Formation of plasma induced surface damage in silica glass etching for optical waveguides

International Nuclear Information System (INIS)

Choi, D.Y.; Lee, J.H.; Kim, D.S.; Jung, S.T.

2004-01-01

Ge, B, P-doped silica glass films are widely used as optical waveguides because of their low losses and inherent compatibility with silica optical fibers. These films were etched by ICP (inductively coupled plasma) with chrome etch masks, which were patterned by reactive ion etching (RIE) using chlorine-based gases. In some cases, the etched surfaces of silica glass were very rough (root-mean square roughness greater than 100 nm) and we call this phenomenon plasma induced surface damage (PISD). Rough surface cannot be used as a platform for hybrid integration because of difficulty in alignment and bonding of active devices. PISD reduces the etch rate of glass and it is very difficult to remove residues on a rough surface. The objective of this study is to elucidate the mechanism of PISD formation. To achieve this goal, PISD formation during different etching conditions of chrome etch mask and silica glass was investigated. In most cases, PISD sources are formed on a glass surface after chrome etching, and metal compounds are identified in theses sources. Water rinse after chrome etching reduces the PISD, due to the water solubility of metal chlorides. PISD is decreased or even disappeared at high power and/or low pressure in glass etching, even if PISD sources were present on the glass surface before etching. In conclusion, PISD sources come from the chrome etching process, and polymer deposition on these sources during the silica etching cause the PISD sources to grow. In the area close to the PISD source there is a higher ion flux, which causes an increase in the etch rate, and results in the formation of a pit

Investigation of cutting-induced damage in CMC bend bars

Directory of Open Access Journals (Sweden)

Neubrand A.

2015-01-01

Full Text Available Ceramic matrix composites (“CMC” with a strong fibre-matrix interface can be made damage-tolerant by introducing a highly porous matrix. Such composites typically have only a low interlaminar shear strength, which can potentially promote damage when preparing specimens or components by cutting. In order to investigate the damage induced by different cutting methods, waterjet cutting with and without abrasives, laser-cutting, wire eroding and cutoff grinding were used to cut plates of two different CMCs with a matrix porosity up to 35 vol.-%. For each combination of cutting method and composite, the flexural and interlaminar shear strength of the resulting specimens was determined. Additionally, the integrity of the regions near the cut surfaces was investigated by high-resolution x-ray computer tomography. It could be shown that the geometrical quality of the cut is strongly affected by the cutting method employed. Laser cut and waterjet cut specimens showed damage and delaminations near the cut surface leading to a reduced interlaminar shear strength of short bend bars in extreme cases.

CEREBRAL CORTEX DAMAGE INDUCED BY ACUTE ORAL ...

African Journals Online (AJOL)

2018-02-28

Feb 28, 2018 ... This study examines alcohol-induced cerebral cortex damage and the association with oxidative ... alcohol has profound effects on the function ... Chronic use of ..... Alcohol induced brain damage and liver damage in young.

Increasing the laser-induced damage threshold of single-crystal ZnGeP{sub 2}

Energy Technology Data Exchange (ETDEWEB)

Zawilski, Kevin T; Setzler, Scott D; Schunemann, Peter G; Pollak, Thomas M [BAE Systems, Advanced Systems and Technology, P.O. Box 868, MER15-1813, Nashua, New Hampshire 03061-0868 (United States)

2006-11-15

The laser-induced damage threshold (LIDT) of single-crystal zinc germanium phosphide (ZGP), ZnGeP{sub 2}, was increased to 2 J/cm{sup 2} at 2.05 {mu}m and a 10 kHz pulse rate frequency (double the previously measured value of 1 J/cm{sup 2}). This increased LIDT was achieved by improving the polishing of ZGP optical parametric oscillator crystals. Two different polishing techniques were evaluated. Surfaces were characterized using scanning white-light interferometry to determine rms surface roughness and sample flatness. The photon backscatter technique was used to determine the degree of surface and subsurface damage in the sample induced through the fabrication process. The effect of subsurface damage in the samples was studied by removing different amounts of material during polishing for otherwise identical samples. Statistical LIDT was measured using a high-average-power, repetitively Q-switched Tm,Ho:YLF 2.05 {mu}m pump laser. On average, lower surface roughness and photon backscatter measurements were a good indicator of ZGP samples exhibiting higher LIDT. The removal of more material during polishing significantly improved the LIDT of otherwise identical samples, indicating the importance of subsurface damage defects in the LIDT of ZGP.

Laser-induced damage of fused silica at 355 and 1065 nm initiated at aluminum contamination particles on the surface

International Nuclear Information System (INIS)

Genin, F.Y.; Michlitsch, K.; Furr, J.; Kozlowski, M.R.; Krulevitch, P.

1997-01-01

1-μm thick circular dots, 10-250 μm dia, were deposited onto 1.14 cm thick fused silica windows by sputtering Al through a mask. Al shavings were also deposited on the windows to investigate effects of particle-substrate adhesion. The silica windows were then illuminated repetitively using a 3-ns, 355 nm and an 8.6-ns, 1064 nm laser. The tests were conducted at near normal incidence with particles on input and output surfaces of the windows. During the first shot, a plasma ignited at the metal particle and damage initiated on the fused silica surface. The morphology of the damage at the metal dots were reproducible but different for input and output surface contamination. For input surface contamination, minor damage occurred where the particle was located; such damage ceased to grow with the removal of contaminant material. More serious damage (pits and cracks) was initiated on the output surface (especially at 355 nm) and grew to catastrophic proportions after few shots. Output surface contaminants were usually ejected on the initial shot, leaving a wave pattern on the surface. No further damage occurred with subsequent shots unless a shot (usually the first shot) cracked the surface; such behavior was mostly observed at 355 nm and occasionally for large shavings at 1064 nm. The size of the damaged area scaled with the size of the particle (except when catastrophic damage occurred). Onset of catastrophic damage on output surface occurred only when particles exceeded a critical size. Damage behavior of the sputtered dots was found to be qualitatively similar to that of the shavings. The artificial contamination technique accelerated the study by allowing better control of the test conditions

Multiple pulse nanosecond laser induced damage threshold on hybrid mirrors

Science.gov (United States)

Vanda, Jan; Muresan, Mihai-George; Bilek, Vojtech; Sebek, Matej; Hanus, Martin; Lucianetti, Antonio; Rostohar, Danijela; Mocek, Tomas; Škoda, Václav

2017-11-01

So-called hybrid mirrors, consisting of broadband metallic surface coated with dielectric reflector designed for specific wavelength, becoming more important with progressing development of broadband mid-IR sources realized using parametric down conversion system. Multiple pulse nanosecond laser induced damage on such mirrors was tested by method s-on-1, where s stands for various numbers of pulses. We show difference in damage threshold between common protected silver mirrors and hybrid silver mirrors prepared by PVD technique and their variants prepared by IAD. Keywords: LIDT,

Laser-Induced Damage Growth on Larger-Aperture Fused Silica Optical Components at 351 nm

International Nuclear Information System (INIS)

Wan-Qing, Huang; Wei, Han; Fang, Wang; Yong, Xiang; Fu-Quan, Li; Bin, Feng; Feng, Jing; Xiao-Feng, Wei; Wan-Guo, Zheng; Xiao-Min, Zhang

2009-01-01

Laser-induced damage is a key lifetime limiter for optics in high-power laser facility. Damage initiation and growth under 351 nm high-fluence laser irradiation are observed on larger-aperture fused silica optics. The input surface of one fused silica component is damaged most severely and an explanation is presented. Obscurations and the area of a scratch on it are found to grow exponentially with the shot number. The area of damage site grows linearly. Micrographs of damage sites support the micro-explosion damage model which could be used to qualitatively explain the phenomena

Cellular Responses to Cisplatin-Induced DNA Damage

Directory of Open Access Journals (Sweden)

Alakananda Basu

2010-01-01

Full Text Available Cisplatin is one of the most effective anticancer agents widely used in the treatment of solid tumors. It is generally considered as a cytotoxic drug which kills cancer cells by damaging DNA and inhibiting DNA synthesis. How cells respond to cisplatin-induced DNA damage plays a critical role in deciding cisplatin sensitivity. Cisplatin-induced DNA damage activates various signaling pathways to prevent or promote cell death. This paper summarizes our current understandings regarding the mechanisms by which cisplatin induces cell death and the bases of cisplatin resistance. We have discussed various steps, including the entry of cisplatin inside cells, DNA repair, drug detoxification, DNA damage response, and regulation of cisplatin-induced apoptosis by protein kinases. An understanding of how various signaling pathways regulate cisplatin-induced cell death should aid in the development of more effective therapeutic strategies for the treatment of cancer.

Pion-induced damage in silicon detectors

CERN Document Server

Bates, S; Glaser, M; Lemeilleur, F; León-Florián, E; Gössling, C; Kaiser, B; Rolf, A; Wunstorf, R; Feick, H; Fretwurst, E; Lindström, G; Moll, Michael; Taylor, G; Chilingarov, A G

1995-01-01

The damage induced by pions in silicon detectors is studied for positive and negative pions for fluence up to 10(14)cm-2 and 10(13) cm-2 respectively. Results on the energy dependence of the damage in the region of 65-330 MeV near to the  resonance are presented. The change in detector characteristics such as leakage current, charge collection efficiency and effective impurity concentration including long-term annealing effects have been studied. Comparisons to neutron and proton-induced damage are presented and discussed.

Study of laser-induced damage on the exit surface of silica components in the nanosecond regime in a multiple wavelengths configuration

International Nuclear Information System (INIS)

Chambonneau, Maxime

2014-01-01

In this thesis, laser-induced damage phenomenon on the surface of fused silica components is investigated in the nanosecond regime. This phenomenon consists in an irreversible modification of the material. In the nanosecond regime, laser damage is tightly correlated to the presence of non-detectable precursor defects which are a consequence of the synthesis and the polishing of the components. In this thesis, we investigate laser damage in a multiple wavelengths configuration. In order to better understand this phenomenon in these conditions of irradiation, three studies are conducted. The first one focuses on damage initiation. The results obtained in the single wavelength configurations highlight a coupling in the multiple wavelengths one. A comparison between the experiments and a model developed during this thesis enables us to improve the knowledge of the fundamental processes involved during this damage phase. Then, we show that post mortem characterizations of damage morphology coupled to an accurate metrology allow us to understand both the nature and also the chronology of the physical mechanisms involved during damage formation. The proposed theoretical scenario is confirmed through various experiments. Finally, we study damage growth in both the single and the multiple wavelengths cases. Once again, this last configuration highlights a coupling between the wavelengths. We show the necessity to account for the spatial characteristics of the laser beams during a growth session. (author) [fr

Quantification of stress-induced damage and post-fire response of 5083 aluminum alloy

International Nuclear Information System (INIS)

Chen, Y.; Puplampu, S.B.; Summers, P.T.; Lattimer, B.Y.; Penumadu, D.; Case, S.W.

2015-01-01

One of the major concerns regarding the use of lightweight materials in ship construction is the response of those materials to fire scenarios, including the residual structural performance after a fire event. This paper presents a study on creep damage evolution in 5083 marine-grade aluminum alloy and its impact on residual mechanical behavior. Tests conducted at 400 °C and pre-selected tensile stress levels were interrupted at target amplitudes of accumulated engineering creep strains to investigate the stress-induced damage using ex-situ characterization. Two-dimensional optical and electron microscopy and three-dimensional X-ray tomography were utilized on samples extracted from these test specimens to characterize the external and internal creep damage. The stress-induced damage is primarily manifested as cavitation and dynamic microstructural evolution. Cavitation morphology, orientation and grain structure evolution were investigated on three perpendicular sample surfaces. A 3D examination of the damage state provided consistent damage information to that obtained from the 2D analysis. The post-fire mechanical properties were also evaluated and linked to the microstructural change. The competing processes of cavitation and grain structure evolution were investigated to develop an understanding of the stress-induced damage associated with high temperature creep

Quantification of stress-induced damage and post-fire response of 5083 aluminum alloy

Energy Technology Data Exchange (ETDEWEB)

Chen, Y., E-mail: yanyun@vt.edu [Department of Engineering Science & Mechanics, Virginia Tech, Blacksburg, VA 24061 (United States); Puplampu, S.B. [Department of Civil and Environmental Engineering, University of Tennessee, Knoxville, TN 37996 (United States); Summers, P.T.; Lattimer, B.Y. [Department of Mechanical Engineering, Virginia Tech, Blacksburg, VA 24061 (United States); Penumadu, D. [Department of Civil and Environmental Engineering, University of Tennessee, Knoxville, TN 37996 (United States); Case, S.W. [Department of Engineering Science & Mechanics, Virginia Tech, Blacksburg, VA 24061 (United States)

2015-08-12

One of the major concerns regarding the use of lightweight materials in ship construction is the response of those materials to fire scenarios, including the residual structural performance after a fire event. This paper presents a study on creep damage evolution in 5083 marine-grade aluminum alloy and its impact on residual mechanical behavior. Tests conducted at 400 °C and pre-selected tensile stress levels were interrupted at target amplitudes of accumulated engineering creep strains to investigate the stress-induced damage using ex-situ characterization. Two-dimensional optical and electron microscopy and three-dimensional X-ray tomography were utilized on samples extracted from these test specimens to characterize the external and internal creep damage. The stress-induced damage is primarily manifested as cavitation and dynamic microstructural evolution. Cavitation morphology, orientation and grain structure evolution were investigated on three perpendicular sample surfaces. A 3D examination of the damage state provided consistent damage information to that obtained from the 2D analysis. The post-fire mechanical properties were also evaluated and linked to the microstructural change. The competing processes of cavitation and grain structure evolution were investigated to develop an understanding of the stress-induced damage associated with high temperature creep.

Flat Surface Damage Detection System (FSDDS)

Science.gov (United States)

Williams, Martha; Lewis, Mark; Gibson, Tracy; Lane, John; Medelius, Pedro; Snyder, Sarah; Ciarlariello, Dan; Parks, Steve; Carrejo, Danny; Rojdev, Kristina

2013-01-01

The Flat Surface Damage Detection system (FSDDS} is a sensory system that is capable of detecting impact damages to surfaces utilizing a novel sensor system. This system will provide the ability to monitor the integrity of an inflatable habitat during in situ system health monitoring. The system consists of three main custom designed subsystems: the multi-layer sensing panel, the embedded monitoring system, and the graphical user interface (GUI). The GUI LABVIEW software uses a custom developed damage detection algorithm to determine the damage location based on the sequence of broken sensing lines. It estimates the damage size, the maximum depth, and plots the damage location on a graph. Successfully demonstrated as a stand alone technology during 2011 D-RATS. Software modification also allowed for communication with HDU avionics crew display which was demonstrated remotely (KSC to JSC} during 2012 integration testing. Integrated FSDDS system and stand alone multi-panel systems were demonstrated remotely and at JSC, Mission Operations Test using Space Network Research Federation (SNRF} network in 2012. FY13, FSDDS multi-panel integration with JSC and SNRF network Technology can allow for integration with other complementary damage detection systems.

Surface Damage and Treatment by Impact of a Low Temperature Nitrogen Jet

Science.gov (United States)

Laribou, Hicham; Fressengeas, Claude; Entemeyer, Denis; Jeanclaude, Véronique; Tazibt, Abdel

2011-01-01

Nitrogen jets under high pressure and low temperature have been introduced recently. The process consists in projecting onto a surface a low temperature jet obtained from releasing the liquid nitrogen stored in a high pressure tank (e.g. 3000 bars) through a nozzle. It can be used in a range of industrial applications, including surface treatment or material removal through cutting, drilling, striping and cleaning. The process does not generate waste other than the removed matter, and it only releases neutral gas into the atmosphere. This work is aimed at understanding the mechanisms of the interaction between the jet and the material surface. Depending on the impacted material, the thermo-mechanical shock and blast effect induced by the jet can activate a wide range of damage mechanisms, including cleavage, crack nucleation and spalling, as well as void expansion and localized ductile failure. The test parameters (standoff distance, dwell time, operating pressure) play a role in selecting the dominant damage mechanism, but combinations of these various modes are usually present. Surface treatment through phase transformation or grain fragmentation in a layer below the surface can also be obtained by adequate tuning of the process parameters. In the current study, work is undertaken to map the damage mechanisms in metallic materials as well as the influence of the test parameters on damage, along with measurements of the thermo-mechanical conditions (impact force, temperature) in the impacted area.

Impact of environmental contamination on laser induced damage of silica optics in Laser MegaJoule

International Nuclear Information System (INIS)

Bien-Aime, K.

2009-11-01

Laser induced damage impact of molecular contamination on fused polished silica samples in a context of high power laser fusion facility, such as Laser MegaJoule (LMJ) has been studied. One of the possible causes of laser induced degradation of optical component is the adsorption of molecular or particular contamination on optical surfaces. In the peculiar case of LMJ, laser irradiation conditions are a fluence of 10 J/cm 2 , a wavelength of 351 nm, a pulse duration of 3 ns for a single shot/days frequency. Critical compounds have been identified thanks to environmental measurements, analysis of material outgassing, and identification of surface contamination in the critical environments. Experiments of controlled contamination involving these compounds have been conducted in order to understand and model mechanisms of laser damage. Various hypotheses are proposed to explain the damage mechanism. (author)

Laser-based structural sensing and surface damage detection

Science.gov (United States)

Guldur, Burcu

this research is to combine useful information extracted from laser scanner data with color information, which provides information in the fourth dimension that enables detection of damage types such as cracks, corrosion, and related surface defects that are generally difficult to detect using only laser scanner data; moreover, the color information also helps to track volumetric changes on structures such as spalling. Although using images with varying resolution to detect cracks is an extensively researched topic, damage detection using laser scanners with and without color images is a new research area that holds many opportunities for enhancing the current practice of visual inspections. The aim is to combine the best features of laser scans and images to create an automatic and effective surface damage detection method, which will reduce the need for skilled labor during visual inspections and allow automatic documentation of related information. This work enables developing surface damage detection strategies that integrate existing condition rating criteria for a wide range damage types that are collected under three main categories: small deformations already existing on the structure (cracks); damage types that induce larger deformations, but where the initial topology of the structure has not changed appreciably (e.g., bent members); and large deformations where localized changes in the topology of the structure have occurred (e.g., rupture, discontinuities and spalling). The effectiveness of the developed damage detection algorithms are validated by comparing the detection results with the measurements taken from test specimens and test-bed bridges.

Transient thermal driven bubble's surface and its potential ultrasound-induced damage

Science.gov (United States)

Movahed, Pooya; Freund, Jonathan B.

2017-11-01

Ultrasound-induced bubble activity in soft tissues is well-known to be a potential injury mechanism in therapeutic ultrasound treatments. We consider damage by transient thermal effects, including a hypothetical mechanism based on transient thermal phenomena, including viscous dissipation. A spherically symmetric compressible Navier-Stokes discretization is developed to solve the full governing equations, both inside and outside of the bubble, without the usual simplifications in the Rayleigh-Plesset bubble dynamics approach. Equations are solved in the Lagrangian framework, which provides a sharp and accurate representation of the interface as well as the viscous dissipation and thermal transport effects, which preclude reduction to the usual Rayleigh-Plesset ordinary differential equation. This method is used to study transient thermal effects at different frequencies and pressure amplitudes relevant to therapeutic ultrasound treatments. High temperatures achieved in the surrounding medium during the violent bubble collapse phase due to the viscous dissipation in the surrounding medium and thermal conduction from the bubble are expected to cause damage. This work was supported by NIH NIDDK Grant P01-DK043881.

A New Experimental Approach to Evaluate Plasma-induced Damage in Microcantilever

Directory of Open Access Journals (Sweden)

Yuki Nishimori

2013-09-01

Full Text Available Plasma  etching,  during  micro-fabrication  processing  is  indispensable  for  fabricating  MEMS  structures.  During  the plasma  processes,  two  major matters,  charged  ions  and  vacuum–ultraviolet  (VUV  irradiation  damage,  take  charge  of reliability  degradation.  The  charged  ions  induce  unwanted  sidewall  etching,  generally  called  as  “notching”,  which causes  degradation  in  brittle  strength.  Furthermore,  the  VUV  irradiation  gives  rise  to  crystal  defects  on  the  etching surface.  To overcome  the  problem,  neutral  beam  etching  (NBE,  which  use  neutral  particles  without  the  VUV irradiation,  has  been  developed.  In  order  to  evaluate  the  effect  of  the  NBE  quantitatively,  we  measured  the  resonance property of a micro-cantilever before and after NBE treatment. The thickness of damage layer (δ times the imaginary part  of  the  complex Young's  modulus  (Eds  were  then  compared,  which  is  a  parameter  of  surface  damage.  Although plasma processes  make the initial surface of cantilevers damaged during their fabrication, the removal of that damage by NBE was confirmed as the reduction in δEds. NBE will realize a damage-free surface for microstructures.

Mitigation technologies for damage induced by pressure waves in high-power mercury spallation neutron sources (1). Material surface improvement

International Nuclear Information System (INIS)

Naoe, Takashi; Futakawa, Masatoshi; Wakui, Takashi; Kogawa, Hiroyuki; Shoubu, Takahisa; Takeuchi, Hirotsugu; Kawai, Masayoshi

2008-01-01

Liquid-mercury target systems for MW-class spallation neutron sources are being developed in the world. Proton beams will be used to induce the spallation reaction. At the moment the proton beam hits the target, pressure waves are generated in the mercury because of the abrupt heat deposition. The pressure waves interact with the target vessel leading to negative pressure that may cause cavitation along the vessel wall. Localized impacts by microjets and/or shock waves that are caused by cavitation bubble collapse impose pitting damage on the vessel wall. Bubble collapse behavior was observed by using a high-speed video camera, as well as simulated numerically. Localized impact due to cavitation bubble collapse was quantitatively estimated through comparison between numerical simulation and experiment. A novel surface treatment technique that consists of carburizing and nitriding processes was developed and the treatment condition was optimized to mitigate the pitting damage due to localized impacts. (author)

Electron backscatter diffraction characterization of laser-induced periodic surface structures on nickel surface

Energy Technology Data Exchange (ETDEWEB)

Sedao, Xxx, E-mail: sedao.xxx@gmail.com [Laboratoire Hubert Curien, Université Jean Monnet, 42000 St-Etienne (France); Maurice, Claire [Laboratoire Georges Friedel, Ecole Nationale Supérieure des Mines, 42023 St-Etienne (France); Garrelie, Florence; Colombier, Jean-Philippe; Reynaud, Stéphanie [Laboratoire Hubert Curien, Université Jean Monnet, 42000 St-Etienne (France); Quey, Romain; Blanc, Gilles [Laboratoire Georges Friedel, Ecole Nationale Supérieure des Mines, 42023 St-Etienne (France); Pigeon, Florent [Laboratoire Hubert Curien, Université Jean Monnet, 42000 St-Etienne (France)

2014-05-01

Graphical abstract: -- Highlight: •Lattice rotation and its distribution in laser-induced periodic surface structures (LIPSS) and the subsurface region on a nickel substrate are revealed using electron backscatter diffraction (EBSD). -- Abstract: We report on the structural investigation of laser-induced periodic surface structures (LIPSS) generated in polycrystalline nickel target after multi-shot irradiation by femtosecond laser pulses. Electron backscatter diffraction (EBSD) is used to reveal lattice rotation caused by dislocation storage during LIPSS formation. Localized crystallographic damages in the LIPSS are detected from both surface and cross-sectional EBSD studies. A surface region (up to 200 nm) with 1–3° grain disorientation is observed in localized areas from the cross-section of the LIPSS. The distribution of the local disorientation is inhomogeneous across the LIPSS and the subsurface region.

Reactive ion beam etching for microcavity surface emitting laser fabrication: technology and damage characterization

International Nuclear Information System (INIS)

Matsutani, A.; Tadokoro, T.; Koyama, F.; Iga, K.

1993-01-01

Reactive ion beam etching (RIBE) is an effective dry etching technique for the fabrication of micro-sized surface emitting (SE) lasers and optoelectronic devices. In this chapter, some etching characteristics for GaAs, InP and GaInAsP with a Cl 2 gas using an RIBE system are discussed. Micro-sized circular mesas including GaInAsP/InP multilayers with vertical sidewalls were fabricated. RIBE-induced damage in InP substrates was estimated by C-V and PL measurement. In addition, the removal of the induced damage by the second RIBE with different conditions for the InP wafer was proposed. The sidewall damage is characterized by photoluminescence emitted from the etched sidewall of a GaInAsP/InP DH wafer. (orig.)

Quercitrin protects skin from UVB-induced oxidative damage

Energy Technology Data Exchange (ETDEWEB)

Yin, Yuanqin [Cancer Institute, The First Affiliated Hospital, China Medical University, Shenyang (China); Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Li, Wenqi; Son, Young-Ok; Sun, Lijuan; Lu, Jian; Kim, Donghern; Wang, Xin [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Yao, Hua [Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang (China); Wang, Lei; Pratheeshkumar, Poyil; Hitron, Andrew J. [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Luo, Jia [Department of Internal Medicine, University of Kentucky, 800 Rose Street, Lexington, KY (United States); Gao, Ning [Department of Pharmacognos, College of Pharmacy, 3rd Military Medical University, Chongqing (China); Shi, Xianglin [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Zhang, Zhuo, E-mail: zhuo.zhang@uky.edu [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States)

2013-06-01

Exposure of the skin to ultraviolet B (UVB) radiation causes oxidative damage to skin, resulting in sunburn, photoaging, and skin cancer. It is generally believed that the skin damage induced by UV irradiation is a consequence of generation of reactive oxygen species (ROS). Recently, there is an increased interest in the use of natural products as chemopreventive agents for non-melanoma skin cancer (NMSC) due to their antioxidants and anti-inflammatory properties. Quercitrin, glycosylated form of quercetin, is the most common flavonoid in nature with antioxidant properties. The present study investigated the possible beneficial effects of quercitrin to inhibit UVB irradiation-induced oxidative damage in vitro and in vivo. Our results showed that quercitrin decreased ROS generation induced by UVB irradiation in JB6 cells. Quercitrin restored catalase expression and GSH/GSSG ratio reduced by UVB exposure, two major antioxidant enzymes, leading to reductions of oxidative DNA damage and apoptosis and protection of the skin from inflammation caused by UVB exposure. The present study demonstrated that quercitrin functions as an antioxidant against UVB irradiation-induced oxidative damage to skin. - Highlights: • Oxidative stress plays a key role in UV-induced cell and tissue injuries. • Quercitrin decreases ROS generation and restores antioxidants irradiated by UVB. • Quercitrin reduces UVB-irradiated oxidative DNA damage, apoptosis, and inflammation. • Quercitrin functions as an antioxidant against UVB-induced skin injuries.

