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Sample records for brain damage allo-trial

  1. Antenatal allopurinol for reduction of birth asphyxia induced brain damage (ALLO-Trial); a randomized double blind placebo controlled multicenter study

    NARCIS (Netherlands)

    Kaandorp, Joepe J.; Benders, Manon J. N. L.; Rademaker, Carin M. A.; Torrance, Helen L.; Oudijk, Martijn A.; de Haan, Timo R.; Bloemenkamp, Kitty W. M.; Rijken, Monique; van Pampus, Maria G.; Bos, Arie F.; Porath, Martina M.; Oetomo, Sidarto Bambang; Willekes, Christine; Gavilanes, A. W. Danilo; Wouters, Maurice G. A. J.; van Elburg, Ruurd M.; Huisjes, Anjoke J. M.; Bakker, Saskia C. M. J. E. R.; van Meir, Claudia A.; von Lindern, Jeannette; Boon, Janine; de Boer, Inge P.; Rijnders, Robbert J. P.; Jacobs, Corrie J. W. F. M.; Uiterwaal, Cuno S. P. M.; Mol, Ben Willem J.; Visser, Gerard H. A.; van Bel, Frank; Derks, Jan B.

    2010-01-01

    Background: Hypoxic-ischaemic encephalopathy is associated with development of cerebral palsy and cognitive disability later in life and is therefore one of the fundamental problems in perinatal medicine. The xanthine-oxidase inhibitor allopurinol reduces the formation of free radicals, thereby limi

  2. Contextualizing aquired brain damage

    DEFF Research Database (Denmark)

    Nielsen, Charlotte Marie Bisgaard

    Contextualizing aquired brain damage Traditional approaches study ’communicational problems’ often in a discourse of disabledness or deficitness. With an ontology of communcation as something unique and a presupposed uniqueness of each one of us, how could an integrational approach (Integrational...... for people with aquired brain injuries will be presented and comparatively discussed in a traditional versus an integrational perspective. Preliminary results and considerations on ”methods” and ”participation” from this study will be presented along with an overview of the project's empirical data....

  3. Brain Damage in School Age Children.

    Science.gov (United States)

    Haywood, H. Carl, Ed.

    The product of a professional workshop, 10 papers discuss brain damage. An introduction to clinical neuropsychology is presented by H. Carl Haywood. A section on neurological foundations includes papers on the organization of the central nervous system by Jack T. Tapp and Lance L. Simpson, on epilepsy by Angela T. Folsom, and on organic language…

  4. Medical Perspectives on Brain Damage and Development. Revised.

    Science.gov (United States)

    McCrae, Marcia Q.

    The author describes damage and normal development of the brain, as well as assessment and intervention with brain-damaged children. After a brief introduction on the complex and delicate process of brain development and a review of incidence, aspects of etiology such as genetic and postnatal causes are discussed. Brain development is examined…

  5. Feedback and neuroplasticity rehabilitation for brain damage

    Institute of Scientific and Technical Information of China (English)

    Eli Carmeli

    2014-01-01

    Neuroplasticity,also known as brain plasticity,refers to the brain tissue's ability to be repaired to reorganized and to create new connections among the nerve cells.It implies that the location of a given function in the brain (for example,certain area in the motor cortex) can displace to another area of the cortex.This transfer ability can be accomplished by sensory motor feedback training.In the case of cerebral palsy (CP) and stroke,neuroplasticity relates to unaffected nerve cells and new synaptogenesis process taking over the functions of damaged nerve cells and their connections.The aim of this overview is to explain how does neuroplasticity work and how intensive sensory motor feedback training can reorganize nerve cells.Although neurorehabilitation offers a series of therapies from the psychological to occupational,speech,teaching or re-training patients on mobility skills,this overview focuses on physical rehabilitation using a comprehensive feedback system to accelerate brain recovery.

  6. Animal imaging studies of potential brain damage

    Science.gov (United States)

    Gatley, S. J.; Vazquez, M. E.; Rice, O.

    To date, animal studies have not been able to predict the likelihood of problems in human neurological health due to HZE particle exposure during space missions outside the Earth's magnetosphere. In ongoing studies in mice, we have demonstrated that cocaine stimulated locomotor activity is reduced by a moderate dose (120 cGy) of 1 GeV 56Fe particles. We postulate that imaging experiments in animals may provide more sensitive and earlier indicators of damage due to HZE particles than behavioral tests. Since the small size of the mouse brain is not well suited to the spatial resolution offered by microPET, we are now repeating some of our studies in a rat model. We anticipate that this will enable us to identify imaging correlates of behavioral endpoints. A specific hypothesis of our studies is that changes in the metabolic rate for glucose in striatum of animals will be correlated with alterations in locomotor activity. We will also evaluate whether the neuroprotective drug L-deprenyl reduces the effect of radiation on locomotor activity. In addition, we will conduct microPET studies of brain monoamine oxidase A and monoamine oxidase B in rats before and at various times after irradiation with HZE particles. The hypothesis is that monoamine oxidase A, which is located in nerve terminals, will be unchanged or decreased after irradiation, while monoamine oxidase B, which is located in glial cells, will be increased after irradiation. Neurochemical effects that could be measured using PET could in principle be applied in astronauts, in terms of detecting and monitoring subtle neurological damage that might have occurred during long space missions. More speculative uses of PET are in screening candidates for prolonged space missions (for example, for adequate reserve in critical brain circuits) and in optimizing medications to treat impairments after missions.

  7. Alcohol-related brain damage in humans.

    Directory of Open Access Journals (Sweden)

    Amaia M Erdozain

    Full Text Available Chronic excessive alcohol intoxications evoke cumulative damage to tissues and organs. We examined prefrontal cortex (Brodmann's area (BA 9 from 20 human alcoholics and 20 age, gender, and postmortem delay matched control subjects. H & E staining and light microscopy of prefrontal cortex tissue revealed a reduction in the levels of cytoskeleton surrounding the nuclei of cortical and subcortical neurons, and a disruption of subcortical neuron patterning in alcoholic subjects. BA 9 tissue homogenisation and one dimensional polyacrylamide gel electrophoresis (PAGE proteomics of cytosolic proteins identified dramatic reductions in the protein levels of spectrin β II, and α- and β-tubulins in alcoholics, and these were validated and quantitated by Western blotting. We detected a significant increase in α-tubulin acetylation in alcoholics, a non-significant increase in isoaspartate protein damage, but a significant increase in protein isoaspartyl methyltransferase protein levels, the enzyme that triggers isoaspartate damage repair in vivo. There was also a significant reduction in proteasome activity in alcoholics. One dimensional PAGE of membrane-enriched fractions detected a reduction in β-spectrin protein levels, and a significant increase in transmembranous α3 (catalytic subunit of the Na+,K+-ATPase in alcoholic subjects. However, control subjects retained stable oligomeric forms of α-subunit that were diminished in alcoholics. In alcoholics, significant loss of cytosolic α- and β-tubulins were also seen in caudate nucleus, hippocampus and cerebellum, but to different levels, indicative of brain regional susceptibility to alcohol-related damage. Collectively, these protein changes provide a molecular basis for some of the neuronal and behavioural abnormalities attributed to alcoholics.

  8. Zika Virus Can Damage Fetal Brain Late in Pregnancy: Study

    Science.gov (United States)

    ... https://medlineplus.gov/news/fullstory_161451.html Zika Virus Can Damage Fetal Brain Late in Pregnancy: Study ... WEDNESDAY, Oct. 12, 2016 (HealthDay News) -- The Zika virus may harm a baby's brain even if the ...

  9. Brain damage in patients with manifest arterial disease

    NARCIS (Netherlands)

    Raamt, Anne Fleur van

    2006-01-01

    In this thesis we assessed whether the risk factors known to affect markers of brain damage in the general population, also effectuate brain damage in patients who already have symptomatic arterial disease. We found that elevated levels of homocysteine were related to slightly lower global cogniti

  10. Experience-Dependent Neural Plasticity in the Adult Damaged Brain

    Science.gov (United States)

    Kerr, Abigail L.; Cheng, Shao-Ying; Jones, Theresa A.

    2011-01-01

    Behavioral experience is at work modifying the structure and function of the brain throughout the lifespan, but it has a particularly dramatic influence after brain injury. This review summarizes recent findings on the role of experience in reorganizing the adult damaged brain, with a focus on findings from rodent stroke models of chronic upper…

  11. TOOL USE DISORDERS AFTER LEFT BRAIN DAMAGE

    Directory of Open Access Journals (Sweden)

    Josselin eBaumard

    2014-05-01

    Full Text Available In this paper we review studies that investigated tool use disorders in left-brain damaged (LBD patients over the last thirty years. Four tasks are classically used in the field of apraxia: Pantomime of tool use, single tool use, real tool use and mechanical problem solving. Our aim was to address two issues, namely, (1 the role of mechanical knowledge in real tool use and (2 the cognitive mechanisms underlying pantomime of tool use, a task widely employed by clinicians and researchers. To do so, we extracted data from 36 papers and computed the difference between healthy subjects and LBD patients. On the whole, pantomime of tool use is the most difficult task and real tool use is the easiest one. Moreover, associations seem to appear between pantomime of tool use, real tool use and mechanical problem solving. These results suggest that the loss of mechanical knowledge is critical in LBD patients, even if all of those tasks (and particularly pantomime of tool use might put differential demands on semantic memory and working memory.

  12. Experience-dependent neural plasticity in the adult damaged brain

    OpenAIRE

    Kerr, Abigail L.; Cheng, Shao-Ying; Jones, Theresa A.

    2011-01-01

    Behavioral experience is at work modifying the structure and function of the brain throughout the lifespan, but it has a particularly dramatic influence after brain injury. This review summarizes recent findings on the role of experience in reorganizing the adult damaged brain, with a focus on findings from rodent stroke models of chronic upper extremity (hand and arm) impairments. A prolonged and widespread process of repair and reorganization of surviving neural circuits is instigated by in...

  13. Perinatal brain damage : The term infant

    NARCIS (Netherlands)

    Hagberg, Henrik; David Edwards, A.; Groenendaal, Floris

    2016-01-01

    Perinatal brain injury at term is common and often manifests with neonatal encephalopathy including seizures. The most common aetiologies are hypoxic–ischaemic encephalopathy, intracranial haemorrhage and neonatal stroke. Besides clinical and biochemical assessment the diagnostic evaluation rely mos

  14. Brain damage in utero after Chernobyl accident

    International Nuclear Information System (INIS)

    Full text: The report presents research study results of neuropsychiatric consequences of the children exposed in utero, who were born just after the Chernobyl accident (between April 26, 1986 and February 26, 1987). The children were under investigation for three stages: in 1990-1992; 1994-1996; 2002-2004. We use the data on health state, IQ level tests and individual dose reconstruction data. First correlation between prenatal acute exposure after atomic bombing and intellectual level decrease was demonstrated by Japanese scientists. It is known that while the Chernobyl whole body irradiation doses are much lower than the Japanese doses, thyroid doses after the Chernobyl accident are significantly higher. During the first stage the five-year-old prenatally exposed children were under examination. The results showed much more somatic diseases and neurofunctional mental disorders. It was also established in this cohort that starting with the 0.3 Sv threshold dose thyroid-stimulating hormone (TSH) level grown along with fetal thyroid dose increase. Thereupon the radiation-induced malfunction of the thyroid-pituitary system was suggested as an important biological mechanism in the genesis of mental disorders in prenatally irradiated children. The epidemiological WHO project 'Brain Damage in Utero' (IPHECA) was implemented in the second stage. The examination of prenatally exposed children from the contaminated territories (555 kBq/m2 and more) resulted in an increased frequency of moderate mental retardation, emotional and behavioral disorders. Increasing of borderline nervous and psychological disorders of parents from the main group was higher than from the control. However it was rather hard to treat these results because individual dosimetric data were not available. Only in the third stage reconstruction of individual doses of children born to mothers evacuated from the Chernobyl exclusion zone was carried out at taking internal and external exposure. It was

  15. Irreversible brain damage caused by methamphetamine

    Directory of Open Access Journals (Sweden)

    Sebastian Moeller

    2016-03-01

    Full Text Available Methamphetamine is an addictive scene substance usage of which is increasing rapidly. While methamphetamine often causes neuropsychiatric symptoms like anxiety, psychosis and hallucinations, reports of structural ongoing cerebral alterations are rare. We here report a case of this kind of damage caused through methamphetamine use.

  16. Damage and repair of irradiated mammalian brain

    Energy Technology Data Exchange (ETDEWEB)

    Frankel, K.; Lo, E.; Phillips, M.; Fabrikant, J.; Brennan, K.; Valk, P.; Poljak, A.; Delapaz, R.; Woodruff, K. (Lawrence Berkeley Lab., CA (USA); Stanford Univ., CA (USA). Medical Center; Brookside Hospital, San Pablo, CA (USA))

    1989-07-01

    We have demonstrated that focal charged particle irradiation of the rabbit brain can create well-defined lesions which are observable by nuclear magnetic resonance imaging (NMR) and positron emission tomography (PET) imaging techniques. These are similar, in terms of location and characteristic NMR and PET features, to those that occur in the brain of about 10% of clinical research human subjects, who have been treated for intracranial vascular malformations with stereotactic radiosurgery. These lesions have been described radiologically as vasogenic edema of the deep white matter,'' and the injury is of variable intensity and temporal duration, can recede or progress to serious neurologic sequelae, and persist for a considerable period of time, frequently 18 mon to 3 yr. 8 refs., 6 figs.

  17. Damage and repair of irradiated mammalian brain

    International Nuclear Information System (INIS)

    We have demonstrated that focal charged particle irradiation of the rabbit brain can create well-defined lesions which are observable by nuclear magnetic resonance imaging (NMR) and positron emission tomography (PET) imaging techniques. These are similar, in terms of location and characteristic NMR and PET features, to those that occur in the brain of about 10% of clinical research human subjects, who have been treated for intracranial vascular malformations with stereotactic radiosurgery. These lesions have been described radiologically as ''vasogenic edema of the deep white matter,'' and the injury is of variable intensity and temporal duration, can recede or progress to serious neurologic sequelae, and persist for a considerable period of time, frequently 18 mon to 3 yr. 8 refs., 6 figs

  18. Rehabilitation of damage to the visual brain

    OpenAIRE

    Ajina, S; Kennard, C

    2012-01-01

    Homonymous visual field loss is a common consequence of stroke and traumatic brain injury. It is associated with an adverse functional prognosis and has implications on day-to-day activities such as driving, reading, and safe navigation. Early recovery is expected in around half of cases, and may be associated with a return in V1 activity. In stable disease, recovery is unlikely beyond three and certainly six months. Rehabilitative approaches generally target three main areas, encompassing a ...

  19. Methadone-Induced Toxic Brain Damage

    OpenAIRE

    Jérôme Corré; Jérôme Pillot; Gilles Hilbert

    2013-01-01

    A 29-year-old man presented with comatose after methadone intoxication. Cerebral tomography only showed cortico-subcortical hypodense signal in the right cerebellar hemisphere. Brain MRI showed a rare imaging of FLAIR and DWI hyperintensities in the two cerebellar hemispheres as well as basal ganglia (globi pallidi), compatible with methadone overdose. To our knowledge this is the first reported case of both cerebellar and basal ganglia involvement in methadone overdose.

  20. Acquired agraphia caused by focal brain damage.

    Science.gov (United States)

    Anderson, S W; Saver, J; Tranel, D; Damasio, H

    1993-03-01

    Motor and linguistic aspects of writing were evaluated in 31 subjects with focal damage in 1 of 3 regions of the left hemisphere: (1) dorsolateral frontal lobe sparing primary motor cortex (group FL), (2) parietal lobe (group PL), or (3) temporal lobe (group TL). A standard procedure was used to evaluate writing for grapheme formation, spatial arrangement, spelling, word selection, grammar, and perseveration. It was predicted that agraphia would be observed in all 3 groups, and that the most severe impairments would be associated with frontal lobe damage, particularly in aspects of writing dependent on sequencing (grapheme formation, spelling, and grammar). It was found that agraphia was common in all groups, particularly in the acute epoch, and that all groups showed considerable recovery of writing by the chronic epoch. Few differences were found between groups. However, the FL group was impaired on spelling and grammar relative to the PL group in the acute epoch and impaired on grammar relative to the TL group in the chronic epoch. The findings are consistent with the notion that writing relies on a distributed neuroanatomical network, which acts in concert to link fragments of visuomotor activity with component linguistic elements.

  1. Neurocomputational models of the remote effects of focal brain damage.

    Science.gov (United States)

    Reggia, James A

    2004-11-01

    Sudden localized brain damage, such as occurs in stroke, produces neurological deficits directly attributable to the damaged site. In addition, other clinical deficits occur due to secondary "remote" effects that functionally impair the remaining intact brain regions (e.g., due to their sudden disconnection from the damaged area), a phenomenon known as diaschisis. The underlying mechanisms of these remote effects, particularly those involving interactions between the left and right cerebral hemispheres, have proven somewhat difficult to understand in the context of current theories of hemispheric specialization. This article describes some recent neurocomputational models done in the author's research group that try to explain diaschisis qualitatively. These studies show that both specialization and diaschisis can be accounted for with a single model of hemispheric interactions. Further, the results suggest that left-right subcortical influences may be much more important in influencing hemispheric specialization than is generally recognized. PMID:15564108

  2. [Neuroendocrine dysfunction and brain damage. A consensus statement].

    Science.gov (United States)

    Leal-Cerro, Alfonso; Rincón, María Dolores; Domingo, Manel Puig

    2009-01-01

    This consensus statement aims to enhance awareness of the incidence and risks of hypopituitarism in patients with traumatic brain injury (TBI) and/or brain hemorrhages among physicians treating patients with brain damage. The importance of this problem is related not only to the frequency of TBI but also to its prevalence in younger populations. The consequences of TBI are characterized by a series of symptoms that depend on the type of sequels related to neuroendocrine dysfunction. The signs and symptoms of hypopituitarism are often confused with those of other sequels of TBI. Consequently, patients with posttraumatic hypopituitarism may receive suboptimal rehabilitation unless the underlying hormone deficiency is identified and treated. This consensus is based on the recommendation supported by expert opinion that patients with a TBI and/or brain hemorrhage should undergo endocrine evaluation in order to assess pituitary function and, if deficiency is detected, should receive hormone replacement therapy.

  3. Hyperschematia after right brain damage: a meaningful entity?

    Directory of Open Access Journals (Sweden)

    Gilles eRode

    2014-01-01

    Full Text Available In recent years we reported three right-brain-damaged patients, who exhibited a left-sided disprortionate expansion of drawings, both by copying and from memory, contralateral to the side of the hemispheric lesion (Neurology, 67: 1801, 2006, Neurocase 14: 369, 2008. We proposed the term hyperschematia for such an expansion, with reference to an interpretation in terms of a lateral leftward distortion of the representation of extra-personal space, with a leftward anisometric expansion (relaxation of the spatial medium. The symptom-complex shown by right-brain-damaged patients with hyperschematia includes: 1 a disproportionate leftward expansion of drawings (with possible addition of details, by copy and from memory (also in clay modeling, in one patient; 2 an overestimation of left lateral extent, when a leftward movement is required, associated with a perceptual underestimation; 4 unawareness of the disorder; 5 no unilateral spatial neglect. In most right-brain-damaged patients, left hyperschematia involves extra-personal space. In one patient the deficit was confined to a body part (left half-face: personal hyperschematia. The neural underpinnings of the disorder include damage to the fronto-temporo-parietal cortices, and subcortical structures in the right cerebral hemisphere, in the vascular territory of the middle cerebral artery. Here, four novel additional patients are reported. Finally, hypeschematia is reconsidered, in its clinical components, the underlying pathological mechanisms, as well as its neural underpinnings.

  4. Patterns of damage in the mature neonatal brain

    Energy Technology Data Exchange (ETDEWEB)

    Triulzi, Fabio; Parazzini, Cecilia; Righini, Andrea [Children' s Hospital ' ' Vittore Buzzi' ' , Departments of Radiology and Neuroradiology, Milan (Italy)

    2006-07-15

    Patterns of damage in the mature neonatal brain can be subdivided into focal, multifocal and diffuse. The main cause of diffuse brain damage in the term newborn is hypoxic-ischaemic encephalopathy (HIE). HIE is still the major recognized perinatal cause of neurological morbidity in full-term newborns. MRI offers today the highest sensitivity in detecting acute anoxic injury of the neonatal brain. Conventional acquisition techniques together with modern diffusion techniques can identify typical patterns of HIE injury, even in the early course of the disease. However, even though highly suggestive, these patterns cannot be considered as pathognomonic. Perinatal metabolic disease such as kernicterus and severe hypoglycaemia should be differentiated from classic HIE. Other conditions, such as infections, non-accidental injury and rarer metabolic diseases can be misinterpreted as HIE in their early course when diffuse brain swelling is still the predominant MRI feature. Diffusion techniques can help to differentiate different types of diffuse brain oedema. Typical examples of focal injuries are arterial or venous infarctions. In arterial infarction, diffusion techniques can define more precisely than conventional imaging the extent of focal infarction, even in the hyperacute phase. Moreover, diffusion techniques provide quantitative data of acute corticospinal tract injury, especially at the level of the cerebral peduncles. Venous infarction should be suspected in every case of unexplained cerebral haematoma in the full-term newborn. In the presence of spontaneous bleeding, venous structures should always be evaluated by MR angiography. (orig.)

  5. Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

    Directory of Open Access Journals (Sweden)

    Ralph Timaru-Kast

    Full Text Available After traumatic brain injury (TBI elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months and old (21 months male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2% compared to young (0%. This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral

  6. Epileptic Encephalopathy in Children with Risk Factors for Brain Damage

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    Josefina Ricardo-Garcell

    2012-01-01

    Full Text Available In the study of 887 new born infants with prenatal and perinatal risk factors for brain damage, 11 children with West syndrome that progressed into Lennox-Gastaut syndrome and another 4 children with Lennox-Gastaut syndrome that had not been preceded by West syndrome were found. In this study we present the main findings of these 15 subjects. In all infants multifactor antecedents were detected. The most frequent risk factors were prematurity and severe asphyxia; however placenta disorders, sepsis, and hyperbilirubinemia were also frequent. In all infants MRI direct or secondary features of periventricular leukomalacia were observed. Followup of all infants showed moderate to severe neurodevelopmental delay as well as cerebral palsy. It is concluded that prenatal and perinatal risk factors for brain damage are very important antecedents that should be taken into account to follow up those infants from an early age in order to detect and treat as early as possible an epileptic encephalopathy.

  7. Epileptic Encephalopathy in Children with Risk Factors for Brain Damage

    Science.gov (United States)

    Ricardo-Garcell, Josefina; Harmony, Thalía; Porras-Kattz, Eneida; Colmenero-Batallán, Miguel J.; Barrera-Reséndiz, Jesús E.; Fernández-Bouzas, Antonio; Cruz-Rivero, Erika

    2012-01-01

    In the study of 887 new born infants with prenatal and perinatal risk factors for brain damage, 11 children with West syndrome that progressed into Lennox-Gastaut syndrome and another 4 children with Lennox-Gastaut syndrome that had not been preceded by West syndrome were found. In this study we present the main findings of these 15 subjects. In all infants multifactor antecedents were detected. The most frequent risk factors were prematurity and severe asphyxia; however placenta disorders, sepsis, and hyperbilirubinemia were also frequent. In all infants MRI direct or secondary features of periventricular leukomalacia were observed. Followup of all infants showed moderate to severe neurodevelopmental delay as well as cerebral palsy. It is concluded that prenatal and perinatal risk factors for brain damage are very important antecedents that should be taken into account to follow up those infants from an early age in order to detect and treat as early as possible an epileptic encephalopathy. PMID:22957240

  8. Resveratrol Protects the Brain of Obese Mice from Oxidative Damage

    Directory of Open Access Journals (Sweden)

    Shraddha D. Rege

    2013-01-01

    Full Text Available Resveratrol (3,5,4′-trihydroxy-trans-stilbene is a polyphenolic phytoalexin that exerts cardioprotective, neuroprotective, and antioxidant effects. Recently it has been shown that obesity is associated with an increase in cerebral oxidative stress levels, which may enhance neurodegeneration. The present study evaluates the neuroprotective action of resveratrol in brain of obese (ob/ob mice. Resveratrol was administered orally at the dose of 25 mg kg−1 body weight daily for three weeks to lean and obese mice. Resveratrol had no effect on body weight or blood glucose levels in obese mice. Lipid peroxides were significantly increased in brain of obese mice. The enzymatic antioxidants superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and nonenzymatic antioxidants tocopherol, ascorbic acid, and glutathione were decreased in obese mice brain. Administration of resveratrol decreased lipid peroxide levels and upregulated the antioxidant activities in obese mice brain. Our findings indicate a neuroprotective effect of resveratrol by preventing oxidative damage in brain tissue of obese mice.

  9. Late damage to brain microvasculature after chronic irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Lyubimova, N. [Institute of Theoretical and Experimental Biophysics, Russian Academy of Science, Moscow (Russian Federation)

    1997-03-01

    The effects on mouse brain microvasculature were examined 12 months after exposure to chronic {gamma}- irradiation at 3 cGy/day for three months. Animals were injected i.p. with 100 mg/kg iproniazid, an inhibitor of mono-amine-oxidase. Six hours later and 15 min before animal sacrifice, 100 mg/kg L-DOPA was also injected. This procedure resulted in the accumulation of catecholamines (CA) in the endothelial cells, a process which otherwise would be prevented by mono-amine-oxidase activity. Animals were killed by decapitation under nembutal anesthesia at various times post irradiation. Dissected pieces of brain were immediately frozen in liquid nitrogen and lyophilized at -20 deg C under vacuum to avoid CA diffusion from the endothelial cell. The reaction between CA and paraformaldehyde gas at 70 % humidity and 80 deg C was used to generate fluorophores which act as endothelial cell markers. Histological specimens were embedded in paraffin was under vacuum and serial section cut. These were assessed under fluorescent microscopy. These studies indicate that in some ways repair of chronic radiation damage may be less complete than repair of damage caused by a single acute exposure. The dystrophic changes seen in the endothelium also suggest the possibility that chronic exposure may be more likely to lead to late functional impairment of brain microcirculation. (author)

  10. Imaging study of brain damage from methanol intoxication of wine

    International Nuclear Information System (INIS)

    Objective: To investigate the imaging of CT and MRI in brain damage caused by methanol intoxication from false wine, and to study the relations between imaging manifestation and different degrees of the methanol intoxication. Method: Thirty nine cases with methanol intoxication from false wine were retrospectively reported, The latent period of these patients was 0-4 days, and the average latent period of these patients was 0.5 days, All cases were performed by serology examination, brain CT scan, and four cases performed by MRI scan after average 2.5 days (range, 1-6 days) the onset of methanol intoxication. Results: Six cases showed hyperintense signals in bilateral putamen, two cases also showed hyperintense signals in biolateral subcortex white substance regions. Four cases showed hyperintense signals in unilateral internal capsule. One case showed hyperintense changess in subcortex white substance regions. Our study showed the positive correlation between CT features and the amount of methanol and stage of clinic manifestation(χ2=4.232, P2=0.001, P>0.05). Conclusions: MRI was better than CT in finding early brain damage caused by methanol intoxication from false wine. The characteristic finding changes of the patients was showed mainly in in bilateral putamen, Prognosis for the patients combined with subcortex white substance lesion wasn't hopeful. (authors)

  11. Brain microvascular endothelial cell transplantation ameliorates ischemic white matter damage.

    Science.gov (United States)

    Puentes, Sandra; Kurachi, Masashi; Shibasaki, Koji; Naruse, Masae; Yoshimoto, Yuhei; Mikuni, Masahiko; Imai, Hideaki; Ishizaki, Yasuki

    2012-08-21

    Ischemic insults affecting the internal capsule result in sensory-motor disabilities which adversely affect the patient's life. Cerebral endothelial cells have been reported to exert a protective effect against brain damage, so the transplantation of healthy endothelial cells might have a beneficial effect on the outcome of ischemic brain damage. In this study, endothelin-1 (ET-1) was injected into the rat internal capsule to induce lacunar infarction. Seven days after ET-1 injection, microvascular endothelial cells (MVECs) were transplanted into the internal capsule. Meningeal cells or 0.2% bovine serum albumin-Hank's balanced salt solution were injected as controls. Two weeks later, the footprint test and histochemical analysis were performed. We found that MVEC transplantation improved the behavioral outcome based on recovery of hind-limb rotation angle (P<0.01) and induced remyelination (P<0.01) compared with the control groups. Also the inflammatory response was repressed by MVEC transplantation, judging from fewer ED-1-positive activated microglial cells in the MVEC-transplanted group than in the other groups. Elucidation of the mechanisms by which MVECs ameliorate ischemic damage of the white matter may provide important information for the development of effective therapies for white matter ischemia. PMID:22771710

  12. Effects ofAstragalus Membranaceus on Ischemia Brain Damage

    Institute of Scientific and Technical Information of China (English)

    Yumin Luo; Zhen Qin

    2000-01-01

    We observed the protective effects of Astragalus Membranaceus on cerebral ischemia. Method: 1. We used intravascular thread rat models with 72hs reperfusion of lh tMCAO for our studies. Astragalus Membranaceus was administrated intraperitoneally in different interval. The rats were sacrificed 72 hours after l h tMCAO. 2. Cerebral infarction volume was determined by TTC staining and image analysis. 3. DTNB method and TBA method were applied to measure the activity of GSH-px and the concentration of MDA respectively. 4. The blood brain barrier damage was evaluated by the area of Evans Blue extravasation. Results:l.The whole brain volume of protective group is larger than its control, but the average infarction volume is significantly less than that of control, and the percentage of average infarction volume to the whole brain is obviously decreased. 2. We found mildly enhanced GSH-px activity and markedly decreased MDA concentration in the protective group compared with its control. But there are no significant changes of GSH-px activity and MDA concentration in the therapy group compared with its control. 3. The area of Evans Blue staining in the protective group is significantly less than that of its control. Conclusion:l.Astragalus Membranaceus can decrease the infarction volume. 2.Astragalus Membranaceus may reduce MDA concentration after cerebral ischemia. 3.Astragalus Membranaceus can protect blood brain barrier.

  13. Ancillary procedure for early diagnosis of brain damage in children

    International Nuclear Information System (INIS)

    CT scan of the head was performed on 14 patients with cerebral palsy, 16 with central coordination disorders, and 16 controls, and findings showing cerebral atrophy and enlargement of the cerebral ventricle were obtained in cases both of cerebral palsy and of central coordination disorders. To objectify these findings, 10 items were selected and evaluated according to 4 grades (0 - 3) and were compared. As a result, it was concluded that CT scan is an excellent ancillary procedure for early diagnosis of brain damages. (Tsunoda, M.)

  14. Dexamethasone alleviates tumor-associated brain damage and angiogenesis.

    Directory of Open Access Journals (Sweden)

    Zheng Fan

    Full Text Available Children and adults with the most aggressive form of brain cancer, malignant gliomas or glioblastoma, often develop cerebral edema as a life-threatening complication. This complication is routinely treated with dexamethasone (DEXA, a steroidal anti-inflammatory drug with pleiotropic action profile. Here we show that dexamethasone reduces murine and rodent glioma tumor growth in a concentration-dependent manner. Low concentrations of DEXA are already capable of inhibiting glioma cell proliferation and at higher levels induce cell death. Further, the expression of the glutamate antiporter xCT (system Xc-; SLC7a11 and VEGFA is up-regulated after DEXA treatment indicating early cellular stress responses. However, in human gliomas DEXA exerts differential cytotoxic effects, with some human glioma cells (U251, T98G resistant to DEXA, a finding corroborated by clinical data of dexamethasone non-responders. Moreover, DEXA-resistant gliomas did not show any xCT alterations, indicating that these gene expressions are associated with DEXA-induced cellular stress. Hence, siRNA-mediated xCT knockdown in glioma cells increased the susceptibility to DEXA. Interestingly, cell viability of primary human astrocytes and primary rodent neurons is not affected by DEXA. We further tested the pharmacological effects of DEXA on brain tissue and showed that DEXA reduces tumor-induced disturbances of the microenvironment such as neuronal cell death and tumor-induced angiogenesis. In conclusion, we demonstrate that DEXA inhibits glioma cell growth in a concentration and species-dependent manner. Further, DEXA executes neuroprotective effects in brains and reduces tumor-induced angiogenesis. Thus, our investigations reveal that DEXA acts pleiotropically and impacts tumor growth, tumor vasculature and tumor-associated brain damage.

  15. MRI findings of brain damage due to neonatal hypoglycemia

    International Nuclear Information System (INIS)

    Objective: To report the MRI findings of brain damage observed in neonatal patients who suffered from isolated hypoglycemia and to explore the value of diffusion-weighted imaging(DWI) in early detection of neonatal hypoglycemic brain injury. Methods: Twelve neonates with isolated hypoglycemia (10 of the 12 were diagnosed to suffer from hypoglycemic encephalopathy) were enrolled in this study. They were first scanned at age from 3 days to 10 days with T1WI, T2WI and DWI(b is 0 s/mm2, 1000 s/mm2), and 4 of them were then scanned from 7 days to 10 days following the initial scan. All acquired MR images were retrospectively analysed. Results: First series of DWI images showed distinct hyperintense signal in 11 cases in several areas including bilateral occipital cortex (2 cases), right occipital cortex (1 case), left occipital cortex and subcortical white matter(1 case), bilateral occipital cortex and subcortical white matter (2 cases), bilateral parieto-occipital cortex (2 cases), bilateral parieto-occipital cortex and subcortical white matter(2 cases), the splenium of corpus callosum (4 cases), bilateral corona radiata( 2 cases), left caudate nucleus and globus pallidus (1 case), bilateral thalamus (1 case), bilaterally posterior limb of internal capsule (1 case). In the initial T1WI and T2WI images, there were subtle hypointensity in the damaged cortical areas (3 cases), hyperintensity in the bilaterally affected occipital cortex( 1 case) on T1 weighted images, and hyperintensity in the affected cortex and subcortical white matter with poor differentiation on T2 weighted images. The followed-up MRI of 4 cases showed regional encephalomalacia in the affected occipital lobes(4 cases), slightly hyperintensity on T2 weighted images in the damaged occipital cortex (2 cases), extensive demyelination (1 case), disappearance of hyperintensity of the splenium of corpus callosum (1 case), and persistent hyperintensity in the splenium of corpus callosum (1 case) on T2 weighted

  16. AMBIENT PARTICULATE MATTER STIMULATES OXIDATIVE STRESS IN BRAIN MICROGLIA AND DAMAGES NEURONS IN CULTURE.

    Science.gov (United States)

    Ambient particulate matter (PM) damages biological targets through oxidative stress (OS) pathways. Several reports indicate that the brain is one of those targets. Since microglia (brain macrophage) are critical to OS-mediated neurodegeneration, their response to concentrated amb...

  17. Mapping neuroplastic potential in brain-damaged patients.

    Science.gov (United States)

    Herbet, Guillaume; Maheu, Maxime; Costi, Emanuele; Lafargue, Gilles; Duffau, Hugues

    2016-03-01

    It is increasingly acknowledged that the brain is highly plastic. However, the anatomic factors governing the potential for neuroplasticity have hardly been investigated. To bridge this knowledge gap, we generated a probabilistic atlas of functional plasticity derived from both anatomic magnetic resonance imaging results and intraoperative mapping data on 231 patients having undergone surgery for diffuse, low-grade glioma. The atlas includes detailed level of confidence information and is supplemented with a series of comprehensive, connectivity-based cluster analyses. Our results show that cortical plasticity is generally high in the cortex (except in primary unimodal areas and in a small set of neural hubs) and rather low in connective tracts (especially associative and projection tracts). The atlas sheds new light on the topological organization of critical neural systems and may also be useful in predicting the likelihood of recovery (as a function of lesion topology) in various neuropathological conditions-a crucial factor in improving the care of brain-damaged patients. PMID:26912646

  18. Sex Differences in the Effects of Unilateral Brain Damage on Intelligence

    Science.gov (United States)

    Inglis, James; Lawson, J. S.

    1981-05-01

    A sexual dimorphism in the functional asymmetry of the damaged human brain is reflected in a test-specific laterality effect in male but not in female patients. This sex difference explains some contradictions concerning the effects of unilateral brain damage on intelligence in studies in which the influence of sex was overlooked.

  19. Environmental enrichment promotes neural remodeling in newborn rats with hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Chuanjun Liu; Yankui Guo; Yalu Li; Zhenying Yang

    2011-01-01

    We evaluated the effect of hypoxic-ischemic brain damage and treatment with early environmental enrichment intervention on development of newborn rats, as evaluated by light and electron microscopy and morphometry. Early intervention with environmental enrichment intelligence training attenuated brain edema and neuronal injury, promoted neuronal repair, and increased neuronal plasticity in the frontal lobe cortex of the newborn rats with hypoxic-ischemic brain damage.

  20. Zika Brain Damage May Occur in Babies with Normal-Sized Heads

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_159621.html Zika Brain Damage May Occur in Babies With Normal- ... 2016 (HealthDay News) -- In the ongoing crisis around Zika-linked birth defects, attention has been largely focused ...

  1. Brain damages in ketamine addicts as revealed by magnetic resonance imaging

    OpenAIRE

    Wang, Chunmei; Zheng, Dong; Xu, Jie; Lam, Waiping; Yew, D. T.

    2013-01-01

    Ketamine, a known antagonist of N-methyl-D-aspartic (NMDA) glutamate receptors, had been used as an anesthetic particularly for pediatric or for cardiac patients. Unfortunately, ketamine has become an abusive drug in many parts of the world while chronic and prolonged usage led to damages of many organs including the brain. However, no studies on possible damages in the brains induced by chronic ketamine abuse have been documented in the human via neuroimaging. This paper described for the fi...

  2. Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

    NARCIS (Netherlands)

    D.C. Engel (Doortje Caroline)

    2008-01-01

    textabstractTraumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and se

  3. White Matter Damage and Cognitive Impairment after Traumatic Brain Injury

    Science.gov (United States)

    Kinnunen, Kirsi Maria; Greenwood, Richard; Powell, Jane Hilary; Leech, Robert; Hawkins, Peter Charlie; Bonnelle, Valerie; Patel, Maneesh Chandrakant; Counsell, Serena Jane; Sharp, David James

    2011-01-01

    White matter disruption is an important determinant of cognitive impairment after brain injury, but conventional neuroimaging underestimates its extent. In contrast, diffusion tensor imaging provides a validated and sensitive way of identifying the impact of axonal injury. The relationship between cognitive impairment after traumatic brain injury…

  4. 45. Damage effects of sulfur dioxide inhalation on DNA of brain cells from mice

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    The damage effects of sulfur dioxide (SO2) inhalation on DNA of brain cells from mice were studied with the single cell microgel electrophoresis tecknique (Comet test). The results show that SO2 inhalation caused the damage effects to DNA of the mouse brain cells in a dose-dependent manner. The results indicate that even under SO2 inhalation at low concentrations as 7 mg SO2/m3, The brain cells with DNA damaged also reached to 98.8%, it implies the brain cells of mammalian animals are very sensitive to SO2 inhalation. The results also indicate that DNA damage of the brain cells from male mice is more serious than that from female mice, that remains to be further studied. These results led us to conclusion SO2 pollution even at low concentrations also has a potential risk to damage genetic material DNA of brain cells from mammalian animals. It might be explained by our conclusion that the recently published epidemiological studies of workers exposed to SO2 or it's derivatives (bi)sulfite) found increased mortality for brain cancer.

  5. Unilateral Brain Damage Effects on Processing Homonymous and Polysemous Words

    Science.gov (United States)

    Klepousniotou, E.; Baum, S.R.

    2005-01-01

    Using an auditory semantic priming paradigm, the present study investigated the abilities of left-hemisphere-damaged (LHD) non-fluent aphasic, right-hemisphere-damaged (RHD) and normal control individuals to access, out of context, the multiple meanings of three types of ambiguous words, namely homonyms (e.g., ''punch''), metonymies (e.g.,…

  6. The immune system mediates blood-brain barrier damage; Possible implications for pathophysiology of neuropsychiatric illnesses

    NARCIS (Netherlands)

    VanderWerf, YD; DeJongste, MJL; terHorst, GJ

    1995-01-01

    The immune system mediates blood-brain barrier damage; possible implications for pathophysiology of neuropsychiatric illnesses. In this investigation the effects of immune activation on the brain are characterized In order to study this, we used a model for chronic immune activation, the myocardial

  7. Expression Profile of DNA Damage Signaling Genes in Proton Exposed Mouse Brain

    Science.gov (United States)

    Ramesh, Govindarajan; Wu, Honglu

    Exposure of living systems to radiation results in a wide assortment of lesions, the most signif-icant of is damage to genomic DNA which induce several cellular functions such as cell cycle arrest, repair, apoptosis etc. The radiation induced DNA damage investigation is one of the im-portant area in biology, but still the information available regarding the effects of proton is very limited. In this report, we investigated the differential gene expression pattern of DNA damage signaling genes particularly, damaged DNA binding, repair, cell cycle arrest, checkpoints and apoptosis using quantitative real-time RT-PCR array in proton exposed mouse brain tissues. The expression profiles showed significant changes in DNA damage related genes in 2Gy proton exposed mouse brain tissues as compared with control brain tissues. Furthermore, we also show that significantly increased levels of apoptotic related genes, caspase-3 and 8 activities in these cells, suggesting that in addition to differential expression of DNA damage genes, the alteration of apoptosis related genes may also contribute to the radiation induced DNA damage followed by programmed cell death. In summary, our findings suggest that proton exposed brain tissue undergo severe DNA damage which in turn destabilize the chromatin stability.

  8. Matching Top–Bottom Parts of Facial Expressions by Brain-Damaged Patients

    OpenAIRE

    Hari S. Asthana; Manas K. Mandal; Tandon, Shiv C.; Sanjay Asthana

    1991-01-01

    Patients with focal brain-damage, right/left hemisphere-damage (RHD/LHD) and anterior/posterior region-damage (ARD/PRD), and normal controls (NC) were asked to match photographs of top–bottom facial parts expressing different emotions, positive (happy, surprise), negative–aroused (fear, anger), negative–nonaroused (sad, disgust). The LHD patients performed significantly worse than the RHD patients, and the ARD patients were significantly worse than the PRD patients, in the perceptual-matching...

  9. Clinical peculiarities of the brain damage in the liquidators of the Chernobyl accident

    International Nuclear Information System (INIS)

    Investigation into the features of the brain damage by the liquidators of the Chernobyl accident has become an urgent issue of today due to a number of circumstances. According to the classical concept dominating radiobiology until recently, the brain being composed of highly - differentiated nerve cells, present a radioresistant structure responsive to radiation injury induced by high and very high radiation doses (10000 rem and higher) only. The results of clinical examinations given to the Chernobyl accident recovery workers at Kiev Institute of Neurosurgery, Academy of Medical Sciences of Ukraine, show that even the so - called ''small - dose'' radiation, when consumed continuously, produces neurological sings of brain damage. 6 figs

  10. Alcohol Alert: Alcohol's Damaging Effects on the Brain

    Science.gov (United States)

    ... R.; et al. Gender differences in moderate drinking effects. Alcohol Research & Health 23:55–64, 1999. (5) Loft, S. ; ... A.; and Sullivan, E. Sex differences in the effects of alcohol on brain structure. American Journal of Psychiatry 158: ...

  11. Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

    OpenAIRE

    Engel, Doortje Caroline

    2008-01-01

    textabstractTraumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and several rare causes e.g. the use of nail guns or lawn mowers have all been described as causes of TBI. The pathology of TBI can be classified by mechanism (closed versus penetrating); clinical severi...

  12. Contralateral and ipsilateral disorders of visual attention in patients with unilateral brain damage.

    Science.gov (United States)

    Gainotti, G; Giustolisi, L; Nocentini, U

    1990-05-01

    To explain the prevalence of unilateral spatial neglect in patients with right brain damage, Heilman et al have suggested that the attentional neurons of the right parietal lobe might have bilateral receptive fields, whereas the homologous cells of the left hemisphere would have strictly contralateral receptive fields. One implication of this theory is that patients with right brain damage should show a prevalence of disorders of visual attention not only in the half space contralateral to the damaged hemisphere, but also in the ipsilateral one. To check this theory, 50 control subjects, 102 right and 125 left brain-damaged patients were given a drawing completion task in which patients were requested to complete the missing parts of a star, a cube and a house. Omissions of lines lying on the sides of the models contralateral and ipsilateral to the damaged hemisphere were taken separately into account. Results did not confirm the hypothesis, since right brain-damaged patients failed to complete the contralateral sides of the models much more frequently than patients with left brain injury, but no difference was found between the two hemispheric groups when ipsilateral disorders of visual attention were taken into account. Furthermore, no correlation was found between omissions of lines lying on the sides of the models contralateral and ipsilateral to the damaged hemisphere. This finding suggests that contralateral and ipsilateral disorders of visual attention are not due to the same mechanism in right brain-damaged patients. The alternative hypothesis viewing ipsilateral disorders as resulting from a widespread lowering of general attention (and only contralateral neglect reflecting a specific disorder of visual attention) was supported by results obtained on a verbal memory test, used to evaluate the general cognitive and attention level of the patients. Patients with clear-cut ipislateral inattention obtained very low scores on this test, whereas patients with

  13. "Neuropeptides in the brain defense against distant organ damage".

    Science.gov (United States)

    Hamasaki, Mike Yoshio; Barbeiro, Hermes Vieira; Barbeiro, Denise Frediani; Cunha, Débora Maria Gomes; Koike, Marcia Kiyomi; Machado, Marcel Cerqueira César; Pinheiro da Silva, Fabiano

    2016-01-15

    Delirium, or acute confusional state, is a common manifestation in diseases that originate outside the central nervous system, affecting 30-40% of elderly hospitalized patients and up to 80% of the critically ill, even though it remains unclear if severe systemic inflammation is able or not to induce cellular disturbances and immune activation in the brain. Neuropeptides are pleotropic molecules heterogeneously distributed throughout the brain and possess a wide spectrum of functions, including regulation of the inflammatory response, so we hypothesized that they would be the major alarm system in the brain before overt microglia activation. In order to investigate this hypothesis, we induced acute pancreatitis in 8-10week old rats and collected brain tissue, 12 and 24h following pancreatic injury, to measure neuropeptide and cytokine tissue levels. We found significantly higher levels of β-endorphin, orexin and oxytocin in the brain of rats submitted to pancreatic injury, when compared to healthy controls. Interestingly, these differences were not associated with increased local cytokine levels, putting in evidence that neuropeptide release occurred independently of microglia activation and may be a pivotal alarm system to initiate neurologic reactions to distant inflammatory non-infectious aggression.

  14. Visceral adipose tissue inflammation is associated with age-related brain changes and ischemic brain damage in aged mice.

    Science.gov (United States)

    Shin, Jin A; Jeong, Sae Im; Kim, Minsuk; Yoon, Joo Chun; Kim, Hee-Sun; Park, Eun-Mi

    2015-11-01

    Visceral adipose tissue is accumulated with aging. An increase in visceral fat accompanied by low-grade inflammation is associated with several adult-onset diseases. However, the effects of visceral adipose tissue inflammation on the normal and ischemic brains of aged are not clearly defined. To examine the role of visceral adipose tissue inflammation, we evaluated inflammatory cytokines in the serum, visceral adipose tissue, and brain as well as blood-brain barrier (BBB) permeability in aged male mice (20 months) underwent sham or visceral fat removal surgery compared with the young mice (2.5 months). Additionally, ischemic brain injury was compared in young and aged mice with sham and visceral fat removal surgery. Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in examined organs were increased in aged mice compared with the young mice, and these levels were reduced in the mice with visceral fat removal. Increased BBB permeability with reduced expression of tight junction proteins in aged sham mice were also decreased in mice with visceral fat removal. After focal ischemic injury, aged mice with visceral fat removal showed a reduction in infarct volumes, BBB permeability, and levels of proinflammatory cytokines in the ischemic brain compared with sham mice, although the neurological outcomes were not significantly improved. In addition, further upregulated visceral adipose tissue inflammation in response to ischemic brain injury was attenuated in mice with visceral fat removal. These results suggest that visceral adipose tissue inflammation is associated with age-related changes in the brain and contributes to the ischemic brain damage in the aged mice. We suggest that visceral adiposity should be considered as a factor affecting brain health and ischemic brain damage in the aged population. PMID:26184082

  15. Visceral adipose tissue inflammation is associated with age-related brain changes and ischemic brain damage in aged mice.

    Science.gov (United States)

    Shin, Jin A; Jeong, Sae Im; Kim, Minsuk; Yoon, Joo Chun; Kim, Hee-Sun; Park, Eun-Mi

    2015-11-01

    Visceral adipose tissue is accumulated with aging. An increase in visceral fat accompanied by low-grade inflammation is associated with several adult-onset diseases. However, the effects of visceral adipose tissue inflammation on the normal and ischemic brains of aged are not clearly defined. To examine the role of visceral adipose tissue inflammation, we evaluated inflammatory cytokines in the serum, visceral adipose tissue, and brain as well as blood-brain barrier (BBB) permeability in aged male mice (20 months) underwent sham or visceral fat removal surgery compared with the young mice (2.5 months). Additionally, ischemic brain injury was compared in young and aged mice with sham and visceral fat removal surgery. Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in examined organs were increased in aged mice compared with the young mice, and these levels were reduced in the mice with visceral fat removal. Increased BBB permeability with reduced expression of tight junction proteins in aged sham mice were also decreased in mice with visceral fat removal. After focal ischemic injury, aged mice with visceral fat removal showed a reduction in infarct volumes, BBB permeability, and levels of proinflammatory cytokines in the ischemic brain compared with sham mice, although the neurological outcomes were not significantly improved. In addition, further upregulated visceral adipose tissue inflammation in response to ischemic brain injury was attenuated in mice with visceral fat removal. These results suggest that visceral adipose tissue inflammation is associated with age-related changes in the brain and contributes to the ischemic brain damage in the aged mice. We suggest that visceral adiposity should be considered as a factor affecting brain health and ischemic brain damage in the aged population.

  16. Prostacyclin infusion may prevent secondary damage in pericontusional brain tissue

    DEFF Research Database (Denmark)

    Reinstrup, Peter; Nordström, Carl-Henrik

    2011-01-01

    Prostacyclin is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation, and has been suggested as therapy for cerebral ischemia. A case of focal traumatic brain lesion that was monitored using intracerebral microdialysis, and bedside analysis and display is reported here........ When biochemical signs of cerebral ischemia progressed, i.v. infusion of prostacyclin was started....

  17. Zingiber officinale Mitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

    Directory of Open Access Journals (Sweden)

    Jintanaporn Wattanathorn

    2011-01-01

    Full Text Available Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect of Zingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO. Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA, superoxide dismutase (SOD, catalase (CAT, and glutathione peroxidase (GSH-Px in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

  18. RXPERIMENTAL AND CLINICAL STUDY OF CREATINE KINASE BB ACTIVITY FOR TH E DIAGNOSIS ON BRAIN DAMAGE

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective To study the differential diagnosis o n cerebral concussion and mild cerebral contusion value of the brain type creati n e kinase isoenzyme(CK-BB),and evaluate the seriousness of brain damage and prog nosis of the patients with acute head injury.Methods Chromatographic separating and fluorometric quant ifying technique was used to detect the CK-BB activity in the cerebrospinal flu id(CSF) of 117 patients with acute head injury and 12 patients with increased in tracranial pressure and 20 normal people.Results The CSF-CK-BB activity of the patients with acu te head injury was remarkably higher than that of the normal people and the CSF -CK-BB activity increased with the seriousness of brain damage.There was a clo se relationship between CSF-CK-BB activity and prognosis,and higher activity o f CSF-CK-BB indicated poor prognosis.Conclusion CSF-CK -BB activity could be used as a new index to diagnose brain damage and evaluate the seriousness of brain damage and prognosis.

  19. Frontal White Matter Damage Impairs Response Inhibition in Children Following Traumatic Brain Injury

    OpenAIRE

    Lipszyc, Jonathan; Levin, Harvey; Hanten, Gerri; Hunter, Jill; Dennis, Maureen; Schachar, Russell

    2014-01-01

    Inhibition, the ability to suppress inappropriate cognitions or behaviors, can be measured using computer tasks and questionnaires. Inhibition depends on the frontal cortex, but the role of the underlying white matter (WM) is unclear. We assessed the specific impact of frontal WM damage on inhibition in 29 children with moderate-to-severe traumatic brain injury (15 with and 14 without frontal WM damage), 21 children with orthopedic injury, and 29 population controls. We used the Stop Signal T...

  20. Radiation-related damage to the developing human brain

    International Nuclear Information System (INIS)

    The authors summarize the significant dose-related effects on brain development which have emerged largely within the last six years of study of prenatally exposed A-bomb survivors. The results are described primarily in terms of the DS86 estimates and differences between these and the older T65DR dose estimates are discussed. The severe mental retardation sample was based on 1598 individuals taken from the PE-86 sample, and the intelligence test scores considered from the same sample involved 1673 children. The authors also discuss some of the recent neurobiological developments that appear relevant to an understanding of the biological bases of dose-related events observed, and suggest future research that may contribute either to further delineation of exposure consequences or to the explanation of the cellular and molecular origins of observed effects. (UK)

  1. Pathophysiology of repetitive head injury in sports. Prevention against catastrophic brain damage

    International Nuclear Information System (INIS)

    The most common head injury in sports is concussion and experiencing multiple concussions in a short period of time sometimes can cause severe brain damage. In this paper, we investigate severe brain damage due to repeated head injury in sports and discuss the pathophysiology of repeated sports injury. The majority of these severe cases are usually male adolescents or young adults that suffer a second head injury before they have recovered from the first head injury. All cases that could be confirmed by brain CT scan after the second injury revealed brain swelling associated with a thin subdural hematoma. We suggested that the existence of subdural hematoma is one of the major causes of brain swelling after repeated head injury in sports. Since repeated concussions occurring within a short period may have a risk for severe brain damage, the diagnosis for initial cerebral concussion should be done appropriately. To prevent catastrophic brain damage, the player who suffered from concussion should not engage in any sports before recovery. The american Academy of Neurology and Colorado Medical Society set a guideline to return to play after cerebral concussion. An international conference on concussion in sports was held at Prague in 2004. The summary and agreement of this meeting was published and the Sports Concussion Assessment Tool (SCAT) was introduced to treat sports-related concussion. In addition, a number of computerized cognitive assessment tests and test batteries have been developed to allow athletes to return to play. It is important that coaches, as well as players and trainers, understand the medical issues involved in concussion. (author)

  2. Macroscopic networks in the human brain: mapping connectivity in healthy and damaged brains

    NARCIS (Netherlands)

    Nijhuis, E.H.J.

    2013-01-01

    The human brain contains a network of interconnected neurons. Recent advances in functional and structural in-vivo magnetic resonance neuroimaging (MRI) techniques have provided opportunities to model the networks of the human brain on a macroscopic scale. This dissertation investigates the possibil

  3. Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure.

    Science.gov (United States)

    Mishra, D; Flora, S J S

    2008-05-01

    Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain - parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50A ppm sodium arsenite in drinking water) for 10A months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

  4. Principles of Experience-Dependent Neural Plasticity: Implications for Rehabilitation after Brain Damage

    Science.gov (United States)

    Kleim, Jeffrey A.; Jones, Theresa A.

    2008-01-01

    Purpose: This paper reviews 10 principles of experience-dependent neural plasticity and considerations in applying them to the damaged brain. Method: Neuroscience research using a variety of models of learning, neurological disease, and trauma are reviewed from the perspective of basic neuroscientists but in a manner intended to be useful for the…

  5. Intranasal mesenchymal stem cell treatment for neonatal brain damage : long-term cognitive and sensorimotor improvement

    NARCIS (Netherlands)

    Donega, Vanessa; van Velthoven, Cindy T J; Nijboer, Cora H; van Bel, Frank; Kas, Martien J H; Kavelaars, Annemieke; Heijnen, Cobi J

    2013-01-01

    Mesenchymal stem cell (MSC) administration via the intranasal route could become an effective therapy to treat neonatal hypoxic-ischemic (HI) brain damage. We analyzed long-term effects of intranasal MSC treatment on lesion size, sensorimotor and cognitive behavior, and determined the therapeutic wi

  6. MLKL inhibition attenuates hypoxia-ischemia induced neuronal damage in developing brain.

    Science.gov (United States)

    Qu, Yi; Shi, Jing; Tang, Ying; Zhao, Fengyan; Li, Shiping; Meng, Junjie; Tang, Jun; Lin, Xuemei; Peng, Xiaodong; Mu, Dezhi

    2016-05-01

    Mixed lineage kinase domain-like protein (MLKL) is a critical molecule mediating cell necroptosis. However, its role in brain injury remains obscure. We first investigated the functions and mechanisms of MLKL in mediating neuronal damage in developing brain after hypoxia-ischemia. Neuronal necroptosis was induced by oxygen-glucose deprivation (OGD) plus caspase inhibitor zVAD treatment (OGD/zVAD). We found that two important necroptosis related proteins, receptor-interacting protein 1 and 3 (RIP1, RIP3) were upregulated. Furthermore, the interaction of RIP1-RIP3 with MLKL increased. Inhibition of MLKL through siRNA diminished RIP1-RIP3-MLKL interaction and attenuated neuronal death induced by OGD/zVAD. The translocation of oligomerized MLKL to the neuronal membrane leading to the injury of cellular membrane is the possible new mechanism of neuronal necroptosis. Animal experiment with neonatal rats further proved that MLKL inhibition attenuated brain damage induced by hypoxia-ischemia. These findings suggest that MLKL is a target to attenuate brain damage in developing brain.

  7. Explorative investigation of biomarkers of brain damage and coagulation system activation in clinical stroke differentiation

    DEFF Research Database (Denmark)

    Undén, Johan; Strandberg, Karin; Malm, Jan;

    2009-01-01

    INTRODUCTION: A simple and accurate method of differentiating ischemic stroke and intracerebral hemorrhage (ICH) is potentially useful to facilitate acute therapeutic management. Blood measurements of biomarkers of brain damage and activation of the coagulation system may potentially serve as nov......: This exploratory study indicated that blood levels of biomarkers GFAP and APC-PCI, prior to neuroimaging, may rule out ICH in a mixed stroke population.......INTRODUCTION: A simple and accurate method of differentiating ischemic stroke and intracerebral hemorrhage (ICH) is potentially useful to facilitate acute therapeutic management. Blood measurements of biomarkers of brain damage and activation of the coagulation system may potentially serve as novel...... diagnostic tools for stroke subtypes. METHODS: Ninety-seven stroke patients were prospectively investigated in a multicenter design with blood levels of brain biomarkers S100B, neuron specific enolase (NSE), glial fibrillary acidic protein (GFAP) as well as a coagulation biomarker, activated protein C...

  8. A protective effect of musical expertise on cognitive outcome following brain damage?

    Science.gov (United States)

    Omigie, Diana; Samson, Severine

    2014-12-01

    The current review examines the possibility that training-related changes that take place in the brains of musicians may have a beneficial effect on their cognitive outcome and recovery following neurological damage. First, we propose three different mechanisms by which training-related brain changes might result in relatively preserved function in musicians as compared to non-musicians with cerebral lesions. Next, we review the neuropsychological literature examining musical ability in professional musicians following brain damage, specifically of vascular, tumoral and epileptic aetiology. Finally, given that assessment of musician patients can greatly inform our understanding of the influence of premorbid experience on postmorbid recovery, we suggest some basic guidelines for the future evaluation of relevant patients. PMID:25380766

  9. Brain damages in ketamine addicts as revealed by magnetic resonance imaging

    Directory of Open Access Journals (Sweden)

    Chunmei eWang

    2013-07-01

    Full Text Available Ketamine, a known antagonist of N-methyl-D-aspartic (NMDA glutamate receptors, had been used as an anesthetic particularly for pediatric or for cardiac patients. Unfortunately, ketamine has become an abusive drug in many parts of the world while chronic and prolonged usage led to damages of many organs including the brain. However, no studies on possible damages in the brains induced by chronic ketamine abuse have been documented in the human via neuroimaging. This paper described for the first time via employing magnetic resonance imaging (MRI the changes in ketamine addicts of 0.5 to 12 years and illustrated the possible brain regions susceptible to ketamine abuse. Twenty-one ketamine addicts were recruited and the results showed that the lesions in the brains of ketamine addicts were located in many regions which appeared 2-4 years after ketamine addiction. Cortical atrophy was usually evident in the frontal, parietal or occipital cortices of addicts. Such study confirmed that many brain regions in the human were susceptible to chronic ketamine injury and presented a diffuse effect of ketamine on the brain which might differ from other central nervous system (CNS drugs, such as cocaine, heroin and methamphetamine.

  10. Tumor necrosis factor α antibody prevents brain damage of rats with acute necrotizing pancreatitis

    Institute of Scientific and Technical Information of China (English)

    Yan-Ling Yang; Ji-Peng Li; Kai-Zong Li; Ke-Feng Dou

    2004-01-01

    AIM: To study the protective effects of tumor necrosis factor á (TNFα) antibody on pancreatic encephalopathy in rats.METHODS:One hundred and twenty SD rats were randomly divided into normal control group,acute necrotizing pancreatitis group and TNFα antibody treated group.Acute hemorrhage necrotizing pancreatitis model in rats was induced by retrograde injection of 50 g/L sodium taurocholate into the pancreatobiliary duct.Serum TNFα was detected and animals were killed 12 h after drug administration.Changes in content of brain water,MDA and SOD as well as leucocyte adhesion of brain microvessels were measured.RESULTS:In TNFα antibody treated group,serum TNFálevel was decreased.Content of brain water,MDA and SOD as well as leucocyte adhesion were decreased significantly in comparison with those of acute necrotizing pancreatitis group (P<0.05).CONCLUSION:TNFα antibody can alleviate the brain damage of rats with acute hemorrhage necrotizing pancreatitis.

  11. Neuroprotective actions of taurine on hypoxic-ischemic brain damage in neonatal rats.

    Science.gov (United States)

    Zhu, Xiao-Yun; Ma, Peng-Sheng; Wu, Wei; Zhou, Ru; Hao, Yin-Ju; Niu, Yang; Sun, Tao; Li, Yu-Xiang; Yu, Jian-Qiang

    2016-06-01

    Taurine is an abundant amino acid in the nervous system, which has been proved to possess antioxidation, osmoregulation and membrane stabilization. Previously it has been demonstrated that taurine exerts ischemic brain injury protective effect. This study was designed to investigate whether the protective effect of taurine has the possibility to be applied to treat neonatal hypoxic-ischemic brain damage. Seven-day-old Sprague-Dawley rats were treated with left carotid artery ligation followed by exposure to 8% oxygen to generate the experimental group. The cerebral damage area was measured after taurine post-treatment with 2,3,5-triphenyltetrazolium chloride (TTC) staining, Hematoxyline-Eosin (HE) staining and Nissl staining. The activities of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), myeloperoxtidase (MPO), ATP and Lactic Acid productions were assayed with ipsilateral hemisphere homogenates. Western-blot and immunofluorescence assay were processed to detect the expressions of AIF, Cyt C, Bax, Bcl-2 in brain. We found that taurine significantly reduced brain infarct volume and ameliorated morphological injury obviously reversed the changes of SOD, MDA, GSH-Px, T-AOC, ATP, MPO, and Lactic Acid levels. Compared with hypoxic-ischemic group, it showed marked reduction of AIF, Cyt C and Bax expressions and increase of Bcl-2 after post-treatment. We conclude that taurine possesses an efficacious neuroprotective effect after cerebral hypoxic-ischemic damage in neonatal rats. PMID:27345710

  12. The effects of chronic smoking on the pathology of alcohol-related brain damage.

    Science.gov (United States)

    McCorkindale, A N; Sheedy, D; Kril, J J; Sutherland, G T

    2016-06-01

    Both pathological and neuroimaging studies demonstrate that chronic alcohol abuse causes brain atrophy with widespread white matter loss limited gray matter loss. Recent neuroimaging studies suggest that tobacco smoking also causes brain atrophy in both alcoholics and neurologically normal individuals; however, this has not been confirmed pathologically. In this study, the effects of smoking and the potential additive effects of concomitant alcohol and tobacco consumption were investigated in autopsied human brains. A total of 44 cases and controls were divided into four groups: 16 non-smoking controls, nine smoking controls, eight non-smoking alcoholics, and 11 smoking alcoholics. The volumes of 26 gray and white matter regions were measured using an established point-counting technique. The results showed trends for widespread white matter loss in alcoholics (p smoking alone had no effect on brain atrophy and the combination of smoking and alcohol showed no additional effect. Neuronal density was analyzed as a more sensitive assay of gray matter integrity. Similar to the volumetric analysis, there was a reduction in neurons (29%) in the prefrontal cortex of alcoholics, albeit this was only a trend when adjusted for potential confounders (p smoking or combinatorial effects on neuronal density in any of the three regions examined. These results do not support the hypothesis that smoking exacerbates alcohol-related brain damage. The trends here support previous studies that alcohol-related brain damage is characterized by focal neuronal loss and generalized white matter atrophy. These disparate effects suggest that two different pathogenic mechanisms may be operating in the alcoholic brain. Future studies using ultrastructural or molecular techniques will be required to determine if smoking has more subtle effects on the brain and how chronic alcohol consumption leads to widespread white matter loss.

  13. Uptake of radiolabeled ions in normal and ischemia-damaged brain

    International Nuclear Information System (INIS)

    The regional concentrations of nine radiochemicals were measured in rat brain after induction of cerebral ischemia to identify tracers concentrated by brain undergoing selective neuronal necrosis. Transient (30 minute) forebrain ischemia was produced in the rat; 24 hours after cerebral recirculation the radiochemicals were injected intravenously and allowed to circulate for 5 hours. The brain concentrations of the radiochemicals in dissected regions were determined by scintillation counting. Forebrain ischemia of this nature will produce extensive injury to striatal neurons but will spare the great majority of neocortical neurons at 24 hours. The regional concentrations of these radiochemicals varied considerably in both control and ischemic animals. In postischemic animals, 4 radionuclides (63Ni, 99TcO4, 22Na, and [3H]tetracycline) were concentrated in the irreversibly damaged striatum in amounts ranging from 1.4 to 2.4 times greater than in normal tissue. The concentrations of 65Zn, 59Fe, 32PO4, and 147Pm in postischemic brain were similar to or less than those in normal brain. The concentration of [14C]EDTA was increased in injured and uninjured brain of postischemic rats. Autoradiographic analysis of the distribution patterns of some of these ions in normal animals showed that 99TcO4, 22Na, 65Zn, and 59Fe were distributed more uniformly throughout the brain than were 32PO4, 63Ni, and 147Pm. At 24 or 48 hours after ischemia, 63Ni, 99TcO4, and 22Na were preferentially concentrated in the damaged striatum and hippocampus, whereas 65Zn, 59Fe, 32PO4, and 147Pm did not accumulate in irreversibly injured tissue. Of the radiochemicals tested to date, Ni, TcO4, and tetracycline may be useful for diagnosing ischemic brain injury in humans, using positron emission tomography

  14. Cocaine induces DNA damage in distinct brain areas of female rats under different hormonal conditions.

    Science.gov (United States)

    de Souza, Marilise F; Gonçales, Tierre A; Steinmetz, Aline; Moura, Dinara J; Saffi, Jenifer; Gomez, Rosane; Barros, Helena M T

    2014-04-01

    We evaluated levels of neuronal DNA damage after acute or repeated cocaine treatment in different brain areas of female rats after ovariectomy or sham surgery. Rats in the control and acute groups were given saline i.p., whereas in the repeated group were given 15 mg/kg, i.p., cocaine for 8 days. After a 10 day washout period, the control group was given saline i.p., whereas rats in the acute and repeated groups were given a challenge dose of 15 mg/kg, i.p., cocaine. After behavioural assessment, rats were killed and the cerebellum, hippocampus, hypothalamus, prefrontal cortex and striatum were dissected for the Comet assay. Acute cocaine exposure induced DNA damage in all brain areas. This effect persisted after repeated administration, except in the hypothalamus, where repeated treatment did not cause increased DNA damage. Sexual hormones exhibited a neuroprotective effect, decreasing cocaine-induced DNA damage in cycling rats in all brain areas. PMID:24552452

  15. Effects of Graded Hypothermia on Hypoxic-ischemic Brain Damage in the Neonatal Rat

    Institute of Scientific and Technical Information of China (English)

    Xiao-yan Xia; Yi-xin Xia

    2011-01-01

    Objective To investigate the effect of graded hypothermia on neuropathologic alteratiors of neonatal rat brain after exposed to hypoxic-ischemic insult at 37℃, 33℃, 31℃, and 28℃, respectively, and to observe the effect of hypothermia on 72-kDa heat shock protein (HSP72) expression after hypoxic-ischemic insult. Methods Seven days old Wistar rats were subjected to unilateral common carotid artery ligation followed by exposure to hypoxia in 8% oxygen for 2 hours at 37℃, 33℃, 31℃, and 28℃, respectively. The brain temperature was monitored indirectly by inserting a mini-thermocouple probe into the temporal muscle during hypoxia. After hypoxia-ischemia their mortality was assessed. Neuronal damage was assessed with HE staining 72 hours after hypoxia. HSP72 expression at 0.5, 24, and 72 hours of recovery was immunohistochemically assessed using a monoclonal antibody to HSP72. Results Hypoxia-ischemia caused 10.5% (2/19) of mortality in rat of 37℃ group, but no death occurred in 33℃, 31℃ or 28℃ groups. HE staining showed neuropathologic damage was extensive in rats exposed to hypoxia-ischemia at 37℃ (more than 80.0%). The incidence of severe brain damage was significantly decreased in 33℃ (53.3%) and 31℃ groups (44.4%), and no histologic injury was seen in the 28℃ group of rats. Expression of HSP72 was manifest and persistent in the rat brain of 37℃ group, but minimum in the rat brain of 28℃ group. Conclusion Mild and moderate hypothermia might prevent cerebral visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing stress response.

  16. Berberine protects against neuronal damage via suppression of glia-mediated inflammation in traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Chien-Cheng Chen

    Full Text Available Traumatic brain injury (TBI triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1 or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain barrier (BBB permeability and brain water content were determined. Expression of PI3K/Akt and Erk signaling and inflammatory mediators were also analyzed. The protective effect of berberine was also investigated in cultured neurons either subjected to stretch injury or exposed to conditioned media with activated microglia. Berberine significantly attenuated functional deficits and brain damage associated with TBI up to day 28 post-injury. Berberine also reduced neuronal death, apoptosis, BBB permeability, and brain edema at day 1 post-injury. These changes coincided with a marked reduction in leukocyte infiltration, microglial activation, matrix metalloproteinase-9 activity, and expression of inflammatory mediators. Berberine had no effect on Akt or Erk 1/2 phosphorylation. In mixed glial cultures, berberine reduced TLR4/MyD88/NF-κB signaling. Berberine also attenuated neuronal death induced by microglial conditioned media; however, it did not directly protect cultured neurons subjected to stretch injury. Moreover, administration of berberine at 3 h post-injury also reduced TBI-induced neuronal damage, apoptosis and inflammation in vivo. Berberine reduces TBI-induced brain damage by limiting the production of inflammatory mediators by glial cells, rather than by a direct neuroprotective effect.

  17. Bacterial cytolysin during meningitis disrupts the regulation of glutamate in the brain, leading to synaptic damage.

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    Carolin Wippel

    Full Text Available Streptococcus pneumoniae (pneumococcal meningitis is a common bacterial infection of the brain. The cholesterol-dependent cytolysin pneumolysin represents a key factor, determining the neuropathogenic potential of the pneumococci. Here, we demonstrate selective synaptic loss within the superficial layers of the frontal neocortex of post-mortem brain samples from individuals with pneumococcal meningitis. A similar effect was observed in mice with pneumococcal meningitis only when the bacteria expressed the pore-forming cholesterol-dependent cytolysin pneumolysin. Exposure of acute mouse brain slices to only pore-competent pneumolysin at disease-relevant, non-lytic concentrations caused permanent dendritic swelling, dendritic spine elimination and synaptic loss. The NMDA glutamate receptor antagonists MK801 and D-AP5 reduced this pathology. Pneumolysin increased glutamate levels within the mouse brain slices. In mouse astrocytes, pneumolysin initiated the release of glutamate in a calcium-dependent manner. We propose that pneumolysin plays a significant synapto- and dendritotoxic role in pneumococcal meningitis by initiating glutamate release from astrocytes, leading to subsequent glutamate-dependent synaptic damage. We outline for the first time the occurrence of synaptic pathology in pneumococcal meningitis and demonstrate that a bacterial cytolysin can dysregulate the control of glutamate in the brain, inducing excitotoxic damage.

  18. Interfacing brain with computer to improve communication and rehabilitation after brain damage.

    Science.gov (United States)

    Riccio, A; Pichiorri, F; Schettini, F; Toppi, J; Risetti, M; Formisano, R; Molinari, M; Astolfi, L; Cincotti, F; Mattia, D

    2016-01-01

    Communication and control of the external environment can be provided via brain-computer interfaces (BCIs) to replace a lost function in persons with severe diseases and little or no chance of recovery of motor abilities (ie, amyotrophic lateral sclerosis, brainstem stroke). BCIs allow to intentionally modulate brain activity, to train specific brain functions, and to control prosthetic devices, and thus, this technology can also improve the outcome of rehabilitation programs in persons who have suffered from a central nervous system injury (ie, stroke leading to motor or cognitive impairment). Overall, the BCI researcher is challenged to interact with people with severe disabilities and professionals in the field of neurorehabilitation. This implies a deep understanding of the disabled condition on the one hand, and it requires extensive knowledge on the physiology and function of the human brain on the other. For these reasons, a multidisciplinary approach and the continuous involvement of BCI users in the design, development, and testing of new systems are desirable. In this chapter, we will focus on noninvasive EEG-based systems and their clinical applications, highlighting crucial issues to foster BCI translation outside laboratories to eventually become a technology usable in real-life realm. PMID:27590975

  19. Platelets recognize brain-specific glycolipid structures, respond to neurovascular damage and promote neuroinflammation.

    Directory of Open Access Journals (Sweden)

    Ilya Sotnikov

    Full Text Available Platelets respond to vascular damage and contribute to inflammation, but their role in the neurodegenerative diseases is unknown. We found that the systemic administration of brain lipid rafts induced a massive platelet activation and degranulation resulting in a life-threatening anaphylactic-like response in mice. Platelets were engaged by the sialated glycosphingolipids (gangliosides integrated in the rigid structures of astroglial and neuronal lipid rafts. The brain-abundant gangliosides GT1b and GQ1b were specifically recognized by the platelets and this recognition involved multiple receptors with P-selectin (CD62P playing the central role. During the neuroinflammation, platelets accumulated in the central nervous system parenchyma, acquired an activated phenotype and secreted proinflammatory factors, thereby triggering immune response cascades. This study determines a new role of platelets which directly recognize a neuronal damage and communicate with the cells of the immune system in the pathogenesis of neurodegenerative diseases.

  20. Recurrent Moderate Hypoglycemia Ameliorates Brain Damage and Cognitive Dysfunction Induced by Severe Hypoglycemia

    OpenAIRE

    Puente, Erwin C.; Silverstein, Julie; Bree, Adam J.; Musikantow, Daniel R.; Wozniak, David F.; Maloney, Susan; Daphna-Iken, Dorit; Fisher, Simon J.

    2010-01-01

    OBJECTIVE Although intensive glycemic control achieved with insulin therapy increases the incidence of both moderate and severe hypoglycemia, clinical reports of cognitive impairment due to severe hypoglycemia have been highly variable. It was hypothesized that recurrent moderate hypoglycemia preconditions the brain and protects against damage caused by severe hypoglycemia. RESEARCH DESIGN AND METHODS Nine-week-old male Sprague-Dawley rats were subjected to either 3 consecutive days of recurr...

  1. Carcinoma cells misuse the host tissue damage response to invade the brain

    OpenAIRE

    Chuang, Han-Ning; van Rossum, Denise; Sieger, Dirk; Siam, Laila; Klemm, Florian; Bleckmann, Annalen; Bayerlová, Michaela; Farhat, Katja; Scheffel, Jörg; Schulz, Matthias; Dehghani, Faramarz; Stadelmann, Christine; Hanisch, Uwe-Karsten; Binder, Claudia; Pukrop, Tobias

    2013-01-01

    The metastatic colonization of the brain by carcinoma cells is still barely understood, in particular when considering interactions with the host tissue. The colonization comes with a substantial destruction of the surrounding host tissue. This leads to activation of damage responses by resident innate immune cells to protect, repair, and organize the wound healing, but may distract from tumoricidal actions. We recently demonstrated that microglia, innate immune cells of the CNS, assist carci...

  2. Frontal lobe syndrome reassessed: comparison of patients with lateral or medial frontal brain damage

    OpenAIRE

    Paradiso, S; Chemerinski, E; Yazici, K.; Tartaro, A.; Robinson, R

    1999-01-01

    Examination of mood and behaviour changes after frontal damage may contribute to understanding the functional role of distinct prefrontal areas in depression and anxiety. Depression and anxiety disorders, symptoms, and behaviour were compared in eight patients with single lateral and eight patients with single medial frontal lesions matched for age, sex, race, education, socioeconomic status, side, and aetiology of lesion 2 weeks and 3 months after brain injury. DSM IV major de...

  3. Changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats

    Institute of Scientific and Technical Information of China (English)

    陈立华; 于嘉; 刘丽旭; 曹美鸿

    2002-01-01

    To explore changes of neuronal calcium channel following brain damage induced by injection of pertussis bacilli in rats, and to investigate the relationship between cytosolic free calcium concentration ( [ Ca2 + ] i ) in the synaptosome and Ca2 + -ATPase activities of mitochondria. Methods: The level of [ Ca2+ ]i in the synaptosome and Ca2+ -ATPase activities of mitochondria in the acute brain damage induced by injection of pertussis bacilli (PB)in rat was determined and nimodipine was administrated to show its effects on [ Ca2+ ]i in the synaptosome and on alteration of Ca2+ -ATPase activity in the mitochondria.Seventy-three rats were randomly divided into four groups,ie, normal control group (Group A ), sham-operation control group (Group B), PB group (Group C) and nimodipine treatment group (Group D). Results: The level of [ Ca2+ ]i was significantly increased in the PB-injected cerebral hemisphere in the Group C as compared with that in the Group A and the Group B at 30 minutes after injection of PB. The level of [ Ca2+ ]i was kept higher in the 4 hours and 24 hours subgroups after the injection in the Group C ( P < 0.05).In contrast, the Ca2+ -ATPase activities were decreased remarkably among all of the subgroups in the Group C.Nimodipine, which was administered after injection of PB,could significantly decrease the [ Ca2+ ]i and increase the activity of Ca2 + -ATPase ( P < 0.05 ). Conclusions: The neuronal calcium channel is opened after injection of PB. There is a negative correlation between activities of Ca2 +-ATPase and [ Ca2 + ]i.Nimodipine can reduce brain damage through stimulating the activities of Ca2+ -ATPase in the mitochondria, and decrease the level of [ Ca2+ ]i in the synaptosome.Treatment with nimodipine dramatically reduces the effects of brain damage induced by injection of PB.

  4. Emotional and non-emotional facial behaviour in patients with unilateral brain damage.

    OpenAIRE

    Borod, J C; Koff, E.; Lorch, M P; Nicholas, M.; Welkowitz, J

    1988-01-01

    Aspects of emotional facial expression (responsivity, appropriateness, intensity) were examined in brain-damaged adults with right or left hemisphere cerebrovascular lesions and in normal controls. Subjects were videotaped during experimental procedures designed to elicit emotional facial expression and non-emotional facial movement (paralysis, mobility, praxis). On tasks of emotional facial expression, patients with right hemisphere pathology were less responsive and less appropriate than pa...

  5. Changes in the permeability of blood brain barrier and endothelial cell damage after cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Ke Liu; Jiansheng Li

    2006-01-01

    OBJECTIVE: To investigate the effect of endothelial cells on the permeability of blood brain barrier (BBB) after brain injury and its effect mechanism.DATA SOURCES: We searched for the articles of permeability of BBB and endothelial cell injury after brain ischemia, which were published between January 1982 and December 2005, with the key words of "cerebral ischemia damage,blood brain barrier ( BBB),permeability,effect of endothelial cell (EC) and its variation mechanism"in English.STUDY SELECTION: The materials were primarily selected. The articles related to the changes in the permeability of BBB and the effect of endothelial cells as well as the change mechanism after cerebral ischemia damage were chosen. Repetitive studies or review articles were excluded.DATA EXTRACTION: Totally 55 related articles were collected, and 35 were excluded due to repetitive or review articles, finally 20 articles were involved.DATA SYNTHESIS: The content or viewpoints of involved literatures were analyzed. Cerebral ischemia had damage for endothelial cells, such as the inflow of a lot of Ca2+, the production of nitrogen monoxide and oxygen free radical, and aggravated destruction of BBB. After acceptors of inflammatory mediators on cerebrovascular endothelial cell membrane, such as histamine, bradykinin , 5-hydroxytryptamine and so on are activated, endothelial cells shrink and the permeability of BBB increases. Its mechanism involves in the inflow of extracellular Ca2+and the release of intracellular Ca2+ in the cells. Glycocalyx molecule on the surface of endothelial cell, having structural polytropy, is the determinative factor of the permeability of BBB. VEGF, intensively increasing the vasopermeability and mainly effecting on postcapillary vein and veinlet, is the strongest known blood vessel permeation reagent. Its chronic overexpression in the brain can lead the destruction of BBB.CONCLUSION: The injury of endothelial cell participants in the pathological mechanism of BBB

  6. Does alcohol damage the adolescent brain? Neuroanatomical and neuropsychological consequences of adolescent drinking

    Directory of Open Access Journals (Sweden)

    Fleming RL

    2015-12-01

    Full Text Available Rebekah L Fleming1,2 1Durham VA Medical Center, 2Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC, USA Abstract: Alcohol drinking is a significant risk factor for morbidity and mortality in adolescents worldwide. Adolescents frequently binge drink, and this pattern of use is associated with poor school performance, injuries, violence, drug use, and a variety of poor psychosocial outcomes in adulthood. These associations have raised concerns that alcohol drinking may damage the adolescent brain and lead to impaired cognition and behavior. Similar to the neurotoxicity seen in adult alcoholics, magnetic resonance imaging studies of brain anatomy in adolescent drinkers have shown that alcohol disrupts the development of temporal and frontal cortices and myelinated fiber tracts throughout the brain. Although adult brains show some recovery with abstinence, at present, no studies have examined brain recovery in adolescents. Studies of neuropsychological function have found deficits in attention and visuospatial ability that show dose-dependent correlations with alcohol exposure and withdrawal symptoms, but visuospatial performance recovers with short-term abstinence. Differences in executive function and decision-making have also been found, but the available evidence suggests that these are not primarily the result of alcohol exposure; instead, they reflect premorbid factors that increase risk-taking and substance use. Nevertheless, alcohol drinking by adolescents remains an important concern because of the potential for brain injury in addition to the many negative consequences associated with acute intoxication. Keywords: adolescence, binge drinking, alcohol, magnetic resonance imaging, neuropsychological function

  7. Chronic hypertension aggravates heat stress-induced brain damage: possible neuroprotection by cerebrolysin.

    Science.gov (United States)

    Muresanu, Dafin Fior; Zimmermann-Meinzingen, Sibilla; Sharma, Hari Shanker

    2010-01-01

    Whole body hyperthermia (WBH) aggravates brain edema formation and cell damage in chronic hypertensive rats compared with normotensive animals. In this investigation, we examined the influence of cerebrolysin on WBH-induced edema formation and brain pathology in hypertensive and normotensive rats. Rats subjected to 4 h WBH at 38 degrees C in a biological oxygen demand (BOD) incubator showed breakdown of the blood-brain barrier (BBB), reduced cerebral blood flow (CBF), edema formation and cell injuries in several parts of the brain. These effects were further aggravated in chronic hypertensive rats (two-kidney one clip model (2K1C), for 4 weeks) subjected to WBH. Pretreatment with cerebrolysin (5 mL/kg, 24 h and 30 min before heat stress) markedly attenuated the BBB dysfunction and brain pathology in normal animals. However, in hypertensive animals, a high dose of cerebrolysin (10 mL/kg, 24 h and 30 min before heat stress) was needed to attenuate WBH-induced BBB dysfunction and brain pathology. These observations indicate that heat stress could affect differently in normal and hypertensive conditions. Furthermore, our results suggest that patients suffering from various chronic cardiovascular diseases may respond differently to hyperthermia and to neuroprotective drugs, e.g., cerebrolysin not reported earlier.

  8. Melatonin Improves Outcomes of Heatstroke in Mice by Reducing Brain Inflammation and Oxidative Damage and Multiple Organ Dysfunction

    Directory of Open Access Journals (Sweden)

    Yu-Feng Tian

    2013-01-01

    Full Text Available We report here that when untreated mice underwent heat stress, they displayed thermoregulatory deficit (e.g., animals display hypothermia during room temperature exposure, brain (or hypothalamic inflammation, ischemia, oxidative damage, hypothalamic-pituitary-adrenal axis impairment (e.g., decreased plasma levels of both adrenocorticotrophic hormone and corticosterone during heat stress, multiple organ dysfunction or failure, and lethality. Melatonin therapy significantly reduced the thermoregulatory deficit, brain inflammation, ischemia, oxidative damage, hypothalamic-pituitary-adrenal axis impairment, multiple organ dysfunction, and lethality caused by heat stroke. Our data indicate that melatonin may improve outcomes of heat stroke by reducing brain inflammation, oxidative damage, and multiple organ dysfunction.

  9. Influence of a brief episode of anesthesia during the induction of experimental brain trauma on secondary brain damage and inflammation.

    Directory of Open Access Journals (Sweden)

    Clara Luh

    Full Text Available It is unclear whether a single, brief, 15-minute episode of background anesthesia already modulates delayed secondary processes after experimental brain injury. Therefore, this study was designed to characterize three anesthesia protocols for their effect on molecular and histological study endpoints. Mice were randomly separated into groups that received sevoflurane (sevo, isoflurane (iso or an intraperitoneal anesthetic combination (midazolam, fentanyl and medetomidine; comb prior to traumatic brain injury (controlled cortical impact, CCI; 8 m/s, 1 mm impact depth, 3 mm diameter. Twenty-four hours after insult, histological brain damage, neurological function (via neurological severity score, cerebral inflammation (via real-time RT-PCR for IL6, COX-2, iNOS and microglia (via immunohistochemical staining for Iba1 were determined. Fifteen minutes after CCI, the brain contusion volume did not differ between the anesthetic regimens (sevo = 17.9±5.5 mm(3; iso = 20.5±3.7 mm(3; comb = 19.5±4.6 mm(3. Within 24 hours after injury, lesion size increased in all groups (sevo = 45.3±9.0 mm(3; iso = 31.5±4.0 mm(3; comb = 44.2±6.2 mm(3. Sevo and comb anesthesia resulted in a significantly larger contusion compared to iso, which was in line with the significantly better neurological function with iso (sevo = 4.6±1.3 pts.; iso = 3.9±0.8 pts.; comb = 5.1±1.6 pts.. The expression of inflammatory marker genes was not significantly different at 15 minutes and 24 hours after CCI. In contrast, significantly more Iba1-positive cells were present in the pericontusional region after sevo compared to comb anesthesia (sevo = 181±48/mm(3; iso = 150±36/mm(3; comb = 113±40/mm(3. A brief episode of anesthesia, which is sufficient for surgical preparations of mice for procedures such as delivering traumatic brain injury, already has a significant impact on the extent of secondary brain damage.

  10. Role of gap junction and connexin-43 in hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Jieying Lin; Niyang Lin

    2006-01-01

    OBJECTEVE:Gap junctin (GJ)is the structural basis for direct intercellular communication of nerve cells . Connexin(Cx) is the protein subunit for constructling GJ channel. Among them, Cx43is closely related with nervous system. Both Cx43 and nervous system play an important role in the pathophysiological development of hypoxic-ischemic injury. We are in attempt to investigate GJ,Cx43 and their correlations with hypoxic-ischemic brain damage by research.DATA SOURCES:Using the terms "brain gap junction"in English and "gap junction"in Chinese, we searched the Medline database and Chinese BioMedical Literature Database as well as China Hospital Knowledge Database to identify the articles published from 1996 to 2006 about GJ and brain hypoxic-ischemic injury.STUDY SELECTION:The articles were selected firstly and abstracts of 250 articles were read thuugh.Articles in which the experimental design met randomized controlled principle were included,and study articles and case reports with repetitve contents were excluded.DATA EXTRACTION:Among 53 included correlative articles, 23 were excluded for repetitive contents and the other 30 were analyzed.DATA SYNTHESIS:GJ,widely esistling in nervous system,plays a key role in maintainling normal differentiation and development as well as physiological function brain tissue.GJ channel is a hydrophilic,low-selectivity and lowohmic channel, which can provide direct channel for intercellular substance transmission and information communication. It plays an important role in the differentiation and development of nerve cells and regulation of physiological function,The funtions of GJ channel are regulated by many factors,which invilved intracellular Ph value, Ca2+concentration, ATP concentration, phosphorylation of Cx, transchannel pressure,some neurohormonal factors,regulatory factors of protein and so on. Cx43 is the main component of GJ channel in the brain tissues. Its expression in the brain tissue of mammal is the strongest

  11. Association between Peripheral Oxidative Stress and White Matter Damage in Acute Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    Wei-Ming Lin

    2014-01-01

    Full Text Available The oxidative stress is believed to be one of the mechanisms involved in the neuronal damage after acute traumatic brain injury (TBI. However, the disease severity correlation between oxidative stress biomarker level and deep brain microstructural changes in acute TBI remains unknown. In present study, twenty-four patients with acute TBI and 24 healthy volunteers underwent DTI. The peripheral blood oxidative biomarkers, like serum thiol and thiobarbituric acid-reactive substances (TBARS concentrations, were also obtained. The DTI metrics of the deep brain regions, as well as the fractional anisotropy (FA and apparent diffusion coefficient, were measured and correlated with disease severity, serum thiol, and TBARS levels. We found that patients with TBI displayed lower FAs in deep brain regions with abundant WMs and further correlated with increased serum TBARS level. Our study has shown a level of anatomic detail to the relationship between white matter (WM damage and increased systemic oxidative stress in TBI which suggests common inflammatory processes that covary in both the peripheral and central reactions after TBI.

  12. Neuroprotection by gonadal steroid hormones in acute brain damage requires cooperation with astroglia and microglia.

    Science.gov (United States)

    Johann, Sonja; Beyer, Cordian

    2013-09-01

    The neuroactive steroids 17β-estradiol and progesterone control a broad spectrum of neural functions. Besides their roles in the regulation of classical neuroendocrine loops, they strongly influence motor and cognitive systems, behavior, and modulate brain performance at almost every level. Such a statement is underpinned by the widespread and lifelong expression pattern of all types of classical and non-classical estrogen and progesterone receptors in the CNS. The life-sustaining power of neurosteroids for tattered or seriously damaged neurons aroused interest in the scientific community in the past years to study their ability for therapeutic use under neuropathological challenges. Documented by excellent studies either performed in vitro or in adequate animal models mimicking acute toxic or chronic neurodegenerative brain disorders, both hormones revealed a high potency to protect neurons from damage and saved neural systems from collapse. Unfortunately, neurons, astroglia, microglia, and oligodendrocytes are comparably target cells for both steroid hormones. This hampers the precise assignment and understanding of neuroprotective cellular mechanisms activated by both steroids. In this article, we strive for a better comprehension of the mutual reaction between these steroid hormones and the two major glial cell types involved in the maintenance of brain homeostasis, astroglia and microglia, during acute traumatic brain injuries such as stroke and hypoxia. In particular, we attempt to summarize steroid-activated cellular signaling pathways and molecular responses in these cells and their contribution to dampening neuroinflammation and neural destruction. This article is part of a Special Issue entitled 'CSR 2013'. PMID:23196064

  13. L-tyrosine induces DNA damage in brain and blood of rats.

    Science.gov (United States)

    De Prá, Samira D T; Ferreira, Gabriela K; Carvalho-Silva, Milena; Vieira, Júlia S; Scaini, Giselli; Leffa, Daniela D; Fagundes, Gabriela E; Bristot, Bruno N; Borges, Gabriela D; Ferreira, Gustavo C; Schuck, Patrícia F; Andrade, Vanessa M; Streck, Emilio L

    2014-01-01

    Mutations in the tyrosine aminotransferase gene have been identified to cause tyrosinemia type II which is inherited in an autosomal recessive manner. Studies have demonstrated that an excessive production of ROS can lead to reactions with macromolecules, such as DNA, lipids, and proteins. Considering that the L-tyrosine may promote oxidative stress, the main objective of this study was to investigate the in vivo effects of L-tyrosine on DNA damage determined by the alkaline comet assay, in brain and blood of rats. In our acute protocol, Wistar rats (30 days old) were killed 1 h after a single intraperitoneal L-tyrosine injection (500 mg/kg) or saline. For chronic administration, the animals received two subcutaneous injections of L-tyrosine (500 mg/kg, 12-h intervals) or saline administered for 24 days starting at postnatal day (PD) 7 (last injection at PD 31), 12 h after the last injection, the animals were killed by decapitation. We observed that acute administration of L-tyrosine increased DNA damage frequency and damage index in cerebral cortex and blood when compared to control group. Moreover, we observed that chronic administration of L-tyrosine increased DNA damage frequency and damage index in hippocampus, striatum, cerebral cortex and blood when compared to control group. In conclusion, the present work demonstrated that DNA damage can be encountered in brain from animal models of hypertyrosinemia, DNA alterations may represent a further means to explain neurological dysfunction in this inherited metabolic disorder and to reinforce the role of oxidative stress in the pathophysiology of tyrosinemia type II.

  14. The mitochondria-targeted antioxidants and remote kidney preconditioning ameliorate brain damage through kidney-to-brain cross-talk.

    Directory of Open Access Journals (Sweden)

    Denis N Silachev

    Full Text Available BACKGROUND: Many ischemia-induced neurological pathologies including stroke are associated with high oxidative stress. Mitochondria-targeted antioxidants could rescue the ischemic organ by providing specific delivery of antioxidant molecules to the mitochondrion, which potentially suffers from oxidative stress more than non-mitochondrial cellular compartments. Besides direct antioxidative activity, these compounds are believed to activate numerous protective pathways. Endogenous anti-ischemic defense may involve the very powerful neuroprotective agent erythropoietin, which is mainly produced by the kidney in a redox-dependent manner, indicating an important role of the kidney in regulation of brain ischemic damage. The goal of this study is to track the relations between the kidney and the brain in terms of the amplification of defense mechanisms during SkQR1 treatment and remote renal preconditioning and provide evidence that the kidney can generate signals inducing a tolerance to oxidative stress-associated brain pathologies. METHODOLOGY/PRINCIPAL FINDINGS: We used the cationic plastoquinone derivative, SkQR1, as a mitochondria-targeted antioxidant to alleviate the deleterious consequences of stroke. A single injection of SkQR1 before cerebral ischemia in a dose-dependent manner reduces infarction and improves functional recovery. Concomitantly, an increase in the levels of erythropoietin in urine and phosphorylated glycogen synthase kinase-3β (GSK-3β in the brain was detected 24 h after SkQR1 injection. However, protective effects of SkQR1 were not observed in rats with bilateral nephrectomy and in those treated with the nephrotoxic antibiotic gentamicin, indicating the protective role of humoral factor(s which are released from functional kidneys. Renal preconditioning also induced brain protection in rats accompanied by an increased erythropoietin level in urine and kidney tissue and P-GSK-3β in brain. Co-cultivation of SkQR1-treated

  15. Relationship between skull asymmetry and CT findings. Supine head position preference and brain damage

    Energy Technology Data Exchange (ETDEWEB)

    Yamori, Yuriko; Yuge, Mariko; Kanda, Toyoko; Ashida, Hiromi; Fukase, Hiroshi

    1987-07-01

    In order to clarify the relationship between brain damage and skull asymmetry or supine head position preference, we classified CT findings of 330 cases with cerebral palsy or risk of motor disturbance into 6 groups according to skull shape. Those were severe (I, n = 37) and mild (II, n = 114) grades in the right occipital flatness, severe (III, n = 34) and mild (IV, n = 58) grades in the left occipital flatness, long skull with temporal flatness (V, n = 33) and symmetric round skull (control, n = 54). It was considered that the asymmetry of cortical atrophy in appearance was formed physicaly by skull asymmetry but that the asymmetric dilatation in appearance of lateral ventricle was related to the asymmetry of brain damage. The severity and the asymmetry of brain damage were tend to increase the grade of skull asymmetry. The incidence of cases with the right occipital flatness was 1.6 times more frequently than the left sided. The incidence of cases whose left (lateral) ventricle was larger than the right was 4.1 times more than the cases whose right ventricle was larger than the left. The cases with occipital flatness in the contralateral side of the larger lateral ventricle were found more than the cases with occipital flatness in the ipsilateral side of the larger ventricle, that is to say, the direction of supine head position preference during early infant was suspected to be the more severely disturbed side of body. These results suggest that the supine head position preference to the right in newborn babies and infants with scoliosis or cerebral palsy might be the result of transient or permanent asymmetric (left > right) brain dysfunction.

  16. Line and word bisection in right-brain-damaged patients with left spatial neglect.

    Science.gov (United States)

    Veronelli, Laura; Vallar, Giuseppe; Marinelli, Chiara V; Primativo, Silvia; Arduino, Lisa S

    2014-01-01

    Right-brain-damaged patients with left unilateral spatial neglect typically set the mid-point of horizontal lines to the right of the objective center. By contrast, healthy participants exhibit a reversed bias (pseudoneglect). The same effect has been described also when bisecting orthographic strings. In particular, for this latter kind of stimulus, some recent studies have shown that visuo-perceptual characteristics, like stimulus length, may contribute to both the magnitude and the direction bias of the bisection performance (Arduino et al. in Neuropsychologia 48:2140-2146, 2010). Furthermore, word stress was shown to modulate reading performances in both healthy participants, and patients with left spatial neglect and neglect dyslexia (Cubelli and Beschin in Brain Lang 95:319-326, 2005; Rusconi et al. in Neuropsychology 18:135-140, 2004). In Experiment I, 22 right-brain-damaged patients (11 with left visuo-spatial neglect) and 11 matched neurologically unimpaired control participants were asked to set the subjective mid-point of word letter strings, and of lines of comparable length. Most patients exhibited an overall disproportionate rightward bias, sensitive to stimulus length, and similar for words and lines. Importantly, in individual patients, biases differed according to stimulus type (words vs. lines), indicating that at least partly different mechanisms may be involved. In Experiment II, the putative effects on the bisection bias of ortho-phonological information (i.e., word stress endings), arising from the non-neglected right hand side of the stimulus were investigated. The orthographic cue induced a rightward shift of the perceived mid-point in both patients and controls, with short words stressed on the antepenultimate final sequence inducing a smaller rightward deviation with respect to short words stressed on the penultimate final sequence. In conclusion, partly different mechanisms, including both visuo-spatial and lexical factors, may support

  17. Organophosphates induce distal axonal damage, but not brain oedema, by inactivating neuropathy target esterase

    International Nuclear Information System (INIS)

    Single doses of organophosphorus compounds (OP) which covalently inhibit neuropathy target esterase (NTE) can induce lower-limb paralysis and distal damage in long nerve axons. Clinical signs of neuropathy are evident 3 weeks post-OP dose in humans, cats and chickens. By contrast, clinical neuropathy in mice following acute dosing with OPs or any other toxic compound has never been reported. Moreover, dosing mice with ethyloctylphosphonofluoridate (EOPF) - an extremely potent NTE inhibitor - causes a different (subacute) neurotoxicity with brain oedema. These observations have raised the possibility that mice are intrinsically resistant to neuropathies induced by acute toxic insult, but may incur brain oedema, rather than distal axonal damage, when NTE is inactivated. Here we provide the first report that hind-limb dysfunction and extensive axonal damage can occur in mice 3 weeks after acute dosing with a toxic compound, bromophenylacetylurea. Three weeks after acutely dosing mice with neuropathic OPs no clinical signs were observed, but distal lesions were present in the longest spinal sensory axons. Similar lesions were evident in undosed nestin-cre:NTEfl/fl mice in which NTE had been genetically-deleted from neural tissue. The extent of OP-induced axonal damage in mice was related to the duration of NTE inactivation and, as reported in chickens, was promoted by post-dosing with phenylmethanesulfonylfluoride. However, phenyldipentylphosphinate, another promoting compound in chickens, itself induced in mice lesions different from the neuropathic OP type. Finally, EOPF induced subacute neurotoxicity with brain oedema in both wild-type and nestin-cre:NTEfl/fl mice indicating that the molecular target for this effect is not neural NTE.

  18. Uptake of radiolabeled ions in normal and ischemia-damaged brain

    Energy Technology Data Exchange (ETDEWEB)

    Dienel, G.A.; Pulsinelli, W.A.

    1986-05-01

    The regional concentrations of nine radiochemicals were measured in rat brain after induction of cerebral ischemia to identify tracers concentrated by brain undergoing selective neuronal necrosis. Transient (30 minute) forebrain ischemia was produced in the rat; 24 hours after cerebral recirculation the radiochemicals were injected intravenously and allowed to circulate for 5 hours. The brain concentrations of the radiochemicals in dissected regions were determined by scintillation counting. Forebrain ischemia of this nature will produce extensive injury to striatal neurons but will spare the great majority of neocortical neurons at 24 hours. The regional concentrations of these radiochemicals varied considerably in both control and ischemic animals. In postischemic animals, 4 radionuclides (/sup 63/Ni, /sup 99/TcO/sub 4/, /sup 22/Na, and (/sup 3/H)tetracycline) were concentrated in the irreversibly damaged striatum in amounts ranging from 1.4 to 2.4 times greater than in normal tissue. The concentrations of /sup 65/Zn, /sup 59/Fe, /sup 32/PO/sub 4/, and /sup 147/Pm in postischemic brain were similar to or less than those in normal brain. The concentration of (14C)EDTA was increased in injured and uninjured brain of postischemic rats. Autoradiographic analysis of the distribution patterns of some of these ions in normal animals showed that /sup 99/TcO/sub 4/, /sup 22/Na, /sup 65/Zn, and /sup 59/Fe were distributed more uniformly throughout the brain than were /sup 32/PO/sub 4/, /sup 63/Ni, and /sup 147/Pm. At 24 or 48 hours after ischemia, /sup 63/Ni, /sup 99/TcO/sub 4/, and /sup 22/Na were preferentially concentrated in the damaged striatum and hippocampus, whereas /sup 65/Zn, /sup 59/Fe, /sup 32/PO/sub 4/, and /sup 147/Pm did not accumulate in irreversibly injured tissue. Of the radiochemicals tested to date, Ni, TcO/sub 4/, and tetracycline may be useful for diagnosing ischemic brain injury in humans, using positron emission tomography.

  19. Brain-peripheral cell crosstalk in white matter damage and repair.

    Science.gov (United States)

    Hayakawa, Kazuhide; Lo, Eng H

    2016-05-01

    White matter damage is an important part of cerebrovascular disease and may be a significant contributing factor in vascular mechanisms of cognitive dysfunction and dementia. It is well accepted that white matter homeostasis involves multifactorial interactions between all cells in the axon-glia-vascular unit. But more recently, it has been proposed that beyond cell-cell signaling within the brain per se, dynamic crosstalk between brain and systemic responses such as circulating immune cells and stem/progenitor cells may also be important. In this review, we explore the hypothesis that peripheral cells contribute to damage and repair after white matter damage. Depending on timing, phenotype and context, monocyte/macrophage can possess both detrimental and beneficial effects on oligodendrogenesis and white matter remodeling. Endothelial progenitor cells (EPCs) can be activated after CNS injury and the response may also influence white matter repair process. These emerging findings support the hypothesis that peripheral-derived cells can be both detrimental or beneficial in white matter pathology in cerebrovascular disease. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia, edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock. PMID:26277436

  20. The Relationship between Localized Brain Damage and Agraphia%脑不同部位损害与失写症

    Institute of Scientific and Technical Information of China (English)

    谢秋幼; 孙红宇; 刘晓加

    2001-01-01

    Writing behavior is affected by many factors and depends on the functional integrity of the nervous system. Its neuropsychological mechanism remains unknown. The agraphic features involving different parts of brain damage are dissimilar. The neuroanatomic location of agraphia and its possible brain mechanism are reviewed.

  1. Implications of astrocytes in mediating the protective effects of Selective Estrogen Receptor Modulators upon brain damage

    Directory of Open Access Journals (Sweden)

    George E. Barreto

    2015-04-01

    Full Text Available Selective Estrogen Receptor Modulators (SERMs are steroidal or non-steroidal compounds that are already used in clinical practice for the treatment of breast cancer, osteoporosis and menopausal symptoms. While SERMs actions in the breast, bone, and uterus have been well characterized, their actions in the brain are less well understood. Previous works have demonstrated the beneficial effects of SERMs in different chronic neurodegenerative diseases like Alzheimer, Parkinson’s disease and Multiple sclerosis, as well as acute degeneration as stroke and traumatic brain injury. Moreover, these compounds exhibit similar protective actions as those of estradiol in the Central Nervous System, overt any secondary effect. For these reasons, in the past few years, there has been a growing interest in the neuroprotective effects exerted directly or indirectly by SERMs in the SNC. In this context, astrocytes play an important role in the maintenance of brain metabolism, and antioxidant support to neurons, thus indicating that better protection of astrocytes are an important asset targeting neuronal protection. Moreover, various clinical and experimental studies have reported that astrocytes are essential for the neuroprotective effects of SERMs during neuronal injuries, as these cells express different estrogen receptors in cell membrane, demonstrating that part of SERMs effects upon injury may be mediated by astrocytes. The present work highlights the current evidence on the protective mechanisms of SERMs, such as tamoxifen and raloxifene, in the SNC, and their modulation of astrocytic properties as promising therapeutic targets during brain damage.

  2. Salvia officinalis l. (sage) Ameliorates Radiation-Induced Oxidative Brain Damage In Rats

    International Nuclear Information System (INIS)

    The present study was designed to investigate the oxidative stress and the role of antioxidant system in the management of gamma irradiation induced whole brain damage in rats . Also, to elucidate the potential role of Salvia officinalis (sage) in alleviating such negative effects. Rats were subjected to gamma radiation (6 Gy). Sage extract was daily given to rats during 14 days before starting irradiation and continued after radiation exposure for another 14 days. The results revealed that the levels of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC) and nitric oxide (NO) content were significantly increased, while the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the reduced glutathione (GSH) content were significantly decreased in the brain homogenate of irradiated rats. Additionally, brain acetylcholinesterase (AChE) as well as alkaline phosphatase (ALP), acid phosphatase (ACP) and lactate dehydrogenase (LDH) activities were significantly increased. On the other hand, the results showed that, administration of sage extract to rats was able to ameliorate the mentioned parameters and the values returned close to the normal ones. It could be concluded that sage extract, by its antioxidant constituents, could modulate radiation induced oxidative stress and enzyme activities in the brain.

  3. Brain damage associated with apraxia of speech: evidence from case studies.

    Science.gov (United States)

    Moser, Dana; Basilakos, Alexandra; Fillmore, Paul; Fridriksson, Julius

    2016-08-01

    The site of crucial damage that causes acquired apraxia of speech (AOS) has been debated in the literature. This study presents five in-depth cases that offer insight into the role of brain areas involved in AOS. Four of the examined participants had a primary impairment of AOS either with (n = 2) or without concomitant mild aphasia (n = 2). The fifth participant presented with a lesion relatively isolated to the left anterior insula (AIns-L), damage that is rarely reported in the literature, but without AOS. Taken together, these cases challenge the role of the AIns-L and implicate the left motor regions in AOS. PMID:27264534

  4. Emotional Processing following Cortical and Subcortical Brain Damage: Contribution of the Fronto-Striatal Circuitry

    Directory of Open Access Journals (Sweden)

    Caterina Breitenstein

    1998-01-01

    Full Text Available The present study examined the differential contribution of cortical and subcortical brain structures in emotional processing by comparing patients with focal cortical lesions (n = 32 to those with primarily subcortical dysregulation of the basal ganglia (Parkinson’s disease n = 14. A standardized measure of emotional perception (Tübingen Affect Battery was used. Only patients in the more advanced stages of Parkinson’s disease and patients with focal damage to the (right frontal lobe differed significantly from controls in both facial expression and affective prosody recognition. The findings imply involvement of the fronto-striatal circuitry in emotional processing.

  5. Candesartan and glycyrrhizin ameliorate ischemic brain damage through downregulation of the TLR signaling cascade.

    Science.gov (United States)

    Barakat, Waleed; Safwet, Nancy; El-Maraghy, Nabila N; Zakaria, Mohamed N M

    2014-02-01

    Stroke is the second leading cause of death in industrialized countries and the most frequent cause of permanent disability in adults worldwide. The final outcome of stroke is determined not only by the volume of the ischemic core, but also by the extent of secondary brain damage inflicted to penumbral tissues by brain swelling, impaired microcirculation, and inflammation. The only drug approved for the treatment ischemic stroke is recombinant tissue plasminogen activator (rt-PA). The current study was designed to investigate the protective effects of candesartan (0.15 mg/kg, orally) and glycyrrhizin (30 mg/kg, orally) experimentally-induced ischemic brain damage in C57BL/6 mice (middle cerebral artery occlusion, MCAO) in comparison to the effects of a standard neuroprotective drug (cerebrolysin, 7.5 mg/kg, IP). All drugs were administered 30 min before and 24h after MCAO. Both candesartan and glycyrrhizin ameliorated the deleterious effects of MCAO as indicated by the improvement in the performance of the animals in behaviour tests, reduction in brain infarction, neuronal degeneration, and leukocyte infiltration. In addition, MCAO induced a significant upregulation in the different elements of the TLR pathway including TLR-2 and TLR-4, Myd88, TRIF and IRF-3 and the downstream effectors TNF-α, IL-1β, IL-6 and NF-kB. All these changes were significantly ameliorated by treatment with candesartan and glycyrrhizin. The results of the current study represent a new indication for both candesartan and glycyrrhizin in the management of ischemic stroke with effects comparable to those of the standard neuroprotective drug cerebrolysin.

  6. Candesartan and glycyrrhizin ameliorate ischemic brain damage through downregulation of the TLR signaling cascade.

    Science.gov (United States)

    Barakat, Waleed; Safwet, Nancy; El-Maraghy, Nabila N; Zakaria, Mohamed N M

    2014-02-01

    Stroke is the second leading cause of death in industrialized countries and the most frequent cause of permanent disability in adults worldwide. The final outcome of stroke is determined not only by the volume of the ischemic core, but also by the extent of secondary brain damage inflicted to penumbral tissues by brain swelling, impaired microcirculation, and inflammation. The only drug approved for the treatment ischemic stroke is recombinant tissue plasminogen activator (rt-PA). The current study was designed to investigate the protective effects of candesartan (0.15 mg/kg, orally) and glycyrrhizin (30 mg/kg, orally) experimentally-induced ischemic brain damage in C57BL/6 mice (middle cerebral artery occlusion, MCAO) in comparison to the effects of a standard neuroprotective drug (cerebrolysin, 7.5 mg/kg, IP). All drugs were administered 30 min before and 24h after MCAO. Both candesartan and glycyrrhizin ameliorated the deleterious effects of MCAO as indicated by the improvement in the performance of the animals in behaviour tests, reduction in brain infarction, neuronal degeneration, and leukocyte infiltration. In addition, MCAO induced a significant upregulation in the different elements of the TLR pathway including TLR-2 and TLR-4, Myd88, TRIF and IRF-3 and the downstream effectors TNF-α, IL-1β, IL-6 and NF-kB. All these changes were significantly ameliorated by treatment with candesartan and glycyrrhizin. The results of the current study represent a new indication for both candesartan and glycyrrhizin in the management of ischemic stroke with effects comparable to those of the standard neuroprotective drug cerebrolysin. PMID:24378346

  7. Are Himalayan Sherpas better protected against brain damage associated with extreme altitude climbs?

    Science.gov (United States)

    Garrido, E; Segura, R; Capdevila, A; Pujol, J; Javierre, C; Ventura, J L

    1996-01-01

    1. The potential risk of brain damage when low-landers attempt to climb the highest summits is a well-known fact. However, very little is known about what occurs to Himalayan natives, perfectly adapted to high altitude, when performing the same type of activity. 2. Taking into account their long-life climbing experience at extreme altitudes, we examined seven of the most recognized Sherpas with the aim of performing a comprehensive neurological evaluation based on medical history, physical examination and magnetic resonance brain imaging. We compared them with one group of 21 lowland elite climbers who had ascended to altitudes of over 8000 m, and another control group of 21 healthy individuals who had never been exposed to high altitude. 3. While all of the lowland climbers presented psychoneurological symptoms during or after the expeditions, and 13 of them (61%) showed magnetic resonance abnormalities (signs of mild cortical atrophy and/or periventricular high-intensity signal areas in the white matter), only one Sherpa (14%) showed similar changes in the scans, presenting neurological symptoms at extreme altitude. The neurological examination was normal in all three groups, and no neuroimaging abnormalities were detected in the control group. 4. The significant differences, in both clinical and neuroimaging terms, suggest that Sherpa highlanders have better brain protection when exposed to extreme altitude. Although the key to protection against cerebral hypoxia cannot be established, it is possible that an increase in the usually short period of acclimatization could minimize brain damage in those low-landers who attempt the highest summits without supplementary oxygen. PMID:8697710

  8. Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

    Directory of Open Access Journals (Sweden)

    S.S. Frassetto

    1999-10-01

    Full Text Available Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10-min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min, followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the

  9. Prevalence, and Intellectual Outcome of Unilateral Focal Cortical Brain Damage as a Function of Age, Sex and Aetiology

    Directory of Open Access Journals (Sweden)

    C. M. J. Braun

    2002-01-01

    Full Text Available Neurologists and neuropsychologists are aware that aging men are more at risk than women for brain damage, principally because of the well known male-predominant risk for cardiovascular disease and related cerebrovascular accidents. However, a disproportion in prevalence of brain damage between the sexes in childhood may be less suspected. Furthermore, sex-specific risk for other aetiologies of brain damage may be little known, whether in the pediatric or adult populations. Proposals of a sex difference in cognitive recovery from brain damage have also been controversial. Six hundred and thirty five “consecutive” cases with cortical focal lesions including cases of all ages and both sexes were reviewed. Aetiology of the lesion was determined for each case as was postlesion IQ. Risk was highly male prevalent in all age groups, with a predominance of cardiovascular aetiology explaining much of the adult male prevalence. However, several other aetiological categories were significantly male prevalent in juveniles (mitotic, traumatic, dysplasic and adults (mitotic, traumatic. There was no sex difference in outcome (i.e., postlesion IQ of these cortical brain lesions for the cohort as a whole, after statistical removal of the influence of lesion extent, aetiology and presence of epilepsy. Mechanisms potentially responsible for sex differences in prevalence, aetiology of brain damage, and recovery, are reviewed and discussed.

  10. Antimicrobial peptides and complement in neonatal hypoxia-ischemia induced brain damage

    Directory of Open Access Journals (Sweden)

    Eridan eRocha-Ferreira

    2015-02-01

    subsequent brain damage.

  11. [The clinical study of the first febrile convulsion in children with brain-damage].

    Science.gov (United States)

    Asoh, M

    1997-05-01

    Forty-nine patients with cerebral palsy, mental retardation, or other congenital neurological disorders who had experienced febrile convulsions and had no previous nonfebrile seizures were presented. They were followed for 1.6 years to 15 years (mean: 6.8 years) after the initial febrile convulsion. The incidence of subsequent epilepsy (two or more afebrile seizures) was 39%, and 80% of them developed epilepsy within 2 years after the first febrile convulsion. The paroxysmal discharges on EEG recorded prior to or after the first febrile convulsion did not predict the occurrence of later epilepsy. Also under 3 years of age, EEG findings led to the same result. There was no definite evidence that administration of anticonvulsive drugs prevented later epilepsy. Pre-existing neurological abnormality was identified as a risk factor for epilepsy, and was an indication of persistent medication. There is no clear prophylactic procedure against long-lasting attacks. Accordingly, medical therapy can be started when epilepsy has developed. Patients with very severe brain damage who could not move except lying comprised only 6% of all cases, and 69% of the epilepsy patients were well controlled. They showed a good prognosis as compared with children with brain-damage in general with epilepsy. PMID:9146028

  12. Piano training in youths with hand motor impairments after damage to the developing brain.

    Science.gov (United States)

    Lampe, Renée; Thienel, Anna; Mitternacht, Jürgen; Blumenstein, Tobias; Turova, Varvara; Alves-Pinto, Ana

    2015-01-01

    Damage to the developing brain may lead to impairment of the hand motor function and negatively impact on patients' quality of life. Development of manual dexterity and finger and hand motor function may be promoted by learning to play the piano. The latter brings together music with the intensive training of hand coordination and fine finger mobility. We investigated if learning to play the piano helped to improve hand motor skills in 18 youths with hand motor disorders resulting from damage during early brain development. Participants trained 35-40 minutes twice a week for 18 months with a professional piano teacher. With the use of a Musical Instrument Digital Interface piano, the uniformity of finger strokes could be objectively assessed from the timing of keystrokes. The analysis showed a significant improvement in the uniformity of keystrokes during the training. Furthermore, the youths showed strong motivation and engagement during the study. This is nevertheless an open study, and further studies remain needed to exclude effects of growth and concomitant therapies on the improvements observed and clarify which patients will more likely benefit from learning to play the piano. PMID:26345312

  13. Dimensions of personality disturbance after focal brain damage: investigation with the Iowa Scales of Personality Change.

    Science.gov (United States)

    Barrash, Joseph; Asp, Erik; Markon, Kristian; Manzel, Kenneth; Anderson, Steven W; Tranel, Daniel

    2011-10-01

    This study employed a multistep, rational-empirical approach to identify dimensions of personality disturbance in brain-damaged individuals: (a) Five dimensions were hypothesized based on empirical literature and conceptual grounds; (b) principal components analysis was performed on the Iowa Scales of Personality Change (ISPC) to determine the pattern of covariance among 30 personality characteristics; (c) when discrepancies existed between principal components analysis results and conceptually based dimensions, empirical findings and clinical considerations were weighed to determine assignment of ISPC scales to dimensions; (d) the fit of data to the refined dimensions was assessed by examination of intercorrelations; (e) differential predictions concerning the relationship of dimensions to ventromedial prefrontal cortex (vmPFC) damage were tested. This process resulted in the specification of five dimensions: Disturbed Social Behavior, Executive/Decision-Making Deficits, Diminished Motivation/Hypo-Emotionality, Irascibility, and Distress. In accord with predictions, the 28 participants with vmPFC lesions, compared to 96 participants with focal lesions elsewhere in the brain, had significantly more Disturbed Social Behavior and Executive/Decision-Making Deficits and tended to have more Diminished Motivation/Hypo-Emotionality. Irascibility was not significantly higher among the vmPFC group, and the groups had very similar levels of Distress. The findings indicate that conceptually distinctive dimensions with differential relationships to vmPFC can be derived from the Iowa Scales of Personality Change. PMID:21500116

  14. Piano training in youths with hand motor impairments after damage to the developing brain.

    Science.gov (United States)

    Lampe, Renée; Thienel, Anna; Mitternacht, Jürgen; Blumenstein, Tobias; Turova, Varvara; Alves-Pinto, Ana

    2015-01-01

    Damage to the developing brain may lead to impairment of the hand motor function and negatively impact on patients' quality of life. Development of manual dexterity and finger and hand motor function may be promoted by learning to play the piano. The latter brings together music with the intensive training of hand coordination and fine finger mobility. We investigated if learning to play the piano helped to improve hand motor skills in 18 youths with hand motor disorders resulting from damage during early brain development. Participants trained 35-40 minutes twice a week for 18 months with a professional piano teacher. With the use of a Musical Instrument Digital Interface piano, the uniformity of finger strokes could be objectively assessed from the timing of keystrokes. The analysis showed a significant improvement in the uniformity of keystrokes during the training. Furthermore, the youths showed strong motivation and engagement during the study. This is nevertheless an open study, and further studies remain needed to exclude effects of growth and concomitant therapies on the improvements observed and clarify which patients will more likely benefit from learning to play the piano.

  15. Vulnerability of premyelinating oligodendrocytes to white-matter damage in neonatal brain injury

    Institute of Scientific and Technical Information of China (English)

    Xiao-Bo Liu; Yan Shen; Jennifer M.Plane; Wenbin Deng

    2013-01-01

    Premature birth is a significant economic and public health burden,and its incidence is rising.Periventricular leukomalacia (PVL) is the predominant form of brain injury in premature infants and the leading cause of cerebral palsy.PVL is characterized by selective white-matter damage with prominent oligodendroglial injury.The maturation-dependent vulnerability of developing and premyelinating oligodendrocytes to excitotoxic,oxidative,and inflammatory forms of injury is a major factor in the pathogenesis of PVL.Recent studies using mouse models of PVL reveal that synapses between axons and developing oligodendrocytes are quickly and profoundly damaged in immature white matter.Axon-glia synapses are highly vulnerable to white-matter injury in the developing brain,and the loss of synapses between axons and premyelinating oligodendrocytes occurs before any cellular loss in the immature white matter.Microglial activation and astrogliosis play important roles in triggering white-matter injury.Impairment of white-matter development and function in the neonatal period contributes critically to functional and behavioral deficits.Preservation of the integrity of the white matter is likely key in the treatment of PVL and subsequent neurological consequences and disabilities.

  16. Assessment of hand after brain damage with the aim of functional surgery.

    Science.gov (United States)

    Romain, M; Benaim, C; Allieu, Y; Pelissier, J; Chammas, M

    1999-01-01

    The semiology of the hand after brain damage is really rich. Its clinical evaluation remains quite difficult and must be integrated in the neuro-orthopedic and cognitive context. Deficiency, neuropsychological, analytic and functional status, must be assessed before any surgical decision aiming the improvement of prehension. Neuropsychological evaluation precise the hemispheric specialization: right hemisphere lesions conduct to unilateral spatial neglect while left hemispherical lesions determine language troubles and gesture impairment (apraxia). The analytical evaluation describes motor and sensitive function and assesses spasticity and pain. Concerning the functional assessment, the Enjalbert's score seems to be the most adapted to the upper limb. The assessment of hand deficiency and its origin is necessary to orientate the surgical decision and includes the Zancolli classification for the fingers and wrist and the House classification for the thumb. These classification used for cerebral palsy seems to be insufficient for all the different situations occurring after brain damage. A new classification is proposed based on 3 parameters: fingers extension, thumb abduction and supination. Surgical decision should be examined only after an adapted rehabilitation program.

  17. Effect of propentofylline on hypoxic-ischaemic brain damage in newborn rat

    Institute of Scientific and Technical Information of China (English)

    XIA Xiao-yan 夏晓艳; SAMESHIMA Hiroshi 鲛岛浩; OTA Arturo 大田Arturo; XIA Yi-xin 夏义欣; IKENOUE Tsuyomu 池ノ上克; TOSHIMORI Kiyotaka 年森清隆; HUANG Xing-hua 黄醒华

    2004-01-01

    Background Studies showed that propentofylline enhances the action of adenosine and protects hippocampal neuronal demage against transient global cerebral ischaemia. Our study was to investigate the effect of propentofylline on hypoxic-ischaemic brain damage in neonatal rat.Methods Seven-day-old Wistar rats were subjected to unilateral common carotid artery ligation and hypoxia in oxygen 8 kPa for two hours at 37℃. Propentofylline (10 mg/kg) was administered intraperitoneally one hour after hypoxia-ischaemia (treated group). Control group rats were received an equivalent volume of saline. The effects of propentofylline were assessed by observing the body mass gain, behavioural alteration and neurohistological changes. The rats were sacrificed at 72 hours after hypoxia-ischaemia, and the brain sections were examined after haematoxylin and eosin staining.Results The propentofylline-treated rats had better body mass gain and better behavioural response than the paired saline-controls did. In the control group, the rats either lost body mass or had little mass gain after the insult, their average body mass gain was 97.3% at 24 h, 100.3% at 48 h, and 114.1% at 72 h of recovery. In propentofylline-treated group, there was a significant improvement of body mass gain at 24 h (100.2%, P<0.05) and 48 h (110.3%, P<0.01) of recovery; the percentage of rats that performed well on behavioural test was significantly higher from 48 h to 72 h of recovery (P<0.05); the incidence of severe brain damage to the cerebral cortex and dentate gyrus was significantly reduced in propentofylline-treated rats (cortex, 93%-70.8%, P<0.01; dentate gyrus 95%-66.7%, P<0.01) as compared with control rats. Conclusions Administration of propentofylline 1 hour after hypoxia-ischaemia significantly attenuates brain damage in both the cerebral cortex and dentate gyrus, and also improves the body mass gain as well as behavioural disturbance in 7-day-old rats.

  18. Pathological and MRI study on experimental heroin-induced brain damage in rats

    International Nuclear Information System (INIS)

    Objective: To study the pathological characteristics of the heroin-induced brain damage in rats, and to assess the diagnostic value of MRI. Methods: A total of 40 adult Wistar rats were studied, 32 rats were used for injecting heroin as heroin group and 8 were used for injecting saline as control group. The heroin dependent rat model was established by administering heroin (ip) in the ascending dosage schedule (0.5 mg/kg), three times a day (at 8:00, 12:00, and 18:00). The control group was established by the same way by injection with saline. The withdrawal scores were evaluated with imp roved criterion in order to estimate the degree of addiction after administering naloxone. Based on the rat model of heroin dependence, the rat model of heroin-induced brain damage was established by the same way with increasing heroin dosage everyday. Two groups were examined by using MRI, light microscope, and electron microscope, respectively in different heroin accumulated dosage (918, 1580, 2686, 3064, 4336, and 4336 mg/kg withdrawal after 2 weeks). Results: There was statistically significant difference (t=9.737, P<0.01) of the withdrawal scores between the heroin dependent group and the saline group (23.0 ± 4.4 and 1.4 ± 0.5, respectively). It suggested that the heroin dependent rat model be established successfully. In different accumulated dosage ( from 1580 mg/kg to 4336 mg/kg), there were degeneration and death of nerve cells in cerebrum and cerebellum of heroin intoxicated rats, and it suggested that the rat model of heroin-induced brain damage was established successfully. The light microscope and electron microscope features of heroin-induced brain damage in rats included: (1) The nerve cells of cerebral cortex degenerated and died. According to the heroin accumulated dosage, there were statistically significant difference of the nerve cell deaths between 4336 mg/kg group and 1580 mg/kg group or control group (P=0.024 and P=0.032, respectively); (2) The main

  19. Moringa Oleifera Lam Mitigates Oxidative Damage and Brain Infarct Volume in Focal Cerebral Ischemia

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    Woranan Kirisattayakul

    2012-01-01

    Full Text Available Problem statement: At present, the therapeutic outcome of cerebral ischemia is still not in the satisfaction level. Therefore, the preventive strategy is considered. Based on the protective effect against oxidative damage of Moringa oleifera Lam. Leaves extract, we hypothesized that this plant extract might protect against cerebral ischemia, one of the challenge problems nowadays. In order to test this hypothesis, we aimed to determine the protective effect of M.oleifera leaves extract in animal model of focal cerebral ischemia induced by permanent occlusion of right middle cerebral artery. Approach: Male Wistar rats, weighing 300-350 g, were orally given the extract once daily at doses of 100, 200 and 400 mg kg-1 BW at a period of 2 weeks, then, they were permanently occluded the right Middle Cerebral Artery (MCAO. The animals were assessed the cerebral infarction volume and oxidative damage markers including MDA level and the activities of SOD, CAT and GSHPx enzymes at 24 h after occlusion. Results: Rats subjected to M.oleifera extract at all doses used in this study significantly decreased brain infarct volume both at cortical and subcortical structures in accompany with the elevation of SOD activity in both hippocampus and striatum while only the rats exposed to the extract at doses of 100 and 400 mg kg-1 BW showed the increased GSHPx activity in hippocampus. No the changes were observed. Therefore, our results demonstrates the potential benefit of M.oleifera leaves to decrease oxidative stress damage and brain infarct volume. Conclusion: This study is the first study to demonstrate the neuroprotective effect against focal cerebral ischemia of M.oleifera leaves. It suggests that M.oleifera may be served as natural resource for developing neuroprotectant against focal cerebral ischemia. However, the precise underlying mechanism and possible active ingredient are still required further study.

  20. Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury.

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    Quan-Guang Zhang

    Full Text Available BACKGROUND: Oxidative stress is known to play an important role in the pathology of traumatic brain injury. Mitochondria are thought to be the major source of the damaging reactive oxygen species (ROS following TBI. However, recent work has revealed that the membrane, via the enzyme NADPH oxidase can also generate the superoxide radical (O(2(-, and thereby potentially contribute to the oxidative stress following TBI. The current study thus addressed the potential role of NADPH oxidase in TBI. METHODOLOGY/PRINCIPAL FINDINGS: The results revealed that NADPH oxidase activity in the cerebral cortex and hippocampal CA1 region increases rapidly following controlled cortical impact in male mice, with an early peak at 1 h, followed by a secondary peak from 24-96 h after TBI. In situ localization using oxidized hydroethidine and the neuronal marker, NeuN, revealed that the O(2(- induction occurred in neurons at 1 h after TBI. Pre- or post-treatment with the NADPH oxidase inhibitor, apocynin markedly inhibited microglial activation and oxidative stress damage. Apocynin also attenuated TBI-induction of the Alzheimer's disease proteins β-amyloid and amyloid precursor protein. Finally, both pre- and post-treatment of apocynin was also shown to induce significant neuroprotection against TBI. In addition, a NOX2-specific inhibitor, gp91ds-tat was also shown to exert neuroprotection against TBI. CONCLUSIONS/SIGNIFICANCE: As a whole, the study demonstrates that NADPH oxidase activity and superoxide production exhibit a biphasic elevation in the hippocampus and cortex following TBI, which contributes significantly to the pathology of TBI via mediation of oxidative stress damage, microglial activation, and AD protein induction in the brain following TBI.

  1. Low intensity microwave radiation induced oxidative stress, inflammatory response and DNA damage in rat brain.

    Science.gov (United States)

    Megha, Kanu; Deshmukh, Pravin Suryakantrao; Banerjee, Basu Dev; Tripathi, Ashok Kumar; Ahmed, Rafat; Abegaonkar, Mahesh Pandurang

    2015-12-01

    Over the past decade people have been constantly exposed to microwave radiation mainly from wireless communication devices used in day to day life. Therefore, the concerns over potential adverse effects of microwave radiation on human health are increasing. Until now no study has been proposed to investigate the underlying causes of genotoxic effects induced by low intensity microwave exposure. Thus, the present study was undertaken to determine the influence of low intensity microwave radiation on oxidative stress, inflammatory response and DNA damage in rat brain. The study was carried out on 24 male Fischer 344 rats, randomly divided into four groups (n=6 in each group): group I consisted of sham exposed (control) rats, group II-IV consisted of rats exposed to microwave radiation at frequencies 900, 1800 and 2450 MHz, specific absorption rates (SARs) 0.59, 0.58 and 0.66 mW/kg, respectively in gigahertz transverse electromagnetic (GTEM) cell for 60 days (2h/day, 5 days/week). Rats were sacrificed and decapitated to isolate hippocampus at the end of the exposure duration. Low intensity microwave exposure resulted in a frequency dependent significant increase in oxidative stress markers viz. malondialdehyde (MDA), protein carbonyl (PCO) and catalase (CAT) in microwave exposed groups in comparison to sham exposed group (pmicrowave exposed groups (pmicrowave exposed animal (pmicrowave exposed groups as compared to their corresponding values in sham exposed group (pmicrowave radiation induces oxidative stress, inflammatory response and DNA damage in brain by exerting a frequency dependent effect. The study also indicates that increased oxidative stress and inflammatory response might be the factors involved in DNA damage following low intensity microwave exposure.

  2. Intrauterine infection and neonatal brain damage%宫内感染与新生儿脑损伤

    Institute of Scientific and Technical Information of China (English)

    石晶; 母得志

    2015-01-01

    宫内感染是导致新生儿脑损伤及神经系统功能障碍的重要危险因素。病毒、细菌和原虫可感染子宫腔并导致胎儿和新生儿脑损伤。炎症反应是宫内感染致新生儿脑损伤的重要致病因素,不同孕期宫内感染导致不同类型脑损害。临床医师应重视孕期宫内感染的预防,有必要进一步加强临床和基础研究,探索宫内感染致新生儿脑损伤的有效干预措施。%Intrauterine infection is an important risk factor for neonatal brain damage and neurological dysfunction. Viruses, bacteria, and protozoa can cause intrauterine infection which results in neonatal brain damage. The inlfammatory response is an important pathogenic factor for neonatal brain damage caused by intrauterine infection. Intrauterine infection in different periods of pregnancy might cause different types of brain damage in neonates. Clinicians should pay attention to the prevention of intrauterine infection during pregnancy. It is necessary to further strengthen the clinical and basic research to explore effective interventions for neonatal brain damage caused by intrauterine infection.

  3. Coefficient of variation of R-R intervals in severe brain damage.

    Science.gov (United States)

    Nezu, A; Kimura, S; Kobayashi, T; Osaka, H; Uehara, S

    1996-01-01

    The coefficient of variation of R-R intervals (CVRR) was studied in 18 children having severe brain damage with a mean +/- standard deviation (s.d.) age of 8.4 +/- 5.9 years, who were divided into ten patients complicated with respiratory insufficiency (RI group) and eight patients with severe athetotic cerebral palsy (SA group). CVRR was obtained in the resting supine position, and was compared with that in 22 neurologically normal controls. CVRR in the RI group (mean +/- S.D., 2.19 +/- 1.28%) was significantly lower than that in controls (5.56 +/- 1.53%), while CVRR in the SA group (11.30 +/- 3.91%) was significantly higher than that in controls (both P < 0.01, ANOVA). In particular, the four patients with brain death showed extremely low CVRR of 1.00-1.29%. Since CVRR was 4.09% in the patient aged 4 years with birth injury of the upper cervical spinal cord causing absence of spontaneous respiration, the extremely low CVRR in patients with brain death may be directly related to brainstem dysfunction. The cause of the high CVRR in the SA group was not determined. Thus, CVRR may be useful for quantitative evaluation of severe neurological disorder.

  4. Microcavitation as a Neuronal Damage Mechanism in Blast Traumatic Brain Injury

    Science.gov (United States)

    Franck, Christian; Estrada, Jonathan

    2015-11-01

    Blast traumatic brain injury (bTBI) is a leading cause of injury in the armed forces. Diffuse axonal injury, the hallmark feature of blunt TBI, has been investigated in direct mechanical loading conditions. However, recent evidence suggests inertial cavitation as a possible bTBI mechanism, particularly in the case of exposure to blasts. Cavitation damage to free surfaces has been well-studied, but bubble interactions within confined 3D environments, in particular their stress and strain signatures are not well understood. The structural damage due to cavitation in living tissues - particularly at the cellular level - are incompletely understood, in part due to the rapid bubble formation and deformation strain rates of up to ~ 105-106 s-1. This project aims to characterize material damage in 2D and 3D cell culture environments by utilizing a novel high-speed red-blue diffraction assisted image correlation method at speeds of up to 106 frames per second. We gratefully acknowledge funding from the Office of Naval Research (POC: Dr. Tim Bentley).

  5. Through metal binding, curcumin protects against lead- and cadmium-induced lipid peroxidation in rat brain homogenates and against lead-induced tissue damage in rat brain.

    Science.gov (United States)

    Daniel, Sheril; Limson, Janice L; Dairam, Amichand; Watkins, Gareth M; Daya, Santy

    2004-02-01

    Curcumin, the major constituent of turmeric is a known, naturally occurring antioxidant. The present study examined the ability of this compound to protect against lead-induced damage to hippocampal cells of male Wistar rats, as well as lipid peroxidation induced by lead and cadmium in rat brain homogenate. The thiobarbituric assay (TBA) was used to measure the extent of lipid peroxidation induced by lead and cadmium in rat brain homogenate. The results show that curcumin significantly protects against lipid peroxidation induced by both these toxic metals. Coronal brain sections of rats injected intraperitoneally with lead acetate (20 mg/kg) in the presence and absence of curcumin (30 mg/kg) were compared microscopically to determine the extent of lead-induced damage to the cells in the hippocampal CA1 and CA3 regions, and to establish the capacity of curcumin to prevent such damage. Lead-induced damage to the neurons was significantly curtailed in the rats injected with curcumin. Possible chelation of lead and cadmium by curcumin as its mechanism of neuroprotection against such heavy metal insult to the brain was investigated using electrochemical, ultraviolet spectrophotometric and infrared spectroscopic analyses. The results of the study show that there is an interaction between curcumin and both cadmium and lead, with the possible formation of a complex between the metal and this ligand. These results imply that curcumin could be used therapeutically to chelate these toxic metals, thus potentially reducing their neurotoxicity and tissue damage.

  6. Biological Signatures of Brain Damage Associated with High Serum Ferritin Levels in Patients with Acute Ischemic Stroke and Thrombolytic Treatment

    Directory of Open Access Journals (Sweden)

    Mónica Millán

    2008-01-01

    Full Text Available Background and purpose: Increased body iron stores have been related to greater oxidative stress and brain injury in clinical and experimental cerebral ischemia and reperfusion. We aimed to investigate the biological signatures of excitotoxicity, inflammation and blood brain barrier disruption potentially associated with high serum ferritin levels-related damage in acute stroke patients treated with i.v. t-PA.