Quercitrin protects skin from UVB-induced oxidative damage

International Nuclear Information System (INIS)

Yin, Yuanqin; Li, Wenqi; Son, Young-Ok; Sun, Lijuan; Lu, Jian; Kim, Donghern; Wang, Xin; Yao, Hua; Wang, Lei; Pratheeshkumar, Poyil; Hitron, Andrew J.; Luo, Jia; Gao, Ning; Shi, Xianglin; Zhang, Zhuo

2013-01-01

Exposure of the skin to ultraviolet B (UVB) radiation causes oxidative damage to skin, resulting in sunburn, photoaging, and skin cancer. It is generally believed that the skin damage induced by UV irradiation is a consequence of generation of reactive oxygen species (ROS). Recently, there is an increased interest in the use of natural products as chemopreventive agents for non-melanoma skin cancer (NMSC) due to their antioxidants and anti-inflammatory properties. Quercitrin, glycosylated form of quercetin, is the most common flavonoid in nature with antioxidant properties. The present study investigated the possible beneficial effects of quercitrin to inhibit UVB irradiation-induced oxidative damage in vitro and in vivo. Our results showed that quercitrin decreased ROS generation induced by UVB irradiation in JB6 cells. Quercitrin restored catalase expression and GSH/GSSG ratio reduced by UVB exposure, two major antioxidant enzymes, leading to reductions of oxidative DNA damage and apoptosis and protection of the skin from inflammation caused by UVB exposure. The present study demonstrated that quercitrin functions as an antioxidant against UVB irradiation-induced oxidative damage to skin. - Highlights: • Oxidative stress plays a key role in UV-induced cell and tissue injuries. • Quercitrin decreases ROS generation and restores antioxidants irradiated by UVB. • Quercitrin reduces UVB-irradiated oxidative DNA damage, apoptosis, and inflammation. • Quercitrin functions as an antioxidant against UVB-induced skin injuries

Ion-induced surface modification of alloys

International Nuclear Information System (INIS)

Wiedersich, H.

1983-11-01

In addition to the accumulation of the implanted species, a considerable number of processes can affect the composition of an alloy in the surface region during ion bombardment. Collisions of energetic ions with atoms of the alloy induce local rearrangement of atoms by displacements, replacement sequences and by spontaneous migration and recombination of defects within cascades. Point defects form clusters, voids, dislocation loops and networks. Preferential sputtering of elements changes the composition of the surface. At temperatures sufficient for thermal migration of point defects, radiation-enhanced diffusion promotes alloy component redistribution within and beyond the damage layer. Fluxes of interstitials and vacancies toward the surface and into the interior of the target induce fluxes of alloying elements leading to depth-dependent compositional changes. Moreover, Gibbsian surface segregation may affect the preferential loss of alloy components by sputtering when the kinetics of equilibration of the surface composition becomes competitive with the sputtering rate. Temperature, time, current density and ion energy can be used to influence the individual processes contributing to compositional changes and, thus, produce a rich variety of composition profiles near surfaces. 42 references

Laser-induced damage of materials in bulk, thin-film, and liquid forms

International Nuclear Information System (INIS)

Natoli, Jean-Yves; Gallais, Laurent; Akhouayri, Hassan; Amra, Claude

2002-01-01

Accurate threshold curves of laser-induced damage (7-ns single shot at 1.064 μm) are measured in bulk and at the surfaces of optical components such as substrates, thin films, multilayers, and liquids. The shapes and the slopes of the curves are related to the spot size and to the densities of the nanodefects that are responsible for damage. First, these densities are reported for bulk substrates. In surfaces and films the recorded extrinsic and intrinsic threshold curves permit the discrimination of the effects of microdefects and nanodefects. In all cases the density of nanocenters is extracted by means of a phenomenological approach. Then we test liquids and mixtures of liquids with controlled defect densities. The results emphasize the agreement between measurement and prediction and demonstrate the validity of the presence of different kinds of nanocenter as the precursors of laser damage

Solar ultraviolet radiation-induced DNA damage in aquatic organisms: potential environmental impact

International Nuclear Information System (INIS)

Haeder, Donat-P.; Sinha, Rajeshwar P.

2005-01-01

Continuing depletion of stratospheric ozone and subsequent increases in deleterious ultraviolet (UV) radiation at the Earth's surface have fueled the interest in its ecological consequences for aquatic ecosystems. The DNA is certainly one of the key targets for UV-induced damage in a variety of aquatic organisms. UV radiation induces two of the most abundant mutagenic and cytotoxic DNA lesions, cyclobutane pyrimidine dimers (CPDs) and pyrimidine pyrimidone photoproducts (6-4PPs) and their Dewar valence isomers. However, aquatic organisms have developed a number of repair and tolerance mechanisms to counteract the damaging effects of UV on DNA. Photoreactivation with the help of the enzyme photolyase is one of the most important and frequently occurring repair mechanisms in a variety of organisms. Excision repair, which can be distinguished into base excision repair (BER) and nucleotide excision repair (NER), also play an important role in DNA repair in several organisms with the help of a number of glycosylases and polymerases, respectively. In addition, mechanisms such as mutagenic repair or dimer bypass, recombinational repair, cell-cycle checkpoints, apoptosis and certain alternative repair pathways are also operative in various organisms. This review deals with the UV-induced DNA damage and repair in a number of aquatic organisms as well as methods of detecting DNA damage

DNA damage-inducible transcripts in mammalian cells

International Nuclear Information System (INIS)

Fornace, A.J. Jr.; Alamo, I. Jr.; Hollander, M.C.

1988-01-01

Hybridization subtraction at low ratios of RNA to cDNA was used to enrich for the cDNA of transcripts increased in Chinese hamster cells after UV irradiation. Forty-nine different cDNA clones were isolated. Most coded for nonabundant transcripts rapidly induced 2- to 10-fold after UV irradiation. Only 2 of the 20 cDNA clones sequenced matched known sequences (metallothionein I and II). The predicted amino acid sequence of one cDNA had two localized areas of homology with the rat helix-destabilizing protein. These areas of homology were at the two DNA-binding sites of this nucleic acid single-strand-binding protein. The induced transcripts were separated into two general classes. Class I transcripts were induced by UV radiation and not by the alkylating agent methyl methanesulfonate. Class II transcripts were induced by UV radiation and by methyl methanesulfonate. Many class II transcripts were induced also by H2O2 and various alkylating agents but not by heat shock, phorbol 12-tetradecanoate 13-acetate, or DNA-damaging agents which do not produce high levels of base damage. Since many of the cDNA clones coded for transcripts which were induced rapidly and only by certain types of DNA-damaging agents, their induction is likely a specific response to such damage rather than a general response to cell injury

Mechanisms of subsidence for induced damage and techniques for analysis

International Nuclear Information System (INIS)

Drumm, E.C.; Bennett, R.M.; Kane, W.F.

1988-01-01

Structural damage due to mining induced subsidence is a function of the nature of the structure and its position on the subsidence profile. A point on the profile may be in the tensile zone, the compressive zone, or the no-deformation zone at the bottom of the profile. Damage to structures in the tension zone is primarily due to a reduction of support during vertical displacement of the ground surface, and to shear stresses between the soil and structure resulting from horizontal displacements. The damage mechanisms due to tension can be investigated effectively using a two-dimensional plane stress analysis. Structures in the compression zone are subjected to positive moments in the footing and large compressive horizontal stresses in the foundation walls. A plane strain analysis of the foundation wall is utilized to examine compression zone damage mechanisms. The structural aspects affecting each mechanism are identified and potential mitigation techniques are summarized

Arcing and surface damage in DITE

International Nuclear Information System (INIS)

Goodall, D.H.J.; McCracken, G.M.

1977-11-01

An investigation into the arcing damage on surfaces exposed to plasmas in the DITE tokamak is described. It has been found that arcing occurs on the fixed limiters, on probes inserted into the plasma and on parts of the torus structure. For surfaces parallel to the toroidal field most of the arcs run across the surface orthogonal to the field direction. Observations in the scanning electron microscope show that the arc tracks are formed by a series of melted craters characteristic of cathode arc spots. The amount of metal removed from the surface is consistent with the concentration of metal observed in the plasma. In plasmas with hydrogen gas puffing during the discharge or with injection of low Z impurities, the arc tracks are observed to be much shallower than in normal low density discharges. Several types of surface damage other than arc tracks have also been observed on probes. These phenomena occur less frequently than arcing and appear to be associated with abnormal discharge conditions. (author)

Surface modification of amorphous nanosilica particles suppresses nanosilica-induced cytotoxicity, ROS generation, and DNA damage in various mammalian cells

International Nuclear Information System (INIS)

Yoshida, Tokuyuki; Yoshioka, Yasuo; Matsuyama, Keigo; Nakazato, Yasutaro; Tochigi, Saeko; Hirai, Toshiro; Kondoh, Sayuri; Nagano, Kazuya; Abe, Yasuhiro; Kamada, Haruhiko; Tsunoda, Shin-ichi; Nabeshi, Hiromi; Yoshikawa, Tomoaki; Tsutsumi, Yasuo

2012-01-01

Highlights: ► There is increasing concern regarding the potential health risks of nanomaterials. ► We evaluated the effect of surface properties of nanomaterials on cellular responses. ► We showed that the surface properties play an important in determining its safety. ► These data provide useful information for producing safer nanomaterials. -- Abstract: Recently, nanomaterials have been utilized in various fields. In particular, amorphous nanosilica particles are increasingly being used in a range of applications, including cosmetics, food technology, and medical diagnostics. However, there is concern that the unique characteristics of nanomaterials might induce undesirable effects. The roles played by the physical characteristics of nanomaterials in cellular responses have not yet been elucidated precisely. Here, by using nanosilica particles (nSPs) with a diameter of 70 nm whose surface was either unmodified (nSP70) or modified with amine (nSP70-N) or carboxyl groups (nSP70-C), we examined the relationship between the surface properties of nSPs and cellular responses such as cytotoxicity, reactive oxygen species (ROS) generation, and DNA damage. To compare the cytotoxicity of nSP70, nSP70-N, or nSP70-C, we examined in vitro cell viability after nSP treatment. Although the susceptibility of each cell line to the nSPs was different, nSP70-C and nSP70-N showed lower cytotoxicity than nSP70 in all cell lines. Furthermore, the generation of ROS and induction of DNA damage in nSP70-C- and nSP70-N-treated cells were lower than those in nSP70-treated cells. These results suggest that the surface properties of nSP70 play an important role in determining its safety, and surface modification of nSP70 with amine or carboxyl groups may be useful for the development of safer nSPs. We hope that our results will contribute to the development of safer nanomaterials.

Surface damage through grazing incidence ions investigated by scanning tunneling microscopy

International Nuclear Information System (INIS)

Redinger, Alex

2009-01-01

Surface damage, caused by grazing incidence ions, is investigated with variable temperature scanning tunneling microscopy. The experiments are carried out on a Pt(111) crystal. The kinetic energy of noble gas ions is varied between 1-15 keV and the angle of incidence can be adjusted between θ = 78.5 and θ = 90 measured with respect to the surface normal. The damage patterns of single ion impacts, on flat terraces and at step edges of monoatomic height, are investigated at low surface temperatures. Ions hitting a flat terrace are usually specular reflected. The energy transfer from the ion to the crystal atoms is small and only little damage is produced. In contrast, at ascending step edges, which are illuminated by the ion beam, large angle scattering events occur. Sputtering, adatom and vacancy production is induced. However, a significant fraction of the ions, which hit step edges, enter the crystal and are guided in between two atomic layers parallel to the surface via small angle binary collisions. This steering process is denoted as subsurface channeling. The energy loss per length scale of the channeled particles is low, which results in long ion trajectories (up to 1000A). During the steering process, the ions produce surface damage. Depending on the ion species and the ion energy, adatom and vacancies or surface vacancy trenches of monoatomic width are observed. The surface damage can be used to track the path of the ion. This makes the whole trajectory of single ions with keV energy visible. The number of sputtered atoms per incident ion at ascending step edges, i.e. the step edge sputtering yield, is measured experimentally for different irradiation conditions. For θ = 86 , the sputtering yield is determined from the fluence dependent retraction of pre-existing illuminated step edges. An alternative method for the step edge sputtering yield determination, is the analysis of the concentration of ascending steps and of the removed amount of material as a

Surface damage through grazing incidence ions investigated by scanning tunneling microscopy

Energy Technology Data Exchange (ETDEWEB)

Redinger, Alex

2009-07-10

Surface damage, caused by grazing incidence ions, is investigated with variable temperature scanning tunneling microscopy. The experiments are carried out on a Pt(111) crystal. The kinetic energy of noble gas ions is varied between 1-15 keV and the angle of incidence can be adjusted between {theta} = 78.5 and {theta} = 90 measured with respect to the surface normal. The damage patterns of single ion impacts, on flat terraces and at step edges of monoatomic height, are investigated at low surface temperatures. Ions hitting a flat terrace are usually specular reflected. The energy transfer from the ion to the crystal atoms is small and only little damage is produced. In contrast, at ascending step edges, which are illuminated by the ion beam, large angle scattering events occur. Sputtering, adatom and vacancy production is induced. However, a significant fraction of the ions, which hit step edges, enter the crystal and are guided in between two atomic layers parallel to the surface via small angle binary collisions. This steering process is denoted as subsurface channeling. The energy loss per length scale of the channeled particles is low, which results in long ion trajectories (up to 1000A). During the steering process, the ions produce surface damage. Depending on the ion species and the ion energy, adatom and vacancies or surface vacancy trenches of monoatomic width are observed. The surface damage can be used to track the path of the ion. This makes the whole trajectory of single ions with keV energy visible. The number of sputtered atoms per incident ion at ascending step edges, i.e. the step edge sputtering yield, is measured experimentally for different irradiation conditions. For {theta} = 86 , the sputtering yield is determined from the fluence dependent retraction of pre-existing illuminated step edges. An alternative method for the step edge sputtering yield determination, is the analysis of the concentration of ascending steps and of the removed amount

Damage at a tungsten surface induced by impacts of self-atoms

Energy Technology Data Exchange (ETDEWEB)

Wu, Yong [Data Center for High Energy Density Physics, Institute of Applied Physics and, Computational Mathematics, P. O. Box 8009, Beijing 100088 (China); Krstic, Predrag, E-mail: predrag.krstic@stonybrook.edu [Institute for Advanced Computational Science, Stony Brook University, Stony Brook, NY 11794-5250 (United States); Zhou, Fu Yang [College of Material Sciences and Optoelectronic Technology, University of the Chinese Academy of Sciences, P. O. Box 4588, Beijing 100049 (China); Meyer, Fred [Physics Division, Oak Ridge National Laboratory, Oak Ridge, TN 37831-6372 (United States)

2015-12-15

We study evolution of the surface defects of a 300 K tungsten surface due to the cumulative impact of 0.25–10 keV self-atoms. The simulation is performed by molecular dynamics with bond-order Tersoff-form potentials. At all studied impact energies the computation shows strong defect-recombination effect of both created Frenkel pairs as well as recombination of the implanted atoms with the vacancies created by the sputtering. This leads to a saturation of the cumulative count of vacancies, evident at energies below 2 keV, as long as the implantation per impact atom exceeds sputtering and to a saturation of the interstitial count when production of the sputtered particles per impact atom becomes larger than 1 (in the energy range 2-4 keV). The number of cumulative defects is fitted as functions of impact fluence and energy, enabling their analytical extrapolation outside the studied range of parameters. - Highlights: • We calculated cumulative creation of defects in tungsten by self-atom impact. • At some energies, the defect count saturate with increasing damage dose. • The defects are accumulated in the first few layers of the tungsten surface. • The interstitials are formed predominantly as adatoms.

Bacterial Cell Surface Damage Due to Centrifugal Compaction

NARCIS (Netherlands)

Peterson, Brandon W.; Sharma, Prashant K.; van der Mei, Henny C.; Busscher, Henk J.

Centrifugal damage has been known to alter bacterial cell surface properties and interior structures, including DNA. Very few studies exist on bacterial damage caused by centrifugation because of the difficulty in relating centrifugation speed and container geometry to the damage caused. Here, we

Blood-induced joint damage: novel targets for therapy

NARCIS (Netherlands)

van Meegeren, M.E.R.

2012-01-01

-induced joint damage can occur due to a trauma but also during surgery when blood leaks into the joint cavity. Besides that, it is one of the major causes of morbidity amongst haemophilia patients. The aims of this thesis were to further unravel the pathogenesis of blood-induced joint damage and to

Bean grain hysteresis with induced mechanical damage

Directory of Open Access Journals (Sweden)

Renata C. Campos

Full Text Available ABSTRACT This study aimed to evaluate the effect of mechanical damage on the hysteresis of beans with induced mechanical damage under different conditions of temperature and relative humidity. Beans (Phaseolus vulgaris L. harvested manually with 35% water content (w.b. were used. Part of this product was subjected to induced mechanical damage by Stein Breakage Tester and controlled drying (damaged and control sample, for sorption processes. The sorption isotherms of water were analyzed for different temperature conditions: 20, 30, 40 and 50 oC; and relative humidity: 0.3; 0.4; 0.5; 0.7 and 0.9 (decimal. Equilibrium moisture content data were correlated with six mathematical models, and the Modified Oswin model was the one that best fitted to the experimental data. According to the above mentioned isotherms, it was possible to observe the phenomenon of hysteresis of damaged and control samples, and this phenomenon was more pronounced in control ones.

He-ion and self-atom induced damage and surface-morphology changes of a hot W target

International Nuclear Information System (INIS)

Meyer, F W; Hijazi, H; Bannister, M E; Dadras, J; Krstic, P S; Meyer, H M III; Parish, C M

2014-01-01

We report results of measurements on the evolution of the surface morphology of a hot tungsten surface due to impacting low-energy (80–12 000 eV) He ions and of simulations of damage caused by cumulative bombardment of 1 and 10 keV W self-atoms. The measurements were performed at the ORNL Multicharged Ion Research Facility, while the simulations were done at the Kraken supercomputing facility of the University of Tennessee. At 1 keV, the simulations show strong defect-recombination effects that lead to a saturation of the total defect number after a few hundred impacts, while sputtering leads to an imbalance of the vacancy and interstitial number. On the experimental side, surface morphology changes were investigated over a broad range of fluences, energies and temperatures for both virgin and pre-damaged W-targets. At the lowest accumulated fluences, small surface-grain features and near-surface He bubbles are observed. At the largest fluences, individual grain characteristics disappear in focused ion beam/scanning electron microscopy (FIB/SEM) scans, and the entire surface is covered by a multitude of near-surface bubbles with a broad range of sizes, and disordered whisker growth, while in top-down SEM imaging the surface is virtually indistinguishable from the nano-fuzz produced on linear plasma devices. These features are evident at progressively lower fluences as the He-ion energy is increased. (paper)

DNA-damage response during mitosis induces whole-chromosome missegregation.

Science.gov (United States)

Bakhoum, Samuel F; Kabeche, Lilian; Murnane, John P; Zaki, Bassem I; Compton, Duane A

2014-11-01

Many cancers display both structural (s-CIN) and numerical (w-CIN) chromosomal instabilities. Defective chromosome segregation during mitosis has been shown to cause DNA damage that induces structural rearrangements of chromosomes (s-CIN). In contrast, whether DNA damage can disrupt mitotic processes to generate whole chromosomal instability (w-CIN) is unknown. Here, we show that activation of the DNA-damage response (DDR) during mitosis selectively stabilizes kinetochore-microtubule (k-MT) attachments to chromosomes through Aurora-A and PLK1 kinases, thereby increasing the frequency of lagging chromosomes during anaphase. Inhibition of DDR proteins, ATM or CHK2, abolishes the effect of DNA damage on k-MTs and chromosome segregation, whereas activation of the DDR in the absence of DNA damage is sufficient to induce chromosome segregation errors. Finally, inhibiting the DDR during mitosis in cancer cells with persistent DNA damage suppresses inherent chromosome segregation defects. Thus, the DDR during mitosis inappropriately stabilizes k-MTs, creating a link between s-CIN and w-CIN. The genome-protective role of the DDR depends on its ability to delay cell division until damaged DNA can be fully repaired. Here, we show that when DNA damage is induced during mitosis, the DDR unexpectedly induces errors in the segregation of entire chromosomes, thus linking structural and numerical chromosomal instabilities. ©2014 American Association for Cancer Research.

An Improved Method of Mitigating Laser Induced Surface Damage Growth in Fused Silica Using a Rastered, Pulsed CO2 Laser

Energy Technology Data Exchange (ETDEWEB)

Bass, I L; Guss, G M; Nostrand, M J; Wegner, P L

2010-10-21

A new method of mitigating (arresting) the growth of large (>200 m diameter and depth) laser induced surface damage on fused silica has been developed that successfully addresses several issues encountered with our previously-reported large site mitigation technique. As in the previous work, a tightly-focused 10.6 {micro}m CO{sub 2} laser spot is scanned over the damage site by galvanometer steering mirrors. In contrast to the previous work, the laser is pulsed instead of CW, with the pulse length and repetition frequency chosen to allow substantial cooling between pulses. This cooling has the important effect of reducing the heat-affected zone capable of supporting thermo-capillary flow from scale lengths on the order of the overall scan pattern to scale lengths on the order of the focused laser spot, thus preventing the formation of a raised rim around the final mitigation site and its consequent down-stream intensification. Other advantages of the new method include lower residual stresses, and improved damage threshold associated with reduced amounts of redeposited material. The raster patterns can be designed to produce specific shapes of the mitigation pit including cones and pyramids. Details of the new technique and its comparison with the previous technique will be presented.

Thermal healing of the sub-surface damage layer in sapphire

International Nuclear Information System (INIS)

Pinkas, Malki; Lotem, Haim; Golan, Yuval; Einav, Yeheskel; Golan, Roxana; Chakotay, Elad; Haim, Avivit; Sinai, Ela; Vaknin, Moshe; Hershkovitz, Yasmin; Horowitz, Atara

2010-01-01

The sub-surface damage layer formed by mechanical polishing of sapphire is known to reduce the mechanical strength of the processed sapphire and to degrade the performance of sapphire based components. Thermal annealing is one of the methods to eliminate the sub-surface damage layer. This study focuses on the mechanism of thermal healing by studying its effect on surface topography of a- and c-plane surfaces, on the residual stresses in surface layers and on the thickness of the sub-surface damage layer. An atomically flat surface was developed on thermally annealed c-plane surfaces while a faceted roof-top topography was formed on a-plane surfaces. The annealing resulted in an improved crystallographic perfection close to the sample surface as was indicated by a noticeable decrease in X-ray rocking curve peak width. Etching experiments and surface roughness measurements using white light interferometry with sub-nanometer resolution on specimens annealed to different extents indicate that the sub-surface damage layer of the optically polished sapphire is less than 3 μm thick and it is totally healed after thermal treatment at 1450 deg. C for 72 h.

Protective effects of vitamin C against gamma-ray induced wholly damage and genetic damage

International Nuclear Information System (INIS)

Fu Chunling; Jiang Weiwei; Zhang Ping; Chen Xiang; Zhu Shengtao

2000-01-01

Objective: Protective effects of supplemental vitamin C against 60 Co-gamma-ray induced wholly damage and genetic damage was investigated in mice. Method: Mice were divided into normal control group, irradiation control group and vitamin C experimental group 1,2,3 (which were orally given vitamin C 15, 30, 45 mg/kg.bw for 10 successive days respectively prior to gamma-ray irradiation). Micronuclei in the bone marrow polychromatophilic erythrocytes in each group of mice were examined and the 30 day survival rate of mice following whole-body 5.0 Gy γ irradiation were also determined. Results: Supplemental vitamin C prior to gamma-rays irradiation can significantly decrease bone marrow PECMN rate of mice and increase 30 day survival rate and prolong average survival time. The protection factor is 2.09. Conclusion: Vitamin C has potent protective effects against gamma irradiation induced damage in mice. In certain dose range, vitamin C can absolutely suppress the gamma-rays induced genetic damage in vivo

Modeling of laser damage initiated by surface contamination

International Nuclear Information System (INIS)

Feit, M.D.; Rubenchik, A.M.; Faux, D.R.; Riddle, R.A.; Shapiro, A.; Eder, D.C.; Penetrante, B.M.; Milam, D.; Genin, F.Y.; Kozlowski, M.R.

1996-11-01

The authors are engaged in a comprehensive effort to understand and model the initiation and growth of laser damage initiated by surface contaminants. This includes, for example, the initial absorption by the contaminant, heating and plasma generation, pressure and thermal loading of the transparent substrate, and subsequent shockwave propagation, 'splashing' of molten material and possible spallation, optical propagation and scattering, and treatment of material fracture. The integration use of large radiation hydrodynamics codes, optical propagation codes and material strength codes enables a comprehensive view of the damage process The following picture of surface contaminant initiated laser damage is emerging from our simulations

Comparison of laser-based mitigation of fused silica surface damage using mid- versus far-infrared lasers

Energy Technology Data Exchange (ETDEWEB)

Yang, S T; Matthews, M J; Elhadj, S; Cooke, D; Guss, G M; Draggoo, V G; Wegner, P J

2009-12-16

Laser induced growth of optical damage can limit component lifetime and therefore operating costs of large-aperture fusion-class laser systems. While far-infrared (IR) lasers have been used previously to treat laser damage on fused silica optics and render it benign, little is known about the effectiveness of less-absorbing mid-IR lasers for this purpose. In this study, they quantitatively compare the effectiveness and efficiency of mid-IR (4.6 {micro}m) versus far-IR (10.6 {micro}m) lasers in mitigating damage growth on fused silica surfaces. The non-linear volumetric heating due to mid-IR laser absorption is analyzed by solving the heat equation numerically, taking into account the temperature-dependent absorption coefficient {alpha}(T) at {lambda} = 4.6 {micro}m, while far-IR laser heating is well-described by a linear analytic approximation to the laser-driven temperature rise. In both cases, the predicted results agree well with surface temperature measurements based on infrared radiometry, as well as sub-surface fictive temperature measurements based on confocal Raman microscopy. Damage mitigation efficiency is assessed using a figure of merit (FOM) relating the crack healing depth to laser power required, under minimally-ablative conditions. Based on their FOM, they show that for cracks up to at least 500 {micro}m in depth, mitigation with a 4.6 {micro}m mid-IR laser is more efficient than mitigation with a 10.6 {micro}m far-IR laser. This conclusion is corroborated by direct application of each laser system to the mitigation of pulsed laser-induced damage possessing fractures up to 225 {micro}m in depth.