  7. Biomarkers of Brain Damage and Postoperative Cognitive Disorders in Orthopedic Patients: An Update

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    Dariusz Tomaszewski

    2015-01-01

    Full Text Available The incidence of postoperative cognitive dysfunction (POCD in orthopedic patients varies from 16% to 45%, although it can be as high as 72%. As a consequence, the hospitalization time of patients who developed POCD was longer, the outcome and quality of life were worsened, and prolonged medical and social assistance were necessary. In this review the short description of such biomarkers of brain damage as the S100B protein, NSE, GFAP, Tau protein, metalloproteinases, ubiquitin C terminal hydrolase, microtubule-associated protein, myelin basic protein, α-II spectrin breakdown products, and microRNA was made. The role of thromboembolic material in the development of cognitive decline was also discussed. Special attention was paid to optimization of surgical and anesthetic procedures in the prevention of postoperative cognitive decline.

  8. Arctigenin Treatment Protects Against Brain Damage Through an Anti-inflammatory and Anti-apoptotic Mechanism After Needle Insertion

    OpenAIRE

    Jie Song; Na Li; Xia Yang; Zhong Gao; Liang Kong; Yingjia Yao; Yanan Jiao; Yuhui Yan; Shaoheng Li; Zhenyu Tao; Guan Lian; Jingxian Yang; Tingguo Kang

    2016-01-01

    Convection enhanced delivery (CED) infuses drugs directly into brain tissue. Needle insertion is required and results in a stab wound injury (SWI). Subsequent secondary injury involves the release of inflammatory and apoptotic cytokines, which have dramatic consequences on the integrity of damaged tissue, leading to the evolution of a pericontusional-damaged area minutes to days after in the initial injury. The present study investigated the capacity for arctigenin (ARC) to prevent secondary ...

  9. Arctigenin Treatment Protects against Brain Damage through an Anti-Inflammatory and Anti-Apoptotic Mechanism after Needle Insertion

    OpenAIRE

    Song, Jie; Li, Na; Xia, Yang; Gao, Zhong; Zou, Sa-feng; Kong, Liang; Yao, Ying-Jia; Jiao, Ya-Nan; Yan, Yu-Hui; Li, Shao-Heng; Tao, Zhen-Yu; Lian, Guan; Yang, Jing-xian; Kang, Ting-Guo

    2016-01-01

    Convection enhanced delivery (CED) infuses drugs directly into brain tissue. Needle insertion is required and results in a stab wound injury (SWI). Subsequent secondary injury involves the release of inflammatory and apoptotic cytokines, which have dramatic consequences on the integrity of damaged tissue, leading to the evolution of a pericontusional-damaged area minutes to days after in the initial injury. The present study investigated the capacity for arctigenin (ARC) to prevent secondary ...

  10. Piano training in youths with hand motor impairments after damage to the developing brain

    Directory of Open Access Journals (Sweden)

    Lampe R

    2015-08-01

    Full Text Available Renée Lampe,1,* Anna Thienel,2 Jürgen Mitternacht,1 Tobias Blumenstein,1 Varvara Turova,1 Ana Alves-Pinto1,* 1Research Unit for Paediatric Neuroorthopaedics and Cerebral Palsy, Orthopaedics Department, Klinikum Rechts der Isar, Technische Universität München, 2Department Sonderpädagogik, Ludwig Maximilians-Universität München, Munich, Germany *These authors contributed equally to this work Abstract: Damage to the developing brain may lead to impairment of the hand motor function and negatively impact on patients’ quality of life. Development of manual dexterity and finger and hand motor function may be promoted by learning to play the piano. The latter brings together music with the intensive training of hand coordination and fine finger mobility. We investigated if learning to play the piano helped to improve hand motor skills in 18 youths with hand motor disorders resulting from damage during early brain development. Participants trained 35–40 minutes twice a week for 18 months with a professional piano teacher. With the use of a Musical Instrument Digital Interface piano, the uniformity of finger strokes could be objectively assessed from the timing of keystrokes. The analysis showed a significant improvement in the uniformity of keystrokes during the training. Furthermore, the youths showed strong motivation and engagement during the study. This is nevertheless an open study, and further studies remain needed to exclude effects of growth and concomitant therapies on the improvements observed and clarify which patients will more likely benefit from learning to play the piano. Keywords: manual skill, cerebral palsy, neurodevelopmental disorder, music, rehabilitation

  11. Damage to Myelin and Oligodendrocytes: A Role in Chronic Outcomes Following Traumatic Brain Injury?

    Directory of Open Access Journals (Sweden)

    William L. Maxwell

    2013-09-01

    Full Text Available There is increasing evidence in the experimental and clinical traumatic brain injury (TBI literature that loss of central myelinated nerve fibers continues over the chronic post-traumatic phase after injury. However, the biomechanism(s of continued loss of axons is obscure. Stretch-injury to optic nerve fibers in adult guinea-pigs was used to test the hypothesis that damage to the myelin sheath and oligodendrocytes of the optic nerve fibers may contribute to, or facilitate, the continuance of axonal loss. Myelin dislocations occur within internodal myelin of larger axons within 1–2 h of TBI. The myelin dislocations contain elevated levels of free calcium. The volume of myelin dislocations increase with greater survival and are associated with disruption of the axonal cytoskeleton leading to secondary axotomy. Waves of Ca2+ depolarization or spreading depression extend from the initial locus injury for perhaps hundreds of microns after TBI. As astrocytes and oligodendrocytes are connected via gap junctions, it is hypothesized that spreading depression results in depolarization of central glia, disrupt axonal ionic homeostasis, injure axonal mitochondria and allow the onset of axonal degeneration throughout an increasing volume of brain tissue; and contribute toward post-traumatic continued loss of white matter.

  12. The DNA damage response molecule MCPH1 in brain development and beyond

    Institute of Scientific and Technical Information of China (English)

    Xiaoqian Liu; Zhong-Wei Zhou; Zhao-Qi Wang

    2016-01-01

    Microcephalin (MCPH1) is identified as being responsible for the neurodevelopmental disorder primary microcephaly type 1,which is characterized by a smaller-than-normal brain size and mental retardation.MCPH1 has originally been identified as an important regulator of telomere integrity and of cell cycle control.Genetic and cellular studies show that MCPH1 controls neurogenesis by coordinating the cell cycle and the centrosome cycle and thereby regulating the division mode of neuroprogenitors to prevent the exhaustion of the progenitor pool and thereby microcephaly.In addition to its role in neurogenesis,MCPH1 plays a role in gonad development.MCPH1 also functions as a tumor suppressor in several human cancers as well as in mouse models.Here,we review the role of MCPH1 in DNA damage response,cell cycle control,chromosome condensation and chromatin remodeling.We also summarize the studies on the biological functions of MCPH1 in brain size determination and in pathologies,including infertility and cancer.

  13. Studies on cerebral protection of digoxin against hypoxic-ischemic brain damage in neonatal rats.

    Science.gov (United States)

    Peng, Kaiwei; Tan, Danfeng; He, Miao; Guo, Dandan; Huang, Juan; Wang, Xia; Liu, Chentao; Zheng, Xiangrong

    2016-08-17

    Hypoxic-ischemic brain damage (HIBD) is a major cause of neonatal acute deaths and chronic nervous system damage. Our present study was designed to investigate the possible neuroprotective effect of digoxin-induced pharmacological preconditioning after hypoxia-ischemia and underlying mechanisms. Neonatal rats were assigned randomly to control, HIBD, or HIBD+digoxin groups. Pharmacological preconditioning was induced by administration of digoxin 72 h before inducing HIBD by carotid occlusion+hypoxia. Behavioral assays, and neuropathological and apoptotic assessments were performed to examine the effects; the expression of Na/K ATPase was also assessed. Rats in the HIBD group showed deficiencies on the T-maze, radial water maze, and postural reflex tests, whereas the HIBD+digoxin group showed significant improvements on all behavioral tests. The rats treated with digoxin showed recovery of pathological conditions, increased number of neural cells and proliferative cells, and decreased number of apoptotic cells. Meanwhile, an increased expression level of Na/K ATPase was observed after digoxin preconditioning treatment. The preconditioning treatment of digoxin contributed toward an improved functional recovery and exerted a marked neuroprotective effect including promotion of cell proliferation and reduction of apoptosis after HIBD, and the neuroprotective action was likely associated with increased expression of Na/K ATPase. PMID:27362436

  14. 660 nm red light-enhanced bone marrow mesenchymal stem cell transplantation for hypoxic-ischemic brain damage treatment

    Institute of Scientific and Technical Information of China (English)

    Xianchao Li; Wensheng Hou; Xiaoying Wu; Wei Jiang; Haiyan Chen; Nong Xiao; Ping Zhou

    2014-01-01

    Bone marrow mesenchymal stem cell transplantation is an effective treatment for neonatal hy-poxic-ischemic brain damage. However, the in vivo transplantation effects are poor and their survival, colonization and differentiation efifciencies are relatively low. Red or near-infrared light from 600-1,000 nm promotes cellular migration and prevents apoptosis. Thus, we hypothesized that the combination of red light with bone marrow mesenchymal stem cell transplantation would be effective for the treatment of hypoxic-ischemic brain damage. In this study, the migra-tion and colonization of cultured bone marrow mesenchymal stem cells on primary neurons after oxygen-glucose deprivation were detected using Transwell assay. The results showed that, after a 40-hour irradiation under red light-emitting diodes at 660 nm and 60 mW/cm2, an increasing number of green lfuorescence-labeled bone marrow mesenchymal stem cells migrated towards hypoxic-ischemic damaged primary neurons. Meanwhile, neonatal rats with hypoxic-ischemic brain damage were given an intraperitoneal injection of 1 × 106 bone marrow mesenchymal stem cells, followed by irradiation under red light-emitting diodes at 660 nm and 60 mW/cm2 for 7 successive days. Shuttle box test results showed that, after phototherapy and bone marrow mesenchymal stem cell transplantation, the active avoidance response rate of hypoxic-ischemic brain damage rats was significantly increased, which was higher than that after bone marrow mesenchymal stem cell transplantation alone. Experimental ifndings indicate that 660 nm red light emitting diode irradiation promotes the migration of bone marrow mesenchymal stem cells, thereby enhancing the contribution of cell transplantation in the treatment of hypox-ic-ischemic brain damage.

  15. 660 nm red light-enhanced bone marrow mesenchymal stem cell transplantation for hypoxic-ischemic brain damage treatment.

    Science.gov (United States)

    Li, Xianchao; Hou, Wensheng; Wu, Xiaoying; Jiang, Wei; Chen, Haiyan; Xiao, Nong; Zhou, Ping

    2014-02-01

    Bone marrow mesenchymal stem cell transplantation is an effective treatment for neonatal hypoxic-ischemic brain damage. However, the in vivo transplantation effects are poor and their survival, colonization and differentiation efficiencies are relatively low. Red or near-infrared light from 600-1,000 nm promotes cellular migration and prevents apoptosis. Thus, we hypothesized that the combination of red light with bone marrow mesenchymal stem cell transplantation would be effective for the treatment of hypoxic-ischemic brain damage. In this study, the migration and colonization of cultured bone marrow mesenchymal stem cells on primary neurons after oxygen-glucose deprivation were detected using Transwell assay. The results showed that, after a 40-hour irradiation under red light-emitting diodes at 660 nm and 60 mW/cm(2), an increasing number of green fluorescence-labeled bone marrow mesenchymal stem cells migrated towards hypoxic-ischemic damaged primary neurons. Meanwhile, neonatal rats with hypoxic-ischemic brain damage were given an intraperitoneal injection of 1 × 10(6) bone marrow mesenchymal stem cells, followed by irradiation under red light-emitting diodes at 660 nm and 60 mW/cm(2) for 7 successive days. Shuttle box test results showed that, after phototherapy and bone marrow mesenchymal stem cell transplantation, the active avoidance response rate of hypoxic-ischemic brain damage rats was significantly increased, which was higher than that after bone marrow mesenchymal stem cell transplantation alone. Experimental findings indicate that 660 nm red light emitting diode irradiation promotes the migration of bone marrow mesenchymal stem cells, thereby enhancing the contribution of cell transplantation in the treatment of hypoxic-ischemic brain damage.

  16. Late radiation damage in bone, bone marrow and brain vasculature, with particular emphasis upon fractionation models

    International Nuclear Information System (INIS)

    X-ray induced changes in rat and human bone and bone marrow vasculature and in rat brain vasculature were measured as a function of time after irradiation and absorbed dose. The absorbed dose in the organ varied from 5 to 25 Gy for single dose irradiations and from 19 to 58 Gy for fractionated irradiations.The number of fractions varied from 3 to 10 for the rats and from 12 to 25 for the human. Blood flow changes were measured using an ''1''2''5I antipyrine or ''8''6RbCl extraction technique. The red blood cell (RBC) volume was examined by ''5''1Cr labelled red cells. Different fractionation models have been compared. Radiation induced reduction of bone and bone marrow blood flow were both time and dose dependent. Reduced blood flow 3 months after irradiation would seem to be an important factor in the subsequent atrophy of bones. With a single dose of 10 Gy the bone marrow blood flow returned to the control level by 7 months after irradiation. In the irradiated bone the RBC volume was about same as that in the control side but in bone marrow the reduction was from 32 to 59%. The dose levels predicted by the nominal standard dose (NSD) formula produced about the same damage to the rat femur seven months after irradiation when the extraction of ''8''6Rb chloride and the dry weight were concerned as the end points. However, the results suggest that the NSB formula underestimates the late radiation damage in bone marrow when a small number of large fractions are used. In the irradiated brains of the rats the blood flow was on average 20.4% higher compared to that in the control group. There was no significant difference in brain blood flow between different fractionation schemes. The value of 0.42 for the exponent of N corresponds to the average value for central nervous system tolerance in the literature. The model used may be sufficiently accurate for clinical work provided the treatment schemes used do not depart too radically from standard practice

  17. Effect of progesterone intervention on the dynamic changes of AQP-4 in hypoxic-ischaemic brain damage.

    Science.gov (United States)

    Li, Xiaojuan; Bai, Ruiying; Zhang, Junhe; Wang, Xiaoyin

    2015-01-01

    To observe the effect of progesterone (PROG) on blood-brain barrier (BBB) permeability, brain tissue water content and dynamic changes of aquaporin-4 (AQP-4) in neonatal rats with hypoxic-ischaemic brain damage (HIBD). 72 neonatal Wistar rats, aged 7 days old, were randomly divided into control, hypoxic-ischaemic (6, 24 and 72 h, and 7 d subgroups) and drug groups (6, 24 and 72 h, and 7 d subgroups). The HIBD animal model was established. BBB was detected via an Evans blue tracer. Brain water content was determined by the dry/wet method. The AQP-4 expression in the cerebral cortex was observed through immunohistochemistry and Western blot. BBB permeability in the cerebral cortex of the neonatal rats, brain water content and AQP-4 expression in the hypoxia-ischaemia group were significantly higher than those of the control group after hypoxia for 6 h (P permeability in the cerebral cortex of the neonatal rats, brain water content and AQP-4 expression in the drug group were significantly lower than those of the hypoxia-ischaemia group after hypoxia for 6, 24 and 72 h (P permeability and BBB expression were positively correlated with the AQP-4 expression. In conclusion, PROG protects the brain of HIBD neonatal rats by alleviating the damage of BBB and cerebral oedema. The protective effect of PROG may be related to the down-regulation of AQP-4 expression in the cerebral cortex of neonatal rats. PMID:26770503

  18. Relationship between Morphofunctional Changes in Open Traumatic Brain Injury and the Severity of Brain Damage in Rats.

    Science.gov (United States)

    Shakova, F M; Barskov, I V; Gulyaev, M V; Prokhorenko, S V; Romanova, G A; Grechko, A V

    2016-07-01

    A correlation between the severity of morphofunctional disturbances and the volume of brain tissue injury determined by MRT was demonstrated on the model of open traumatic brain injury in rats. A relationship between the studied parameters (limb placing and beam walking tests and histological changes) and impact force (the height of load fell onto exposed brain surface) was revealed.

  19. Comparison of the Bender Gestalt Test for Both Black and White Brain-Damaged Patients Using Two Scoring Systems

    Science.gov (United States)

    Butler, Oliver T.; And Others

    1976-01-01

    This study tested for cultural bias in the Bender Visual Motor Gestalt Test. Subjects were 72 black and white patients diagnosed as either brain damaged or psychiatric. Bender protocols were scored by Pascal-Suttell and Hain systems. No race effect appeared except for the Pascal-Suttell system for which blacks scored significantly better. (Author)

  20. Relationship between AQP4 expression and structural damage to the blood-brain barrier at early stages of traumatic brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    LU Hong; LEI Xiao-yan; HU Hui; HE Zhan-ping

    2013-01-01

    Background Although some studies have reported that aquaporin-4 (AQP4) plays an important role in the brain edema after traumatic brain injury (TBI),little is known about the AQP4 expression in the early stage of TBI,or about the correlation between the structural damage to the blood-brain barrier (BBB) and angioedema.The aim of this project was to investigate the relationship between AQP4 expression and damage to the BBB at early stages of TBI.Methods One hundred and twenty healthy adult Wistar rats were randomly divided into two greups:sham operation group (SO) and TBI group.The TBI group was divided into five sub-groups according to the different time intervals:1,3,6,12,and 24 hours.The brains of the animals were taken out at different time points after TBI to measure brain water content.The cerebral edema and BBB changes in structure were examined with an optical microscopy (OM) and transmission electron microscopy (TEM),and the IgG content and AQP4 protein expression in traumatic brain tissue were determined by means of immunohistochemistry and Western blotting.The data were analyzed with SPSS 13.0statistical software.Results In the SO greup,tissue was negative for IgG,and there were no abnormalities in brain water content or AQP4 expression.In the TBI group,brain water content significantly increased at 6 hours and peaked at 24 hours following injury.IgG expression significantly increased from 1 to 6 hours following injury,and remained at a high level at 24 hours.Pathological observation revealed BBB damage at 1 hour following injury.Angioedema appeared at 1 hour,was gradually aggravated,and became obvious at 6 hours.Intracellular edema occurred at 3 hours,with the presence of large glial cell bodies and mitochondrial swelling.These phenomena were aggravated with time and became obvious at 12 hours.In addition,microglial proliferation was visible at 24 hours.AQP4 protein expression were reduced at 1 hour,lowest at 6 hours,and began to increase at 12 hours

  1. Development of brain damage as measured by brain impedance recordings, and changes in heart rate, and blood pressure induced by different stunning and killing methods.

    Science.gov (United States)

    Savenije, B; Lambooij, E; Gerritzen, M A; Korf, J

    2002-04-01

    Poultry are electrically stunned before slaughter to induce unconsciousness and to immobilize the chickens for easier killing. From a welfare point of view, electrical stunning should induce immediate and lasting unconsciousness in the chicken. As an alternative to electroencephalography, which measures brain electrical activity, this study used brain impedance recordings, which measure brain metabolic activity, to determine the onset and development of brain damage. Fifty-six chickens were surgically equipped with brain electrodes and a canula in the wing artery and were subjected to one of seven stunning and killing methods: whole body electrical stunning; head-only electrical stunning at 50, 100 or 150 V; or an i.v. injection with MgCl2. After 30 s, the chickens were exsanguinated. Brain impedance and blood pressure were measured. Extracellular volume was determined from the brain impedance data and heart rate from the blood pressure data. An immediate and progressive reduction in extracellular volume in all chickens was found only with whole body stunning at 150 V. This treatment also caused cardiac fibrillation or arrest in all chickens. With all other electrical stunning treatments, extracellular volume was immediately reduced in some but not all birds, and cardiac fibrillation or arrest was not often found. Ischemic conditions, caused by cessation of the circulation, stimulated this epileptic effect. A stunner setting of 150 V is therefore recommended to ensure immediate and lasting unconsciousness, which is a requirement for humane slaughter. PMID:11989758

  2. Elevated endogenous erythropoietin concentrations are associated with increased risk of brain damage in extremely preterm neonates.

    Directory of Open Access Journals (Sweden)

    Steven J Korzeniewski

    Full Text Available We sought to determine, in very preterm infants, whether elevated perinatal erythropoietin (EPO concentrations are associated with increased risks of indicators of brain damage, and whether this risk differs by the co-occurrence or absence of intermittent or sustained systemic inflammation (ISSI.Protein concentrations were measured in blood collected from 786 infants born before the 28th week of gestation. EPO was measured on postnatal day 14, and 25 inflammation-related proteins were measured weekly during the first 2 postnatal weeks. We defined ISSI as a concentration in the top quartile of each of 25 inflammation-related proteins on two separate days a week apart. Hypererythropoietinemia (hyperEPO was defined as the highest quartile for gestational age on postnatal day 14. Using logistic regression and multinomial logistic regression models, we compared risks of brain damage among neonates with hyperEPO only, ISSI only, and hyperEPO+ISSI, to those who had neither hyperEPO nor ISSI, adjusting for gestational age.Newborns with hyperEPO, regardless of ISSI, were more than twice as likely as those without to have very low (< 55 Mental (OR 2.3; 95% CI 1.5-3.5 and/or Psychomotor (OR 2.4; 95% CI 1.6-3.7 Development Indices (MDI, PDI, and microcephaly at age two years (OR 2.4; 95%CI 1.5-3.8. Newborns with both hyperEPO and ISSI had significantly increased risks of ventriculomegaly, hemiparetic cerebral palsy, microcephaly, and MDI and PDI < 55 (ORs ranged from 2.2-6.3, but not hypoechoic lesions or other forms of cerebral palsy, relative to newborns with neither hyperEPO nor ISSI.hyperEPO, regardless of ISSI, is associated with elevated risks of very low MDI and PDI, and microcephaly, but not with any form of cerebral palsy. Children with both hyperEPO and ISSI are at higher risk than others of very low MDI and PDI, ventriculomegaly, hemiparetic cerebral palsy, and microcephaly.

  3. Implicit and Explicit Routes to Recognize the Own Body: Evidence from Brain Damaged Patients.

    Science.gov (United States)

    Candini, Michela; Farinelli, Marina; Ferri, Francesca; Avanzi, Stefano; Cevolani, Daniela; Gallese, Vittorio; Northoff, Georg; Frassinetti, Francesca

    2016-01-01

    Much research suggested that recognizing our own body-parts and attributing a body-part to our physical self-likely involve distinct processes. Accordingly, facilitation for self-body-parts was found when an implicit, but not an explicit, self-recognition was required. Here, we assess whether implicit and explicit bodily self-recognition is mediated by different cerebral networks and can be selectively impaired after brain lesion. To this aim, right- (RBD) and left- (LBD) brain damaged patients and age-matched controls were presented with rotated pictures of either self- or other-people hands. In the Implicit task participants were submitted to hand laterality judgments. In the Explicit task they had to judge whether the hand belonged, or not, to them. In the Implicit task, controls and LBD patients, but not RBD patients, showed an advantage for self-body stimuli. In the Explicit task a disadvantage emerged for self-compared to others' body stimuli in controls as well as in patients. Moreover, when we directly compared the performance of patients and controls, we found RBD, but not LBD, patients to be impaired in both the implicit and explicit recognition of self-body-part stimuli. Conversely, no differences were found for others' body-part stimuli. Crucially, 40% RBD patients showed a selective deficit for implicit processing of self-body-part stimuli, whereas 27% of them showed a selective deficit in the explicit recognition of their own body. Additionally, we provide anatomical evidence revealing the neural basis of this dissociation. Based on both behavioral and anatomical data, we suggest that different areas of the right hemisphere underpin implicit and explicit self-body knowledge. PMID:27630550

  4. Implicit and Explicit Routes to Recognize the Own Body: Evidence from Brain Damaged Patients

    Science.gov (United States)

    Candini, Michela; Farinelli, Marina; Ferri, Francesca; Avanzi, Stefano; Cevolani, Daniela; Gallese, Vittorio; Northoff, Georg; Frassinetti, Francesca

    2016-01-01

    Much research suggested that recognizing our own body-parts and attributing a body-part to our physical self-likely involve distinct processes. Accordingly, facilitation for self-body-parts was found when an implicit, but not an explicit, self-recognition was required. Here, we assess whether implicit and explicit bodily self-recognition is mediated by different cerebral networks and can be selectively impaired after brain lesion. To this aim, right- (RBD) and left- (LBD) brain damaged patients and age-matched controls were presented with rotated pictures of either self- or other-people hands. In the Implicit task participants were submitted to hand laterality judgments. In the Explicit task they had to judge whether the hand belonged, or not, to them. In the Implicit task, controls and LBD patients, but not RBD patients, showed an advantage for self-body stimuli. In the Explicit task a disadvantage emerged for self-compared to others' body stimuli in controls as well as in patients. Moreover, when we directly compared the performance of patients and controls, we found RBD, but not LBD, patients to be impaired in both the implicit and explicit recognition of self-body-part stimuli. Conversely, no differences were found for others' body-part stimuli. Crucially, 40% RBD patients showed a selective deficit for implicit processing of self-body-part stimuli, whereas 27% of them showed a selective deficit in the explicit recognition of their own body. Additionally, we provide anatomical evidence revealing the neural basis of this dissociation. Based on both behavioral and anatomical data, we suggest that different areas of the right hemisphere underpin implicit and explicit self-body knowledge.

  5. The perception of peripersonal space in right and left brain damage hemiplegic patients.

    Science.gov (United States)

    Bartolo, Angela; Carlier, Mauraine; Hassaini, Sabrina; Martin, Yves; Coello, Yann

    2014-01-01

    Peripersonal space, as opposed to extrapersonal space, is the space that contains reachable objects and in which multisensory and sensorimotor integration is enhanced. Thus, the perception of peripersonal space requires combining information on the spatial properties of the environment with information on the current capacity to act. In support of this, recent studies have provided converging evidences that perceiving objects in peripersonal space activates a neural network overlapping with that subtending voluntary motor action and motor imagery. Other studies have also underlined the dominant role of the right hemisphere (RH) in motor planning and of the left hemisphere (LH) in on-line motor guiding, respectively. In the present study, we investigated the effect of a right or left hemiplegia in the perception of peripersonal space. 16 hemiplegic patients with brain damage to the left (LH) or right (RH) hemisphere and eight matched healthy controls performed a color discrimination, a motor imagery and a reachability judgment task. Analyses of response times and accuracy revealed no variation among the three groups in the color discrimination task, suggesting the absence of any specific perceptual or decisional deficits in the patient groups. In contrast, the patient groups revealed longer response times in the motor imagery task when performed in reference to the hemiplegic arm (RH and LH) or to the healthy arm (RH). Moreover, RH group showed longer response times in the reachability judgment task, but only for stimuli located at the boundary of peripersonal space, which was furthermore significantly reduced in size. Considered together, these results confirm the crucial role of the motor system in motor imagery task and the perception of peripersonal space. They also revealed that RH damage has a more detrimental effect on reachability estimates, suggesting that motor planning processes contribute specifically to the perception of peripersonal space.

  6. The perception of peripersonal space in right and left brain damage hemiplegic patients

    Directory of Open Access Journals (Sweden)

    Angela eBartolo

    2014-01-01

    Full Text Available Peripersonal space, as opposed to extrapersonal space, is the space that contains reachable objects and in which multisensory and sensorimotor integration is enhanced. Thus, the perception of peripersonal space requires combining information on the spatial properties of the environment with information on the current capacity to act. In support of this, recent studies have provided converging evidences that perceiving objects in peripersonal space activates a neural network overlapping with that subtending voluntary motor action and motor imagery. Other studies have also underlined the dominant role of the right hemisphere in motor planning and of the left hemisphere in on-line motor guiding, respectively. In the present study, we investigated the effect of a right or left hemiplegia in the perception of peripersonal space. 16 hemiplegic patients with brain damage to the left (LH or right (RH hemisphere and 8 matched healthy controls (HC performed a colour discrimination, a motor imagery and a reachability judgment task. Analyses of response times and accuracy revealed no variation among the three groups in the colour discrimination task, suggesting the absence of any specific perceptual or decisional deficits in the patient groups. In contrast, the patient groups revealed longer response times in the motor imagery task when performed in reference to the hemiplegic arm (RH and LH or to the healthy arm (RH. Moreover, RH group showed longer response times in the reachability judgement task, but only for stimuli located at the boundary of peripersonal space, which was furthermore significantly reduced in size. Considered together, these results confirm the crucial role of the motor system in motor imagery task and the perception of peripersonal space. They also revealed that right hemisphere damage has a more detrimental effect on reachability estimates, suggesting that motor planning processes contribute specifically to the perception of

  7. Investigation of cavitation as a possible damage mechanism in blast-induced traumatic brain injury.

    Science.gov (United States)

    Goeller, Jacques; Wardlaw, Andrew; Treichler, Derrick; O'Bruba, Joseph; Weiss, Greg

    2012-07-01

    Cavitation was investigated as a possible damage mechanism for war-related traumatic brain injury (TBI) due to an improvised explosive device (IED) blast. When a frontal blast wave encounters the head, a shock wave is transmitted through the skull, cerebrospinal fluid (CSF), and tissue, causing negative pressure at the contrecoup that may result in cavitation. Numerical simulations and shock tube experiments were conducted to determine the possibility of cranial cavitation from realistic IED non-impact blast loading. Simplified surrogate models of the head consisted of a transparent polycarbonate ellipsoid. The first series of tests in the 18-inch-diameter shock tube were conducted on an ellipsoid filled with degassed water to simulate CSF and tissue. In the second series, Sylgard gel, surrounded by a layer of degassed water, was used to represent the tissue and CSF, respectively. Simulated blast overpressure in the shock tube tests ranged from a nominal 10-25 pounds per square inch gauge (psig; 69-170 kPa). Pressure in the simulated CSF was determined by Kulite thin line pressure sensors at the coup, center, and contrecoup positions. Using video taken at 10,000 frames/sec, we verified the presence of cavitation bubbles at the contrecoup in both ellipsoid models. In all tests, cavitation at the contrecoup was observed to coincide temporally with periods of negative pressure. Collapse of the cavitation bubbles caused by the surrounding pressure and elastic rebound of the skull resulted in significant pressure spikes in the simulated CSF. Numerical simulations using the DYSMAS hydrocode to predict onset of cavitation and pressure spikes during cavity collapse were in good agreement with the tests. The numerical simulations and experiments indicate that skull deformation is a significant factor causing cavitation. These results suggest that cavitation may be a damage mechanism contributing to TBI that requires future study.

  8. Influence of the extracellular matrix on endogenous and transplanted stem cells after brain damage

    Directory of Open Access Journals (Sweden)

    Lars eRoll

    2014-08-01

    Full Text Available The limited regeneration capacity of the adult central nervous system requires strategies to improve recovery of patients. In this context, the interaction of endogenous as well as transplanted stem cells with their environment is crucial. An understanding of the molecular mechanisms could help to improve regeneration by targeted manipulation.In the course of reactive gliosis, astrocytes upregulate Glial fibrillary acidic protein (GFAP and start, in many cases, to proliferate. Beside GFAP, subpopulations of these astroglial cells coexpress neural progenitor markers like Nestin. Although cells express these markers, the proportion of cells that eventually give rise to neurons is limited in many cases in vivo compared to the situation in vitro. In the first section, we present the characteristics of endogenous progenitor-like cells and discuss the differences in their neurogenic potential in vitro and in vivo.As the environment plays an important role for survival, proliferation, migration, and other processes, the second section of the review describes changes in the extracellular matrix (ECM, a complex network that contains numerous signaling molecules. It appears that signals in the damaged central nervous system lead to an activation and de-differentiation of astrocytes, but do not effectively promote neuronal differentiation of these cells. Factors that influence stem cells during development are upregulated in the damaged brain as part of an environment resembling a stem cell niche. We give a general description of the ECM composition, with focus on stem cell-associated factors like the glycoprotein Tenascin-C.Stem cell transplantation is considered as potential treatment strategy. Interaction of transplanted stem cells with the host environment is critical for the outcome of stem cell-based therapies. Possible mechanisms involving the ECM by which transplanted stem cells might improve recovery are discussed in the last section.

  9. Narrating stroke: the life-writing and fiction of brain damage.

    Science.gov (United States)

    Zimmermann, Martina

    2012-12-01

    Cerebro-vascular events are, after neurodegenerative disorders, the most frequent cause of brain damage that leads to the patient's impaired cognitive and/or bodily functioning. While the medico-scientific discourse related to stroke suggests that patients experience a change in identity and self-concept, the present analysis focuses on the patients' personal presentation of their experience to, first, highlight their way of thinking and feeling and, second, contribute to the clinician's actual understanding of the meaning of stroke within the life of each individual. As stroke 'victims' necessarily speak from the position of having undergone very abrupt degeneration followed by being confronted with a gradual relocation within their 'recovery', the present study addresses how narrative texts describe the condition, that is, the insult itself and its impairing consequences for body and mind, and how patients portray themselves within their illness. Furthermore, given that all illness narrative must remain non-representative, especially when exploring conditions that impair cognitive abilities, autobiographically inspired fiction, equally, contributes to neuroscientific perspectives on embodiment: it gives further insight into how the condition is perceived and alerts us to those aspects of the experience that are understood as particularly momentous.

  10. Radiation damage to the normal monkey brain. Experimental study induced by interstitial irradiation

    International Nuclear Information System (INIS)

    Radiation damage to normal brain tissue induced by interstitial irradiation with iridium-192 seeds was sequentially evaluated by computed tomography (CT), magnetic resonance imaging (MRI), and histological examination. This study was carried out in 14 mature Japanese monkeys. The experimental area received more than 200-260 Gy of irradiation developed coagulative necrosis. Infiltration of macrophages to the periphery of the necrotic area was seen. In addition, neovascularization, hyalinization of vascular walls, and gliosis were found in the periphery of the area invaded by the macrophages. All sites at which the vascular walls were found to have acute stage fibrinoid necrosis eventually developed coagulative necrosis. The focus of necrosis was detected by MRI starting 1 week after the end of radiation treatment, and the size of the necrotic area did not change for 6 months. The peripheral areas showed clear ring enhancement with contrast material. Edema surrounding the lesions was the most significant 1 week after radiation and was reduced to a minimum level 1 month later. However, the edema then expanded once again and was sustained for as long as 6 months. CT did not provide as clear of a presentation as MRI, but it did reveal similar findings for the most part, and depicted calcification in the necrotic area. This experimental model is considered useful for conducting basic research on brachytherapy, as well as for achieving a better understanding of delayed radiation necrosis. (author)

  11. Alteration in rectification of potassium channels in perinatal hypoxia ischemia brain damage.

    Science.gov (United States)

    Chen, Penghui; Wang, Liyan; Deng, Qiyue; Ruan, Huaizhen; Cai, Wenqin

    2015-01-15

    Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day-old rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch-clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K(+) channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential, membrane resistance, and membrane capacitance of OPCs were increased in both the gray and white matter of the cerebral cortex. OPCs in both the gray and white matter exhibited voltage-dependent K(+) currents, which consisted of the initiated rectified potassium currents (IA) and the sustained rectified currents (IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.

  12. Radiation damage to the normal monkey brain: experimental study induced by interstitial irradiation.

    Directory of Open Access Journals (Sweden)

    Mishima N

    2003-06-01

    Full Text Available Radiation damage to normal brain tissue induced by interstitial irradiation with iridium-192 seeds was sequentially evaluated by computed tomography (CT, magnetic resonance imaging (MRI, and histological examination. This study was carried out in 14 mature Japanese monkeys. The experimental area received more than 200-260 Gy of irradiation developed coagulative necrosis. Infiltration of macrophages to the periphery of the necrotic area was seen. In addition, neovascularization, hyalinization of vascular walls, and gliosis were found in the periphery of the area invaded by the macrophages. All sites at which the vascular walls were found to have acute stage fibrinoid necrosis eventually developed coagulative necrosis. The focus of necrosis was detected by MRI starting 1 week after the end of radiation treatment, and the size of the necrotic area did not change for 6 months. The peripheral areas showed clear ring enhancement with contrast material. Edema surrounding the lesions was the most significant 1 week after radiation and was reduced to a minimum level 1 month later. However, the edema then expanded once again and was sustained for as long as 6 months. CT did not provide as clear of a presentation as MRI, but it did reveal similar findings for the most part, and depicted calcification in the necrotic area. This experimental model is considered useful for conducting basic research on brachytherapy, as well as for achieving a better understanding of delayed radiation necrosis.

  13. Partially flexible MEMS neural probe composed of polyimide and sucrose gel for reducing brain damage during and after implantation

    International Nuclear Information System (INIS)

    This paper presents a flexible microelectromechanical systems (MEMS) neural probe that minimizes neuron damage and immune response, suitable for chronic recording applications. MEMS neural probes with various features such as high electrode densities have been actively investigated for neuron stimulation and recording to study brain functions. However, successful recording of neural signals in chronic application using rigid silicon probes still remains challenging because of cell death and macrophages accumulated around the electrodes over time from continuous brain movement. Thus, in this paper, we propose a new flexible MEMS neural probe that consists of two segments: a polyimide-based, flexible segment for connection and a rigid segment composed of thin silicon for insertion. While the flexible connection segment is designed to reduce the long-term chronic neuron damage, the thin insertion segment is designed to minimize the brain damage during the insertion process. The proposed flexible neural probe was successfully fabricated using the MEMS process on a silicon on insulator wafer. For a successful insertion, a biodegradable sucrose gel is coated on the flexible segment to temporarily increase the probe stiffness to prevent buckling. After the insertion, the sucrose gel dissolves inside the brain exposing the polyimide probe. By performing an insertion test, we confirm that the flexible probe has enough stiffness. In addition, by monitoring immune responses and brain histology, we successfully demonstrate that the proposed flexible neural probe incurs fivefold less neural damage than that incurred by a conventional silicon neural probe. Therefore, the presented flexible neural probe is a promising candidate for recording stable neural signals for long-time chronic applications. (paper)

  14. Association of retinal and macular damage with brain atrophy in multiple sclerosis.

    Directory of Open Access Journals (Sweden)

    Jan Dörr

    Full Text Available Neuroaxonal degeneration in the central nervous system contributes substantially to the long term disability in multiple sclerosis (MS patients. However, in vivo determination and monitoring of neurodegeneration remain difficult. As the widely used MRI-based approaches, including the brain parenchymal fraction (BPF have some limitations, complementary in vivo measures for neurodegeneration are necessary. Optical coherence tomography (OCT is a potent tool for the detection of MS-related retinal neurodegeneration. However, crucial aspects including the association between OCT- and MRI-based atrophy measures or the impact of MS-related parameters on OCT parameters are still unclear. In this large prospective cross-sectional study on 104 relapsing remitting multiple sclerosis (RRMS patients we evaluated the associations of retinal nerve fiber layer thickness (RNFLT and total macular volume (TMV with BPF and addressed the impact of disease-determining parameters on RNFLT, TMV or BPF. BPF, normalized for subject head size, was estimated with SIENAX. Relations were analyzed primarily by Generalized Estimating Equation (GEE models considering within-patient inter-eye relations. We found that both RNFLT (p = 0.019, GEE and TMV (p = 0.004, GEE associate with BPF. RNFLT was furthermore linked to the disease duration (p<0.001, GEE but neither to disease severity nor patients' age. Contrarily, BPF was rather associated with severity (p<0.001, GEE than disease duration and was confounded by age (p<0.001, GEE. TMV was not associated with any of these parameters. Thus, we conclude that in RRMS patients with relatively short disease duration and rather mild disability RNFLT and TMV reflect brain atrophy and are thus promising parameters to evaluate neurodegeneration in MS. Furthermore, our data suggest that RNFLT and BPF reflect different aspects of MS. Whereas BPF best reflects disease severity, RNFLT might be the better parameter for monitoring axonal

  15. The recently identified P2Y-like receptor GPR17 is a sensor of brain damage and a new target for brain repair.

    Directory of Open Access Journals (Sweden)

    Davide Lecca

    Full Text Available Deciphering the mechanisms regulating the generation of new neurons and new oligodendrocytes, the myelinating cells of the central nervous system, is of paramount importance to address new strategies to replace endogenous damaged cells in the adult brain and foster repair in neurodegenerative diseases. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl-leukotrienes (cysLTs, two families of endogenous signaling molecules, are markedly increased at the site of damage, suggesting that they may act as "danger signals" to alert responses to tissue damage and start repair. Here we show that, in brain telencephalon, GPR17, a recently deorphanized receptor for both uracil nucleotides and cysLTs (e.g., UDP-glucose and LTD(4, is normally present on neurons and on a subset of parenchymal quiescent oligodendrocyte precursor cells. We also show that induction of brain injury using an established focal ischemia model in the rodent induces profound spatiotemporal-dependent changes of GPR17. In the lesioned area, we observed an early and transient up-regulation of GPR17 in neurons expressing the cellular stress marker heat shock protein 70. Magnetic Resonance Imaging in living mice showed that the in vivo pharmacological or biotechnological knock down of GPR17 markedly prevents brain infarct evolution, suggesting GPR17 as a mediator of neuronal death at this early ischemic stage. At later times after ischemia, GPR17 immuno-labeling appeared on microglia/macrophages infiltrating the lesioned area to indicate that GPR17 may also acts as a player in the remodeling of brain circuitries by microglia. At this later stage, parenchymal GPR17+ oligodendrocyte progenitors started proliferating in the peri-injured area, suggesting initiation of remyelination. To confirm a specific role for GPR17 in oligodendrocyte differentiation, the in vitro exposure of cortical pre-oligodendrocytes to the GPR17 endogenous ligands UDP-glucose and LTD(4

  16. Minimal Brain Damage/Dysfunction (MBD) en de ontwikkeling van de wetenschappelijke kinderstudie in Nederland, ca. 1950–1990

    OpenAIRE

    Nelleke Bakker

    2014-01-01

    This paper discusses the reception in the Netherlands of Minimal Brain Damage/Dysfunction (MBD) and related labels for normally gifted children with learning disabilities and behavioural problems by child scientists of all sorts from the 1950s up to the late 1980s, when MBD was replaced with Attention Deficit Hyperactivity Disorder (ADHD). Unlike what has been suggested, as compared to ADHD, MBD turns out to have been all but a rare diagnosis for children who were not handicapped more serious...

  17. 660 nm red light-enhanced bone marrow mesenchymal stem cell transplantation for hypoxic-ischemic brain damage treatment

    OpenAIRE

    Li, Xianchao; Hou, Wensheng; Wu, Xiaoying; Jiang, Wei; Chen, Haiyan; Xiao, Nong; Zhou, Ping

    2014-01-01

    Bone marrow mesenchymal stem cell transplantation is an effective treatment for neonatal hypoxic-ischemic brain damage. However, the in vivo transplantation effects are poor and their survival, colonization and differentiation efficiencies are relatively low. Red or near-infrared light from 600–1,000 nm promotes cellular migration and prevents apoptosis. Thus, we hypothesized that the combination of red light with bone marrow mesenchymal stem cell transplantation would be effective for the tr...

  18. Multimodal deficits in right brain damaged patients with and without neglect and their modulation by sensory stimulation techniques

    OpenAIRE

    Rosenthal, Alisha

    2015-01-01

    Spatial neglect is a neurological disorder most often caused by vascular, right hemispheric brain damage. It is mainly characterized by a failure to attend, orient to or react to stimuli presented in the contralesional hemispace. By definition, neglect is seen as a higher order spatial disorder not merely caused by a sensory (e.g. hemianopia) or motor (e.g. hemiplegia) deficit. This definition includes the aspect of multimodality, which plays a central role in the assessment and therapy of th...

  19. Is There Chronic Brain Damage in Retired NFL Players? Neuroradiology, Neuropsychology, and Neurology Examinations of 45 Retired Players

    OpenAIRE

    Casson, Ira R.; Viano, David C.; Haacke, E. Mark; Kou, Zhifeng; LeStrange, Danielle G.

    2014-01-01

    Background: Neuropathology and surveys of retired National Football League (NFL) players suggest that chronic brain damage is a frequent result of a career in football. There is limited information on the neurological statuses of living retired players. This study aimed to fill the gap in knowledge by conducting in-depth neurological examinations of 30- to 60-year-old retired NFL players. Hypothesis: In-depth neurological examinations of 30- to 60-year-old retired players are unlikely to dete...

  20. Evidence for a therapeutic effect of Braintone on ischemic brain damage***

    Institute of Scientific and Technical Information of China (English)

    Yuanyuan Qin; Yu Luo; Weiwei Gu; Lei Yang; Xikun Shen; Zhenlun Gu; Huiling Zhang; Xiumei Gao

    2013-01-01

    This study used a novel combination of in vivo and in vitro experiments to show that Braintone had neuroprotective effects and clarified the molecular mechanisms underlying its efficacy. The Chinese herbal extract Braintone is composed of Radix Rhodiolase Essence, Radix Notoginseng Essence, Folium Ginkgo Essence and Rhizoma Chuanxiong. In vivo experiments showed that cerebral in-farction volume was reduced, hemispheric water content decreased, and neurological deficits were al eviated in a rat model of permanent middle cerebral artery occlusion after administration of 87.5, 175 or 350 mg/kg Braintone for 7 consecutive days. Western blot analysis showed that Braintone enhanced the expression of hypoxia-inducible factor 1α, heme oxygenase-1 and vascular endothe-lial growth factor in the ischemic cortex of these rats. The 350 mg/kg dose of Braintone produced the most dramatic effects. For the in vitro experiments, prior to oxygen-glucose deprivation, rats were intragastrical y injected with 440, 880 or 1 760 mg/kg Braintone to prepare a Braintone-co-ntaining serum, which was used to pre-treat human umbilical vein endothelial cel s for 24 hours. Human umbilical vein endothelial cel injury was al eviated with this pre-treatment. Western blot and real-time PCR analysis showed that the Braintone-containing serum increased the levels of hypox-ia-inducible factor 1α mRNA and protein, heme oxygenase-1 protein and vascular endothelial growth factor mRNA in oxygen-glucose deprived human umbilical vein endothelial cel s. The 1 760 mg/kg dose produced the greatest increases in expression. Col ectively, these experimental findings suggest that Braintone has neuroprotective effects on ischemia-induced brain damage via the up-regulation of hypoxia-inducible factor 1α, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cel s.

  1. BRAIN DAMAGE AND OXIDATIVE STRESS IN THE PERINATAL PERIOD: MELATONIN AS A NEUROPROTECTIVE NEW DRUG

    Directory of Open Access Journals (Sweden)

    S. Perrone

    2012-08-01

    Full Text Available Prenatal factors represent the main determinants of hypoxicischemic encephalopathy (HIE rather than intra- or post-partum conditions in perinatal period. Oxidative stress (OS plays a key role in perinatal brain damage. The development of therapeutic strategies to improve the outcomes of babies with HIE is still mandatory. Aim: to evaluate the effectiveness of melatonin as a neuroprotective drug. To investigate the influence of Melatonin on the OS biomarkers production in an animal model of cerebral hypoxia-ischemia. Methods: 30 rat pups were subjected to ligation of the right common carotid artery and exposed for 2.5 hours at an hypoxic condition. A group of 15 rats was administered melatonin at a dose of 15 mg/kg 5 minutes after the procedure (Mel GROUP. At the same time 15 rats received placebo (HI GROUP. A group of 5 healthy rats was used as sham operated (S GROUP. Isoprostanes (IsoPs, neuroprostanes (NPs and neurofurans (NFs, all markers of OS were measured at 1, 24 and 48 h from ischemic injury in homogenized cerebral cortex of the two sides, right (hypoxia and ischemia and left (hypoxia. Results: In the HI group were observed: a significant increase of IsoPs on the left side of cortex after 1 h from HI injury (p<0.001; a significant increase of NPs on both sides after 24 h (p<0.05 and a significant increase of NFs on the left (p<0.05 after 24 h. After 48 h in the Mel group was observed a significant increase of IsoPs on the left (p<0.05 and of NPs on both sides of cerebral cortex (p<0.05. Conclusions: Melatonin reduces OS biomarkers in cerebral cortex of HI rats after 24 h from its administration. The drug is no longer effective after 48 h. These results lay the groundwork for future clinical studies in infants.

  2. Right-sided representational neglect after left brain damage in a case without visuospatial working memory deficits.

    Science.gov (United States)

    van Dijck, Jean-Philippe; Gevers, Wim; Lafosse, Christophe; Fias, Wim

    2013-10-01

    Brain damaged patients suffering from representational neglect (RN) fail to report, orient to, or verbally describe contra-lesional elements of imagined environments or objects. So far this disorder has only been reported after right brain damage, leading to the idea that only the right hemisphere is involved in this deficit. A widely accepted account attributes RN to a lateralized impairment in the visuospatial component of working memory. So far, however, this hypothesis has not been tested in detail. In the present paper, we describe, for the first time, the case of a left brain damaged patient suffering from right-sided RN while imagining both known and new environments and objects. An in-depth evaluation of her visuospatial working memory abilities, with special focus on the presence of a lateralized deficit, did not reveal any abnormality. In sharp contrast, her ability to memorize visual information was severely compromised. The implications of these results are discussed in the light of recent insights in the neglect syndrome.

  3. Vojta and Bobath combined treatment for high risk infants with brain damage at early period

    Institute of Scientific and Technical Information of China (English)

    Chunyan Wu; Xiaohui Peng; Xuesong Li; Qingling Niu; Hong Guo; Huitao Huang

    2007-01-01

    BACKGROUND: In the process of early screening and interventions to high risk infants with brain damage,the occasion and choosing methods of interventions and the combined application of different interventions are still at the exploratory phase.OBJECTIVE: To observe the efficacy of early intervention using Vojta and Bobath combined treatment in high risk infants with brain damage, and investigate the effect of early rehabilitation on the prognosis.DESIGN: A randomized controlled comparative observation.SETTING: Daqing Oil Field General Hospital of Heilongjiang Province.PARTICIPANTS: Eighty-four high risk infants younger than 1 year were selected from the Department of Pediatrics, Daqing Oil Field General Hospital of Heilongjiang Province from October 2005 to October 2006,including 52 boys (62%) and 32 girls (38%). The treatment started at the age of 0 - 3 months in 11 cases (13%), 4 - 6 months in 28 cases (33%), 7 - 9 months in 35 cases (42%), and 10 - 12 months in 10 cases (12%). Infants with at least two of the followings were enrolled, including 7 Vojta abnormal postural reflexes,slow or disorder of motor development, increase of muscular tension, postural abnormality, primary reflection residual and CT/MRI abnormalities. Informed consents were obtained from their guardians. The 84 infants were randomly divided into treatment group (n =42) and control group (n =42).METHODS: All the children were intravenously injected with cerebroprotein hydrolysate injection or cattle encephalon glycoside and ignotin injection, 10 times as a course for 2 - 5 courses; Besides, the infants in the treatment group also received early rehabilitative training of Vojta and Bobath combined treatment, once a day, 40 minutes per time, 5 times a week followed by a 2-day rest, 1 month as a course, and totally 2 - 5 courses. The Vojta method was to facilitate the automatic regulation by reflexlocomotion. Bobath method was to inhibit abnormal posture but facilitate the normal one, thus it is

  4. Amifostine, a radioprotectant agent, protects rat brain tissue lipids against ionizing radiation induced damage: An FTIR microspectroscopic imaging study

    Energy Technology Data Exchange (ETDEWEB)

    Cakmak G.; Miller L.; Zorlu, F.; Severcan, F.

    2012-03-03

    Amifostine is the only approved radioprotective agent by FDA for reducing the damaging effects of radiation on healthy tissues. In this study, the protective effect of amifostine against the damaging effects of ionizing radiation on the white matter (WM) and grey matter (GM) regions of the rat brain were investigated at molecular level. Sprague-Dawley rats, which were administered amifostine or not, were whole-body irradiated at a single dose of 800 cGy, decapitated after 24 h and the brain tissues of these rats were analyzed using Fourier transform infrared microspectroscopy (FTIRM). The results revealed that the total lipid content and CH{sub 2} groups of lipids decreased significantly and the carbonyl esters, olefinic=CH and CH{sub 3} groups of lipids increased significantly in the WM and GM after exposure to ionizing radiation, which could be interpreted as a result of lipid peroxidation. These changes were more prominent in the WM of the brain. The administration of amifostine before ionizing radiation inhibited the radiation-induced lipid peroxidation in the brain. In addition, this study indicated that FTIRM provides a novel approach for monitoring ionizing radiation induced-lipid peroxidation and obtaining different molecular ratio images can be used as biomarkers to detect lipid peroxidation in biological systems.

  5. Negative regulation of miRNA-9 on oligodendrocyte lineage gene 1 during hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Lijun Yang; Hong Cui; Ting Cao

    2014-01-01

    Oligodendrocyte lineage gene 1 plays a key role in hypoxic-ischemic brain damage and myelin repair. miRNA-9 is involved in the occurrence of many related neurological disorders. Bioin-formatics analysis demonstrated that miRNA-9 complementarily, but incompletely, bound oligodendrocyte lineage gene 1, but whether miRNA-9 regulates oligodendrocyte lineage gene 1 remains poorly understood. Whole brain slices of 3-day-old Sprague-Dawley rats were cultured and divided into four groups:control group;oxygen-glucose deprivation group (treatment with 8% O2+ 92%N2 and sugar-free medium for 60 minutes);transfection control group (after oxygen and glucose deprivation for 60 minutes, transfected with control plasmid) and miRNA-9 transfection group (after oxygen and glucose deprivation for 60 minutes, transfected with miRNA-9 plasmid). From the third day of transfection, and with increasing culture days, oligodendrocyte lineage gene 1 expression increased in each group, peaked at 14 days, and then decreased at 21 days. Real-time quantitative PCR results, however, demonstrated that oligoden-drocyte lineage gene 1 expression was lower in the miRNA-9 transfection group than that in the transfection control group at 1, 3, 7, 14, 21 and 28 days after transfection. Results suggested that miRNA-9 possibly negatively regulated oligodendrocyte lineage gene 1 in brain tissues during hypoxic-ischemic brain damage.

  6. Study on CT changes in autistic children; Anatomical correlation of the damaged brain and delay of psychomotor development

    Energy Technology Data Exchange (ETDEWEB)

    Yaguchi, Katsumi (Juntendo Univ., Tokyo (Japan). School of Medicine)

    1993-05-01

    Since 1979 we have performed CT examinations on 132 autistic children. Neurological diagnosis of the lesion was established by Dr. Segawa's group. On the CT of many autistic children, we found a small low density change located in the anterior wall of the temporal horn, or localized dilatation of the inferior horn near the damaged brain. We reviewed 96 of these patients who all had the obvious low density changes, or localized irregular dilatations in the anterior wall of the temporal horn. By measuring the distance of damage from the midline, we divided the 96 cases into two groups. Group 1 consisted of those with damage located laterally more than 30 mm line from the midline. Group 2 consisted of those with damage medially to the 30 mm line from the midline. Those cases with a large lesion both laterally and medially of the 30 mm line were categorized into group 1. In the adult brain the lateral border of the amygdaloid nucleus was never located laterally more than 30 mm from the midline. Laterally over the 30 mm line there were two marked fiber systems running near the anterior wall of the temporal horn: the fiber of the anterior commissure and the uncinate fascicle. Group 1 consisted of 62 patients and group 2 of 34 patients. The majority of the two group patients were pure autism children. This suggested that the main lesion in autism was in the amygdala. (author).

  7. Magnetic resonance imaging of post-ischemic blood-brain barrier damage with PEGylated iron oxide nanoparticles

    Science.gov (United States)

    Liu, Dong-Fang; Qian, Cheng; An, Yan-Li; Chang, Di; Ju, Sheng-Hong; Teng, Gao-Jun

    2014-11-01

    Blood-brain barrier (BBB) damage during ischemia may induce devastating consequences like cerebral edema and hemorrhagic transformation. This study presents a novel strategy for dynamically imaging of BBB damage with PEGylated supermagnetic iron oxide nanoparticles (SPIONs) as contrast agents. The employment of SPIONs as contrast agents made it possible to dynamically image the BBB permeability alterations and ischemic lesions simultaneously with T2-weighted MRI, and the monitoring could last up to 24 h with a single administration of PEGylated SPIONs in vivo. The ability of the PEGylated SPIONs to highlight BBB damage by MRI was demonstrated by the colocalization of PEGylated SPIONs with Gd-DTPA after intravenous injection of SPION-PEG/Gd-DTPA into a mouse. The immunohistochemical staining also confirmed the leakage of SPION-PEG from cerebral vessels into parenchyma. This study provides a novel and convenient route for imaging BBB alteration in the experimental ischemic stroke model.

  8. A Review of the Bender Gestalt Test as a Screening Instrument for Brain Damage with School-Aged Children of Normal Intelligence Since 1970.

    Science.gov (United States)

    Eno, Larry; Deichmann, John

    1980-01-01

    All methods reviewed significantly discriminate between groups of brain damaged and unimpaired children. No method, however, provides successful predictive rates high enough to warrant the use of the Bender as the sole diagnostic instrument in individual cases. (Author)

  9. Pomegranate Alleviates Oxidative Damage and Neurotransmitter Alterations in Rats Brain Exposed to Aluminum Chloride and/or Gamma Radiation

    International Nuclear Information System (INIS)

    Aluminum and gamma radiation, both are potent neurotoxins and have been implicated in many human neuro degenerative diseases. The present study was designed to investigate the role of pomegranate in alleviating oxidative damage and alteration of neurotransmitters in the brain of rats exposed to aluminum chloride (AlCl3), and/or gamma radiation (IR). The results revealed that rats whole body exposed to γ- rays, (1 Gy/week up to 4 Gy), and/or administered aluminum chloride (35 mg/kg body weight), via gavages for 4 weeks, resulted in brain tissue damage, featuring by significant increase of the level of thiobarbituric acid reactive substances (TBARS), and advanced oxidation protein products (AOPP), associated with significant decrease of superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) content indicating occurrence of oxidative stress. A significant decrease of serotonin (5-HT) level associated with a significant increase of 5-hydroxyindole acetic acid (5-HIAA), in addition to a significant decrease in dopamine (DA), norepinephrine (NE) and epinephrine (EPI) contents recorded at the 1st, 7th and 14th day post-irradiation, indicating alterations in the metabolism of brain monoamines. On the other hand, the results exhibited that, supplementation of rats with pomegranate, via gavages, at a dose of 3 ml /kg body weight/ day, for 4 weeks along with AlCl3 with or without radiation has significantly ameliorated the changes occurred in the mentioned parameters and the values returned close to the normal ones. It could be concluded that pomegranate, by its antioxidant constituents might antagonize brain oxidative damage and minimize the severity of aluminum (Al), and/or radiation-induced neurotransmitters disorders

  10. Does any aspect of mind survive brain damage that typically leads to a persistent vegetative state? Ethical considerations

    Directory of Open Access Journals (Sweden)

    Fuchs Thomas

    2007-12-01

    Full Text Available Abstract Recent neuroscientific evidence brings into question the conclusion that all aspects of consciousness are gone in patients who have descended into a persistent vegetative state (PVS. Here we summarize the evidence from human brain imaging as well as neurological damage in animals and humans suggesting that some form of consciousness can survive brain damage that commonly causes PVS. We also raise the issue that neuroscientific evidence indicates that raw emotional feelings (primary-process affects can exist without any cognitive awareness of those feelings. Likewise, the basic brain mechanisms for thirst and hunger exist in brain regions typically not damaged by PVS. If affective feelings can exist without cognitive awareness of those feelings, then it is possible that the instinctual emotional actions and pain "reflexes" often exhibited by PVS patients may indicate some level of mentality remaining in PVS patients. Indeed, it is possible such raw affective feelings are intensified when PVS patients are removed from life-supports. They may still experience a variety of primary-process affective states that could constitute forms of suffering. If so, withdrawal of life-support may violate the principle of nonmaleficence and be tantamount to inflicting inadvertent "cruel and unusual punishment" on patients whose potential distress, during the process of dying, needs to be considered in ethical decision-making about how such individuals should be treated, especially when their lives are ended by termination of life-supports. Medical wisdom may dictate the use of more rapid pharmacological forms of euthanasia that minimize distress than the de facto euthanasia of life-support termination that may lead to excruciating feelings of pure thirst and other negative affective feelings in the absence of any reflective awareness.

  11. CT findings of the brain damages resulting from the high voltage electric injuries

    Energy Technology Data Exchange (ETDEWEB)

    Kim, So Eun; Kim, Young Keun; Shim, Hyang Yi; Lee, Shin Hyung; Lee, Chang Joon [National Medical Center, Seoul (Korea, Republic of)

    1994-02-15

    The purpose of this study is to evaluate the CT features and pathogenesis of the electric brain injuries. We reviewed the CT scans of 3 patients injured by high-voltage electricity. We evaluated the findings early and delayed periods in each patients. The early CT findings were diffuse brain edema, scalp swelling, and focal hemorrhagic contusion. The findings of delayed period were cerebral infarction, pneumocephalus, brain abscess, and pneumatocele. CT was useful to correlate the pathogenesis and variable features of electric brain injuries.

  12. [Arm Motor Function Recovery during Rehabilitation with the Use of Hand Exoskeleton Controlled by Brain-Computer Interface: a Patient with Severe Brain Damage].

    Science.gov (United States)

    Biryukova, E V; Pavlova, O G; Kurganskaya, M E; Bobrov, P D; Turbina, L G; Frolov, A A; Davydov, V I; Sil'tchenko, A V; Mokienko, O A

    2016-01-01

    We studied the dynamics of motor function recovery in a patient with severe brain damage in the course of neurorehabilitation using hand exoskeleton controlled by brain-computer interface. For estimating the motor function of paretic arm, we used the biomechanical analysis of movements registered during the course of rehabilitation. After 15 weekly sessions of hand exoskeleton control, the following results were obtained: a) the velocity profile of goal-directed movements of paretic hand became bell-shaped, b) the patient began to extend and abduct the hand which was flexed and adducted in the beginning of rehabilitation, and c) the patient began to supinate the forearm which was pronated in the beginning of rehabilitation. The first result is an evidence of the general improvement of the quality of motor control, while the second and third results prove that the spasticity of paretic arm has decreased. PMID:27188144

  13. Systemic inflammatory challenges compromise survival after experimental stroke via augmenting brain inflammation, blood- brain barrier damage and brain oedema independently of infarct size

    OpenAIRE

    Dénes Ádám; Ferenczi Szilamér; Kovács Krisztina J.

    2011-01-01

    Abstract Background Systemic inflammation impairs outcome in stroke patients and experimental animals via mechanisms which are poorly understood. Circulating inflammatory mediators can activate cerebrovascular endothelium or glial cells in the brain and impact on ischaemic brain injury. One of the most serious early clinical complications of cerebral ischaemia is brain oedema, which compromises survival in the first 24-48 h. It is not understood whether systemic inflammatory challenges impair...

  14. Effect of montelukast on the expression of interleukin-18, telomerase reverse transcriptase, and Bcl-2 in the brain tissue of neonatal rats with hypoxic-ischemic brain damage.

    Science.gov (United States)

    Liu, J L; Zhao, X H; Zhang, D L; Zhang, J B; Liu, Z H

    2015-01-01

    The aim of this study was to investigate the effect of montelukast on the expression of interleukin (IL)-18, telomerase reverse transcriptase (TERT), and Bcl-2 in the brain tissue of neonatal rats with hypox-ic-ischemic brain damage (HIBD). To establish the model of HIBD, 8% oxygen was applied to rats after the unilateral carotid artery was ligated. Twenty rats were randomly assigned to the control group, while another 40 were used to establish the HIBD model and were randomly divided equally into model group and treatment group. A 0.1 mg/kg dose of montelukast or an equal volume of saline was intraperitoneally injected to the rats in the treatment group and the model group, respectively. Brain tissue from 4 rats in each group was sampled at 0, 6, 12, 24, and 72 h after brain damage, and immunohistochemistry was used to measure IL-18, TERT and Bcl-2 expressions. IL-18, TERT, and Bcl-2 levels increased after 12 h in both the model group and treatment group, peaked after 48 h, and then decreased. Although not statistically significant, IL-18, TERT, and Bcl-2 expressions after 24, 48, and 96 h were all lower in the treatment group than those in the model group. In conclusion, montelukast has a protective effect on the cerebral tissue of neonatal rats with HIBD, and may mediate an increase of TERT and Bcl-2 levels but not of IL-18. Further study is required to elucidate the mechanism of the protective effect of montelukast on HIBD. PMID:26345821

  15. Neuroprotective effect of developmental docosahexaenoic acid supplement against excitotoxic brain damage in infant rats

    NARCIS (Netherlands)

    Hogyes, E; Nyakas, C; Kiliaan, A; Farkas, T; Penke, B; Luiten, PGM; Högyes, E.

    2003-01-01

    Long-chain polyunsaturated fatty acid (LC-PUFA) composition of neural membranes is a key factor for brain development, in chemical communication of neurons and probably also their survival in response to injury. Viability of cholinergic neurons was tested during brain development following dietary s

  16. Neuroprotective effect of developmental docosahexaenoic acid supplement against excitotoxic brain damage in infant rats.

    NARCIS (Netherlands)

    Hogyes, E.; Nyakas, C.; Kiliaan, A.J.; Farkas, T.; Penke, B.; Luiten, P.G.M.

    2003-01-01

    Long-chain polyunsaturated fatty acid (LC-PUFA) composition of neural membranes is a key factor for brain development, in chemical communication of neurons and probably also their survival in response to injury. Viability of cholinergic neurons was tested during brain development following dietary s

  17. Beneficial Effects of Teucrium polium and Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

    Directory of Open Access Journals (Sweden)

    S. Mojtaba Mousavi

    2015-01-01

    Full Text Available Objective. The effects of hydroalcoholic extract of Teucrium polium and metformin on diabetes-induced memory impairment and brain tissues oxidative damage were investigated. Methods. The rats were divided into: (1 Control, (2 Diabetic, (3 Diabetic-Extract 100 (Dia-Ext 100, (4 Diabetic-Extract 200 (Dia-Ext 200, (5 Diabetic-Extract 400 (Dia-Ext 400, and (6 Diabetic-Metformin (Dia-Met. Groups 3–6 were treated by 100, 200, and 400 mg/kg of the extract or metformin, respectively, for 6 weeks (orally. Results. In passive avoidance test, the latency to enter the dark compartment in Diabetic group was lower than that of Control group (P<0.01. In Dia-Ext 100, Dia-Ext 200, and Dia-Ext 400 and Metformin groups, the latencies were higher than those of Diabetic group (P<0.01. Lipid peroxides levels (reported as malondialdehyde, MDA, concentration in the brain of Diabetic group were higher than Control (P<0.001. Treatment by all doses of the extract and metformin decreased the MDA concentration (P<0.01. Conclusions. The results of present study showed that metformin and the hydroalcoholic extract of Teucrium polium prevent diabetes-induced memory deficits in rats. Protection against brain tissues oxidative damage might have a role in the beneficial effects of the extract and metformin.

  18. Early environmental enrichment affects neurobehavioral development and prevents brain damage in rats submitted to neonatal hypoxia-ischemia.

    Science.gov (United States)

    Schuch, Clarissa Pedrini; Diaz, Ramiro; Deckmann, Iohanna; Rojas, Joseane Jiménez; Deniz, Bruna Ferrary; Pereira, Lenir Orlandi

    2016-03-23

    Our previous results demonstrated improved cognition in adolescent rats housed in environmental enrichment (EE) that underwent neonatal hypoxia-ischemia (HI). The aim of this study was to investigate the effects of early EE on neurobehavioral development and brain damage in rats submitted to neonatal HI. Wistar rats were submitted to the HI procedure on the 7th postnatal day (PND) and housed in an enriched environment (8th-20th PND). The maturation of physical characteristics and the neurological reflexes were evaluated and the volume of striatum, corpus callosum and neocortex was measured. Data analysis demonstrated a clear effect of EE on neurobehavioral development; also, daily performance was improved in enriched rats on righting, negative geotaxis and cliff aversion reflex. HI caused a transient motor deficit on gait latency. Brain atrophy was found in HI animals and this damage was partially prevented by the EE. In conclusion, early EE stimulated neurobehavioral development in neonate rats and also protects the neocortex and the corpus callosum from atrophy following HI. These findings reinforce the potential of EE as a strategy for rehabilitation following neonatal HI and provide scientific support to the use of this therapeutic strategy in the treatment of neonatal brain injuries in humans.

  19. False memories to emotional stimuli are not equally affected in right- and left-brain-damaged stroke patients.

    Science.gov (United States)

    Buratto, Luciano Grüdtner; Zimmermann, Nicolle; Ferré, Perrine; Joanette, Yves; Fonseca, Rochele Paz; Stein, Lilian Milnitsky

    2014-10-01

    Previous research has attributed to the right hemisphere (RH) a key role in eliciting false memories to visual emotional stimuli. These results have been explained in terms of two right-hemisphere properties: (i) that emotional stimuli are preferentially processed in the RH and (ii) that visual stimuli are represented more coarsely in the RH. According to this account, false emotional memories are preferentially produced in the RH because emotional stimuli are both more strongly and more diffusely activated during encoding, leaving a memory trace that can be erroneously reactivated by similar but unstudied emotional items at test. If this right-hemisphere hypothesis is correct, then RH damage should result in a reduction in false memories to emotional stimuli relative to left-hemisphere lesions. To investigate this possibility, groups of right-brain-damaged (RBD, N=15), left-brain-damaged (LBD, N=15) and healthy (HC, N=30) participants took part in a recognition memory experiment with emotional (negative and positive) and non-emotional pictures. False memories were operationalized as incorrect responses to unstudied pictures that were similar to studied ones. Both RBD and LBD participants showed similar reductions in false memories for negative pictures relative to controls. For positive pictures, however, false memories were reduced only in RBD patients. The results provide only partial support for the right-hemisphere hypothesis and suggest that inter-hemispheric cooperation models may be necessary to fully account for false emotional memories. PMID:25129810

  20. Processing Homonymy and Polysemy: Effects of Sentential Context and Time-Course Following Unilateral Brain Damage

    Science.gov (United States)

    Klepousniotou, Ekaterini; Baum, Shari R.

    2005-01-01

    The present study investigated the abilities of left-hemisphere-damaged (LHD) non-fluent aphasic, right-hemisphere-damaged (RHD), and normal control individuals to access, in sentential biasing contexts, the multiple meanings of three types of ambiguous words, namely homonyms (e.g., ''punch''), metonymies (e.g., ''rabbit''), and metaphors (e.g.,…

  1. Metallic gold reduces TNFalpha expression, oxidative DNA damage and pro-apoptotic signals after experimental brain injury

    DEFF Research Database (Denmark)

    Pedersen, Mie Ostergaard; Larsen, Agnete; Pedersen, Dan Sonne;

    2009-01-01

    -45 microm in size or the vehicle (placebo) were implanted in the cortical tissue followed by a cortical freeze-lesioning. At 1-2 weeks post-injury, brains were analyzed by using immunohistochemistry and markers of inflammation, oxidative stress and apoptosis. This study shows that gold treatment...... significantly reduces the cerebral levels of tumor necrosis factor alpha (TNFalpha), oxidative DNA damage (as judged by 8-oxoguanine levels), and pro-apoptotic markers (cleaved caspase-3, cytochrome c leakage), when compared to those of controls. The data presented here points toward gold particles as a tool...

  2. MRI at 3 Tesla detects no evidence for ischemic brain damage in intensively treated patients with homozygous familial hypercholesterolemia

    International Nuclear Information System (INIS)

    Homozygous familial hypercholesterolemia (FH) is considered a model disease for excessive plasma cholesterol levels. Patients with untreated homozygous FH have a markedly increased risk for premature atherosclerosis. The frequency and extent of ischemic brain damage detectable by high-field magnetic resonance imaging (MRI) after long-term intensive treatment are unknown. In a case control study, five patients with homozygous FH (one male and four females; mean age: 23.6 ± 9.2, range: 12-36 years; mean pre-treatment serum total cholesterol level: 26.9 ± 3.24 mmol/L; all patients with documented atherosclerotic plaques in the carotid arteries) and five age- and sex-matched healthy controls were studied. All patients had been on maximal lipid-lowering medication since early childhood, and four of them were also on treatment with low-density lipoprotein (LDL) apheresis at bi-weekly intervals. Brain MRI was performed at 3 Tesla field strength with fluid-attenuated T2-weighted inversion recovery and T1-weighted spin-echo MR pulse sequences and subsequently evaluated by two independent readers. The maximal lipid-lowering treatment reduced the total serum cholesterol by more than 50% in the patients, but their serum concentrations were still 3.6-fold higher than those found in the controls (11.9 ± 4.2 vs. 4.5 ± 0.5 mmol/L; p < 0.0047). No brain abnormality was observed in any of the patients with homozygous FH. Homozygous FH patients on intensive cholesterol-lowering therapy have no evidence of ischemic brain damage at 3 Tesla MRI despite the remaining high cholesterol levels. (orig.)

  3. MRI at 3 Tesla detects no evidence for ischemic brain damage in intensively treated patients with homozygous familial hypercholesterolemia

    Energy Technology Data Exchange (ETDEWEB)

    Schmitz, Stephan A.; O' Regan, Declan P.; Fitzpatrick, Julie; Hajnal, Joseph V. [Hammersmith Hospital Campus, Imaging Sciences Department, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, London (United Kingdom); Neuwirth, Clare; Potter, Elizabeth; Tosi, Isabella; Naoumova, Rossi P. [MRC Clinical Sciences Centre, Clinical Research Facility, London (United Kingdom); Hammersmith Hospital, Lipid Clinic, London (United Kingdom)

    2007-11-15

    Homozygous familial hypercholesterolemia (FH) is considered a model disease for excessive plasma cholesterol levels. Patients with untreated homozygous FH have a markedly increased risk for premature atherosclerosis. The frequency and extent of ischemic brain damage detectable by high-field magnetic resonance imaging (MRI) after long-term intensive treatment are unknown. In a case control study, five patients with homozygous FH (one male and four females; mean age: 23.6 {+-} 9.2, range: 12-36 years; mean pre-treatment serum total cholesterol level: 26.9 {+-} 3.24 mmol/L; all patients with documented atherosclerotic plaques in the carotid arteries) and five age- and sex-matched healthy controls were studied. All patients had been on maximal lipid-lowering medication since early childhood, and four of them were also on treatment with low-density lipoprotein (LDL) apheresis at bi-weekly intervals. Brain MRI was performed at 3 Tesla field strength with fluid-attenuated T2-weighted inversion recovery and T1-weighted spin-echo MR pulse sequences and subsequently evaluated by two independent readers. The maximal lipid-lowering treatment reduced the total serum cholesterol by more than 50% in the patients, but their serum concentrations were still 3.6-fold higher than those found in the controls (11.9 {+-} 4.2 vs. 4.5 {+-} 0.5 mmol/L; p < 0.0047). No brain abnormality was observed in any of the patients with homozygous FH. Homozygous FH patients on intensive cholesterol-lowering therapy have no evidence of ischemic brain damage at 3 Tesla MRI despite the remaining high cholesterol levels. (orig.)

  4. Berberine Protects against Neuronal Damage via Suppression of Glia-Mediated Inflammation in Traumatic Brain Injury

    OpenAIRE

    Chien-Cheng Chen; Tai-Ho Hung; Chao Yu Lee; Liang-Fei Wang; Chun-Hu Wu; Chia-Hua Ke; Szu-Fu Chen

    2014-01-01

    Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain ba...

  5. Rehabilitation of Executive Functioning in Patients with Frontal Lobe Brain Damage with Goal Management Training

    OpenAIRE

    Brian eLevine; Schweizer, Tom A.; Charlene eO'Connor; Gary eTurner; Susan eGillingham; Stuss, Donald T.; Tom eManly; Robertson, Ian H.

    2011-01-01

    PUBLISHED Executive functioning deficits due to brain disease affecting frontal lobe functions cause significant real-life disability, yet solid evidence in support of executive functioning interventions is lacking. Goal Management Training (GMT), an executive functioning intervention that draws upon theories concerning goal processing and sustained attention, has received empirical support in studies of patients with traumatic brain injury, normal aging, and case studies. GMT promotes a m...

  6. Pentosan polysulfate protects brain endothelial cells against bacterial lipopolysaccharide-induced damages.

    Science.gov (United States)

    Veszelka, Szilvia; Pásztói, Mária; Farkas, Attila E; Krizbai, István; Ngo, Thi Khue Dung; Niwa, Masami; Abrahám, Csongor S; Deli, Mária A

    2007-01-01

    Peripheral inflammation can aggravate local brain inflammation and neuronal death. The blood-brain barrier (BBB) is a key player in the event. On a relevant in vitro model of primary rat brain endothelial cells co-cultured with primary rat astroglia cells lipopolysaccharide (LPS)-induced changes in several BBB functions have been investigated. LPS-treatment resulted in a dose- and time-dependent decrease in the integrity of endothelial monolayers: transendothelial electrical resistance dropped, while flux of permeability markers fluorescein and albumin significantly increased. Immunostaining for junctional proteins ZO-1, claudin-5 and beta-catenin was significantly weaker in LPS-treated endothelial cells than in control monolayers. LPS also reduced the intensity and changed the pattern of ZO-1 immunostaining in freshly isolated rat brain microvessels. The activity of P-glycoprotein, an important efflux pump at the BBB, was also inhibited by LPS. At the same time production of reactive oxygen species and nitric oxide was increased in brain endothelial cells treated with LPS. Pentosan polysulfate, a polyanionic polysaccharide could reduce the deleterious effects of LPS on BBB permeability, and P-glycoprotein activity. LPS-stimulated increase in the production of reactive oxygen species and nitric oxide was also decreased by pentosan treatment. The protective effect of pentosan for brain endothelium can be of therapeutical significance in bacterial infections affecting the BBB.

  7. The effects of chronic smoking on the pathology of alcohol-related brain damage.

    Science.gov (United States)

    McCorkindale, A N; Sheedy, D; Kril, J J; Sutherland, G T

    2016-06-01

    Both pathological and neuroimaging studies demonstrate that chronic alcohol abuse causes brain atrophy with widespread white matter loss limited gray matter loss. Recent neuroimaging studies suggest that tobacco smoking also causes brain atrophy in both alcoholics and neurologically normal individuals; however, this has not been confirmed pathologically. In this study, the effects of smoking and the potential additive effects of concomitant alcohol and tobacco consumption were investigated in autopsied human brains. A total of 44 cases and controls were divided into four groups: 16 non-smoking controls, nine smoking controls, eight non-smoking alcoholics, and 11 smoking alcoholics. The volumes of 26 gray and white matter regions were measured using an established point-counting technique. The results showed trends for widespread white matter loss in alcoholics (p contrast, smoking alone had no effect on brain atrophy and the combination of smoking and alcohol showed no additional effect. Neuronal density was analyzed as a more sensitive assay of gray matter integrity. Similar to the volumetric analysis, there was a reduction in neurons (29%) in the prefrontal cortex of alcoholics, albeit this was only a trend when adjusted for potential confounders (p generalized white matter atrophy. These disparate effects suggest that two different pathogenic mechanisms may be operating in the alcoholic brain. Future studies using ultrastructural or molecular techniques will be required to determine if smoking has more subtle effects on the brain and how chronic alcohol consumption leads to widespread white matter loss. PMID:27286935

  8. Brain

    Science.gov (United States)

    ... will return after updating. Resources Archived Modules Updates Brain Cerebrum The cerebrum is the part of the ... the outside of the brain and spinal cord. Brain Stem The brain stem is the part of ...

  9. Attenuation of Oxidative Damage by Boerhaavia diffusa L. Against Different Neurotoxic Agents in Rat Brain Homogenate.

    Science.gov (United States)

    Ayyappan, Prathapan; Palayyan, Salin Raj; Kozhiparambil Gopalan, Raghu

    2016-01-01

    Due to a high rate of oxidative metabolic activity in the brain, intense production of reactive oxygen metabolite occurs, and the subsequent generation of free radicals is implicated in the pathogenesis of traumatic brain injury, epilepsy, and ischemia as well as chronic neurodegenerative diseases. In the present study, protective effects of polyphenol rich ethanolic extract of Boerhaavia diffusa (BDE), a neuroprotective edible medicinal plant against oxidative stress induced by different neurotoxic agents, were evaluated. BDE was tested against quinolinic acid (QA), 3-nitropropionic acid (NPA), sodium nitroprusside (SNP), and Fe (II)/EDTA complex induced oxidative stress in rat brain homogenates. QA, NPA, SNP, and Fe (II)/EDTA treatment caused an increased level of thiobarbituric acid reactive substances (TBARS) in brain homogenates along with a decline in the activities of antioxidant enzymes. BDE treatment significantly decreased the production of TBARS (p brain. Since many of the neurological disorders are associated with free radical injury, these data may imply that B. diffusa, functioning as an antioxidant agent, may be beneficial for reducing various neurodegenerative complications.

  10. Dizocilpine (MK-801) arrests status epilepticus and prevents brain damage induced by Soman. (Reannouncement with new availability information)

    Energy Technology Data Exchange (ETDEWEB)

    Sparenborg, S.; Brennecke, L.H.; Jaax, N.K.; Braitman, D.J.

    1992-12-31

    The involvement of the NMDA receptor in the neurotoxicity induced by soman, an organophosphorus compound which irreversibly inhibits cholinesterase, was studied in guinea pigs. The drug MK-801 (0.5, 1 or 5 mg/kg, i.p.) was given as a pretreatment before a convulsant dose of soman or as a post treatment (30, 100 or 300 micron g/kg, i.m.) 5 min after the development of soman-induced status epilepticus. Pyridostigmine, atropine and pralidoxime chloride were also given to each subject to counteract the lethality of soman. All subjects that were challenged with soman and given the vehicle for MK-801 (saline) exhibited severe convulsions and electrographic seizure activity. Neuronal necrosis was found in the hippocampus, amygdala, thalamus and the pyriform and cerebral cortices of those subjects surviving for 48 hr. Pretreatment with 0.5 or 1 mg/kg doses of MK-801 did not prevent nor delay the onset of seizure activity but did diminish its intensity and led to its early arrest. At the largest dose (5 mg/kg), MK-801 completely prevented the development of seizure activity and brain damage. Post treatment with MK-801 prevented, arrested or reduced seizure activity, convulsions and neuronal necrosis in a dose-dependent manner. The NMDA receptor may play a more critical role in the spread and maintenance, rather than the initiation of cholinergically-induced seizure activity....Seizure-related brain damage, Organophosphorus compound, Nerve agent, Cholinesterase inhibition, Excitotoxicity, Guinea pig.

  11. Diagnostic and prognostic value of asphyxia, Sarnat's clinical classification, and CT-scan in perinatal brain damage

    International Nuclear Information System (INIS)

    A retrospective review was made of 145 babies, excluding those with congenital heart disease or chromosome aberration, admitted for CT scanning. The study was done to determine the diagnostic and prognostic value of CT findings, as well as the presence of asphyxia and the clinical stage based on the Sarnat's classification, in perinatal brain damage. The patients had a minimum follow up of 2 years for the evaluation of neurologic manifestations, such as cerebral palsy, epilepsy and mental retardation. Among babies weighing 2,000 g or more at birth, neonatal asphyxia was significantly correlated with neurologic prognosis. In addition, both clinical stages and CT findings were significantly correlated with neurologic prognosis, irrespective of birth weight. The correlation between clinical stages and CT findings was significant, irrespective of body weight, however, a significant correlation between clinical stages and neonatal asphyxia was restricted to those weighing 2,000 g or more. These findings suggest that the presence of asphyxia, clinical stages and CT findings are complementary in the diagnosis and prognosis evaluation of perinatal brain damage. (N.K.)

  12. Organotypic hippocampal slice cultures for studies of brain damage, neuroprotection and neurorepair

    DEFF Research Database (Denmark)

    Noraberg, Jens; Poulsen, Frantz Rom; Blaabjerg, Morten;

    2005-01-01

    Slices of developing brain tissue can be grown for several weeks as so-called organotypic slice cultures. Here we summarize and review studies using hippocampal slice cultures to investigate mechanisms and treatment strategies for the neurodegenerative disorders like stroke (cerebral ischemia......), Alzheimer's disease (AD) and epilepsia. Studies of non-excitotoxic neurotoxic compounds and the experimental use of slice cultures in studies of HIV neurotoxicity, traumatic brain injury (TBI) and neurogenesis are included. For cerebral ischemia, experimental models with oxygen-glucose deprivation (OGD...... in vitro models using dispersed cell cultures, experimental in vivo models, and in some instances, clinical trials. New techniques including slice culturing of hippocampal tissue from transgenic mice as well as more mature brain tissue, and slice cultures coupled to microelectrode arrays (MEAs), on...

  13. Aging aggravates ischemic stroke-induced brain damage in mice with chronic peripheral infection.

    Science.gov (United States)

    Dhungana, Hiramani; Malm, Tarja; Denes, Adam; Valonen, Piia; Wojciechowski, Sara; Magga, Johanna; Savchenko, Ekaterina; Humphreys, Neil; Grencis, Richard; Rothwell, Nancy; Koistinaho, Jari

    2013-10-01

    Ischemic stroke is confounded by conditions such as atherosclerosis, diabetes, and infection, all of which alter peripheral inflammatory processes with concomitant impact on stroke outcome. The majority of the stroke patients are elderly, but the impact of interactions between aging and inflammation on stroke remains unknown. We thus investigated the influence of age on the outcome of stroke in animals predisposed to systemic chronic infection. Th1-polarized chronic systemic infection was induced in 18-22 month and 4-month-old C57BL/6j mice by administration of Trichuris muris (gut parasite). One month after infection, mice underwent permanent middle cerebral artery occlusion and infarct size, brain gliosis, and brain and plasma cytokine profiles were analyzed. Chronic infection increased the infarct size in aged but not in young mice at 24 h. Aged, ischemic mice showed altered plasma and brain cytokine responses, while the lesion size correlated with plasma prestroke levels of RANTES. Moreover, the old, infected mice exhibited significantly increased neutrophil recruitment and upregulation of both plasma interleukin-17α and tumor necrosis factor-α levels. Neither age nor infection status alone or in combination altered the ischemia-induced brain microgliosis. Our results show that chronic peripheral infection in aged animals renders the brain more vulnerable to ischemic insults, possibly by increasing the invasion of neutrophils and altering the inflammation status in the blood and brain. Understanding the interactions between age and infections is crucial for developing a better therapeutic regimen for ischemic stroke and when modeling it as a disease of the elderly.

  14. An investigation of body part as object (BPO) responses in normal and brain-damaged adults.

    Science.gov (United States)

    Duffy, R J; Duffy, J R

    1989-07-01

    A test of simple pantomime was administered to three groups of adults and comparisons were made across groups of the incidence of subjects who exhibited body part as object (BPO) responses and of the mean frequency of occurrence of BPO in each group. The three groups were left-hemisphere-damaged aphasics (N = 28), right-hemisphere-damaged (N = 24), and normal controls (N = 28). The results indicated no significant differences among groups on the BPO measures. Also, to test the strength of association between the frequency of occurrence of BPO and measures of limb apraxia and severity of aphasia for the left-hemisphere-damaged aphasic group, correlation coefficients were obtained. The correlations were low and nonsignificant. The results of this investigation do not support the common clinical assumption that the occurrence of BPO during the performance of simple pantomimes is pathognomic for left-hemisphere pathology or associated with limb apraxia.

  15. GCR Transport in the Brain: Assessment of Self-Shielding, Columnar Damage, and Nuclear Reactions on Cell Inactivation Rates

    Science.gov (United States)

    Shavers, M. R.; Atwell, W.; Cucinotta, F. A.; Badhwar, G. D. (Technical Monitor)

    1999-01-01

    Radiation shield design is driven by the need to limit radiation risks while optimizing risk reduction with launch mass/expense penalties. Both limitation and optimization objectives require the development of accurate and complete means for evaluating the effectiveness of various shield materials and body-self shielding. For galactic cosmic rays (GCR), biophysical response models indicate that track structure effects lead to substantially different assessments of shielding effectiveness relative to assessments based on LET-dependent quality factors. Methods for assessing risk to the central nervous system (CNS) from heavy ions are poorly understood at this time. High-energy and charge (HZE) ion can produce tissue events resulting in damage to clusters of cells in a columnar fashion, especially for stopping heavy ions. Grahn (1973) and Todd (1986) have discussed a microlesion concept or model of stochastic tissue events in analyzing damage from HZE's. Some tissues, including the CNS, maybe sensitive to microlesion's or stochastic tissue events in a manner not illuminated by either conventional dosimetry or fluence-based risk factors. HZE ions may also produce important lateral damage to adjacent cells. Fluences of high-energy proton and alpha particles in the GCR are many times higher than HZE ions. Behind spacecraft and body self-shielding the ratio of protons, alpha particles, and neutrons to HZE ions increases several-fold from free-space values. Models of GCR damage behind shielding have placed large concern on the role of target fragments produced from tissue atoms. The self-shielding of the brain reduces the number of heavy ions reaching the interior regions by a large amount and the remaining light particle environment (protons, neutrons, deuterons. and alpha particles) may be the greatest concern. Tracks of high-energy proton produce nuclear reactions in tissue, which can deposit doses of more than 1 Gv within 5 - 10 cell layers. Information on rates of

  16. Clinical pragmatism and the care of brain damaged patients: toward a palliative neuroethics for disorders of consciousness.

    Science.gov (United States)

    Fins, Joseph J

    2005-01-01

    Unraveling the mysteries of consciousness, lost and regained, and perhaps even intervening so as to prompt recovery are advances for which neither the clinical nor the lay community are prepared. These advances will shake existing expectations about severe brain damage and will find an unprepared clinical context, perhaps even one inhospitable to what should clearly be viewed as important advances. This could be the outcome of this line of inquiry, if this exceptionally imaginative research can continue at all. This work faces a restrictive research environment that has the potential to imperil it. Added to the complexity of the scientific challenges that must be overcome is the societal context in which these investigations must occur. Research on human consciousness goes to the heart of our humanity and asks us to grapple with fundamental questions about the self. Added to this is the regulatory complexity of research on subjects who may be unable to provide their own consent because of impaired decision-making capacity, itself a function of altered or impaired consciousness. These factors can lead to a restrictive view of research that can favor risk aversion over discovery. In this paper, I attempt to explain systematically some of these challenges. I suggest that some of the resistance might be tempered if we view the needs of patients with severe brain injury through the prism of palliative care and adopt that field's ethos and methods when caring for and conducting research on individuals with severe brain damage and disorders of consciousness. To make this argument I draw upon the American pragmatic tradition and utilize clinical pragmatism, a method of moral problem-solving that my colleagues and I have developed to address ethical challenges in clinical care and research. PMID:16186050

  17. Progressive brain damage, synaptic reorganization and NMDA activation in a model of epileptogenic cortical dysplasia.

    Directory of Open Access Journals (Sweden)

    Francesca Colciaghi

    Full Text Available Whether severe epilepsy could be a progressive disorder remains as yet unresolved. We previously demonstrated in a rat model of acquired focal cortical dysplasia, the methylazoxymethanol/pilocarpine - MAM/pilocarpine - rats, that the occurrence of status epilepticus (SE and subsequent seizures fostered a pathologic process capable of modifying the morphology of cortical pyramidal neurons and NMDA receptor expression/localization. We have here extended our analysis by evaluating neocortical and hippocampal changes in MAM/pilocarpine rats at different epilepsy stages, from few days after onset up to six months of chronic epilepsy. Our findings indicate that the process triggered by SE and subsequent seizures in the malformed brain i is steadily progressive, deeply altering neocortical and hippocampal morphology, with atrophy of neocortex and CA regions and progressive increase of granule cell layer dispersion; ii changes dramatically the fine morphology of neurons in neocortex and hippocampus, by increasing cell size and decreasing both dendrite arborization and spine density; iii induces reorganization of glutamatergic and GABAergic networks in both neocortex and hippocampus, favoring excitatory vs inhibitory input; iv activates NMDA regulatory subunits. Taken together, our data indicate that, at least in experimental models of brain malformations, severe seizure activity, i.e., SE plus recurrent seizures, may lead to a widespread, steadily progressive architectural, neuronal and synaptic reorganization in the brain. They also suggest the mechanistic relevance of glutamate/NMDA hyper-activation in the seizure-related brain pathologic plasticity.

  18. Calcium antagonists decrease capillary wall damage in aging hypertensive rat brain

    NARCIS (Netherlands)

    Farkas, E.; de Jong, G.I.; Apro, E.; Keuker, J.I.H.; Luiten, P.G.M.

    2001-01-01

    Chronic hypertension during aging is a serious threat to the cerebral vasculature. The larger brain arteries can react to hypertension with an abnormal wall thickening, a loss of elasticity and a narrowed lumen. However, little is known about the hypertension-induced alterations of cerebral capillar

  19. Rehabilitation of executive functioning in patients with frontal lobe brain damage with Goal Management Training

    Directory of Open Access Journals (Sweden)

    Brian eLevine

    2011-02-01

    Full Text Available Executive functioning deficits due to brain disease affecting frontal lobe functions cause significant real-life disability, yet solid evidence in support of executive functioning interventions is lacking. Goal Management Training (GMT, an executive functioning intervention that draws upon theories concerning goal processing and sustained attention, has received empirical support in studies of patients with traumatic brain injury, normal aging, and case studies. GMT promotes a mindful approach to complex real-life tasks that pose problems for patients with executive functioning deficits, with a main goal of periodically stopping ongoing behavior to monitor and adjust goals. In this controlled trial, an expanded version of GMT was compared to an alternative intervention, Brain Health Workshop (BHW that was matched to GMT on non-specific characteristics that can affect intervention outcome. Participants included 19 individuals in the chronic phase of recovery from brain disease (predominantly stroke affecting frontal lobe function. Outcome data indicated specific effects of GMT on the Sustained Attention to Response Task (SART as well as the Tower Test, a visuospatial problem solving measure that reflected far transfer of training effects. There were no significant effects on self-report questionnaires, likely owing to the complexity of these measures in this heterogeneous patient sample. Overall, these data support the efficacy of GMT in the rehabilitation of executive functioning deficits.

  20. EEG Delta Band as a Marker of Brain Damage in Aphasic Patients after Recovery of Language

    Science.gov (United States)

    Spironelli, Chiara; Angrilli, Alessandro

    2009-01-01

    In this study spectral delta percentage was used to assess both brain dysfunction/inhibition and functional linguistic impairment during different phases of word processing. To this aim, EEG delta amplitude was measured in 17 chronic non-fluent aphasic patients while engaged in three linguistic tasks: Orthographic, Phonological and Semantic.…

  1. Role of Toll-like receptor 4 and Janus kinase and signal transducer and activator of transcription signal transduction pathway in sepsis-induced brain damage

    Institute of Scientific and Technical Information of China (English)

    Haiyan Yin; Jianrui Wei; Rui Zhang; Xiaoling Ye; Youfeng Zhu

    2011-01-01

    The Janus kinase and signal transducer and activator of transcription (JAK/STAT) signal transduction pathway is involved in sepsis-induced functional damage to the heart, liver, kidney, and other organs.However, the cellular and molecular mechanisms underlying sepsis-induced brain damage remain elusive.In the present study, we found severe loss of neurons in the hippocampal CA1 region in rats with sepsis-induced brain damage following intraperitoneal injection of endotoxin, The expression of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 was significantly increased in brain tissues following lipopolysaccharide exposure.AG490 (JAK2 antagonist) and rapamycin (STAT3 antagonist) significantly reduced neuronal loss and suppressed the increased expression of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 in the hippocampal CA1 region in sepsis-induced brain damaged rats.Overall, these data suggest that blockade of the JAK/STAT signal transduction pathway is neuroprotective in sepsis-induced brain damage via the inhibition of toll-like receptor 4, tumor necrosis factor α, and interleukin-6 expression.

  2. [Effect of salvianolic acid B on neural cells damage and neurogenesis after brain ischemia-reperfusion in rats].

    Science.gov (United States)

    Zhong, Jing; Tang, Min-ke; Zhang, Yan; Xu, Qiu-ping; Zhang, Jun-tian

    2007-07-01

    This study is to observe the effect of salvianolic acid B (Sal B) on neural cells damage and neurogenesis in sub-granular zone (SGZ) and sub-ventricular zone (SVZ) after brain ischemia-reperfusion (I/R) in rats. A modified middle cerebral artery occlusion (MCAO) model of focal cerebral ischemia-reperfusion was used. The rats were divided into four groups: sham control group, ischemia-reperfusion group, Sal B 1 and 10 mg x kg(-1) groups. Sal B was consecutively administrated once a day by ip injection after MCAO. The neurogenesis in SGZ and SVZ was investigated by BrdU method 7 days after MCAO. The Nissl staining for neurons in the hippocampal CA1 and cerebral cortex was performed 14 days after MCAO. A beam-walking test was used to monitor the motor function recovery. We found that brain ischemia resulted in an increase of BrdU positive cells both in ipsilateral SGZ and SVZ at 7th day after MCAO. Sal B (10 mg x kg(-1)) significantly increased further the number of BrdU positive cells both in SGZ and SVZ (P loss and improved motor function recovery after brain ischemia in rats.

  3. Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Zhichun Feng; Jing Liu; Rong Ju

    2013-01-01

    Hyperbaric oxygen therapy for the treatment of neonatal hypoxic-ischemic brain damage has been used clinically for many years, but its effectiveness remains controversial. In addition, the mechanism of this potential neuroprotective effect remains unclear. This study aimed to investigate the influence of hyperbaric oxygen on the proliferation of neural stem cells in the subventricular zone of neonatal Sprague-Dawley rats (7 days old) subjected to hypoxic-ischemic brain damage. Six hours after modeling, rats were treated with hyperbaric oxygen once daily for 7 days. Immunohistochemistry revealed that the number of 5-bromo-2′-deoxyuridine positive and nestin positive cells in the subventricular zone of neonatal rats increased at day 3 after hypoxic-ischemic brain damage and peaked at day 5. After hyperbaric oxygen treatment, the number of 5-bromo-2′- deoxyuridine positive and nestin positive cells began to increase at day 1, and was significantly higher than that in normal rats and model rats until day 21. Hematoxylin-eosin staining showed that hyperbaric oxygen treatment could attenuate pathological changes to brain tissue in neonatal rats, and reduce the number of degenerating and necrotic nerve cells. Our experimental findings indicate that hyperbaric oxygen treatment enhances the proliferation of neural stem cells in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage, and has therapeutic potential for promoting neurological recovery following brain injury.

  4. Cerebral white matter injury and damage to myelin sheath following whole-brain ischemia.

    Science.gov (United States)

    Chen, Yingzhu; Yi, Qiong; Liu, Gang; Shen, Xue; Xuan, Lihui; Tian, Ye

    2013-02-01

    Myelin sheath, either in white matter or in other regions of brain, is vulnerable to ischemia. The specific events involved in the progression of ischemia in white matter have not yet been elucidated. The aim of this study was to determine histopathological alterations in cerebral white matter and levels of myelin basic protein (MBP) in ischemia-injured brain tissue during the acute and subacute phases of central nervous injury following whole-brain ischemia. The whole cerebral ischemia model (four-vessel occlusion (4-VO)) was established in adult Sprague-Dawley rats and MBP gene expression and protein levels in the brain tissue were measured using reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA) at 2 days, 4 days, 7 days, 14 days, and 28 days following ischemia. Demyelination was determined by Luxol fast blue myelin staining, routine histopathological staining, and electron microscopy in injured brain tissue. Results showed that edema, vascular dilation, focal necrosis, demyelination, adjacent reactive gliosis and inflammation occurred 7 days after ischemia in HE staining and recovered to control levels at 28 days. The absence of Luxol fast blue staining and vacuolation was clearly visible at 7 days, 14 days, and 28 days. Semiquantitative analysis showed that the transparency of myelin had decreased significantly by 7 days, 14 days, and 28 days. Demyelination and ultrastructual changes were detected 7 days after ischemia. The relative levels of MBP mRNA decreased 2 days after ischemia and this trend continued throughout the remaining four points in time. The MBP levels measured using ELISA also decreased significantly at 2 days and 4 days, but they recovered by 7 days and returned to control levels by 14 days. These results suggest that the impact of ischemia on cerebral white matter is time-sensitive and that different effects may follow different courses over time.

  5. Suppression and Narrative Time Shifts in Adults with Right-Hemisphere Brain Damage

    Science.gov (United States)

    Scharp, Victoria L.; Tompkins, Connie A.

    2013-01-01

    Purpose: This study examined the functioning of a central comprehension mechanism, suppression, in adults with right-hemisphere damage (RHD) while they processed narratives that cued a shift in time frame. In normal language comprehension, mental activation of concepts from a prior time frame is suppressed. The (re)activation of information…

  6. Functional reorganization of the large-scale brain networks that support high-level cognition following brain damage in aphasia

    Directory of Open Access Journals (Sweden)

    Idan Asher Blank

    2015-05-01

    Full Text Available Over the last decade, a number of large-scale networks in the human cortex that support high-level cognition have been identified. Here, we focus on two of these networks: the fronto-temporal language network (e.g., Fedorenko et al., 2010, and the fronto-parietal “multiple demand (MD” network (e.g., Duncan, 2010. These two networks are clearly distinct from one another: first, their respective regions show distinct functional profiles, with language regions showing selective responses to language stimuli (Fedorenko et al., 2011; Monti et al., 2012 and MD regions showing domain-general responses to cognitive effort across a wide range of tasks (Duncan & Owen, 2001; Fedorenko et al., 2013. Second, during “rest” and cognitive processing, each network shows strong activity synchronization among its constituent regions, whereas regions across the two networks are not synchronized (Blank et al., 2014; Lee et al., 2012; Mantini et al., 2013. In the current study, we examined how these functional characteristics of the two networks were affected following aphasia-inducing strokes. In particular, we asked whether damage to the language network would alter the involvement of the MD network in linguistic processing, and whether such damage would alter the patterns of synchronization across the two networks. Four male individuals with aphasia (age: M=53, having suffered a single left MCA CVA, were scanned in fMRI on two paradigms that enable basic functional characterization of language and MD regions: (i a language localizer task, where they passively read sentences and sequences of pseudowords (Fedorenko et al., 2010; and (ii a spatial working memory task, where they had to remember fewer (easy or more (hard locations in a grid (Fedorenko et al., 2013. Language and MD regions were defined in each individual using the sentences > pseudowords contrast and the hard > easy contrast, respectively. Subjects were also scanned while listening to

  7. Neuropharmacology – Special Issue on Cerebral Ischemia Mechanisms of Ischemic Brain Damage – Review Article

    OpenAIRE

    Doyle, Kristian P.; Simon, Roger P.; Stenzel-Poore, Mary P

    2008-01-01

    Each year in the United States approximately 700,000 individuals are afflicted with a stroke and currently there are almost 2 million survivors of stroke living in the US with prolonged disability. In China 1.5 million people die from stroke each year and in developed nations stroke is the third leading cause of death, only surpassed by heart disease and cancer. Brain injury following stroke results from the complex interplay of multiple pathways including excitotoxicity, acidotoxicity, ionic...

  8. Role of Endoplasmic Reticulum Stress in Brain Damage After Cardiopulmonary Resuscitation in Rats.

    Science.gov (United States)

    Zhang, Jincheng; Xie, Xuemeng; Pan, Hao; Wu, Ziqian; Lu, Wen; Yang, Guangtian

    2015-07-01

    Postcardiac arrest syndrome yields poor neurological outcomes, but the mechanisms underlying this condition remain poorly understood. This study investigated whether endoplasmic reticulum (ER) stress-mediated apoptosis is induced in injured brain after resuscitation. Sprague-Dawley rats were subjected to 6 min of cardiac arrest (CA) and then resuscitated successfully. In the first experiment, animals were sacrificed 1, 3, 6, 12, or 24 h (n = 3 per group) after successful cardiopulmonary resuscitation. Brain tissues were analyzed by real-time polymerase chain reaction and Western blotting. In the second experiment, either dimethyl sulfoxide or salubrinal (Sal; 1 mg/kg), an ER stress inhibitor, was injected 30 min before the induction of CA (n = 10 per group). Neurological deficits were evaluated 24 h after CA. Brain specimens were analyzed using electron microscopy, terminal deoxynucleotidyl transferase dUTP nick end labeling assays and immunohistochemistry. We found that the messenger RNA and protein levels of glucose-regulated protein 78, X-box binding protein 1, C/EBP homologous protein, and caspase 12 were significantly elevated after resuscitation. We also observed that rats treated with Sal exhibited an improved neurological deficit score (32.3 ± 15.5 in the Sal group vs. 49.8 ± 20.9 in controls, P < 0.05). In addition, morphological improvements in the hippocampal ER were observed in the Sal group compared with the dimethyl sulfoxide group 24 h after reperfusion. Furthermore, in situ immunostaining revealed that markers of ER stress were significantly inhibited by Sal pretreatment. Our findings suggested that ER stress and the associated apoptotic pathways were activated in the hippocampus after resuscitation. Administration of Sal 30 min before cardiopulmonary resuscitation ameliorated neurological dysfunction 24 h after CA, possibly through the inhibition of ER stress after postresuscitation brain injury. PMID:25705860

  9. The accumulation of brain water-free sodium is associated with ischemic damage independent of the blood pressure in female rats.

    Science.gov (United States)

    Sumiyoshi, Manabu; Kitazato, Keiko T; Yagi, Kenji; Miyamoto, Takeshi; Kurashiki, Yoshitaka; Matsushita, Nobuhisa; Kinouchi, Tomoya; Kuwayama, Kazuyuki; Satomi, Junichiro; Nagahiro, Shinji

    2015-08-01

    Estrogen deficiency worsens ischemic stroke outcomes. In ovariectomized (OVX(+)) rats fed a high-salt diet (HSD), an increase in the body Na(+)/water ratio, which characterizes water-free Na(+) accumulation, was associated with detrimental vascular effects independent of the blood pressure (BP). We hypothesized that an increase in brain water-free Na(+) accumulation is associated with ischemic brain damage in OVX(+)/HSD rats. To test our hypothesis we divided female Wistar rats into 4 groups, OVX(+) and OVX(-) rats fed HSD or a normal diet (ND), and subjected them to transient cerebral ischemia. The brain Na(+)/water ratio was increased even in OVX(+)/ND rats and augmented in OVX(+)/HSD rats. The increase in the brain Na(+)/water ratio was positively correlated with expansion of the cortical infarct volume without affecting the BP. Interestingly, OVX(+) was associated with the decreased expression of ATP1α3, a subtype of the Na(+) efflux pump. HSD increased the expression of brain Na(+) influx-related molecules and the mineralocorticoid receptor (MR). The pretreatment of OVX(+)/HSD rats with the MR antagonist eplerenone reduced brain water-free Na(+) accumulation, up-regulated ATP1α3, down-regulated MR, and reduced the cortical infarct volume. Our findings show that the increase in the brain Na(+)/water ratio elicited by estrogen deficiency or HSD is associated with ischemic brain damage BP-independently, suggesting the importance of regulating the accumulation of brain water-free Na(+). The up-regulation of ATP1α3 and the down-regulation of MR may provide a promising therapeutic strategy to attenuate ischemic brain damage in postmenopausal women.

  10. Brain Malformations

    Science.gov (United States)

    Most brain malformations begin long before a baby is born. Something damages the developing nervous system or causes it ... medicines, infections, or radiation during pregnancy interferes with brain development. Parts of the brain may be missing, ...

  11. Head injuries in the 18th century: the management of the damaged brain.

    Science.gov (United States)

    Ganz, Jeremy C

    2013-07-01

    The 18th century was the time when trauma neurosurgery began to develop into the modern discipline. Before this, the management had, for the most part, changed little from the days of Hippocrates, Celsus, and Galen. Attention was directed to skull injuries, and the brain was treated as the seat of the rational soul but without other function. Symptoms after trauma were attributed to injuries to the bone and meninges. Following the lead of the Royal Academy of Surgery in Paris, it was accepted from the 1730s that the brain was the seat of symptoms after cranial trauma. During the 18th century, at least 12 surgeons published articles on cranial injury, 6 describing significant clinical series on this topic. They were Henri-François Le Dran (1685-1770) of Paris, Percival Pott (1714-1788) of London, James Hill (1703-1776) from Dumfries, Sylvester O'Halloran (1728-1807) of Limerick (Ireland), William Dease (1750-1798) of Dublin, and John Abernethy (1764-1831) of London. This article analyzes these series. Each individual made a different contribution. It is suggested that the relatively lesser-known James Hill in Scotland demonstrated the greatest understanding of the management of brain trauma and achieved the best results. A product of the Scottish Enlightenment, he adapted his management to his own experience and was not tied to the accepted authorities of his day, but he improved the management of each case following his experience with previous patients. He deserves to be remembered.

  12. Metformin Prevents Cisplatin-Induced Cognitive Impairment and Brain Damage in Mice.

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    Wenjun Zhou

    Full Text Available Chemotherapy-induced cognitive impairment, also known as 'chemobrain', is now widely recognized as a frequent adverse side effect of cancer treatment that often persists into survivorship. There are no drugs available to prevent or treat chemotherapy-induced cognitive deficits. The aim of this study was to establish a mouse model of cisplatin-induced cognitive deficits and to determine the potential preventive effects of the anti-diabetic drug metformin.Treatment of C57/BL6J mice with cisplatin (cumulative dose 34.5 mg/kg impaired performance in the novel object and place recognition task as well as in the social discrimination task indicating cognitive deficits. Co-administration of metformin prevented these cisplatin-induced cognitive impairments. At the structural level, we demonstrate that cisplatin reduces coherency of white matter fibers in the cingulate cortex. Moreover, the number of dendritic spines and neuronal arborizations as quantified on Golgi-stained brains was reduced after cisplatin treatment. Co-administration of metformin prevented all of these structural abnormalities in cisplatin-treated mice. In contrast to what has been reported in other models of chemobrain, we do not have evidence for persistent microglial or astrocyte activation in the brains of cisplatin-treated mice. Finally, we show that co-administration of metformin also protects against cisplatin-induced peripheral neuropathy.In summary, we show here for the first time that treatment of mice with cisplatin induces cognitive deficits that are associated with structural abnormalities in the brain. Moreover, we present the first evidence that the widely used and safe anti-diabetic drug metformin protects against these deleterious effects of cancer treatment. In view of the ongoing clinical trials to examine the potential efficacy of metformin as add-on therapy in patients treated for cancer, these findings should allow rapid clinical translation.

  13. Human umbilical cord blood cells restore brain damage induced changes in rat somatosensory cortex.

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    Maren Geissler

    Full Text Available Intraperitoneal transplantation of human umbilical cord blood (hUCB cells has been shown to reduce sensorimotor deficits after hypoxic ischemic brain injury in neonatal rats. However, the neuronal correlate of the functional recovery and how such a treatment enforces plastic remodelling at the level of neural processing remains elusive. Here we show by in-vivo recordings that hUCB cells have the capability of ameliorating the injury-related impairment of neural processing in primary somatosensory cortex. Intact cortical processing depends on a delicate balance of inhibitory and excitatory transmission, which is disturbed after injury. We found that the dimensions of cortical maps and receptive fields, which are significantly altered after injury, were largely restored. Additionally, the lesion induced hyperexcitability was no longer observed in hUCB treated animals as indicated by a paired-pulse behaviour resembling that observed in control animals. The beneficial effects on cortical processing were reflected in an almost complete recovery of sensorimotor behaviour. Our results demonstrate that hUCB cells reinstall the way central neurons process information by normalizing inhibitory and excitatory processes. We propose that the intermediate level of cortical processing will become relevant as a new stage to investigate efficacy and mechanisms of cell therapy in the treatment of brain injury.

  14. Human Umbilical Cord Blood Cells Restore Brain Damage Induced Changes in Rat Somatosensory Cortex

    Science.gov (United States)

    Geißler, Maren; Dinse, Hubert R.; Neuhoff, Sandra; Kreikemeier, Klaus; Meier, Carola

    2011-01-01

    Intraperitoneal transplantation of human umbilical cord blood (hUCB) cells has been shown to reduce sensorimotor deficits after hypoxic ischemic brain injury in neonatal rats. However, the neuronal correlate of the functional recovery and how such a treatment enforces plastic remodelling at the level of neural processing remains elusive. Here we show by in-vivo recordings that hUCB cells have the capability of ameliorating the injury-related impairment of neural processing in primary somatosensory cortex. Intact cortical processing depends on a delicate balance of inhibitory and excitatory transmission, which is disturbed after injury. We found that the dimensions of cortical maps and receptive fields, which are significantly altered after injury, were largely restored. Additionally, the lesion induced hyperexcitability was no longer observed in hUCB treated animals as indicated by a paired-pulse behaviour resembling that observed in control animals. The beneficial effects on cortical processing were reflected in an almost complete recovery of sensorimotor behaviour. Our results demonstrate that hUCB cells reinstall the way central neurons process information by normalizing inhibitory and excitatory processes. We propose that the intermediate level of cortical processing will become relevant as a new stage to investigate efficacy and mechanisms of cell therapy in the treatment of brain injury. PMID:21673795

  15. Correlation between Patent Foramen Ovale, Cerebral "Lesions" and Neuropsychometric Testing in Experienced Sports Divers: Does Diving Damage the Brain?

    Science.gov (United States)

    Balestra, Costantino; Germonpré, Peter

    2016-01-01

    SCUBA diving exposes divers to decompression sickness (DCS). There has been considerable debate whether divers with a Patent Foramen Ovale of the heart have a higher risk of DCS because of the possible right-to-left shunt of venous decompression bubbles into the arterial circulation. Symptomatic neurological DCS has been shown to cause permanent damage to brain and spinal cord tissue; it has been suggested that divers with PFO may be at higher risk of developing subclinical brain lesions because of repeated asymptomatic embolization of decompression-induced nitrogen bubbles. These studies however suffer from several methodological flaws, including self-selection bias. We recruited 200 volunteer divers from a recreational diving population who had never suffered from DCS; we then randomly selected 50 of those for further investigation. The selected divers underwent brain Magnetic Resonance Imaging to detect asymptomatic brain lesions, contrast trans-oesophageal echocardiography for PFO, and extensive neuro-psychometric testing. Neuro-psychometry results were compared with a control group of normal subjects and a separate control group for subjects exposed to neurotoxic solvents. Forty two divers underwent all the tests and are included in this report. Grade 2 Patent Foramen Ovale was found in 16 (38%) of the divers; brain Unidentified Bright Objects (UBO's) were found in 5 (11.9%). There was no association between PFO and the presence of UBO's (P = 0.693) or their size (p = 0.5) in divers. Neuropsychometric testing in divers was significantly worse from controls in two tests, Digit Span Backwards (DSB; p Coordination (EYE) tests. There was no correlation between PFO, number of UBO's and any of the neuro-psychometric tests. We conclude that for uneventful recreational diving, PFO does not appear to influence the presence of UBO's. Diving by itself seems to cause some decrease of short-term memory and higher cognitive function, including visual-motor skills; this

  16. Triethyllead-induced peroxidative damage in various regions of the rat brain

    Energy Technology Data Exchange (ETDEWEB)

    Ali, S.F. (Univ. of Arkansas for Medical Sciences, Little Rock (USA)); Bondy, S.C. (Univ. of California, Irvine (USA))

    1989-01-01

    Adult male Fisher 344 rats (8-10 wk old) were dosed ip with 1.75 mg/kg body weight of triethyllead chloride (TEL) for 5 consecutive days. Rats were sacrificed 1, 7, or 21 d after the last injection. The rate of lipid peroxidation was significantly elevated in frontal cortex at all three time points assayed (1, 7, or 21 d). However, hippocampal and cerebellar membranes showed no changes in peroxidative capacity at these time points. In order to determine whether cortical membrane damage was reflected in alteration of a restricted protein population, a series of high-affinity receptor binding sites was determined in cortical membranes derived from treated rats 7 d after the last injection of triethyllead. The rate of lipid peroxidation was significantly increased in the frontal cortex of triethyllead treated rats; however, no changes in the binding of ({sup 3}H)spiroperidol, ({sup 3}H)quinuclidinyl benzilate, and ({sup 3}H)benzodiazepine were seen in animals exposed to triethyllead. The cortical wet weight, protein content, and cell number were also unchanged by TEL treatment, reflecting an absence of gross damage.

  17. S100B Protein, a Damage-Associated Molecular Pattern Protein in the Brain and Heart, and Beyond

    Directory of Open Access Journals (Sweden)

    Guglielmo Sorci

    2010-01-01

    Full Text Available S100B belongs to a multigenic family of Ca2+-binding proteins of the EF-hand type and is expressed in high abundance in the brain. S100B interacts with target proteins within cells thereby altering their functions once secreted/released with the multiligand receptor RAGE. As an intracellular regulator, S100B affects protein phosphorylation, energy metabolism, the dynamics of cytoskeleton constituents (and hence, of cell shape and migration, Ca2+ homeostasis, and cell proliferation and differentiation. As an extracellular signal, at low, physiological concentrations, S100B protects neurons against apoptosis, stimulates neurite outgrowth and astrocyte proliferation, and negatively regulates astrocytic and microglial responses to neurotoxic agents, while at high doses S100B causes neuronal death and exhibits properties of a damage-associated molecular pattern protein. S100B also exerts effects outside the brain; as an intracellular regulator, S100B inhibits the postinfarction hypertrophic response in cardiomyocytes, while as an extracellular signal, (high S100B causes cardiomyocyte death, activates endothelial cells, and stimulates vascular smooth muscle cell proliferation.

  18. The effects of different fractions of Coriandrum sativum on pentylenetetrazole-induced seizures and brain tissues oxidative damage in rats

    Directory of Open Access Journals (Sweden)

    Akbar Anaeigoudari

    2016-03-01

    Full Text Available Objective: In the present work, the effects of different fractions of Coriandrum sativum (C. sativum, on pentylenetetrazole (PTZ-induced seizures and brain tissues oxidative damage were investigated in rats. Materials and Methods: The rats were divided into the following groups: (1 vehicle, (2 PTZ (90 mg/kg, (3 water fraction (WF of C. sativum (25 and 100 mg/kg, (4 n-butanol fraction (NBF of C. sativum (25 and 100 mg/kg, and (5 ethyl acetate fraction (EAF of C. sativum (25 and 100 mg/kg. Results: The first generalized tonic-clonic seizures (GTCS latency in groups treated with 100 mg /kg of WF or EAF was significantly higher than that of PTZ group (p< 0.01. In contrast to WF, the EAF and NBF were not effective in increasing the first minimal clonic seizure (MCS latency. Malondialdehyde (MDA levels in both cortical and hippocampal tissues of PTZ group were significantly higher than those of control animals (p< 0.001. Pretreatment with WF, NBF, or EAF resulted in a significant reduction in the MDA levels of hippocampi (pConclusion: The present study showed that different fractions of C. sativum possess antioxidant activity in the brain and WF and EAF of this plant have anticonvulsant effects.

  19. Simulated Microgravity and Low-Dose/Low-Dose-Rate Radiation Induces Oxidative Damage in the Mouse Brain.

    Science.gov (United States)

    Mao, Xiao Wen; Nishiyama, Nina C; Pecaut, Michael J; Campbell-Beachler, Mary; Gifford, Peter; Haynes, Kristine E; Becronis, Caroline; Gridley, Daila S

    2016-06-01

    Microgravity and radiation are stressors unique to the spaceflight environment that can have an impact on the central nervous system (CNS). These stressors could potentially lead to significant health risks to astronauts, both acutely during the course of a mission or chronically, leading to long-term, post-mission decrements in quality of life. The CNS is sensitive to oxidative injury due to high concentrations of oxidizable, unsaturated lipids and low levels of antioxidant defenses. The purpose of this study was to evaluate oxidative damage in the brain cortex and hippocampus in a ground-based model for spaceflight, which includes prolonged unloading and low-dose radiation. Whole-body low-dose/low-dose-rate (LDR) gamma radiation using (57)Co plates (0.04 Gy at 0.01 cGy/h) was delivered to 6 months old, mature, female C57BL/6 mice (n = 4-6/group) to simulate the radiation component. Anti-orthostatic tail suspension was used to model the unloading, fluid shift and physiological stress aspects of the microgravity component. Mice were hindlimb suspended and/or irradiated for 21 days. Brains were isolated 7 days or 9 months after irradiation and hindlimb unloading (HLU) for characterization of oxidative stress markers and microvessel changes. The level of 4-hydroxynonenal (4-HNE) protein, an oxidative specific marker for lipid peroxidation, was significantly elevated in the cortex and hippocampus after LDR + HLU compared to controls (P environment-induced oxidative stress. PMID:27243749

  20. Relationship between opioid therapy, tissue-damaging procedures, and brain metabolites as measured by proton MRS in asphyxiated term neonates.

    Science.gov (United States)

    Angeles, Danilyn M; Ashwal, Stephen; Wycliffe, Nathaniel D; Ebner, Charlotte; Fayard, Elba; Sowers, Lawrence; Holshouser, Barbara A

    2007-05-01

    To examine the effects of opioid and tissue-damaging procedures (TDPs) [i.e. procedures performed in the neonatal intensive care unit (NICU) known to result in pain, stress, and tissue damage] on brain metabolites, we reviewed the medical records of 28 asphyxiated term neonates (eight opioid-treated, 20 non-opioid treated) who had undergone magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (MRS) within the first month of life as well as eight newborns with no clinical findings of asphyxial injury. We found that lower creatine (Cr), myoinositol (Ins), and N-acetylaspartate (NAA)/choline (Cho) (p OGM) NAA/Cr was decreased (p = 0.03) and lactate (Lac) was present in a significantly higher amount (40%; p = 0.03) in non-opioid-treated neonates compared with opioid-treated neonates. Compared with controls, untreated neonates showed larger changes in more metabolites in basal ganglia (BG), thalami (TH), and OGM with greater significance than treated neonates. Our data suggest that TDPs affect spectral metabolites and that opioids do not cause harm in asphyxiated term neonates exposed to repetitive TDPs in the first 2-4 DOL and may provide a degree of neuroprotection.

  1. Research progress in apoptosis and hypoxic - ischemic brain damage%缺氧缺血性脑损伤与凋亡的进展

    Institute of Scientific and Technical Information of China (English)

    陈敏榕; 陈燕惠

    2004-01-01

    Apoptosis is one of the most important causes, which results in the central neuronal system complication in hypoxic- ischemic brain damage (HIBD). Apoptosis occurs in the developing brain more than in the developed brain. Apoptosis can last several weeks and may be inverted its pathology by appropriate therapy. Caspase inhibitor, neurotrophic factors, anti-apoptosis gene Bcl-2, mild hypothermia, and early intervention play important roles in promoting neuronal cell survival and preventing from apoptosis through different mechanisms. It may be a new way for rehabilitation of HIBD.

  2. Reversible brain damage following acute organic solvents' poisoning determined by magnetic resonance

    Directory of Open Access Journals (Sweden)

    Dujmović Irena

    2005-01-01

    Full Text Available Introduction. Acute exposure to the effects of volatile solvents is characterized by the abrupt onset of symptoms and signs of poisoning, and relatively fast recovery in the majority of cases. Case report. We report a 24-year-old patient with an acute, accidental poisoning with a mixture of volatile organic solvents (most probably toluene, styrene and xylene, which led to the development of upward gaze paresis, diplopia, hemiparesis, ataxic gate, and the late onset truncal ataxia episodes. After 6 weeks, he recovered completely, while his extensive brain MRI lesions in the caudate nuclei, laterobasal putaminal regions, bilateral anterior insular cortex, central midbrain tegmental area withdrew completely after 4 months. Conclusion. Acute toxic encephalopathy should be a part of the differential diagnosis in any patient with acute neurobehavioral and neurological deficit.

  3. A link between vascular damage and cognitive deficits after whole-brain radiation therapy for cancer: A clue to other types of dementia?

    Science.gov (United States)

    Yamada, Maki K

    2016-01-01

    Whole brain radiation therapy for the treatment of tumors can sometimes cause cognitive impairment. Memory deficits were noted in up to 50% of treated patients over a short period of several months. In addition, an increased rate of dementia in young patients has been noted over the longer term, i.e. years. A deficit in neurogenesis after irradiation has been postulated to be the main cause of cognitive decline in patients, but recent data on irradiation therapy for limited parts of the brain appear to indicate other possibilities. Irradiation can directly damage various types of cells other than neuronal stem cells. However, this paper will focus on injury to brain vasculature leading to cognitive decline since vessels represent a better therapeutic target for drug development than other cells in the brain because of the blood-brain barrier. PMID:27087553

  4. Differences in supratentorial white matter diffusion after radiotherapy - New biomarker of normal brain tissue damage?

    Energy Technology Data Exchange (ETDEWEB)

    Ravn, Soeren; Jens Broendum Froekaer, Jens [Dept. of Radiology, Aalborg Univ. Hospital, Aalborg (Denmark)], e-mail: sorl@rn.dk; Holmberg, Mats [Dept. of Oncology, Aalborg Univ. Hospital, Aalborg (Denmark); Soerensen, Preben [Dept. of Neurosurgery, Aalborg Univ. Hospital, Aalborg (Denmark); Carl, Jesper [Dept. of Neurosurgery, Aalborg Univ. Hospital, Aalborg (Denmark)

    2013-10-15

    Introduction: Therapy-induced injury to normal brain tissue is a concern in the treatment of all types of brain tumours. The purpose of this study was to investigate if magnetic resonance diffusion tensor imaging (DTI) could serve as a potential biomarker for the assessment of radiation-induced long-term white matter injury. Material and methods: DTI- and T1-weighted images of the brain were obtained in 19 former radiotherapy patients [nine men and 10 women diagnosed with astrocytoma (4), pituitary adenoma (6), meningioma (8) and craniopharyngioma (1), average age 57.8 (range 35-71) years]. Average time from radiotherapy to DTI scan was 4.6 (range 2.0-7.1) years. NordicICE software (NIC) was used to calculate apparent diffusion coefficient maps (ADC-maps). The co-registration between T1 images and ADC-maps were done using the auto function in NIC. The co-registration between the T1 images and the patient dose plans were done using the auto function in the treatment planning system Eclipse from Varian. Regions of interest were drawn on the T1-weighted images in NIC based on iso curves from Eclipse. Data was analysed by t-test. Estimates are given with 95 % CI. Results: A mean ADC difference of 4.6(0.3;8.9) X 10{sup -5} mm{sup 2}/s, p = 0.03 was found between paired white matter structures with a mean dose difference of 31.4 Gy. Comparing the ADC-values of the areas with highest dose from the paired data (dose > 33 Gy) with normal white matter (dose < 5 Gy) resulted in a mean dose difference of 44.1 Gy and a mean ADC difference of 7.87(3.15;12.60) X 10{sup -5} mm{sup 2}/s, p = 0.003. Following results were obtained when looking at differences between white matter mean ADC in average dose levels from 5 to 55 Gy in steps of 10 Gy with normal white matter mean ADC: 5 Gy; 1.91(-1.76;5.58) X 10{sup -5} mm{sup 2}/s, p = 0.29; 15 Gy; 5.81(1.53;10.11) X 10{sup -5} mm{sup 2}/s, p = 0.01; 25 Gy; 5.80(2.43;9.18) X 10{sup -5} mm{sup 2}/s, p = 0.002; 35 Gy; 5.93(2.89;8.97) X 10

  5. A high-affinity, dimeric inhibitor of PSD-95 bivalently interacts with PDZ1-2 and protects against ischemic brain damage

    DEFF Research Database (Denmark)

    Bach, Anders*; Clausen, Bettina H; Møller, Magda;

    2012-01-01

    Inhibition of the ternary protein complex of the synaptic scaffolding protein postsynaptic density protein-95 (PSD-95), neuronal nitric oxide synthase (nNOS), and the N-methyl-d-aspartate (NMDA) receptor is a potential strategy for treating ischemic brain damage, but high-affinity inhibitors...

  6. Melatonin reduces membrane rigidity and oxidative damage in the brain of SAMP8 mice.

    Science.gov (United States)

    García, J J; Piñol-Ripoll, G; Martínez-Ballarín, E; Fuentes-Broto, L; Miana-Mena, F J; Venegas, C; Caballero, B; Escames, G; Coto-Montes, A; Acuña-Castroviejo, D

    2011-11-01

    We evaluated the autophagy-lysosomal pathway and membrane fluidity in brain cells and mitochondrial membranes obtained from senescence-accelerated (SAMP(8)) and senescence-resistant (SAMR(1)) mice at 5 and 10 months of age. Moreover, we studied whether chronic treatment from age 1 to 10 months with melatonin stabilizes membrane fluidity. Fluidity was measured by polarization changes of 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene-p-toluene sulfonate. Results showed that in untreated animals at 5 months of age, synaptosomal and mitochondrial fluidity was decreased in SAMP(8) compared to SAMR(1), as was the cathepsin D/B ratio, indicating dysfunction of the autophagy-lysosomal pathway. Moreover, we detected synaptosomal rigidity and programmed cell death capability in both groups at 10 months of age. Mitochondrial fluidity, however, did not show a significant age-dependent change but was lower in SAMP(8) than in SAMR(1) at the 5- and 10-month time points. Melatonin administration prevented rigidity in the mitochondrial membrane and seemed to decrease age-related autophagy-lysosomal alterations. These data suggest that melatonin may act to slow down the aging process because of its ability to enhance membrane fluidity and maintain structural pathways. PMID:20096480

  7. Dental management in dysphagia syndrome patients with previously acquired brain damages

    Directory of Open Access Journals (Sweden)

    Ennio Bramanti

    2012-01-01

    Full Text Available Dysphagia is defined as difficulty in swallowing food (semi-solid or solid, liquid, or both. Difficulty in swallowing affects approximately 7% of population, with risk incidence increasing with age. There are many disorder conditions predisposing to dysphagia such as mechanical strokes or esophageal diseases even if neurological diseases represent the principal one. Cerebrovascular pathology is today the leading cause of death in developing countries, and it occurs most frequently in individuals who are at least 60 years old. Swallowing disorders related to a stroke event are common occurrences. The incidence ranging is estimated from 18% to 81% in the acute phase and with a prevalence of 12% among such patients. Cerebral, cerebellar, or brain stem strokes can influence swallowing physiology while cerebral lesions can interrupt voluntary control of mastication and bolus transport during the oral phase. Among the most frequent complications of dysphagia are increased mortality and pulmonary risks such as aspiration pneumonia, dehydration, malnutrition, and long-term hospitalization. This review article discusses the epidemiology of dysphagia, the normal swallowing process, pathophysiology, signs and symptoms, diagnostics, and dental management of patients affected.

  8. A clinically relevant model of perinatal global ischemic brain damage in rats.

    Science.gov (United States)

    Yang, Ting; Zhuang, Lei; Terrando, Niccolò; Wu, Xinmin; Jonhson, Mark R; Maze, Mervyn; Ma, Daqing

    2011-04-01

    We have designed a clinically relevant model of perinatal asphyxia providing intrapartum hypoxia in rats. On gestation day 22 SD rats were anesthetized and the uterine horns were exteriorized and placed in a water bath at 37°C for up to 20min. After this, pups were delivered from the uterus and manually stimulated to initiate breathing in an incubator at 37°C for 1 h in air. Brains were harvested and stained with cresyl violet, caspase-3, and TUNEL to detect morphological and apoptotic changes on postnatal days (PND) 1, 3, and 7. Separate cohorts were maintained until PND 50 and tested for learning and memory using Morris water maze (WM). Survival rate was decreased with longer hypoxic time, and 100% mortality was noted when hypoxia time was beyond 18min. Apoptosis was increased with the duration of hypoxia with neuronal loss and cell shrinkage in the CA1 of hippocampus. The time taken for the juveniles to locate the hidden platform during WM was increased in animals subjected to hypoxia. These data demonstrate that perinatal ischemic injury leads to neuronal death in the hippocampus and long-lasting cognitive dysfunction. This model mimics hypoxic ischemic encephalopathy in humans and may be appropriate for investigating therapeutic interventions. PMID:21281606

  9. Neuroendocrine Disturbances after Brain Damage: An Important and Often Undiagnosed Disorder.

    Science.gov (United States)

    Tanriverdi, Fatih; Kelestimur, Fahrettin

    2015-04-28

    Traumatic brain injury (TBI) is a common and significant public health problem all over the world. Until recently, TBI has been recognized as an uncommon cause of hypopituitarism. The studies conducted during the last 15 years revealed that TBI is a serious cause of hypopituitarism. Although the underlying pathophysiology has not yet been fully clarified, new data indicate that genetic predisposition, autoimmunity and neuroinflammatory changes may play a role in the development of hypopituitarism. Combative sports, including boxing and kickboxing, both of which are characterized by chronic repetitive head trauma, have been shown as new causes of neuroendocrine abnormalities, mainly hypopituitarism, for the first time during the last 10 years. Most patients with TBI-induced pituitary dysfunction remain undiagnosed and untreated because of the non-specific and subtle clinical manifestations of hypopituitarism. Replacement of the deficient hormones, of which GH is the commonest hormone lost, may not only reverse the clinical manifestations and neurocognitive dysfunction, but may also help posttraumatic disabled patients resistant to classical treatment who have undiagnosed hypopituitarism and GH deficiency in particular. Therefore, early diagnosis, which depends on the awareness of TBI as a cause of neuroendocrine abnormalities among the medical community, is crucially important.

  10. Neuroendocrine Disturbances after Brain Damage: An Important and Often Undiagnosed Disorder

    Directory of Open Access Journals (Sweden)

    Fatih Tanriverdi

    2015-04-01

    Full Text Available Traumatic brain injury (TBI is a common and significant public health problem all over the world. Until recently, TBI has been recognized as an uncommon cause of hypopituitarism. The studies conducted during the last 15 years revealed that TBI is a serious cause of hypopituitarism. Although the underlying pathophysiology has not yet been fully clarified, new data indicate that genetic predisposition, autoimmunity and neuroinflammatory changes may play a role in the development of hypopituitarism. Combative sports, including boxing and kickboxing, both of which are characterized by chronic repetitive head trauma, have been shown as new causes of neuroendocrine abnormalities, mainly hypopituitarism, for the first time during the last 10 years. Most patients with TBI-induced pituitary dysfunction remain undiagnosed and untreated because of the non-specific and subtle clinical manifestations of hypopituitarism. Replacement of the deficient hormones, of which GH is the commonest hormone lost, may not only reverse the clinical manifestations and neurocognitive dysfunction, but may also help posttraumatic disabled patients resistant to classical treatment who have undiagnosed hypopituitarism and GH deficiency in particular. Therefore, early diagnosis, which depends on the awareness of TBI as a cause of neuroendocrine abnormalities among the medical community, is crucially important.

  11. Association of retinal and macular damage with brain atrophy in multiple sclerosis.

    Science.gov (United States)

    Dörr, Jan; Wernecke, Klaus D; Bock, Markus; Gaede, Gunnar; Wuerfel, Jens T; Pfueller, Caspar F; Bellmann-Strobl, Judith; Freing, Alina; Brandt, Alexander U; Friedemann, Paul

    2011-01-01

    Neuroaxonal degeneration in the central nervous system contributes substantially to the long term disability in multiple sclerosis (MS) patients. However, in vivo determination and monitoring of neurodegeneration remain difficult. As the widely used MRI-based approaches, including the brain parenchymal fraction (BPF) have some limitations, complementary in vivo measures for neurodegeneration are necessary. Optical coherence tomography (OCT) is a potent tool for the detection of MS-related retinal neurodegeneration. However, crucial aspects including the association between OCT- and MRI-based atrophy measures or the impact of MS-related parameters on OCT parameters are still unclear. In this large prospective cross-sectional study on 104 relapsing remitting multiple sclerosis (RRMS) patients we evaluated the associations of retinal nerve fiber layer thickness (RNFLT) and total macular volume (TMV) with BPF and addressed the impact of disease-determining parameters on RNFLT, TMV or BPF. BPF, normalized for subject head size, was estimated with SIENAX. Relations were analyzed primarily by Generalized Estimating Equation (GEE) models considering within-patient inter-eye relations. We found that both RNFLT (p = 0.019, GEE) and TMV (p = 0.004, GEE) associate with BPF. RNFLT was furthermore linked to the disease duration (pdamage longitudinally. Longitudinal studies are necessary for validation of data and to further clarify the relevance of TMV. PMID:21494659

  12. Planning for selective amygdalohippocampectomy involving less neuronal ifber damage based on brain connectivity using tractography

    Institute of Scientific and Technical Information of China (English)

    Seung-Hak Lee; Mansu Kim; Hyunjin Park

    2015-01-01

    Temporal lobe resection is an important treatment option for epilepsy that involves removal of potentially essential brain regions. Selective amygdalohippocampectomy is a widely performed temporal lobe surgery. We suggest starting the incision for selective amygdalohippocampec-tomy at the inferior temporal gyrus based on diffusion magnetic resonance imaging (MRI) tractography. Diffusion MRI data from 20 normal participants were obtained from Parkinson’s Progression Markers Initiative (PPMI) database (www.ppmi-info.org). A tractography algorithm was applied to extract neuronal fiber information for the temporal lobe, hippocampus, and amygdala. Fiber information was analyzed in terms of the number of fibers and betweenness centrality. Distances between starting incisions and surgical target regions were also considered to explore the length of the surgical path. Middle temporal and superior temporal gyrus regions have higher connectivity values than the inferior temporal gyrus and thus are not good candi-dates for starting the incision. The distances between inferior temporal gyrus and surgical target regions were shorter than those between middle temporal gyrus and target regions. Thus, the in-ferior temporal gyrus is a good candidate for starting the incision. Starting the incision from the inferior temporal gyrus would spare the important (in terms of betweenness centrality values) middle region and shorten the distance to the target regions of the hippocampus and amygdala.

  13. Chronic cocaine administration causes extensive white matter damage in brain: diffusion tensor imaging and immunohistochemistry studies.