Zinc protects HepG2 cells against the oxidative damage and DNA damage induced by ochratoxin A

Energy Technology Data Exchange (ETDEWEB)

Zheng, Juanjuan; Zhang, Yu [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); Xu, Wentao, E-mail: xuwentaoboy@sina.com [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); The Supervision, Inspection and Testing Center of Genetically Modified Organisms, Ministry of Agriculture, Beijing 100083 (China); Luo, YunBo [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); The Supervision, Inspection and Testing Center of Genetically Modified Organisms, Ministry of Agriculture, Beijing 100083 (China); Hao, Junran [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); Shen, Xiao Li [The Supervision, Inspection and Testing Center of Genetically Modified Organisms, Ministry of Agriculture, Beijing 100083 (China); Yang, Xuan [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); Li, Xiaohong [The Supervision, Inspection and Testing Center of Genetically Modified Organisms, Ministry of Agriculture, Beijing 100083 (China); Huang, Kunlun, E-mail: hkl009@163.com [Laboratory of Food Safety and Molecular Biology, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083 (China); The Supervision, Inspection and Testing Center of Genetically Modified Organisms, Ministry of Agriculture, Beijing 100083 (China)

2013-04-15

Oxidative stress and DNA damage are the most studied mechanisms by which ochratoxin A (OTA) induces its toxic effects, which include nephrotoxicity, hepatotoxicity, immunotoxicity and genotoxicity. Zinc, which is an essential trace element, is considered a potential antioxidant. The aim of this paper was to investigate whether zinc supplement could inhibit OTA-induced oxidative damage and DNA damage in HepG2 cells and the mechanism of inhibition. The results indicated that that exposure of OTA decreased the intracellular zinc concentration; zinc supplement significantly reduced the OTA-induced production of reactive oxygen species (ROS) and decrease in superoxide dismutase (SOD) activity but did not affect the OTA-induced decrease in the mitochondrial membrane potential (Δψ{sub m}). Meanwhile, the addition of the zinc chelator N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) strongly aggravated the OTA-induced oxidative damage. This study also demonstrated that zinc helped to maintain the integrity of DNA through the reduction of OTA-induced DNA strand breaks, 8-hydroxy-2′-deoxyguanosine (8-OHdG) formation and DNA hypomethylation. OTA increased the mRNA expression of metallothionein1-A (MT1A), metallothionein2-A (MT2A) and Cu/Zn superoxide dismutase (SOD1). Zinc supplement further enhanced the mRNA expression of MT1A and MT2A, but it had no effect on the mRNA expression of SOD1 and catalase (CAT). Zinc was for the first time proven to reduce the cytotoxicity of OTA through inhibiting the oxidative damage and DNA damage, and regulating the expression of zinc-associated genes. Thus, the addition of zinc can potentially be used to reduce the OTA toxicity of contaminated feeds. - Highlights: ► OTA decreased the intracellular zinc concentration. ► OTA induced the formation of 8-OHdG in HepG2 cells. ► It was testified for the first time that OTA induced DNA hypomethylation. ► Zinc protects against the oxidative damage and DNA damage induced by

Zinc protects HepG2 cells against the oxidative damage and DNA damage induced by ochratoxin A

International Nuclear Information System (INIS)

Zheng, Juanjuan; Zhang, Yu; Xu, Wentao; Luo, YunBo; Hao, Junran; Shen, Xiao Li; Yang, Xuan; Li, Xiaohong; Huang, Kunlun

2013-01-01

Oxidative stress and DNA damage are the most studied mechanisms by which ochratoxin A (OTA) induces its toxic effects, which include nephrotoxicity, hepatotoxicity, immunotoxicity and genotoxicity. Zinc, which is an essential trace element, is considered a potential antioxidant. The aim of this paper was to investigate whether zinc supplement could inhibit OTA-induced oxidative damage and DNA damage in HepG2 cells and the mechanism of inhibition. The results indicated that that exposure of OTA decreased the intracellular zinc concentration; zinc supplement significantly reduced the OTA-induced production of reactive oxygen species (ROS) and decrease in superoxide dismutase (SOD) activity but did not affect the OTA-induced decrease in the mitochondrial membrane potential (Δψ m ). Meanwhile, the addition of the zinc chelator N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) strongly aggravated the OTA-induced oxidative damage. This study also demonstrated that zinc helped to maintain the integrity of DNA through the reduction of OTA-induced DNA strand breaks, 8-hydroxy-2′-deoxyguanosine (8-OHdG) formation and DNA hypomethylation. OTA increased the mRNA expression of metallothionein1-A (MT1A), metallothionein2-A (MT2A) and Cu/Zn superoxide dismutase (SOD1). Zinc supplement further enhanced the mRNA expression of MT1A and MT2A, but it had no effect on the mRNA expression of SOD1 and catalase (CAT). Zinc was for the first time proven to reduce the cytotoxicity of OTA through inhibiting the oxidative damage and DNA damage, and regulating the expression of zinc-associated genes. Thus, the addition of zinc can potentially be used to reduce the OTA toxicity of contaminated feeds. - Highlights: ► OTA decreased the intracellular zinc concentration. ► OTA induced the formation of 8-OHdG in HepG2 cells. ► It was testified for the first time that OTA induced DNA hypomethylation. ► Zinc protects against the oxidative damage and DNA damage induced by OTA in

Mechanisms of free radical-induced damage to DNA.

Science.gov (United States)

Dizdaroglu, Miral; Jaruga, Pawel

2012-04-01

Endogenous and exogenous sources cause free radical-induced DNA damage in living organisms by a variety of mechanisms. The highly reactive hydroxyl radical reacts with the heterocyclic DNA bases and the sugar moiety near or at diffusion-controlled rates. Hydrated electron and H atom also add to the heterocyclic bases. These reactions lead to adduct radicals, further reactions of which yield numerous products. These include DNA base and sugar products, single- and double-strand breaks, 8,5'-cyclopurine-2'-deoxynucleosides, tandem lesions, clustered sites and DNA-protein cross-links. Reaction conditions and the presence or absence of oxygen profoundly affect the types and yields of the products. There is mounting evidence for an important role of free radical-induced DNA damage in the etiology of numerous diseases including cancer. Further understanding of mechanisms of free radical-induced DNA damage, and cellular repair and biological consequences of DNA damage products will be of outmost importance for disease prevention and treatment.

Damage-induced nonassociated inelastic flow in rock salt

International Nuclear Information System (INIS)

Chan, K.S.; Bodner, S.R.; Brodsky, N.S.; Fossum, A.F.; Munson, D.E.

1993-01-01

The multi-mechanism deformation coupled fracture model recently developed by CHAN, et al. (1992), for describing time-dependent, pressure-sensitive inelastic flow and damage evolution in crystalline solids was evaluated against triaxial creep experiments on rock salt. Guided by experimental observations, the kinetic equation and the flow law for damage-induced inelastic flow in the model were modified to account for the development of damage and inelastic dilatation in the transient creep regime. The revised model was then utilized to obtain the creep response and damage evolution in rock salt as a function of confining pressure and stress difference. Comparison between model calculation and experiment revealed that damage-induced inelastic flow is nonassociated, dilatational, and contributes significantly to the macroscopic strain rate observed in rock salt deformed at low confining pressures. The inelastic strain rate and volumetric strain due to damage decrease with increasing confining pressures, and all are suppressed at sufficiently high confining pressures

Surface analysis of transition metal oxalates: Damage aspects

Energy Technology Data Exchange (ETDEWEB)

Chenakin, S.P., E-mail: chenakin@imp.kiev.ua [Université Libre de Bruxelles (ULB), Chimie-Physique des Matériaux, B-1050 Bruxelles (Belgium); Institute of Metal Physics, Nat. Acad. Sci. of Ukraine, Akad. Vernadsky Blvd. 36, 03680 Kiev (Ukraine); Szukiewicz, R. [Université Libre de Bruxelles (ULB), Chimie-Physique des Matériaux, B-1050 Bruxelles (Belgium); Barbosa, R.; Kruse, N. [Université Libre de Bruxelles (ULB), Chimie-Physique des Matériaux, B-1050 Bruxelles (Belgium); Voiland School of Chemical Engineering and Bioengineering, Washington State University, 155 Wegner Hall, Pullman, WA 99164-6515 (United States)

2016-05-15

Highlights: • Gas evolution from the Mn, Co, Ni and Cu oxalate hydrates in vacuum, during exposure to X-rays and after termination of X-ray irradiation is studied. • A comparative study of the damage caused by X-rays in NiC{sub 2}O{sub 4} and CuC{sub 2}O{sub 4} is carried out. • Effect of Ar{sup +} bombardment on the structure and composition of CoC{sub 2}O{sub 4} is studied. - Abstract: The behavior of transition metal oxalates in vacuum, under X-ray irradiation and low-energy Ar{sup +} ion bombardment was studied. A comparative mass-spectrometric analysis was carried out of gas evolution from the surface of Mn, Co, Ni and Cu oxalate hydrates in vacuum, during exposure to X-rays and after termination of X-ray irradiation. The rates of H{sub 2}O and CO{sub 2} liberation from the oxalates were found to be in an inverse correlation with the temperatures of dehydration and decomposition, respectively. X-ray photoelectron spectroscopy (XPS) was employed to study the X-ray induced damage in NiC{sub 2}O{sub 4} and CuC{sub 2}O{sub 4} by measuring the various XP spectral characteristics and surface composition of the oxalates as a function of time of exposure to X-rays. It was shown that Cu oxalate underwent a significantly faster degradation than Ni oxalate and demonstrated a high degree of X-ray induced reduction from the Cu{sup 2+} to the Cu{sup 1+} chemical state. 500 eV Ar{sup +} sputter cleaning of CoC{sub 2}O{sub 4} for 10 min was found to cause a strong transformation of the oxalate structure which manifested itself in an appreciable alteration of the XP core-level and valence band spectra. The analysis of changes in stoichiometry and comparison of XP spectra of bombarded oxalate with respective spectra of a reference carbonate CoCO{sub 3} implied that the bombardment-induced decomposition of CoC{sub 2}O{sub 4} gave rise to the formation of CoO-like and disordered CoCO{sub 3}-like phases.

High-Density Plasma-Induced Etch Damage of GaN

International Nuclear Information System (INIS)

Baca, A.G.; Han, J.; Lester, L.F.; Pearton, S.J.; Ren, F.; Shul, R.J.; Willison, C.G.; Zhang, L.; Zolper, J.C.

1999-01-01

Anisotropic, smooth etching of the group-III nitrides has been reported at relatively high rates in high-density plasma etch systems. However, such etch results are often obtained under high de-bias and/or high plasma flux conditions where plasma induced damage can be significant. Despite the fact that the group-III nitrides have higher bonding energies than more conventional III-V compounds, plasma-induced etch damage is still a concern. Attempts to minimize such damage by reducing the ion energy or increasing the chemical activity in the plasma often result in a loss of etch rate or anisotropy which significantly limits critical dimensions and reduces the utility of the process for device applications requiring vertical etch profiles. It is therefore necessary to develop plasma etch processes which couple anisotropy for critical dimension and sidewall profile control and high etch rates with low-damage for optimum device performance. In this study we report changes in sheet resistance and contact resistance for n- and p-type GaN samples exposed to an Ar inductively coupled plasma (ICP). In general, plasma-induced damage was more sensitive to ion bombardment energies as compared to plasma flux. In addition, p-GaN was typically more sensitive to plasma-induced damage as compared to n-GaN

Effect of Cavitation on Surface Damage of 16.7Cr-10Ni-2Mo Stainless Steel in Marine Environment

Energy Technology Data Exchange (ETDEWEB)

Chong, Sang-Ok; Han, Min-Su; Kim, Seong-Jong [Mokpo National Maritime University, Mokpo (Korea, Republic of)

2015-10-15

Stainless steel is generally known to have characteristics of excellent corrosion resistance and durability, but in a marine environment it can suffer from localized corrosion due to the breakdown of passivity film due to chloride ion in seawater. Furthermore, the damage behaviors are sped up under a cavitation environment because of complex damage from electrochemical corrosion and cavitation-erosion. In this study the characteristics of electrochemical corrosion and cavitation erosion behavior were evaluated on 16.7Cr-10Ni-2Mo stainless steel under a cavitation environment in natural seawater. The electrochemical experiments have been conducted at both static conditions and dynamic conditions inducing cavitation with different current density parameters. The surface morphology and damage behaviors were compared after the experiment. After the cavitation test with time variables morphological examinations on damaged specimens were analyzed by using a scanning electron microscope and a 3D microscope. the galvanostatic experiment gave a cleaner surface morphology presented with less damage depth at high current density regions. It is due to the effect of water cavitation peening under the cavitation condition. In the cavitation experiment, with amplitude of 30 μm and seawater temperature of 25 ℃, weight loss and cavitation-erosion damage depth were dramatically increased after 5 hours inducing cavitation.

Calculation of femtosecond pulse laser induced damage threshold for broadband antireflective microstructure arrays.

Science.gov (United States)

Jing, Xufeng; Shao, Jianda; Zhang, Junchao; Jin, Yunxia; He, Hongbo; Fan, Zhengxiu

2009-12-21

In order to more exactly predict femtosecond pulse laser induced damage threshold, an accurate theoretical model taking into account photoionization, avalanche ionization and decay of electrons is proposed by comparing respectively several combined ionization models with the published experimental measurements. In addition, the transmittance property and the near-field distribution of the 'moth eye' broadband antireflective microstructure directly patterned into the substrate material as a function of the surface structure period and groove depth are performed by a rigorous Fourier model method. It is found that the near-field distribution is strongly dependent on the periodicity of surface structure for TE polarization, but for TM wave it is insensitive to the period. What's more, the femtosecond pulse laser damage threshold of the surface microstructure on the pulse duration taking into account the local maximum electric field enhancement was calculated using the proposed relatively accurate theoretical ionization model. For the longer incident wavelength of 1064 nm, the weak linear damage threshold on the pulse duration is shown, but there is a surprising oscillation peak of breakdown threshold as a function of the pulse duration for the shorter incident wavelength of 532 nm.

Surface hardening induced by high flux plasma in tungsten revealed by nano-indentation

Energy Technology Data Exchange (ETDEWEB)

Terentyev, D., E-mail: dterenty@sckcen.be [SCK-CEN, Nuclear Materials Science Institute, Boeretang 200, 2400 Mol (Belgium); Bakaeva, A. [SCK-CEN, Nuclear Materials Science Institute, Boeretang 200, 2400 Mol (Belgium); Department of Applied Physics, Ghent University, St. Pietersnieuwstraat 41, 9000 Ghent (Belgium); Pardoen, T.; Favache, A. [Institute of Mechanics, Materials and Civil Engineering, Université catholique de Louvain, Place Sainte Barbe 2 L5.02.02, 1348 Louvain-la-Neuve (Belgium); Zhurkin, E.E. [Department of Experimental Nuclear Physics K-89, Faculty of Physics and Mechanics, St. Petersburg State Polytechnical University, 29 Polytekhnicheskaya str., 195251 St. Petersburg (Russian Federation)

2016-08-01

Surface hardness of tungsten after high flux deuterium plasma exposure has been characterized by nanoindentation. The effect of plasma exposure was rationalized on the basis of available theoretical models. Resistance to plastic penetration is enhanced within the 100 nm sub-surface region, attributed to the pinning of geometrically necessary dislocations on nanometric deuterium cavities – signature of plasma-induced defects and deuterium retention. Sub-surface extension of thereby registered plasma-induced damage is in excellent agreement with the results of alternative measurements. The study demonstrates suitability of nano-indentation to probe the impact of deposition of plasma-induced defects in tungsten on near surface plasticity under ITER-relevant plasma exposure conditions.

Wavelength dependence of femtosecond laser-induced damage threshold of optical materials

Energy Technology Data Exchange (ETDEWEB)

Gallais, L., E-mail: laurent.gallais@fresnel.fr; Douti, D.-B.; Commandré, M. [Aix-Marseille Université, CNRS, Centrale Marseille, Institut Fresnel UMR 7249, 13013 Marseille (France); Batavičiūtė, G.; Pupka, E.; Ščiuka, M.; Smalakys, L.; Sirutkaitis, V.; Melninkaitis, A. [Laser Research Center, Vilnius University, Saulétekio aléja 10, LT-10223 Vilnius (Lithuania)

2015-06-14

An experimental and numerical study of the laser-induced damage of the surface of optical material in the femtosecond regime is presented. The objective of this work is to investigate the different processes involved as a function of the ratio of photon to bandgap energies and compare the results to models based on nonlinear ionization processes. Experimentally, the laser-induced damage threshold of optical materials has been studied in a range of wavelengths from 1030 nm (1.2 eV) to 310 nm (4 eV) with pulse durations of 100 fs with the use of an optical parametric amplifier system. Semi-conductors and dielectrics materials, in bulk or thin film forms, in a range of bandgap from 1 to 10 eV have been tested in order to investigate the scaling of the femtosecond laser damage threshold with the bandgap and photon energy. A model based on the Keldysh photo-ionization theory and the description of impact ionization by a multiple-rate-equation system is used to explain the dependence of laser-breakdown with the photon energy. The calculated damage fluence threshold is found to be consistent with experimental results. From these results, the relative importance of the ionization processes can be derived depending on material properties and irradiation conditions. Moreover, the observed damage morphologies can be described within the framework of the model by taking into account the dynamics of energy deposition with one dimensional propagation simulations in the excited material and thermodynamical considerations.

Continuum damage mechanics method for fatigue growth of surface cracks

International Nuclear Information System (INIS)

Feng Xiqiao; He Shuyan

1997-01-01

With the background of leak-before-break (LBB) analysis of pressurized vessels and pipes in nuclear plants, the fatigue growth problem of either circumferential or longitudinal semi-elliptical surface cracks subjected to cyclic loading is studied by using a continuum damage mechanics method. The fatigue damage is described by a scalar damage variable. From the damage evolution equation at the crack tip, a crack growth equation similar to famous Paris' formula is derived, which shows the physical meaning of Paris' formula. Thereby, a continuum damage mechanics approach is developed to analyze the configuration evolution of surface cracks during fatigue growth

Impact damage reduction by structured surface geometry

DEFF Research Database (Denmark)

Kusano, Yukihiro; Fedorov, Vladimir; McGugan, Malcolm

2018-01-01

performance was observed for polyurethane-coated fibre composites with structured geometries at the back surfaces. Repeated impacts by rubber balls on the coated side caused damage and delamination of the coating. The laminates with structured back surfaces showed longer durability than those with a flat back...

An extended sequence specificity for UV-induced DNA damage.

Science.gov (United States)

Chung, Long H; Murray, Vincent

2018-01-01

The sequence specificity of UV-induced DNA damage was determined with a higher precision and accuracy than previously reported. UV light induces two major damage adducts: cyclobutane pyrimidine dimers (CPDs) and pyrimidine(6-4)pyrimidone photoproducts (6-4PPs). Employing capillary electrophoresis with laser-induced fluorescence and taking advantages of the distinct properties of the CPDs and 6-4PPs, we studied the sequence specificity of UV-induced DNA damage in a purified DNA sequence using two approaches: end-labelling and a polymerase stop/linear amplification assay. A mitochondrial DNA sequence that contained a random nucleotide composition was employed as the target DNA sequence. With previous methodology, the UV sequence specificity was determined at a dinucleotide or trinucleotide level; however, in this paper, we have extended the UV sequence specificity to a hexanucleotide level. With the end-labelling technique (for 6-4PPs), the consensus sequence was found to be 5'-GCTC*AC (where C* is the breakage site); while with the linear amplification procedure, it was 5'-TCTT*AC. With end-labelling, the dinucleotide frequency of occurrence was highest for 5'-TC*, 5'-TT* and 5'-CC*; whereas it was 5'-TT* for linear amplification. The influence of neighbouring nucleotides on the degree of UV-induced DNA damage was also examined. The core sequences consisted of pyrimidine nucleotides 5'-CTC* and 5'-CTT* while an A at position "1" and C at position "2" enhanced UV-induced DNA damage. Crown Copyright © 2017. Published by Elsevier B.V. All rights reserved.

Effects of focused ion beam induced damage on the plasticity of micropillars

International Nuclear Information System (INIS)

El-Awady, Jaafar A.; Woodward, Christopher; Dimiduk, Dennis M.; Ghoniem, Nasr M.

2009-01-01

The hardening effects of focused ion beam (FIB) induced damage produced during the fabrication of micropillars are examined by introducing a surface layer of nanosized obstacles into a dislocation dynamics simulation. The influence of the depth and strength of the obstacles as a function of pillar diameter is assessed parametrically. We show that for a selected set of sample sizes between 0.5 and 1.0 μm, the flow strength can increase by 10-20 %, for an obstacle strength of 750 MPa, and damage depth of 100 nm. On the other hand, for sizes larger and smaller than this range, the effect of damage is negligible. Results show that the obstacles formed during the FIB milling may be expected to alter the microstructure of micropillars, however, they have a negligible effect on the observed size-strength scaling laws.

Laser-induced damage study of polymer PMMA

International Nuclear Information System (INIS)

Mansour, N.

2001-01-01

This article presents the results of bulk laser-induced damage measurements in polymer PMMA at 532 nm and 1064 nm for nanosecond laser pulses. The damage thresholds were measured for focused spot sizes ranging over two orders of magnitude. In this work, self-focusing effects were verified to be absent by measurements of breakdown thresholds using both linearly and circularly polarized light. At both 1064 nm and 532 nm, the dependence of the breakdown field, E B , on the spot size, ω, was empirically determined to be E B = C/√ω, where C depends on the wavelength. The extracted value for C(λ) at 1064 nm is larger by a factor of 5 than at 532 nm. Possible reasons for this strong dispersion and mechanism for laser-induced damage in polymer materials will be discussed

Mitigation of waterlogging-induced damages to pepper by exogenous meja

International Nuclear Information System (INIS)

Jun, O.; Bin, L.; Zhi, Y.B.

2017-01-01

In this study, we studied the mitigation effects of exogenous Methyl jasmonate (MeJA) on waterlogging-induced damages to Xinyou No.5 wrinkled skin pepper cultivar by spraying MeJA on leave's surface at different waterlogging periods and investigated its underlying mechanisms. The results showed that administration of MeJA increased antioxidant enzymes' activities, proline and soluble sugar contents and alcohol dehydrogenase (ADH) activity, reduced relative conductivity, malondialdehyde (MDA) and hydroxyl free radical (.OH) accumulation, lactate dehydrogenase (LDH) activity and lactic acid and acetaldehyde accumulation, and maintained high root malate dehydrogenase (MDH) and succinate dehydrogenase (SDH) activities and certain aerobic respiratory metabolism. The study also found that there were significant differences among exogenous MeJA treatments at different waterlogging periods. Peppers treated with exogenous MeJA 1 day and 2 days prior to waterlogging had optimal agronomic traits, higher chlorophyll content, enzymatic activities and osmolytic substances, as well as lower relative conductivity, MDA and ·OH accumulation. Overall, the results suggest that MeJA mitigates waterlogging-induced damages to pepper by adjusting osmolytic substances contents, antioxidant enzymatic activities and root respiration and metabolism and achieves better alleviation effects by spraying prior to waterlogging. (author)

Experiment and numerical simulation of welding induced damage: stainless steel 15-5PH

International Nuclear Information System (INIS)

Wu, T.

2007-11-01

The objective of this study is the prediction of damage and residual stresses induced by hot processing which leads to phase transformation in martensitic stainless steel. This study firstly concerns the modelling of the damage of material induced by a complex history of thermo-elastoplastic multiphase in heat-affected-zone (HAZ) of welding. In this work, a two-scale mode of elastoplastic damage multiphase was developed in the framework of thermodynamics of irreversible process. The constitutive equations are coupling with ductile damage, elasto-plasticity, phase transformation, and transformation plasticity. Besides, a damage equation was proposed based on the Lemaitre's damage model in the framework of continuum damage mechanics. The experiments of 15-5PH were implemented for the identification of phase transformation, transformation plasticity and damage models. Tensile tests of round specimens were used to identify the parameters of damage model as well as mechanical behaviours at various temperatures. Tests of flat notched specimen were designed to provide the validation of damage model and strain localization using three dimensional image correlation technologies. In addition, microscopic analysis was performed to provide microstructure characterization of 15-5PH and to discover the damage mechanism. Finally the numerical simulation was performed in the code CAST3M of CEA. On the one hand, numerical verification of the flat notched plates was implemented and compared with experimental results. On the other hand, we used the two-scale model including phase transformation, transformation plasticity and damage to simulate the level of residual stresses of a disk made of 15-5PH metal heated by laser. The internal variables, such as strain, stress, damage, were successfully traced in the simulation of two-scale model. The simulation results showed the transformation plasticity changes the level of residual stresses and should not be negligible; damage decreases

Automated analysis of damages for radiation in plastics surfaces; Analisis automatizado de danos por radiacion en superficies plasticas

Energy Technology Data Exchange (ETDEWEB)

Andrade, C; Camacho M, E; Tavera, L; Balcazar, M [ININ, 52045 Ocoyoacac, Estado de Mexico (Mexico)

1990-02-15

Analysis of damages done by the radiation in a polymer characterized by optic properties of polished surfaces, of uniformity and chemical resistance that the acrylic; resistant until the 150 centigrade grades of temperature, and with an approximate weight of half of the glass. An objective of this work is the development of a method that analyze in automated form the superficial damages induced by radiation in plastic materials means an images analyst. (Author)

MDM2 Antagonists Counteract Drug-Induced DNA Damage

Directory of Open Access Journals (Sweden)

Anna E. Vilgelm

2017-10-01

Full Text Available Antagonists of MDM2-p53 interaction are emerging anti-cancer drugs utilized in clinical trials for malignancies that rarely mutate p53, including melanoma. We discovered that MDM2-p53 antagonists protect DNA from drug-induced damage in melanoma cells and patient-derived xenografts. Among the tested DNA damaging drugs were various inhibitors of Aurora and Polo-like mitotic kinases, as well as traditional chemotherapy. Mitotic kinase inhibition causes mitotic slippage, DNA re-replication, and polyploidy. Here we show that re-replication of the polyploid genome generates replicative stress which leads to DNA damage. MDM2-p53 antagonists relieve replicative stress via the p53-dependent activation of p21 which inhibits DNA replication. Loss of p21 promoted drug-induced DNA damage in melanoma cells and enhanced anti-tumor activity of therapy combining MDM2 antagonist with mitotic kinase inhibitor in mice. In summary, MDM2 antagonists may reduce DNA damaging effects of anti-cancer drugs if they are administered together, while targeting p21 can improve the efficacy of such combinations.

Smeared crack modelling approach for corrosion-induced concrete damage

DEFF Research Database (Denmark)

Thybo, Anna Emilie Anusha; Michel, Alexander; Stang, Henrik

2017-01-01

In this paper a smeared crack modelling approach is used to simulate corrosion-induced damage in reinforced concrete. The presented modelling approach utilizes a thermal analogy to mimic the expansive nature of solid corrosion products, while taking into account the penetration of corrosion...... products into the surrounding concrete, non-uniform precipitation of corrosion products, and creep. To demonstrate the applicability of the presented modelling approach, numerical predictions in terms of corrosion-induced deformations as well as formation and propagation of micro- and macrocracks were......-induced damage phenomena in reinforced concrete. Moreover, good agreements were also found between experimental and numerical data for corrosion-induced deformations along the circumference of the reinforcement....

Morphologies of laser-induced damage in hafnia-silica multilayer mirror and polarizer coatings

International Nuclear Information System (INIS)

Genin, F.Y.; Stolz, C.J.

1996-08-01

Hafnium-silica multilayer mirrors and polarizers were deposited by e-beam evaporation onto BK7 glass substrates. The mirrors and polarizers were coated for operation at 1053 nm at 45 degree and at Brewster's angle (56 degree), respectively. They were tested with a single 3-ns laser pulse. Morphology of the laser-induced damage was characterized by optical and scanning electron microscopy. Four distinct damage morphologies were found: pits, flatbottom pits, scalds, and delaminates. The pits and flat bottom pits ( 2 ). The pits seemed to result from ejection of nodular defects by causing local enhancement of the electric field. Scalds and delaminates could be observed at higher fluences (above 13 J/cm 2 ) and seemed to result from the formation of plasmas on the surface. These damage types often originated at pits and were less than 300 μm diameter; their size increased almost linearly with fluence. Finally, effects of the damage on the beam (reflectivity degradation and phase modulations) were measured

Laser damage in optical components: metrology, statistical and photo-induced analysis of precursor centres

International Nuclear Information System (INIS)

Gallais, L.