    Science.gov (United States)

    Narayana, Ponnada A; Herrera, Juan J; Bockhorst, Kurt H; Esparza-Coss, Emilio; Xia, Ying; Steinberg, Joel L; Moeller, F Gerard

    2014-03-30

    The effect of chronic cocaine exposure on multiple white matter structures in rodent brain was examined using diffusion tensor imaging (DTI), locomotor behavior, and end point histology. The animals received either cocaine at a dose of 100mg/kg (N=19), or saline (N=17) for 28 days through an implanted osmotic minipump. The animals underwent serial DTI scans, locomotor assessment, and end point histology for determining the expressions of myelin basic protein (MBP), neurofilament-heavy protein (NF-H), proteolipid protein (PLP), Nogo-A, aquaporin-4 (AQP-4), and growth associated protein-43 (GAP-43). Differences in the DTI measures were observed in the splenium (scc) and genu (gcc) of the corpus callosum (cc), fimbria (fi), and the internal capsule (ic). A significant increase in the activity in the fine motor movements and a significant decrease in the number of rearing events were observed in the cocaine-treated animals. Reduced MBP and Nogo-A and increased GAP-43 expressions were most consistently observed in these structures. A decrease in the NF-H expression was observed in fi and ic. The reduced expression of Nogo-A and the increased expression of GAP-43 may suggest destabilization of axonal connectivity and increased neurite growth with aberrant connections. Increased GAP-43 suggests drug-induced plasticity or a possible repair mechanism response. The findings indicated that multiple white matter tracts are affected following chronic cocaine exposure. PMID:24507117

  14. The assessment of pragmatics in Iranian patients with right brain damage.

    Directory of Open Access Journals (Sweden)

    Davood Sobhani-Rad

    2014-06-01

    Full Text Available Pragmatics is appropriate use of language across a variety of social contexts that provides accurate interpretation of intentions. The occurrence of the right hemisphere lesions can interfere with pragmatic abilities, and particularly with the processing of nonliteral speech acts.Since the objective of this study was to assess different aspects of pragmatic competence in the right hemisphere damage (RHD patients, 20 Iranian patients with right hemisphere lesions were examined by adult pragmatic profile (APP and a novel checklist was introduced for Persian language speaking individuals. Meanwhile, 40 healthy adult individuals, who were age and gender matched with RHD patients, were considered as the control group. After obtaining video records, all subjects were evaluated for 35 pragmatic skills, including 24 verbal, 5 paralinguistic, and 6 nonverbal aspects, by a two-point scale system.Studying RHD patients and their healthy counterparts revealed that the performance by participants with right hemisphere lesions exhibited a high degree of inappropriate pragmatic abilities compared with controls in all domains. Furthermore, RHD patients showed a trend of increasing difficulty in understanding and producing different pragmatic phenomena, including standard communication acts.Present results indicated that the right hemisphere lesions significantly affected pragmatic abilities in verbal, paralinguistic and nonverbal aspects. Such a pattern of performance, which is in line with deficits previously reported for RHD, proved the unquestioned role of the right hemisphere in processing nonliteral language.

  15. Monitoring stroke progression: in vivo imaging of cortical perfusion, blood-brain barrier permeability and cellular damage in the rat photothrombosis model.

    Science.gov (United States)

    Schoknecht, Karl; Prager, Ofer; Vazana, Udi; Kamintsky, Lyn; Harhausen, Denise; Zille, Marietta; Figge, Lena; Chassidim, Yoash; Schellenberger, Eyk; Kovács, Richard; Heinemann, Uwe; Friedman, Alon

    2014-11-01

    Focal cerebral ischemia is among the main causes of death and disability worldwide. The ischemic core often progresses, invading the peri-ischemic brain; however, assessing the propensity of the peri-ischemic brain to undergo secondary damage, understanding the underlying mechanisms, and adjusting treatment accordingly remain clinically unmet challenges. A significant hallmark of the peri-ischemic brain is dysfunction of the blood-brain barrier (BBB), yet the role of disturbed vascular permeability in stroke progression is unclear. Here we describe a longitudinal in vivo fluorescence imaging approach for the evaluation of cortical perfusion, BBB dysfunction, free radical formation and cellular injury using the photothrombosis vascular occlusion model in male Sprague Dawley rats. Blood-brain barrier dysfunction propagated within the peri-ischemic brain in the first hours after photothrombosis and was associated with free radical formation and cellular injury. Inhibiting free radical signaling significantly reduced progressive cellular damage after photothrombosis, with no significant effect on blood flow and BBB permeability. Our approach allows a dynamic follow-up of cellular events and their response to therapeutics in the acutely injured cerebral cortex.

  16. Processing of visual gravitational motion in the peri-sylvian cortex: Evidence from brain-damaged patients.

    Science.gov (United States)

    Maffei, Vincenzo; Mazzarella, Elisabetta; Piras, Fabrizio; Spalletta, Gianfranco; Caltagirone, Carlo; Lacquaniti, Francesco; Daprati, Elena

    2016-05-01

    Rich behavioral evidence indicates that the brain estimates the visual direction and acceleration of gravity quite accurately, and the underlying mechanisms have begun to be unraveled. While the neuroanatomical substrates of gravity direction processing have been studied extensively in brain-damaged patients, to our knowledge no such study exists for the processing of visual gravitational motion. Here we asked 31 stroke patients to intercept a virtual ball moving along the vertical under either natural gravity or artificial reversed gravity. Twenty-seven of them also aligned a luminous bar to the vertical direction (subjective visual vertical, SVV). Using voxel-based lesion-symptom mapping as well as lesion subtraction analysis, we found that lesions mainly centered on the posterior insula are associated with greater deviations of SVV, consistent with several previous studies. Instead, lesions mainly centered on the parietal operculum decrease the ability to discriminate natural from unnatural gravitational acceleration with a timed motor response in the interception task. Both the posterior insula and the parietal operculum belong to the vestibular cortex, and presumably receive multisensory information about the gravity vector. We speculate that an internal model estimating the effects of gravity on visual objects is constructed by transforming the vestibular estimates of mechanical gravity, which are computed in the brainstem and cerebellum, into internalized estimates of virtual gravity, which are stored in the cortical vestibular network. The present lesion data suggest a specific role for the parietal operculum in detecting the mismatch between predictive signals from the internal model and the online visual signals. PMID:27007069

  17. Pre-ischemic treadmill training alleviates brain damage via GLT-1-mediated signal pathway after ischemic stroke in rats.

    Science.gov (United States)

    Wang, X; Zhang, M; Yang, S-D; Li, W-B; Ren, S-Q; Zhang, J; Zhang, F

    2014-08-22

    Physical exercise could play a neuroprotective role in both human and animals. However, the involved signal pathways underlying the neuroprotective effect are still not well established. This study was to investigate the possible signal pathways involved in the neuroprotection of pre-ischemic treadmill training after ischemic stroke. Seventy-two SD rats were randomly assigned into three groups (n=24/group): sham surgery group, middle cerebral artery occlusion (MCAO) group and MCAO with exercise group. Following three weeks of treadmill training exercise, ischemic stroke was induced by occluding the middle cerebral artery (MCA) in rat for 2 h, followed by reperfusion. Twenty-four hours after MCAO/reperfusion, 12 rats in each group were evaluated for neurological deficit scores and then sacrificed to measure the infarct volume (n=6) and cerebral edema (n=6). Six rats in each group were sacrificed to measure the expression level of glutamate transporter-1 (GLT-1), protein kinase C-α (PKC-α), Akt, and phosphatidylinositol 3 kinase (PI3K) (n=6). Two hundred and eighty minutes (4.67 h) after occlusion, six rats in each group were decapitated to detect the mRNA expression level of metabotropic glutamate receptor 5 (mGluR5) and N-methyl-D-aspartate receptor subunit type 2B (NR2B) (n=6).The results demonstrated that pre-ischemic treadmill training exercise reduced brain infarct volume, cerebral edema and neurological deficits, also decreased the over expression of PKC-α and increased the expression level of GLT-1, Akt and PI3K after ischemic stroke (pexercise (pexercise preconditioning ameliorated brain damage after ischemic stroke, which might be involved in two signal pathways: PKC-α-GLT-1-Glutamate and PI3K/Akt-GLT-1-Glutamate. PMID:24907601

  18. Willed-movement training reduces brain damage and enhances synaptic plasticity related proteins synthesis after focal ischemia.

    Science.gov (United States)

    Nie, Jingjing; Yang, Xiaosu; Tang, Qingping; Shen, Qin; Li, Simin

    2016-01-01

    It has been wildly accepted that willed movement(WM) training promotes neurological rehabilitation in patients with stroke. However, it was not clear whether the effect of WM is better than other forms of exercise. The purpose of this study is to assess different effects of WM and other forms of exercise on rats with focal ischemia. The subjects are all had right middle cerebral artery occlusion (MCAO) surgery and randomly allocated to three groups of training and one control group with no training. Infarct volume by 2,3,5-triphenyltetrazolium chloride (TTC) dye, expression of PICK1 and synaptophysin in cerebral cortex and striatum of injured side by western blotting and immunofluorescence performed are analyzed. Exercise has done respectively on rats in each group for 15 days and 30 days. Compared with the control group, the brain damage is reduced in other groups after 15 days exercise. The protein expressions levels of synaptophysin and PICK1 are upregulated after exercise. Concentration of PICK1 protein in WM is greater than other exercise groups, and the expression of synaptophysin in WM and SM groups are higher than EM groups. The number of PICK1 positive cells, synaptophysin and PICK1 co-positive cells are increased by exercise. Synaptophysin is widely distributed in cortex surrounding the injury area in WM and EM. It is indicated in our result that willed-movement training is the most effective intervention in enhancing the PICK1-mediated synaptic plasticity in the area adjacent to the damage region of ischemic rats. PMID:26556240

  19. The impact of acquired brain damage in terms of epidemiology, economics and loss in quality of life

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    Larrañaga Isabel

    2011-04-01

    Full Text Available Abstract Background Patients with acquired brain damage (ABD have suffered a brain lesion that interrupts vital development in the physical, psychological and social spheres. Stroke and traumatic brain injury (TBI are the two main causes. The objectives of this study were to estimate the incidence and prevalence of ABD in the population of the Basque Country and Navarre in 2008, to calculate the associated cost of the care required and finally to assess the loss in health-related quality of life. Methods On the one hand, a cross-sectional survey was carried out, in order to estimate the incidence of ABD and its consequences in terms of costs and loss in quality of life from the evolution of a sample of patients diagnosed with stroke and TBI. On the other hand, a discrete event simulation model was built that enabled the prevalence of ABD to be estimated. Finally, a calculation was made of the formal and informal costs of ABD in the population of the Basque Country and Navarre (2,750,000 people. Results The cross-sectional study showed that the incidences of ABD caused by stroke and TBI were 61.8 and 12.5 cases per 100,000 per year respectively, while the overall prevalence was 657 cases per 100,000 people. The SF-36 physical and mental component scores were 28.9 and 44.5 respectively. The total economic burden was calculated to be 382.14 million euro per year, distributed between 215.27 and 166.87 of formal and informal burden respectively. The average cost per individual was 21,040 € per year. Conclusions The main conclusion of this study is that ABD has a high impact in both epidemiological and economic terms as well as loss in quality of life. The overall prevalence obtained is equivalent to 0.7% of the total population. The substantial economic burden is distributed nearly evenly between formal and informal costs. Specifically, it was found that the physical dimensions of quality of life are the most severely affected. The prevalence

  20. Dapsone improves functional deficit and diminishes brain damage evaluated by 3-Tesla magnetic resonance image after transient cerebral ischemia and reperfusion in rats.

    Science.gov (United States)

    Diaz-Ruiz, Araceli; Roldan-Valadez, Ernesto; Ortiz-Plata, Alma; Mondragón-Lozano, Rodrigo; Heras-Romero, Yessica; Mendez-Armenta, Marisela; Osorio-Rico, Laura; Nava-Ruiz, Concepción; Ríos, Camilo

    2016-09-01

    Stroke is a frequent cause of death and the first of disability in the world population. We have shown that dapsone acts as an antioxidant, antiinflammatory and antiapoptotic agent after brain Ischemia reperfusion (I/R) in rats; however, its therapeutic efficacy, measured by imaging has not been characterized. In this context, the aim of this study was to evaluate the neuroprotective effect of dapsone by magnetic resonance imaging (MRI) and to correlate imaging markers with motor function and oxidative stress after transient cerebral ischemia and reperfusion (I/R). We used male rats throughout the experiment. Functional deficit after I/R was assessed by using Longa scale. The area of brain tissue damage was measured by histology. The nuclear factor erythroid 2-related factor 2 (Nrf-2) and the amount of reactive oxygen species (ROS) were measured as biomarkers of oxidative stress. Finally, difussion tensor MRI was employed to measure the fractional anisotropy (FA), as a MRI marker of the pathophysiologic brain status. Results showed a better functional recovery and less damaged tissue in animals treated with dapsone vs control group. The values of FA were higher in animals receiving treatment, indicating a better preservation of brain structure. At early stages of the damage, dapsone was able to reduce both oxidative markers (Nrf-2 and ROS). Our findings provide new evidence for the efficacy of dapsone when administered during the acute phase after I/R and that quantitative sequences of MRI are useful for characterizing its potential therapeutic benefits after stroke. PMID:27321157

  1. Protective Effect of Calendula officinalis L. Flowers Against Monosodium Glutamate Induced Oxidative Stress and Excitotoxic Brain Damage in Rats.

    Science.gov (United States)

    Shivasharan, B D; Nagakannan, P; Thippeswamy, B S; Veerapur, V P

    2013-07-01

    Monosodium glutamate (MSG) is a popular flavour enhancer used in food industries; however, excess MSG is neurotoxic. Oxidative stress is well documented in MSG induced neurotoxicity. The compounds having antioxidant and anti-inflammatory properties reportedly possess beneficial effects against various neurotoxic insults. Calendula officinalis Linn. flower extract (COE) is known for its potent antioxidant and anti-inflammatory activities. Hence, this present study has been designed to evaluate the neuroprotective effect of COE on MSG-induced neurotoxicity in rats. Adult Wistar rats were administered systemically for 7 days with MSG and after one h of MSG injection, rats were treated with COE (100 and 200 mg/kg) orally. At the end the treatment period, animals were assessed for locomotor activity and were sacrificed; brains were isolated for estimation of LPO, GSH, CAT, TT, GST, Nitrite and histopathological studies. MSG caused a significant alteration in animal behavior, oxidative defense (raised levels of LPO, nitrite concentration, depletion of antioxidant levels) and hippocampal neuronal histology. Treatment with COE significantly attenuated behavioral alterations, oxidative stress, and hippocampal damage in MSG-treated animals. Hence, this study demonstrates that COE protects against MSG-induced neurotoxicity in rats. The antioxidant and anti-inflammatory properties of COE may be responsible for its observed neuroprotective action. PMID:24426226

  2. Protein kinase C inhibition attenuates vascular ETB receptor upregulation and decreases brain damage after cerebral ischemia in rat

    Directory of Open Access Journals (Sweden)

    Vikman Petter

    2007-01-01

    Full Text Available Abstract Background Protein kinase C (PKC is known to be involved in the pathophysiology of experimental cerebral ischemia. We have previously shown that after transient middle cerebral artery occlusion, there is an upregulation of endothelin receptors in the ipsilateral middle cerebral artery. The present study aimed to examine the effect of the PKC inhibitor Ro-32-0432 on endothelin receptor upregulation, infarct volume and neurology outcome after middle cerebral artery occlusion in rat. Results At 24 hours after transient middle cerebral artery occlusion (MCAO, the contractile endothelin B receptor mediated response and the endothelin B receptor protein expression were upregulated in the ipsilateral but not the contralateral middle cerebral artery. In Ro-32-0432 treated rats, the upregulated endothelin receptor response was attenuated. Furthermore, Ro-32-0432 treatment decreased the ischemic brain damage significantly and improved neurological scores. Immunohistochemistry showed fainter staining of endothelin B receptor protein in the smooth muscle cells of the ipsilateral middle cerebral artery of Ro-32-0432 treated rats compared to control. Conclusion The results suggest that treatment with Ro-32-0432 in ischemic stroke decreases the ischemic infarction area, neurological symptoms and associated endothelin B receptor upregulation. This provides a new perspective on possible mechanisms of actions of PKC inhibition in cerebral ischemia.

  3. New light on white matter damage of the premature brain: a neonatologist’s point of view

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    Maria Antonietta Marcialis

    2014-06-01

    Full Text Available Periventricular leucomalacia (PVL is traditionally considered a multifactorial lesion related to three main mechanisms: ischemia, inflammation and excitotoxicity. For years it was believed that hypoperfusion, associated with the peculiar vascular anatomy of the premature brain (border zones, was the conditio sine qua non in the pathogenesis of PVL. More recently this theory has been questioned. Many studies have stressed the importance of the association between inflammation/infection and white matter injury and have supported the multi hit hypothesis according to which several (genetic, hormonal, immune and nutritional factors may team up in a multi-hit fashion. The emerging concept is that the fetal white cell activation together with the interaction between the innate and adaptive immune system play a main role in white matter damage. Currently there are increasing evidence that PVL is a disease of connectivity. In this article we review the news in the basics of pathogenesis, the incidence, the definition and the diagnosis of PVL. Furthermore, recent follow-up studies and neuroprotective therapies are mentioned. Proceedings of the International Course on Perinatal Pathology (part of the 10th International Workshop on Neonatology · October 22nd-25th, 2014 · Cagliari (Italy · October 25th, 2014 · The role of the clinical pathological dialogue in problem solving Guest Editors: Gavino Faa, Vassilios Fanos, Peter Van Eyken

  4. H2O2-mediated DNA damage and repair in the brain cells in the aging rats detected by comet assay

    Institute of Scientific and Technical Information of China (English)

    Suming ZhangM.D., Ph.D; Zongchao Han, M.D.; Siyu Fang, M.D.; Ruan Yang, M.D; Wei Wang, M.D., Ph. D

    2000-01-01

    Objective: To identify the relation between DNA damage susceptibility/ DNA repair capability and aging process after insults, an observation of H2O2_induced DNA damage and the kinetics of DNA repair in senescent murine brain cells with the alkaline single cell gel electrophoresis (SCGE/Comet assay) was made. Methods: The dissociated brain cells harvested in the area of the cerebral cortex, hippocampus, basal gang]ion from 3-month (n=10), 8-month (n=8) and 26-month (n=5) old rats were respectively treated with H2O2 in gradient doses for 10 min, or without H2O2 as controls. The cells embedded in agarose were lysed, helix-untied, electrophoresed, stained with a fluorescence DNA binding stain, viewed under a fluorescence microscope. Individual image was optically recorded. The frequency of the tailed cells and the grade of tails wereused to analyze single strand breaks of DNA and injury intensity. Results: By the cell and DNA image like comets, a linear increase was noticed in vulnerability of DNA both to H2O2 doses and to the age. Regarding the damaged region of the brain, the cortex cells were more vulnerable to the insult than the hippocampus/basal ganglionic cells. Whatever aging or not the cells were, the maximum of ratio of DNA repair was only within 1 hour during the incubation for 0.5-4 hours after the insults. Furthermore, the more aging, the less ratio of DNA repair of sick cells. Conclusion: The DNA damagesusceptibility and the DNA repair capability of individual cells, whatever its age is, can be detected by this brain cell injury model. Comet assay is a sensitive way to find out DNA damage and repair of the cells. It should be more difficult for the cells to cope with an acute and excessive than with a persistent, chronic and mild DNA damage which is more related to an accumulating injury, the aging.

  5. Early (N170/M170 face-sensitivity despite right lateral occipital brain damage in acquired prosopagnosia

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    Esther eAlonso Prieto

    2011-12-01

    Full Text Available Compared to objects, pictures of faces elicit a larger early electromagnetic response at occipito-temporal sites on the human scalp, with an onset of 130 ms and a peak at about 170 ms. This N170 face effect is larger in the right than the left hemisphere and has been associated with the early categorization of the stimulus as a face. Here we tested whether this effect can be observed in the absence of some of the visual areas showing a preferential response to faces as typically identified in neuroimaging. Event related potentials were recorded in response to faces, cars and their phase-scrambled versions in a well-known brain-damaged case of prosopagnosia (PS. Despite the patient’s right inferior occipital gyrus lesion encompassing the most posterior cortical area showing preferential response to faces (occipital face area, OFA, we identified an early face-sensitive component over the right occipito-temporal hemisphere of the patient that was identified as the N170. A second experiment supported this conclusion, showing the typical N170 increase of latency and amplitude in response to inverted faces. In contrast, there was no N170 in the left hemisphere, where PS has a lesion to the middle fusiform gyrus and shows no evidence of face-preferential response in neuroimaging (no left fusiform face area, or lFFA. These results were replicated by a magneto-encephalographic (MEG investigation of the patient, disclosing a M170 component only in the right hemisphere. These observations indicate that face preferential activation in the inferior occipital cortex is not necessary to elicit early visual responses associated with face perception (N170/M170 on the human scalp. These results further suggest that when the right inferior occipital cortex is damaged, the integrity of the middle fusiform gyrus and/or the superior temporal sulcus – two areas showing face preferential responses in the patient’s right hemisphere - might be necessary to generate

  6. Cooperative effect of angiotensin AT(1) and endothelin ET(A) receptor antagonism limits the brain damage after ischemic stroke in rat

    DEFF Research Database (Denmark)

    Stenman, Emelie; Jamali, Roya; Henriksson, Marie;

    2007-01-01

    ) and endothelin ET(A) receptors however decreased the brain damage and improved the neurological scores (both Psmooth muscle cells......Cerebral ischemia results in enhanced expression of smooth muscle cell endothelin and angiotensin receptors in cerebral arteries. We hypothesise that this phenomenon may be detrimental and that acute treatment with a combined non-hypotensive dose of the angiotensin AT(1) receptor inhibitor.......05 mg/kg/day), ZD1611 (0.15 mg/kg/day), both combined or vehicle with start immediately after the occlusion. After 48 h the rats were sacrificed, the brains sliced and stained with 1% 2, 3, 5-triphenyltetrazolium chloride (TTC) and the volume of ischemic damage determined. The middle cerebral arteries...

  7. Moderately delayed post-insult treatment with normobaric hyperoxia reduces excitotoxin-induced neuronal degeneration but increases ischemia-induced brain damage

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    Haelewyn Benoit

    2011-04-01

    Full Text Available Abstract Background The use and benefits of normobaric oxygen (NBO in patients suffering acute ischemic stroke is still controversial. Results Here we show for the first time to the best of our knowledge that NBO reduces both NMDA-induced calcium influxes in vitro and NMDA-induced neuronal degeneration in vivo, but increases oxygen and glucose deprivation-induced cell injury in vitro and ischemia-induced brain damage produced by middle cerebral artery occlusion in vivo. Conclusions Taken together, these results indicate that NBO reduces excitotoxin-induced calcium influx and subsequent neuronal degeneration but favors ischemia-induced brain damage and neuronal death. These findings highlight the complexity of the mechanisms involved by the use of NBO in patients suffering acute ischemic stroke.

  8. Decreased levels of pNR1 S897 protein in the cortex of neonatal Sprague Dawley rats with hypoxic-ischemic or NMDA-induced brain damage

    International Nuclear Information System (INIS)

    Our objective was to investigate the protein level of phosphorylated N-methyl-D-aspartate (NMDA) receptor-1 at serine 897 (pNR1 S897) in both NMDA-induced brain damage and hypoxic-ischemic brain damage (HIBD), and to obtain further evidence that HIBD in the cortex is related to NMDA toxicity due to a change of the pNR1 S897 protein level. At postnatal day 7, male and female Sprague-Dawley rats (13.12 ± 0.34 g) were randomly divided into normal control, phosphate-buffered saline (PBS) cerebral microinjection, HIBD, and NMDA cerebral microinjection groups. Immunofluorescence and Western blot (N = 10 rats per group) were used to examine the protein level of pNR1 S897. Immunofluorescence showed that control and PBS groups exhibited significant neuronal cytoplasmic staining for pNR1 S897 in the cortex. Both HIBD and NMDA-induced brain damage markedly decreased pNR1 S897 staining in the ipsilateral cortex, but not in the contralateral cortex. Western blot analysis showed that at 2 and 24 h after HIBD, the protein level of pNR1 S897 was not affected in the contralateral cortex (P > 0.05), whereas it was reduced in the ipsilateral cortex (P < 0.05). At 2 h after NMDA injection, the protein level of pNR1 S897 in the contralateral cortex was also not affected (P > 0.05). The levels in the ipsilateral cortex were decreased, but the change was not significant (P > 0.05). The similar reduction in the protein level of pNR1 S897 following both HIBD and NMDA-induced brain damage suggests that HIBD is to some extent related to NMDA toxicity possibly through NR1 phosphorylation of serine 897

  9. Decreased levels of pNR1 S897 protein in the cortex of neonatal Sprague Dawley rats with hypoxic-ischemic or NMDA-induced brain damage

    Directory of Open Access Journals (Sweden)

    Ming-Yan Hei

    2012-10-01

    Full Text Available Our objective was to investigate the protein level of phosphorylated N-methyl-D-aspartate (NMDA receptor-1 at serine 897 (pNR1 S897 in both NMDA-induced brain damage and hypoxic-ischemic brain damage (HIBD, and to obtain further evidence that HIBD in the cortex is related to NMDA toxicity due to a change of the pNR1 S897 protein level. At postnatal day 7, male and female Sprague Dawley rats (13.12 ± 0.34 g were randomly divided into normal control, phosphate-buffered saline (PBS cerebral microinjection, HIBD, and NMDA cerebral microinjection groups. Immunofluorescence and Western blot (N = 10 rats per group were used to examine the protein level of pNR1 S897. Immunofluorescence showed that control and PBS groups exhibited significant neuronal cytoplasmic staining for pNR1 S897 in the cortex. Both HIBD and NMDA-induced brain damage markedly decreased pNR1 S897 staining in the ipsilateral cortex, but not in the contralateral cortex. Western blot analysis showed that at 2 and 24 h after HIBD, the protein level of pNR1 S897 was not affected in the contralateral cortex (P > 0.05, whereas it was reduced in the ipsilateral cortex (P 0.05. The levels in the ipsilateral cortex were decreased, but the change was not significant (P > 0.05. The similar reduction in the protein level of pNR1 S897 following both HIBD and NMDA-induced brain damage suggests that HIBD is to some extent related to NMDA toxicity possibly through NR1 phosphorylation of serine 897.

  10. The discrepancy between the absence of copper deposition and the presence of neuronal damage in the brain of Atp7b(-/-) mice.

    Science.gov (United States)

    Dong, Yi; Shi, Sheng-Sheng; Chen, Sheng; Ni, Wang; Zhu, Min; Wu, Zhi-Ying

    2015-02-01

    Wilson's disease (WD) is caused by mutations within the copper-transporting ATPase (ATP7B), characterized by copper deposition in various organs, principally the liver and the brain. With the availability of Atp7b(-/-) mice, the valid animal model of WD, the mechanism underlying copper-induced hepatocyte necrosis has been well understood. Nonetheless, little is known about the adverse impact of copper accumulation on the brain in WD. Therefore, the aim of this study was to identify copper disturbances according to various brain compartments and further dissect the causal relationship between copper storage and neuronal damage using Atp7b(-/-) mice. Copper levels in the liver, whole brain, brain compartments and basal ganglia mitochondria of Atp7b(-/-) mice and age-matched controls were measured by atomic absorption spectroscopy. Delicate electron microscopic studies on hepatocytes and neurons in the basal ganglia were performed. Here we further confirmed the remarkably elevated copper content and abnormal ultrastructure findings in livers of Atp7b(-/-) mice. Interestingly, we found the ultrastructure abnormalities in neurons of the basal ganglia of Atp7b(-/-) mice, whereas copper deposition was not detected in the whole brain, even within the basal ganglia and its mitochondria. The disparity provided a new understanding of neuronal dysfunction in WD, and strongly indicated that copper might not be the sole causative player and other unidentified pathogenic factors could enhance the toxic effects of copper on neurons in WD.

  11. Regulation of endogenous neural stem/progenitor cells for neural repair - factors that promote neurogenesis and gliogenesis in the normal and damaged brain

    Directory of Open Access Journals (Sweden)

    Kimberly eChristie

    2013-01-01

    Full Text Available Neural stem/precursor cells in the adult brain reside in the subventricular zone (SVZ of the lateral ventricles and the subgranular zone (SGZ of the dentate gyrus in the hippocampus. These cells primarily generate neuroblasts that normally migrate to the olfactory bulb and the dentate granule cell layer respectively. Following brain damage, such as traumatic brain injury, ischemic stroke or in degenerative disease models, neural precursor cells from the SVZ in particular, can migrate from their normal route along the rostral migratory stream to the site of neural damage. This neural precursor cell response to neural damage is mediated by release of endogenous factors, including cytokines and chemokines produced by the inflammatory response at the injury site, and by the production of growth and neurotrophic factors. Endogenous hippocampal neurogenesis is frequently also directly or indirectly affected by neural damage. Administration of a variety of factors that regulate different aspects of neural stem/precursor biology often leads to improved functional motor and/or behavioural outcomes. Such factors can target neural stem/precursor proliferation, survival, migration and differentiation into appropriate neuronal or glial lineages. Newborn cells also need to subsequently survive and functionally integrate into extant neural circuitry, which may be the major bottleneck to the current therapeutic potential of neural stem/precursor cells. This review will cover the effects of a range of intrinsic and extrinsic factors that regulate neural stem /precursor cell functions. In particular it focuses on factors that may be harnessed to enhance the endogenous neural stem/precursor cell response to neural damage, highlighting those that have already shown evidence of preclinical effectiveness and discussing others that warrant further preclinical investigation.

  12. First Autologous Cell Therapy of Cerebral Palsy Caused by Hypoxic-Ischemic Brain Damage in a Child after Cardiac Arrest—Individual Treatment with Cord Blood

    Science.gov (United States)

    Jensen, A.; Hamelmann, E.

    2013-01-01

    Each year, thousands of children incur brain damage that results in lifelong sequelae. Therefore, based on experimental evidence, we explored the therapeutic potential of human cord blood, known to contain stem cells, to examine the functional neuroregeneration in a child with cerebral palsy after cardiac arrest. The boy, whose cord blood was stored at birth, was 2.5 years old and normally developed when global ischemic brain damage occurred resulting in a persistent vegetative state. Nine weeks later, he received autologous cord blood (91.7 mL, cryopreserved, 5.75 × 10e8 mononuclear cells) intravenously. Active rehabilitation (physio- and ergotherapy) was provided daily, follow-up at 2, 5, 12, 24, 30, and 40 months. At 2-months follow-up the boy's motor control improved, spastic paresis was largely reduced, and eyesight was recovered, as did the electroencephalogram. He smiled when played with, was able to sit and to speak simple words. At 40 months, independent eating, walking in gait trainer, crawling, and moving from prone position to free sitting were possible, and there was significantly improved receptive and expressive speech competence (four-word sentences, 200 words). This remarkable functional neuroregeneration is difficult to explain by intense active rehabilitation alone and suggests that autologous cord blood transplantation may be an additional and causative treatment of pediatric cerebral palsy after brain damage. PMID:23762741

  13. First autologous cell therapy of cerebral palsy caused by hypoxic-ischemic brain damage in a child after cardiac arrest-individual treatment with cord blood.

    Science.gov (United States)

    Jensen, A; Hamelmann, E

    2013-01-01

    Each year, thousands of children incur brain damage that results in lifelong sequelae. Therefore, based on experimental evidence, we explored the therapeutic potential of human cord blood, known to contain stem cells, to examine the functional neuroregeneration in a child with cerebral palsy after cardiac arrest. The boy, whose cord blood was stored at birth, was 2.5 years old and normally developed when global ischemic brain damage occurred resulting in a persistent vegetative state. Nine weeks later, he received autologous cord blood (91.7 mL, cryopreserved, 5.75 × 10e8 mononuclear cells) intravenously. Active rehabilitation (physio- and ergotherapy) was provided daily, follow-up at 2, 5, 12, 24, 30, and 40 months. At 2-months follow-up the boy's motor control improved, spastic paresis was largely reduced, and eyesight was recovered, as did the electroencephalogram. He smiled when played with, was able to sit and to speak simple words. At 40 months, independent eating, walking in gait trainer, crawling, and moving from prone position to free sitting were possible, and there was significantly improved receptive and expressive speech competence (four-word sentences, 200 words). This remarkable functional neuroregeneration is difficult to explain by intense active rehabilitation alone and suggests that autologous cord blood transplantation may be an additional and causative treatment of pediatric cerebral palsy after brain damage. PMID:23762741

  14. Right Hemisphere Brain Damage

    Science.gov (United States)

    ... or focusing on what is said or seen. Perception: Visual perception deficits causing a person to have difficulty perceiving ... recalling previously learned information and learning new information. Social communication (pragmatics): Difficulty interpreting abstract language such as ...

  15. Quantitative MRI analysis of the brain after twenty-two years of neuromyelitis optica indicates focal tissue damage

    DEFF Research Database (Denmark)

    Aradi, Mihaly; Koszegi, Edit; Orsi, Gergely;

    2013-01-01

    BACKGROUND: The long-term effect of neuromyelitis optica (NMO) on the brain is not well established. METHODS: After 22 years of NMO, a patient's brain was examined by quantitative T1- and T2-weighted mono- and biexponential diffusion and proton spectroscopy. It was compared to 3 cases with short...

  16. Rapamycin Reduced Ischemic Brain Damage in Diabetic Animals Is Associated with Suppressions of mTOR and ERK1/2 Signaling

    Science.gov (United States)

    Liu, Ping; Yang, Xiao; Hei, Changchun; Meli, Yvonne; Niu, Jianguo; Sun, Tao; Li, P. Andy

    2016-01-01

    The objectives of the present study are to investigate the activation of mTOR and ERK1/2 signaling after cerebral ischemia in diabetic rats and to examine the neuroprotective effects of rapamycin. Ten minutes transient global cerebral ischemia was induced in straptozotocin-induced diabetic hyperglycemic rats and non-diabetic, euglycemic rats. Brain samples were harvested after 16 h of reperfusion. Rapamycin or vehicle was injected 1 month prior to the induction of ischemia. The results showed that diabetes increased ischemic neuronal cell death and associated with elevations of p-P70S6K and Ras/ERK1/2 and suppression of p-AMPKα. Rapamycin ameliorated diabetes-enhanced ischemic brain damage and suppressed phosphorylation of P70S6K and ERK1/2. It is concluded that diabetes activates mTOR and ERK1/2 signaling pathways in rats subjected to transient cerebral ischemia and inhibition of mTOR by rapamycin reduces ischemic brain damage and suppresses the mTOR and ERK1/2 signaling in diabetic settings. PMID:27489506

  17. Cerebral Visual Impairment: Which Perceptive Visual Dysfunctions Can Be Expected in Children with Brain Damage? A Systematic Review

    Science.gov (United States)

    Boot, F. H.; Pel, J. J. M.; van der Steen, J.; Evenhuis, H. M.

    2010-01-01

    The current definition of Cerebral Visual Impairment (CVI) includes all visual dysfunctions caused by damage to, or malfunctioning of, the retrochiasmatic visual pathways in the absence of damage to the anterior visual pathways or any major ocular disease. CVI is diagnosed by exclusion and the existence of many different causes and symptoms make…

  18. The relationship between emotion regulation capacity, heart rate variability, and quality of life in individuals with alcohol-related brain damage

    Directory of Open Access Journals (Sweden)

    Steinmetz JP

    2016-08-01

    Full Text Available Jean-Paul Steinmetz,1,2 Claus Vögele,3,4 Christiane Theisen-Flies,5 Carine Federspiel,1,2 Stefan Sütterlin6,7 1Department of Research and Development, ZithaSenior, 2Centre for Memory and Mobility, ZithaSenior, 3Institute for Health and Behaviour, Integrative Research Unit on Social and Individual Development (INSIDE, University of Luxembourg, Luxembourg; 4Research Group Health Psychology, University of Leuven, Leuven, Belgium; 5Home St Joseph, ZithaSenior, Luxembourg; 6Department of Psychology, Lillehammer University College, Lillehammer, 7Division of Surgery and Clinical Neuroscience, Department of Psychosomatic Medicine, Oslo University Hospital – Rikshospitalet, Oslo, Norway Abstract: The reliable measurement of quality of life (QoL presents a challenge in individuals with alcohol-related brain damage. This study investigated vagally mediated heart rate variability (vmHRV as a physiological predictor of QoL. Self- and proxy ratings of QoL and dysexecutive symptoms were collected once, while vmHRV was repeatedly assessed over a 3-week period at weekly intervals in a sample of nine alcohol-related brain damaged patients. We provide robustness checks, bootstrapped correlations with confidence intervals, and standard errors for mean scores. We observed low to very low heart rate variability scores in our patients in comparison to norm values found in healthy populations. Proxy ratings of the QoL scale “subjective physical and mental performance” and everyday executive dysfunctions were strongly related to vmHRV. Better proxy-rated QoL and fewer dysexecutive symptoms were observed in those patients with higher vmHRV. Overall, patients showed low parasympathetic activation favoring the occurrence of dysfunctional emotion regulation strategies. Keywords: heart rate variability, emotion regulation, alcohol-related brain damage, quality of life

  19. Duration and numerical estimation in right brain-damaged patients with and without neglect: Lack of support for a mental time line.

    Science.gov (United States)

    Masson, Nicolas; Pesenti, Mauro; Dormal, Valérie

    2016-08-01

    Previous studies have shown that left neglect patients are impaired when they have to orient their attention leftward relative to a standard in numerical comparison tasks. This finding has been accounted for by the idea that numerical magnitudes are represented along a spatial continuum oriented from left to right with small magnitudes on the left and large magnitudes on the right. Similarly, it has been proposed that duration could be represented along a mental time line that shares the properties of the number continuum. By comparing directly duration and numerosity processing, this study investigates whether or not the performance of neglect patients supports the hypothesis of a mental time line. Twenty-two right brain-damaged patients (11 with and 11 without left neglect), as well as 11 age-matched healthy controls, had to judge whether a single dot presented visually lasted shorter or longer than 500 ms and whether a sequence of flashed dots was smaller or larger than 5. Digit spans were also assessed to measure verbal working memory capacities. In duration comparison, no spatial-duration bias was found in neglect patients. Moreover, a significant correlation between verbal working memory and duration performance was observed in right brain-damaged patients, irrespective of the presence or absence of neglect. In numerical comparison, only neglect patients showed an enhanced distance effect for numerical magnitude smaller than the standard. These results do not support the hypothesis of the existence of a mental continuum oriented from left to right for duration. We discuss an alternative account to explain the duration impairment observed in right brain-damaged patients. PMID:26395357

  20. Twenty-year brain magnetic resonance imaging follow-up study in Systemic Lupus Erythematosus: Factors associated with accrual of damage and central nervous system involvement.

    Science.gov (United States)

    Piga, Matteo; Peltz, Maria Teresa; Montaldo, Carlo; Perra, Daniela; Sanna, Giovanni; Cauli, Alberto; Mathieu, Alessandro

    2015-06-01

    To evaluate the long-term progression of cerebral MRI abnormalities in patients with longstanding SLE, 30 patients (age 53.5 ± 11.3) underwent brain MRI at baseline (b-MRI) and after 19.4 ± 3.7 years of follow-up (fu-MRI). Two neuroradiologists visually analyzed the MRIs comparing: 1) white matter hyperintensities (WMHIs), 2) cerebral volume, and 3) parenchymal defects; these outcomes were also built in a modified MRI scoring system (mMSS) to estimate the cumulative parenchymal damage. The independent risk factors for accrual of MRI brain damage, as well as the association between MRI abnormalities and the development of new neuropsychiatric (NP) manifestations classified according to the 1999 ACR case definition were also analyzed. Twenty-three patients (76.7%) showed worsening of mMSS; 19 (63.3%) had increased number and volume of WMHIs, 8 (26.7%) had significant cerebral volume loss, and 6 (20%) showed new ischemic parenchymal lesions. Only 6 patients had normal MRI. Antimalarial agents (p=0.006; OR 0.08) were protective against worsening of WMHIs. High cumulative dose of corticosteroids (p=0.026; OR 8.8) and dyslipidemia (p=0.044; OR 10.1) were associated with increased mMSS and cerebral volume loss, respectively. Higher mMSS score at baseline was independently associated with worsening of WMHIs (p=0.001; OR 5.7) and development of new NP events (p=0.019; OR 2.0); higher load of deep WMHIs at b-MRI (p=0.018; OR 2.0) was independently associated with stroke risk. This study shows that MRI brain damage in SLE patients progresses independently from NP involvement as effect of potentially modifiable risk factors and it is associated with increased risk of new NP events. PMID:25617815

  1. Involvement of the JNK/FOXO3a/Bim Pathway in Neuronal Apoptosis after Hypoxic-Ischemic Brain Damage in Neonatal Rats.

    Directory of Open Access Journals (Sweden)

    Deyuan Li

    Full Text Available c-Jun N-terminal kinase (JNK plays a key role in the regulation of neuronal apoptosis. Previous studies have revealed that forkhead transcription factor (FOXO3a is a critical effector of JNK-mediated tumor suppression. However, it is not clear whether the JNK/FOXO3a pathway is involved in neuronal apoptosis in the developing rat brain after hypoxia-ischemia (HI. In this study, we generated an HI model using postnatal day 7 rats. Fluorescence immunolabeling and Western blot assays were used to detect the distribution and expression of total and phosphorylated JNK and FOXO3a and the pro-apoptotic proteins Bim and CC3. We found that JNK phosphorylation was accompanied by FOXO3a dephosphorylation, which induced FOXO3a translocation into the nucleus, resulting in the upregulation of levels of Bim and CC3 proteins. Furthermore, we found that JNK inhibition by AS601245, a specific JNK inhibitor, significantly increased FOXO3a phosphorylation, which attenuated FOXO3a translocation into the nucleus after HI. Moreover, JNK inhibition downregulated levels of Bim and CC3 proteins, attenuated neuronal apoptosis and reduced brain infarct volume in the developing rat brain. Our findings suggest that the JNK/FOXO3a/Bim pathway is involved in neuronal apoptosis in the developing rat brain after HI. Agents targeting JNK may offer promise for rescuing neurons from HI-induced damage.

  2. Brain-Specific Cytoskeletal Damage Markers in Cerebrospinal Fluid: Is There a Common Pattern between Amyotrophic Lateral Sclerosis and Primary Progressive Multiple Sclerosis?

    Science.gov (United States)

    Abdelhak, Ahmed; Junker, Andreas; Brettschneider, Johannes; Kassubek, Jan; Ludolph, Albert C; Otto, Markus; Tumani, Hayrettin

    2015-01-01

    Many neurodegenerative disorders share a common pathophysiological pathway involving axonal degeneration despite different etiological triggers. Analysis of cytoskeletal markers such as neurofilaments, protein tau and tubulin in cerebrospinal fluid (CSF) may be a useful approach to detect the process of axonal damage and its severity during disease course. In this article, we review the published literature regarding brain-specific CSF markers for cytoskeletal damage in primary progressive multiple sclerosis and amyotrophic lateral sclerosis in order to evaluate their utility as a biomarker for disease progression in conjunction with imaging and histological markers which might also be useful in other neurodegenerative diseases associated with affection of the upper motor neurons. A long-term benefit of such an approach could be facilitating early diagnostic and prognostic tools and assessment of treatment efficacy of disease modifying drugs.

  3. Brain-Specific Cytoskeletal Damage Markers in Cerebrospinal Fluid: Is There a Common Pattern between Amyotrophic Lateral Sclerosis and Primary Progressive Multiple Sclerosis?

    Directory of Open Access Journals (Sweden)

    Ahmed Abdelhak

    2015-07-01

    Full Text Available Many neurodegenerative disorders share a common pathophysiological pathway involving axonal degeneration despite different etiological triggers. Analysis of cytoskeletal markers such as neurofilaments, protein tau and tubulin in cerebrospinal fluid (CSF may be a useful approach to detect the process of axonal damage and its severity during disease course. In this article, we review the published literature regarding brain-specific CSF markers for cytoskeletal damage in primary progressive multiple sclerosis and amyotrophic lateral sclerosis in order to evaluate their utility as a biomarker for disease progression in conjunction with imaging and histological markers which might also be useful in other neurodegenerative diseases associated with affection of the upper motor neurons. A long-term benefit of such an approach could be facilitating early diagnostic and prognostic tools and assessment of treatment efficacy of disease modifying drugs.

  4. CGP 35348, GABA B Receptor Antagonist, Has a Potential to Improve Neuromuscular Coordination and Spatial Learning in Albino Mouse following Neonatal Brain Damage

    OpenAIRE

    Gillani, Q.; M. Ali; Iqbal, F.

    2014-01-01

    To study the effect of CGP 35348 on learning and memory in albino mice following hypoxia ischemia insult, 10 days old albino mice were subjected to right common carotid artery ligation followed by 8% hypoxia for 25 minutes. Following brain damage, mice were fed on normal rodent diet till they were 13 week old. At this time point, mice were divided into two groups. Group 1 received saline and group 2 intrapertoneally CGP 35348 (1 mg/mL solvent/Kg body weight) for 12 days. A battery of tests us...

  5. Bilateral cerebellar and brain stem infarction resulting from vertebral artery injury following cervical trauma without radiographic damage of the spinal column: A case report

    Energy Technology Data Exchange (ETDEWEB)

    Mimata, Yoshikuni; Sato, Kotaro; Suzuki, Yoshiaki [Iwate Prefectural Chubu Hospital, Department of Orthopaedic Surgery, Kitakami (Japan); Murakami, Hideki [Iwate Medical University, Department of Orthopaedic Surgery, School of Medicine, Morioka (Japan)

    2014-01-15

    Vertebral artery injury can be a complication of cervical spine injury. Although most cases are asymptomatic, the rare case progresses to severe neurological impairment and fatal outcomes. We experienced a case of bilateral cerebellar and brain stem infarction with fatal outcome resulting from vertebral artery injury associated with cervical spine trauma. A 69-year-old male was admitted to our hospital because of tetraplegia after falling down the stairs and hitting his head on the floor. Marked bony damage of the cervical spine was not apparent on radiographs and CT scans, so the injury was initially considered to be a cervical cord injury without bony damage. However, an intensity change in the intervertebral disc at C5/C6, and a ventral epidural hematoma were observed on MRI. A CT angiogram of the neck showed the right vertebral artery was completely occluded at the C4 level of the spine. Forty-eight hours after injury, the patient lapsed into drowsy consciousness. The cranial CT scan showed a massive low-density area in the bilateral cerebellar hemispheres and brain stem. Anticoagulation was initiated after a diagnosis of the right vertebral artery injury, but the patient developed bilateral cerebellar and brain stem infarction. The patient's brain herniation progressed and the patient died 52 h after injury. We considered that not only anticoagulation but also treatment for thrombosis would have been needed to prevent cranial embolism. We fully realize that early and appropriate treatment are essential to improve the treatment results, and constructing a medical system with a team of orthopedists, radiologists, and neurosurgeons is also very important. (orig.)

  6. DNA damage induced by phenylalanine and its analogue p-chlorophenylalanine in blood and brain of rats subjected to a model of hyperphenylalaninemia.

    Science.gov (United States)

    Simon, Kellen R; Dos Santos, Rosane M; Scaini, Giselli; Leffa, Daniela D; Damiani, Adriani P; Furlanetto, Camila B; Machado, Jéssica L; Cararo, José H; Macan, Tamires P; Streck, Emilio L; Ferreira, Gustavo C; Andrade, Vanessa M; Schuck, Patrícia F

    2013-10-01

    Phenylketonuria (PKU) is a disease caused by a deficiency of phenylalanine hydroxylase (PAH), resulting in an accumulation of phenylalanine (Phe) in the brain tissue, cerebrospinal fluid, and other tissues of PKU patients. Considering that high levels of Phe are associated with neurological dysfunction and that the mechanisms underlying the neurotoxicity in PKU remain poorly understood, the main objective of this study was to investigate the in vivo and in vitro effects of Phe on DNA damage, as determined by the alkaline comet assay. The results showed that, compared to control group, the levels of DNA migration were significantly greater after acute administration of Phe, p-chlorophenylalanine (p-Cl-Phe, an inhibitor of PAH), or a combination thereof in cerebral cortex and blood, indicating DNA damage. These treatments also provoked increase of carbonyl content. Additionally, when Phe or p-Cl-Phe was present in the incubation medium, we observed an increase in the frequency and index of DNA damage in the cerebral cortex and blood, without affecting lactate dehydrogenase (LDH) release. Our in vitro and in vivo findings indicate that DNA damage occurs in the cerebral cortex and blood of rats receiving Phe, suggesting that this mechanism could be, at least in part, responsible for the neurological dysfunction in PKU patients.

  7. Differential effects of fresh frozen plasma and normal saline on secondary brain damage in a large animal model of polytrauma, hemorrhage and traumatic brain injury

    DEFF Research Database (Denmark)

    Hwabejire, John O; Imam, Ayesha M; Jin, Guang;

    2013-01-01

    We have previously shown that the extent of traumatic brain injury (TBI) in large animal models can be reduced with early infusion of fresh frozen plasma (FFP), but the precise mechanisms remain unclear. In this study, we investigated whether resuscitation with FFP or normal saline differed...

  8. 性别对新生缺氧缺血性脑损伤大鼠学习记忆功能及脑组织损伤的影响%The effect of sex differences on the ability of learning and memory and brain tissue damage of newborn rats with hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    唐华兵; 温晓红; 黄会芝; 刘惠

    2015-01-01

    Objective To explore the effect of sex difference on learning and memory function and the brain tissue damage of neonatal SD rats with hypoxic-ischemic brain damage.Methods Sixty,7-day-old neonatal Sprague-Dawley rats,were divided into randomly:male control group (M group,n=15),female control group (F group,n=15),male hypoxic-ischemic brain damage group (MHIBD group,n=15) and female hypoxic-ischemic brain damage group (FHIBD group,n=15).A modified newborn rat model that had a combined hypoxic-ischemic brain damage as described by Rice-Vannucci was used.The Morris water maze was used to evaluate the ability of learning and memory.The brain MRI and transmission electron microscope(TEM) was used to evaluate the scope of brain tissue damage and the change of the synaptic ultrastructure.Results There were no differences in swimming distance,escape latency,synaptic cleft and damage brain volume between M group and F group(P>0.05).Compare with M group and F group,MHIBD group and FHIBD group showed significant brain injury,longer escape latency ((39.38±11.40) s vs (14.86±4.42) s,(30.14±7.18)s vs (18.41±5.03) s),longer swimming distance ((15.31± 1.77) cm vs (3.68±1.50) cm,(13.18±1.79) cm vs (4.61±1.61) cm),and TEM showed the synaptic cleft was widened ((23.18± 1.36) nm vs (19.24± 1.51) nm,(21.40± 1.71) nm vs (19.87±0.94) nm),P<0.05).MHIBD group was more seriously compromised than the FHIBD group(P<0.05).The brain MRI showed the damage brain volume of MHIBD group were significantly larger than FHIBD group(P<0.05).Conclusion After bypoxic ischemic brain damage,the tolerance of brain damage and / or post-injury recovery capabilities of female rats are stronger than males.%目的 探讨不同性别新生大鼠缺氧缺血性脑损伤(hypoxic ischemic brain damage,HIBD)后学习记忆功能及脑组织损伤的改变.方法 新生7d龄SD大鼠60只,采用随机数表法分为雄性对照组、雌性对照组、雄性HIBD组、雌性HIBD组,每组15

  9. Vulnerability of the Developing Brain to Hypoxic-Ischemic Damage: Contribution of the Cerebral Vasculature to Injury and Repair?

    Directory of Open Access Journals (Sweden)

    Ana eBaburamani

    2012-11-01

    Full Text Available As clinicians attempt to understand the underlying reasons for the vulnerability of different regions of the developing brain to injury, it is apparent that little is known as to how hypoxia-ischemia may affect the cerebrovasculature in the developing infant. Most of the research investigating the pathogenesis of perinatal brain injury following hypoxia-ischemia has focussed on excitotoxicity, oxidative stress and inflammatory response, with the response of the developing cerebrovasculature receiving less attention. This is surprising as the presentation of devastating and permanent injury such as germinal matrix-intraventricular haemorrhage (GM-IVH and perinatal stroke are of vascular origin, and the origin of periventricular leukomalacia (PVL may also arise from poor perfusion of the white matter. This highlights that cerebrovasculature injury following hypoxia could primarily be responsible for the injury seen in the brain of many infants diagnosed with hypoxic-ischemic encephalopathy (HIE.Interestingly the highly dynamic nature of the cerebral blood vessels in the fetus, and the fluctuations of cerebral blood flow and metabolic demand that occur following hypoxia suggest that the response of blood vessels could explain both regional protection and vulnerability in the developing brain. However research into how blood vessels respond following hypoxia-ischemia have mostly been conducted in adult models of ischemia or stroke, further highlighting the need to investigate how the developing cerebrovasculature responds and the possible contribution to perinatal brain injury following hypoxia. This review discusses the current concepts on the pathogenesis of perinatal brain injury, the development of the fetal cerebrovasculature and the blood brain barrier (BBB, and key mediators involved with the response of cerebral blood vessels to hypoxia.

  10. Surviving Brain Damage After Assault Wilson Barbara A Dhamapurkar Samira Kashinath and Rose Anita Surviving Brain Damage After Assault 154pp £19.99 Psychology Press/Routledge 9781138824584 1138824585 [Formula: see text].

    Science.gov (United States)

    2016-09-01

    This book documents the journey of Gary, a young man who sustained a severe traumatic brain injury in an attack by a gang armed with hammers and baseball bats. Gary spent 19 months with minimal awareness of his surroundings before showing signs of recovery and, after nearly three years of rehabilitation, a return to independence.

  11. The relationship between emotion regulation capacity, heart rate variability, and quality of life in individuals with alcohol-related brain damage.

    Science.gov (United States)

    Steinmetz, Jean-Paul; Vögele, Claus; Theisen-Flies, Christiane; Federspiel, Carine; Sütterlin, Stefan

    2016-01-01

    The reliable measurement of quality of life (QoL) presents a challenge in individuals with alcohol-related brain damage. This study investigated vagally mediated heart rate variability (vmHRV) as a physiological predictor of QoL. Self- and proxy ratings of QoL and dysexecutive symptoms were collected once, while vmHRV was repeatedly assessed over a 3-week period at weekly intervals in a sample of nine alcohol-related brain damaged patients. We provide robustness checks, bootstrapped correlations with confidence intervals, and standard errors for mean scores. We observed low to very low heart rate variability scores in our patients in comparison to norm values found in healthy populations. Proxy ratings of the QoL scale "subjective physical and mental performance" and everyday executive dysfunctions were strongly related to vmHRV. Better proxy-rated QoL and fewer dysexecutive symptoms were observed in those patients with higher vmHRV. Overall, patients showed low parasympathetic activation favoring the occurrence of dysfunctional emotion regulation strategies. PMID:27616894

  12. The relationship between emotion regulation capacity, heart rate variability, and quality of life in individuals with alcohol-related brain damage

    Science.gov (United States)

    Steinmetz, Jean-Paul; Vögele, Claus; Theisen-Flies, Christiane; Federspiel, Carine; Sütterlin, Stefan

    2016-01-01

    The reliable measurement of quality of life (QoL) presents a challenge in individuals with alcohol-related brain damage. This study investigated vagally mediated heart rate variability (vmHRV) as a physiological predictor of QoL. Self- and proxy ratings of QoL and dysexecutive symptoms were collected once, while vmHRV was repeatedly assessed over a 3-week period at weekly intervals in a sample of nine alcohol-related brain damaged patients. We provide robustness checks, bootstrapped correlations with confidence intervals, and standard errors for mean scores. We observed low to very low heart rate variability scores in our patients in comparison to norm values found in healthy populations. Proxy ratings of the QoL scale “subjective physical and mental performance” and everyday executive dysfunctions were strongly related to vmHRV. Better proxy-rated QoL and fewer dysexecutive symptoms were observed in those patients with higher vmHRV. Overall, patients showed low parasympathetic activation favoring the occurrence of dysfunctional emotion regulation strategies.

  13. Value of serum brain natriuretic peptide levels in the prognosis of brain damage after cardiopulmonary resuscitation%血清脑钠肽水平对心肺复苏后脑损伤的预测价值研究

    Institute of Scientific and Technical Information of China (English)

    李钦浩; 巩晓娜; 周娆娆; 刘朋; 张磊; 亓雪梅; 蒋芳杰

    2013-01-01

    OBJECTIVE To evaluate the effect of serum brain natriuretic peptide levels on brain damage at the early stage after cardiopulmonary resuscitation (CPR). METHODS There were 34 patients with restoration of spontaneous circulation after successful CPR.After 2 months of successful cardiopulmonary resuscitation (CPR) , patients with GCS score ≥ 12 were mild brain damage (I group, male 6 cases, female 8 cases); GCS score 9 ≤ GCS ≤ 11 were moderate brain damage (II group, male 4 cases, female 6 cases); GCS score 3 ≤ GCS ≤ 8 were severe brain damage (Ⅲ group, male 5 cases, and female 5 cases) . Control group was consisted of 15 healthy volunteers. All of the patients' venous blood were respectively collected and BNP was detected by enzyme linked immunosorbent assay at 2, 8, 12, 24 and 48 h after restoring of independent circulation. RESULTS Compared the age, sex, start time of cardiac arrest to recovery in cardiopulmonary resuscitation (CPR) group and control group, differences were not statistically significant (P> 0.05); at 2, 8, 12, 24 and 48 h, serum BNP levels in I , II and Ⅲ groups were significantly higher than the control group (P < 0.05); And in the trail group, I group was significantly lower than the II group (P< 0.05); II group and was significantly lower than the HI group (P< 0.05). CONCLUSION Serum BNP levels can reflect cardiopulmonary resuscitation (CPR) early after HPC ischemia brain damage, and for the assessment of the recovery cardiopulmonary resuscitation (CPR) has an important value.%目的 探讨血清脑钠肽(BNP)对心肺复苏后脑损伤的预测的价值.方法 34例经心肺复苏后自主循环恢复的患者,以心肺复苏成功后2个月格拉斯哥昏迷评分(GCS)≥12为轻度脑损伤(Ⅰ组),男6例,女8例;9≤GCS≤11为中度脑损伤(Ⅱ组),男4例,女6例;3≤GCS≤8为重度脑损伤(Ⅲ组),男5例,女5例.另外选取14例健康者(女8例,男6例)作为对照组.所有患者均在自主循环恢复后2、8

  14. Reversible lesions in the brain parenchyma in Wilson's disease confirmed by magnetic resonance imaging: earlier administration of chelating therapy can reduce the damage to the brain.

    Science.gov (United States)

    Kozić, Duško B; Petrović, Igor; Svetel, Marina; Pekmezović, Tatjana; Ragaji, Aleksandar; Kostić, Vladimir S

    2014-11-01

    The aim of this study was to evaluate the resolution of brain lesions in patients with Wilson's disease during the long-term chelating therapy using magnetic resonance imaging and a possible significance of the time latency between the initial symptoms of the disease and the introduction of this therapy. Initial magnetic resonance examination was performed in 37 patients with proven neurological form of Wilson's disease with cerebellar, parkinsonian and dystonic presentation. Magnetic resonance reexamination was done 5.7 ± 1.3 years later in 14 patients. Patients were divided into: group A, where chelating therapy was initiated < 24 months from the first symptoms and group B, where the therapy started ≥ 24 months after the initial symptoms. Symmetry of the lesions was seen in 100% of patients. There was a significant difference between groups A and B regarding complete resolution of brain stem and putaminal lesions (P = 0.005 and P = 0.024, respectively). If the correct diagnosis and adequate treatment are not established less than 24 months after onset of the symptoms, irreversible lesions in the brain parenchyma could be expected. Signal abnormalities on magnetic resonance imaging might therefore, at least in the early stages, represent reversible myelinolisis or cytotoxic edema associated with copper toxicity.

  15. Flunarizine and lamotngine propnyiaxis effects on neuron-specific enolase,S-100,and brain-specific creatine kinase in a fetal rat model of hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Li He; Jingyi Deng; Wendan He

    2008-01-01

    BACKGROUND:Calcium antagonists may act as neuroprotectants,diminishing the influx of calcium ions through voltage-sensitive calcium channels. When administered prophylactically,they display neuroprotective effects against hypoxic-ischemic brain damage in newborn rats.OBJECTIVE:To investigate the neuroprotective effects of flunarizine(FNZ),lamotrigine (LTG)and the combination of both drugs,on hypoxic-ischemic brain damage in fetal rats.DESIGN AND SETTING:This randomized,complete block design was performed at the Department of Pediatrics.Shenzhen Fourth People's Hospital,Guangdong Medical College.MATERIALS:Forty pregnant Wistar rats,at gestational day 20,were selected for the experiment and were randomly divided into FNZ,LTG,FNZ+LTG,and model groups,with 10 rats in each group.METHODS:Rats in the FNZ.LTG,and FNZ+LTG groups received intragastric injections of FNZ (0.5 mg/kg/d),LTG(10 mg/kg/d),and FNZ(0.5 mg/kg/d)+LTG(10 mg/kg/d),respectively.Drugs were administered once a day for 3 days prior to induction of hypoxia-ischemia.Rats in the modeJ group were not administered any drugs.Three hours after the final administration,eight pregnant rats from each group underwent model establishment hypoxia-ischemia brain damage to the fetal rats.Cesareans were performed at 6,12,24,and 48 hours later;and 5 fetal rats were removed from each mother and kept warm.Twe fetuses without model establishment were removed by planned cesarean at the same time and served as controls.A total of 0.3 mL serum was collected from fetal rats at 6,12,24,and 48 hours,respectively,following birth.MAIN OUTCOME MEASURES:Serum protein concentrations of neuron-specific enolase and S-100 were measured by ELISA.Serum concentrations of brain-specific creatine kinase were measured using an electrogenerated chemiluminescence method.RESULTS:Serum concentrations of neuron-specific enolase,S-100,and brain-specific creatine kinase were significantly higher in the hypoxic-ischemic fetal rats.compared with the non

  16. Orally Administrated Ascorbic Acid Suppresses Neuronal Damage and Modifies Expression of SVCT2 and GLUT1 in the Brain of Diabetic Rats with Cerebral Ischemia-Reperfusion

    Directory of Open Access Journals (Sweden)

    Naohiro Iwata

    2014-04-01

    Full Text Available Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2 and glucose transporter 1 (GLUT1 after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o. for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.

  17. Temporal dynamics of cerebral blood flow, cortical damage, apoptosis, astrocyte-vasculature interaction and astrogliosis in the pericontusional region after traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Sonia eVillapol

    2014-06-01

    Full Text Available Traumatic brain injury (TBI results in a loss of brain tissue at the moment of impact in the cerebral cortex. Subsequent secondary injury involves the release of molecular signals with dramatic consequences for the integrity of damaged tissue, leading to the evolution of a pericontusional-damaged area minutes to days after in the initial injury. The mechanisms behind the progression of tissue loss remain under investigation. In this study, we analyzed the spatial-temporal profile of blood flow, apoptotic and astrocytic-vascular events in the cortical regions around the impact site at time points ranging from 5 hours to 2 months after TBI. We performed a mild-moderate controlled cortical impact injury in young adult mice and analyzed the glial and vascular response to injury. We observed a dramatic decrease in perilesional cerebral blood flow (CBF immediately following the cortical impact that lasted until days later. CBF finally returned to baseline levels by 30 days post-injury (dpi. The initial impact also resulted in an immediate loss of tissue and cavity formation that gradually increased in size until 3 dpi. An increase in dying cells localized in the pericontusional region and a robust astrogliosis were also observed at 3 dpi. A strong vasculature interaction with astrocytes was established at 7 dpi. Glial scar formation began at 7 dpi and seemed to be compact by 60 dpi. Altogether, these results suggest that TBI results in a progression from acute neurodegeneration that precedes astrocytic activation, reformation of the neurovascular unit to glial scar formation. Understanding the multiple processes occurring after TBI is critical to the ability to develop neuroprotective therapeutics to ameliorate the short and long-term consequences of brain injury.

  18. Ameliorating reactive oxygen species-induced in vitro lipid peroxidation in brain, liver, mitochondria and DNA damage by Zingiber officinale Roscoe.

    Science.gov (United States)

    Ajith, T A

    2010-01-01

    Iron is an essential nutrient for a number of cellular activities. However, excess cellular iron can be toxic by producing reactive oxygen species (ROS) such as superoxide anion (O(2) (-)) and hydroxyl radical (HO(·)) that damage proteins, lipids and DNA. Mutagenic and genotoxic end products of lipid peroxidation can induce the decline of mitochondrial respiration and are associated with various human ailments including aging, neurodegenerative disorders, cancer etc. Zingiber officinale Roscoe (ginger) is a widely used spice around the world. The protective effect of aqueous ethanol extract of Z. officinale against ROS-induced in vitro lipid peroxidation and DNA damage was evaluated in this study. The lipid peroxidation was induced by hydroxyl radical generated from Fenton's reaction in rat liver and brain homogenates and mitochondrial fraction (isolated from rat liver). The DNA protection was evaluated using H(2)O(2)-induced changes in pBR-322 plasmid and Fenton reaction-induced DNA fragmentation in rat liver. The results indicated that Z. officinale significantly (Pofficinale in the liver homogenate was 94 %. However, the extract could partially alleviate the DNA damage. The protective mechanism can be correlated to the radical scavenging property of Z. officinale. The results of the study suggest the possible nutraceutical role of Z. officinale against the oxidative stress induced human ailments. PMID:23105887

  19. Traumatic Brain Injury

    Science.gov (United States)

    Traumatic brain injury (TBI) happens when a bump, blow, jolt, or other head injury causes damage to the brain. Every year, millions of people in the U.S. suffer brain injuries. More than half are bad enough that ...

  20. Cortical hypoxic-ischemic brain damage in shaken-baby (shaken impact) syndrome: value of diffusion-weighted MRI

    Energy Technology Data Exchange (ETDEWEB)

    Parizel, Paul M.; Oezsarlak, Oezkan; Goethem, Johan W. van [Department of Radiology, University of Antwerp, Wilrijkstraat 10, 2650, Edegem (Belgium); Ceulemans, Berten; Laridon, Annick [Department of Pediatric Neurology, University of Antwerp, Wilrijkstraat 10, 2650, Edegem (Belgium); Jorens, Philippe G. [Department of Pediatric Intensive Care Medicine, University of Antwerp, Wilrijkstraat 10, 2650, Edegem (Belgium)

    2003-12-01

    Shaken-baby syndrome (SBS) is a type of child abuse caused by violent shaking of an infant, with or without impact, and characterized by subdural hematomas, retinal hemorrhages, and occult bone fractures. Parenchymal brain lesions in SBS may be missed or underestimated on CT scans, but can be detected at an earlier stage with diffusion-weighted MRI (DW-MRI) as areas of restricted diffusion. We demonstrate the value of DW-MRI in a 2-month-old baby boy with suspected SBS. The pattern of diffusion abnormalities indicates that the neuropathology of parenchymal lesions in SBS is due to hypoxic-ischemic brain injuries, and not to diffuse axonal injury. (orig.)

  1. Age-dependent loss of cholinergic neurons in learning and memory-related brain regions and impaired learning in SAMP8 mice with trigeminal nerve damage.

    Science.gov (United States)

    He, Yifan; Zhu, Jihong; Huang, Fang; Qin, Liu; Fan, Wenguo; He, Hongwen

    2014-11-15

    The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory behaviors and structural changes in related brain regions, in a mouse model of Alzheimer's disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged (4-month-old) or elderly (7-month-old) senescence-accelerated mouse prone 8 (SAMP8) mice. When the middle-aged mice reached 8 months (middle-aged group 1) or 11 months (middle-aged group 2), and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learning and memory were performed, and the cholinergic system was examined in the hippocampus (Nissl staining and acetylcholinesterase histochemistry) and basal forebrain (choline acetyltransferase immunohistochemistry). In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic fibers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no significant differences in histology or behavior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present findings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer's disease, and indicate that

  2. Endoplasmic reticulum stress-induced apoptosis in the penumbra aggravates secondary damage in rats with traumatic brain injur y

    Institute of Scientific and Technical Information of China (English)

    Guo-zhu Sun; Fen-fei Gao; Zong-mao Zhao; Hai Sun; Wei Xu; Li-wei Wu; Yong-chang He

    2016-01-01

    Neuronal apoptosis is mediated by intrinsic and extrinsic signaling pathways such as the membrane-mediated, mitochondrial, and endo-plasmic reticulum stress pathways. Few studies have examined the endoplasmic reticulum-mediated apoptosis pathway in the penumbra after traumatic brain injury, and it remains unclear whether endoplasmic reticulum stress can activate the caspase-12-dependent apoptotic pathway in the traumatic penumbra. Here, we established rat models of lfuid percussion-induced traumatic brain injury and found that protein expression of caspase-12, caspase-3 and the endoplasmic reticulum stress marker 78 kDa glucose-regulated protein increased in the traumatic penumbra 6 hours after injury and peaked at 24 hours. Furthermore, numbers of terminal deoxynucleotidyl transferase-mediat-ed dUTP nick end labeling-positive cells in the traumatic penumbra also reached peak levels 24 hours after injury. These ifndings suggest that caspase-12-mediated endoplasmic reticulum-related apoptosis is activated in the traumatic penumbra, and may play an important role in the pathophysiology of secondary brain injury.

  3. Disulfiram is a direct and potent inhibitor of human O6-methylguanine-DNA methyltransferase (MGMT) in brain tumor cells and mouse brain and markedly increases the alkylating DNA damage

    Science.gov (United States)

    Srivenugopal, Kalkunte S.