2002-11-01

This thesis deals with laser damage phenomena for nanosecond pulses, in optical components such as glasses, dielectric and metallic thin films. Firstly, a work is done on the laser damage metrology, in order to obtain accurate and reliable measurement of laser-induced damage probabilities, with a rigorous control of test parameters. Then, with the use of a specific model, we find densities of laser damage precursors in the case of bulk glasses (few tens by (100μm) 3 ) and in the case of glass surfaces (one precursor by μm 3 ). Our analysis is associated to morphology studies by Atomic Force Microscope to discuss about precursor nature and damage process. Influence of wavelength (from 355 to 1064 nm) and cumulated shots is also studied. Simulations are performed to study initiation mechanisms on these inclusions. This work gives an estimation of complex index and size of the precursor, which permits to discuss about possible detection by non-destructive tools. (author)

Parvovirus infection-induced DNA damage response

Science.gov (United States)

Luo, Yong; Qiu, Jianming

2014-01-01

Parvoviruses are a group of small DNA viruses with ssDNA genomes flanked by two inverted terminal structures. Due to a limited genetic resource they require host cellular factors and sometimes a helper virus for efficient viral replication. Recent studies have shown that parvoviruses interact with the DNA damage machinery, which has a significant impact on the life cycle of the virus as well as the fate of infected cells. In addition, due to special DNA structures of the viral genomes, parvoviruses are useful tools for the study of the molecular mechanisms underlying viral infection-induced DNA damage response (DDR). This review aims to summarize recent advances in parvovirus-induced DDR, with a focus on the diverse DDR pathways triggered by different parvoviruses and the consequences of DDR on the viral life cycle as well as the fate of infected cells. PMID:25429305

Temperature dependence on plasma-induced damage and chemical reactions in GaN etching processes using chlorine plasma

Science.gov (United States)

Liu, Zecheng; Ishikawa, Kenji; Imamura, Masato; Tsutsumi, Takayoshi; Kondo, Hiroki; Oda, Osamu; Sekine, Makoto; Hori, Masaru

2018-06-01

Plasma-induced damage (PID) on GaN was optimally reduced by high-temperature chlorine plasma etching. Energetic ion bombardments primarily induced PID involving stoichiometry, surface roughness, and photoluminescence (PL) degradation. Chemical reactions under ultraviolet (UV) irradiation and chlorine radical exposure at temperatures higher than 400 °C can be controlled by taking into account the synergism of simultaneous photon and radical irradiations to effectively reduce PID.

Ceramide Production Mediates Aldosterone-Induced Human Umbilical Vein Endothelial Cell (HUVEC Damages.

Directory of Open Access Journals (Sweden)

Yumei Zhang

Full Text Available Here, we studied the underlying mechanism of aldosterone (Aldo-induced vascular endothelial cell damages by focusing on ceramide. We confirmed that Aldo (at nmol/L inhibited human umbilical vein endothelial cells (HUVEC survival, and induced considerable cell apoptosis. We propose that ceramide (mainly C18 production might be responsible for Aldo-mediated damages in HUVECs. Sphingosine-1-phosphate (S1P, an anti-ceramide lipid, attenuated Aldo-induced ceramide production and following HUVEC damages. On the other hand, the glucosylceramide synthase (GCS inhibitor PDMP or the ceramide (C6 potentiated Aldo-induced HUVEC apoptosis. Eplerenone, a mineralocorticoid receptor (MR antagonist, almost completely blocked Aldo-induced C18 ceramide production and HUVEC damages. Molecularly, ceramide synthase 1 (CerS-1 is required for C18 ceramide production by Aldo. Knockdown of CerS-1 by targeted-shRNA inhibited Aldo-induced C18 ceramide production, and protected HUVECs from Aldo. Reversely, CerS-1 overexpression facilitated Aldo-induced C18 ceramide production, and potentiated HUVEC damages. Together, these results suggest that C18 ceramide production mediates Aldo-mediated HUVEC damages. MR and CerS-1 could be the two signaling molecule regulating C18 ceramide production by Aldo.

Contribution of endogenous and exogenous damage to the total radiation-induced damage in the bacterial spore

International Nuclear Information System (INIS)

Jacobs, G.P.; Samuni, A.; Czapski, G.

1980-01-01

Radical scavengers such as polyethylene glycol 4000 and bovine albumin have been used to define the contribution of exogenous and endogenous damage to the total radiation-induced damage in aqueous buffered suspensions of Bacillus pumilus spores. The results indicate that this damage in the bacterial spore is predominantly endogenous

Cuticular surface damage of Ascaridia galli adult worms treated with Veitchia merrillii betel nuts extract in vitro.

Science.gov (United States)

Balqis, Ummu; Hambal, Muhammad; Rinidar; Athaillah, Farida; Ismail; Azhar; Vanda, Henni; Darmawi

2017-07-01

The objective of this research was to in vitro evaluate the cuticular surface damage of Ascaridia galli adult worms treated with ethanolic extract of betel nuts Veitchia merrillii . Phytochemical screening was done using FeCl 3 , Wagner and Dragendorff reagents, NaOH, MgHCl, and Liebermann-Burchard reaction test. Amount of 16 worms were segregated into four groups with three replicates. Four worms of each group submerged into phosphate buffered saline, 25 mg/ml, and 75 mg/ml crude ethanolic extract of V. merrillii , and 15 mg/ml albendazole. The effect of these extract was observed 40 h after incubation as soon as worms death. The worms were sectioned transversally and were explored for any cuticular histopathological changes in their body surface under microscope. We found that the ethanolic extract of V. merrillii betel nuts contains tannins, alkaloids, flavonoids, triterpenoids, and saponins. The ethanolic extract of betel nuts V. merrillii induces surface alterations caused cuticular damage of A. galli adult worms. We concluded that ethanolic extract of betel nuts V. merrillii possess anthelmintic activity caused cuticular damage of A. galli adult worms.

Radiation-induced DNA damage as a function of DNA hydration

International Nuclear Information System (INIS)

Swarts, S.G.; Miao, L.; Wheeler, K.T.; Sevilla, M.D.; Becker, D.

1995-01-01

Radiation-induced DNA damage is produced from the sum of the radicals generated by the direct ionization of the DNA (direct effect) and by the reactions of the DNA with free radicals formed in the surrounding environment (indirect effect). The indirect effect has been believed to be the predominant contributor to radiation-induced intracellular DNA damage, mainly as the result of reactions of bulk water radicals (e.g., OH·) with DNA. However, recent evidence suggests that DNA damage, derived from the irradiation of water molecules that are tightly bound in the hydration layer, may occur as the result of the transfer of electron-loss centers (e.g. holes) and electrons from these water molecules to the DNA. Since this mechanism for damaging DNA more closely parallels that of the direct effect, the irradiation of these tightly bound water molecules may contribute to a quasi-direct effect. These water molecules comprise a large fraction of the water surrounding intracellular DNA and could account for a significant proportion of intracellular radiation-induced DNA damage. Consequently, the authors have attempted to characterize this quasi-direct effect to determine: (1) the extent of the DNA hydration layer that is involved with this effect, and (2) what influence this effect has on the types and quantities of radiation-induced DNA damage

Impact of mechanical stress induced in silica vacuum windows on laser-induced damage.

Science.gov (United States)

Gingreau, Clémence; Lanternier, Thomas; Lamaignère, Laurent; Donval, Thierry; Courchinoux, Roger; Leymarie, Christophe; Néauport, Jérôme

2018-04-15

At the interface between vacuum and air, optical windows must keep their optical properties, despite being subjected to mechanical stress. In this Letter, we investigate the impact of such stress on the laser-induced damage of fused silica windows at the wavelength of 351 nm in the nanosecond regime. Different stress values, from 1 to 30 MPa, both tensile and compressive, were applied. No effect of the stress on the laser-induced damage was evidenced.

Growth behavior of laser-induced damage on fused silica optics under UV, ns laser irradiation.

Science.gov (United States)

Negres, Raluca A; Norton, Mary A; Cross, David A; Carr, Christopher W

2010-09-13

The growth behavior of laser-induced damage sites is affected by a large number of laser parameters as well as site morphology. Here we investigate the effects of pulse duration on the growth rate of damage sites located on the exit surface of fused silica optics. Results demonstrate a significant dependence of the growth parameters on laser pulse duration at 351 nm from 1 ns to 15 ns, including the observation of a dominant exponential versus linear, multiple-shot growth behavior for long and short pulses, respectively. These salient behaviors are tied to the damage morphology and suggest a shift in the fundamental growth mechanisms for pulses in the 1-5 ns range.

Surface damage of W exposed to combined stationary D plasma and ELMs-like pulsed plasma

Energy Technology Data Exchange (ETDEWEB)

Jia, Y.Z., E-mail: jaja880816@aliyun.com [Science and Technology on Reactor Fuel and Materials Laboratory, Nuclear Power Institute of China, Chengdu, Sichuan 610213 (China); Laboratory of Advanced Materials, School of Materials Science and Engineering, Tsinghua University, Beijing 100084 (China); Liu, W., E-mail: liuw@mail.tsinghua.edu.cn [Laboratory of Advanced Materials, School of Materials Science and Engineering, Tsinghua University, Beijing 100084 (China); Xu, B.; Qu, S.L. [Laboratory of Advanced Materials, School of Materials Science and Engineering, Tsinghua University, Beijing 100084 (China); Morgan, T.W. [FOM Institute DIFFER-Dutch Institute for Fundamental Energy Research, 5612AJ Eindhoven (Netherlands)

2017-04-15

The surface damage of W under D plasma and ELMs-like transient heat loads was studied by combined stationary and pulsed D plasma. Low-flux transient heat loads will promote blister formation due to the gas expansion inside the blisters. On the contrary, high-flux transient heat loads will mitigate blistering due to the high surface temperature. Therefore, blistering on W surface first increased and then decreased with the increasing transient heat loads. The promotion effect of pulsed plasma on blistering is more obvious on [001] and [110] surfaces than on [111] surface, and the orientation dependence of blisters was mitigated by the transient heat loads. Surface modification induced by transient heat loads only formed on [001] and [110] surfaces, but did not form on [111] surface. The orientation dependence of surface modification was mainly due to the slipping system of dislocations.

Picosecond laser damage of fused silica at 355 nm

International Nuclear Information System (INIS)

Meng Xiangjie; Liu Hongjie; Wang Fang; Zhang Zhen; An Xinyou; Huang Jin; Jiang Xiaodong; Wu Weidong; Ren Weiyi

2013-01-01

This paper studies the initiated damage threshold, the damage morphology and the subsequent damage growth on fused silica's input-surface and exit-surface under picosecond laser irradiation at 355 nm. Defects induced fluorescence on surface of the optical component is observed. The results demonstrate a significant dependence of the initiated damage on pulse duration and surface defects, and that of the damage growth on self-focusing, sub-surface defects. The damage-threshold is 3.98 J/cm 2 of input surface and 2.91 J/cm 2 of exit surface. The damage morphologies are quite different between input surface and exit surface. Slow growth behavior appears for the diameter of exit-surface and linear growth one for the depth of exit-surface in the lateral side of damage site with the increase of shot number. Defects have changed obviously compared with nanosecond laser damage in the damage area. Several main reasons such as electric intensification and self-focusing for the observed initiated damage and damage growth behavior are discussed. (authors)

Chemical determination of free radical-induced damage to DNA.

Science.gov (United States)

Dizdaroglu, M

1991-01-01

Free radical-induced damage to DNA in vivo can result in deleterious biological consequences such as the initiation and promotion of cancer. Chemical characterization and quantitation of such DNA damage is essential for an understanding of its biological consequences and cellular repair. Methodologies incorporating the technique of gas chromatography/mass spectrometry (GC/MS) have been developed in recent years for measurement of free radical-induced DNA damage. The use of GC/MS with selected-ion monitoring (SIM) facilitates unequivocal identification and quantitation of a large number of products of all four DNA bases produced in DNA by reactions with hydroxyl radical, hydrated electron, and H atom. Hydroxyl radical-induced DNA-protein cross-links in mammalian chromatin, and products of the sugar moiety in DNA are also unequivocally identified and quantitated. The sensitivity and selectivity of the GC/MS-SIM technique enables the measurement of DNA base products even in isolated mammalian chromatin without the necessity of first isolating DNA, and despite the presence of histones. Recent results reviewed in this article demonstrate the usefulness of the GC/MS technique for chemical determination of free radical-induced DNA damage in DNA as well as in mammalian chromatin under a vast variety of conditions of free radical production.

Ultrasound-induced cavitation damage to external epithelia of fish skin.

Science.gov (United States)

Frenkel, V; Kimmel, E; Iger, Y

1999-10-01

Transmission electron microscopy was used to show the effects of therapeutic ultrasound (fish skin. Exposures of up to 90 s produced damage to 5 to 6 of the outermost layers. Negligible temperature elevations and lack of damage observed when using degassed water indicated that the effects were due to cavitation. The minimal intensity was determined for inducing cellular damage, where the extent and depth of damage to the tissues was correlated to the exposure duration. The results may be interpreted as a damage front, advancing slowly from the outer cells inward, presumably in association with the slow replacement of the perforated cell contents with the surrounding water. This study illustrates that a controlled level of microdamage may be induced to the outer layers of the tissues.

Induced surface stress at crystal surfaces

International Nuclear Information System (INIS)

Dahmen, K.

2002-05-01

Changes of the surfaces stress Δτ (s) can be studied by observing the bending of thin crystalline plates. With this cantilever method one can gain the induced change of surface stress Δτ (s) from the bending of plates with the help of elasticity theory. For elastic isotropic substrates the relevant relations are known. Here the relations are generalized to elastic anisotropic crystals with a C 2v - Symmetry. The equilibrium shapes of crystalline plates oriented along the (100)-, (110)-, or (111)-direction which are clamped along one edge are calculated with a numeric method under the load of a homogeneous but pure isotropic or anisotropic surface stress. The results can be displayed with the dimensionality, so that the effect of clamping can be described in a systematic way. With these tabulated values one can evaluate cantilever experiments exactly. These results are generalized to cantilever methods for determining magnetoelastic constants. It is shown which magnetoelastic constants are measured in domains of thin films with ordered structures. The eigenshape and the eigenfrequency of plates constraint through a clamping at one side are calculated. These results give a deeper understanding of the elastic anisotropy. The induced surface stress of oxygen on the (110)-surface of molybdenum is measured along the principle directions Δτ [001] and Δτ [ anti 110] . The anisotropy of the surface stress is found for the p(2 x 2)-reconstruction. Lithium induces a tensile surface stress on the Molybdenum (110)-surface up to a coverage of Θ = 0, 3 monolayer. For a higher coverage the induced stress drops and reaches a level of less than -1, 2 N/m at one monolayer. It is shown, that cobalt induces a linear increasing stress with respect to the coverage on the (100)-surface of copper with a value of 2, 4GPa. The copper (100)-surface is bombarded with accelerated ions in the range between 800-2200 eV. The resulting induced compressive stress (Δτ (s) < 0) of the order

[Challenge and treatment strategy for ocular surface damage in patients with long term use of antiglaucoma drugs].

Science.gov (United States)

He, Xiang-Ge

2011-02-01

Long term use of topical anti-glaucoma drugs has been shown to induce chronic conjunctivitis, superficial punctate keratitis (SPK) and dry eye symptom. Under these conditions, a loss of goblet cells in conjunctiva, epithelial squamous metaplasia and apoptosis were morphologically revealed. Benzalkonium Chloride (BKC), a most frequently used preservative in eye drops, has been found to be an important factor causing ocular surface damage. Furthermore, a big challenge for ophthalmologists is that toxic damage of medication to ocular surface tissues is mild, poor specificity, and delayed manifestation in patients, especially when coexisting with other ocular surface diseases. Impairment of ocular surface tissues greatly impacts the life quality of patients and subsequently influences compliance with glaucoma therapy. This paper emphasizes to take measures to prevent ocular surface tissue damage resulted from chronic use of topical anti-glaucoma drugs and further discusses the treatment strategy. Effective and long-lasting action drugs should always be selected for glaucomatous patients in order to decrease the frequency of topical instillation or at a more expensive medication, a fixed combination formula can be considered for glaucoma therapy. An early surgery or laser treatment is also proposed for the patients who require an IOP reduction with an existing ocular surface impairment. Future investigation and development of new medications with long-term efficacy and appropriate BKC are suggested and preservative-free or drugs with new preservative materials recommended.

Surface Contaminant Control Technologies to Improve Laser Damage Resistance of Optics

Directory of Open Access Journals (Sweden)

Xiaofeng Cheng

2014-01-01

Full Text Available The large high-power solid lasers, such as the National Ignition Facility (NIF of America and the Shenguang-III (SG-III laser facility of China, can output over 2.1 MJ laser pulse for the inertial confinement fusion (ICF experiments. Because of the enhancement of operating flux and the expansion of laser driver scale, the problem of contamination seriously influences their construction period and operation life. During irradiation by intense laser beams, the contaminants on the metallic surface of beam tubes can be transmitted to the optical surfaces and lead to damage of optical components. For the high-power solid-state laser facilities, contamination control focuses on the slab amplifiers, spatial filters, and final-optical assemblies. In this paper, an effective solution to control contaminations including the whole process of the laser driver is put forward to provide the safe operation of laser facilities, and the detailed technical methods of contamination control such as washing, cleanliness metrology, and cleanliness protecting are also introduced to reduce the probability of laser-induced damage of optics. The experimental results show that the cleanliness level of SG-III laser facility is much better to ensure that the laser facility can safely operate at high energy flux.

Vorinostat induces reactive oxygen species and DNA damage in acute myeloid leukemia cells.

Directory of Open Access Journals (Sweden)

Luca A Petruccelli

Full Text Available Histone deacetylase inhibitors (HDACi are promising anti-cancer agents, however, their mechanisms of action remain unclear. In acute myeloid leukemia (AML cells, HDACi have been reported to arrest growth and induce apoptosis. In this study, we elucidate details of the DNA damage induced by the HDACi vorinostat in AML cells. At clinically relevant concentrations, vorinostat induces double-strand breaks and oxidative DNA damage in AML cell lines. Additionally, AML patient blasts treated with vorinostat display increased DNA damage, followed by an increase in caspase-3/7 activity and a reduction in cell viability. Vorinostat-induced DNA damage is followed by a G2-M arrest and eventually apoptosis. We found that pre-treatment with the antioxidant N-acetyl cysteine (NAC reduces vorinostat-induced DNA double strand breaks, G2-M arrest and apoptosis. These data implicate DNA damage as an important mechanism in vorinostat-induced growth arrest and apoptosis in both AML cell lines and patient-derived blasts. This supports the continued study and development of vorinostat in AMLs that may be sensitive to DNA-damaging agents and as a combination therapy with ionizing radiation and/or other DNA damaging agents.

Vorinostat Induces Reactive Oxygen Species and DNA Damage in Acute Myeloid Leukemia Cells

Science.gov (United States)

Pettersson, Filippa; Retrouvey, Hélène; Skoulikas, Sophia; Miller, Wilson H.

2011-01-01

Histone deacetylase inhibitors (HDACi) are promising anti-cancer agents, however, their mechanisms of action remain unclear. In acute myeloid leukemia (AML) cells, HDACi have been reported to arrest growth and induce apoptosis. In this study, we elucidate details of the DNA damage induced by the HDACi vorinostat in AML cells. At clinically relevant concentrations, vorinostat induces double-strand breaks and oxidative DNA damage in AML cell lines. Additionally, AML patient blasts treated with vorinostat display increased DNA damage, followed by an increase in caspase-3/7 activity and a reduction in cell viability. Vorinostat-induced DNA damage is followed by a G2-M arrest and eventually apoptosis. We found that pre-treatment with the antioxidant N-acetyl cysteine (NAC) reduces vorinostat-induced DNA double strand breaks, G2-M arrest and apoptosis. These data implicate DNA damage as an important mechanism in vorinostat-induced growth arrest and apoptosis in both AML cell lines and patient-derived blasts. This supports the continued study and development of vorinostat in AMLs that may be sensitive to DNA-damaging agents and as a combination therapy with ionizing radiation and/or other DNA damaging agents. PMID:21695163

Curcumin Attenuates Methotrexate-Induced Hepatic Oxidative Damage in Rats

International Nuclear Information System (INIS)

HEMEIDA, R.A.M.; MOHAFEZ, O.M.

2008-01-01

In the present study, we have addressed the ability of curcumin to suppress MTX-induced liver damage. Hepatotoxicity was induced by injection of a single dose of MTX (20 mg/kg I.P.). MTX challenge induced liver damage that was well characterized histopathologically and biochemically. MTX increased relative liver/body weight ratio. Histologically, MTX produced fatty changes in hepatocytes and sinusoidal lining cells, mild necrosis and inflammation. Biochemically, the test battery entailed elevated activities of serum ALT and AST. Liver activities of superoxide dismutase (SOD), catalase (CAT) and level of reduced glutathione (GSH), were notably reduced, while lipid peroxidation, expressed as malondialdhyde (MDA) level was significantly increased. Administration of curcumin (100mg/kg, I.P.) once daily for 5 consecutive days after MTX challenge mitigated the injurious effects of MTX and ameliorated all the altered biochemical parameters. These results showed that administration of curcumin decreases MTX-induced liver damage probably via regulation of oxidant/anti-oxidant balance. In conclusion, the present study indicates that curcumin may be of therapeutic benefit against MTX-cytotoxicity.

Current study on ionizing radiation-induced mitochondial DNA damage and mutations

International Nuclear Information System (INIS)

Zhou Xin; Wang Zhenhua; Zhang Hong

2012-01-01

Current advance in ionizing radiation-induced mitochondrial DNA damage and mutations is reviewed, in addition with the essential differences between mtDNA and nDNA damage and mutations. To extent the knowledge about radiation induced mitochondrial alterations, the researchers in Institute of Modern Physics, Chinese Academy of Sciences developed some technics such as real-time PCR, long-PCR for accurate quantification of radiation induced damage and mutations, and in-depth investigation about the functional changes of mitochondria based on mtDNA damage and mutations were also carried out. In conclusion, the important role of mitochondrial study in radiation biology is underlined, and further study on mitochondrial study associated with late effect and metabolism changes in radiation biology is pointed out. (authors)

Beam-induced damage to the Tevatron components and what has been done about it

International Nuclear Information System (INIS)

Mokhov, N.V.; Czarapata, P.C.; Drozhdin, A.I.; Still, D.A.; Samulyak, R.V.

2007-01-01

A beam-induced damage to the Tevatron collimators happened in December 2003 was induced by a failure in the CDF Roman Pot detector positioning during the collider run. Possible scenarios of this failure resulted in an excessive halo generation and superconducting magnet quench have been studied via realistic simulations using the STRUCT and MARS14 codes. It is shown that the interaction of a misbehaved proton beam with the collimators result in a rapid local heating and a possible damage. A detailed consideration is given to the ablation process for the collimator material taking place in high vacuum. It is shown that ablation of tungsten (primary collimator) and stainless steel (secondary collimator) jaws results in creation of a groove in the jaw surface as was observed after the December's accident. The actions undertaken to avoid such an accident in future are described in detail. (author)

Beam-induced damage to the Tevatron components and what has been done about it

International Nuclear Information System (INIS)

Mokhov, N.V.; Czarapata, P.C.; Drozhdin, A.I.; Still, D.A.; Samulyak, R.V.

2006-01-01

A beam-induced damage to the Tevatron collimators happened in December 2003 was induced by a failure in the CDF Roman Pot detector positioning during the collider run. Possible scenarios of this failure resulted in an excessive halo generation and superconducting magnet quench have been studied via realistic simulations using the STRUCT and MARS14 codes. It is shown that the interaction of a misbehaved proton beam with the collimators result in a rapid local heating and a possible damage. A detailed consideration is given to the ablation process for the collimator material taking place in high vacuum. It is shown that ablation of tungsten (primary collimator) and stainless steel (secondary collimator) jaws results in creation of a groove in the jaw surface as was observed after the December's accident. The actions undertaken to avoid such an accident in future are described in detail

Study of Surface Wear and Damage Induced by Dry Sliding of Tempered AISI 4140 Steel against Hardened AISI 1055 Steel

Directory of Open Access Journals (Sweden)

A. Elhadi

2016-12-01

Full Text Available In industry, the sliding mechanical systems are subject to friction and wear phenomena. These phenomena can be the origin of a reduction of the efficiency of the mechanical system even to be responsible for its incapacity. Generally, the materials of the parts which are moving relative (tribological couple of these systems are low alloy steels and carbon steels, thanks to their good mechanical and tribological properties. The present work aimed to study, the surface wear and damage induced by dry sliding of hard carbon steel AISI 1055 (disc against tempered low alloy steel AISI 4140 (pin with different hardness and applied loads was investigated. The results revealed that the interaction between the applied load and pin hardness result in complex thermo-mechanical behaviour of the worn surfaces. When a lower hardness pin is used, the main wear mechanisms observed on the discs were abrasion, adhesion, and oxidation. When a higher hardness pin is used, the wear of the discs is governed by delamination, oxidation, and plastic deformation. In particular, third-body wear occurs at high applied load resulting in higher wear rate of high hardness pins compared to low hardness pins.

Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture

Energy Technology Data Exchange (ETDEWEB)

Romano, M.; Razandi, M.; Ivey, K.J. (Long Beach VA Medical Center, CA (USA))

1990-04-01

The present study evaluated the effect of sucralfate and its components, sucrose octasulfate and aluminum hydroxide, on: (1) damage to rat cultured gastric mucosal cells induced by sodium taurocholate in a neutral environment and in conditions independent of systemic factors, (2) prostaglandin E2 and on 6-keto prostaglandin F1 alpha release by cultured cells, and (3) sulfhydryl content of cultured cells. Cell damage was quantitated by chromium-51 release assay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were measured by radioimmunoassay. Total sulfhydryl content of cultured cells was determined calorimetrically. Microscopically, sucralfate was found to adhere tightly to epithelial cell surfaces despite frequent washings. Sucralfate 2 mg/ml and 5 mg/ml significantly decreased taurocholate-induced damage, reducing taurocholate-induced specific 51Cr release by 11.8 points (equal to 29% decrease in cell damage, P less than 0.01) and 22.9 points (equal to 56% decrease in cell damage, P less than 0.001), respectively. Sucrose octasulfate and aluminum hydroxide did not exert significant protection against damage induced by sodium taurocholate. The protective effect of sucralfate was not prevented by indomethacin, nor was it counteracted by the sulfhydryl blocker, iodoacetamide. Sucralfate, but not its components, significantly and dose-dependently stimulated prostaglandin E2 (r = 0.94, P less than 0.05) and 6-keto prostaglandin F1 alpha (r = 0.89, P less than 0.05) production by cultured cells. Neither sucralfate nor its components affected sulfhydryl content of cultured cells. In conclusion, sucralfate, but not its components, (1) protects rat gastric mucosal cells against taurocholate-induced damage in conditions independent of systemic factors and in a neutral environment and (2) significantly stimulates prostaglandin production by cultured cells.

Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture

International Nuclear Information System (INIS)

Romano, M.; Razandi, M.; Ivey, K.J.

1990-01-01

The present study evaluated the effect of sucralfate and its components, sucrose octasulfate and aluminum hydroxide, on: (1) damage to rat cultured gastric mucosal cells induced by sodium taurocholate in a neutral environment and in conditions independent of systemic factors, (2) prostaglandin E2 and on 6-keto prostaglandin F1 alpha release by cultured cells, and (3) sulfhydryl content of cultured cells. Cell damage was quantitated by chromium-51 release assay. Prostaglandin E2 and 6-keto prostaglandin F1 alpha were measured by radioimmunoassay. Total sulfhydryl content of cultured cells was determined calorimetrically. Microscopically, sucralfate was found to adhere tightly to epithelial cell surfaces despite frequent washings. Sucralfate 2 mg/ml and 5 mg/ml significantly decreased taurocholate-induced damage, reducing taurocholate-induced specific 51Cr release by 11.8 points (equal to 29% decrease in cell damage, P less than 0.01) and 22.9 points (equal to 56% decrease in cell damage, P less than 0.001), respectively. Sucrose octasulfate and aluminum hydroxide did not exert significant protection against damage induced by sodium taurocholate. The protective effect of sucralfate was not prevented by indomethacin, nor was it counteracted by the sulfhydryl blocker, iodoacetamide. Sucralfate, but not its components, significantly and dose-dependently stimulated prostaglandin E2 (r = 0.94, P less than 0.05) and 6-keto prostaglandin F1 alpha (r = 0.89, P less than 0.05) production by cultured cells. Neither sucralfate nor its components affected sulfhydryl content of cultured cells. In conclusion, sucralfate, but not its components, (1) protects rat gastric mucosal cells against taurocholate-induced damage in conditions independent of systemic factors and in a neutral environment and (2) significantly stimulates prostaglandin production by cultured cells

Modelling of settlement induced building damage

NARCIS (Netherlands)

Giardina, G.

2013-01-01

This thesis focuses on the modelling of settlement induced damage to masonry buildings. In densely populated areas, the need for new space is nowadays producing a rapid increment of underground excavations. Due to the construction of new metro lines, tunnelling activity in urban areas is growing.

DNA damage-induced inflammation and nuclear architecture.

Science.gov (United States)

Stratigi, Kalliopi; Chatzidoukaki, Ourania; Garinis, George A

2017-07-01

Nuclear architecture and the chromatin state affect most-if not all- DNA-dependent transactions, including the ability of cells to sense DNA lesions and restore damaged DNA back to its native form. Recent evidence points to functional links between DNA damage sensors, DNA repair mechanisms and the innate immune responses. The latter raises the question of how such seemingly disparate processes operate within the intrinsically complex nuclear landscape and the chromatin environment. Here, we discuss how DNA damage-induced immune responses operate within chromatin and the distinct sub-nuclear compartments highlighting their relevance to chronic inflammation. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Ultraviolet radiation-induced interleukin 6 release in HeLa cells is mediated via membrane events in a DNA damage-independent way.

Science.gov (United States)

Kulms, D; Pöppelmann, B; Schwarz, T

2000-05-19

Evidence exists that ultraviolet radiation (UV) affects molecular targets in the nucleus or at the cell membrane. UV-induced apoptosis was found to be mediated via DNA damage and activation of death receptors, suggesting that nuclear and membrane effects are not mutually exclusive. To determine whether participation of nuclear and membrane components is also essential for other UV responses, we studied the induction of interleukin-6 (IL-6) by UV. Exposing HeLa cells to UV at 4 degrees C, which inhibits activation of surface receptors, almost completely prevented IL-6 release. Enhanced repair of UV-mediated DNA damage by addition of the DNA repair enzyme photolyase did not affect UV-induced IL-6 production, suggesting that in this case membrane events predominant over nuclear effects. UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release. Transfection with a dominant negative mutant of the signaling protein TRAF-2 reduced IL-6 release upon exposure to UV, indicating that UV-induced IL-6 release is mediated by activation of the tumor necrosis factor receptor-1. These data demonstrate that UV can exert biological effects mainly by affecting cell surface receptors and that this is independent of its ability to induce nuclear DNA damage.

Damage-induced DNA repair processes in Escherichia coli cells

International Nuclear Information System (INIS)

Slezarikova, V.

1986-01-01

The existing knowledge is summed up of the response of Escherichia coli cells to DNA damage due to various factors including ultraviolet radiation. So far, three inducible mechanisms caused by DNA damage are known, viz., SOS induction, adaptation and thermal shock induction. Greatest attention is devoted to SOS induction. Its mechanism is described and the importance of the lexA recA proteins is shown. In addition, direct or indirect role is played by other proteins, such as the ssb protein binding the single-strand DNA sections. The results are reported of a study of induced repair processes in Escherichia coli cells repeatedly irradiated with UV radiation. A model of induction by repeated cell irradiation discovered a new role of induced proteins, i.e., the elimination of alkali-labile points in the daughter DNA synthetized on a damaged model. The nature of the alkali-labile points has so far been unclear. In the adaptation process, regulation proteins are synthetized whose production is induced by the presence of alkylation agents. In the thermal shock induction, new proteins synthetize in cells, whose function has not yet been clarified. (E.S.)

A new surface fractal dimension for displacement mode shape-based damage identification of plate-type structures

Science.gov (United States)

Shi, Binkai; Qiao, Pizhong

2018-03-01

Vibration-based nondestructive testing is an area of growing interest and worthy of exploring new and innovative approaches. The displacement mode shape is often chosen to identify damage due to its local detailed characteristic and less sensitivity to surrounding noise. Requirement for baseline mode shape in most vibration-based damage identification limits application of such a strategy. In this study, a new surface fractal dimension called edge perimeter dimension (EPD) is formulated, from which an EPD-based window dimension locus (EPD-WDL) algorithm for irregularity or damage identification of plate-type structures is established. An analytical notch-type damage model of simply-supported plates is proposed to evaluate notch effect on plate vibration performance; while a sub-domain of notch cases with less effect is selected to investigate robustness of the proposed damage identification algorithm. Then, fundamental aspects of EPD-WDL algorithm in term of notch localization, notch quantification, and noise immunity are assessed. A mathematical solution called isomorphism is implemented to remove false peaks caused by inflexions of mode shapes when applying the EPD-WDL algorithm to higher mode shapes. The effectiveness and practicability of the EPD-WDL algorithm are demonstrated by an experimental procedure on damage identification of an artificially-induced notched aluminum cantilever plate using a measurement system of piezoelectric lead-zirconate (PZT) actuator and scanning laser Doppler vibrometer (SLDV). As demonstrated in both the analytical and experimental evaluations, the new surface fractal dimension technique developed is capable of effectively identifying damage in plate-type structures.

Clustered DNA damage induced by proton and heavy ion irradiation

International Nuclear Information System (INIS)

Davidkova, M.; Pachnerova Brabcova, K; Stepan, V.; Vysin, L.; Sihver, L.; Incerti, S.

2014-01-01

Ionizing radiation induces in DNA strand breaks, damaged bases and modified sugars, which accumulate with increasing density of ionizations in charged particle tracks. Compared to isolated DNA damage sites, the biological toxicity of damage clusters can be for living cells more severe. We investigated the clustered DNA damage induced by protons (30 MeV) and high LET radiation (C 290 MeV/u and Fe 500 MeV/u) in pBR322 plasmid DNA. To distinguish between direct and indirect pathways of radiation damage, the plasmid was irradiated in pure water or in aqueous solution of one of the three scavengers (coumarin-3-carboxylic acid, dimethylsulfoxide, and glycylglycine). The goal of the contribution is the analysis of determined types of DNA damage in dependence on radiation quality and related contribution of direct and indirect radiation effects. The yield of double strand breaks (DSB) induced in the DNA plasmid-scavenger system by heavy ion radiation was found to decrease with increasing scavenging capacity due to reaction with hydroxyl radical, linearly with high correlation coefficients. The yield of non-DSB clusters was found to occur twice as much as the DSB. Their decrease with increasing scavenging capacity had lower linear correlation coefficients. This indicates that the yield of non-DSB clusters depends on more factors, which are likely connected to the chemical properties of individual scavengers. (authors)

Study on DNA damages induced by UV radiation

International Nuclear Information System (INIS)

Doan Hong Van; Dinh Ba Tuan; Tran Tuan Anh; Nguyen Thuy Ngan; Ta Bich Thuan; Vo Thi Thuong Lan; Tran Minh Quynh; Nguyen Thi Thom

2015-01-01

DNA damages in Escherichia coli (E. coli) exposed to UV radiation have been investigated. After 30 min of exposure to UV radiation of 5 mJ/cm"2, the growth of E. coli in LB broth medium was about only 10% in compared with non-irradiated one. This results suggested that the UV radiation caused the damages for E. coli genome resulted in reduction in its growth and survival, and those lesions can be somewhat recovered. For both solutions of plasmid DNAs and E. coli cells containing plasmid DNA, this dose also caused the breakage on single and double strands of DNA, shifted the morphology of DNA plasmid from supercoiled to circular and linear forms. The formation of pyrimidine dimers upon UV radiation significantly reduced when the DNA was irradiated in the presence of Ganoderma lucidum extract. Thus, studies on UV-induced DNA damage at molecular level are very essential to determine the UV radiation doses corresponding to the DNA damages, especially for creation and selection of useful radiation-induced mutants, as well as elucidation the protective effects of the specific compounds against UV light. (author)

UV-induced skin damage

International Nuclear Information System (INIS)

Ichihashi, M.; Ueda, M.; Budiyanto, A.; Bito, T.; Oka, M.; Fukunaga, M.; Tsuru, K.; Horikawa, T.

2003-01-01

Solar radiation induces acute and chronic reactions in human and animal skin. Chronic repeated exposures are the primary cause of benign and malignant skin tumors, including malignant melanoma. Among types of solar radiation, ultraviolet B (290-320 nm) radiation is highly mutagenic and carcinogenic in animal experiments compared to ultraviolet A (320-400 nm) radiation. Epidemiological studies suggest that solar UV radiation is responsible for skin tumor development via gene mutations and immunosuppression, and possibly for photoaging. In this review, recent understanding of DNA damage caused by direct UV radiation and by indirect stress via reactive oxygen species (ROS) and DNA repair mechanisms, particularly nucleotide excision repair of human cells, are discussed. In addition, mutations induced by solar UV radiation in p53, ras and patched genes of non-melanoma skin cancer cells, and the role of ROS as both a promoter in UV-carcinogenesis and an inducer of UV-apoptosis, are described based primarily on the findings reported during the last decade. Furthermore, the effect of UV on immunological reaction in the skin is discussed. Finally, possible prevention of UV-induced skin cancer by feeding or topical use of antioxidants, such as polyphenols, vitamin C, and vitamin E, is discussed

Modelling low velocity impact induced damage in composite laminates

Science.gov (United States)

Shi, Yu; Soutis, Constantinos

2017-12-01

The paper presents recent progress on modelling low velocity impact induced damage in fibre reinforced composite laminates. It is important to understand the mechanisms of barely visible impact damage (BVID) and how it affects structural performance. To reduce labour intensive testing, the development of finite element (FE) techniques for simulating impact damage becomes essential and recent effort by the composites research community is reviewed in this work. The FE predicted damage initiation and propagation can be validated by Non Destructive Techniques (NDT) that gives confidence to the developed numerical damage models. A reliable damage simulation can assist the design process to optimise laminate configurations, reduce weight and improve performance of components and structures used in aircraft construction.

Ion-induced damage and amorphization in Si

International Nuclear Information System (INIS)

Holland, O.W.; White, C.W.

1990-01-01

Ion-induced damage growth in high-energy, self-ion irradiated Si was studied using electron microscopy and Rutherford backscattering spectroscopy. The results show that there is a marked variation in the rate of damage growth, as well as the damage morphology, along the path of the ion. Near the ion end-of-range (eor), damage increases monotonically with ion fluence until a buried amorphous layer is formed, while damage growth saturates at a low level in the region ahead. The morphology of the damage in the saturated region is shown to consist predominantly of simple defect clusters such as the divacancy. Damage growth remains saturated ahead of the eor until expansion of the buried amorphous layer encroaches into the region. A homogeneous growth model is presented which accounts for damage saturation, and accurately predicts the dose-rate dependence of the saturation level. Modifications of the model are discussed which are needed to account for the rapid growth in the eor region and near the interface of the buried amorphous layer. Two important factors contributing to rapid damage growth are identified. Spatial separation of the Frenkel defect pairs (i.e. interstitials and vacancies) due to the momentum of the interstitials is shown to greatly impact damage growth near the eor, while uniaxial strain in the interfacial region of the amorphous layer is identified as an important factor contributing to growth at that location. 20 refs., 10 figs

2-Aminopurine hairpin probes for the detection of ultraviolet-induced DNA damage

International Nuclear Information System (INIS)

El-Yazbi, Amira F.; Loppnow, Glen R.

2012-01-01

Highlights: ► Molecular beacon with 2AP bases detects DNA damage in a simple mix-and-read assay. ► Molecular beacons with 2AP bases detect damage at a 17.2 nM limit of detection. ► The 2AP molecular beacon is linear over a 0–3.5 μM concentration range for damage. - Abstract: Nucleic acid exposure to radiation and chemical insults leads to damage and disease. Thus, detection and understanding DNA damage is important for elucidating molecular mechanisms of disease. However, current methods of DNA damage detection are either time-consuming, destroy the sample, or are too specific to be used for generic detection of damage. In this paper, we develop a fluorescence sensor of 2-aminopurine (2AP), a fluorescent analogue of adenine, incorporated in the loop of a hairpin probe for the quantification of ultraviolet (UV) C-induced nucleic acid damage. Our results show that the selectivity of the 2AP hairpin probe to UV-induced nucleic acid damage is comparable to molecular beacon (MB) probes of DNA damage. The calibration curve for the 2AP hairpin probe shows good linearity (R 2 = 0.98) with a limit of detection of 17.2 nM. This probe is a simple, fast and economic fluorescence sensor for the quantification of UV-induced damage in DNA.

Radiation induced genetic damage in Aspergillus nidulans

International Nuclear Information System (INIS)

Georgiou, J.T.

1984-01-01

The mechanism by which ionizing radiation induces genetic damage in haploid and diploid conidia of Aspergillus nidulans was investigated. Although the linear dose-response curves obtained following low LET irradiation implied a 'single-hit' action of radiation, high LET radiations were much more efficient than low LET radiations, which suggests the involvement of a multiple target system. It was found that the RBE values for non-disjunction and mitotic crossing-over were very different. Unlike mitotic crossing-over, the RBE values for non-disjunction were much greater than for cell killing. This suggests that non-disjunction is a particularly sensitive genetical endpoint that is brought about by damage to a small, probably non-DNA target. Radiosensitisers were used to study whether radiation acts at the level of the DNA or some other cellular component. The sensitisation to electrons and/or X-rays by oxygen, and two nitroimidazoles (metronidazole and misonidazole) was examined for radiation induced non-disjunction, mitotic crossing-over, gene conversion, point mutation and cell killing. It was found that these compounds sensitised the cells considerably more to genetic damage than to cell killing. (author)

Preventing Ultraviolet Light-Induced Damage: The Benefits of Antioxidants

Science.gov (United States)

Yip, Cheng-Wai

2007-01-01

Extracts of fruit peels contain antioxidants that protect the bacterium "Escherichia coli" against damage induced by ultraviolet light. Antioxidants neutralise free radicals, thus preventing oxidative damage to cells and deoxyribonucleic acid. A high survival rate of UV-exposed cells was observed when grapefruit or grape peel extract was…

The ovarian DNA damage repair response is induced prior to phosphoramide mustard-induced follicle depletion, and ataxia telangiectasia mutated inhibition prevents PM-induced follicle depletion

Energy Technology Data Exchange (ETDEWEB)

Ganesan, Shanthi, E-mail: shanthig@iastate.edu; Keating, Aileen F., E-mail: akeating@iastate.edu

2016-02-01

Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide and destroys primordial and primary follicles potentially by DNA damage induction. The temporal pattern by which PM induces DNA damage and initiation of the ovarian response to DNA damage has not yet been well characterized. This study investigated DNA damage initiation, the DNA repair response, as well as induction of follicular demise using a neonatal rat ovarian culture system. Additionally, to delineate specific mechanisms involved in the ovarian response to PM exposure, utility was made of PKC delta (PKCδ) deficient mice as well as an ATM inhibitor (KU 55933; AI). Fisher 344 PND4 rat ovaries were cultured for 12, 24, 48 or 96 h in medium containing DMSO ± 60 μM PM or KU 55933 (48 h; 10 nM). PM-induced activation of DNA damage repair genes was observed as early as 12 h post-exposure. ATM, PARP1, E2F7, P73 and CASP3 abundance were increased but RAD51 and BCL2 protein decreased after 96 h of PM exposure. PKCδ deficiency reduced numbers of all follicular stages, but did not have an additive impact on PM-induced ovotoxicity. ATM inhibition protected all follicle stages from PM-induced depletion. In conclusion, the ovarian DNA damage repair response is active post-PM exposure, supporting that DNA damage contributes to PM-induced ovotoxicity. - Highlights: • PM exposure induces DNA damage repair gene expression. • Inhibition of ATM prevented PM-induced follicle depletion. • PKCδ deficiency did not impact PM-induced ovotoxicity.

Myostatin as a Marker for Doxorubicin Induced Cardiac Damage.

Science.gov (United States)

Kesik, Vural; Honca, Tevfik; Gulgun, Mustafa; Uysal, Bulent; Kurt, Yasemin Gulcan; Cayci, Tuncer; Babacan, Oguzhan; Gocgeldi, Ercan; Korkmazer, Nadir

2016-01-01

Doxorubicin (DXR) is an effective chemotherapeutic agent but causes severe cardiac failure over known doses. Thus, early detection and prevention of cardiac damage is important. Various markers have been tested for early detection of cardiac damage. Myostatin is a protein produced in skeletal muscle cells inhibits muscle differentiation and growth during myogenesis. We evaluated the role of myostatin as a marker for showing DXR induced cardiac damage and compared with well known cardiac markers like NT-proBNP, hs-TnT and CK in a rat model of chronic DXR cardiotoxicity. Myostatin, NT-proBNP, and hs-TnT but not CK rose significantly during DXR treatment. Myostatin can be used as an early marker of DXR induced cardiotoxicity. © 2016 by the Association of Clinical Scientists, Inc.

Surface Damage Mechanism of Monocrystalline Si Under Mechanical Loading

Science.gov (United States)

Zhao, Qingliang; Zhang, Quanli; To, Suet; Guo, Bing

2017-03-01

Single-point diamond scratching and nanoindentation on monocrystalline silicon wafer were performed to investigate the surface damage mechanism of Si under the contact loading. The results showed that three typical stages of material removal appeared during dynamic scratching, and a chemical reaction of Si with the diamond indenter and oxygen occurred under the high temperature. In addition, the Raman spectra of the various points in the scratching groove indicated that the Si-I to β-Sn structure (Si-II) and the following β-Sn structure (Si-II) to amorphous Si transformation appeared under the rapid loading/unloading condition of the diamond grit, and the volume change induced by the phase transformation resulted in a critical depth (ductile-brittle transition) of cut (˜60 nm ± 15 nm) much lower than the theoretical calculated results (˜387 nm). Moreover, it also led to abnormal load-displacement curves in the nanoindentation tests, resulting in the appearance of elbow and pop-out effects (˜270 nm at 20 s, 50 mN), which were highly dependent on the loading/unloading conditions. In summary, phase transformation of Si promoted surface deformation and fracture under both static and dynamic mechanical loading.

NDE of Damage in Aircraft Flight Control Surfaces

International Nuclear Information System (INIS)

Hsu, David K.; Barnard, Daniel J.; Dayal, Vinay

2007-01-01

Flight control surfaces on an aircraft, such as ailerons, flaps, spoilers and rudders, are typically adhesively bonded composite or aluminum honeycomb sandwich structures. These components can suffer from damage caused by hail stone, runway debris, or dropped tools during maintenance. On composites, low velocity impact damages can escape visual inspection, whereas on aluminum honeycomb sandwich, budding failure of the honeycomb core may or may not be accompanied by a disbond. This paper reports a study of the damage morphology in such structures and the NDE methods for detecting and characterizing them. Impact damages or overload failures in composite sandwiches with Nomex or fiberglass core tend to be a fracture or crinkle or the honeycomb cell wall located a distance below the facesheet-to-core bondline. The damage in aluminum honeycomb is usually a buckling failure, propagating from the top skin downward. The NDE methods used in this work for mapping out these damages were: air-coupled ultrasonic scan, and imaging by computer aided tap tester. Representative results obtained from the field will be shown

Gravity-induced rock mass damage related to large en masse rockslides: Evidence from Vajont

Science.gov (United States)

Paronuzzi, Paolo; Bolla, Alberto

2015-04-01

The Vajont landslide is a well-known, reservoir-induced slope failure that occurred on 9 October 1963 and was characterized by an 'en masse' sliding motion that triggered various large waves, determining catastrophic consequences for the nearby territory and adjacent villages. During the Vajont dam construction, and especially after the disaster, some researchers identified widespread field evidence of heavy rock mass damage involving the presumed prehistoric rockslide and/or the 1963 failed mass. This paper describes evidence of heavy gravitational damage, including (i) folding, (ii) fracturing, (iii) faulting, and (iv) intact rock disintegration. The gravity-induced rock mass damage (GRMD) characterizes the remnants of the basal shear zone, still resting on the large detachment surface, and the 1963 failed rock mass. The comprehensive geological study of the 1963 Vajont landslide, based on the recently performed geomechanical survey (2006-present) and on the critical analysis of the past photographic documentation (1959-1964), allows us to recognize that most GRMD evidence is related to the prehistoric multistage Mt. Toc rockslide. The 1963 catastrophic en masse remobilization induced an increase to the prehistoric damage, reworking preexisting structures and creating additional gravity-driven features (folds, fractures, faults, and rock fragmentation). The gravity-induced damage was formed during the slope instability phases that preceded the collapse (static or quasi-static GRMD) and also as a consequence of the sliding motion and of the devastating impact between the failed blocks (dynamic GRMD). Gravitational damage originated various types of small drag folds such as flexures, concentric folds, chevron, and kink-box folds, all having a radius of 1-5 m. Large buckle folds (radius of 10-50 m) are related to the dynamic damage and were formed during the en masse motion as a consequence of deceleration and impact processes that involved the sliding mass. Prior

Micro-mechanisms of Surface Defects Induced on Aluminum Alloys during Plastic Deformation at Elevated Temperatures

Science.gov (United States)

Gali, Olufisayo A.

Near-surface deformed layers developed on aluminum alloys significantly influence the corrosion and tribological behavior as well as reduce the surface quality of the rolled aluminum. The evolution of the near-surface microstructures induced on magnesium containing aluminum alloys during thermomechanical processing has been investigated with the aim generating an understanding of the influence of individual forming parameters on its evolution and examine the microstructure of the roll coating induced on the mating steel roll through material transfer during rolling. The micro-mechanisms related to the various features of near-surface microstructure developed during tribological conditions of the simulated hot rolling process were identified. Thermomechanical processing experiments were performed with the aid of hot rolling (operating temperature: 550 to 460 °C, 4, 10 and 20 rolling pass schedules) and hot forming (operating temperature: 350 to 545 °C, strain rate: 4 x 10-2 s-1) tribo-simulators. The surface, near-surface features and material transfer induced during the elevated temperature plastic deformation were examined and characterized employing optical interferometry, SEM/EDS, FIB and TEM. Near-surface features characterized on the rolled aluminum alloys included; cracks, fractured intermetallic particles, aluminum nano-particles, oxide decorated grain boundaries, rolled-in oxides, shingles and blisters. These features were related to various individual rolling parameters which included, the work roll roughness, which induced the formation of shingles, rolling marks and were responsible for the redistribution of surface oxide and the enhancements of the depth of the near-surface damage. The enhanced stresses and strains experienced during rolling were related to the formation and propagation of cracks, the nanocrystalline structure of the near-surface layers and aluminum nano-particles. The mechanism of the evolution of the near-surface microstructure were

Surface-structure dependence of healing radiation-damage mechanism in nanoporous tungsten

Science.gov (United States)

Duan, Guohua; Li, Xiangyan; Sun, Jingjing; Hao, Congyu; Xu, Yichun; Zhang, Yange; Liu, Wei; Liu, C. S.

2018-01-01

Under nuclear fusion environments, displacement damage in tungsten (W) is usually caused by neutrons irradiation through producing large quantities of vacancies (Vs) and self-interstitial atoms (SIAs). These defects not only affect the mechanical properties of W, but also act as the trap sites for implanted hydrogen isotopes and helium. Nano-porous (NP) W with a high fraction of free surfaces has been developed to mitigate the radiation damage. However, the mechanism of the surface reducing defects accumulation is not well understood. By using multi-scale simulation methods, we investigated the interaction of the SIA and V with different surfaces on across length and time scales. We found that, at a typical operation temperature of 1000 K, surface (1 1 0) preferentially heals radiation damage of W compared with surface (1 0 0) and boundary (3 1 0). On surface (1 1 0), the diffusion barrier for the SIA is only 0.68 eV. The annihilation of the SIA-V happens via the coupled motion of the V segregation towards the surface from the bulk and the two-dimensional diffusion of the SIA on the surface. Such mechanism makes the surface (1 1 0) owe better healing capability. On surface (1 0 0), the diffusion energy barrier for the SIA is 2.48 eV, higher than the diffusion energy barrier of the V in bulk. The annihilation of the SIA-V occurs via the V segregation and recombination. The SIA was found to migrate one-dimensionally along a boundary (3 1 0) with a barrier of 0.21 eV, leading to a lower healing efficiency in the boundary. This study suggested that the on-surface process plays an important role in healing radiation damage of NP W in addition to surface-enhanced diffusion and annihilation near the surface. A certain surface structure renders nano-structured W more radiation-tolerant.

Damage to underground coal mines caused by surface blasting

International Nuclear Information System (INIS)

Fourie, A.B.; Green, R.W.

1993-01-01

An investigation of the potential damage to underground coal workings as a result of surface blasting at an opencast coal mine is described. Seismometers were installed in a worked out area of an underground mine, in the eastern Transvaal region of South Africa, and the vibration caused by nearby surface blasting recorded. These measurements were used to derive peak particle velocities. These velocities were correlated with observed damage underground in order to establish the allowable combination of the two blasting parameters of charge mass per relay, and blast-to-gage point distance. An upper limit of 110mm/sec peak particle velocity was found to be sufficient to ensure that the damage to the particular workings under consideration was minimal. It was further found that a cube-root scaling law provided a better fit to the field data than the common square-root law. 11 refs., 6 figs., 5 tabs

Characterization of the damage produced on different materials surfaces

International Nuclear Information System (INIS)

Dellavale Clara, Hector Damian

2004-01-01

In the present work the characterization techniques of surfaces ULOI and RIMAPS have been applied on laboratory samples made from aluminium, stainless steel and material based on fiberglass.The resultant surfaces of, chemical etching with corrosive agents Keller and Tucker, mechanic damage from the wear and tear of abrasive paper and sandrubbing with alumina particles, are analyzed to different level of damage.The systematic application of the above mentioned techniques is carried out with the objective of finding information, which allows to characterize the superficial damage, both in its incipient state as in the extreme situation revealed by the presence of etch pits. Important results have been obtained, in the characterization of the incipient stage of the chemical etching, using the curves of the normalized area.In addition, it was possible to verify the capacity of the techniques in the early detection of the preferential directions generated by the etch pits

Stress response of Escherichia coli induced by surface streamer discharge in humid air

International Nuclear Information System (INIS)

Doležalová, Eva; Prukner, Václav; Lukeš, Petr; Šimek, Milan

2016-01-01

Inactivation of Escherichia coli by means of surface streamer discharge has been investigated to obtain new insights into the key mechanisms involved, with a particular emphasis placed on the microbial response to plasma-induced stress. The surface streamer discharge was produced in coplanar dielectric barrier discharge electrode geometry, and was driven by an amplitude-modulated ac high voltage in humid synthetic air at atmospheric pressure. The response to plasma-induced stress was evaluated by using conventional cultivation, sublethal injury and resazurin assay and the LIVE/DEAD ® BacLight ™ Bacterial Viability kit. Compared to conventional cultivation, the LIVE/DEAD ® test labels bacteria with damaged membranes, while resazurin assay tracks their metabolic activity. Our results clearly demonstrate that the treated bacteria partly lost their ability to grow properly, i.e. they became injured and culturable, or even viable but nonculturable (VBNC). The ability to develop colonies could have been lost due to damage of the bacterial membrane. Damage of the membranes was mainly caused by the lipid peroxidation, evidencing the key role of oxygen reactive species, in particular ozone. We conclude that the conventional cultivation method overestimates the decontamination efficiency of various plasma sources, and must therefore be complemented by alternative techniques capable of resolving viable but nonculturable bacteria. (paper)

Photoexcited riboflavin induces oxidative damage to human serum albumin

Science.gov (United States)

Hirakawa, Kazutaka; Yoshioka, Takuto

2015-08-01

Photoexcited riboflavin induced damage of human serum albumin (HSA), a water soluble protein, resulting in the diminishment of fluorescence from the tryptophan residue. Because riboflavin hardly photosensitized singlet oxygen generation and sodium azide, a singlet oxygen quencher, did not inhibit protein damage, electron transfer-mediated oxidation of HSA was speculated. Fluorescence lifetime of riboflavin was not affected by HSA, suggesting that the excited triplet state of riboflavin is responsible for protein damage through electron transfer. In addition, the preventive effect of xanthone derivatives, triplet quenchers, on photosensitized protein damage could be evaluated using this photosensitized reaction system of riboflavin and HSA.