    2014-01-01

    The alcohol aversion drug disulfiram (DSF) reacts and conjugates with the protein-bound nucleophilic cysteines and is known to elicit anticancer effects alone or improve the efficacy of many cancer drugs. We investigated the effects of DSF on human O6-methylguanine-DNA methyltransferase (MGMT), a DNA repair protein and chemotherapy target that removes the mutagenic O6-akyl groups from guanines, and thus confers resistance to alkylating agents in brain tumors. We used DSF, copper-chelated DSF or CuCl2–DSF combination and found that all treatments inhibited the MGMT activity in two brain tumor cell lines in a rapid and dose-dependent manner. The drug treatments resulted in the loss of MGMT protein from tumor cells through the ubiquitin-proteasome pathway. Evidence showed that Cys145, a reactive cysteine, critical for DNA repair was the sole site of DSF modification in the MGMT protein. DSF was a weaker inhibitor of MGMT, compared with the established O6-benzylguanine; nevertheless, the 24–36h suppression of MGMT activity in cell cultures vastly increased the alkylation-induced DNA interstrand cross-linking, G2/M cell cycle blockade, cytotoxicity and the levels of apoptotic markers. Normal mice treated with DSF showed significantly attenuated levels of MGMT activity and protein in the liver and brain tissues. In nude mice bearing T98 glioblastoma xenografts, there was a preferential inhibition of tumor MGMT. Our studies demonstrate a strong and direct inhibition of MGMT by DSF and support the repurposing of this brain penetrating drug for glioma therapy. The findings also imply an increased risk for alkylation damage in alcoholic patients taking DSF. PMID:24193513

  4. Nutri-epigenetics ameliorates blood-brain barrier damage and neurodegeneration in hyperhomocysteinemia: role of folic acid.

    Science.gov (United States)

    Kalani, Anuradha; Kamat, Pradip K; Givvimani, Srikanth; Brown, Kasey; Metreveli, Naira; Tyagi, Suresh C; Tyagi, Neetu

    2014-02-01

    Epigenetic mechanisms underlying nutrition (nutrition epigenetics) are important in understanding human health. Nutritional supplements, for example folic acid, a cofactor in one-carbon metabolism, regulate epigenetic alterations and may play an important role in the maintenance of neuronal integrity. Folic acid also ameliorates hyperhomocysteinemia, which is a consequence of elevated levels of homocysteine. Hyperhomocysteinemia induces oxidative stress that may epigenetically mediate cerebrovascular remodeling and leads to neurodegeneration; however, the mechanisms behind such alterations remain unclear. Therefore, the present study was designed to observe the protective effects of folic acid against hyperhomocysteinemia-induced epigenetic and molecular alterations leading to neurotoxic cascades. To test this hypothesis, we employed 8-weeks-old male wild-type (WT) cystathionine-beta-synthase heterozygote knockout methionine-fed (CBS+/− + Met), WT, and CBS+/− + Met mice supplemented with folic acid (FA) [WT + FA and CBS+/− + Met + FA, respectively, 0.0057-μg g−1 day−1 dose in drinking water/4 weeks]. Hyperhomocysteinemia in CBS+/− + Met mouse brain was accompanied by a decrease in methylenetetrahydrofolate reductase and an increase in S-adenosylhomocysteine hydrolase expression, symptoms of oxidative stress, upregulation of DNA methyltransferases, rise in matrix metalloproteinases, a drop in the tissue inhibitors of metalloproteinases, decreased expression of tight junction proteins, increased permeability of the blood-brain barrier, neurodegeneration, and synaptotoxicity. Supplementation of folic acid to CBS+/− + Met mouse brain led to a decrease in the homocysteine level and rescued pathogenic and epigenetic alterations, showing its protective efficacy against homocysteine-induced neurotoxicity.

  5. [Peloid therapy in the complex sanatorium treatment of children of early age with complications of perinatal brain damage].

    Science.gov (United States)

    Ponomareva, S O; Babina, L M

    2003-01-01

    The search for novel approaches to multimodality prophylaxis and treatment of sequelae of perinatal nervous system affection as well as introduction of the early diagnostic criteria are topical problems in present-day pediatric neurology. Peloid therapy efficacy in combined sanatorium treatment was studied (Peloterm unit) in 44 infants aged 1 to 3 years. They suffered from sequelae of perinatal affections of the central nervous system including infantile cerebral paralysis. A positive effect (improvement of motor and psychic-speech development) was achieved in 98% cases. This indicates validity of this method in the treatment of CNS affections following perinatal affection of the brain in infants over 1 year of age. PMID:14753007

  6. Towards a new analytical approach to the challenges of communication difficulties and aquired brain damage in everyday practices

    DEFF Research Database (Denmark)

    Klemmensen, Charlotte Marie Bisgaard

    in everyday life. A sense-making-in-practice approach may help form a new discourse. How may a new analytical approach be designed? May ‘communication’ be described as ‘participation abilities’, using the framework from language psychology combined with discursive psychology and the conventions......The approach of language psychology is grounded in the persons communicating; where as the approach of discursive psychology is grounded in social interaction. There is a lack of scientific knowledge on the social/communicative/interactional challenges of communication difficulties and brain injury...

  7. Use of biomarker S100B for traumatic brain damage in the emergency department may change observation strategy

    DEFF Research Database (Denmark)

    Hansen-Schwartz, Jacob; Bouchelouche, Pierre Nourdine

    2014-01-01

    INTRODUCTION: The revised Scandinavian Neurotrauma Committee (SNC) guidelines on management of patients with head trauma include an option for measurement of S100B in peripheral blood with 100% sensitivity for neurosurgical intervention. A medical technology assessment was conducted to evaluate any...... impact of using S100B on the use of computed tomographies (CT) of the brain and admission for observation. MATERIAL AND METHODS: Patients referred for assessment of head injury over a period of 1.5 months had their blood sampled for measurement of S100B in serum. Results were not available...

  8. Parkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance

    OpenAIRE

    Keeney Paula M; Dunham Lisa D; Morton Stephanie L; Arthur Charles R; Bennett James P

    2009-01-01

    Abstract Background Sporadic Parkinson's disease (sPD) is a nervous system-wide disease that presents with a bradykinetic movement disorder and is frequently complicated by depression and cognitive impairment. sPD likely has multiple interacting causes that include increased oxidative stress damage to mitochondrial components and reduced mitochondrial bioenergetic capacity. We analyzed mitochondria from postmortem sPD and CTL brains for evidence of oxidative damage to mitochondrial DNA (mtDNA...

  9. Immediate S-100B and neuron-specific enolase plasma measurements for rapid evaluation of primary brain damage in alcohol-intoxicated, minor head-injured patients.

    Science.gov (United States)

    Mussack, Thomas; Biberthaler, Peter; Kanz, Karl Georg; Heckl, Ute; Gruber, Rudolf; Linsenmaier, Ulrich; Mutschler, Wolf; Jochum, Marianne

    2002-11-01

    The neuroproteins S-100B and neuron-specific enolase (NSE) released into the circulation are suggested to be reliable markers for primary brain damage. However, safe identification of relevant post-traumatic complications after minor head injury (MHI) is often hampered by acute intoxication of the patients. The objective of this study was to determine the diagnostic validity of immediate plasma measurements of S-100B and NSE in comparison with neurological examinations and cerebral computed tomography (CCT) findings in alcohol-intoxicated MHI patients. One hundered thrity-nine MHI individuals were enrolled in this prospective study during Munich's Oktoberfest 2000. Plasma levels of S-100B and NSE as well as serum alcohol and glucose values were determined by fully automated assays immediately after admission. The results were compared with Glasgow Coma Scale score, a brief neurological examination, and the CCT findings. Without being influenced by alcohol, median S-100B levels of the CCT+ group were significantly increased compared with those of the CCT- group (P < 0.001). NSE, alcohol, and glucose levels showed no significant group differences. As calculated by the ROC analysis, a cutoff value of 0.21 ng/mL with an area under the curve of 0.864 clearly differentiates between CCT+ and CCT- patients at a sensitivity of 100%, a specificity of 50.0%, and a positive likelihood ratio of 2.0. Although acute alcohol intoxication did not confound plasma measurements of S-100B and NSE, only S-100B levels below the cutoff level of 0.21 ng/mL seem to indicate absence of primary brain damage. Thus, in addition to routine neurological examinations, S-100B measurements immediately after admission might help to reduce CCT scans in alcohol-intoxicated patients early after MHI.

  10. Diffusion tensor and volumetric magnetic resonance measures as biomarkers of brain damage in a small animal model of HIV.

    Directory of Open Access Journals (Sweden)

    Margaret R Lentz

    Full Text Available There are currently no widely accepted neuro-HIV small animal models. We wanted to validate the HIV-1 Transgenic rat (Tg as an appropriate neuro-HIV model and then establish in vivo imaging biomarkers of neuropathology, within this model, using MR structural and diffusion tensor imaging (DTI.Young and middle-aged Tg and control rats were imaged using MRI. A subset of middle-aged animals underwent longitudinal repeat imaging six months later. Total brain volume (TBV, ventricular volume (VV and parenchymal volume (PV = TBV-VV were measured. Fractional anisotropy (FA and mean diffusivity (MD values of the corpus callosum (CC were calculated from DTI data.TBV and PV were smaller in Tg compared to control rats in young and middle-aged cohorts (p0.05.We detected brain volume loss in the Tg rat, probably due to astrocytic dysfunction/loss, loss of structural/axonal matrix and striatal neuronal loss as suggested by immunofluorescence. Increased MD and decreased FA in the CC probably reflect microstructural differences between the Tg and Control rats which could include increased extracellular space between white matter tracts, demyelination and axonal degeneration, among other pathologies. We believe that the Tg rat is an adequate model of neuropathology in HIV and that volumetric MR and DTI measures can be potentially used as biomarkers of disease progression.

  11. Curcumin reduces oxidative damage by increasing reduced glutathione and preventing membrane permeability transition in isolated brain mitochondria.

    Science.gov (United States)

    Jat, D; Parihar, P; Kothari, S C; Parihar, M S

    2013-12-31

    Mitochondria are critical regulators of energy metabolism and programmed cell death pathways. Mitochondria are also the major site for the production of reactive oxygen species which make this organelle more susceptible to oxidative damage and impairments of mitochondrial functions. Antioxidants have been of limited therapeutic success to ameliorate the toxic effects of oxidative stress in mitochondria. One reason may be the inability of mitochondria to selectively take up antioxidants. In the present study we synthesized mitochondrially targeted curcumin with an aim of delivering this polyphenolic compound to isolated mitochondria. Our observations show the strong anti-oxidative effects of curcumin and mitochondrially targeted curcumin against the lipid peroxidation, protein carbonylation and mitochondrial permeability transition induced by tert-butylhydroperoxide. Both curcumin and mitochondrially targeted curcumin significantly enhanced endogenous reduced glutathione level in the mitochondria thus preserving mitochondrial defense system against oxidative stress. We concluded that curcumin and mitochondrially targeted curcumin protected mitochondria against tert-butylhydroperoxide by lowering the oxidative damage, increasing the availability of endogenous reduced glutathione and preserving the mitochondrial integrity. Importantly, mitochondrially targeted curcumin was found most effective in ameliorating oxidative stress and preserving mitochondrial integrity than curcumin.

  12. Brain Basics

    Medline Plus

    Full Text Available ... the brain, which is linked to thought and emotion. It is also linked to reward systems in ... stay focused on a task, and managing proper emotional reactions. Reduced ACC activity or damage to this ...

  13. CGP 35348, GABAB Receptor Antagonist, Has a Potential to Improve Neuromuscular Coordination and Spatial Learning in Albino Mouse following Neonatal Brain Damage

    Directory of Open Access Journals (Sweden)

    Q. Gillani

    2014-01-01

    Full Text Available To study the effect of CGP 35348 on learning and memory in albino mice following hypoxia ischemia insult, 10 days old albino mice were subjected to right common carotid artery ligation followed by 8% hypoxia for 25 minutes. Following brain damage, mice were fed on normal rodent diet till they were 13 week old. At this time point, mice were divided into two groups. Group 1 received saline and group 2 intrapertoneally CGP 35348 (1 mg/mL solvent/Kg body weight for 12 days. A battery of tests used to assess long term neurofunction (Morris water maze, Rota rod and open field along with brain infarct measurement. Overall CGP 35348 has improved the motor function in male and female albino mice but effects were more pronounced in female albino mice. In open field, CGP 35348 treated female albino mice had demonstrated poor exploratory behavior. During Morris water maze test, gender specific effects were observed as CGP 35348 had improved spatial learning and memory and swimming speed in male albino mice but had no effect in female albino mice following hypoxia ischemia encephalopathy (HIE. We concluded that GABAB receptor antagonists CGP 35348 can be used to improve gender based spatial memory.

  14. In vivo evaluation of brain damage in the course of systemic lupus erythematosus using magnetic resonance spectroscopy, perfusion-weighted and diffusion-tensor imaging.

    Science.gov (United States)

    Zimny, A; Szmyrka-Kaczmarek, M; Szewczyk, P; Bladowska, J; Pokryszko-Dragan, A; Gruszka, E; Wiland, P; Sasiadek, M

    2014-01-01

    Twenty-two neuropsychiatric (NPSLE) and 13 systemic lupus erythematosus (SLE) patients with a normal appearing brain on plain magnetic resonance (MR) as well as 20 age-matched healthy controls underwent MR spectroscopy (MRS), perfusion-weighted (PWI) and diffusion-tensor imaging (DTI). In MRS NAA/Cr, Cho/Cr and mI/Cr ratios were calculated from the posterior cingulate cortex and left parietal white matter. In PWI, values of cerebral blood volume (CBV) were assessed from 14 regions, including gray and white matter. In DTI fractional anisotropy (FA) values were obtained from 14 white matter tracts including projection, commissural and association fibers. All MR measurements were correlated with clinical data. SLE and NPSLE patients showed significantly (p < 0.05) lower NAA/Cr ratios within both evaluated regions and FA values within the cingulum, as well as a tendency to cortical hypoperfusion. Compared to SLE, NPSLE subjects revealed lower FA values within a wide range of association fibers and corpus callosum. Advanced MR techniques are capable of in vivo detection of complex microstructural brain damage in SLE and NPSLE subjects regarding neuronal loss, mild hypoperfusion and white matter disintegrity. MRS and DTI seem to show the highest usefulness in depicting early changes in normal appearing gray and white matter in SLE patients. PMID:24192079

  15. Effect of different resuscitation strategies on post-resuscitation brain damage in a porcine model of prolonged cardiac arrest

    Institute of Scientific and Technical Information of China (English)

    Gu Wei; Hou Xiaomin; Li Chunsheng

    2014-01-01

    Background The choice of a defibrillation or a cardiopulmonary resuscitation (CPR)-first strategy in the treatment of prolonged cardiac arrest (CA) is still controversial.The purpose of this study was to compare the effects of defibrillation or CPR administered first on neurological prognostic markers in a porcine model of prolonged CA.Methods After 8 minutes of untreated ventricular fibrillation (VF),24 inbred Chinese Wuzhishan minipigs were randomized to receive either defibrillation first (ID group,n=12) or chest compression first (IC group,n=12).In the ID group,a shock was delivered immediately.If defibrillation failed to attain restoration of spontaneous circulation (ROSC),manual chest compressions were rapidly initiated at a rate of 100 compressions/min and a compression-to-ventilation ratio of 30:2.If VF persisted after five cycles of CPR,a second defibrillation attempt was made.In the IC group,chest compressions were delivered first,followed by a shock.After successful ROSC,hemodynamic status and blood samples were obtained at 0.5,1,2,4,6,and 24 hours after ROSC.Porcine-specific neuron-specific enolase (NSE) and S100B were measured from sera using enzyme-linked immunosorbent assays.Porcine cerebral performance category scores were used to evaluate preliminary neurological function following 24 hours recovery.Surviving pigs were sacrificed at 24 hours after ROSC and brains were removed for electron microscopy analysis.Results The number of shocks,total defibrillation energy,and time to ROSC were significantly lower in the ID group compared with the IC group.Compared with the IC group,S100B expression was decreased at 2 and 4 hours after ROSC,and NSE expression decreased at 6 and 24 hours after ROSC in the ID group.Brain tissue analysis showed that injury was attenuated in the ID group compared with the IC group.There were no significant differences between 6 and 24 hours survival rates.Conclusion Defibrillation first may result in a shorter time to ROSC and

  16. Methods for assisting recovery of damaged brain and spinal cord using arrays of X-ray microplanar beams

    Energy Technology Data Exchange (ETDEWEB)

    Dilmanian, F. Avraham; McDonald, III, John W.

    2007-01-02

    A method of assisting recovery of an injury site of brain or spinal cord injury includes providing a therapeutic dose of X-ray radiation to the injury site through an array of parallel microplanar beams. The dose at least temporarily removes regeneration inhibitors from the irradiated regions. Substantially unirradiated cells surviving between the microplanar beams migrate to the in-beam irradiated portion and assist in recovery. The dose may be administered in dose fractions over several sessions, separated in time, using angle-variable intersecting microbeam arrays (AVIMA). Additional doses may be administered by varying the orientation of the microplanar beams. The method may be enhanced by injecting stem cells into the injury site.

  17. Methods for assisting recovery of damaged brain and spinal cord using arrays of X-Ray microplanar beams

    Science.gov (United States)

    Dilmanian, F. Avraham; McDonald, III, John W.

    2007-12-04

    A method of assisting recovery of an injury site of brain or spinal cord injury includes providing a therapeutic dose of X-ray radiation to the injury site through an array of parallel microplanar beams. The dose at least temporarily removes regeneration inhibitors from the irradiated regions. Substantially unirradiated cells surviving between the microplanar beams migrate to the in-beam irradiated portion and assist in recovery. The dose may be administered in dose fractions over several sessions, separated in time, using angle-variable intersecting microbeam arrays (AVIMA). Additional doses may be administered by varying the orientation of the microplanar beams. The method may be enhanced by injecting stem cells into the injury site.

  18. Age-dependent loss of cholinergic neurons in learning and memory-related brain regions and impaired learning in SAMP8 mice with trigeminal nerve damage

    Institute of Scientific and Technical Information of China (English)

    Yifan He; Jihong Zhu; Fang Huang; Liu Qin; Wenguo Fan; Hongwen He

    2014-01-01

    The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory be-haviors and structural changes in related brain regions, in a mouse model of Alzheimer’s disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged (4-month-old) or elderly (7-month-old) senescence-accelerated mouse prone 8 (SAMP8) mice. When the middle-aged mice reached 8 months (middle-aged group 1) or 11 months (middle-aged group 2), and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learn-ing and memory were performed, and the cholinergic system was examined in the hippocampus (Nissl staining and acetylcholinesterase histochemistry) and basal forebrain (choline acetyltrans-ferase immunohistochemistry). In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic ifbers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no signiifcant differences in histology or be-havior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present ifndings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer’s disease, and

  19. Entrenamiento en actividades de la vida diaria en un paciente con daño cerebral adquirido = Activities of daily living training in brain damage patient

    Directory of Open Access Journals (Sweden)

    Ruiz Sancho, A

    2007-09-01

    Full Text Available RESUMENLas personas que se ven afectadas por un daño cerebral adquirido pueden sufrir secuelas físicas, cognitivas, conductuales y emocionales. La gravedad de las mismas varía en función de la magnitud y naturaleza del daño, dificultando que la persona mantenga su autonomía y que requiera de terceras personas durante el desempeño de sus tareas cotidianas.Dentro del proceso rehabilitador es función del terapeuta ocupacional intervenir en el entrenamiento de las actividades de la vida diaria básicas e instrumentales para lograr el nivel más alto de independencia posible. Cuánto más ecológico sea el tratamiento más posibilidades tendremos de que éste se generalice, sobre todo en los casos en que la gravedad de la lesión sea importante.El siguiente artículo describe el tratamiento en terapia ocupacional de una persona con daño cerebral adquirido mediante el entrenamiento en la realización de las actividades de la vida diaria básicas, permitiendo así la generalización de los aprendizajes en su entorno cotidiano con el fin de favorecer su autonomía personal. SUMARYPeople who have been affected by a cerebral acquired damage could suffer physical, cognitive, behavioural and emotional sequels. The gravity of these sequels changes depending on the magnitude and nature of the damage. And it makes more difficult that the person supports his/her autonomy and it could be necessary third persons for his/her daily care.By this way, in the rehabilitation process, the occupational therapist has to intervene in the training of the daily life basic and instrumental activities to get the highest possible level of independence. The more ecological it is the treatment, the more possibilities we will have that this one is generalized, especially the more serious is the person damage.The following article intents to describe an occupational therapy intervention with a person who has suffered an acquired brain damage, especially working by the

  20. Lignans from Schisandra chinensis ameliorate cognition deficits and attenuate brain oxidative damage induced by D-galactose in rats.

    Science.gov (United States)

    Yan, Tingxu; Shang, Lei; Wang, Mengshi; Zhang, Chenning; Zhao, Xu; Bi, Kaishun; Jia, Ying

    2016-06-01

    The aim of this study was to explore the neuroprotective effects of active compounds from Schisandra chinensis (Trucz.) Baill. (Magnoliaceae) against the D-galactose (D-gal)-induced neurotoxicity in rat. The Wistar rats were subcutaneously injected with D-gal (150 mg/(kg day)) for six weeks and orally administered with water extract or 95 % ethanol extract (partitioned with petroleum ether (PE), chloroform (CF), ethyl acetate (EA) and n-Butanol (NB), respectively) of the fruits of Schisandra chinensis simultaneously. The alteration of cognitive functions was assessed by using Morris water maze and Step-down type passive avoidance test. The results demonstrated that PE fraction was the most effective fraction to ameliorate cognitive deficits. Further biochemical examination indicated that PE could attenuate the activities decreasing of superoxide dismutase (SOD), catalase (CAT), the total antioxidant (T-AOC) induced by D-gal, and maintain the normal levels of glutathione (GSH), malondialdehyde (MDA) and nitric oxide (NO) in the serum, prefrontal cortex, striatum and hippocampus of the brain of related rat, selectively. Meanwhile, the compounds of PE fraction were also identified as mainly lignans, thus, these results suggest that lignans from the PE fraction of Schisandra chinensis represented a potential source of medicine for the treatment of the aging-associated neurodegenerative diseases. PMID:26847610

  1. Lignans from Schisandra chinensis ameliorate cognition deficits and attenuate brain oxidative damage induced by D-galactose in rats.

    Science.gov (United States)

    Yan, Tingxu; Shang, Lei; Wang, Mengshi; Zhang, Chenning; Zhao, Xu; Bi, Kaishun; Jia, Ying

    2016-06-01

    The aim of this study was to explore the neuroprotective effects of active compounds from Schisandra chinensis (Trucz.) Baill. (Magnoliaceae) against the D-galactose (D-gal)-induced neurotoxicity in rat. The Wistar rats were subcutaneously injected with D-gal (150 mg/(kg day)) for six weeks and orally administered with water extract or 95 % ethanol extract (partitioned with petroleum ether (PE), chloroform (CF), ethyl acetate (EA) and n-Butanol (NB), respectively) of the fruits of Schisandra chinensis simultaneously. The alteration of cognitive functions was assessed by using Morris water maze and Step-down type passive avoidance test. The results demonstrated that PE fraction was the most effective fraction to ameliorate cognitive deficits. Further biochemical examination indicated that PE could attenuate the activities decreasing of superoxide dismutase (SOD), catalase (CAT), the total antioxidant (T-AOC) induced by D-gal, and maintain the normal levels of glutathione (GSH), malondialdehyde (MDA) and nitric oxide (NO) in the serum, prefrontal cortex, striatum and hippocampus of the brain of related rat, selectively. Meanwhile, the compounds of PE fraction were also identified as mainly lignans, thus, these results suggest that lignans from the PE fraction of Schisandra chinensis represented a potential source of medicine for the treatment of the aging-associated neurodegenerative diseases.

  2. Lack of adrenomedullin in mouse endothelial cells results in defective angiogenesis, enhanced vascular permeability, less metastasis, and more brain damage.

    Science.gov (United States)

    Ochoa-Callejero, Laura; Pozo-Rodrigálvarez, Andrea; Martínez-Murillo, Ricardo; Martínez, Alfredo

    2016-01-01

    Adrenomedullin (AM) is a vasodilating peptide involved in the regulation of circulatory homeostasis and in the pathophysiology of certain cardiovascular diseases. AM plays critical roles in blood vessels, including regulation of vascular stability and permeability. To elucidate the autocrine/paracrine function of AM in endothelial cells (EC) in vivo, a conditional knockout of AM in EC (AM(EC-KO)) was used. The amount of vascularization of the matrigel implants was lower in AM(EC-KO) mice indicating a defective angiogenesis. Moreover, ablation of AM in EC revealed increased vascular permeability in comparison with wild type (WT) littermates. In addition, AM(EC-KO) lungs exhibited significantly less tumor growth than littermate WT mice using a syngeneic model of metastasis. Furthermore, following middle cerebral artery permanent occlusion, there was a significant infarct size decrease in animals lacking endothelial AM when compared to their WT counterparts. AM is an important regulator of EC function, angiogenesis, tumorigenesis, and brain response to ischemia. Studies of AM should bring novel approaches to the treatment of vascular diseases. PMID:27640364

  3. Different visual exploration of tool-related gestures in left hemisphere brain damaged patients is associated with poor gestural imitation.

    Science.gov (United States)

    Vanbellingen, Tim; Schumacher, Rahel; Eggenberger, Noëmi; Hopfner, Simone; Cazzoli, Dario; Preisig, Basil C; Bertschi, Manuel; Nyffeler, Thomas; Gutbrod, Klemens; Bassetti, Claudio L; Bohlhalter, Stephan; Müri, René M

    2015-05-01

    According to the direct matching hypothesis, perceived movements automatically activate existing motor components through matching of the perceived gesture and its execution. The aim of the present study was to test the direct matching hypothesis by assessing whether visual exploration behavior correlate with deficits in gestural imitation in left hemisphere damaged (LHD) patients. Eighteen LHD patients and twenty healthy control subjects took part in the study. Gesture imitation performance was measured by the test for upper limb apraxia (TULIA). Visual exploration behavior was measured by an infrared eye-tracking system. Short videos including forty gestures (20 meaningless and 20 communicative gestures) were presented. Cumulative fixation duration was measured in different regions of interest (ROIs), namely the face, the gesturing hand, the body, and the surrounding environment. Compared to healthy subjects, patients fixated significantly less the ROIs comprising the face and the gesturing hand during the exploration of emblematic and tool-related gestures. Moreover, visual exploration of tool-related gestures significantly correlated with tool-related imitation as measured by TULIA in LHD patients. Patients and controls did not differ in the visual exploration of meaningless gestures, and no significant relationships were found between visual exploration behavior and the imitation of emblematic and meaningless gestures in TULIA. The present study thus suggests that altered visual exploration may lead to disturbed imitation of tool related gestures, however not of emblematic and meaningless gestures. Consequently, our findings partially support the direct matching hypothesis. PMID:25841335

  4. [A careful course of action in a conflict regarding useful treatment of a newborn infant with severe brain damage].

    Science.gov (United States)

    van Beek, R H T; Buiting, H P J; de Haan, F H; van Goudoever, J B

    2005-11-26

    In a newborn female infant, it was concluded that severe perinatal asphyxia had caused such extensive cerebral damage that further medical treatment was useless. Based on their religious beliefs, the parents disagreed, despite the fact that the requested second opinions supported the conclusion of the medical staff. Since the parents persisted, a period of inurement was agreed upon during which reanimation would be performed if necessary. After several months, there was no change in the attitude of the parents towards the policy not to reanimate, even though it was clear that there was no improvement whatsoever in the patient's neurological status, while everyone agreed that she showed signs of increased suffering. The decision regarding the determination of a situation in which further medical treatment was useless was re-evaluated carefully. In a legal procedure started by the parents, the judge supported the decision of the attending physicians. In order to prevent the parents from taking their child home, in which case a situation could arise in which she would be deprived of adequate sedation or analgesia, which the attending physicians were obliged to provide, the Dutch Child Protection Council was consulted and the parents were deprived of their parental authority. Ultimately, the patient died suddenly due to respiratory and circulatory arrest without another situation in which reanimation might have been indicated. PMID:16358621

  5. Chagas cardiomyopathy: the potential of diastolic dysfunction and brain natriuretic peptide in the early identification of cardiac damage.

    Directory of Open Access Journals (Sweden)

    Ana Garcia-Alvarez

    Full Text Available INTRODUCTION: Chagas disease remains a major cause of mortality in several countries of Latin America and has become a potential public health problem in non-endemic countries as a result of migration flows. Cardiac involvement represents the main cause of mortality, but its diagnosis is still based on nonspecific criteria with poor sensitivity. Early identification of patients with cardiac involvement is desirable, since early treatment may improve prognosis. This study aimed to assess the role of diastolic dysfunction, abnormal myocardial strain and elevated brain natriuretic peptide (BNP in the early identification of cardiac involvement in Chagas disease. METHODOLOGY/PRINCIPAL FINDINGS: Fifty-four patients divided into 3 groups--group 1 (undetermined form: positive serology without ECG or 2D-echocardiographic abnormalities; N = 32, group 2 (typical ECG abnormalities of Chagas disease but normal 2D-echocardiography; N = 14, and group 3 (regional wall motion abnormalities, left ventricular [LV] end-diastolic diameter >55 mm or LV ejection fraction 37 pg/ml were noted in 0%, 13%, 29% and 63% in controls and groups 1 to 3, respectively. Half of patients in the undetermined form had impaired relaxation patterns, whereas half of patients with ECG abnormalities suggestive of Chagas cardiomyopathy had normal diastolic function. In group 1, BNP levels were statistically higher in patients with diastolic dysfunction as compared to those with normal diastolic function (27 ± 26 vs. 11 ± 8 pg/ml, p = 0.03. CONCLUSION/SIGNIFICANCE: In conclusion, the combination of diastolic function and BNP measurement adds important information that could help to better stratify patients with Chagas disease.

  6. Exercise pre‑conditioning alleviates brain damage via excitatory amino acid transporter 2 and extracellular signal‑regulated kinase 1/2 following ischemic stroke in rats.

    Science.gov (United States)

    Wang, Xiao; Zhang, Min; Feng, Rui; Li, Wen-Bin; Ren, Shi-Qing; Zhang, Feng

    2015-02-01

    Previous studies have reported that physical exercise may exert a neuroprotective effect in humans as well as animals. However, the detailed mechanisms underlying the neuroprotective effect of exercise has remained to be elucidated. The aim of the present study was to explore the possible signaling pathways involved in the protective effect of pre‑ischemic treadmill training for ischemic stroke in rats. A total of 36 male Sprague‑Dawley rats were divided at random into three groups as follows (n=12 for each): Sham surgery group; middle cerebral artery occlusion (MCAO) group; and exercise with MCAO group. Following treadmill training for three weeks, the middle cerebral artery was occluded for 90 min in order to induce ischemic stroke, followed by reperfusion. Following 24 h post‑reperfusion, six rats from each group were assessed for neurological deficits and then sacrificed to calculate the infarct volume. The remaining rats (n=6 for each group) were sacrificed and the expression levels of excitatory amino acid transporter 2 (EAAT‑2) and extracellular signal‑regulated kinase 1/2 (ERK1/2) were detected using western blot analysis. The results of the present study demonstrated that rats that underwent pre‑ischemic exercise intervention had a significantly decreased brain infarct volume and neurological deficits; in addition, the pre‑ischemic exercise group showed decreased overexpression of phosphorylated ERK1/2 and increased expression of EAAT‑2 following ischemic stroke. In conclusion, treadmill training exercise prior to ischemic stroke alleviated brain damage in rats via regulation of EAAT‑2 and ERK1/2. PMID:25370789

  7. The protective effect of heat acclimation from hypoxic damage in the brain involves changes in the expression of glutamate receptors

    Science.gov (United States)

    Yacobi, Assaf; Stern Bach, Yael; Horowitz, Michal

    2014-01-01

    Long-term heat acclimation (34 °C, 30d) alters the physiological responses and the metabolic state of organisms. It also improves ability to cope with hypoxic stress via a cross-tolerance mechanism. Within the brain, the hippocampal and frontal cortex neurons are the most sensitive to hypoxia and cell death is mainly caused by calcium influx via glutamate-gated ion channels, specifically NMDA and AMPA receptors. GluN1 subunit levels of NMDA-R correspond to NMDA-R levels. GluN2B/GluN2A subunit ratio is a qualitative index of channel activity; a higher ratio implies lower calcium permeability. The GluA2 subunit of AMPA-R controls channel permeability by inhibiting calcium penetration. Here, in rats model we (i)used behavioral-assessment tests to evaluate heat acclimation mediated hypoxic (15’ 4.5 ± 0.5% O2) neuroprotection, (ii) measured protein and transcript levels of NMDA-R and AMPA-R subunits before and after hypoxia in the hippocampus and the frontal cortex, to evaluate the role of Ca2+ in neuro-protection/cross-tolerance. Behavioral tests confirmed hypoxic tolerance in long-term (30d) but not in short-term (2d) heat acclimated rats. Hypoxic tolerance in the long-term acclimated phenotype was accompanied by a significant decrease in basal NMDA receptor GluN1 protein and an increase in its mRNA. The long-term acclimated rats also showed post ischemic increases in the GluN2B/GluN2A subunit ratio and GluA2 subunit of the AMPA receptor, supporting the hypothesis that reduced calcium permeability contributes to heat acclimation mediated hypoxia cross-tolerance. Abrupt post ischemic change in GluN2B/GluN2A subunit ratio with no change in NMDA-R subunits transcript levels implies that post-translational processes are inseparable acclimatory cross-tolerance mechanism.

  8. Parkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance

    Directory of Open Access Journals (Sweden)

    Keeney Paula M

    2009-09-01

    Full Text Available Abstract Background Sporadic Parkinson's disease (sPD is a nervous system-wide disease that presents with a bradykinetic movement disorder and is frequently complicated by depression and cognitive impairment. sPD likely has multiple interacting causes that include increased oxidative stress damage to mitochondrial components and reduced mitochondrial bioenergetic capacity. We analyzed mitochondria from postmortem sPD and CTL brains for evidence of oxidative damage to mitochondrial DNA (mtDNA, heteroplasmic mtDNA point mutations and levels of electron transport chain proteins. We sought to determine if sPD brains possess any mtDNA genotype-respiratory phenotype relationships. Results Treatment of sPD brain mtDNA with the mitochondrial base-excision repair enzyme 8-oxyguanosine glycosylase-1 (hOGG1 inhibited, in an age-dependent manner, qPCR amplification of overlapping ~2 kbase products; amplification of CTL brain mtDNA showed moderate sensitivity to hOGG1 not dependent on donor age. hOGG1 mRNA expression was not different between sPD and CTL brains. Heteroplasmy analysis of brain mtDNA using Surveyor nuclease® showed asymmetric distributions and levels of heteroplasmic mutations across mtDNA but no patterns that statistically distinguished sPD from CTL. sPD brain mitochondria displayed reductions of nine respirasome proteins (respiratory complexes I-V. Reduced levels of sPD brain mitochondrial complex II, III and V, but not complex I or IV proteins, correlated closely with rates of NADH-driven electron flow. mtDNA levels and PGC-1α expression did not differ between sPD and CTL brains. Conclusion PD brain mitochondria have reduced mitochondrial respiratory protein levels in complexes I-V, implying a generalized defect in respirasome assembly. These deficiencies do not appear to arise from altered point mutational burden in mtDNA or reduction of nuclear signaling for mitochondrial biogenesis, implying downstream etiologies. The origin of age

  9. MRI征像分析在新生儿缺氧缺血性脑损伤诊断中的临床价值%Clinical Value of MRI in Diagnosis of Neonatal Hypoxic Ischemic Brain Damage

    Institute of Scientific and Technical Information of China (English)

    马菲; 张欣贤; 刘畅畅

    2016-01-01

    Objective To investigate the clinical value of MRI in diagnosis of neonatal hypoxic ischemic brain damage.Methods MRI data of 711 cases of neonatal hypoxic ischemic brain injury in our hospital from May 2015 to February 2013 were retrospectively analyzed.Results Neonatal hypoxic ischemic brain damage occurs mainly in different periods of prenatal, birth and postpartum period, In this group of 711 cases, there were 583 cases of asphyxia during birth and birth, 128 cases after birth, 682 cases of brain injury (95.92%, 682/711),The most common type was white matter damage (590/711, 82.98%), followed by gray matter damage, including cortical damage (369/711, 51.89%),Basal ganglia thalamic injury (298/711, 41.91%) and brain stem damage (263/711, 36.99%);There were statistically significant differences in the scores of 1 min and 5 Apgar (P<0.05) in mild and moderate and severe groups with different degrees of injury. Conclusion The most common type of neonatal hypoxic ischemic brain damage is white matter damage, and the MRI imaging of the patients with moderate and severe brain injury is more serious, and the basal ganglia and thalamus damage is the most important. MRI image analysis is very important for the diagnosis of neonatal hypoxic ischemic brain damage.%目的:探讨MRI征像分析在新生儿缺氧缺血性脑损伤诊断中的临床价值。方法回顾性分析2013年2月至2015年5月在我院新生儿科住院的711例缺氧缺血性脑损伤新生儿MRI资料。结果新生儿缺氧缺血性脑损伤主要发生于产前、产时及产后不同时期,本组711例新生儿中,产前及产时窒息有583例,产后为128例;682例患儿头颅MRI证实脑损伤(95.92%,682/711),最常见的类型为白质损伤(590/711,82.98%),其次为灰质损伤,包括皮层损伤(369/711,51.89%),基底节-丘脑损伤(298/711,41.91%)及脑干损伤(263/711,36.99%);不同程度损伤的轻度组、中度组、重度组之间间1 min、5 min

  10. Effect of microglia in alcohol-induced brain damage%小胶质细胞在酒精性脑损伤中的作用

    Institute of Scientific and Technical Information of China (English)

    李锦程; 赵海苹; 罗玉敏

    2014-01-01

    Alcohol has a significant effect on the central nervous system, as the key immune effector cells in the brain, some studies proved that microglia plays an important role in the neurotoxicity of alcohol, which can lead to neuronal death and degeneration. Some investigations demonstrated that microglia is beneficial to maintain a steady state rather than causing nerve degeneration, microglia activation is the end of the damage induced by the alcohol rather than cause. This paper reviews the microglial response and related mechanism in neuronal death and degeneration caused by alcohol.%饮酒对中枢神经系统有重大影响,小胶质细胞是脑内原位免疫效应细胞,它在乙醇引起的神经毒性中有重要作用,可导致神经元死亡与退行性变;小胶质细胞有利于维持稳态而不是导致神经退行性变,小胶质细胞活化是乙醇引起损害的结果而不是损害的原因。本文对乙醇引起的神经元死亡和退行性变中小胶质细胞的反应及相应机制作一综述。

  11. 新生儿低血糖脑损伤振幅整合脑电图特征研究%Characteristics of amplitude integrated EEG in neonates with hypoglycemic brain damage

    Institute of Scientific and Technical Information of China (English)

    郭志梅; 刘芳; 周春风; 暴丽莎; 吕少广; 杜志方

    2013-01-01

    目的:探讨新生儿低血糖脑损伤的临床特征,研究低血糖脑损伤时振幅整合脑电图(aEEG)的变化特点,探讨aEEG在低血糖脑损伤时的预测作用。方法选取24例低血糖新生儿,在诊断低血糖当天行MRI检查,当天或隔天行aEEG描记,分析aEEG背景波的变异性、睡眠-觉醒周期、下边界及振幅等变化特点,并与MRI结果比较。结果严重低血糖脑损伤新生儿出现不同程度的癫发作,并在血糖纠正后继续存在。低血糖脑损伤时aEEG的表现为帽状或锯齿形癫发作,睡眠-觉醒周期消失,而对下边界及振幅的影响不大。睡眠-觉醒周期恢复提示脑功能恢复良好。在监测低血糖脑损伤方面, aEEG与MRI有很好的一致性。结论 aEEG在监测低血糖脑损伤时有其特征意义的变化,可用来动态监测低血糖脑损伤。%Objectives To investigate the clinical characteristics of hypoglycemic brain damage, and to assess the ifndings of amplitude-integrated electroencephalography (aEEG) and its predictive value in hypoglycemic brain damage. Methods Twenty-four neonates diagnosed with hypoglycaemia were selected. 12-hour continuous aEEG recordings were performed on the day when hypoglycaemia was diagnosed and second aEEG tracings was performed on the same day or the day after. The variability of aEEG background, appearance of sleep-wake cycling, bandwidth span and amplitude of lower border were analysed and compared with the results of brain MRI. Results Different degrees of epileptic seizures were found in neonates with severe hypoglycemic brain damage and were persisted after the blood sugar was corrected. aEEG in hypoglycemic brain damage was characterized by calyptriform or jagged epileptiform activity, disappearance of the sleep-wake cycle, but little impact on amplitude of lower border and bandwidth span. The recovery of sleep-wake cycle was a sign of brain function recovery. The aEEG and MRI had a

  12. MRI findings of brain damage due to neonatal hypoglycemia%新生儿低血糖脑损伤的MRI表现

    Institute of Scientific and Technical Information of China (English)

    王璐; 范国光; 冀旭; 孙宝海; 郭启勇

    2009-01-01

    Objective To report the MRI findings of brain damage obsenrved in neonatal patients who suffered from isolated hypoglycemia and to explore the value of diffusion-weighted imaging(DWI) inearly detection of neonatal hypoglycemic brain iniun,. Methods Twelve neonates with isolated hypoglycemia(10 of the 12 were diagnosed to suffer from hypoglycemic encephalopathy)were enrolled in this study.They were first scanned at age from 3 days to 10 days with Tl WI,T,WI and DWI(b is 0 s/mm2,1000 s/mm2),and 4 of them were then scanned from 7 days to 10 days following the initial scan.All acquired MR images were retrospectively analysed.Results First series of DWl images showed distinct hyperintense signal in 11 cases in several areas including bi lateral occipital cortex(2 cases),right occipital cortex(1 case),left occipital cortex and subcortical white matter(1 case),biIateral occipital cortex and flubcortical white matter(2 cases),bilateral parieto-occipital cortex(2 cases),bilateral parieto-occipital cortex and subcortical white matter(2 cases),the splenium of corpus catlosum(4 cases),bilateral corona radiata(2 cases),left eaudate nucleus and globus pallidus(1 case),bilateral thalamus(1 case),bilaterally posterior limb of internal capsule(1 ease).In the initial T1 WI and T2,WI images,there were subtle hypointensity in the damaged cortical areas(3 cases),hyperintensity in the bilaterally affected occipital cortex(1 case)on T1 weighted images,and hyperintensity in the affected cortex and subcortieal white matter with poor differentiation on T2 weighted images.The followed-up MRI of 4 cases showed regional encephalomalaeia in the affected occipital lobes(4 cases),slightly hyperintensity on T2 weighted images in the damaged occipital cortex(2 cases),extensive demyelination(1 case).disappearance of hyperintensity of the splenium of corpus callosum(1 case),and persistent hyperintensity in the splenium of corpus callosum (1 case)on T2 weighted images.Conclusion The findings suggest

  13. No Increases in Biomarkers of Genetic Damage or Pathological Changes in Heart and Brain Tissues in Male Rats Administered Methylphenidate Hydrochloride (Ritalin) for 28 Days

    OpenAIRE

    Witt, Kristine L.; Malarkey, David E; Hobbs, Cheryl A.; Davis, Jeffrey P.; Kissling, Grace E.; Caspary, William; Travlos, Gregory; Recio, Leslie

    2010-01-01

    Following a 2005 report of chromosomal damage in children with attention deficit/hyperactivity disorder (ADHD) who were treated with the commonly prescribed medication methylphenidate (MPH), numerous studies have been conducted to clarify the risk for MPH-induced genetic damage. Although most of these studies reported no changes in genetic damage endpoints associated with exposure to MPH, one recent study (Andreazza et al. 2007) reported an increase in DNA damage detected by the Comet assay i...

  14. SECONDARY BRAIN INJURY

    OpenAIRE

    Ida Ayu Basmatika

    2013-01-01

    Secondary brain injury is a condision that occurs at some times after the primary impact and can be largely prevented and treated. Most brain injury ends with deadly consequences which is caused by secondary damage to the brain. Traumatic brain injured still represents the leading cause of morbidity and mortality in individuals under the age of 45 years in the world. The classification of secondary brain injured is divided into extracranial and intracranial causes. The cause of extracranial s...

  15. The neuroprotective effect of miRNA-132 against amyloid β-protein-induced neuronal damage via upregulation of brain-derived neurotrophic factor

    Directory of Open Access Journals (Sweden)

    Lei XIANG

    2016-08-01

    Full Text Available Background Brain-derived neurotrophic factor (BDNF plays a crucial role in the pathogenesis of Alzheimer's disease (AD. MicroRNA (miRNA-132, which is widely expressed in neurons, is involved in BDNF-mediated neural development by regulating the expression of target gene. This study aims to investigate the effect of miRNA-132 on BDNF and its neuroprotective effect.  Methods The hippocampal neurons were transfected by miRNA-132 after 72 h in vitro, then exposed to amyloid β-protein (Aβ on the 7th day to build AD models. The difference of miRNA-132 expression between AD group and control group was detected by real-time fluorescent quantitative polymerase chain reaction (PCR. The alterations of BDNF mRNA were observed in the neurons of different groups. Finally, the cell viability was observed by methyl thiazolyl tetrazolium (MTT assay in AD neurons transfected with miRNA-132 or incubated with BDNF. Results 1 MiRNA-132 was significantly decreased (t = 13.888, P = 0.000, and the expression of BDNF mRNA was also reduced in AD group (t = -12.274, P = 0.000. 2 Green fluorescence was clearly visible by inverted phase-contrast fluorescence microscopy after transfected with miRNA-132. BDNF mRNA was upregulated when miRNA-132 overexpression both in control group (t = 16.135, P = 0.000 and AD group (t = 8.656, P = 0.000. 3 Cell viability was obviously decreased in neurons exposed to Aβ (t = -6.023, P = 0.000, which was improved when transfected with miRNA-132 (t = 3.385, P = 0.007 or incubated with BDNF (t = 3.672, P = 0.004.  Conclusions The expression of miRNA-132 and BDNF was reduced in neuronal AD model. MiRNA-132 played an important role on neuroprotection against A β-induced neuronal damage via upregulation of BDNF. It could be expected to provide new perspective for the diagnosis and treatment of AD. DOI: 10.3969/j.issn.1672-6731.2016.07.009

  16. 高血压性脑出血后血浆凝血酶的动态变化与脑损害的关系%The relation between the developmental change of plasma thrombin and brain damage after hypertension intracerebral hemorrhage

    Institute of Scientific and Technical Information of China (English)

    2002-01-01

    @@ Background:After intracerebral hemorrhage,besides take part in blood coagulation,plasma thrombin also is an important neural media.It can cause cerebral edema, damage blood brain barrier,and have cytotoxicity.We analysed the amount and the release law of plasma thrombin,and their relation to brain damage on the inpatients with hypertension intracerebral hemorrhage (HCH) who came to our hospital from 1999 to 2001.

  17. Monitoring arterio-venous differences of glucose and lactate in the anesthetized rat with or without brain damage with ultrafiltration and biosensor technology

    NARCIS (Netherlands)

    Leegsma-Vogt, G; Venema, K; Postema, F; Korf, J

    2001-01-01

    Continuous monitoring of arterio-venous glucose and lactate differences may serve as a diagnostic tool to assess normal brain function and brain pathology. We describe a method and some results obtained with arterio-venous measurements of glucose and lactate in the blood of the halothane-anesthetize

  18. Brain Basics

    Medline Plus

    Full Text Available ... ADHD , schizophrenia , and depression . Hippocampus —Helps create and file new memories. When the hippocampus is damaged, a ... portion of the brain involved in creating and filing new memories. hypothalmic-pituitary-adrenal (HPA) axis —A ...

  19. Stem cell therapy for neonatal brain injury : Perspectives and Challenges

    NARCIS (Netherlands)

    Titomanlio, Luigi; Kavelaars, Annemieke; Dalous, Jeremie; Mani, Shyamala; El Ghouzzi, Vincent; Heijnen, Cobi; Baud, Olivier; Gressens, Pierre

    2011-01-01

    Cerebral palsy is a major health problem caused by brain damage during pregnancy, delivery, or the immediate postnatal period. Perinatal stroke, intraventricular hemorrhage, and asphyxia are the most common causes of neonatal brain damage. Periventricular white matter damage (periventricular leukoma

  20. Categorization skills and recall in brain damaged children: a multiple case study Habilidades de categorização e recordação em crianças com lesões cerebrais: um estudo de casos multiplos

    Directory of Open Access Journals (Sweden)

    Claudia Berlim de Mello

    2009-09-01

    Full Text Available During development, children become capable of categorically associating stimuli and of using these relationships for memory recall. Brain damage in childhood can interfere with this development. This study investigated categorical association of stimuli and recall in four children with brain damages. The etiology, topography and timing of the lesions were diverse. Tasks included naming and immediate recall of 30 perceptually and semantically related figures, free sorting, delayed recall, and cued recall of the same material. Traditional neuropsychological tests were also employed. Two children with brain damage sustained in middle childhood relied on perceptual rather than on categorical associations in making associations between figures and showed deficits in delayed or cued recall, in contrast to those with perinatal lesions. One child exhibited normal performance in recall despite categorical association deficits. The present results suggest that brain damaged children show deficits in categorization and recall that are not usually identified in traditional neuropsychological tests.No desenvolvimento, as crianças tornam-se capazes de associar estímulos em categorias e de se beneficiar dessas associações para sua recordação posterior. Lesões cerebrais na infância podem interferir nesse desenvolvimento. Neste estudo, essas habilidades foram avaliadas em crianças com lesões cerebrais. A etiologia, topografia e época de instalação da lesão variaram. As tarefas incluíram: nomeação e recordação imediata de 30 figuras relacionadas perceptual e semanticamente; associação livre; recordação tardia e recordação com pistas. Testes neuropsicológicos tradicionais também foram usados. Duas crianças com lesões adquiridas na fase escolar associaram as figuras baseadas em relações perceptivas e não categóricas e apresentaram déficits de recordação tardia e com pistas, ao contrario das outras duas com lesões perinatais

  1. CK-MB在新生儿窒息脑损伤诊断中的价值研究%Study on value of CK - MB% in diagnosing Neonatal Asphyxia with brain damage

    Institute of Scientific and Technical Information of China (English)

    郑佳音; 章利群; 应俊; 周伟丽; 陈筱菲; 杨建荣

    2011-01-01

    目的:研究CK-MB在反映新生儿窒息所致的脑损伤中的临床意义及诊断价值.方法:收集49例实验组及20例对照组,其中将实验组分成合并脑损伤(27例)和不合并脑损伤(22例)两对比组,分别采用自动生化分析仪法与琼脂糖凝胶电泳法检测其总CK活性、同工酶活性和CK-MB%.结果:(1)对照组两方法测定结果比较,自动生化分析仪法测定的CK-MB%高于琼脂糖凝胶电泳法(简称电泳法)检测的结果(P0.05).(2)实验组中合并脑损伤组中CK-MB%和不合并脑损伤组比较,测定结果无差别(P>0.05).结论:自动生化分析仪法测定的CK-MB%明显高于电泳法检测的CK-MB%.上述两种方法检测的CK-MB%在实验组和对照组间以及在新生儿窒息中是否合并脑损伤并无显著性差异,不宜作为诊断新生儿窒息所致的脑损伤的生化指标.%Objective:To study the value of CK - MB in diagnosing neonatal asphyxia with brain damage. Methods: 69 patients(22 neonatal asphyxia,27 neonatal asphyxia with brain damage,20 normal) were evaluated with total CK,CK -MB,calculate CK - MB ratio using automatic biochemical analyser and agarose sugar electrophoresis method. Results: ( 1 ) The results of CK- MB% measured by automatic biochemical analyser were higher than the agarose sugar electrophoresis in the control group and the test group( P < 0.01 ). Compared between two groups, results were indifferent ( P > 0.05 ). ( 2 ) Compared the brain damage group with neonatal asphyxia group, results were indifferent( P > 0.05 ). Conclusion: The results of CK - MB% measured by automatic biochemical analyser were significantly higher than the agarose sugar electrophoresis. The results of CK - MB%may not be regarded as a biochemical indicator in diagnosing neonatal asphyxia with brain damage.

  2. Protective effects of riboflavin and selenium on brain microsomal Ca2+-ATPase and oxidative damage caused by glyceryl trinitrate in a rat headache model.

    Science.gov (United States)

    Nazıroğlu, Mustafa; Çelik, Ömer; Uğuz, Abdulhadi Cihangir; Bütün, Ayşe

    2015-03-01

    Migraine headaches are considered to be associated with increased mitochondrial energy metabolism. Mitochondrial oxidative stress is also important in migraine headache pathophysiology although riboflavin and selenium (Se) induced a modulator role on mitochondrial oxidative stress in the brain. The current study aimed to determine the effects of Se with/without riboflavin on the microsomal membrane Ca(2+)-ATPase (MMCA), lipid peroxidation, antioxidant, and electroencephalography (EEG) values in glyceryl trinitrate (GTN)-induced brain injury rats. Thirty-two rats were randomly divided into four groups. The first group was used as the control, and the second group was the GTN group. Se and Se plus oral riboflavin were administered to rats constituting the third and fourth groups for 10 days prior to GTN administration. The second, third, and fourth groups received GTN to induce headache. Ten hours after the administration of GTN, the EEG records and brain cortex samples were obtained for all groups. Brain cortex microsomes were obtained from the brain samples. The brain and microsomal lipid peroxidation levels were higher in the GTN group compared to the control group, whereas they were decreased by selenium and selenium + riboflavin treatments. Vitamin A, vitamin C, vitamin E, and reduced glutathione (GSH) concentrations of the brain and MMCA, GSH and glutathione peroxidase values of microsomes were decreased by the GTN administration, although the values and β-carotene concentrations were increased by Se and Se + riboflavin treatments. There was no significant change in EEG records of the four groups. In conclusion, Se with/without riboflavin administration protected against GTN-induced brain oxidative toxicity by inhibiting free radicals and the modulation of MMCA activity and supporting the antioxidant redox system.

  3. 静息态功能磁共振在新生儿脑损伤中的应用研究%Application research of resting state functional magnetic resonance imaging in newborn brain damage

    Institute of Scientific and Technical Information of China (English)

    李红新; 屠文娟; 高敏; 江凯华; 董选

    2014-01-01

    新生儿脑损伤是新生儿死亡和儿童期致残的主要原因,现阶段的主要问题是对该部分患儿脑损伤的特点、客观的预后评估和早期干预的定位判断及康复后的疗效分析等方面存在一定困难,静息态功能磁共振(rs-fMRI)不需要受试者完成复杂的任务,适合新生儿脑功能的研究.目前关于rs-fMRI脑损伤方面的报道多是来自成人的研究,新生儿方面的研究甚少,国外目前也主要集中在新生儿脑发育的研究上.如果能够对新生儿脑损伤方面开展此项的研究,并获得有价值的研究成果,将不仅有助于更加全面、准确地了解新生儿缺氧缺血性脑病患儿脑损伤组织的结构和功能,而且还可以为临床提供更多更有价值的信息.%Newborn brain damage is the main cause of new-borns' death and disabilities.Current research difficulties lie in analyzing characteristics of cerebral injuries,making objective prognosis and early intervention,as well as analysis of therapeutic effects after recovery.Since subjects are not requested to complete complex tasks while doing resting state functional MRI (rs-fMRI) tests,rs-fMRI is reckoned to be suitable for neonatal brain function research.So far,most rs-fMRI reports regarding cerebral injury are for adults,with only a few have been done on neonates.Foreign research are mainly focused on new borns' brain development.If relevant rs-fMRI research can be done on newborn brain damage,it would be helpful to accurately evaluate structure and function of patients' brain tissue damage.Further research can provide more valuable information in clinics.

  4. Differential effects of HIF-1 inhibition by YC-1 on the overall outcome and blood-brain barrier damage in a rat model of ischemic stroke.

    Directory of Open Access Journals (Sweden)

    Jingqi Yan

    Full Text Available Hypoxia-inducible factor 1 (HIF-1 is a master regulator of cellular adaptation to hypoxia and has been suggested as a potent therapeutic target in cerebral ischemia. Here we show in an ischemic stroke model of rats that inhibiting HIF-1 and its downstream genes by 3-(5'-hydroxymethyl-2'-furyl-1-benzylindazole (YC-1 significantly increases mortality and enlarges infarct volume evaluated by MRI and histological staining. Interestingly, the HIF-1 inhibition remarkably ameliorates ischemia-induced blood-brain barrier (BBB disruption determined by Evans blue leakage although it does not affect brain edema. The result demonstrates that HIF-1 inhibition has differential effects on ischemic outcomes and BBB permeability. It indicates that HIF-1 may have different functions in different brain cells. Further analyses show that ischemia upregulates HIF-1 and its downstream genes erythropoietin (EPO, vascular endothelial growth factor (VEGF, and glucose transporter (Glut in neurons and brain endothelial cells and that YC-1 inhibits their expression. We postulate that HIF-1-induced VEGF increases BBB permeability while certain other proteins coded by HIF-1's downstream genes such as epo and glut provide neuroprotection in an ischemic brain. The results indicate that YC-1 lacks the potential as a cerebral ischemic treatment although it confers certain protection to the cerebral vascular system.

  5. Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study

    Energy Technology Data Exchange (ETDEWEB)

    Rourke, Elizabeth A.; Lopez, Mirtha S.; Monroy, Claudia M. [Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030 (United States); Scheurer, Michael E. [Department of Pediatrics and Dan L. Duncan Cancer Center, The Baylor College of Medicine, Houston, TX 77030 (United States); Etzel, Carol J. [Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030 (United States); Albrecht, Thomas [Department of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555 (United States); Bondy, Melissa L.; El-Zein, Randa A., E-mail: relzein@mdanderson.org [Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030 (United States)

    2010-04-12

    Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in the presence of γ-radiation; an established risk factor for gliomas. We tested the hypothesis that HCMV infection modifies the sensitivity of cells to γ-radiation-induced genetic damage. We used peripheral blood lymphocytes (PBLs) from 110 glioma patients and 100 controls to measure the level of chromosome damage and cell death. We evaluated baseline, HCMV-, γ-radiation and HCMV + γ-radiation induced genetic instability with the comprehensive Cytokinesis-Blocked Micronucleus Cytome (CBMN-CYT). HCMV, similar to radiation, induced a significant increase in aberration frequency among cases and controls. PBLs infected with HCMV prior to challenge with γ-radiation led to a significant increase in aberrations as compared to baseline, γ-radiation and HCMV alone. With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis.

  6. Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study

    International Nuclear Information System (INIS)

    Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in the presence of γ-radiation; an established risk factor for gliomas. We tested the hypothesis that HCMV infection modifies the sensitivity of cells to γ-radiation-induced genetic damage. We used peripheral blood lymphocytes (PBLs) from 110 glioma patients and 100 controls to measure the level of chromosome damage and cell death. We evaluated baseline, HCMV-, γ-radiation and HCMV + γ-radiation induced genetic instability with the comprehensive Cytokinesis-Blocked Micronucleus Cytome (CBMN-CYT). HCMV, similar to radiation, induced a significant increase in aberration frequency among cases and controls. PBLs infected with HCMV prior to challenge with γ-radiation led to a significant increase in aberrations as compared to baseline, γ-radiation and HCMV alone. With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis

  7. The mechanism of oligodendrocyte precursor cell death passway in hypoxic - ischemic brain damage.%缺氧缺血性脑损伤中的少突胶质前体细胞死亡通路机制

    Institute of Scientific and Technical Information of China (English)

    杨雪; 郝艳秋

    2011-01-01

    缺氧缺血性脑损伤( hypoxic - ischemic brain damage,HIBD)是围产期常见疾病,致病机制尚未完全明确,治疗困难,预后差.少突胶质前体细胞( Oligodendrocyte precursor cell,OPC)是HIBD的主要靶细胞之一.缺氧缺血可以通过凋亡、氧自由基、兴奋毒性损伤等途径引发OPC死亡.亚低温、神经营养因子、OPC移植等方法可以通过抑制凋亡、抗氧化应激、拮抗兴奋毒性损伤等机制用于临床治疗HIBD.%Hypoxic - ischemic brain damage is a common disease in perinatal period, and it's pathogenic mechanism is not defi-nite completly. It is difficult to treat HIBD and the prognosis is not ideal. Oligodendrocyte precursor cell is the main target of HIBD. Hypoxic - ischemia can induce OPC to die through apoptosis, oxygen radicals and exitotoxicity. Mild hypothermia, neurotrophic factors and OPC transplantation can be applied to treat HIBD through depressing apoptosis, confronting oxygen radicals and inhibitting exito-toxicity.

  8. White matter damage and brain network alterations in concussed patients: a review of recent diffusion tensor imaging and resting-state functional connectivity data.

    Science.gov (United States)

    Chong, Catherine D; Schwedt, Todd J

    2015-05-01

    Over 2 million people are diagnosed with concussion each year in the USA, resulting in substantial individual and societal burdens. Although 'routine' clinical neuroimaging is useful for the diagnosis of more severe forms of traumatic brain injury, it is insensitive for detecting pathology associated with concussion. Diffusion tensor imaging (DTI) and blood-oxygenation-level-dependent (BOLD) resting-state functional connectivity magnetic resonance imaging (rs-fMRI) are techniques that allow for investigation of brain structural and functional connectivity patterns. DTI and rs-fMRI may be more sensitive than routine neuroimaging for detecting brain sequelae of concussion. This review summarizes recent DTI and rs-fMRI findings of altered structural and functional connectivity patterns in concussed patients.

  9. Is brain copper deficiency in Alzheimer's, Lewy body, and Creutzfeldt Jakob diseases the common key for a free radical mechanism and oxidative stress-induced damage?

    Science.gov (United States)

    Deloncle, Roger; Guillard, Olivier

    2015-01-01

    In Alzheimer's (AD), Lewy body (LBD), and Creutzfeldt Jakob (CJD) diseases, similar pathological hallmarks have been described, one of which is brain deposition of abnormal protease-resistant proteins. For these pathologies, copper bound to proteins is able to protect against free radicals by reduction from cupric Cu++ to cupreous Cu+. We have previously demonstrated in bovine brain homogenate that free radicals produce proteinase K-resistant prion after manganese is substituted for copper. Since low brain copper levels have been described in transmissible spongiform encephalopathies, in substantia nigra in Parkinson's disease, and in various brain regions in AD, LBD, and CJD, a mechanism has been proposed that may underlie the neurodegenerative processes that occur when copper protection against free radicals is impaired. In peptide sequences, the alpha acid proton near the peptide bond is highly mobile and can be pulled out by free radicals. It will produce a trivalent α-carbon radical and induce a free radical chain process that will generate a D-amino acid configuration in the peptide sequence. Since only L-amino acids are physiologically present in mammalian (human) proteins, it may be supposed that only physiological L-peptides can be recycled by physiological enzymes such as proteases. If a D-amino acid is found in the peptide sequence subsequent to deficient copper protection against free radicals, it will not be recognized and might alter the proteasome L-amino acid recycling from brain peptides. In the brain, there will result an accumulation of abnormal protease-resistant proteins such as those observed in AD, LBD, and CJD.

  10. Early MEK1/2 Inhibition after Global Cerebral Ischemia in Rats Reduces Brain Damage and Improves Outcome by Preventing Delayed Vasoconstrictor Receptor Upregulation

    DEFF Research Database (Denmark)

    Johansson, Sara Ellinor; Larsen, Stine Schmidt; Povlsen, Gro Klitgaard;

    2014-01-01

    neuronal cell death after global cerebral ischemia. The aim was to characterize the time-course of receptor upregulation and associated neuronal damage after global ischemia and investigate whether treatment with the MEK1/2 inhibitor U0126 can prevent cerebrovascular receptor upregulation and thereby...... with U0126 normalised cerebrovascular ETB and 5-HT1B receptor expression and contractile function, reduced hippocampal cell death and improved survival rate compared to vehicle treated animals.CONCLUSIONS: Excessive cerebrovascular expression of contractile ETB and 5-HT1B receptors is a delayed response...... to global cerebral ischemia peaking 3 days after the insult, which likely contributes to the development of delayed neuronal damage. The enhanced cerebrovascular contractility can be prevented by treatment with the MEK1/2 inhibitor U0126, diminishes neuronal damage and improves survival rate, suggesting MEK...

  11. Protective Effect of Selenoarginine on D-galactose-induced Brain Damage Mice%硒精氨酸对D-半乳糖诱导脑损伤小鼠的防护作用

    Institute of Scientific and Technical Information of China (English)

    马艳弘; 黄开红; 王英; 刘安军

    2011-01-01

    目的:研究硒精氨酸(selenoarginine,SeArg)对D-半乳糖(D-gal)所致脑损伤的防护作用.方法:将40只昆明种小鼠随机分成4组:正常组、模型组、低硒剂量组、高硒剂量组.通过后颈背部皮下注射D-半乳糖建立脑损伤模型,以灌胃方式加入SeArg,连续处理6周,采用原子荧光法检测各组小鼠脑Se和血清Se含量,生化分析法检测脑组织匀浆GSH-Px、GSH、SOD、MDA、NO、NOS和血清NO与NOS水平,流式细胞仪检测脑细胞凋亡率,同时对脑组织切片做HE染色及Nissl染色,光镜下观察脑组织病理学变化.结果:与模型组相比,SeArg组小鼠Se、GSH含量和GSH-Px、SOD活性明显上调,MDA、NO含量以及NOS活性显著降低,脑细胞凋亡率明显下调.脑组织染色结果与生化检测结果一致.其中,低剂量的SeArg作用效果更佳.结论:SeArg对D-半乳糖所致的小鼠脑损伤有明显的防护作用,这种保护效应与SeArg能够清除自由基,提高抗氧化酶活性,增强抗氧化防御机制有关.%Objective: To investigate the preventive effects of SeArg on D-gal-induced brain damage mice. Methods:Mice were randomly divided into four groups (n=10): normal group, model group, low dose SeArg group [8.35 μgSe(kg·d)] and high dose SeArg group [16.78 μgSe (kg·d)]. The SeArg was added by ig. administration, brain damage model was induced by sc. injection D-gal. After 6 weeks of treatment, the level of Se in serum and brain tissues were measured by atomic fluorescence spectrum, and the level of GSH-Px, GSH, SOD, MDA、NO and NOS were measured by biochemical method. The apoptotic rate of cerebral cells was measured by flow cytometer. Brain tissue was isolated for HE and Nissl staining and pathological change of brain tissue was observed by light microscope. Results: Compared with the model group, the level of Se, GSH-Px, GSH and SOD were significantly increased, the level of MDA, NO and NOS obviously reduced, the apoptotic rate of cerebral cells

  12. Deficiency of complement receptors CR2/CR1 in Cr2⁻/⁻ mice reduces the extent of secondary brain damage after closed head injury.

    Science.gov (United States)

    Neher, Miriam D; Rich, Megan C; Keene, Chesleigh N; Weckbach, Sebastian; Bolden, Ashley L; Losacco, Justin T; Patane, Jenée; Flierl, Michael A; Kulik, Liudmila; Holers, V Michael; Stahel, Philip F

    2014-01-01

    Complement activation at the C3 convertase level has been associated with acute neuroinflammation and secondary brain injury after severe head trauma. The present study was designed to test the hypothesis that Cr2-/- mice, which lack the receptors CR2/CD21 and CR1/CD35 for complement C3-derived activation fragments, are protected from adverse sequelae of experimental closed head injury. Adult wild-type mice and Cr2-/- mice on a C57BL/6 genetic background were subjected to focal closed head injury using a standardized weight-drop device. Head-injured Cr2-/- mice showed significantly improved neurological outcomes for up to 72 hours after trauma and a significantly decreased post-injury mortality when compared to wild-type mice. In addition, the Cr2-/- genotype was associated with a decreased extent of neuronal cell death at seven days post-injury. Western blot analysis revealed that complement C3 levels were reduced in the injured brain hemispheres of Cr2-/- mice, whereas plasma C3 levels remained unchanged, compared to wild-type mice. Finally, head-injured Cr2-/- had an attenuated extent of post-injury C3 tissue deposition, decreased astrocytosis and microglial activation, and attenuated immunoglobulin M deposition in injured brains compared to wild-type mice. Targeting of these receptors for complement C3 fragments (CR2/CR1) may represent a promising future approach for therapeutic immunomodulation after traumatic brain injury. PMID:24885042

  13. Long-term streptozotocin-induced diabetes in rats leads to severe damage of brain blood vessels and neurons via enhanced oxidative stress.