Processing of radiation-induced clustered DNA damage generates DSB in mammalian cells

International Nuclear Information System (INIS)

Gulston, M.K.; De Lara, C.M.; Davis, E.L.; Jenner, T.J.; O'Neill, P.

2003-01-01

Full text: Clustered DNA damage sites, in which two or more lesions are formed within a few helical turns of the DNA after passage of a single radiation track, are signatures of DNA modifications induced by ionizing radiation in mammalian cell. With 60 Co-radiation, the abundance of clustered DNA damage induced in CHO cells is ∼4x that of prompt double strand breaks (DSB) determined by PFGE. Less is known about the processing of non-DSB clustered DNA damage induced in cells. To optimize observation of any additional DSB formed during processing of DNA damage at 37 deg C, xrs-5 cells deficient in non-homologous end joining were used. Surprisingly, ∼30% of the DSB induced by irradiation at 37 deg C are rejoined within 4 minutes in both mutant and wild type cells. No significant mis-repair of these apparent DSB was observed. It is suggested that a class of non-DSB clustered DNA damage is formed which repair correctly within 4 min but, if 'trapped' prior to repair, are converted into DSB during the lysis procedure of PFGE. However at longer times, a proportion of non-DSB clustered DNA damage sites induced by γ-radiation are converted into DSB within ∼30 min following post-irradiation incubation at 37 deg C. The corresponding formation of additional DSB was not apparent in wild type CHO cells. From these observations, it is estimated that only ∼10% of the total yield of non DSB clustered DNA damage sites are converted into DSB through cellular processing. The biological consequences that the majority of non-DSB clustered DNA damage sites are not converted into DSBs may be significant even at low doses, since a finite chance exists of these clusters being formed in a cell by a single radiation track

Plasmid DNA damage induced by helium atmospheric pressure plasma jet

Science.gov (United States)

Han, Xu; Cantrell, William A.; Escobar, Erika E.; Ptasinska, Sylwia

2014-03-01

A helium atmospheric pressure plasma jet (APPJ) is applied to induce damage to aqueous plasmid DNA. The resulting fractions of the DNA conformers, which indicate intact molecules or DNA with single- or double-strand breaks, are determined using agarose gel electrophoresis. The DNA strand breaks increase with a decrease in the distance between the APPJ and DNA samples under two working conditions of the plasma source with different parameters of applied electric pulses. The damage level induced in the plasmid DNA is also enhanced with increased plasma irradiation time. The reactive species generated in the APPJ are characterized by optical emission spectra, and their roles in possible DNA damage processes occurring in an aqueous environment are also discussed.

Damage to cellular and isolated DNA induced by a metabolite of aspirin

Energy Technology Data Exchange (ETDEWEB)

Oikawa, Shinji [Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Mie 514-8507 (Japan)], E-mail: s-oikawa@doc.medic.mie-u.ac.jp; Kobayashi, Hatasu; Tada-Oikawa, Saeko [Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Mie 514-8507 (Japan); JSPS Research Fellow (Japan); Isono, Yoshiaki [Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Mie 514-8507 (Japan); Kawanishi, Shosuke [Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Mie 514-8507 (Japan); Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie 513-8670 (Japan)

2009-02-10

Aspirin has been proposed as a possible chemopreventive agent. On the other hand, a recent cohort study showed that aspirin may increase the risk for pancreatic cancer. To clarify whether aspirin is potentially carcinogenic, we investigated the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), which is correlated with the incidence of cancer, in cultured cells treated with 2,3-dihydroxybenzoic acid (2,3-DHBA), a metabolite of aspirin. 2,3-DHBA induced 8-oxodG formation in the PANC-1 human pancreatic cancer cell line. 2,3-DHBA-induced DNA single-strand breaks were also revealed by comet assay using PANC-1 cells. Flow cytometric analyses showed that 2,3-DHBA increased the levels of intracellular reactive oxygen species (ROS) in PANC-1 cells. The 8-oxodG formation and ROS generation were also observed in the HL-60 leukemia cell line, but not in the hydrogen peroxide (H{sub 2}O{sub 2})-resistant clone HP100 cells, suggesting the involvement of H{sub 2}O{sub 2}. In addition, an hprt mutation assay supported the mutagenicity of 2,3-DHBA. We investigated the mechanism underlying the 2,3-DHBA-induced DNA damage using {sup 32}P-labeled DNA fragments of human tumor suppressor genes. 2,3-DHBA induced DNA damage in the presence of Cu(II) and NADH. DNA damage induced by 2,3-DHBA was enhanced by the addition of histone peptide-6 [AKRHRK]. Interestingly, 2,3-DHBA and histone peptide-6 caused base damage in the 5'-ACG-3' and 5'-CCG-3' sequences, hotspots of the p53 gene. Bathocuproine, a Cu(I) chelator, and catalase inhibited the DNA damage. Typical hydroxyl radical scavengers did not inhibit the DNA damage. These results suggest that ROS derived from the reaction of H{sub 2}O{sub 2} with Cu(I) participate in the DNA damage. In conclusion, 2,3-DHBA induces oxidative DNA damage and mutations, which may result in carcinogenesis.

Damage to cellular and isolated DNA induced by a metabolite of aspirin

International Nuclear Information System (INIS)

Oikawa, Shinji; Kobayashi, Hatasu; Tada-Oikawa, Saeko; Isono, Yoshiaki; Kawanishi, Shosuke

2009-01-01

Aspirin has been proposed as a possible chemopreventive agent. On the other hand, a recent cohort study showed that aspirin may increase the risk for pancreatic cancer. To clarify whether aspirin is potentially carcinogenic, we investigated the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), which is correlated with the incidence of cancer, in cultured cells treated with 2,3-dihydroxybenzoic acid (2,3-DHBA), a metabolite of aspirin. 2,3-DHBA induced 8-oxodG formation in the PANC-1 human pancreatic cancer cell line. 2,3-DHBA-induced DNA single-strand breaks were also revealed by comet assay using PANC-1 cells. Flow cytometric analyses showed that 2,3-DHBA increased the levels of intracellular reactive oxygen species (ROS) in PANC-1 cells. The 8-oxodG formation and ROS generation were also observed in the HL-60 leukemia cell line, but not in the hydrogen peroxide (H 2 O 2 )-resistant clone HP100 cells, suggesting the involvement of H 2 O 2 . In addition, an hprt mutation assay supported the mutagenicity of 2,3-DHBA. We investigated the mechanism underlying the 2,3-DHBA-induced DNA damage using 32 P-labeled DNA fragments of human tumor suppressor genes. 2,3-DHBA induced DNA damage in the presence of Cu(II) and NADH. DNA damage induced by 2,3-DHBA was enhanced by the addition of histone peptide-6 [AKRHRK]. Interestingly, 2,3-DHBA and histone peptide-6 caused base damage in the 5'-ACG-3' and 5'-CCG-3' sequences, hotspots of the p53 gene. Bathocuproine, a Cu(I) chelator, and catalase inhibited the DNA damage. Typical hydroxyl radical scavengers did not inhibit the DNA damage. These results suggest that ROS derived from the reaction of H 2 O 2 with Cu(I) participate in the DNA damage. In conclusion, 2,3-DHBA induces oxidative DNA damage and mutations, which may result in carcinogenesis

Impact induced damage assessment by means of Lamb wave image processing

Science.gov (United States)

Kudela, Pawel; Radzienski, Maciej; Ostachowicz, Wieslaw

2018-03-01

The aim of this research is an analysis of full wavefield Lamb wave interaction with impact-induced damage at various impact energies in order to find out the limitation of the wavenumber adaptive image filtering method. In other words, the relation between impact energy and damage detectability will be shown. A numerical model based on the time domain spectral element method is used for modeling of Lamb wave propagation and interaction with barely visible impact damage in a carbon-epoxy laminate. Numerical studies are followed by experimental research on the same material with an impact damage induced by various energy and also a Teflon insert simulating delamination. Wavenumber adaptive image filtering and signal processing are used for damage visualization and assessment for both numerical and experimental full wavefield data. It is shown that it is possible to visualize and assess the impact damage location, size and to some extent severity by using the proposed technique.

Excision of x-ray-induced thymine damage in chromatin from heated cells

International Nuclear Information System (INIS)

Warters, R.L.; Roti Roti, J.L.

1979-01-01

Experiments were performed to distinguish between two possible modes of hyperthermia-induced inhibition of thymine base damage excision from the DNA of CHO cells: (1) heat denaturation of excision enzyme(s) or (2) heat-induced alteration of the substrate for damage excision (chromatin). While hyperthermia (45 0 C, 15 min) had no apparent effect on the capacity of the excision enzymes to excise damage from DNA it had a dramatic effect (ca. 80% inhibition) on the ability of chromatin to serve as a substrate for unheated enzymes. These results suggest that hyperthermia-induced radiosensitization of CHO cells may be due primarily to lesions in the cellular chromatin

Graphite surface topography induced by Ta cluster impact and oxidative etching

International Nuclear Information System (INIS)

Reimann, C.T.; Olsson, L.; Erlandsson, R.; Henkel, M.; Urbassek, H.M.

1998-01-01

Freshly cleaved highly oriented pyrolytic graphite (HOPG), when baked in air at ∝630 C, forms one-monolayer(ML)-deep circular pits due to oxidation initiated at surface defect sites. We found that the areal density and depths of these pits could be modulated by deliberately introducing surface and sub-surface defects by energetic ion bombardment prior to baking. Bombardment by 555-eV/atom Ta 1 + , Ta 2 + , Ta 4 + , or Ta 9 + , always enhanced the areal density of etch pits, but only bombardment by Ta 4 + , or Ta 9 + significantly enhanced the depths of the pits. We performed molecular dynamics simulations of Ta n cluster bombardment of HOPG (n = 1, 2, 4, and 9) with the aim of characterizing the damage structures induced by the bombardment and correlating them with the experimental data. For Ta 9 + , the simulations showed a high level of damage extending from the surface down to nine MLs, in agreement with the most probable etch pit depth observed. For other cluster species, predicted etch pit depths were deeper than the observed ones. Annealing or steric requirements for initiating oxidation may account for some of the differences between simulations and experimental results. (orig.)

Effect of Mercuric Nitrate on Repair of Radiation-induced DNA Damage

Energy Technology Data Exchange (ETDEWEB)

Paneka, Agnieszka; Antonina, Cebulska Wasilewska [The Henryk Niewodniczanski Institute of Nuclear Physics, Krakow (Poland); Han, Min; Kim, Jin Kyu [Korea Atomic Energy Research Institute, Jeongeup (Korea, Republic of)

2009-10-15

High concentrations of mercury can cause serious damage to the nervous system, immune system, kidneys and liver in humans. And mercury is toxic to developing embryos because mercury ions can penetrate the blood.placenta barrier to reach the embryo. Studies from human monitoring of occupational exposure to mercury vapours have shown that mercury can alter the ability of lymphocytes to repair radiation-induced DNA damage. The aim of this in vitro study was to investigate, on the molecular and cytogenetic levels, the effect of exposure to mercury ions on the kinetics of the repair process of DNA damage induced by ionising radiation.

Organic honey supplementation reverses pesticide-induced genotoxicity by modulating DNA damage response.

Science.gov (United States)

Alleva, Renata; Manzella, Nicola; Gaetani, Simona; Ciarapica, Veronica; Bracci, Massimo; Caboni, Maria Fiorenza; Pasini, Federica; Monaco, Federica; Amati, Monica; Borghi, Battista; Tomasetti, Marco

2016-10-01

Glyphosate (GLY) and organophosphorus insecticides such as chlorpyrifos (CPF) may cause DNA damage and cancer in exposed individuals through mitochondrial dysfunction. Polyphenols ubiquitously present in fruits and vegetables, have been viewed as antioxidant molecules, but also influence mitochondrial homeostasis. Here, honey containing polyphenol compounds was evaluated for its potential protective effect on pesticide-induced genotoxicity. Honey extracts from four floral organic sources were evaluated for their polyphenol content, antioxidant activity, and potential protective effects on pesticide-related mitochondrial destabilization, reactive oxygen and nitrogen species formation, and DNA damage response in human bronchial epithelial and neuronal cells. The protective effect of honey was, then evaluated in a residential population chronically exposed to pesticides. The four honey types showed a different polyphenol profile associated with a different antioxidant power. The pesticide-induced mitochondrial dysfunction parallels ROS formation from mitochondria (mtROS) and consequent DNA damage. Honey extracts efficiently inhibited pesticide-induced mtROS formation, and reduced DNA damage by upregulation of DNA repair through NFR2. Honey supplementation enhanced DNA repair activity in a residential population chronically exposed to pesticides, which resulted in a marked reduction of pesticide-induced DNA lesions. These results provide new insight regarding the effect of honey containing polyphenols on pesticide-induced DNA damage response. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Laser-induced damage to thin film dielectric coatings

International Nuclear Information System (INIS)

Walker, T.W.

1980-01-01

The laser-induced damage thresholds of dielectric thin film coatings have been found to be more than an order of magnitude lower than the bulk material damage thresholds. Prior damage studies have been inconclusive in determining the damage mechanism which is operative in thin films. A program was conducted in which thin film damage thresholds were measured as a function of laser wavelength (1.06 μm, 0.53 μm, 0.35 μm and 0.26 μm), laser pulse length (5 and 15 nanoseconds), film materials and film thickness. The large matrix of data was compared to predictions given by avalanche ionization, multiphoton ionization and impurity theories of laser damage. When Mie absorption cross-sections and the exact thermal equations were included into the impurity theory excellent agreement with the data was found. The avalanche and multiphoton damage theories could not account for most parametric variations in the data. For example, the damage thresholds for most films increased as the film thickness decreased and only the impurity theory could account for this behavior. Other observed changes in damage threshold with changes in laser wavelength, pulse length and film material could only be adequately explained by the impurity theory. The conclusion which results from this study is that laser damage in thin film coatings results from absorbing impurities included during the deposition process

Multi-scale fracture damage associated with underground chemical explosions

Science.gov (United States)

Swanson, E. M.; Sussman, A. J.; Wilson, J. E.; Townsend, M. J.; Prothro, L. B.; Gang, H. E.

2018-05-01

Understanding rock damage induced by explosions is critical for a number of applications including the monitoring and verification of underground nuclear explosions, mine safety issues, and modeling fluid flow through fractured rock. We use core observations, televiewer logs, and thin section observations to investigate fracture damage associated with two successive underground chemical explosions (SPE2 and SPE3) in granitic rock at both the mesoscale and microscale. We compare the frequency and orientations of core-scale fractures, and the frequency of microfractures, between a pre-experiment core and three post-experiment cores. Natural fault zones and explosion-induced fractures in the vicinity of the explosive source are readily apparent in recovered core and in thin sections. Damage from faults and explosions is not always apparent in fracture frequency plots from televiewer logs, although orientation data from these logs suggests explosion-induced fracturing may not align with the pre-existing fracture sets. Core-scale observations indicate the extent of explosion-induced damage is 10.0 m after SPE2 and 6.8 m after SPE3, despite both a similar size and location for both explosions. At the microscale, damage is observed to a range distance of 10.2 ± 0.9 m after SPE2, and 16.6 ± 0.9 and 11.2 ± 0.6 in two different cores collected after SPE3. Additional explosion-induced damage, interpreted to be the result of spalling, is readily apparent near the surface, but only in the microfracture data. This depth extent and intensity of damage in the near-surface region also increased after an additional explosion. This study highlights the importance of evaluating structural damage at multiple scales for a more complete characterization of the damage, and particularly shows the importance of microscale observations for identifying spallation-induced damage.

Inductively Coupled Plasma-Induced Etch Damage of GaN p-n Junctions

International Nuclear Information System (INIS)

SHUL, RANDY J.; ZHANG, LEI; BACA, ALBERT G.; WILLISON, CHRISTI LEE; HAN, JUNG; PEARTON, S.J.; REN, F.

1999-01-01

Plasma-induced etch damage can degrade the electrical and optical performance of III-V nitride electronic and photonic devices. We have investigated the etch-induced damage of an Inductively Coupled Plasma (ICP) etch system on the electrical performance of mesa-isolated GaN pn-junction diodes. GaN p-i-n mesa diodes were formed by Cl 2 /BCl 3 /Ar ICP etching under different plasma conditions. The reverse leakage current in the mesa diodes showed a strong relationship to chamber pressure, ion energy, and plasma flux. Plasma induced damage was minimized at moderate flux conditions (≤ 500 W), pressures ≥2 mTorr, and at ion energies below approximately -275 V

DNA-damage-inducible (din) loci are transcriptionally activated in competent Bacillus subtilis

International Nuclear Information System (INIS)

Love, P.E.; Lyle, M.J.; Yasbin, R.E.

1985-01-01

DNA damage-inducible (din) operon fusions were generated in Bacillus subtilis by transpositional mutagenesis. These YB886(din::Tn917-lacZ) fusion isolates produced increased β-galactosidase when exposed to mitomycin C, UV radiation, or ethyl methanesulfonate, indicating that the lacZ structural gene had inserted into host transcriptional units that are induced by a variety of DNA-damaging agents. One of the fusion strains was DNA-repair deficient and phenotypically resembled a UV-sensitive mutant of B. subtilis. Induction of β-galactosidase also occurred in the competent subpopulation of each of the din fusion strains, independent of exposure to DNA-damaging agents. Both the DNA-damage-inducible and competence-inducible components of β-galactosidase expression were abolished by the recE4 mutation, which inhibits SOS-like (SOB) induction but does not interfere with the development of the component state. The results indicate that gene expression is stimulated at specific loci within the B. subtilis chromosome both by DNA-damaging agents and by the development of competence and that this response is under the control of the SOB regulatory system. Furthermore, they demonstrate that at the molecular level SOB induction and the development of competence are interrelated cellular events

Pathology of radiation induced lung damage

International Nuclear Information System (INIS)

Kawabata, Yoshinori; Murata, Yoshihiko; Ogata, Hideo; Katagiri, Shiro; Sugita, Hironobu; Iwai, Kazuo; Sakurai, Isamu.

1985-01-01

We examined pathological findings of radiation induced lung damage. Twenty-three cases are chosen from our hospital autopsy cases for 9 years, which fulfil strict criteria of radiation lung damage. Lung damage could be classified into 3 groups : 1) interstitial pneumonia type (9 cases), 2) intermediate pneumonia type (8 cases), and 3) alveolar pneumonia type (6 cases), according to the degree of intra-luminal exudation. These classification is well correlated with clinical findings. Pathological alveolar pneumonia type corresponds to symptomatic, radiologic ground glass pneumonic shadow. And pathologic interstitial type corresponds to clinical asymptomatic, radiologic reticulo-nodular shadow. From the clinico-pathological view point these classification is reasonable one. Radiation affects many lung structures and showed characteristic feature of repair. Elastofibrosis of the alveolar wall is observed in every cases, obstructive bronchiolitis are observed in 5 cases, and obstructive bronchiolitis in 9 cases. They are remarkable additional findings. Thickening of the interlobular septum, broncho-vascular connective tissue, and pleural layer are observed in every cases together with vascular lesions. (author)

Ultrasound-induced DNA damage and signal transductions indicated by gammaH2AX

Science.gov (United States)

Furusawa, Yukihiro; Fujiwara, Yoshisada; Zhao, Qing-Li; Hassan, Mariame Ali; Ogawa, Ryohei; Tabuchi, Yoshiaki; Takasaki, Ichiro; Takahashi, Akihisa; Ohnishi, Takeo; Kondo, Takashi

2011-09-01

Ultrasound (US) has been shown to induce cancer cell death via different forms including apoptosis. Here, we report the potential of low-intensity pulsed US (LIPUS) to induce genomic DNA damage and subsequent DNA damage response. Using the ionizing radiation-induced DNA double-strand breaks (DSBs) as the positive control, we were able to observe the induction of DSBs (as neutral comet tails) and the subsequent formation of gammaH2AX-positive foci (by immunofluorescence detection) in human leukemia cells following exposure to LIPUS. The LIPUS-induced DNA damage arose most likely from the mechanical, but not sonochemical, effect of cavitation, based on our observation that the suppression of inertial cavitation abrogated the gammH2AX foci formation, whereas scavenging of free radical formation (e.g., hydroxyl radical) had no protective effect on it. Treatment with the specific kinase inhibitor of ATM or DNA-PKcs, which can phosphorylate H2AX Ser139, revealed that US-induced gammaH2AX was inhibited more effectively by the DNA-PK inhibitor than ATM kinase inhibitor. Notably, these inhibitor effects were opposite to those with radiation-induced gammH2AX. In conclusion, we report, for the first time that US can induce DNA damage and the DNA damage response as indicated by gammaH2AX was triggered by the cavitational mechanical effects. Thus, it is expected that the data shown here may provide a better understanding of the cellular responses to US.

Effect of Shock-Induced Cavitation Bubble Collapse on the damage in the Simulated Perineuronal Net of the Brain.

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Wu, Yuan-Ting; Adnan, Ashfaq

2017-07-13

The purpose of this study is to conduct modeling and simulation to understand the effect of shock-induced mechanical loading, in the form of cavitation bubble collapse, on damage to the brain's perineuronal nets (PNNs). It is known that high-energy implosion due to cavitation collapse is responsible for corrosion or surface damage in many mechanical devices. In this case, cavitation refers to the bubble created by pressure drop. The presence of a similar damage mechanism in biophysical systems has long being suspected but not well-explored. In this paper, we use reactive molecular dynamics (MD) to simulate the scenario of a shock wave induced cavitation collapse within the perineuronal net (PNN), which is the near-neuron domain of a brain's extracellular matrix (ECM). Our model is focused on the damage in hyaluronan (HA), which is the main structural component of PNN. We have investigated the roles of cavitation bubble location, shockwave intensity and the size of a cavitation bubble on the structural evolution of PNN. Simulation results show that the localized supersonic water hammer created by an asymmetrical bubble collapse may break the hyaluronan. As such, the current study advances current knowledge and understanding of the connection between PNN damage and neurodegenerative disorders.

Surface damage studies of ETFE polymer bombarded with low energy Si ions (≤100 keV)

International Nuclear Information System (INIS)

Minamisawa, Renato Amaral; Almeida, Adelaide De; Budak, Satilmis; Abidzina, Volha; Ila, Daryush

2007-01-01

Surface studies of ethylenetetrafluoroethylene (ETFE), bombarded with Si in a high-energy tandem Pelletron accelerator, have recently been reported. Si ion bombardment with a few MeV to a few hundred keV energies was shown to be sufficient to produce damage on ETFE film. We report here the use of a low energy implanter with Si ion energies lower than 100 keV, to induce changes on ETFE films. In order to determine the radiation damage, ETFE bombarded films were simulated with SRIM software and analyzed with optical absorption photometry (OAP), Raman and Fourier transform infrared-attenuated total reflectance (FTIR-ATR) spectroscopy to show quantitatively the physical and chemical property changes. Carbonization occurs following higher dose implantation, and hydroperoxides were formed following dehydroflorination of the polymer

Prevention of Severe Hypoglycemia-Induced Brain Damage and Cognitive Impairment with Verapamil.

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Jackson, David A; Michael, Trevin; Vieira de Abreu, Adriana; Agrawal, Rahul; Bortolato, Marco; Fisher, Simon J

2018-05-03

People with insulin-treated diabetes are uniquely at risk for severe hypoglycemia-induced brain damage. Since calcium influx may mediate brain damage, we tested the hypothesis that the calcium channel blocker, verapamil, would significantly reduce brain damage and cognitive impairment caused by severe hypoglycemia. Ten-week-old Sprague-Dawley rats were randomly assigned to one of three treatments; 1) control hyperinsulinemic (200 mU.kg -1 min -1 ) euglycemic (80-100mg/dl) clamps (n=14), 2) hyperinsulinemic hypoglycemic (10-15mg/dl) clamps (n=16), or 3) hyperinsulinemic hypoglycemic clamps followed by a single treatment with verapamil (20mg/kg) (n=11). As compared to euglycemic controls, hypoglycemia markedly increased dead/dying neurons in the hippocampus and cortex, by 16-fold and 14-fold, respectively. Verapamil treatment strikingly decreased hypoglycemia-induced hippocampal and cortical damage, by 87% and 94%, respectively. Morris Water Maze probe trial results demonstrated that hypoglycemia induced a retention, but not encoding, memory deficit (noted by both abolished target quadrant preference and reduced target quadrant time). Verapamil treatment significantly rescued spatial memory as noted by restoration of target quadrant preference and target quadrant time. In summary, a one-time treatment with verapamil following severe hypoglycemia prevented neural damage and memory impairment caused by severe hypoglycemia. For people with insulin treated diabetes, verapamil may be a useful drug to prevent hypoglycemia-induced brain damage. © 2018 by the American Diabetes Association.

Metoprolol induces oxidative damage in common carp (Cyprinus carpio).

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Martínez-Rodríguez, Héctor; Donkor, Kingsley; Brewer, Sharon; Galar-Martínez, Marcela; SanJuan-Reyes, Nely; Islas-Flores, Hariz; Sánchez-Aceves, Livier; Elizalde-Velázquez, Armando; Gómez-Oliván, Leobardo Manuel

2018-04-01

During the last decade, β-blockers such as metoprolol (MTP) have been frequently detected in surface water, aquatic systems and municipal water at concentrations of ng/L to μg/L. Only a small number of studies exist on the toxic effects induced by this group of pharmaceuticals on aquatic organisms. Therefore, the present study aimed to evaluate the oxidative damage induced by MTP in the common carp Cyprinus carpio, using oxidative stress biomarkers. To this end, indicators of cellular oxidation such as hydroperoxide content (HPC), lipid peroxidation (LPX) and protein carbonyl content (PCC) were determined, as well as the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Also, concentrations of MTP and its metabolite O-desmethyl metoprolol were determined in water as well as carp gill, liver, kidney, brain and blood, along with the partial uptake pattern of these compounds. Results show that carp takes up MTP and its metabolite in the different organs evaluated, particularly liver and gill. The oxidative stress biomarkers, HPC, LPX, and PCC, as well as SOD and CAT activity all increased significantly at most exposure times in all organs evaluated. Results indicate that MTP and its metabolite induce oxidative stress on the teleost C. carpio and that the presence of these compounds may constitute a risk in water bodies for aquatic species. Copyright © 2018 Elsevier B.V. All rights reserved.

Determination of ultra-short laser induced damage threshold of KH2PO4 crystal: Numerical calculation and experimental verification

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Jian Cheng

2016-03-01

Full Text Available Rapid growth and ultra-precision machining of large-size KDP (KH2PO4 crystals with high laser damage resistance are tough challenges in the development of large laser systems. It is of high interest and practical significance to have theoretical models for scientists and manufacturers to determine the laser-induced damage threshold (LIDT of actually prepared KDP optics. Here, we numerically and experimentally investigate the laser-induced damage on KDP crystals in ultra-short pulse laser regime. On basis of the rate equation for free electron generation, a model dedicated to predicting the LIDT is developed by considering the synergistic effect of photoionization, impact ionization and decay of electrons. Laser damage tests are performed to measure the single-pulse LIDT with several testing protocols. The testing results combined with previously reported experimental data agree well with those calculated by the model. By taking the light intensification into consideration, the model is successfully applied to quantitatively evaluate the effect of surface flaws inevitably introduced in the preparation processes on the laser damage resistance of KDP crystals. This work can not only contribute to further understanding of the laser damage mechanisms of optical materials, but also provide available models for evaluating the laser damage resistance of exquisitely prepared optical components used in high power laser systems.

Oxidative damage and neurodegeneration in manganese-induced neurotoxicity

International Nuclear Information System (INIS)

Milatovic, Dejan; Zaja-Milatovic, Snjezana; Gupta, Ramesh C.; Yu, Yingchun; Aschner, Michael

2009-01-01

Exposure to excessive manganese (Mn) levels results in neurotoxicity to the extrapyramidal system and the development of Parkinson's disease (PD)-like movement disorder, referred to as manganism. Although the mechanisms by which Mn induces neuronal damage are not well defined, its neurotoxicity appears to be regulated by a number of factors, including oxidative injury, mitochondrial dysfunction and neuroinflammation. To investigate the mechanisms underlying Mn neurotoxicity, we studied the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates (HEP), neuroinflammation mediators and associated neuronal dysfunctions both in vitro and in vivo. Primary cortical neuronal cultures showed concentration-dependent alterations in biomarkers of oxidative damage, F 2 -isoprostanes (F 2 -IsoPs) and mitochondrial dysfunction (ATP), as early as 2 h following Mn exposure. Treatment of neurons with 500 μM Mn also resulted in time-dependent increases in the levels of the inflammatory biomarker, prostaglandin E 2 (PGE 2 ). In vivo analyses corroborated these findings, establishing that either a single or three (100 mg/kg, s.c.) Mn injections (days 1, 4 and 7) induced significant increases in F 2 -IsoPs and PGE 2 in adult mouse brain 24 h following the last injection. Quantitative morphometric analyses of Golgi-impregnated striatal sections from mice exposed to single or three Mn injections revealed progressive spine degeneration and dendritic damage of medium spiny neurons (MSNs). These findings suggest that oxidative stress, mitochondrial dysfunction and neuroinflammation are underlying mechanisms in Mn-induced neurodegeneration.

Effect of SOS-induced levels of imuABC on spontaneous and damage-induced mutagenesis in Caulobacter crescentus.

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Alves, Ingrid R; Lima-Noronha, Marco A; Silva, Larissa G; Fernández-Silva, Frank S; Freitas, Aline Luiza D; Marques, Marilis V; Galhardo, Rodrigo S

2017-11-01

imuABC (imuAB dnaE2) genes are responsible for SOS-mutagenesis in Caulobacter crescentus and other bacterial species devoid of umuDC. In this work, we have constructed operator-constitutive mutants of the imuABC operon. We used this genetic tool to investigate the effect of SOS-induced levels of these genes upon both spontaneous and damage-induced mutagenesis. We showed that constitutive expression of imuABC does not increase spontaneous or damage-induced mutagenesis, nor increases cellular resistance to DNA-damaging agents. Nevertheless, the presence of the operator-constitutive mutation rescues mutagenesis in a recA background, indicating that imuABC are the only genes required at SOS-induced levels for translesion synthesis (TLS) in C. crescentus. Furthermore, these data also show that TLS mediated by ImuABC does not require RecA, unlike umuDC-dependent mutagenesis in E. coli. Copyright © 2017 Elsevier B.V. All rights reserved.

Retention and features of deuterium detrapping from radiation-induced damages in steels

International Nuclear Information System (INIS)

Tolstolutskaya, G.D.; Ruzhytskiy, V.V.; Karpov, S.A.; Kopanets, I.E.

2009-01-01

The accelerators and ion-beam analysis techniques are used for simulation of displacement damage and detailed investigation of distribution profiles of damage and impurity gas atoms (especially helium and hydrogen) in the irradiation of targets for a wide ranges of doses and particle energies. The influence of preimplanted helium and heavy ion-induced damage on deuterium trapping in austenitic and ferritic/martensitic steels was studied. The results obtained for 18Cr10NiTi stainless steel show that ion-implanted deuterium is weakly trapped by defects produced in 5 keV D + displacement cascades. The effective trapping temperature interval is between 300 and 600 K. The characteristics of trapping and the temperature range of hydrogen isotopes retention in traps formed by prior implantation of helium depend on the concentration of implanted helium and on the type of defects developed. The formation of helium bubbles in 18Cr10NiTi steel causes an order of magnitude increase in the content of retained deuterium atoms in the range of temperature 300-600 K and extends the interval of effective trapping temperatures to 1000 K. Energetic heavy-ion irradiation (1.4 MeV Ar + ) has been used for modeling defect cluster formation under displacement cascade conditions to simulate fusion reactor environments. It was found that retention of hydrogen and deuterium strongly increased in this case. It is shown that the presence of a surface-passive film considerably shifts the gas release interval to higher temperatures and reduces the deuterium surface recombination coefficient by several orders of magnitude.

Low energy Ar ion bombardment damage of Si, GaAs, and InP surfaces

International Nuclear Information System (INIS)

Williams, R.S.

1982-01-01

Argon bombardment damage to (100) surfaces of Si, GaAs, and InP for sputter ion-gun potentials of 1, 2, and 3 kilovolts was studied using Rutherford backscattering. Initial damage rates and saturation damage levels were determined. Bombardment damage sensitivity increased for the sequence Si, GaAs, and InP. Saturation damage levels for Si and GaAs correspond reasonably to LSS projected range plus standard deviation estimates; damage to InP exceeded this level significantly. For an ion-gun potential of 3 keV, the initial sputter yield of P from an InP surface exceeded the sputter yield of In by four atoms per incident Ar projectile. (author)

Role of endothelium in radiation-induced normal tissue damages

International Nuclear Information System (INIS)

Milliat, F.

2007-05-01

More than half of cancers are treated with radiation therapy alone or in combination with surgery and/or chemotherapy. The goal of radiation therapy is to deliver enough ionising radiation to destroy cancer cells without exceeding the level that the surrounding healthy cells can tolerate. Unfortunately, radiation-induced normal tissue injury is still a dose limiting factor in the treatment of cancer with radiotherapy. The knowledge of normal tissue radiobiology is needed to determine molecular mechanisms involved in normal tissue pathogenic pathways in order to identify therapeutic targets and develop strategies to prevent and /or reduce side effects of radiation therapy. The endothelium is known to play a critical role in radiation-induced injury. Our work shows that endothelial cells promote vascular smooth muscle cell proliferation, migration and fibro-genic phenotype after irradiation. Moreover, we demonstrate for the first time the importance of PAI-1 in radiation-induced normal tissue damage suggesting that PAI-1 may represent a molecular target to limit injury following radiotherapy. We describe a new role for the TGF-b/Smad pathway in the pathogenesis of radiation-induced damages. TGF-b/Smad pathway is involved in the fibro-genic phenotype of VSMC induced by irradiated EC as well as in the radiation-induced PAI-1 expression in endothelial cells. (author)

Quantification of high-power ultrasound induced damage on potato starch granules using light microscopy.

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Zuo, Yue Yue J; Hébraud, Pascal; Hemar, Yacine; Ashokkumar, Muthupandian

2012-05-01

A simple light microscopic technique was developed in order to quantify the damage inflicted by high-power low-frequency ultrasound (0-160 W, 20 kHz) treatment on potato starch granules in aqueous dispersions. The surface properties of the starch granules were modified using ethanol and SDS washing methods, which are known to displace proteins and lipids from the surface of the starch granules. The study showed that in the case of normal and ethanol-washed potato starch dispersions, two linear regions were observed. The number of defects first increased linearly with an increase in ultrasound power up to a threshold level. This was then followed by another linear dependence of the number of defects on the ultrasound power. The power threshold where the change-over occurred was higher for the ethanol-washed potato dispersions compared to non-washed potato dispersions. In the case of SDS-washed potato starch, although the increase in defects was linear with the ultrasound power, the power threshold for a second linear region was not observed. These results are discussed in terms of the different possible mechanisms of cavitation induced-damage (hydrodynamic shear stresses and micro-jetting) and by taking into account the hydrophobicity of the starch granule surface. Copyright © 2011 Elsevier B.V. All rights reserved.

Diclofenac protects cultured human corneal epithelial cells against hyperosmolarity and ameliorates corneal surface damage in a rat model of dry eye.

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Sawazaki, Ryoichi; Ishihara, Tomoaki; Usui, Shinya; Hayashi, Erika; Tahara, Kayoko; Hoshino, Tatsuya; Higuchi, Akihiro; Nakamura, Shigeru; Tsubota, Kazuo; Mizushima, Tohru

2014-04-21

Dry eye syndrome (DES) is characterized by an increase in tear osmolarity and induction of the expression and nuclear localization of an osmoprotective transcription factor (nuclear factor of activated T-cells 5 [NFAT5]) that plays an important role in providing protection against hyperosmotic tears. In this study, we screened medicines already in clinical use with a view of finding compounds that protect cultured human corneal epithelial cells against hyperosmolarity-induced cell damage. Viable cell number was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method and cellular NFAT5 level was measured by immunoblotting. The rat model for DES was developed by removal of the lacrimal glands, with an assessment of corneal surface damage based on levels of fluorescein staining and epithelial apoptosis. Some nonsteroidal anti-inflammatory drugs (NSAIDs), including diclofenac sodium (diclofenac), were identified during the screening procedure. These NSAIDs were able to suppress hyperosmolarity-induced apoptosis and cell growth arrest. In contrast, other NSAIDs, including bromfenac sodium (bromfenac), did not exert such a protective action. Treatment of cells with diclofenac, but not bromfenac, stimulated both the nuclear localization and expression of NFAT5 under hyperosmotic conditions. In the rat model for DES, topical administration of diclofenac (but not bromfenac) to eyes reduced corneal surface damage without affecting the volume of tear fluid. Diclofenac appears to protect cells against hyperosmolarity-induced cell damage and NFAT5 would play an important role in this protective action. The findings reported here may also indicate that the topical administration of diclofenac to eyes may be therapeutically beneficial for DES patients.

Cytoprotective effect of phloroglucinol on oxidative stress induced cell damage via catalase activation.

Science.gov (United States)

Kang, Kyoung Ah; Lee, Kyoung Hwa; Chae, Sungwook; Zhang, Rui; Jung, Myung Sun; Ham, Young Min; Baik, Jong Seok; Lee, Nam Ho; Hyun, Jin Won

2006-02-15

We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown alga), against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Phloroglucinol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydrogen peroxide (H(2)O(2)), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, phloroglucinol reduced H(2)O(2) induced apoptotic cells formation in V79-4 cells. In addition, phloroglucinol inhibited cell damage induced by serum starvation and radiation through scavenging ROS. Phloroglucinol increased the catalase activity and its protein expression. In addition, catalase inhibitor abolished the protective effect of phloroglucinol from H(2)O(2) induced cell damage. Furthermore, phloroglucinol increased phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular catalase activity and modulating ERK signal pathway. (c) 2005 Wiley-Liss, Inc.

Endomorphin 1 effectively protects cadmium chloride-induced hepatic damage in mice

International Nuclear Information System (INIS)

Gong Pin; Chen Fuxin; Ma Guofen; Feng Yun; Zhao Qianyu; Wang Rui

2008-01-01

The antioxidative capacity of endomorphin 1 (EM1), an endogenous μ-opioid receptor agonist, has been demonstrated by in vivo assays. The present study reports the effect of EM1 on hepatic damage induced by cadmium chloride (Cd(II)) in adult male mouse. Mouse were given intraperitoneally (i.p.) a single dose of Cd(II) (1 mg/kg body weight per day) and the animals were co-administrated with a dose of EM1 (50 μM/kg body weight per day) for 6 days. Since hepatic damage induced by Cd(II) is related to oxidative stress, lipid peroxidation (LPO), protein carbonyl (PCO), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) were evaluated. The parameter indicating tissue damage such as liver histopathology was also determined. In addition, the concentrations of Cd and zinc (Zn) in the liver were analyzed. The intoxication of Cd(II) lead to the enhanced production of LPO and PCO, treatment with EM1 can effectively ameliorate the increase of LPO and PCO compared to the Cd(II) group. The increased activities of CAT, SOD and the elevated GSH induced by Cd(II) may relate to an adaptive-response to the oxidative damage, the effect of EM1 can restore the elevated antioxidant defense. Our results suggested that the structure features and the ability of chelating metal of EM1 may play a major role in the antioxidant effect of EM1 in vivo and opioid receptors may be involved in the protection of hepatic damage induced by Cd(II)

The effect of phytosterol protects rats against 4-nitrophenol-induced liver damage.

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Chen, Jiaqin; Song, Meiyan; Li, Yansen; Zhang, Yonghui; Taya, Kazuyoshi; Li, ChunMei

2016-01-01

We investigated the effect of phytosterol (PS) in regard to liver damage induced by 4-nitrophenol (PNP). Twenty rats were randomly divided into four groups (Control, PS, PNP, and PNP+PS). The PS and PNP+PS groups were pretreated with PS for one week. The PNP and PNP+PS groups were injected subcutaneously with PNP for 28 days. The control group received a basal diet and was injected with vehicle alone. Treatment with PS prevented the elevation of the total bilirubin levels, as well as an increase in serum alkaline transaminase and aspartate transaminase, which are typically caused by PNP-induced liver damage. Histopathologically showed that liver damage was significantly mitigated by PS treatment. However, there was no significant change in antioxidant enzyme activities, and the Nrf2-antioxidant system was not activated after treatment with PS. These results suggest that PS could mitigate liver damage induced by PNP, but does not enhance antioxidant capacity. Copyright © 2015 Elsevier B.V. All rights reserved.

Methimazole-induced hypothyroidism causes cellular damage in the spleen, heart, liver, lung and kidney.

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Cano-Europa, Edgar; Blas-Valdivia, Vanessa; Franco-Colin, Margarita; Gallardo-Casas, Carlos Angel; Ortiz-Butrón, Rocio

2011-01-01

It is known that a hypothyroidism-induced hypometabolic state protects against oxidative damage caused by toxins. However, some workers demonstrated that antithyroid drug-induced hypothyroidism can cause cellular damage. Our objective was to determine if methimazole (an antithyroid drug) or hypothyroidism causes cellular damage in the liver, kidney, lung, spleen and heart. Twenty-five male Wistar rats were divided into 5 groups: euthyroid, false thyroidectomy, thyroidectomy-induced hypothyroidism, methimazole-induced hypothyroidism (60 mg/kg), and treatment with methimazole (60 mg/kg) and a T₄ injection (20 μg/kg/d sc). At the end of the treatments (4 weeks for the pharmacological groups and 8 weeks for the surgical groups), the animals were anesthetized with sodium pentobarbital and they were transcardially perfused with 10% formaldehyde. The spleen, heart, liver, lung and kidney were removed and were processed for embedding in paraffin wax. Coronal sections were stained with hematoxylin-eosin. At the end of treatment, animals with both the methimazole- and thyroidectomy-induced hypothyroidism had a significant reduction of serum concentration of thyroid hormones. Only methimazole-induced hypothyroidism causes cellular damage in the kidney, lung, liver, heart, kidney and spleen. In addition, animals treated with methimazole and T₄ showed cellular damage in the lung, spleen and renal medulla with lesser damage in the liver, renal cortex and heart. The thyroidectomy only altered the lung structure. The alterations were prevented by T₄ completely in the heart and partially in the kidney cortex. These results indicate that tissue damage found in hypothyroidism is caused by methimazole. Copyright © 2009 Elsevier GmbH. All rights reserved.

Damage Mechanism in Counter Pairs Caused by Bionic Non-smoothed Surface

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ZHANG Zhan-hui

2016-08-01

Full Text Available Four biomimetic non-smoothed surface specimens with different shapes were prepared by laser processing. Tests were conducted on MMU-5G wear and abrasion test machine to study the influencing rule of non-smoothed surfaces on counter pairs. The results show that the mass loss of the friction pair matching with the non-smoothed units is much greater than the ones matching with the smooth specimens. The pairs matching with different non-smoothed units suffer differently. The non-smoothed surface protruding zone exerts micro cutting on counter pairs. The striation causes the greatest mass loss of the pairs than the other non-smoothed units, which almost doubles the damage of the grid ones suffering the least. The difference in pairs damage is attributed to the different mechanism of undertaking the load in the process of wear. The damage can be alleviated effectively by changing the shapes of the units without increasing or decreasing the area ratio of the non-smoothed units.

Ginsenoside Rg3 induces DNA damage in human osteosarcoma cells and reduces MNNG-induced DNA damage and apoptosis in normal human cells.

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Zhang, Yue-Hui; Li, Hai-Dong; Li, Bo; Jiang, Sheng-Dan; Jiang, Lei-Sheng

2014-02-01

Panax ginseng is a Chinese medicinal herb. Ginsenosides are the main bioactive components of P. ginseng, and ginsenoside Rg3 is the primary ginsenoside. Ginsenosides can potently kill various types of cancer cells. The present study was designed to evaluate the potential genotoxicity of ginsenoside Rg3 in human osteosarcoma cells and the protective effect of ginsenoside Rg3 with respect to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced DNA damage and apoptosis in a normal human cell line (human fibroblasts). Four human osteosarcoma cell lines (MG-63, OS732, U-2OS and HOS cells) and a normal human cell line (human fibroblasts) were employed to investigate the cytotoxicity of ginsenosides Rg3 by MTT assay. Alkaline comet assay and γH2AX focus staining were used to detect the DNA damage in MG-63 and U-2OS cells. The extent of cell apoptosis was determined by flow cytometry and a DNA ladder assay. Our results demonstrated that the cytotoxicity of ginsenoside Rg3 was dose-dependent in the human osteosarcoma cell lines, and MG-63 and U-2OS cells were the most sensitive to ginsenoside Rg3. As expected, compared to the negative control, ginsenoside Rg3 significantly increased DNA damage in a concentration-dependent manner. In agreement with the comet assay data, the percentage of γH2AX-positive MG-63 and U-2OS cells indicated that ginsenoside Rg3 induced DNA double-strand breaks in a concentration-dependent manner. The results also suggest that ginsenoside Rg3 reduces the extent of MNNG-induced DNA damage and apoptosis in human fibroblasts.

UV and ionizing radiations induced DNA damage, differences and similarities

Science.gov (United States)

Ravanat, Jean-Luc; Douki, Thierry

2016-11-01

Both UV and ionizing radiations damage DNA. Two main mechanisms, so-called direct and indirect pathways, are involved in the degradation of DNA induced by ionizing radiations. The direct effect of radiation corresponds to direct ionization of DNA (one electron ejection) whereas indirect effects are produced by reactive oxygen species generated through water radiolysis, including the highly reactive hydroxyl radicals, which damage DNA. UV (and visible) light damages DNA by again two distinct mechanisms. UVC and to a lesser extend UVB photons are directly absorbed by DNA bases, generating their excited states that are at the origin of the formation of pyrimidine dimers. UVA (and visible) light by interaction with endogenous or exogenous photosensitizers induce the formation of DNA damage through photosensitization reactions. The excited photosensitizer is able to induce either a one-electron oxidation of DNA (type I) or to produce singlet oxygen (type II) that reacts with DNA. In addition, through an energy transfer from the excited photosensitizer to DNA bases (sometime called type III mechanism) formation of pyrimidine dimers could be produced. Interestingly it has been shown recently that pyrimidine dimers are also produced by direct absorption of UVA light by DNA, even if absorption of DNA bases at these wavelengths is very low. It should be stressed that some excited photosensitizers (such as psoralens) could add directly to DNA bases to generate adducts. The review will described the differences and similarities in terms of damage formation (structure and mechanisms) between these two physical genotoxic agents.

Topical application of ST266 reduces UV-induced skin damage

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Guan L

2017-11-01

Full Text Available Linna Guan,1 Amanda Suggs,1 Emily Galan,1 Minh Lam,1 Elma D Baron1,2 1Department of Dermatology, Case Western Reserve University, 2Cleveland Veterans Affairs Medical Center, Cleveland, OH, USA Abstract: Ultraviolet radiation (UVR has a significant impact on human skin and is the major environmental factor for skin cancer formation. It is also believed that 80% of the signs of skin aging are attributed to UVR. UVR induces inflammatory changes in the skin via the increase in oxidative stress, DNA damage vascular permeability, and fluctuation in a myriad of cytokines. Acutely, UVR causes skin inflammation and DNA damage, which manifest as sunburn (erythema. ST266 is the secretome of proprietary amnion-derived cells that have been shown to reduce inflammation and accelerate healing of various wounds by promoting migration of keratinocytes and fibroblasts in preclinical animal studies. We hypothesized that ST266 has anti-inflammatory effects that can be used to reduce ultraviolet (UV erythema and markers of inflammation. In this study, we examined the in vivo effects of ST266 on post UV-irradiated skin by measuring erythema, level of cyclobutane pyrimidine dimer (CPD, and expression level of xeroderma pigmentosum, complementation group A (XPA. We demonstrated that ST266 has the potential to reduce the acute effects of UV-induced skin damage when applied immediately after the initial exposure. In addition, ST266 is shown to reduce erythema, increase XPA DNA repair protein, and decrease damaged DNA. Keywords: ST266, photoaging, erythema, CPD, XPA, UV-induced DNA damage

Elastoplastic simulation coupled to the induced anisotropic damage for argilites

International Nuclear Information System (INIS)

Chiarelli, A.S.; Shao, J.F.

2002-01-01

A constitutive model coupling plastic deformation and induced damage is proposed to describe the mechanical behaviour of a shale rock, the argilites of East. The plastic behaviour is produced by a typical cohesive-frictional model. The material damage is represented by a second rank symmetric tensor. The damage criterion and evolution rate is related to tensile strains. The damage effect on plastic flow is also considered by an anisotropic transformation. The model formulation and a simple procedure for the determination of model parameters from standards tests is proposed. The validity of the model is checked against experimental data in various loading conditions. (author)

Decrease of FIB-induced lateral damage for diamond tool used in nano cutting

Energy Technology Data Exchange (ETDEWEB)

Wu, Wei [State Key Laboratory of Precision Measuring Technology and Instruments, Centre of MicroNano Manufacturing Technology, Tianjin University, Tianjin 300072 (China); Xu, Zongwei, E-mail: zongweixu@163.com [State Key Laboratory of Precision Measuring Technology and Instruments, Centre of MicroNano Manufacturing Technology, Tianjin University, Tianjin 300072 (China); Fang, Fengzhou, E-mail: fzfang@gmail.com [State Key Laboratory of Precision Measuring Technology and Instruments, Centre of MicroNano Manufacturing Technology, Tianjin University, Tianjin 300072 (China); Liu, Bing; Xiao, Yinjing; Chen, Jinping [State Key Laboratory of Precision Measuring Technology and Instruments, Centre of MicroNano Manufacturing Technology, Tianjin University, Tianjin 300072 (China); Wang, Xibin [School of Mechanical Engineering, Beijing Institute of Technology, Beijing 100081 (China); Liu, Hongzhong [State Key Laboratory for Manufacturing Systems Engineering, Xi’an Jiaotong University, Xi’an 710049 (China)

2014-07-01

Highlights: • We mainly aim to characterize and decrease the FIB-induced damage on diamond tool. • Raman and XPS methods were used to characterize the nanoscale FIB-induced damage. • Lower energy FIB can effectively lessen the FIB-induced damage on diamond tool. • The diamond tools’ performance was greatly improved after FIB process optimization. • 6 nm chip thickness of copper was achieved by diamond tool with 22 nm edge radius. - Abstract: Diamond cutting tools with nanometric edge radius used in ultra-precision machining can be fabricated by focused ion beam (FIB) technology. However, due to the nanoscale effects, the diamond tools performance and the cutting edge lifetime in nano cutting would be degraded because of the FIB-induced nanoscale lateral damage. In this study, the methods of how to effectively characterize and decrease the FIB-induced lateral damage for diamond tool are intensively studied. Based on the performance optimization diamond machining tools, the controllable chip thickness of less than 10 nm was achieved on a single-crystal copper in nano cutting. In addition, the ratio of minimum thickness of chip (MTC) to tool edge radius of around 0.3–0.4 in nano cutting is achieved. Methods for decreasing the FIB-induced damage on diamond tools and adding coolant during the nano cutting are very beneficial in improving the research of nano cutting and MTC. The nano cutting experiments based on the sharp and high performance of diamond tools would validate the nano cutting mechanisms that many molecular dynamic simulation studies have put forward and provide new findings for nano cutting.

Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

Directory of Open Access Journals (Sweden)

José A. Hernández

2016-01-01

Full Text Available The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.

Edaravone Protect against Retinal Damage in Streptozotocin-Induced Diabetic Mice

Science.gov (United States)

Liu, Xiaoyi; Chen, Xi; Xie, Ping; Yuan, Songtao; Zhang, Weiwei; Lin, Xiaojun; Liu, Qinghuai

2014-01-01

Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger, is used for the clinical treatment of retinal injury. In this study, we investigated the protective effects of edaravone against diabetic retinal damage in the mouse. Diabetic retinopathy in the mouse was induced by injection of streptozotocin. Edaravone was given once-daily and was intraperitoneally (i.p.) treated at a dose of 3 mg/kg from streptozotocin injection to 4 weeks after onset of diabetes. Retinal ganglion cells (RGCs) damage was evaluated by recording the pattern electroretinogram (ERG). RGCs damage was also detected by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and the levels of reactive oxygen species (ROS) were determined fluorometrically. The expressions of phosporylated-ERK1/2, BDNF, and caspase-3 were determined by Western blot analysis. Retinal levels of ROS, phosphorylated ERK1/2, and cleaved caspase-3 were significantly increased, whereas the expression of BDNF was significantly decreased in the retinas of diabetic mice, compared to nondiabetic mice. Administration of edaravone significantly attenuated diabetes induced RGCs death, upregulation of ROS, ERK1/2 phosphorylation, and cleaved caspase-3 and downregulation of BDNF. These findings suggest that oxidative stress plays a pivotal role in diabetic retinal damage and that systemic administration of edaravone may slow the progression of retinal neuropathy induced by diabetes. PMID:24897298

Edaravone protect against retinal damage in streptozotocin-induced diabetic mice.