    Science.gov (United States)

    Yang, Hongying; Fan, Shourui; Song, Dianping; Wang, Zhuo; Ma, Shungao; Li, Shuqing; Li, Xiaohong; Xu, Mian; Xu, Min; Wang, Xianmo

    2013-02-01

    The aim of this study was to investigate pathophysiological alterations and oxidative stress in various stages of streptozotocin (STZ)‑induced diabetes mellitus (DM) in rats. Male Sprague-Dawley rats (120) were randomized into DM and control groups. Body mass, plasma glucose, glycated hemoglobin (HbA1c), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) levels, as well as aldose reductase (AR) activities, in brain tissue and serum were determined. Electron microscopy was used to observe neuron and vessel changes in the brain. In STZ‑treated rats, blood glucose, low density lipoproteins, triglycerides and total cholesterol levels increased 1.43‑3.0‑fold and high density lipoprotein, HbA1c and insulin sensitivity index increased 1.1‑1.23‑fold compared with control. At week 16 following treatment, DM rat serum H2O2 concentration was increased, indicating oxidative stress and mRNA levels of GPx and SOD were 2‑fold higher than the control. Protein GPx and SOD levels were reduced (Pblood vessels in the DM rat brains became increasingly abnormal over time with altered Golgi bodies, mitochondria and endoplasmic reticulum cisterns, concurrent with SOD inactivation and AR protein accumulation. Disease progression in rats with STZ‑induced DM included brain pathologies with vascular and neuron cell abnormalities, associated with the reduction of SOD, CAT and GPx activities and also AR accumulation.

  14. Deficiency of complement receptors CR2/CR1 in Cr2⁻/⁻ mice reduces the extent of secondary brain damage after closed head injury.

    Science.gov (United States)

    Neher, Miriam D; Rich, Megan C; Keene, Chesleigh N; Weckbach, Sebastian; Bolden, Ashley L; Losacco, Justin T; Patane, Jenée; Flierl, Michael A; Kulik, Liudmila; Holers, V Michael; Stahel, Philip F

    2014-05-24

    Complement activation at the C3 convertase level has been associated with acute neuroinflammation and secondary brain injury after severe head trauma. The present study was designed to test the hypothesis that Cr2-/- mice, which lack the receptors CR2/CD21 and CR1/CD35 for complement C3-derived activation fragments, are protected from adverse sequelae of experimental closed head injury. Adult wild-type mice and Cr2-/- mice on a C57BL/6 genetic background were subjected to focal closed head injury using a standardized weight-drop device. Head-injured Cr2-/- mice showed significantly improved neurological outcomes for up to 72 hours after trauma and a significantly decreased post-injury mortality when compared to wild-type mice. In addition, the Cr2-/- genotype was associated with a decreased extent of neuronal cell death at seven days post-injury. Western blot analysis revealed that complement C3 levels were reduced in the injured brain hemispheres of Cr2-/- mice, whereas plasma C3 levels remained unchanged, compared to wild-type mice. Finally, head-injured Cr2-/- had an attenuated extent of post-injury C3 tissue deposition, decreased astrocytosis and microglial activation, and attenuated immunoglobulin M deposition in injured brains compared to wild-type mice. Targeting of these receptors for complement C3 fragments (CR2/CR1) may represent a promising future approach for therapeutic immunomodulation after traumatic brain injury.

  15. The nuclear retention of transcription factor FOXO3a correlates with a DNA damage response and increased glutamine synthetase expression by astrocytes suggesting a neuroprotective role in the ageing brain.

    Science.gov (United States)

    Fluteau, Adeline; Ince, Paul G; Minett, Thais; Matthews, Fiona E; Brayne, Carol; Garwood, Claire J; Ratcliffe, Laura E; Morgan, Sarah; Heath, Paul R; Shaw, Pamela J; Wharton, Stephen B; Simpson, Julie E

    2015-11-16

    The accumulation of reactive oxygen species leading to oxidative damage and cell death plays an important role in a number of neurodegenerative disorders. FOXO3a, the main isoform of FOXO transcription factors, mediates the cellular response to oxidative stress by regulating the expression of genes involved in DNA repair and glutamine metabolism, including glutamine synthetase (GS). Immunohistochemical investigation of the population-based neuropathology cohort of the Medical Research Council's Cognitive Function and Ageing Study (MRC CFAS) demonstrates that nuclear retention of FOXO3a significantly correlates with a DNA damage response and with GS expression by astrocytes. Furthermore, we show that GS expression correlates with increasing Alzheimer-type pathology in this ageing cohort. Our findings suggest that in response to oxidative stress, the nuclear retention of FOXO3a in astrocytes upregulates expression of GS as a neuroprotective mechanism. However, the activity of GS may be compromised by increasing levels of oxidative stress in the ageing brain resulting in dysfunctional enzyme activity, neuronal excitotoxic damage and cognitive impairment.

  16. 近足月胎兔持续宫内缺氧缺血性脑损伤模型的建立%Establishment of intrauterine hypoxic-ischemic brain damage model in near term fetal rabbits

    Institute of Scientific and Technical Information of China (English)

    王能里; 南燕; 柳艳丽; 林素; 叶伟; 唐震海; 林锦; 林振浪

    2012-01-01

    目的:建立近足月(29 d胎龄)胎兔持续宫内缺氧缺血性脑损伤模型,为深入研究新生儿缺氧缺血性脑损伤发病机制和治疗提供合适模型.方法:选择孕29 d健康新西兰白兔24只,联合全身麻醉和腰麻对孕兔进行麻醉,从左侧股动脉插入4F Fogarty动脉取栓导管,实验组向导管球囊内注入生理盐水0.3 mL阻断孕兔子宫血供,阻断时间分别为20 min、25 min、28 min、30 min和40 min,每组4只;对照组插管后不注入生理盐水,共4只.24 h后行剖宫产,记录新生兔一般情况,评估新生兔神经行为学和脑组织病理学改变.结果:麻醉过程中孕兔生命体征稳定,未发生低氧血症,对麻醉耐受性良好.实验组向导管球囊内注入生理盐水0.3 mL后孕兔右侧股动脉搏动消失,血压测不出;而对照组血压无明显波动(P>0.05).持续阻断子宫血供导致胎兔和新生兔死亡,存活新生兔神经行为学异常,脑细胞发生凋亡.阻断子宫血供20 min时,未发现死胎,新生兔行为学和脑组织病理学改变不明显;阻断子宫血供25 min和28 min时,死胎率分别为12.9%和40.6%,存活新生兔出现不同程度的神经行为异常,脑组织切片发现神经元细胞肿胀,小胶质细胞活化,脑细胞凋亡;而阻断子宫血供超过30 min时,死胎率高达80.0%.结论:持续阻断孕兔子宫血供导致胎兔死亡、新生兔神经行为学异常及脑组织病理学改变,且不同阻断时间引起不同程度的脑损伤;持续阻断子宫血供25~28 min,可为缺氧缺血性脑损伤的相关研究提供合适的胎儿期全身性缺氧缺血性脑损伤胎兔模型.%AIM: To establish intrauterine hypoxic - ischemic brain damage ( HIBD) model in near term fetal rabbits at 29 d gestation age for the investigation of the pathogenesis and treatment of newborn HIBD . METHODS: Twenty - four pregnant New Zealand white rabbits at 29th gestational day were chosen for this project. Under combined general

  17. EGb761 provides a protective effect against Aβ1-42 oligomer-induced cell damage and blood-brain barrier disruption in an in vitro bEnd.3 endothelial model.

    Directory of Open Access Journals (Sweden)

    Wen-bin Wan

    Full Text Available Alzheimer's disease (AD is the most common form of senile dementia which is characterized by abnormal amyloid beta (Aβ accumulation and deposition in brain parenchyma and cerebral capillaries, and leads to blood-brain barrier (BBB disruption. Despite great progress in understanding the etiology of AD, the underlying pathogenic mechanism of BBB damage is still unclear, and no effective treatment has been devised. The standard Ginkgo biloba extract EGb761 has been widely used as a potential cognitive enhancer for the treatment of AD. However, the cellular mechanism underlying the effect remain to be clarified. In this study, we employed an immortalized endothelial cell line (bEnd.3 and incubation of Aβ(1-42 oligomer, to mimic a monolayer BBB model under conditions found in the AD brain. We investigated the effect of EGb761 on BBB and found that Aβ1-42 oligomer-induced cell injury, apoptosis, and generation of intracellular reactive oxygen species (ROS, were attenuated by treatment with EGb761. Moreover, treatment of the cells with EGb761 decreased BBB permeability and increased tight junction scaffold protein levels including ZO-1, Claudin-5 and Occludin. We also found that the Aβ(1-42 oligomer-induced upregulation of the receptor for advanced glycation end-products (RAGE, which mediates Aβ cytotoxicity and plays an essential role in AD progression, was significantly decreased by treatment with EGb761. To our knowledge, we provide the first direct in vitro evidence of an effect of EGb761 on the brain endothelium exposed to Aβ(1-42 oligomer, and on the expression of tight junction (TJ scaffold proteins and RAGE. Our results provide a new insight into a possible mechanism of action of EGb761. This study provides a rational basis for the therapeutic application of EGb761 in the treatment of AD.

  18. 牛磺酸对哺乳动物大脑发育及抗缺氧缺血性脑损伤的作用%Effects of taurine on the development of the mammalian brain and anti-hypoxic ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    罗济璇; 舒斯云; 马林; 吴升

    2014-01-01

    As an inhibitory amino acid similar to gama-aminobutyric acid,taurine can activate the corticostriatal pathway as an endogenous ligand for glycine receptors,establishing equilibrium between the excitatory and inhibitory processes in the brain.In mammalian brains,taurine concentrations increase during the developmental period of the brain until weaning,and subsequently decline reaching stable concentrations in adulthood.With abilities of anti-oxidative stress,anti-inflammatory and anti-apoptosis,taurine can improve the hypoxic-ischemic brain injury,promote the proliferation and differentiation of neurons and affect brain development,It needs more investigations to prove when and how taurine supplementation during gestation,baby,children or adult can assist the development of the brain and prevent the damage of the brain from hypoxic and ischemic damage.%牛磺酸是存在于哺乳动物大脑中类似γ-氨基丁酸的抑制性氨基酸,可与甘氨酸受体结合激活皮质纹状体通路,发挥着平衡大脑兴奋性和抑制性过程的重要作用.它的浓度在哺乳动物大脑发育过程中持续升高至断奶期,到成年后达到稳定水平.牛磺酸具有强大的抗氧化应激、抗炎和抗凋亡作用,并且可以改善缺氧缺血性脑损伤,促进神经细胞增殖分化,影响胎儿脑发育.动物实验表明补充牛磺酸可促进新生儿脑发育,有保护或减轻脑缺氧缺血性和氧化应激脑损伤的作用.但对于人类能否补充牛磺酸来促进脑发育保护脑损伤,以及在何时补充、补充的剂量和途径的研究资料并不充分,有待于进一步深入研究.

  19. Hippocampal damage and kainic acid injection induce a rapid increase in mRNA for BDNF and NGF in the rat brain.

    Science.gov (United States)

    Ballarín, M; Ernfors, P; Lindefors, N; Persson, H

    1991-10-01

    In situ hybridization and Northern blots were used to study expression of mRNAs for members of the nerve growth factor family in the rat brain following an excitatory stimulus. One hour after a unilateral needle insertion or saline injection into the dorsal hippocampus, the level of brain-derived neurotrophic factor (BDNF) mRNA increased markedly in granular neurons of the dentate gyrus and in the piriform cortex ipsilateral to the injection. The same treatment also increased the level of NGF mRNA in granular neurons of the ipsilateral dentate gyrus. The rapid increase in BDNF and NGF mRNA after a needle insertion or injection of saline was transient and preceded by an increase in c-fos mRNA in the same brain regions. In contrast to a needle insertion per se or a saline injection, 7 h after a unilateral injection of kainic acid into the dorsal hippocampus, the level of BDNF mRNA was dramatically increased in the ipsilateral hippocampus, as well as in the ipsilateral frontoparietal, piriform and perihinal cortex, the amygdaloid complex, claustrum, and ventromedial hypothalamus. A less pronounced increase was also seen in these brain areas on the contralateral side. Northern blots revealed that the level of BDNF mRNA increased 5- and 40-fold in the contra- and ipsilateral hippocampus, respectively, compared to sham-operated control animals. In contrast to BDNF and NGF, the level of hippocampus-derived neurotrophic factor/neurotrohin-3 (HDNF/NT-3) mRNA was not altered by either needle insertion or injection of saline or kainic acid.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:1915733

  20. Reversible lesions in the brain parenchyma in Wilson’s disease conifrmed by magnetic resonance imaging:earlier administration of chelating therapy can reduce the damage to the brain

    Institute of Scientific and Technical Information of China (English)

    Duko B Kozi; Igor Petrovi; Marina Svetel; Tatjana Pekmezovi; Aleksandar Ragaji; Vladimir S Kosti

    2014-01-01

    The aim of this study was to evaluate the resolution of brain lesions in patients with Wilson’s disease during the long-term chelating therapy using magnetic resonance imaging and a possible signiifcance of the time latency between the initial symptoms of the disease and the introduction of this therapy. Initial magnetic resonance examination was performed in 37 patients with proven neurological form of Wilson’s disease with cerebellar, parkinsonian and dystonic presentation. Magnetic resonance reexamination was done 5.7 ± 1.3 years later in 14 patients. Patients were divided into: group A, where chelating therapy was initiated < 24 months from the ifrst symp-toms and group B, where the therapy started≥ 24 months after the initial symptoms. Symmetry of the lesions was seen in 100% of patients. There was a signiifcant difference between groups A and B regarding complete resolution of brain stem and putaminal lesions (P= 0.005 andP=0.024, respectively). If the correct diagnosis and adequate treatment are not established less than 24 months after onset of the symptoms, irreversible lesions in the brain parenchyma could be ex-pected. Signal abnormalities on magnetic resonance imaging might therefore, at least in the early stages, represent reversible myelinolisis or cytotoxic edema associated with copper toxicity.

  1. Deficiency of complement receptors CR2/CR1 in Cr2 -/- mice reduces the extent of secondary brain damage after closed head injury

    OpenAIRE

    Neher, Miriam D.; Rich, Megan C; Keene, Chesleigh N; Weckbach, Sebastian; Bolden, Ashley L; Losacco, Justin T; Patane, Jenée; Flierl, Michael A; Kulik, Liudmila; Holers, V. Michael; Stahel, Philip F

    2014-01-01

    Complement activation at the C3 convertase level has been associated with acute neuroinflammation and secondary brain injury after severe head trauma. The present study was designed to test the hypothesis that Cr2 -/- mice, which lack the receptors CR2/CD21 and CR1/CD35 for complement C3-derived activation fragments, are protected from adverse sequelae of experimental closed head injury. Adult wild-type mice and Cr2 -/- mice on a C57BL/6 genetic background were subjected to focal closed head ...

  2. Purple Sweet Potato Color Ameliorates Cognition Deficits and Attenuates Oxidative Damage and Inflammation in Aging Mouse Brain Induced by D-Galactose

    Directory of Open Access Journals (Sweden)

    Qun Shan

    2009-01-01

    Full Text Available Purple sweet potato color (PSPC, a naturally occurring anthocyanin, has a powerful antioxidant activity in vitro and in vivo. This study explores whether PSPC has the neuroprotective effect on the aging mouse brain induced by D-galactose (D-gal. The mice administrated with PSPC (100 mg/kg.day, 4 weeks, from 9th week via oral gavage showed significantly improved behavior performance in the open field and passive avoidance test compared with D-gal-treated mice (500 mg/kg.day, 8 weeks. We further investigate the mechanism involved in neuroprotective effects of PSPC on mouse brain. Interestingly, we found, PSPC decreased the expression level of glial fibrillary acidic protein (GFAP, inducible nitric oxide synthase (iNOS, and cyclooxygenase-2 (COX-2, inhibited nuclear translocation of nuclear factor-kappaB (NF-κB, increased the activity of copper/zinc superoxide dismutase (Cu/Zn-SOD and catalase (CAT, and reduced the content of malondialdehyde (MDA, respectively. Our data suggested that PSPC attenuated D-gal-induced cognitive impairment partly via enhancing the antioxidant and anti-inflammatory capacity.

  3. Neural network plasticity in the human brain

    OpenAIRE

    Rizk, Sviatlana

    2013-01-01

    The human brain is highly organized within networks. Functionally related neural-assemblies communicate by oscillating synchronously. Intrinsic brain activity contains information on healthy and damaged brain functioning. This thesis investigated the relationship between functional networks and behavior. Furthermore, we assessed functional network plasticity after brain damage and as a result of brain stimulation. In different groups of patients we observed reduced functional connectivity bet...

  4. Effect of hypertensive disorder complicating pregnancy on neonate brain damage and brain development%妊娠期高血压对新生儿脑损伤及脑发育影响的研究

    Institute of Scientific and Technical Information of China (English)

    姚烨; 洪金玲; 陈琪; 吴长君

    2015-01-01

    ObjectiveTo analyze the craniocerebrum ultrasonographic images of the infants born by women with hypertension in pregnancy and investigate the effect of hypertension in pregnancy on neonate brain injury and brain development.MethodsTo assess the brain injury and brain development, 106 infants born by women with hypertension in pregnancy (study group) and 200 infants born by women without high risk factors during perinatal period (control group) in the neonatal intensive care unit of First Affiliated Hospital of Harbin Medical University between 2013 and 2014 underwent brain ultrasonography. The abnormal ultrasound images and the constitution of abnormal ultrasound images distribution in two groups were compared. The relationship between the abnormal ultrasound images and the degree of hypertension in pregnancy were analyzed.ResultsThe brain ultrasonographic result of the infants : (1) In the group with hypertension in pregnancy, the abnormal ultrasound images were found in 78 cases (73.6%). For the preterm infants, the solitary abnormality was found in 41 cases (25 cases of cerebral white matter injury, 14 cases of peri-intraventricular hemorrhage and 2 case of brain hypoevolutism) and multiple abnormalities were found in 15 cases; for the full-term infants, the solitary abnormality was found in 17 cases (12 cases of peri-intraventricular hemorrhage, 3 cases of hypoxic-ischemic encephalopathy and 2 case of brain hypoevolutism) and multiple abnormalities were found in 5 cases. (2) In the group without high risk factors, abnormalities were found in 73 cases (36.5 %). For the preterm infants, abnormal ultrasound images were found in 45 cases, including solitary abnormality found in 30 cases (24 cases of cerebral white matter injury, 4 cases of peri-intraventricular hemorrhage and 2 case of brain hypoevolutism) and multiple abnormalities found in 15 cases; for the full-term infants, the abnormal ultrasound images were found in 30 cases, including solitary abnormality

  5. The association atorvastatin-meloxicam reduces brain damage, attenuating reactive gliosis subsequent to arterial embolism = La asociación atorvastatina-meloxicam reduce el daño cerebral, atenuando la gliosis reactiva consecuente a embolismo arterial

    Directory of Open Access Journals (Sweden)

    Marcela Hernández Torres

    2013-10-01

    Full Text Available The association atorvastatin-meloxicam reduces brain damage, attenuating reactive gliosis subsequent to arterial embolism Introduction: Stroke is the leading cause of disability and the third of death in Colombia and in the world and it is associated with neurodegenerative and mental diseases. Objective: To determine the effects of the atorvastatin- meloxicam association on reactive gliosis in a model of cerebral ischemia produced by arterial embolization. Materials and methods: 56 adult male Wistar rats were used, divided into four ischemic and four control groups, plus 10 additional animals to determine the distribution and extent of infarction by injury in six of them and simulation (sham in the remaining four. The treatments were: placebo, atorvastatin (ATV, meloxicam (MELOX and ATV + MELOX in ischemic and simulated animals. 24 hours post-ischemia mitochondrial enzymatic activity was evaluated with triphenyl- tetrazolium (TTC, and at 120 hours astrocytic reactivity (anti-GFAP was analyzed by conventional immunohistochemistry. Results: The association ATV + MELOX favored the modulation of the response of protoplasmatic and fibrous astrocytes in both the hippocampus and the paraventricular zone by reducing their hypereactivity. Conclusion: Atorvastatin and meloxicam, either individually or associated, reduce cerebral damage by lessening the reactive gliosis produced by arterial embolization; this suggests new mechanisms of neuroprotection against thromboembolic cerebral ischemia, and opens new perspectives in its early treatment.

  6. Effect of rehabilitation therapy on intelligence and motor development of children with brain damage syndrome%康复治疗对脑损伤综合征患儿智力及运动发育的影响

    Institute of Scientific and Technical Information of China (English)

    赵志霞

    2016-01-01

    Objective To investigate the effect of rehabilitation therapy on intelligence and motor development of children with brain damage syndrome.Methods From October 2012 to October 2014, 80 patients with brain damage syndrome were selected and divided into two groups according to therapeutic method with 40 cases in each group.The control group were given nerve growth factor injection treatment, while the observation group were given the scheme of comprehensive rehabilitation training on the basis of observation group.Gesell and Peabody score in the two groups was compared.Results After treatment, the GMQ of the children in observation group increased to (75.9 ± 10.3) and DQ (58.9 ± 8.1) , which was better than control group (P < 0.05).The total effective rate was 92.5 % , which was higher than the control group of 62.5 % , and the difference was statistically significant (P <0.05).Conclusions Using modern rehabilitation program in the clinical treatment of brain injury syndrome can promote the normal development of children and their motor function and intelligence, promoting neurological function recovery, which is worthy of promotion.%目的 探讨康复治疗对脑损伤综合征患儿智力及运动发育的影响.方法 选取2012年10月至2014年10月脑损伤综合征患儿80例,依据治疗方法分为两组,每组40例.对照组给予神经生长因子注射治疗,观察组则在对照组基础上加用综合康复训练,比较两组Gesell与Peabody评分.结果 治疗后,观察组患儿GMQ提升至(75.9±10.3)分,DQ提升至(58.9±8.1)分,均优于对照组(P<0.05);观察组总有效率为92.5%,高于对照组的62.5%,差异有统计学意义(P<0.05).结论 康复治疗可促进脑损伤综合征患儿运动功能及智力的正常发育,促进其神经功能的恢复,值得推广.

  7. M-CSF deficiency leads to reduced metallothioneins I and II expression and increased tissue damage in the brain stem after 6-aminonicotinamide treatment

    DEFF Research Database (Denmark)

    Penkowa, Milena; Poulsen, Christian; Carrasco, Javier;

    2002-01-01

    6-Aminonicotinamide (6-AN) is a niacin antagonist, which leads to degeneration of gray-matter astrocytes followed by a vigorous inflammatory response. Macrophage colony stimulating factor (M-CSF) is important during inflammation, and in order to further clarify the roles for M-CSF...... in neurodegeneration and brain cell death, we have examined the effect of 6-AN on osteopetrotic mice with genetic M-CSF deficiency (op/op mice). The 6-AN-induced degeneration of gray-matter areas was comparable in control and op/op mice, but the numbers of reactive astrocytes, macrophages, and lymphocytes...... for caspases and cytochrome c) were significantly increased in 6-AN-injected op/op mice relative to controls. From a number of antioxidant factors assayed, only metallothioneins I and II (MT-I+II) were decreased in op/op mice in comparison to controls. Thus, the present results indicate that M-CSF...

  8. A novel rat model of blast-induced traumatic brain injury simulating different damage degree: implications for morphological, neurological, and biomarker changes

    Directory of Open Access Journals (Sweden)

    Mengdong eLiu

    2015-05-01

    Full Text Available In current military conflicts and civilian terrorism, blast-induced traumatic brain injury (bTBI is the primary cause of neurotrauma. However, the effects and mechanisms of bTBI are poorly understood. Although previous researchers have made significant contributions to establishing animal models for the simulation of bTBI, the precision and controllability of blast-induced injury in animal models must be improved. Therefore, we established a novel rat model to simulate blast-wave injury to the brain. To simulate different extents of bTBI injury, the animals were divided into moderate and severe injury groups. The miniature spherical explosives (PETN used in each group were of different sizes (2.5 mm diameter in the moderate injury group and 3.0 mm diameter in the severe injury group. A specially designed apparatus was able to precisely adjust the positions of the miniature explosives and create eight rats with bTBI simultaneously, using a single electric detonator. Neurological functions, gross pathologies, histopathological changes and the expression levels of various biomarkers were examined after the explosion. Compared with the moderate injury group, there were significantly more neurological dysfunctions, cortical contusions, intraparenchymal hemorrhages, cortical expression of S-100β, MBP, NSE, IL-8, IL-10, iNOS and HIF-1α in the severe injury group. These results demonstrate that we have created a reliable and reproducible bTBI model in rats. This model will be helpful for studying the mechanisms of bTBI and developing strategies for clinical bTBI treatment.

  9. Physical exercise prevents short and long-term deficits on aversive and recognition memory and attenuates brain oxidative damage induced by maternal deprivation.

    Science.gov (United States)

    Neves, Ben-Hur; Menezes, Jefferson; Souza, Mauren Assis; Mello-Carpes, Pâmela B

    2015-12-01

    It is known from previous research that physical exercise prevents long-term memory deficits induced by maternal deprivation in rats. But we could not assume similar effects of physical exercise on short-term memory, as short- and long-term memories are known to result from some different memory consolidation processes. Here we demonstrated that, in addition to long-term memory deficit, the short-term memory deficit resultant from maternal deprivation in object recognition and aversive memory tasks is also prevented by physical exercise. Additionally, one of the mechanisms by which the physical exercise influences the memory processes involves its effects attenuating the oxidative damage in the maternal deprived rats' hippocampus and prefrontal cortex.

  10. Attenuation of the bacterial load in blood by pretreatment with granulocyte-colony-stimulating factor protects rats from fatal outcome and brain damage during Streptococcus pneumoniae meningitis

    DEFF Research Database (Denmark)

    Brandt, Christian T; Lundgren, Jens D; Lund, Søren Peter;

    2004-01-01

    A model of pneumococcal meningitis in young adult rats receiving antibiotics once the infection was established was developed. The intent was to mimic clinical and histopathological features of pneumococcal meningitis in humans. The primary aim of the present study was to evaluate whether medical...... boosting of the peripheral neutrophil count affected the outcome of the meningitis. The risk of terminal illness over the first 7 days after infection was significantly reduced for rats who had elevated peripheral white blood cell counts after receiving granulocyte-colony-stimulating factor (G-CSF) prior...... to the infection compared to that for untreated rats (P = 0.039 by the log rank test). The improved outcome was associated with reduced signs of cerebral cortical damage (P = 0.008). Furthermore, the beneficial effects of G-CSF were associated with reduced bacterial loads in the cerebrospinal fluid (median, 1.1 x...

  11. 枕区脑损伤影像学与临床转归特点分析%The image and clinical outcome of brain structure damage in occipital lobe

    Institute of Scientific and Technical Information of China (English)

    王三梅; 杨常栓; 侯豫; 肖丽丽; 何芳; 马秀伟; 廖玉珍

    2011-01-01

    Objective To explore the impact of brain structure damage in occipital lobe on developmental aspects in children. Methods The imaging of brain structure damage in occipital lobe of 17 cases was analyzed. Evaluation was on classification of epilepsy, performance, and EEG monitoring, efficacy analysis, growth monitoring by comparing the different areas of injury with clinical follow-up. Results Perinatal hypoglycemia is the common cause (73.8% - 58.8%) for occipital lobe brain structure damage; 3 cases had simple brain white matter injury, fourteen cases had cortical and subcortical white matter damage; Sixteen of the total 17 cases had eye abnormal manifestation with various forms and change over time. Fourteen cases (82.4%) had epilepsy, baby spasms developed in 11 cases ( 64.7%) , with EEG performance of asymmetry part origin and height disorders. Treatment with ACTH was effective in 8 cases. Fourteen cases ( 82.4% ) had abnormal jitter attack, and all of them showed pure white matter damage in imaging. Five cases had motor development retardation by DDST assessment. The sport ability markedly improved in 8 cases after epilepsy had been controlled. Two cases had high muscle tension and serious backward sports development with congenital corpus callosum demonstrated stunted growth in imaging. Conclusions Perinatal hypoglycemia is a common cause of occipital lobe brain structure damage , which of'ten results in abnormal ocular performance and infancy systemic jitter attack, usually as pre-epilepsy signs. Baby spasm is a f'requent complication. Control of epilepsy is important to developmental improvement.%目的 探讨影像学提示脑枕区结构损伤患儿的智能发育轨迹特点.方法 收集头颅影像学提示枕区结构损伤患儿17例,按枕区损伤部位分类,采用临床随访,对癫(疒间)表现、脑电图表现、药效及生长发育等方面进行监测评价.结果 围生期低血糖为枕区脑损伤常见病因(58.8% ~ 70

  12. Neuroprotective effect of melatonin on preterm rat after hypoxia-ischemia brain damage%褪黑素对新生大鼠缺血缺氧后脑损伤的保护作用

    Institute of Scientific and Technical Information of China (English)

    乔丽丽; 沈伟勤; 陈国宏

    2012-01-01

    目的 探讨褪黑素对新生大鼠缺氧缺血性脑损伤 (HIBD) 的保护作用.方法 Wistar大鼠 48 只,5日龄时结扎左侧颈总动脉,吸入氧氮混合气体 50 min 制作成HIBD模型,随机分成生理盐水组,褪黑素组,缺血缺氧 (HI)+生理盐水组,HI+褪黑素组.褪黑素腹腔注射共 3 次,每次 5 mg/kg,第 1 次在结扎动脉前,第 2 次在吸入氧氮混合气体前给予,第 3 次在HIBD模型制作 24 h 后给予.大鼠在HIBD模型制作后 72 h 被处死,取脑作免疫组化染色,判断脑灰质 (microtubule-associatedprotein-2,MAP-2)、脑白质 (myelin basic protein,MBP) 损伤;HIBD模型制作后 7 周作Y迷宫记忆功能测试.结果 褪黑素能明显减轻HIBD大鼠脑灰质MAP-2和脑白质MBP损伤,还可提高大鼠的长期记忆能力和运动协调能力.结论 褪黑素对HIBD大鼠大脑损伤有明显的短期和长期保护作用.%Objective To investigate neuroprotective effect of melatonin on newborn rat brain after hypoxia-ischemia brain damage (HIBD). Methods Forty-eight 5-day-old Wistar rats were randomly divided into physiological saline group, melatonin group, hypoxia-ischemia (HI) + saline group and HI + melatonin group. The HIBD rat models were induced by unilateral ligation of the left common carotid artery followed by 50 min inhalation of mixed oxygen and nitrogen. Melatonin was intraperitoneally injected three times with a dose of 5mg/kg before artery ligation, before ischemia and after 24h HI immediately. The rats were sacrified after 72h HI and the immunohistochemical staining was applied to brain tissue. Microtubule-associated protein-2 (MAP-2) and myelin basic protein (MBP) were evaluated as indicators for damages in grey matter and white matter, respectively. The memory abilities of the rats were measured through Y maze test at 7 weeks after HI. Results Melatonin treatment reduced the injury of grey matter and white matter significantly, and improved the long-term memory ability and motor

  13. Influence of Quadruple Intervention Treatment on Development Process of Children with Brain Damage Syndrome%四联干预疗法对脑损伤综合征患儿神经运动发育的影响

    Institute of Scientific and Technical Information of China (English)

    张勇; 兰瑞; 谢巧玲

    2013-01-01

    目的:观察四联干预疗法治疗脑损伤综合征患儿的临床疗效.方法:纳入符合诊断标准的脑损伤综合征患儿145例,运用四联干预疗法进行干预治疗,60天1个疗程,每干预治疗20天休息20天,干预前后分别进行Gesell神经运动发育评估(DQ)、粗大运动功能(GMFM)评估,观察患儿干预后智力测试、GMFM得分改善情况;以患儿干预介入时机分组进行协方差分析,探讨干预介入时机及患儿治疗前各项分值水平对患儿预后的影响.结果:干预治疗后Gesell智力测试5个能区、GMFM粗大运动功能A、B、C3个能区得分在α=0.05水准上与治疗前相比均有统计学意义(P<0.05),治疗后较治疗前各项得分均有提高;介入时机及治疗前Gesell发育量表DQ的社会适应、大运动、精细运动、语言各项得分对患儿预后均有影响.结论:四联干预疗法对脑损伤综合征患儿的神经运动发育有较好的促进作用,早期介入四联干预对预防患儿神经伤残有一定的临床价值.%Objective:To observe the clinical curative effect of quadruple intervention therapy in the treatment of cerebral damage syndrome patients.Methods:145 children conformed to the criteria of the diagnosis of brain damage syndrome were selected,using quadruple intervention therapy intervention,60 days was a course,between each 20 days treatment course there was a rest for 20 days.After a period of treatment all the children had Gesell intelligence test and GMFM gross motor evaluation,observing the improvement of the situation after treatment and making covariance analysis according to the intervention of children age group,to discuss the effects of intervention time and the score before treatment on the prognosis of children.Results:After the intervention,the scores of five area in the Gesell intelligence test and three scores of GMFM compared with before treatment were statistically significant(P < 0.05)at the level of α =0.05,the

  14. Experimental Study on Brain Damage Following Extensive Bridging Vein Injury during Surgery%术中桥静脉广泛损伤后继发性脑损害实验研究

    Institute of Scientific and Technical Information of China (English)

    邓志锋; 郭华; 李明; 张铭文; 袁丰; 吴绮明

    2001-01-01

    目的:用动物模拟开颅术,持续牵拉脑组织,切断引流之桥静脉,在术后数小时引起淤血性脑实质损害。病理 观察此种静脉淤血性脑损害的发生情况。方法:成年家猫18只,随机分为A、B、C三组,A、B组各5只,C组8只。 A组开颅后在靠近上矢状窦处将一侧所有桥静脉电凝切断,5 h后缝合手术切口;B组开颅后将一50克重物加压 于外侧裂中段,5 h后缝合手术切口;C组则为切断一侧所有桥静脉并将一50 g重物加压于外侧裂中段,5 h后缝合 手术切口。24 h后静注伊文氏蓝染料后处死动物,取脑标本检查。结果:A、B和C组脑组织伊文氏蓝染色面积分 别为3.80%、2.93%和24.83%,A、B组与C组之间存在显著差异(P<0.0l、P<0.01);C组镜下可见蛛网膜下腔、 脑实质区有出血现象,A、B组则未见明显出血现象。结论:持续牵拉脑组织合并桥静脉切断可导致血脑屏障功能 受损,通透性增加。术中应注重回流桥静脉的保护、减少脑组织牵拉,从而减少淤血性脑损害的发生。%Objective:Animal models were used for craniotomy. Brain retraction and drainage bridging veins were severed to induce postoperative congestive brain damage several hours later, and the specimens of brain were observed pathologically. Methods: Eighteen adult cats were divided into group A, B and C. In group A(five cats), after craniotomy all bridging veins of the left cerebral hemisphere were coagulated elec trically near the superior sagittal sinus and five hours later the surgical wound was closed. In group B(five cats), a round plate weighing 50 g was pressed on the middle segment of the left Sylvian fissure for 5 hours and then the wound was closed. In group C(eight cats), both of the above interventions were performed. Twenty four hours later Evans blue was injected intravenously, then all animals were killed and the brains were removed for photography

  15. Attenuation of the bacterial load in blood by pretreatment with granulocyte-colony-stimulating factor protects rats from fatal outcome and brain damage during Streptococcus pneumoniae meningitis

    DEFF Research Database (Denmark)

    Brandt, Christian T; Lundgren, Jens D; Lund, Søren Peter;

    2004-01-01

    boosting of the peripheral neutrophil count affected the outcome of the meningitis. The risk of terminal illness over the first 7 days after infection was significantly reduced for rats who had elevated peripheral white blood cell counts after receiving granulocyte-colony-stimulating factor (G-CSF) prior...... to the infection compared to that for untreated rats (P = 0.039 by the log rank test). The improved outcome was associated with reduced signs of cerebral cortical damage (P = 0.008). Furthermore, the beneficial effects of G-CSF were associated with reduced bacterial loads in the cerebrospinal fluid (median, 1.1 x...... 10(5) versus 2.9 x 10(5) CFU/ml; P = 0.023) and in blood (median, 2.9 x 10(2) versus 6.3 x 10(2) CFU/ml; P = 0.024), as well as attenuated pleocytosis (median, 800 x 10(6) versus 1,231 x 10(6) cells/liter; P = 0.025), 24 h after the infection. Conversely, initiation of G-CSF therapy 28 h...

  16. SECONDARY BRAIN INJURY

    Directory of Open Access Journals (Sweden)

    Ida Ayu Basmatika

    2013-03-01

    Full Text Available Secondary brain injury is a condision that occurs at some times after the primary impact and can be largely prevented and treated. Most brain injury ends with deadly consequences which is caused by secondary damage to the brain. Traumatic brain injured still represents the leading cause of morbidity and mortality in individuals under the age of 45 years in the world. The classification of secondary brain injured is divided into extracranial and intracranial causes. The cause of extracranial such as hipoxia, hypotensi, hyponatremia, hypertermia, hypoglycemia or hyperglycemia. The cause of intracranial such as extradural, subdural, intraserebral, intraventrikular, dan subarachnoid hemorrhage. Beside that secondary injury can also be caused by edema and infection. Post-traumatic cerebral injured is characterized by direct tissue damage, impaired regulation of cerebral blood flow (cerebral blood flow / CBF, and disruption of metabolism. Manifestations of secondary brain injured include increased intracranial pressure, ischemic brain damage, cerebral hypoxia and hypercarbi, as well as disruption of cerebral autoregulation. The first priority is to stabilize the patient's cervical spine injury, relieve and maintain airway, ensure adequate ventilation (breathing, and making venous access for fluid resuscitation pathways (circulation and assessing the level of awareness and disability. This steps is crucial in patients with head injured to prevent hypoxia and hypotension, which is the main cause of secondary brain injury.

  17. Anticipation of Brain Shift in Deep Brain Stimulation Automatic Planning

    OpenAIRE

    Hamzé, Noura; Bilger, Alexandre; Duriez, Christian; Cotin, Stéphane; Essert, Caroline

    2015-01-01

    International audience Deep Brain Stimulation is a neurosurgery procedure consisting in implanting an electrode in a deep structure of the brain. This intervention requires a preoperative planning phase, with a millimetric accuracy, in which surgeons decide the best placement of the electrode depending on a set of surgical rules. However, brain tissues may deform during the surgery because of the brain shift phenomenon, leading the electrode to mistake the target, or moreover to damage a v...

  18. Effect of erythropoietin on the expression of NSE in neonatal rats with hypoxic ischemic brain damage%EPO对新生大鼠缺氧缺血性脑损伤NSE表达的影响

    Institute of Scientific and Technical Information of China (English)

    刘青; 曾志; 周卓妍; 蔡岳鞠; 陈美苑; 宋燕燕

    2011-01-01

    目的:观察促红细胞生成素(EPO)对新生大鼠缺氧缺血性脑损伤后神经元特异性烯醇化酶表达的影响.方法:7日龄SD大鼠随机分成假手术对照组、EPO治疗组、缺氧缺血(HIBD)组.造模后在不同时间点检测脑质量损伤百分比、皮层脑组织HE染色、免疫组化观察皮层神经元特异性烯醇化酶(NSE)的表达.结果:与假手术对照组相比较,HIBD组大鼠脑组织病理变化明显,EPO治疗组能明显改善大鼠脑组织形态变化和脑质量损伤百分比(P<0.05);HIBD组大鼠造模48 h后可见部分NSE阳性表达出现在神经元外,造模后第4天NSE的阳性表达达到高峰;在相同时间点EPO治疗组可明显减少NSE阳性表达颗粒在神经元间隙的出现;HIBD组大鼠在造模后48h和8 d NSE阳性细胞数目均少于同日龄对照组和EPO组(P<0.05).结论:EPO在HIBD发生早期起到神经保护的作用,减少神经元的坏死,减轻缺氧缺血导致的脑功能损伤.%Aim:To observe the effect of erythropoietin on the expression of NSE ( neuron specific eno-lase) in neonatal rats with hypoxic ischemic brain damage. Methods: Sprague-Dawley rats (7-day old) were randomly divided into sham operation group, EPO treatment group and HIBD group. The histologi-cal (HE staining) and immunohistochemistry methods were used to determine the pathological changes and the NSE expression levels in the brain at different time points. Results: Compared to the sham operation group, the rats of HIBD group showed significant pathological change, and the histological changes and the brain damage were improved significantly in EPO treatment group (P<0.05) at every sampling point. 48 h after modeling , NSE expressions were observed in intercellular spaces in the HIBD group. After 96h, NSE expression increased sharply in intercellular spaces in the HIBD group. However, NSE expressions were significantly reduced in the EPO treatment group at the same sampling point. The

  19. 低照度光疗法在脑损伤疾病治疗方面的研究进展%Progress of Low Level Light Therapy to Treat Brain Damage Diseases

    Institute of Scientific and Technical Information of China (English)

    王德田; 陈图南; 朱礼国; 彭其先; 李泽仁; 冯华; 刘仓理; 赵剑衡

    2015-01-01

    Low level light therapy is a steady developing therapeutic approach to treat brain damage diseases due to the limits of traditional method. It is using low power laser or quasi-monochromatic light with the wavelength from 600nm to 1100nm to modulate biological function in a nondestructive and non-thermal manner. It has been used for wound healing, pain relief, treatment of inflammation and swelling. And recently, it has been explored for treatment of brain damage dis-eases. The mechanism, applications and therapeutic parameters of low level light were reviewed.%由于传统方法在脑疾病治疗方面的局限性,低照度光疗法越来越受到重视。低照度光疗法利用波长在600 nm-1100 nm的低功率激光或者准单色光以非破坏和非热行为来调制生物过程,用于促进伤口愈合,抑制感染、水肿以及减轻疼痛等。近来,研究者进行了大量低照度光治疗脑损伤疾病方面的实验,研究对象从细胞、动物模型到人类,病症从卒中,急性脑创伤到慢性脑损伤以及神经退行性病变等。研究结果表明,低照度光疗法有可能应用于脑部损伤疾病的治疗。介绍了低照度光疗法的机理、应用,并对低照度光疗法的治疗参数,包括治疗窗口、波长以及剂量等进行了回顾。

  20. Lesões isquêmicas cerebrais no recém-nascido pré-termo de muito baixo peso Ischemic brain damage in very low birth weight preterm newborn infants

    Directory of Open Access Journals (Sweden)

    Rita C. Silveira

    2005-03-01

    Full Text Available OBJETIVO: Apresentar uma revisão crítica e atualizada sobre as lesões cerebrais isquêmicas no recém-nascido pré-termo de muito baixo peso. FONTES DE DADOS: As referências foram obtidas através do banco de dados MEDLINE, sendo selecionadas as mais representativas a critério dos autores. SÍNTESE DOS DADOS: A hemorragia com evolução para lesão isquêmica cerebral, a leucomalácia periventricular cística e a lesão difusa da substância branca cerebral são as lesões isquêmicas mais freqüentes em recém-nascidos pré-termo de muito baixo peso. Todas são doenças de causas multifatoriais, em que podem estar envolvidos fatores vasculares, hemodinâmicos, inflamatórios e infecciosos. São doenças que podem causar seqüelas neuropsicomotoras importantes e levar à paralisia cerebral e/ou déficit cognitivo e comportamental. CONCLUSÕES: O diagnóstico precoce e uma estratégia terapêutica adequada podem minimizar as seqüelas causadas por essas doenças. A prevenção da prematuridade é a principal medida preventiva a ser tomada.OBJECTIVE: To present a critical and up-to-date review of ischemic brain damage in premature, very low birth weight infants. SOURCES OF DATA: Articles were obtained by means of a search of the MEDLINE database, with those considered most representative by the authors being selected. SUMMARY OF THE FINDINGS: The most frequent ischemic injuries among preterm, very low birth weight neonates are hemorrhage progressing to with ischemic brain damage, cystic periventricular leukomalacia and diffuse lesions of the cerebral white matter. All of these conditions have multiple causative factors, which may include vascular, hemodynamic, inflammatory and infectious factors. These are disorders that can cause significant neuropsychomotor sequelae and lead to cerebral palsy and/or cognitive and behavioral deficits. CONCLUSIONS: Early diagnosis and adequate management of the patient can minimize long-term problems caused

  1. 鱼藤酮对大鼠脑内多巴胺能神经元损伤的机制研究%The damaged mechanism of rotenone on dopaminergic neuron of brain in rat

    Institute of Scientific and Technical Information of China (English)

    吴艳芬; 王永春; 苏军红; 张延平; 王伟

    2014-01-01

    目的:研究鱼藤酮对大鼠脑内多巴胺能神经元的毒性作用机制。方法健康成年雄性Wistar大鼠背部皮下注射鱼藤酮制备帕金森病动物模型。采用免疫细胞化学、透射电镜技术及分光光度法技术检测大鼠脑内多巴胺能神经元的损伤及纹状体中氧化应激参数的改变。结果鱼藤酮组大鼠中脑酪氨酸羟化酶(TH)免疫反应阳性神经元数明显少于对照组(P<0.01),纹状体中TH免疫反应强度明显降低(P<0.05),透射电镜可见鱼藤酮组黑质多巴胺能神经元内线粒体损伤,树突变性,其内微粒、微管聚集,同时纹状体发生了明显的氧化损伤。结论氧化应激和超微结构改变是鱼藤酮对大鼠脑内多巴胺能神经元损伤的主要发病机制。%Objective The study of the toxic mechanism about rotenone on dopaminergic neurons of brain in rats.Methods Healthy adult male Wistar rats were injected rotenone subcutaneous to prepare for Parkinson 's disease animal model.The damage of dopaminergic neurons of substantia nigra and striatum in rats brain was detected using immunocytochemistry , transmission electron microscopy and spectrophotometry .Results The TH immune response positive neuron numbers were significantly less in the midbrain of rotenone group as compared with control group ( P <0.01) .The TH strength of immune response in striatum significantly decreased in rotenone group ras ( P <0.05 ) .In the experimental group The microfilament microtubules gathered in the midbrain dopaminergic neurons, and oxidative damage significantly increased in striatum of rotenone group rats .Conclusions Oxidative stress and ultrastructure changes are the main pathogenesis of rotenone on dopaminergic neurons in rats .

  2. Changes of biological clock protein in neonatal rats with hypoxic-ischemic brain damage%缺氧缺血性脑损伤新生大鼠松果体钟基因表达的变化

    Institute of Scientific and Technical Information of China (English)

    李永富; 金美芳; 孙斌; 冯星

    2013-01-01

    Objective To study the effects of biological clock protein on circadian disorders in hypoxic-ischemic brain damage ( HIBD) by examining levels of CLOCK and BMAL1 proteins in the pineal gland of neonatal rats. Methods Seventy-two 7-day-old Sprague-Dawley (SD) rats were randomly divided into sham-operated and HIBD groups. HIBD model was prepared according to the modified Levine method. Western blot analysis was used to measure the levels of CLOCK and BMAL1 in the pineal gland at 0, 2, 12, 24, 36 and 48 hours after operation. Results Both CLOCK and BMAL levels in the pineal gland increased significantly 48 hours after HIBD compared with the sham-operated group ( P 0. 05 ) . Conclusions Levels of CLOCK and BMAL1 proteins in the pineal gland of rats increase significantly 48 hours after HIBD, suggesting that both CLOCK and BMAL1 may be involved the regulatory mechanism of circadian disorders in rats with HIBD.%目的 观察缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)新生大鼠松果体中CLOCK、BMAL1蛋白表达的变化,探讨钟基因表达异常在HIBD导致的昼夜节律紊乱中的作用.方法 72只7日龄新生Sprague-Dawley大鼠随机分为假手术组与HIBD模型组,每组36只.采用改良Levine法建立HIBD模型,用Western blot方法测定两组新生大鼠术后0、2、12、24、36、48 h松果体中CLOCK、BMAL1蛋白水平.结果 HIBD模型组松果体的CLOCK及BMAL1蛋白表达水平在HIBD后48 h高于假手术组(P<0.05),在0、2、12、24、36 h CLOCK及BMAL1蛋白表达水平与假手术组相比差异均无统计学意义(P>0.05).结论 HIBD新生大鼠松果体中CLOCK和BMAL1蛋白在损伤48 h后有显著升高,提示两者可能共同参与缺氧缺血时昼夜节律紊乱的发生.

  3. Neuroprotective effects of recombinant human erythropoietin on hypoxic-ischemic brain damage in neonatal rats%rhEPO 对新生鼠缺氧缺血性脑损伤的神经保护作用

    Institute of Scientific and Technical Information of China (English)

    张娟利; 陈晨; 于淑群

    2013-01-01

    Objective To explore the protective effects of recombinant human erythropoietin ( rhEPO) on hypoxic-ischemic brain damage in neonatal rats .Methods Fifty-seven 7-day-old Sprague-Dawley rats were randomly assigned to 3 groups: sham-operated group ( control group), hypoxic-ischemic brain damage model (HIBD group) and rhEPO-intervention group.Immediately after reparation of HIBD model , the rhEPO-intervention group was injected 3 000U/kg of rhEPO into the abdominal cavity , and the HIBD group was injected the same dose of normal saline .After 24 hours histological changes in brain tissue were observed with electron microscope .Apoptosis of damage neuron was measured by flow cytometry (FCM).Four separate reflexes were evaluated at 7day.Results Compared with the sham-operated group, the rats in HIBD group showed obvious histo-pathological damage in left brain.The apoptosis of neuron increased (28.30 ±4.80 vs 47.14 ± 6.97, P<0.05) and the survived cells decreased (72.42 ±7.93 vs 48.33 ±8.39, P<0.05).Compared with the HIBD group, the neuronal apoptosis decreased (47.14 ±6.97 vs 36.88 ±9.43,P<0.05) and survived cells increased (48.33 ±8.39 vs 60.06 ±8.32, P<0.05) in rhEPO-intervention group.The evaluation on four reflections ( suspension test, righting reflex, cliff aversion reflex and tendency reflection ) in HIBD group was worse than that in the control group , which indicated nerve function injury .Compared with the HIBD group, the righting reflex and cliff aversion reflex were shortened in rhEPO-intervention group (4.59 ±0.11 vs 2.84 ±0.13, 10.84 ± 1.26 vs 8.49 ±1.03, P<0.05).The differences between groups and among groups were all significant .Conclusion Extrinsic rhEPO can reduce pathologic injury of brain tissues in HIBD rats and plays a neuroprotective role through stabilizing cell structure , inhibiting cell apoptosis and improving short-term behavioral assessment .%目的:探讨重组人促红细胞生成素( rhEPO)对新生鼠缺氧缺血性

  4. Utilidad de un programa de rehabilitación neuropsicológica de la memoria en daño cerebral adquirido (Usefulness of a Program of Neuropsychological Rehabilitation of Memory in Acquired Brain Damage

    Directory of Open Access Journals (Sweden)

    Carlos José De los Reyes-Aragón

    2013-12-01

    Full Text Available RESUMEN: Este estudio evaluó la utilidad de un programa de rehabilitación cognitiva y funcional de memoria para pacientes con daño cerebral adquirido. Diez participantes con deterioro cognitivo leve o moderado participaron en el estudio, cinco de ellos asistieron durante cuatro meses a un programa semanal de rehabilitación, mientras que los otros cinco no recibieron intervención neuropsicológica. Los resultados mostraron que el grupo de rehabilitación mejoró la puntuación en la Escala de Memoria de Wechsler III. De igual forma, se encontró que la puntuación en la escala de fallos de memoria de la vida diaria solo mejoró en el grupo que recibió rehabilitación. Los resultados sugieren que el programa de rehabilitación de la memoria resulta útil en el tratamiento de las secuelas tanto cognitivas como funcionales resultantes del daño cerebral adquirido. ABSTRACT: This study evaluated the usefulness of a cognitive and functional rehabilitation of memory program for patients with acquired brain injury. Ten participants with mild- to -moderate cognitive impairment participated in the study; five of them for four months attended a weekly rehabilitation program, while the other five did not receive any neuropsychological intervention. The results showed that the rehabilitation group improved the score in the Wechsler III Memory Scale. Similarly, it was found that the score on the memory scale of failure of the daily life only improved in the group that received rehabilitation. The results suggest that memory rehabilitation program is useful in the treatment of both cognitive and functional sequels resulting from acquired brain damage.

  5. Change of G-protein expression in the myocardial damage induced by acute brain injury%急性脑损伤致心肌损害中心肌G蛋白表达的改变

    Institute of Scientific and Technical Information of China (English)

    郭彩霞; 曾翔俊; 杜凤和; 陈步星

    2015-01-01

    Objective To test the effect of Gs-protein and Gq-protein on cardiac damage induced by acute brain injury,and the contribution ofβ1-ARB and 5-HT2A RB to G-protein.Methods The Wistar rat model of acute brain injury was built.The mRNA level of Gsαand Gqαwere evaluated with real time PCR,and the protein level of Gsαand Gqαwere detected by Western blotting assay.Results Compared with NORMgroup,the mRNA level of Gsαwas (92.6 ±24)%in SHAMgroup,(39.7 ±30)%in ABI group and (80.1 ± 1 2)% in BETA group,respectively.The mRNA level of Gsαwas significantly decreased in ABI group compared to SHAM group,but significantly increased in β1-ARB treated BETA group,and there is no difference of GsαmRNA level betweenβ1-ARB treated BETA and SHAM groups.Compared with NORM group,the protein level of Gqαwas (1 05 ±30)% in SHAM group,(1 1 0 ±1 4)% in ABI group and (1 07 ±23)% in BETA group.There was no statistical difference among three groups.Conclusion The mRNA and protein of Gsαwere significantly decreased after acute brain injury,which indicates the occurrence of myocardial damage induced by acute brain injury may be related to the inhibition in signal transduction pathway mediated Gs-protein.Gs-protein may be in the form of expression change involved in the occurrence of myocardial damage induced by acute brain injury.%目的:建立动物急性脑损伤(acute brain injury,ABI)模型,观察心肌Gs 蛋白α亚基(αsubunite of Gs ,Gsα)和Gq 蛋白α亚基(αsubunite of Gq ,Gqα)的变化,探讨Gs 和Gq 在急性脑损伤致心肌损伤中的作用及其β1肾上腺素受体阻断剂(adrenalinβ1 receptor blocker,β1-ARB)和5-羟色胺受体2A阻断剂(5-hydroxytryptamine 2A receptor blocker,5-HT2ARB)对G蛋白的影响。方法复制Wistar大鼠ABI模型(n=8)。采用数字表法随机分为正常组(NORM)、假手术对照组(SHAM)、急性脑损伤模型组(ABI)、β1-ARB组(BETA)和5-HT2A RB组(KETA组

  6. Sun Damage

    Science.gov (United States)

    ... rash and rashes clinical tools newsletter | contact Share | Sun Damage A A A The sun has a profound effect over years of exposure ... changes. Exposure to ultraviolet (UV) light from the sun accounts for most premature skin aging. Many skin ...

  7. Damage Distributions

    DEFF Research Database (Denmark)

    Lützen, Marie

    2001-01-01

    The purpose of Task 2.2 of the HARDER project is according to the work package description: For various structural configurations of the struck ship and using the results of Task 2.1, the probability distributions for the damage location and size will be derived. The format will be similar to the...... damage statistics and bow height statistics for vessels in the world fleet. The proposals for the p-, r-, and v-factors have been compared to factors from current regulation by examples.......The purpose of Task 2.2 of the HARDER project is according to the work package description: For various structural configurations of the struck ship and using the results of Task 2.1, the probability distributions for the damage location and size will be derived. The format will be similar to the p...... between the damage location, the damage sizes and the main particulars of the struck vessel. From the numerical simulation and the analyse of the damage statistics it is found that the current formulation from the IMO SLF 43/3/2 can be used as basis for determination of the p-, r-, and v...

  8. 围生期窒息新生儿脑损伤早期超声的临床诊断价值%Diagnostic value of cerebral ultrasound in early brain damage of asphyxia children in perinatal period

    Institute of Scientific and Technical Information of China (English)

    李静波; 王建荣; 张海峰

    2015-01-01

    目的:对围生期窒息病史的新生儿,72h内行床旁颅脑超声检查,观察脑组织结构及血流动力学改变,探讨此类患儿早期常见脑损伤类型及超声表现。方法方患儿出生后72h内行首次颅脑超声检查,多普勒技术经颞囟检测大脑前动脉、中动脉血流动力学变化,主要参数:收缩期峰值血流速度(Vs)、舒张末期血流速度(Vd)、阻力指数(RI)。结果生后72h内超声检查,60例患儿中47例表现不同程度的脑损伤,阳性率78.3%。结论围生期窒息患儿易造成缺氧缺血性脑损伤,颅脑超声可早期发现脑组织结构改变及血流动力学变化,72h内检查阳性率高,对NICU中的重症患儿,超声具有床旁检查的优势。%Objective In this work ,the newborn babies with the history of asphyxia in the perinatal period were subjec‐ted to the bedside cerebral ultrasound examination within 72 h .The brain structure and hemodynamic changes were ob‐served so as to early explore the the common type of brain injury and sonographic findings in these children .Methods Children born within 72 h underwent the bedeside cerebral ultrasound examination for the first time .The main parame‐ters ,which reflected the blood flow dynamic changes in anterior cerebral artery and middle cerebral artery ,in terms of the peak systolic blood flow velocity (Vs) ,end‐diastolic velocity (Vd) ,and resistance index (RI) ,were detected with doppler technique via temporal fontanelle .Results By the Ultrasound test within 72 h after birth ,47 out of 60 cases were shown brain injury at different extent .The positive rate was 78 .3% .Conclusion Children with asphyxia in the perinatal period are prone to hypoxic ischemic brain damage .Cerebral ultrasound can early detect the changes of brain tissue structure and hemodynamics .Checking within 72 h ,the positive rate is high .For the severe patients in NICU ,ultrasound has the ad‐vantages for

  9. Brain Basics

    Medline Plus

    Full Text Available ... News About Us Home > Health & Education > Educational Resources Brain Basics Introduction The Growing Brain The Working Brain ... to mental disorders, such as depression. The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are ...

  10. Brain Basics

    Science.gov (United States)

    ... News About Us Home > Health & Education > Educational Resources Brain Basics Introduction The Growing Brain The Working Brain ... to mental disorders, such as depression. The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are ...

  11. Brain Basics

    Medline Plus

    Full Text Available ... Brain Basics provides information on how the brain works, how mental illnesses are disorders of the brain, ... learning more about how the brain grows and works in healthy people, and how normal brain development ...

  12. 早期干预对早产儿脑损伤预后的临床观察%Clinical Research on Early Intervention to Prognosis of Premature Infants with Brain Damage

    Institute of Scientific and Technical Information of China (English)

    杨泽艳; 吴素凤; 蒋淑珍

    2011-01-01

    Objective: To explore the clinical effects of early comprehensive intervention on development of intelligence and motor in preterm infants with brain injury. Meihods: 80 infants with brain damage were divided into two groups, the control group (n=40) received conventional therapy and health care instruction, and the intervention group (n=40) also received early synthesis intervention (GM-1+rehabilitation training). The infants in both groups were followed up regularly for 2 years, and were examined neonatal behavioral neurological assessments (NBNA) in the correction age of the 40 weeks, as well as the development assessments of intelligence and motor. Results: The difference of NBNA scores in the correction age of 40 weeks between the control group (30.95 ± 0.88) and the intervention group (33.04± 1.12) had statistical significance (P<0.05); the mental development index (MDI) of 9 months old infants and the physical development index (PDI) of 6 months old infants in intervention group were significantly higher than those in control group (P<0.05 or P<0,01); when the infants were 1 year old, there were significant differences in gross motor, fine motor, adaptive, language and personal-social function areas between the two groups, especially better in the intervention group (P<0.01); The sequelae rate of the intervention groups (17.5%) were less than that of the control group (32.5%) (P<0.01). Conclusion: The early comprehensive intervention may obviously rehabilitate the damaged neurological system of premature infants with brain injury, promote the development of intelligence and motor and reduce the rate of disability.%目的:探讨早期联合干预对脑损伤早产儿智能及运动发育的影响.方法:80例存在脑损伤的早产儿随机分为干预组与对照组,每组各40例,对照组给予常规治疗与保健指导,干预组在此基础上联合神经节苷脂治疗与早期康复训练,定期随访两年,观察比较患儿纠正胎龄40周时神

  13. Hypertension and cerebrovascular damage.

    Science.gov (United States)

    Veglio, Franco; Paglieri, Cristina; Rabbia, Franco; Bisbocci, Daniela; Bergui, Mauro; Cerrato, Paolo

    2009-08-01

    Hypertension is the most important modifiable factor for cerebrovascular disease. Stroke and dementia are growing health problems that have considerable social and economical consequences. Hypertension causes brain lesions by several mechanisms predisposing to lacunar infarctions, leucoaraiosis, and white matter changes as well as to intracerebral haemorrhages. These parenchymal damages determine evident or silent neurological alterations that often precede the onset of cognitive decline. It is important to recognize cerebrovascular disease and, above all, to correlate typical lesions to hypertension. Antihypertensive therapy has shown clinical benefits in primary and secondary prevention of stroke. These drugs represent important instruments against cerebrovascular disease but their effects on cognition are still matter of debate. Cerebral parenchymal and functional damages have to be considered together to make medical intervention more incisive. PMID:19100549

  14. 丰富与贫瘠环境对新生鼠脑损伤后脑功能的影响%Effects of enriched environment and impoverished environment on brain function of premature rats after hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    鲁利群; 江俊; 杨欣; 刘松梅

    2009-01-01

    Objective To investigate the effects of enriched environment and impoverished environment on brain function after hypoxie-ischemic brain damage (HIBD). Methods Three-day-old SD rats, which weredivided into enriched environment group (EE), standard environment group (SE) and impoverished environ-ment group (IE) by random digits table were used to establish HIBD model. The sham-operation rats served as control group. Different environment stimulations were administrated to the rats respectively since the 2nd day after HIBD. On the 32nd day, hanging test and incline plane test were carried out to evaluate the sensorimotor function. Morris water maze was used to evaluate the learning and memory ability. The expression of GFAP in the cortex and hippocampus was measured by the method of immunohistochemistry. Results The brain func-tion of IE group was much worse than that of SE group (P 0.05). Immunohistochemical analysis showed the expression of GFAP in the cortex and hippocampus of Sham group was significantly lower than that of other groups (P 0.05).皮层和海马GFAP免疫组织化学染色结果 显示,Sham组GFAP阳性细胞数分别低于其他3组(P<0.01),而SE组低于EE组,高于IE组(P<0.01).结论 丰富环境增加新生鼠脑损伤后GFAP的表达,改善脑功能;贫瘠环境加重脑功能的损害.

  15. [Brain abscess - overview].

    Science.gov (United States)

    Sveinsson, Olafur Arni; Asgeirsson, Hilmir; Olafsson, Ingvar H

    2013-01-01

    Brain abscess is a life threatening illness, demanding rapid diagnosis and treatment. Its development requires seeding of an organism into the brain parenchyma, often in an area of damaged brain tissue or in a region with poor microcirculation. The lesion evolves from a cerebritis stage to capsule formation. Brain abscesses can be caused by contiguous or haematogenous spread of an infection, or by head trauma/ neurosurgical procedure. The most common presentation is that of headache and vomiting due to raised intracranial pressure. Seizures have been reported in up to 50% of cases. Focal neurological deficits may be present, depending on the location of the lesion. Treatment of a brain abscess involves aspiration or excision, along with parenteral antibiotic therapy. The outcome has improved dramatically in the last decades due to improvement in diagnostic techniques, neurosurgery, and broad-spectrum antibiotics. The authors provide an overview of the pathogenesis, diagnosis and management of brain abscesses. PMID:23341403

  16. 非结合胆红素/白蛋白比值与脑干诱发电位相关性及对胆红素脑损伤预测价值%Correlation and predictive value between non conjugated bilirubin/albumin ratio and brain stem evoked potential in predicting bilirubin brain damage

    Institute of Scientific and Technical Information of China (English)

    扈志银; 郑小亮; 户振军

    2015-01-01

    目的:研究新生儿非结合胆红素/白蛋白比值与ABR相关性及对胆红素脑损伤的预测价值,为防治提供临床依据. 方法:以2013年1月至2014年12月在庆阳市妇幼保健院新生儿病房收住的113例足月高胆红素血症患儿为观察对象,检查血清总胆红素、非结合胆红素水平、计算总胆红素/白蛋白(B/A)、非结合胆红素/白蛋白(UCB/A)比值, ABR,并监测其伴随疾病. 结果:观察时间内,113例高胆红素血症的足月新生儿中合并胆红素脑病31例,无胆红素脑病患儿82例. 分析了B/A、UCB/A及ABR诊断胆红素脑病的灵敏度、特异性及Youden指数. 提示UCB/A及ABR作为诊断胆红素脑病的指标有一定价值. 结论:UCB/A值与ABR对胆红素脑损伤有诊断价值,可作为目前临床检测新生儿胆红素脑损伤的方法.%Objective:To study the predictive value of neonatal bilirubin/albumin ratio with ABR correlation to bilirubin brain damage in order to provide the clinical basis for the prevention and control. Methods:113 cases of full-term neonatal hyperbilirubinemia in Qingyang maternal and child care from Jan 2013 to Dec 2014 were checked levels of the serum total bilirubin and the combination of bilirubin, calculates ratio of total bilirubin/albumin(B/A) and the combination of bilirubin/albumin(UCB/A), ABR and its associated with disease. Results: In the observation period, there were 31 cases of bilirubin encephalopathy and no bilirubin encephalopathy of 82 cases. The sensitivity and specificity of B/A, UCB/A, ABR and Youden index in the diagnosis of neonatal hyperbilirubinemia were analyzed. Conclusion:UCB/A value and ABR have diagnostic value to the bilirubin brain damage, which can be used as a method to detect neonatal bilirubin brain injury at present.

  17. Radiation damage

    CERN Document Server

    Heijne, Erik H M; CERN. Geneva

    1998-01-01

    a) Radiation damage in organic materials. This series of lectures will give an overview of radiation effects on materials and components frequently used in accelerator engineering and experiments. Basic degradation phenomena will be presented for organic materials with comprehensive damage threshold doses for commonly used rubbers, thermoplastics, thermosets and composite materials. Some indications will be given for glass, scintillators and optical fibres. b) Radiation effects in semiconductor materials and devices. The major part of the time will be devoted to treat radiation effects in semiconductor sensors and the associated electronics, in particular displacement damage, interface and single event phenomena. Evaluation methods and practical aspects will be shown. Strategies will be developed for the survival of the materials under the expected environmental conditions of the LHC machine and detectors. I will describe profound revolution in our understanding of black holes and their relation to quantum me...

  18. Brain herniation

    Science.gov (United States)

    ... herniation; Uncal herniation; Subfalcine herniation; Tonsillar herniation; Herniation - brain ... Brain herniation occurs when something inside the skull produces pressure that moves brain tissues. This is most ...

  19. Inhibitory action of antioxidants (ascorbic acid or α-tocopherol) on seizures and brain damage induced by pilocarpine in rats Ação inibitória de antioxidantes (ácido ascórbico e α-tocoferol) nas convulsões e dano cerebral em ratos induzidos pela pilocarpina

    OpenAIRE

    Adriana da Rocha Tomé; Paulo Michel Pinheiro Ferreira; Rivelilson Mendes de Freitas

    2010-01-01

    Temporal lobe epilepsy is the most common form of epilepsy in humans. Oxidative stress is a mechanism of cell death induced by seizures. Antioxidant compounds have neuroprotective effects due to their ability to inhibit free radical production. The objectives of this work were to comparatively study the inhibitory action of antioxidants (ascorbic acid or α-tocopherol) on behavioral changes and brain damage induced by high doses of pilocarpine, aiming to further clarify the mechanism of a...

  20. 促红细胞生成素联合头部亚低温治疗新生儿脑损伤的评价%Evaluation of Combined Treatment with Erythropoietin and Cephalosome Subhypothermia on Neonatal Brain Damage

    Institute of Scientific and Technical Information of China (English)

    杨军; 牛美真; 董擎宇

    2012-01-01

    目的:探讨促红细胞生成素(EP0)联合头部亚低温治疗新生儿脑损伤(NBD)的疗效.方法:脑损伤新生儿86例随机分为治疗组46例和对照组40例.治疗组应用重组人促红细胞生成素(rhEPO) 100 U/kg肌肉或静脉注射,每周3次,应用2周;治疗组同时采用FX-2000亚低温治疗仪(深圳)头部亚低温治疗持续72 h,亚低温治疗结束后自然复温.对照组按HIE治疗方案进行.对各组于生后7d、14 d、21 d、28 d进行新生儿行为神经测定(NBNA),并对生后3个月、6个月智能发育评估(CDCC)及6个月的随访情况进行分析.结果:生后7d、14 d、21 d、28 d时治疗组NBNA评分高于对照组(t分别为2.008、5.341、6.238、7.485,P均<0.05);治疗组3个月与6个月智力发育指数(MDI)、心理运动发育指数(PDI)均高于对照组(P<0.05).结论:头部亚低温与EPO的联合治疗新生儿脑损伤短期和远期效果优于常规治疗.%Objective:To evaluate the effect of combined treatment with erythropoietin and cephalosome subhypothermia on neonatal brain damage (NBD). Methods; Eighty-six brain damaged newborns enrolled in this study were divided randomly into combination group (n=46) and conventional group (n=40). The effect was evaluated by neonatal behavioral neurological assessment (NBNA) (on days 7, 14,21 and 28), and the long-term effect was evaluated by using intellectual development table made by Children's Development Center of China (CDCC) at 3 and 6 months of age. Results: On days 7, 14, 21 and 28, NBNA evaluation was much higher in combination group than that in conventional group (t = 2.008, t = 5. 341, t = 6.238, t = 7.485, P<0.05). The scores of mental developmental index (MDI) at 3 months of age as well as MDI and psycho-motor developmental index (PDI) at 6 months of age in combination group were much higher than those of the conventional group (P<0.05 ). Conclusions: Combination therapy with systemic subhypothermia and erythropoietin exerts

  1. 促红细胞生成素对新生鼠缺氧缺血性脑损伤的保护作用%Neuroprotective effect of erythropoietin on hypoxic-ischemic brain damage in neonatal rats

    Institute of Scientific and Technical Information of China (English)

    邝素华; 史雪川; 马廉; 李建宏

    2008-01-01

    目的:探讨促红细胞生成素(Erythropoietin,EPO)对新生大鼠缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)的保护作用及其可能的机制.方法:新生7天大鼠随机分3组:假手术组、HIBD模型组和EPO治疗组(HIBD+EPO组).观察缺氧缺血后脑组织含水量、病理改变、免疫组织化学检测凋亡因子Bd-2的表达以及脑萎缩程度.结果:EPO治疗能显著减轻缺氧缺血侧(左侧)大脑半球水肿、病理学改变和大脑半球萎缩程度.左大脑半球含水量降至(85.93±1.19)%.显著低于HIBD模型组(86.75±0.87)%(P<0.05),左脑组织萎缩比(14.95±14.15)%,显著低于模型组(28.26±19.39)%(P<0.01).HIBD+EPO组大鼠缺血侧皮层Bcl-2阳性细胞表达较HIBD模型组及假手术组均显著增多.结论:EPO对新生鼠缺氧缺血性脑损伤具有保护作用,其机制与提高抑制细胞凋亡的发生有关.

  2. Oxidative damage of mouse brain cells induced by pesticide chlorpyrifos%农药毒死蜱对小鼠脑细胞氧化损伤的研究

    Institute of Scientific and Technical Information of China (English)

    马萍; 焦铭; 尤会会; 赵静云; 杜娟; 罗清; 杨旭

    2013-01-01

    Chlorpyrifos is an efficient, low toxicity, broad-spectrum organophosphorus insecticide acaricide. This study aims at identifying the oxidative stress effects of chlorpyrifos on organisms. Kunming mice were orally administrated with chlorpyrifos daily for seven days at the concentration of 3 , 6 and 12 mg·kg-1 , respectively. The contents of reactive oxygen species (ROS) , glutathione (GSH) and malondialdehyde (MDA) in the brain homogenate and DNA-protein Crosslink (DPC) coefficients in the brain cells were measured to indicate the oxidative damages. The experimental results showed that the contents of ROS, MDA and DPC coefficients increased gradually while GSH content decreased with the increasing exposure dose, and all the biomarkers were in the exposure dose-response manner. When the exposure dose was at 6 mg·kg-1 , DPC coefficient was significantly higher than the control group (p < 0. 05 ) , and MDA contents had extremely significant differences (p < 0. 01). In the higher dose groups (12 mg·kg-1) , ROS content and DPC coefficient indicated significant differences compared with the control group (p <0.05) , and GSH and MDA contents had extremely significant differences (p <0.01 ). These experimental results demonstrated that chlorpyrifos can increase the oxidative stress and DNA-protein crosslinks in mouse brain at a higher dose.%毒死蜱是一种高效、低毒、广谱的有机磷杀虫杀螨剂.为研究其对生物体的氧化损伤,以昆明小鼠为受试体,毒死蜱按3、6和12 mg·kg-13个剂量水平灌胃染毒小鼠7d,以脑组织匀浆测定活性氧(Reactive oxygen species,ROS)、还原型谷胱甘肽(Glutathione,GSH)和丙二醛(Malondialdehyde,MDA)的含量,以脑细胞测定DNA-蛋白质交联(DNA-protein Crosslink,DPC)系数.实验结果表明,随着毒死蜱染毒剂量的升高,ROS和MDA含量及DPC系数逐渐上升,GSH含量逐渐降低,各指标呈一定的剂量-效应关系.染毒剂量为6 mg·kg-1时,与对

  3. Oxidative Stress Damage from Nanometer Titanium Dioxide in Goldfish Brain Tissue%纳米二氧化钛对金鱼脑组织的氧化应激损伤

    Institute of Scientific and Technical Information of China (English)

    孙慧群; 张群; 陈书琴; 操璟璟

    2015-01-01

    In order to investigate the oxidative damage mechanism of photocatalytic type nano-TiO2 on goldfish brain tissue,a test involving the content of malondialdehyde (MDA),protein carbonyl (PC) and H2O2 in goldfish brain tissues together with the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the expression of Cu/Zn-SOD protein was determined after goldfishes were exposed to different nano-TiO2 concentrations of 0,16,32,64 and 128 mg/L.The results showed that the Cu/Zn-SOD activity in goldfish brain tissues decreased fiom 1.70 × 10-3 kat/kg to 0.35 × 10-3 kat/kg,and then rebounded to 0.46 × 10-3 kat/kg with the nano-TiO2 concentration varying from 0 to 128 mg/L.Meanwhile,the Mn-SOD activity presented a decrease-increase-decrease trend;the MDA content increased from 0.85 to 2.83 nmol/g,and then decreased to 2.54 nmol/g.The PC content increased all the way when the H2O2 content increased from 4.32 to 9.28 μ mol/g,and then decreased to 8.38 μmol/g.When the nano-TiO2 concentration increased,the expression of Cu/Zn-SOD decreased gradually.The research indicated that nano-TiO2 strongly affected the oxidative damage in goldfish brain tissues.The increase of the MDA and PC content was associated with the decreasing of the Cu/Zn-SOD and GPx activity,while H2O2 has a bearing on the GPx activity and other factors.%为探讨光催化型nano-TiO2(纳米二氧化钛)对金鱼(Carassius auratus L.)脑组织的氧化应激损伤效应,以5 nm的锐钛型钛白粉为试验材料,分别在ρ(nano-TiO2)为0、16、32、64、128 mg/L下对金鱼进行处理,测定金鱼脑组织MDA(丙二醛)、PC(羰基化蛋白)和H2O2含量,SOD(超氧化物歧化酶)和GPx(谷胱甘肽过氧化物酶)活性以及Cu/Zn-SOD蛋白表达量.结果表明:ρ(nano-TiO2)从0 mg/L升至128 mg/L,金鱼脑组织Cu/Zn-SOD活性从1.70×10-3 kat/kg(以鲜质量计,下同)降至0.35×10 3kat/kg,再回升至0.46×10 3 kat/kg;Mn-SOD活性呈降—升—降趋势,MDA含量从0.85 nmol

  4. Brains on video games

    OpenAIRE

    Bavelier, Daphne; Green, C. Shawn; Han, Doug Hyun; Renshaw, Perry F.; Merzenich, Michael M.; Gentile, Douglas A.

    2011-01-01

    The popular press is replete with stories about the effects of video and computer games on the brain. Sensationalist headlines claiming that video games ‘damage the brain’ or ‘boost brain power’ do not do justice to the complexities and limitations of the studies involved, and create a confusing overall picture about the effects of gaming on the brain. Here, six experts in the field shed light on our current understanding of the positive and negative ways in which playing video games can affe...

  5. Study on the protective function and its mechanism of cyclosporin A to immature brain tissue with convulsive brain damage%环孢素A对未成熟脑惊厥性损伤的保护作用及机制研究

    Institute of Scientific and Technical Information of China (English)

    郭亚乐; 黄绍平; 李丹; 杨琳; 周戬平

    2009-01-01

    Objective To investigate the protective function and its mechanisms of eyclosporin A to immature brain tissue with convulsive brain damage. Methods 21-day-old SD rats were given lithium-pilocarpine to make the epilepsy model. Total 67 male rats had been investigated. Cyclosporin A (CsA) were injected three times at 6, 30, 54 hrs after model had been established. Three dosages had been chosen: 5, 10 and 25 mg/kg each time. The level of apoptotic cells, P-glycoprotein (P-gp), glial fibrillary acidic protein (GFAP) in CA1 area of hippocampus had been determined, and compared with the rats without giving CsA. Results Rats from epilepsy model group had higher level of apoptosis, P-gp, GFAP expression than those from pseudo-model group. CsA injection by dose 5 mg/kg each time for three times reduced the level of P-gp, GFAP. Model group and pseudo-model group were same. Both the interventions of CsA injection by 10 mg/kg and 25 mg/kg can reduce the level of P-gp, GFAP, however neither of their effectiveness was better than CsA 5 mg/kg each time. Conclusions Small dosage of CsA may protect the immature brain tissue from convulsive brain damage by reducing the level of P-gp, GFAP in CA1 area of hippocampus.%目的 探讨环孢素A(CsA)对未成熟脑惊厥性损伤的保护作用及机制.方法 21日龄SD雄性大鼠67只,制作氯化锂-匹鲁卡品癫(癎)模型,分别于制模后6、30、54 h采用CsA干预,分5、10、25 ms/(kg·次),三个干预剂量,与模型不干预组对比,观察制模后72 h脑海马CA1区凋亡细胞、多药耐药基因产物P-糖蛋白(P-gp)、星形胶质细胞纤维酸性蛋白(GFAP)表达情况等.结果 模型组比假手术组海马CA1区凋亡细胞、P-gP、GFAP表达明显增加,CsA 5 me,/(kg·次)干预组可显著减少P-gP、GFAP表达,且与假手术组水平接近,CsA 10 ms/(kg·次)、CsA 25 me,/(kg·次)有相似效果,但不及CsA 5 ms/(kg·次)效果明显.CsA干预不能减少凋亡细胞.结论 中小剂量Cs

  6. 新生期注射谷氨酸单钠对大鼠脑区损伤程度的比较观察%Comparative Study of Damage to Different Parts of Brain with Injected Monosodium Glutamate in Newborn Rat

    Institute of Scientific and Technical Information of China (English)

    张金平; 史玉兰; 金凤霞; 白文忠; 高志国

    2000-01-01

    The damage to 16 parts of brain is comparatively researched in the adult rat. Those experimental animals are injected intraperitoneal different dose monosodium glutamate in the newborn period. The neurons are decrease markedly in most parts of the brain in the experimental rats. But some parts of brain are protected from the neurotoxicity of monosodium glutamate.%比较观察了在新生期腹腔内注射不同剂量谷氨酸单钠后,成年大鼠16个脑区的神经元损伤程度.发现大多数脑区的神经元显著减少,但有的脑区对谷氨酸单钠的神经毒性具有一定保护作用.

  7. DNA damage in neurodegenerative diseases

    Energy Technology Data Exchange (ETDEWEB)

    Coppedè, Fabio, E-mail: fabio.coppede@med.unipi.it; Migliore, Lucia, E-mail: lucia.migliore@med.unipi.it

    2015-06-15

    Highlights: • Oxidative DNA damage is one of the earliest detectable events in the neurodegenerative process. • The mitochondrial DNA is more vulnerable to oxidative attack than the nuclear DNA. • Cytogenetic damage has been largely documented in Alzheimer's disease patients. • The question of whether DNA damage is cause or consequence of neurodegeneration is still open. • Increasing evidence links DNA damage and repair with epigenetic phenomena. - Abstract: Following the observation of increased oxidative DNA damage in nuclear and mitochondrial DNA extracted from post-mortem brain regions of patients affected by neurodegenerative diseases, the last years of the previous century and the first decade of the present one have been largely dedicated to the search of markers of DNA damage in neuronal samples and peripheral tissues of patients in early, intermediate or late stages of neurodegeneration. Those studies allowed to demonstrate that oxidative DNA damage is one of the earliest detectable events in neurodegeneration, but also revealed cytogenetic damage in neurodegenerative conditions, such as for example a tendency towards chromosome 21 malsegregation in Alzheimer's disease. As it happens for many neurodegenerative risk factors the question of whether DNA damage is cause or consequence of the neurodegenerative process is still open, and probably both is true. The research interest in markers of oxidative stress was shifted, in recent years, towards the search of epigenetic biomarkers of neurodegenerative disorders, following the accumulating evidence of a substantial contribution of epigenetic mechanisms to learning, memory processes, behavioural disorders and neurodegeneration. Increasing evidence is however linking DNA damage and repair with epigenetic phenomena, thereby opening the way to a very attractive and timely research topic in neurodegenerative diseases. We will address those issues in the context of Alzheimer's disease

  8. DNA damage in neurodegenerative diseases

    International Nuclear Information System (INIS)

    Highlights: • Oxidative DNA damage is one of the earliest detectable events in the neurodegenerative process. • The mitochondrial DNA is more vulnerable to oxidative attack than the nuclear DNA. • Cytogenetic damage has been largely documented in Alzheimer's disease patients. • The question of whether DNA damage is cause or consequence of neurodegeneration is still open. • Increasing evidence links DNA damage and repair with epigenetic phenomena. - Abstract: Following the observation of increased oxidative DNA damage in nuclear and mitochondrial DNA extracted from post-mortem brain regions of patients affected by neurodegenerative diseases, the last years of the previous century and the first decade of the present one have been largely dedicated to the search of markers of DNA damage in neuronal samples and peripheral tissues of patients in early, intermediate or late stages of neurodegeneration. Those studies allowed to demonstrate that oxidative DNA damage is one of the earliest detectable events in neurodegeneration, but also revealed cytogenetic damage in neurodegenerative conditions, such as for example a tendency towards chromosome 21 malsegregation in Alzheimer's disease. As it happens for many neurodegenerative risk factors the question of whether DNA damage is cause or consequence of the neurodegenerative process is still open, and probably both is true. The research interest in markers of oxidative stress was shifted, in recent years, towards the search of epigenetic biomarkers of neurodegenerative disorders, following the accumulating evidence of a substantial contribution of epigenetic mechanisms to learning, memory processes, behavioural disorders and neurodegeneration. Increasing evidence is however linking DNA damage and repair with epigenetic phenomena, thereby opening the way to a very attractive and timely research topic in neurodegenerative diseases. We will address those issues in the context of Alzheimer's disease

  9. Protective effect of c-fos antisense oligonucleotides on brain damage induced by glutamate%c-fos反义寡核苷酸对谷氨酸神经毒性鼠脑损伤的防护

    Institute of Scientific and Technical Information of China (English)

    岳少杰; 陶永光; 罗自强; 冯德云; 伍赶球

    2001-01-01

    Objective To investigate the relation between glutamate neurotoxicity and c-fos gene expression. Methods c-fos antisense oligonucleotides (AS ODN) was injected into the right lateral ventricles of 9 SD rats to block the c-fos gene expression in brain tissue. c-fos sense oligonucleotides (S ODN)was used a control. The numbers and morphology of neurons in both cerebral cortex and hippocampal CA1 were detected by MIAS-300 image analysing instrument. c-fos gene expression in brain was observed by immunohistochemical method. The content of water and electrolytes in the brain tissue and Ca2+ in the synapse were measured. Results The c-fos AS ODN blocked the c-fos gene expression and reduced the content of both water and sodium in brain tissue and Ca2+ in symptosome, thus alleviating the morphological damage in neuron. S ODN did not have such effect. Conclusion c-fos gene expression plays an important role in mediating the effect of glutamate neurotoxicity. Blocking the c-fos gene expression could antagonize glutamate neurotoxicity.%目的 探讨c-fos基因的表达在谷氨酸神经毒性中的作用。方法 在9只SD大鼠侧脑室注射c-fos反义寡核苷酸以阻断脑组织c-fos基因的表达,并用c-fos正义寡核苷酸为对照。观察脑组织中水、电解质含量和突触体内Ca2+浓度的变化,并采用细胞形态计量分析及免疫组织化学方法,观察大脑皮质、海马CA1区神经细胞数目、形态的变化及c-fos基因的表达。结果 c-fos反义寡核苷酸可有效地阻断脑组织c-fos基因的表达,降低脑组织c-fos阳性细胞率(9.4%±2.8%和74%±3%,P<0.01),抑制谷氨酸神经毒性所致的脑组织含水量(79.9%±0.4%和82.3%±0.8%,P<0.01)、钠(5.05 mg/g干重±0.39 mg/g干重和5.98 mg/g干重±0.50 mg/g干重,P<0.01)及细胞内Ca2+(176 nmol/L±35 nmol/L和344.12±50.13,P<0.01)含量的增加,抑制谷氨酸所致大脑皮质(157±10和145±7,P<0

  10. Brain Fingerprinting

    Directory of Open Access Journals (Sweden)

    Ravi Kumar

    2012-12-01

    Full Text Available Brain Fingerprinting is a scientific technique to determine whether or not specific information is stored in an individual's brain by measuring a electrical brain wave response to Word, phrases, or picture that are presented on computer screen. Brain Fingerprinting is a controversial forensic science technique that uses electroencephalography (EEG to determine whether specific information is stored in a subject's brain.

  11. Brain Fingerprinting

    Directory of Open Access Journals (Sweden)

    ravi kumar

    2012-12-01

    Full Text Available Brain Fingerprinting is a scientific technique to determine whether or not specific information is stored in an individual's brain by measuring a electrical brain wave response to Word, phrases, or picture that are presented on computer screen. Brain Fingerprinting is a controversial forensic science technique that uses electroencephalograph y (EEG to determine whether specific information is stored in a subject's brain

  12. Brain Tumors

    Science.gov (United States)

    A brain tumor is a growth of abnormal cells in the tissues of the brain. Brain tumors can be benign, with no cancer cells, ... cancer cells that grow quickly. Some are primary brain tumors, which start in the brain. Others are ...

  13. 热休克蛋白表达对缺血性脑损伤的保护作用%The protection effectiveness of the expression of heat shock protein on ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    许川山; 余茜; 吴士明; 唐建民

    2003-01-01

    Heat shock protein is a group of stress protein produced under ill state. It can protect normal cells from damages caused by bad stimulates. It is thought as one of substance basis that remain in the process of evolution and take effect of anti damage. Now it is paid attentions as neuron protective substance induced by cerebral ischemic preconditioning.

  14. Brains on video games.

    Science.gov (United States)

    Bavelier, Daphne; Green, C Shawn; Han, Doug Hyun; Renshaw, Perry F; Merzenich, Michael M; Gentile, Douglas A

    2011-11-18

    The popular press is replete with stories about the effects of video and computer games on the brain. Sensationalist headlines claiming that video games 'damage the brain' or 'boost brain power' do not do justice to the complexities and limitations of the studies involved, and create a confusing overall picture about the effects of gaming on the brain. Here, six experts in the field shed light on our current understanding of the positive and negative ways in which playing video games can affect cognition and behaviour, and explain how this knowledge can be harnessed for educational and rehabilitation purposes. As research in this area is still in its early days, the contributors of this Viewpoint also discuss several issues and challenges that should be addressed to move the field forward.

  15. Brains on video games.

    Science.gov (United States)

    Bavelier, Daphne; Green, C Shawn; Han, Doug Hyun; Renshaw, Perry F; Merzenich, Michael M; Gentile, Douglas A

    2011-12-01

    The popular press is replete with stories about the effects of video and computer games on the brain. Sensationalist headlines claiming that video games 'damage the brain' or 'boost brain power' do not do justice to the complexities and limitations of the studies involved, and create a confusing overall picture about the effects of gaming on the brain. Here, six experts in the field shed light on our current understanding of the positive and negative ways in which playing video games can affect cognition and behaviour, and explain how this knowledge can be harnessed for educational and rehabilitation purposes. As research in this area is still in its early days, the contributors of this Viewpoint also discuss several issues and challenges that should be addressed to move the field forward. PMID:22095065

  16. Brain Basics

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    Full Text Available ... as depression. The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are the basic working unit of the brain ... specialized for the function of conducting messages. A neuron has three basic parts: Cell body which includes ...

  17. Brain surgery

    Science.gov (United States)

    Craniotomy; Surgery - brain; Neurosurgery; Craniectomy; Stereotactic craniotomy; Stereotactic brain biopsy; Endoscopic craniotomy ... cut depends on where the problem in the brain is located. The surgeon creates a hole in ...

  18. Brain Basics

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    Full Text Available ... Brain Basics provides information on how the brain works, how mental illnesses are disorders of the brain, ... others live with symptoms of mental illness every day. They can be moderate, or serious and cause ...

  19. Brain Basics

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    Full Text Available ... The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are the basic working unit of the ... distant nerve cells (via axons) to form brain circuits. These circuits control specific body functions such as ...

  20. Brain Basics

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    Full Text Available ... Basics will introduce you to some of this science, such as: How the brain develops How genes and the environment affect the brain The basic structure of the brain How different parts of ...

  1. Brain Basics

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    Full Text Available ... science, such as: How the brain develops How genes and the environment affect the brain The basic ... that with brain development in people mental disorders. Genes and environmental cues both help to direct this ...

  2. Protective effect of carboxymethyl chitosan(CMC)on the liver and brain in mice damaged by Dgalactose%羧甲基壳聚糖对D-半乳糖诱导氧化损伤模型小鼠肝、脑的保护作用

    Institute of Scientific and Technical Information of China (English)

    付青姐; 李明春; 李强

    2011-01-01

    目的:探索羧甲基壳聚糖(CMC)对D-半乳糖诱导氧化损伤模型小鼠肝、脑的作用.方法:实验分为4组:对照组、CMC组、D-半乳糖模型组、D-半乳糖+ CMC组.测定各组小鼠肝、脑超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性、丙二醛(MDA)的含量及蛋白质羰基化程度.结果:D-半乳糖可诱导小鼠蛋白质羰基化,诱导小鼠氧化损伤,CMC可使小鼠蛋白质羰基化含量降低,SOD,CAT活性增加,MDA含量降低.结论:CMC对D-半乳糖引起的氧化损伤有一定的保护作用.%OBJECTIVE To investigate the protective effect of CMC on the liver and brain in mice damaged by D-galactose. METHODS Animals were divided into four groups: control group; D-galactose treated animals; control + CMC group; D-galactose + CMC group. Protein carbonyl and SOD, CAT, MDA of the liver and brain were detected. RESULTS D-galactose induced protein carbonyl of brain and liver, CMC decreased it. CMC increased the activity of SOD and CAT and decreased the MDA content. CONCLUSION CMC might play a protective effect on the oxidative protein damage of brain and liver in mice.

  3. Cannabinoids on the Brain

    Directory of Open Access Journals (Sweden)

    Andrew J. Irving

    2002-01-01

    Full Text Available Cannabis has a long history of consumption both for recreational and medicinal uses. Recently there have been significant advances in our understanding of how cannabis and related compounds (cannabinoids affect the brain and this review addresses the current state of knowledge of these effects. Cannabinoids act primarily via two types of receptor, CB1 and CB2, with CB1 receptors mediating most of the central actions of cannabinoids. The presence of a new type of brain cannabinoid receptor is also indicated. Important advances have been made in our understanding of cannabinoid receptor signaling pathways, their modulation of synaptic transmission and plasticity, the cellular targets of cannabinoids in different central nervous system (CNS regions and, in particular, the role of the endogenous brain cannabinoid (endocannabinoid system. Cannabinoids have widespread actions in the brain: in the hippocampus they influence learning and memory; in the basal ganglia they modulate locomotor activity and reward pathways; in the hypothalamus they have a role in the control of appetite. Cannabinoids may also be protective against neurodegeneration and brain damage and exhibit anticonvulsant activity. Some of the analgesic effects of cannabinoids also appear to involve sites within the brain. These advances in our understanding of the actions of cannabinoids and the brain endocannabinoid system have led to important new insights into neuronal function which are likely to result in the development of new therapeutic strategies for the treatment of a number of key CNS disorders.

  4. Neuroprotective role of ibuprofen in hypoxic-ischemic brain damage in neonatal rats%布洛芬对新生大鼠缺氧缺血后脑损伤的保护作用

    Institute of Scientific and Technical Information of China (English)

    乔丽丽; 沈伟勤

    2013-01-01

    Objective To investigate neuroprotective effect of ibuprofen on neonatal rats brain damage after hypoxia-ischemia (HI). Methods Fourty 7-day-old mice were divided to normal saline (NS) group, ibuprofen group, HI+NS group, and Hl+ibuprofen group. The HI+NS group and Hl+ibuprofen group subjected to unilateral ligation of the left common carotid artery (ischemia) and 50 min of hypoxia for set up HI model. An initial dose of ibuprofen lOOmg/kg was administered 2 hours after HI followed by a maintenance dose 50mg/kg every 24 hours for 6 days in Hl+ibuprofen group and ibupreofen group. The mice were sacrificed 7 days after HI. The grey matter, microtubule-associated protein-2 (MAP-2) and white matter, myeline basic protein (MBP) and neurofilameng (NF) injury were detected by immunohistochemical staining. The number of galectin-3 positive cells were counted in Cortex, DG, CA area. Results In NS group and ibuprofen group, the grey matter was normal and does not appear infarct. In Hl+ibuprofen group, the infarct area was (33.18+4.57) mm and the infarct volume was (39.18+4.29) mm3. In HI+NS group, the infarct area was (35.23+4.15) mm2 and the infarct volume was (40.23+4.65) mm3. There was no difference between two groups (t=34.54, 42.38, P>0.05). In Hl+ibuprofen group, the loss of MBP was (42.32+7.56)% and the loss of neurofilament (NF) was (40.34+6.83)%. In HI+NS group, the loss of MBP was (31.34+5.67)% and the loss of NF was (30.82+5.24)%. There were significant differences between two groups (t=13.51, 11.56, P0.05).HI+生理盐水组脑白质MBP损失为(42.32±7.56)%,NF为(40.34±6.83)%;HI+布洛芬组分别为(31.34±5.67)%、(30.82±5.24)%,两组差异有统计学意义(t=13.51、11.56,P均<0.05).HI+布洛芬组Cortex区的galectin-3细胞较HI+生理盐水组明显下降,差异有统计学意义(U=11.52,P<0.05).结论 布洛芬对HI后大脑的白质有明显保护作用,可能与降低小胶质细胞活性有关;但对大脑灰质无明显保护作用.

  5. Cortisol Excess and the Brain.

    Science.gov (United States)

    Resmini, Eugenia; Santos, Alicia; Webb, Susan M

    2016-01-01

    Until the last decade, little was known about the effects of chronic hypercortisolism on the brain. In the last few years, new data have arisen thanks to advances in imaging techniques; therefore, it is now possible to investigate brain activity in vivo. Memory impairments are present in patients with Cushing's syndrome (CS) and are related to hippocampal damage; functional dysfunctions would precede structural abnormalities as detected by brain imaging. Earlier diagnosis and rapid normalization of hypercortisolism could stop the progression of hippocampal damage and memory impairments. Impairments of executive functions (including decision-making) and other functions such as visuoconstructive skills, language, motor functions and information processing speed are also present in CS patients. There is controversy concerning the reversibility of brain impairment. It seems that longer disease duration and older age are associated with less recovery of brain functioning. Conversely, earlier diagnosis and rapid normalization of hypercortisolism appear to stop progression of brain damage and functional impairments. Moreover, brain tissue functioning and neuroplasticity can be influenced by many factors. Currently available studies appear to be complementary, evaluating the same phenomenon from different points of view, but are often not directly comparable. Finally, CS patients have a high prevalence of psychopathology, such as depression and anxiety which do not completely revert after cure. Thus, psychological or psychiatric evaluation could be recommended in CS patients, so that treatment may be prescribed if required. PMID:27210466

  6. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HU Hua; YAO Hong-tian; ZHANG Wei-ping; ZHANG LEI; DING Wei; ZHANG Shi-hong; CHEN Zhong; WEI Er-qing

    2005-01-01

    Objective: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. Methods: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. Results: AQP4 expression was increased from 15h to at least 8 d after injury. AQP4immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.Conclusion: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

  7. Brain Basics

    Medline Plus

    Full Text Available ... Welcome. Brain Basics provides information on how the brain works, how mental illnesses are disorders of the brain, ... highly developed area at the front of the brain that, in humans, plays a role in executive functions such as ...

  8. Brain Basics

    Medline Plus

    Full Text Available ... Research Modern research tools and techniques are giving scientists a more detailed understanding of the brain than ever before. Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses magnetic fields to take pictures of the brain's structure, studies ...

  9. Mathematical modelling of blood-brain barrier failure and edema

    Science.gov (United States)

    Waters, Sarah; Lang, Georgina; Vella, Dominic; Goriely, Alain

    2015-11-01

    Injuries such as traumatic brain injury and stroke can result in increased blood-brain barrier permeability. This increase may lead to water accumulation in the brain tissue resulting in vasogenic edema. Although the initial injury may be localised, the resulting edema causes mechanical damage and compression of the vasculature beyond the original injury site. We employ a biphasic mixture model to investigate the consequences of blood-brain barrier permeability changes within a region of brain tissue and the onset of vasogenic edema. We find that such localised changes can indeed result in brain tissue swelling and that the type of damage that results (stress damage or strain damage) depends on the ability of the brain to clear edema fluid.

  10. 99mTc HM-PAO brain perfusion SPECT in brain death

    International Nuclear Information System (INIS)

    We have easily carried out and interpreted 99mTc HM-PAO SPECT in a consecutive series of 40 comatose patients with brain damage, without discontinuing therapy. Brain death was diagnosed in 7 patients, by recognising absence of brain perfusion, as shown by no intracranial radionuclide uptake. In patients in whom perfusion was seen on brain scans, HM-PAO SPECT improved assessment of the extent of injury, which in general was larger than suggested by CT. (orig.)

  11. Contraction-induced muscle fiber damage is increased in soleus muscle of streptozotocin-diabetic rats and is associated with elevated expression of brain-derived neurotrophic factor mRNA in muscle fibers and activated satellite cells

    NARCIS (Netherlands)

    Copray, S; Liem, R; Brouwer, N; Greenhaff, P; Habens, F; Fernyhough, P

    2000-01-01

    The expression of brain-derived neurotrophic factor (BDNF) is elevated in the soleus muscle of streptozotocin-diabetic rats. To determine whether this diabetes-induced elevation was associated with or enhanced by muscle activity we have induced high-intensity muscle contraction by electrically stimu

  12. Respiratory mechanics in brain injury: A review

    OpenAIRE

    Koutsoukou, Antonia; Katsiari, Maria; Orfanos, Stylianos E; Kotanidou, Anastasia; Daganou, Maria; Kyriakopoulou, Magdalini; Koulouris, Nikolaos G.; Rovina, Nikoletta

    2016-01-01

    Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients (BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case ...

  13. Relationship of plasma S100B and myelin basic protein level with brain damage in preterm infants%血浆S100B蛋白和髓鞘碱性蛋白与早产儿脑损伤的关系

    Institute of Scientific and Technical Information of China (English)

    陈珊; 李薇; 瞿柳红; 唐娟; 荣箫; 周伟

    2014-01-01

    .早产儿出生后血浆S100B、MBP蛋白的增高对判断是否发生早期脑损伤及PVL具有一定的临床意义.%Objective To study the relationships of plasma myelin basic protein (MBP) and S100B level with periventricular hemorrhage-intraventricular hemorrhage (PVH-IVH) and periventricular leucumalacia (PVL) in preterm infants.Methods There were 385 cases of preterm infants whose gestational age was less than 34 weeks and were admitted in NICUs of Guangzhou Women and Children's Medical Center of Guangzhou Medical University,Guangzhou Huadu District Maternal and Child Health Hospital and Dongguan Hospital Affiliated to Jinan University from Jan.2010 to Jun.2013,enrolled in the study.The plasma levels of S100B and MBP protein were detected within 24 hours and on the 3rd,7th,14th day after birth.Cranial ultrasound (US) was preformed 2-3 d,1 week,2 weeks,3 weeks and 4 weeks after birth.They also received Cranial MRI examination before discharge or when the correct gestational age reached 40 weeks.According to the exclusion standard 73 cases were excluded.The included 312 cases were divided into 3 groups (no brain damage group,PVH-IVH group and PVL group) according to the result of cranial US and MRI.The differences of the plasma levels of S100B and MBP protein among each groups were compared,and the relationship of the plasma levels of S100B and MBP protein in no brain damage group with gestational age were analyzed.Results The results of cranial ultrasound and/or MRI showed:204 cases had no brain damage (put in no brain damage group),69 cases had PVH-IVH (put in PVH-IVH group),and 27 cases had PVL,12 cases had PVL and PVH-IVH (both put in PVL group).The plasma level of S100B:within 24h and 3 d after birth,the serum levels of S100B in PVH-IVH group were significantly higher than those in no brain damage group (P < 0.05) ; and the plasma levels of S100B in PVL group were significantly higher than those in no brain damage group and PVH-IVH group (all P < 0.05).On 7 d and 14 d after

  14. Neurobiology: Language By, In, Through and Across the Brain

    Science.gov (United States)

    Müller, Ralph-Axel

    Language has come to be commonly understood as something accomplished by the brain. Much scientific investigation has consequently focused in looking for language in the brain. Although it may sound intuitive, this approach suggests that language is an object located inside another object. This spatial metaphor has generated important insights into the brain sites important for language, from nineteenth century studies of brain-damaged patients to more recent and refined evidence from brain imaging.

  15. Brain connectivity and sensory stimulation in disorders of consciousness

    OpenAIRE

    Heine, Lizette

    2016-01-01

    This thesis explores brain connectivity and sensory stimulation in patients with disorders of consciousness (DOC). These are serious conditions where massive brain damage can lead to a dissociation between arousal and awareness (e.g., UWS and MCS). Part I explores brain connectivity. We highlight that brain function and structure are intimately related to each other, and to consciousness. The decrease in brain function can be used to distinguish between the clinically indicated states of ...

  16. Repeated mild injury causes cumulative damage to hippocampal cells

    NARCIS (Netherlands)

    E.J. Matser; C.I. de Zeeuw (Chris); J.T. Weber (John)

    2002-01-01

    textabstractAn interesting hypothesis in the study of neurotrauma is that repeated traumatic brain injury may result in cumulative damage to cells of the brain. However, post-injury sequelae are difficult to address at the cellular level in vivo. Therefore, it is necessary to compl

  17. Brain Basics

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    Full Text Available ... all. She was happily married and successful in business. Then, after a serious setback at work, she ... than ever before. Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses ...

  18. Brain Basics

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    Full Text Available ... the anatomy, physiology, and chemistry of the nervous system. When the brain cannot effectively coordinate the billions ... basic working unit of the brain and nervous system. These cells are highly specialized for the function ...

  19. Brain Basics

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    Full Text Available ... the brain cannot effectively coordinate the billions of cells in the body, the results can affect many ... unit of the brain and nervous system. These cells are highly specialized for the function of conducting ...

  20. Brain Basics

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    Full Text Available ... Trials — Participants Statistics Help for Mental Illnesses Outreach Research Priorities Funding Labs at NIMH News About Us Home > Health & Education > Educational Resources Brain Basics Introduction The Growing Brain The ...

  1. Brain Basics

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    Full Text Available ... brain may play a role in disorders like schizophrenia or attention deficit hyperactivity disorder (ADHD) . Glutamate —the ... mental disorders, including autism , obsessive compulsive disorder (OCD) , schizophrenia , and depression . Brain Regions Just as many neurons ...

  2. Brain Basics

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    Full Text Available ... body, the results can affect many aspects of life. Scientists are continually learning more about how the brain grows and works in healthy people, and how normal brain development and function ...

  3. Brain Basics

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    Full Text Available ... Brain Basics will introduce you to some of this science, such as: How the brain develops How ... cell, and responds to signals from the environment; this all helps the cell maintain its balance with ...

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    Full Text Available ... How the brain develops How genes and the environment affect the brain The basic structure of the ... inside contents of the cell from its surrounding environment and controls what enters and leaves the cell, ...

  5. Brain Basics

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    Full Text Available ... affect many aspects of life. Scientists are continually learning more about how the brain grows and works ... early brain development. It may also assist in learning and memory. Problems in making or using glutamate ...

  6. Brain Basics

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    Full Text Available ... have been linked to many mental disorders, including autism , obsessive compulsive disorder (OCD) , schizophrenia , and depression . Brain ... studies show that brain growth in children with autism appears to peak early. And as they grow ...

  7. Brain Basics

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    Full Text Available ... may help improve treatments for anxiety disorders like phobias or post-traumatic stress disorder (PTSD) . Prefrontal cortex ( ... brain's structure, studies show that brain growth in children with autism appears to peak early. And as ...

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    Full Text Available ... body, the results can affect many aspects of life. Scientists are continually learning more about how the brain grows and works in healthy people, and how normal brain development ...

  9. Brain Basics

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    Full Text Available ... medications could reduce the amount of trial and error and frustration that many people with depression experience ... early brain development, and may also assist in learning and memory. hippocampus —A portion of the brain ...

  10. Brain Diseases

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    The brain is the control center of the body. It controls thoughts, memory, speech, and movement. It regulates the function of many organs. When the brain is healthy, it works quickly and automatically. However, ...

  11. Brain Basics

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    Full Text Available ... than ever before. Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses ... depression experience when starting treatment. Gene Studies Advanced technologies are also making it faster, easier, and more ...

  12. Brain Basics

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    Full Text Available ... mainly involved in controlling movement and aiding the flow of information to the front of the brain, ... the neuron will fire. This enhances the electrical flow among brain cells required for normal function and ...

  13. Brain Basics

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    Full Text Available ... works in healthy people, and how normal brain development and function can go awry, leading to mental ... and are working to compare that with brain development in people mental disorders. Genes and environmental cues ...

  14. Brain Basics

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    Full Text Available ... and epigenetic changes can be passed on to future generations. Further understanding of genes and epigenetics may ... than ever before. Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses ...

  15. Brain Basics

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    Full Text Available ... neurons, the most highly specialized cells of all, conduct messages. Every cell in our bodies contains a ... brain's structure, studies show that brain growth in children with autism appears to peak early. And as ...

  16. Brain Basics

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    Full Text Available ... can be related to changes in the anatomy, physiology, and chemistry of the nervous system. When the ... healthy people, and how normal brain development and function can go awry, leading to mental illnesses. Brain ...

  17. Brain Basics

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    Full Text Available ... Real Life Brain Basics in Real Life—How Depression affects the Brain Meet Sarah Sarah is a ... blues" from time to time. In contrast, major depression is a serious disorder that lasts for weeks. ...

  18. Material Induced Anisotropic Damage

    NARCIS (Netherlands)

    Niazi, M.S.; Wisselink, H.H.; Meinders, V.T.; Boogaard, van den A.H.; Hora, P.

    2012-01-01

    The anisotropy in damage can be driven by two different phenomena; anisotropic defor-mation state named Load Induced Anisotropic Damage (LIAD) and anisotropic (shape and/or distribution) second phase particles named Material Induced Anisotropic Damage (MIAD). Most anisotropic damage models are based

  19. Brain Basics

    Medline Plus

    Full Text Available ... pituitary-adrenal (HPA) axis. Brain Basics in Real Life Brain Basics in Real Life—How Depression affects the Brain Meet Sarah Sarah ... having trouble coping with the stresses in her life. She began to think of suicide because she ...

  20. Brain Basics

    Medline Plus

    Full Text Available ... Life Brain Basics in Real Life—How Depression affects the Brain Meet Sarah Sarah is a middle-aged woman ... new memories. hypothalmic-pituitary-adrenal (HPA) axis —A brain-body ... stress. impulse —An electrical communication signal sent between neurons ...

  1. Brain Aneurysm

    Science.gov (United States)

    A brain aneurysm is an abnormal bulge or "ballooning" in the wall of an artery in the brain. They are sometimes called berry aneurysms because they ... often the size of a small berry. Most brain aneurysms produce no symptoms until they become large, ...

  2. Tau 的病理性修饰与新生儿缺氧缺血性脑损伤%Abnormally modified tau and hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    肖婕; 李凡

    2015-01-01

    Tau is the most abundant microtubule-associated protein in the brain .If tau protein lost the normal function, the toxic effect should be showed and plays an important role in various central nervous system lesions .Hypoxic-ischemic encephalopathy ( HIE) is an important cause of mortality in the neonatal period and it is mainly characterized by neurological deficits such as cognitive limitations .However , the mechanism still needs further study , and the underlying re-lationship between tau protein and HIE lacks direct evidence .Some recent clinical study reported that tau protein expres-sion elevated in the serum of asphyxia children and had a high correlation with behavior deficient .In this review , we focus on 3 key points to provide new insights to understand the tau protein-related pathogenesis of HIE as followed:(1) tau pro-tein and its phosphorylation change during central nervous system development ;(2) comparison of tau protein expression in developing brain and adult brain under some neurological disorders;(3) potential pathological change of tau in HIE related pathological conditions , such as dysmyelination , inflammation response and glutamate metabolism .

  3. 果糖二磷酸钠镁对鼠脑缺血-再灌注损伤的保护作用%Protective Effects of Sodium Magnesium Fructose Diphosphate on Brain Damage of Rats Subjected to Focal Cerebral Ischemia and Reperfusion

    Institute of Scientific and Technical Information of China (English)

    董志; 曾凡新; 周岐新; 傅洁民; 薛春生

    2002-01-01

    目的:三究果糖二磷酸钠镜头(FDPM)对大鼠脑缺备一再灌注引起脑损伤的保护作用.方法:自大鼠颈总动脉插入尼龙线栓栓塞大脑中动脉,造成大脑缺血,拔出线栓实线灌注.脑缺血10 min后给予400 mg·kg-1FDPM,400 mg·kg-1FDP及30mg·kg-1MgSO4,分别于脑缺血1h再灌注2h,5h和23h分别进行神经病学评分,并于脑缺血1h再灌注23h时测定脑梗塞面积及脑组织MDA含量,观察大脑组织病理学变化.结果:FDPM降低脑血一再灌注大鼠神经病学评分,缩小脑梗塞面积,降低脑组织MDA含量,减轻光镜下脑组织的病理改变.其作用强于FDP或MgSO4.结论:FDPM可显著保护大脑缺血再灌注引起的脑损伤,其作用单用FDP或MgSO4.%Objective: To study the effects of sodium magnesiusm fructose diphesphate(FDPM) on brain dsmage of rais after ischemia-reperfusion. Methods: Rats were subjected to cerebral ischemia-reperfusion induced by inserting a nylon thread into internal carotid artery to block the origin of middle cerebral artery and removing the thread later.FDPM (400 mg·kg-1)fructose-l,6-diphosphate(FDP, 400 mg·kg- 1)and magnesium sulfate (MgSO4, 30 mg·kg-1) were administrated 10 min af ter the onset of ischemia. Neurological scale, brain infarct area, Malondialdehyde(MDA) content and histopathological chang es of brain tissue were studied. Results: FDPM decreased neurological scale, diminished brain infarct area, reduced MDA content and relieved histopathologial change of rat brain tissue subjJected to ischemia-repefusion. These effecis were more powerful than that of FDP or MgSO4.Conclusions:It is suggested that FDPM markedly preventad rats against brain damage after cerebral ischmia-reperfusion,and its effect was better than that of FDP or MgSO4.

  4. The brain's best friend : microglial neurotoxicity revisited

    NARCIS (Netherlands)

    Hellwig, Sabine; Heinrich, Annette; Biber, Knut

    2013-01-01

    One long standing aspect of microglia biology was never questioned; their involvement in brain disease. Based on morphological changes (retracted processes and amoeboid shape) that inevitably occur in these cells in case of damage in the central nervous system, microglia in the diseased brain were c

  5. Brain MRI in Type 2 Diabetes

    OpenAIRE

    Tiehuis, A.M.

    2009-01-01

    In recent years is has become clear that type 2 diabetes affects the central nervous system. These long-term complications manifest as structural changes on brain imaging, cognitive decrements and a 1.5-2 fold increased risk for the development of dementia, in particular in the elderly. The pathogenesis of diabetes-induced brain damage is not completely understood. Both vascular and metabolic disturbances may play an important role in the impact of diabetes on the brain. The course of develop...

  6. [Asterixis in focal brain lesions].

    Science.gov (United States)

    Velasco, F; Gomez, J C; Zarranz, J J; Lambarri, I; Ugalde, J

    2004-05-01

    Asterixis is a motor control disorder characterized by the presence of abnormal movements of the lower limbs in the vertical plane during posture maintenance. Asterixis is usually bilateral and associated with toxic-metabolic metabolic encephalopathies. Unilateral asterixis is less frequent and it normally indicates focal brain damage. We report the cases of four patients (two males/two females), aged 57 to 83 years, suffering from uni or bilateral asterixis associated with focal brain damage. All patients underwent CT brain scan and a neurophysiological study (parietal EMG and/or PES). In addition, any toxic-metabolic cause that could be produced by this clinical phenomenon was ruled out with the appropriate testing. Unilateral asterixis is a clinical symptom that may indicate the presence of focal brain damage. Often, it is ignored or overlooked during routine neurological examinations. On the other hand, the presence of a bilateral asterixis is not always indicative of a toxic-metabolic encephalopathy.Rarely, such as in one of the cases herein presented, bilateral asterixis can also appear associated with structural brain lesions. Although asterixis diagnosis is fundamentally clinical, the neurophysiological study contributes to verify the diagnosis.

  7. Brain and Cognitive-Behavioural Development after Asphyxia at Term Birth

    Science.gov (United States)

    de Haan, Michelle; Wyatt, John S.; Roth, Simon; Vargha-Khadem, Faraneh; Gadian, David; Mishkin, Mortimer

    2006-01-01

    Perinatal asphyxia occurs in approximately 1-6 per 1000 live full-term births. Different patterns of brain damage can result, though the relation of these patterns to long-term cognitive-behavioural outcome remains under investigation. The hippocampus is one brain region that can be damaged (typically not in isolation), and this site of damage has…

  8. Brain glycogen

    DEFF Research Database (Denmark)

    Obel, Linea Lykke Frimodt; Müller, Margit S; Walls, Anne B;

    2012-01-01

    Glycogen is a complex glucose polymer found in a variety of tissues, including brain, where it is localized primarily in astrocytes. The small quantity found in brain compared to e.g., liver has led to the understanding that brain glycogen is merely used during hypoglycemia or ischemia....... In this review evidence is brought forward highlighting what has been an emerging understanding in brain energy metabolism: that glycogen is more than just a convenient way to store energy for use in emergencies-it is a highly dynamic molecule with versatile implications in brain function, i.e., synaptic...... activity and memory formation. In line with the great spatiotemporal complexity of the brain and thereof derived focus on the basis for ensuring the availability of the right amount of energy at the right time and place, we here encourage a closer look into the molecular and subcellular mechanisms...

  9. Prehospital Care of Traumatic Brain Injury

    Directory of Open Access Journals (Sweden)

    TVSP Murthy

    2008-01-01

    Full Text Available Traumatic brain injury (TBI occurs when a sudden trauma causes brain damage. Depending on the severity, outcome can be anything from complete recovery to permanent disability or death. Emergency medical services play a dominant role in provision of primary care at the site of injury. Since little can be done to reverse the initial brain damage due to trauma, attempts to prevent further brain damage and stabilize the patient before he can be brought to a specialized trauma care centre play a pivotal role in the final outcome. Recognition and early treatment of hypoten-sion, hypoxemia, and hypoglycemia, objective neurological assessment based on GCS and pupils, and safe transport to an optimal care centre are the key elements of prehospital care of a TBI patient.

  10. Word Recognition in Individuals with Left and Right Hemisphere Damage: The Role of Lexical Stress.

    Science.gov (United States)

    Baum, Shari R.

    2002-01-01

    Employed a lexical decision task to asses whether left hemisphere damaged (LHD) and right hemisphere damaged (RHD) patients are similarly sensitive to stress patterns in lexical access. Results confirmed that individuals without brain damage are influenced by stress patterns, as indicated by increased lexical decision latencies to incorrectly…

  11. Brain Basics

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    Full Text Available ... as they grow there are differences in brain development in children who develop bipolar disorder than children who do not. Studies comparing such children to those with normal brain development may help scientists to pinpoint when and where ...

  12. Brain Basics

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    Full Text Available ... PTSD) . Prefrontal cortex (PFC) —Seat of the brain's executive functions, such as judgment, decision making, and problem solving. ... brain that, in humans, plays a role in executive functions such as judgment, decision making and problem solving, ...

  13. Brain Basics

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    Full Text Available ... Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses magnetic fields to take pictures of ... to slow or stop them from progressing. Functional magnetic resonance imaging (fMRI) is another important research tool in understanding ...

  14. Brain Basics

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    Full Text Available ... little dopamine or problems using dopamine in the thinking and feeling regions of the brain may play ... axis —A brain-body circuit which plays a critical role in the body's response to stress. impulse — ...

  15. Brain Basics

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    Full Text Available ... Brain Imaging Using brain imaging technologies such as magnetic resonance imaging (MRI), which uses magnetic fields to take ... to slow or stop them from progressing. Functional magnetic resonance imaging (fMRI) is another important research tool in ...

  16. Brain Basics

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    Full Text Available ... Basics in Real Life Brain Basics in Real Life—How Depression affects the Brain Meet Sarah Sarah is a middle-aged woman who seemed to have it all. She was happily married and successful in business. Then, after a serious setback at work, she lost interest ...

  17. CHARACTERIZATION OF DAMAGED MATERIALS

    Energy Technology Data Exchange (ETDEWEB)

    Hsu, P C; Dehaven, M; McClelland, M; Chidester, S; Maienschein, J L

    2006-06-23

    Thermal damage experiments were conducted on LX-04, LX-10, and LX-17 at high temperatures. Both pristine and damaged samples were characterized for their material properties. A pycnometer was used to determine sample true density and porosity. Gas permeability was measured in a newly procured system (diffusion permeameter). Burn rate was measured in the LLNL strand burner. Weight losses upon thermal exposure were insignificant. Damaged pressed parts expanded, resulting in a reduction of bulk density by up to 10%. Both gas permeabilities and burn rates of the damaged samples increased by several orders of magnitude due to higher porosity and lower density. Moduli of the damaged materials decreased significantly, an indication that the materials became weaker mechanically. Damaged materials were more sensitive to shock initiation at high temperatures. No significant sensitization was observed when the damaged samples were tested at room temperature.

  18. Aging and oxidatively damaged nuclear DNA in animal organs

    DEFF Research Database (Denmark)

    Møller, Peter; Løhr, Mille; Folkmann, Janne K;

    2010-01-01

    Oxidative stress is considered to contribute to aging and is associated with the generation of oxidatively damaged DNA, including 8-oxo-7,8-dihydroguanine. We have identified 69 studies that have measured the level of oxidatively damaged DNA in organs of animals at various ages. In general, organs...... with limited cell proliferation, i.e., liver, kidney, brain, heart, pancreas, and muscle, tended to show accumulation of DNA damage with age, whereas organs with highly proliferating cells, such as intestine, spleen, and testis, showed more equivocal or no effect of age. A restricted analysis of studies...... evidence for aging-associated accumulation of oxidatively damaged DNA in organs with limited cell proliferation....

  19. Brain peroxisomes.

    Science.gov (United States)

    Trompier, D; Vejux, A; Zarrouk, A; Gondcaille, C; Geillon, F; Nury, T; Savary, S; Lizard, G

    2014-03-01

    Peroxisomes are essential organelles in higher eukaryotes as they play a major role in numerous metabolic pathways and redox homeostasis. Some peroxisomal abnormalities, which are often not compatible with life or normal development, were identified in severe demyelinating and neurodegenerative brain diseases. The metabolic roles of peroxisomes, especially in the brain, are described and human brain peroxisomal disorders resulting from a peroxisome biogenesis or a single peroxisomal enzyme defect are listed. The brain abnormalities encountered in these disorders (demyelination, oxidative stress, inflammation, cell death, neuronal migration, differentiation) are described and their pathogenesis are discussed. Finally, the contribution of peroxisomal dysfunctions to the alterations of brain functions during aging and to the development of Alzheimer's disease is considered.

  20. H-和L-铁蛋白在脑膜炎中抑制由于自由铁增高造成的脑损伤%The Inhibitory Effect of H-and L-ferritin on Increased free Iron-induced Brain Damage in Experimental Meningitis

    Institute of Scientific and Technical Information of China (English)

    任昊; 翟效月

    2011-01-01

    Objective To study the changes of ferritin and free iron in brains of meningitis,and to investigate the protective effect of ferritin against inflammatory brain injuries.Methods Forty Wistar rats were used as models of meningitis,which were divided into two groups randomly with equal number of both sexes.Brain samples were extracted according to the requirements of morphological and quantitative analysis.Cerebral free iron was measured with Ferene-S method,and expression of ferritin was measured by western blot.Confocal microscopy was applied for the detection of RNA peroxidation product 8-hydroxy-guanosine(8-OHdG).Results Compared with control group,cerebral free iron levels in the infected brains were significantly increased,as well as H- and L-ferritin levels.Ferritin expression coexisted with cerebral iron in terms of cell types.Brain RNA peroxidation indicator of 8-OhdG didn't increase significantly.Conclusion Pneumococcal meningitis was associated with an increase of cerebral iron level in rats, but without an increase of brain oxidation.H-and L-ferritin could combine with the free iron and thus protected the brain from oxidative damage.%目的 检测铁蛋白与自由铁在脑膜炎大鼠大脑中的改变.探讨H-和L-型铁蛋白对该炎性病变脑损伤的保护作用.方法 40只新生Wistar大鼠作脑膜炎动物模型,雌雄各半,随机分组.大脑材料分别按形态学石蜡切片和定量分析的要求进行取材.利用Ferene-S方法测脑自由铁,免疫印迹测铁蛋白的表达,共聚焦显微镜观察RNA过氧化产物8-羟基鸟苷酸荧光信号.结果 与对照组比较,脑自由铁在感染组中显著上升.H-和L-铁蛋白水平同时增加,且在大脑皮质与脑铁有共存关系.RNA过氧化指标8-羟基鸟苷酸无显著增加.结论 大鼠脑膜炎病变过程伴随着脑自由铁的增加,但并未发生脑的过氧化损伤.H-和L-铁蛋白的表达能够结合自由铁从而保护大脑.

  1. Traumatic brain injury and reserve.

    Science.gov (United States)

    Bigler, Erin D; Stern, Yaakov

    2015-01-01

    The potential role of brain and cognitive reserve in traumatic brain injury (TBI) is reviewed. Brain reserve capacity (BRC) refers to preinjury quantitative measures such as brain size that relate to outcome. Higher BRC implies threshold differences when clinical deficits will become apparent after injury, where those individuals with higher BRC require more pathology to reach that threshold. Cognitive reserve (CR) refers to how flexibly and efficiently the individual makes use of available brain resources. The CR model suggests the brain actively attempts to cope with brain damage by using pre-existing cognitive processing approaches or by enlisting compensatory approaches. Standard proxies for CR include education and IQ although this has expanded to include literacy, occupational attainment, engagement in leisure activities, and the integrity of social networks. Most research on BRC and CR has taken place in aging and degenerative disease but these concepts likely apply to the effects of TBI, especially with regards to recovery. Since high rates of TBI occur in those under age 35, both CR and BRC factors likely relate to how the individual copes with TBI over the lifespan. These factors may be particularly relevant to the relationship of developing dementia in the individual who has sustained a TBI earlier in life.

  2. Systemic LPS administration induces brain inflammation but not dopaminergic neuronal death in the substantia nigra

    OpenAIRE

    Jeong, Hey-Kyeong; Jou, Ilo; Joe, Eun-hye

    2010-01-01

    It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including Parkinson's disease (PD). Recently, systemic inflammation has also emerged as a risk factor for PD. In the present study, we evaluated how systemic inflammation induced by intravenous (iv) lipopolysaccharides (LPS) injection affected brain inflammation and neuronal damage in the rat. Interestingly, almost all brain inflammatory response...

  3. DNA Damage Response

    OpenAIRE

    Giglia-Mari, Giuseppina; Zotter, Angelika; Vermeulen, Wim

    2011-01-01

    Structural changes to DNA severely affect its functions, such as replication and transcription, and play a major role in age-related diseases and cancer. A complicated and entangled network of DNA damage response (DDR) mechanisms, including multiple DNA repair pathways, damage tolerance processes, and cell-cycle checkpoints safeguard genomic integrity. Like transcription and replication, DDR is a chromatin-associated process that is generally tightly controlled in time and space. As DNA damag...

  4. Inhibitory action of antioxidants (ascorbic acid or α-tocopherol on seizures and brain damage induced by pilocarpine in rats Ação inibitória de antioxidantes (ácido ascórbico e α-tocoferol nas convulsões e dano cerebral em ratos induzidos pela pilocarpina

    Directory of Open Access Journals (Sweden)

    Adriana da Rocha Tomé

    2010-06-01

    Full Text Available Temporal lobe epilepsy is the most common form of epilepsy in humans. Oxidative stress is a mechanism of cell death induced by seizures. Antioxidant compounds have neuroprotective effects due to their ability to inhibit free radical production. The objectives of this work were to comparatively study the inhibitory action of antioxidants (ascorbic acid or α-tocopherol on behavioral changes and brain damage induced by high doses of pilocarpine, aiming to further clarify the mechanism of action of these antioxidant compounds. In order to determinate neuroprotective effects, we studied the effects of ascorbic acid (250 or 500 mg/kg, i.p. and α-tocopherol (200 or 400 mg/kg, i.p. on the behavior and brain lesions observed after seizures induced by pilocarpine (400 mg/kg, i.p., P400 model in rats. Ascorbic acid or α-tocopherol injections prior to pilocarpine suppressed behavioral seizure episodes. These findings suggested that free radicals can be produced during brain damage induced by seizures. In the P400 model, ascorbic acid and α-tocopherol significantly decreased cerebral damage percentage. Antioxidant compounds can exert neuroprotective effects associated with inhibition of free radical production. These results highlighted the promising therapeutic potential of ascorbic acid and α-tocopherol in treatments for neurodegenerative diseases.A epilepsia de lobo temporal é a mais comum forma de epilepsia em humanos. O estresse oxidativo é um dos mecanismos de morte celular induzida pelas crises convulsivas. Os compostos antioxidantes apresentam efeitos neuroprotetores devido à sua capacidade de inibir a produção de radicais livres. Os objetivos do presente trabalho foram estudar de forma comparativa a ação inibitória de antioxidantes (ácido ascórbico e α-tocoferol sobre as alterações comportamentais e histopatológicas no hipocampo de ratos após convulsões induzidas pela pilocarpina. A fim de determinar os efeitos neuroprotetores

  5. Brain tumor - primary - adults

    Science.gov (United States)

    ... Vestibular schwannoma (acoustic neuroma) - adults; Meningioma - adults; Cancer - brain tumor (adults) ... Primary brain tumors include any tumor that starts in the brain. Primary brain tumors can start from brain cells, ...

  6. Brain radiation - discharge

    Science.gov (United States)

    Radiation - brain - discharge; Cancer-brain radiation; Lymphoma - brain radiation; Leukemia - brain radiation ... Decadron) while you are getting radiation to the brain. It may make you hungrier, cause leg swelling ...

  7. Brain and Addiction

    Science.gov (United States)

    ... Teens / Drug Facts / Brain and Addiction Brain and Addiction Print Your Brain Your brain is who you ... is taken over and over. What Is Drug Addiction? Addiction is a chronic brain disease that causes ...

  8. Brain imaging in type 2 diabetes.

    Science.gov (United States)

    Brundel, Manon; Kappelle, L Jaap; Biessels, Geert Jan

    2014-12-01

    Type 2 diabetes mellitus (T2DM) is associated with cognitive dysfunction and dementia. Brain imaging may provide important clues about underlying processes. This review focuses on the relationship between T2DM and brain abnormalities assessed with different imaging techniques: both structural and functional magnetic resonance imaging (MRI), including diffusion tensor imaging and magnetic resonance spectroscopy, as well as positron emission tomography and single-photon emission computed tomography. Compared to people without diabetes, people with T2DM show slightly more global brain atrophy, which increases gradually over time compared with normal aging. Moreover, vascular lesions are seen more often, particularly lacunar infarcts. The association between T2DM and white matter hyperintensities and microbleeds is less clear. T2DM has been related to diminished cerebral blood flow and cerebrovascular reactivity, particularly in more advanced disease. Diffusion tensor imaging is a promising technique with respect to subtle white matter involvement. Thus, brain imaging studies show that T2DM is associated with both degenerative and vascular brain damage, which develops slowly over the course of many years. The challenge for future studies will be to further unravel the etiology of brain damage in T2DM, and to identify subgroups of patients that will develop distinct progressive brain damage and cognitive decline.

  9. MRI of fetal acquired brain lesions

    Energy Technology Data Exchange (ETDEWEB)

    Prayer, Daniela [Department of Radiodiagnostics, Medical University of Vienna (Austria)]. E-mail: daniela.prayer@meduniwien.ac.at; Brugger, Peter C. [Center of Anatomy and Cell Biology, Medical University of Vienna (Austria); Kasprian, Gregor [Department of Radiodiagnostics, Medical University of Vienna (Austria); Witzani, Linde [Department of Radiodiagnostics, Medical University of Vienna (Austria); Helmer, Hanns [Department of Obstetrics and Gynecology, Medical University of Vienna (Austria); Dietrich, Wolfgang [Department of Neurosurgery, Medical University of Vienna (Austria); Eppel, Wolfgang [Department of Obstetrics and Gynecology, Medical University of Vienna (Austria); Langer, Martin [Department of Obstetrics and Gynecology, Medical University of Vienna (Austria)

    2006-02-15

    Acquired fetal brain damage is suspected in cases of destruction of previously normally formed tissue, the primary cause of which is hypoxia. Fetal brain damage may occur as a consequence of acute or chronic maternal diseases, with acute diseases causing impairment of oxygen delivery to the fetal brain, and chronic diseases interfering with normal, placental development. Infections, metabolic diseases, feto-fetal transfusion syndrome, toxic agents, mechanical traumatic events, iatrogenic accidents, and space-occupying lesions may also qualify as pathologic conditions that initiate intrauterine brain damage. MR manifestations of acute fetal brain injury (such as hemorrhage or acute ischemic lesions) can easily be recognized, as they are hardly different from postnatal lesions. The availability of diffusion-weighted sequences enhances the sensitivity in recognizing acute ischemic lesions. Recent hemorrhages are usually readily depicted on T2 (*) sequences, where they display hypointense signals. Chronic fetal brain injury may be characterized by nonspecific changes that must be attributable to the presence of an acquired cerebral pathology. The workup in suspected acquired fetal brain injury also includes the assessment of extra-CNS organs that may be affected by an underlying pathology. Finally, the placenta, as the organ that mediates oxygen delivery from the maternal circulation to the fetus, must be examined on MR images.

  10. MRI of fetal acquired brain lesions

    International Nuclear Information System (INIS)

    Acquired fetal brain damage is suspected in cases of destruction of previously normally formed tissue, the primary cause of which is hypoxia. Fetal brain damage may occur as a consequence of acute or chronic maternal diseases, with acute diseases causing impairment of oxygen delivery to the fetal brain, and chronic diseases interfering with normal, placental development. Infections, metabolic diseases, feto-fetal transfusion syndrome, toxic agents, mechanical traumatic events, iatrogenic accidents, and space-occupying lesions may also qualify as pathologic conditions that initiate intrauterine brain damage. MR manifestations of acute fetal brain injury (such as hemorrhage or acute ischemic lesions) can easily be recognized, as they are hardly different from postnatal lesions. The availability of diffusion-weighted sequences enhances the sensitivity in recognizing acute ischemic lesions. Recent hemorrhages are usually readily depicted on T2 (*) sequences, where they display hypointense signals. Chronic fetal brain injury may be characterized by nonspecific changes that must be attributable to the presence of an acquired cerebral pathology. The workup in suspected acquired fetal brain injury also includes the assessment of extra-CNS organs that may be affected by an underlying pathology. Finally, the placenta, as the organ that mediates oxygen delivery from the maternal circulation to the fetus, must be examined on MR images

  11. Brain Basics

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    Full Text Available ... related to changes in the anatomy, physiology, and chemistry of the nervous system. When the brain cannot ... who can diagnose mental disorders are psychologists or clinical social workers. The psychiatrist asked Sarah and her ...

  12. Brain Basics

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    Full Text Available ... begun to chart how the brain develops over time in healthy people and are working to compare ... listless, and had no appetite most of the time. Weeks later, Sarah realized she was having trouble ...

  13. Brain Basics

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    Full Text Available ... as in areas of the brain that control movement. When electrical signals are abnormal, they can cause ... normal mood functioning. Dopamine —mainly involved in controlling movement and aiding the flow of information to the ...

  14. Brain Basics

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    Full Text Available ... Statistics Help for Mental Illnesses Outreach Outreach Home Public Involvement Outreach Partners Alliance for Research Progress Coalition ... also linked to reward systems in the brain. Problems in producing dopamine can result in Parkinson's disease, ...

  15. Brain Basics

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    Full Text Available ... related to changes in the anatomy, physiology, and chemistry of the nervous system. When the brain cannot ... husband questions about Sarah's symptoms and family medical history. Epigenetic changes from stress or early-life experiences ...

  16. Brain Basics

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    Full Text Available ... at the front of the brain that, in humans, plays a role in executive functions such as ... to another. Share Science News Connectome Re-Maps Human Cortex ECT Lifts Depression, Sustains Remission in Older ...

  17. Brain Basics

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    Full Text Available ... treatments, and possibly prevention of such illnesses. The Working Brain Neurotransmitters Everything we do relies on neurons ... depression, can occur when this process does not work correctly. Communication between neurons can also be electrical, ...

  18. Brain Basics

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    Full Text Available ... in controlling movement, managing the release of various hormones, and aiding the flow of information to the ... at the front of the brain that, in humans, plays a role in executive functions such as ...

  19. Brain Basics

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    Full Text Available ... the understanding of how the brain grows and works and the effects of genes and environment on mental health. This knowledge is allowing scientists to make important discoveries that ...

  20. Brain Basics

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    Full Text Available ... may help improve treatments for anxiety disorders like phobias or post-traumatic stress disorder (PTSD) . Prefrontal cortex ( ... doctor, who ran some tests. After deciding her symptoms were not caused by a stroke, brain tumor, ...

  1. Brain Basics

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    Full Text Available ... related to changes in the anatomy, physiology, and chemistry of the nervous system. When the brain cannot ... NIMH Strategic Plan in 2016 August 31, 2016, 2:00-3:00 PM ET General Health Information ...

  2. Brain Basics

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    Full Text Available ... sends impulses and extends from cell bodies to meet and deliver impulses to another nerve cell. Axons ... in Real Life—How Depression affects the Brain Meet Sarah Sarah is a middle-aged woman who ...

  3. Brain Basics

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    Full Text Available ... Director’s Blog Budget Strategic Plan Offices and Divisions Careers@NIMH Advisory Boards and Groups Staff Directories Getting ... works in healthy people, and how normal brain development and function can go awry, leading to mental ...

  4. Brain Basics

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    Full Text Available ... little dopamine or problems using dopamine in the thinking and feeling regions of the brain may play ... but can still remember past events and learned skills, and carry on a conversation, all which rely ...

  5. Brain Basics

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    Full Text Available ... and plays an important role during early brain development. It may also assist in learning and memory. ... but can still remember past events and learned skills, and carry on a conversation, all which rely ...

  6. Brain Basics

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    Full Text Available ... These factors may act alone or together in complex ways, to change the way a gene is ... little dopamine or problems using dopamine in the thinking and feeling regions of the brain may play ...

  7. Brain Basics

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    Full Text Available ... the brain, which is linked to thought and emotion. It is also linked to reward systems in ... or-flight response and is also involved in emotions and memory. anterior cingulate cortex —Is involved in ...

  8. Brain Basics

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    Full Text Available ... or serious and cause severe disability. Through research, we know that mental disorders are brain disorders. Evidence ... many different types of cells in the body. We say that cells differentiate as the embryo develops, ...

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  10. Brain Health

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  20. 急性脑损伤致心肌损害的内源性NE及心肌β_1-AR变化%Endogenetic NE and Myocardial β_1-AR in the myocardial damage after acute brain injury

    Institute of Scientific and Technical Information of China (English)

    郭彩霞; 张立克; 王红霞; 芦玲巧; 杜凤和

    2010-01-01

    目的 探讨急性脑损伤(acute brain injury,ABI)致心肌损害的内源性去甲肾上腺素(noradrenaline,NE)和β_1肾上腺素受体(adrenalin β_1 receptor,β_1-AR)变化,为了解ABI致心肌损害的发生机制提供理论依据.方法 采用动物模型观察肌酸磷酸激酶同工酶(MB isoenzyme of creatine kinase,CK-MB)含量判断心肌损害与否及损伤程度,采用高效液相色谱-电化学检测(high performance liquid chromatogramphy-electrical conductivity detector,HPLC-ECD)测定血浆及心肌组织NE水平,观察1、6、24和48 h时间点的变化.采用反转录多聚酶链反应(reverse transcriptase polymerase chain reaction,RT-PCR)和实时定量反转录多聚酶链反应(real-time RT-PCR,rt-RT-PCR)测定β_1-AR mRNA表达.实验分为正常组、假手术组、ABI组和β_1肾上腺素受体阻断剂(adrenalin β_1 receptor blocker,β_1-ARB)组.结果 ABI致心肌损害表现为CK-MB含量显著增加(P<0.05),脑损伤后24 h心肌损害最严重.血浆和心肌组织NE水平显著升高(P<0.05),血浆NE水平与CK-MB含量呈正相关(P<0.05).ABI及预先应用β_1-AR阻断剂后心肌组织β_1-AR mRNA表达与对照组相比差异无统计学意义.结论 ABI可导致心肌损害的发生,可增加内源性NE,NE可能是参与急性脑损伤后心肌损害的机制之一.