Directory of Open Access Journals (Sweden)

Dongqing Yuan

Full Text Available Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one, a free radical scavenger, is used for the clinical treatment of retinal injury. In this study, we investigated the protective effects of edaravone against diabetic retinal damage in the mouse. Diabetic retinopathy in the mouse was induced by injection of streptozotocin. Edaravone was given once-daily and was intraperitoneally (i.p. treated at a dose of 3 mg/kg from streptozotocin injection to 4 weeks after onset of diabetes. Retinal ganglion cells (RGCs damage was evaluated by recording the pattern electroretinogram (ERG. RGCs damage was also detected by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL staining, and the levels of reactive oxygen species (ROS were determined fluorometrically. The expressions of phosporylated-ERK1/2, BDNF, and caspase-3 were determined by Western blot analysis. Retinal levels of ROS, phosphorylated ERK1/2, and cleaved caspase-3 were significantly increased, whereas the expression of BDNF was significantly decreased in the retinas of diabetic mice, compared to nondiabetic mice. Administration of edaravone significantly attenuated diabetes induced RGCs death, upregulation of ROS, ERK1/2 phosphorylation, and cleaved caspase-3 and downregulation of BDNF. These findings suggest that oxidative stress plays a pivotal role in diabetic retinal damage and that systemic administration of edaravone may slow the progression of retinal neuropathy induced by diabetes.

Feasibility and safety of inducing modest hypothermia in awake patients with acute stroke through surface cooling

DEFF Research Database (Denmark)

Kammersgaard, L P; Rasmussen, B H; Jørgensen, Henrik Stig

2000-01-01

Hypothermia reduces neuronal damage in animal stroke models. Whether hypothermia is neuroprotective in patients with acute stroke remains to be clarified. In this case-control study, we evaluated the feasibility and safety of inducing modest hypothermia by a surface cooling method in awake patients...

Enhanced thermomechanical stability on laser-induced damage by functionally graded layers in quasi-rugate filters

Science.gov (United States)

Pu, Yunti; Ma, Ping; Lv, Liang; Zhang, Mingxiao; Lu, Zhongwen; Qiao, Zhao; Qiu, Fuming

2018-05-01

Ta2O5-SiO2 quasi-rugate filters with a reasonable optimization of rugate notch filter design were prepared by ion-beam sputtering. The optical properties and laser-induced damage threshold are studied. Compared with the spectrum of HL-stacks, the spectrum of quasi-rugate filters have weaker second harmonic peaks and narrower stopbands. According to the effect of functionally graded layers (FGLs), 1-on-1 and S-on-1 Laser induced damage threshold (LIDT) of quasi-rugate filters are about 22% and 50% higher than those of HL stacks, respectively. Through the analysis of the damage morphologies, laser-induced damage of films under nanosecond multi-pulse are dominated by a combination of thermal shock stress and thermomechanical instability due to nodules. Compared with catastrophic damages, the damage sits of quasi-rugate filters are developed in a moderate way. The damage growth behavior of defect-induced damage sites have been effectively restrained by the structure of FGLs. Generally, FGLs are used to reduce thermal stress by the similar thermal-expansion coefficients of neighboring layers and solve the problems such as instability and cracking raised by the interface discontinuity of nodular boundaries, respectively.

Noninvasive assessment of articular cartilage surface damage using reflected polarized light microscopy

Science.gov (United States)

Huynh, Ruby N.; Nehmetallah, George; Raub, Christopher B.

2017-06-01

Articular surface damage occurs to cartilage during normal aging, osteoarthritis, and in trauma. A noninvasive assessment of cartilage microstructural alterations is useful for studies involving cartilage explants. This study evaluates polarized reflectance microscopy as a tool to assess surface damage to cartilage explants caused by mechanical scraping and enzymatic degradation. Adult bovine articular cartilage explants were scraped, incubated in collagenase, or underwent scrape and collagenase treatments. In an additional experiment, cartilage explants were subject to scrapes at graduated levels of severity. Polarized reflectance parameters were compared with India ink surface staining, features of histological sections, changes in explant wet weight and thickness, and chondrocyte viability. The polarized reflectance signal was sensitive to surface scrape damage and revealed individual scrape features consistent with India ink marks. Following surface treatments, the reflectance contrast parameter was elevated and correlated with image area fraction of India ink. After extensive scraping, polarized reflectance contrast and chondrocyte viability were lower than that from untreated explants. As part of this work, a mathematical model was developed and confirmed the trend in the reflectance signal due to changes in surface scattering and subsurface birefringence. These results demonstrate the effectiveness of polarized reflectance microscopy to sensitively assess surface microstructural alterations in articular cartilage explants.

Reduction of arsenite-enhanced ultraviolet radiation-induced DNA damage by supplemental zinc

Energy Technology Data Exchange (ETDEWEB)

Cooper, Karen L.; King, Brenee S.; Sandoval, Monica M.; Liu, Ke Jian; Hudson, Laurie G., E-mail: lhudson@salud.unm.edu

2013-06-01

Arsenic is a recognized human carcinogen and there is evidence that arsenic augments the carcinogenicity of DNA damaging agents such as ultraviolet radiation (UVR) thereby acting as a co-carcinogen. Inhibition of DNA repair is one proposed mechanism to account for the co-carcinogenic actions of arsenic. We and others find that arsenite interferes with the function of certain zinc finger DNA repair proteins. Furthermore, we reported that zinc reverses the effects of arsenite in cultured cells and a DNA repair target protein, poly (ADP-ribose) polymerase-1. In order to determine whether zinc ameliorates the effects of arsenite on UVR-induced DNA damage in human keratinocytes and in an in vivo model, normal human epidermal keratinocytes and SKH-1 hairless mice were exposed to arsenite, zinc or both before solar-simulated (ss) UVR exposure. Poly (ADP-ribose) polymerase activity, DNA damage and mutation frequencies at the Hprt locus were measured in each treatment group in normal human keratinocytes. DNA damage was assessed in vivo by immunohistochemical staining of skin sections isolated from SKH-1 hairless mice. Cell-based findings demonstrate that ssUVR-induced DNA damage and mutagenesis are enhanced by arsenite, and supplemental zinc partially reverses the arsenite effect. In vivo studies confirm that zinc supplementation decreases arsenite-enhanced DNA damage in response to ssUVR exposure. From these data we can conclude that zinc offsets the impact of arsenic on ssUVR-stimulated DNA damage in cells and in vivo suggesting that zinc supplementation may provide a strategy to improve DNA repair capacity in arsenic exposed human populations. - Highlights: • Low levels of arsenite enhance UV-induced DNA damage in human keratinocytes. • UV-initiated HPRT mutation frequency is enhanced by arsenite. • Zinc supplementation offsets DNA damage and mutation frequency enhanced by arsenite. • Zinc-dependent reduction of arsenite enhanced DNA damage is confirmed in vivo.

Radiation induced DNA damage and repair in mutagenesis

International Nuclear Information System (INIS)

Strniste, G.F.; Chen, D.J.; Okinaka, R.T.

1987-01-01

The central theme in cellular radiobiological research has been the mechanisms of radiation action and the physiological response of cells to this action. Considerable effort has been directed toward the characterization of radiation-induced DNA damage and the correlation of this damage to cellular genetic change that is expressed as mutation or initiating events leading to cellular transformation and ultimately carcinogenesis. In addition, there has been a significant advancement in their understanding of the role of DNA repair in the process of mutation leading to genetic change in cells. There is extensive literature concerning studies that address radiation action in both procaryotic and eucaryotic systems. This brief report will make no attempt to summarize this voluminous data but will focus on recent results from their laboratory of experiments in which they have examined, at both the cellular and molecular levels, the process of ionizing radiation-induced mutagenesis in cultured human cells

Growth of Laser Initiated Damage in Fused Silica at 527 nm

International Nuclear Information System (INIS)

Norton, M A; Donohue, E E; Hollingsworth, W G; McElroy, J N; Hackel, R P

2003-01-01

The effective lifetime of optics is limited by both laser-induced damage and the subsequent growth of laser initiated damage sites. We have measured the growth rate of laser-induced damage in fused silica in both air and vacuum at 527 nm. For damage on the exit surface, the data shows exponential growth in the lateral size of the damage site with shot number. The exponential growth coefficient depends linearly on the laser fluence. The behavior at the fluence threshold for growth is contrasted to that observed at 351 nm. The growth rate was not significantly affected by either the wavelength of the initiating fluence or the presence of 10 torr of air as compared to vacuum. When the damage is located on the input surface, it has both a higher threshold for growth and does not grow exponentially

Simultaneous impact of neutron irradiation and sputtering on the surface structure of self–damaged ITER–grade tungsten

Energy Technology Data Exchange (ETDEWEB)

Belyaeva, A. I., E-mail: aibelyaeva@mail.ru; Savchenko, A. A. [National Technical University “Kharkov Politechnical Institute”, Kharkov, 61002 (Ukraine); Galuza, A. A.; Kolenov, I. V. [Institute of Electrophysics and Radiation Technologies, National Academy of Science of Ukraine, Kharkov, 61024 (Ukraine)

2014-07-15

Simultaneous effects of neutron irradiation and long–term sputtering on the surface relief of ITER–grade tungsten were studied. The effects of neutron–induced displacement damage have been simulated by irradiation of tungsten target with W{sup 6+} ions of 20 MeV energy. Ar{sup +} ions with energy 600 eV were used as imitation of charge exchange atoms in ITER. The surface relief was studied after each sputtering act. The singularity in the WJ–IG surface relief was ascertained experimentally at the first time, which determines the law of roughness extension under sputtering. As follows from the experimental data, the neutron irradiation has not to make a decisive additional contribution in the processes developing under impact of charge exchange atoms only.

Mono and sequential ion irradiation induced damage formation and damage recovery in oxide glasses: Stopping power dependence of the mechanical properties

International Nuclear Information System (INIS)

Mir, A.H.; Monnet, I.; Toulemonde, M.; Bouffard, S.; Jegou, C.; Peuget, S.

2016-01-01

Simple and complex borosilicate glasses were irradiated with single and double ion beams of light and heavy ions over a broad fluence and stopping power range. As a result of the heavy ion irradiation (U, Kr, Au), the hardness was observed to diminish and saturate after a decrease by 35 ± 1%. Unlike slow and swift heavy ion irradiation, irradiation with light ions (He,O) induced a saturation hardness decrease of 18 ± 1% only. During double ion beam irradiation; where glasses were first irradiated with a heavy ion (gold) and then by a light ion (helium), the light ion irradiation induced partial damage recovery. As a consequence of the recovery effect, the hardness of the pre-irradiated glasses increased by 10–15% depending on the chemical composition. These results highlight that the nuclear energy loss and high electronic energy loss (≥4 keV/nm) result in significant and similar modifications whereas light ions with low electronic energy loss (≤1 keV/nm) result in only mild damage formation in virgin glasses and recovery in highly pre-damaged glasses. These results are important to understand the damage formation and recovery in actinide bearing minerals and in glasses subjected to self-irradiation by alpha decays. - Highlights: • Behavior of glasses strongly depends on the electronic energy loss (Se) of the ions. • High Se (≥4 keV/nm) induces large changes in comparison to lower Se values. • Apart from mild damage formation, low Se causes recovery of pre-existing damage. • Alpha induced partial recovery of the damage would occur in nuclear waste glasses.

Ketoconazole-induced testicular damage in rats reduced by Gentiana extract.

Science.gov (United States)

Amin, Amr

2008-04-01

Ketoconazole (KET) is an antifungal drug with a broad spectrum of activity that also induces reproductive toxicity in humans and animals. The protective effect of Gentiana (GEN) extract (Gentiana lutea) against KET-induced testicular damage was evaluated in male Wistar rats. GEN extract was administered orally (1g/kgbwt/day) for 26 days. Three weeks after extract administration, KET was co-administered intraperitoneally at a dose of 100mg/kg once a day for 5 days. KET-induced reproductive toxicity was associated with clear reductions of the weights of testes and epididymides, sperm indices and serum testosterone levels. KET also induced severe testicular histopathological lesions such as degeneration of the seminiferous tubules and depletion of germ cells. In addition, marked oxidative damage to testicular lipids and alterations of natural antioxidants (catalase (CAT) and superoxide dismutase (SOD)) were reported in association with KET toxicity. Most of the KET-induced effects were greatly decreased with the concomitant application of GEN extract. This study suggests a protective role of GEN extract that could be attributed to its antioxidant properties.

Effect of temperature on surface error and laser damage threshold for self-healing BK7 glass.

Science.gov (United States)

Wang, Chu; Wang, Hongxiang; Shen, Lu; Hou, Jing; Xu, Qiao; Wang, Jian; Chen, Xianhua; Liu, Zhichao

2018-03-20

Cracks caused during the lapping and polishing process can decrease the laser-induced damage threshold (LIDT) of the BK7 glass optical elements, which would shorten the lifetime and limit the output power of the high-energy laser system. When BK7 glass is heated under appropriate conditions, the surface cracks can exhibit a self-healing phenomenon. In this paper, based on thermodynamics and viscous fluid mechanics theory, the mechanisms of crack self-healing are explained. The heat-healing experiment was carried out, and the effect of water was analyzed. The multi-spatial-frequency analysis was used to investigate the effect of temperature on surface error for self-healing BK7 glass, and the lapped BK7 glass specimens before and after heat healing were detected by an interferometer and atomic force microscopy. The low-spatial-frequency error was analyzed by peak to valley and root mean square, the mid-spatial-frequency error was analyzed by power spectral density, and the high-spatial-frequency error was analyzed by surface roughness. The results showed that the optimal heating temperature for BK7 was 450°C, and when the heating temperature was higher than the glass transition temperature (555°C), the surface quality decreased a lot. The laser damage test was performed, and the specimen heated at 450°C showed an improvement in LIDT.

Frost induced damages within porous materials - from concrete technology to fuel cells technique

Science.gov (United States)

Palecki, Susanne; Gorelkov, Stanislav; Wartmann, Jens; Heinzel, Angelika

2017-12-01

Porous media like concrete or layers of membrane electrode assemblies (MEA) within fuel cells are affected by a cyclic frost exposure due to different damage mechanisms which could lead to essential degradation of the material. In general, frost damages can only occur in case of a specific material moisture content. In fuel cells, residual water is generally available after shut down inside the membrane i.e. the gas diffusion layer (GDL). During subsequent freezing, this could cause various damage phenomena such as frost heaves and delamination effects of the membrane electrode assembly, which depends on the location of pore water and on the pore structure itself. Porous materials possess a pore structure that could range over several orders of magnitudes with different properties and freezing behaviour of the pore water. Latter can be divided into macroscopic, structured and pre-structured water, influenced by surface interactions. Therefore below 0 °C different water modifications can coexist in a wide temperature range, so that during frost exposure a high amount of unfrozen and moveable water inside the pore system is still available. This induces transport mechanisms and shrinkage effects. The physical basics are similar for porous media. While the freezing behaviour of concrete has been studied over decades of years, in order to enhance the durability, the know-how about the influence of a frost attack on fuel cell systems is not fully understood to date. On the basis of frost damage models for concrete structures, an approach to describe the impact of cyclic freezing and thawing on membrane electrode assemblies has been developed within this research work. Major aim is beyond a better understanding of the frost induced mechanisms, the standardization of a suitable test procedure for the assessment of different MEA materials under such kind of attack. Within this contribution first results will be introduced.

Modeling DNA?damage-induced pneumopathy in mice: insight from danger signaling cascades

OpenAIRE

Wirsd?rfer, Florian; Jendrossek, Verena

2017-01-01

Radiation-induced pneumonitis and fibrosis represent severe and dose-limiting side effects in the radiotherapy of thorax-associated neoplasms leading to decreased quality of life or - as a consequence of treatment with suboptimal radiation doses - to fatal outcomes by local recurrence or metastatic disease. It is assumed that the initial radiation-induced damage to the resident cells triggers a multifaceted damage-signalling cascade in irradiated normal tissues including a multifactorial secr...

Is there a role for leukotrienes as mediators of ethanol-induced gastric mucosal damage?

International Nuclear Information System (INIS)

Wallace, J.L.; Beck, P.L.; Morris, G.P.

1988-01-01

The role of leukotriene (LT) C 4 as a mediator of ethanol-induced gastric mucosal damage was investigated. Rats were pretreated with a number of compounds, including inhibitors of leukotriene biosynthesis and agents that have previously been shown to reduce ethanol-induced damage prior to oral administration of absolute ethanol. Ethanol administration resulted in a fourfold increase in LTC 4 synthesis. LTC 4 synthesis could be reduced significantly by pretreatment with L651,392 or dexamethosone without altering the susceptibility of the gastric mucosa to ethanol-induced damage. Furthermore, changes in LBT 4 synthesis paralleled the changes in LTC 4 synthesis observed after ethanol administration. The effects of ethanol on gastric eicosanoid synthesis were further examined using an ex vivo gastric chamber preparation that allowed for application of ethanol to only one side of the stomach. These studies confirm that ethanol can stimulate gastric leukotriene synthesis independent of the production of hemorrhagic damage. Inhibition of LTC 4 synthesis does not confer protection to the mucosa, suggesting that LTC 4 does not play an important role in the etiology of ethanol-induced gastric damage

Spontaneous perseverative turning in rats with radiation-induced hippocampal damage

International Nuclear Information System (INIS)

Mickley, G.A.; Ferguson, J.L.; Nemeth, T.J.; Mulvihill, M.A.; Alderks, C.E.

1989-01-01

This study found a new behavioral correlate of lesions specific to the dentate granule cell layer of the hippocampus: spontaneous perseverative turning. Irradiation of a portion of the neonatal rat cerebral hemispheres produced hypoplasia of the granule cell layer of the hippocampal dentate gyrus while sparing the rest of the brain. Radiation-induced damage to the hippocampal formation caused rats placed in bowls to spontaneously turn in long, slow bouts without reversals. Irradiated subjects also exhibited other behaviors characteristic of hippocampal damage (e.g., perseveration in spontaneous exploration of the arms of a T-maze, retarded acquisition of a passive avoidance task, and increased horizontal locomotion). These data extend previously reported behavioral correlates of fascia dentata lesions and suggest the usefulness of a bout analysis of spontaneous bowl turning as a measure of nondiscrete-trial spontaneous alternation and a sensitive additional indicator of radiation-induced hippocampal damage

Dunnione ameliorates cisplatin-induced small intestinal damage by modulating NAD{sup +} metabolism

Energy Technology Data Exchange (ETDEWEB)

Pandit, Arpana; Kim, Hyung-Jin; Oh, Gi-Su; Shen, AiHua; Lee, Su-Bin; Khadka, Dipendra; Lee, SeungHoon [Center for Metabolic Function Regulation & Department of Microbiology, Wonkwang University, Iksan, Jeonbuk 570-749 (Korea, Republic of); Shim, Hyeok; Yang, Sei-Hoon; Cho, Eun-Young [Department of Internal Medicine, School of Medicine, Wonkwang University, Iksan, Jeonbuk 570-749 (Korea, Republic of); Kwon, Kang-Beom [Department of Oriental Medical Physiology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 570-749 (Korea, Republic of); Kwak, Tae Hwan [PAEAN Biotechnology, 160 Techno-2 Street, Yuseong-gu, Daejeon 305-500 (Korea, Republic of); Choe, Seong-Kyu; Park, Raekil [Center for Metabolic Function Regulation & Department of Microbiology, Wonkwang University, Iksan, Jeonbuk 570-749 (Korea, Republic of); So, Hong-Seob, E-mail: jeanso@wku.ac.kr [Center for Metabolic Function Regulation & Department of Microbiology, Wonkwang University, Iksan, Jeonbuk 570-749 (Korea, Republic of)

2015-11-27

Although cisplatin is a widely used anticancer drug for the treatment of a variety of tumors, its use is critically limited because of adverse effects such as ototoxicity, nephrotoxicity, neuropathy, and gastrointestinal damage. Cisplatin treatment increases oxidative stress biomarkers in the small intestine, which may induce apoptosis of epithelial cells and thereby elicit damage to the small intestine. Nicotinamide adenine dinucleotide (NAD{sup +}) is a cofactor for various enzymes associated with cellular homeostasis. In the present study, we demonstrated that the hyper-activation of poly(ADP-ribose) polymerase-1 (PARP-1) is closely associated with the depletion of NAD{sup +} in the small intestine after cisplatin treatment, which results in downregulation of sirtuin1 (SIRT1) activity. Furthermore, a decrease in SIRT1 activity was found to play an important role in cisplatin-mediated small intestinal damage through nuclear factor (NF)-κB p65 activation, facilitated by its acetylation increase. However, use of dunnione as a strong substrate for the NADH:quinone oxidoreductase 1 (NQO1) enzyme led to an increase in intracellular NAD{sup +} levels and prevented the cisplatin-induced small intestinal damage correlating with the modulation of PARP-1, SIRT1, and NF-κB. These results suggest that direct modulation of cellular NAD{sup +} levels by pharmacological NQO1 substrates could be a promising therapeutic approach for protecting against cisplatin-induced small intestinal damage. - Highlights: • NAD{sup +} acts as a cofactor for numerous enzymes including Sirtuins and PARP. • Up-regulation of SIRT1 could attenuate the cisplatin-induced intestinal damage. • Modulation of the cellular NAD{sup +} could be a promising therapeutic approach.

Activation of protein kinase A and clustering of cell surface receptors by N-methyl-N'-nitro-N-nitrosoguanidine are independent of genomic DNA damage

Energy Technology Data Exchange (ETDEWEB)

Wang Zheng; Wang Guliang; Yang Jun; Guo Lei; Yu Yingnian

2003-07-25

Alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces cellular stress leading to chromosomal aberrations, mutations and cell death. Previous reports from our laboratory have shown that low concentration of MNNG induces untargeted mutation (UTM), which occurs on intact DNA in mammalian cells through changes in gene expression profile. It also causes the activation of cAMP-protein kinase A (PKA) and up-regulation of POL-{beta}, which is demonstrated to play a role in DNA repair system. In order to find out the possible initial signal involved in UTM, we try to investigate whether the activation of PKA-CREB signal pathway is closely related to DNA damage. Our data shows that the treatment of low concentration MNNG (0.2 {mu}M) activates PKA-CREB pathway in a comparable level both in a nuclear and enucleated cell system. And similar to the cell response caused by UV, the clustering of cell surface receptors of epidermal growth factor (EGF) and tumor necrosis factor {alpha} (TNF{alpha}) was also observed in cells exposed to MNNG. It was further demonstrated that the clustering of the surface receptors is independent of the genomic DNA damage, as this phenomenon was also observed in enucleated cells. These observations indicate that the initiation of signal cascades induced by low concentration of MNNG might be associated with its interaction with cell surface receptors and/or direct activation of related signal proteins but not its DNA damaging property.

Electron Beam Induced Radiation Damage of the Semiconductor Radiation Detector based on Silicon

International Nuclear Information System (INIS)

Kim, Han Soo; Kim, Yong Kyun; Park, Se Hwan; Haa, Jang Ho; Kang, Sang Mook; Chung, Chong Eun; Cho, Seung Yeon; Park, Ji Hyun; Yoon, Tae Hyung

2005-01-01

A Silicon Surface Barrier (SSB) semiconductor detector which is generally used to detect a charged particle such as an alpha particle was developed. The performance of the developed SSB semiconductor detector was measured with an I-V curve and an alpha spectrum. The response for an alpha particle was measured by Pu-238 sources. A SSB semiconductor detector was irradiated firstly at 30sec, at 30μA and secondly 40sec, 40μA with a 2MeV pulsed electron beam generator in KAERI. And the electron beam induced radiation damage of a homemade SSB detector and the commercially available PIN photodiode were investigated. An annealing effect of the damaged SSB and PIN diode detector were also investigated using a Rapid Thermal Annealing (RTA). This data may assist in designing the silicon based semiconductor radiation detector when it is operated in a high radiation field such as space or a nuclear power plant

Study of surface damage on cell envelope assessed by AFM and flow cytometry of Lactobacillus plantarum exposed to ethanol and dehydration.

Science.gov (United States)

Bravo-Ferrada, B M; Gonçalves, S; Semorile, L; Santos, N C; Tymczyszyn, E E; Hollmann, A

2015-06-01

In this work, we evaluated freeze-drying damage at the surface level of oenological strain Lactobacillus plantarum UNQLp155, as well as its ability to grow in a synthetic wine with and without pre-acclimation. Damage on cell surface was studied by flow cytometry, zeta potential and atomic force microscopy, and cell survival was analysed by plate count. Results showed that beside cells acclimated at lower ethanol concentration (6% v/v) became more susceptible to drying than nonacclimated ones, after rehydration they maintain their increased ability to grow in a synthetic wine. Acclimation at a higher ethanol concentration (10% v/v) produces several damages on the cell surface losing its ability to grow in a synthetic wine. In this work, we showed for the first time that sublethal alterations on bacterial surface induced by a pre-acclimation with a low ethanol concentration (6%), upon a freeze-drying process, result in a better bacterial adaptation to the stress conditions of wine-like medium, as well as to the preservation process. Understanding the adaptation to ethanol of oenological strains and their effects on the preservation process has a strong impact on winemaking process and allows to define the most appropriate conditions to obtain malolactic starters cultures. © 2015 The Society for Applied Microbiology.

Robust optimization of the laser induced damage threshold of dielectric mirrors for high power lasers.

Science.gov (United States)

Chorel, Marine; Lanternier, Thomas; Lavastre, Éric; Bonod, Nicolas; Bousquet, Bruno; Néauport, Jérôme

2018-04-30

We report on a numerical optimization of the laser induced damage threshold of multi-dielectric high reflection mirrors in the sub-picosecond regime. We highlight the interplay between the electric field distribution, refractive index and intrinsic laser induced damage threshold of the materials on the overall laser induced damage threshold (LIDT) of the multilayer. We describe an optimization method of the multilayer that minimizes the field enhancement in high refractive index materials while preserving a near perfect reflectivity. This method yields a significant improvement of the damage resistance since a maximum increase of 40% can be achieved on the overall LIDT of the multilayer.

Ku70 inhibits gemcitabine-induced DNA damage and pancreatic cancer cell apoptosis

International Nuclear Information System (INIS)

Ma, Jiali; Hui, Pingping; Meng, Wenying; Wang, Na; Xiang, Shihao

2017-01-01

The current study focused on the role of Ku70, a DNA-dependent protein kinase (DNA-PK) complex protein, in pancreatic cancer cell resistance to gemcitabine. In both established cell lines (Mia-PaCa-2 and PANC-1) and primary human pancreatic cancer cells, shRNA/siRNA-mediated knockdown of Ku70 significantly sensitized gemcitabine-induced cell death and proliferation inhibition. Meanwhile, gemcitabine-induced DNA damage and subsequent pancreatic cancer cell apoptosis were also potentiated with Ku70 knockdown. On the other hand, exogenous overexpression of Ku70 in Mia-PaCa-2 cells suppressed gemcitabine-induced DNA damage and subsequent cell apoptosis. In a severe combined immune deficient (SCID) mice Mia-PaCa-2 xenograft model, gemcitabine-induced anti-tumor activity was remarkably pontificated when combined with Ku70 shRNA knockdown in the xenografts. The results of this preclinical study imply that Ku70 might be a primary resistance factor of gemcitabine, and Ku70 silence could significantly chemo-sensitize gemcitabine in pancreatic cancer cells. - Highlights: • Ku70 knockdown sensitizes gemcitabine-induced killing of pancreatic cancer cells. • Ku70 knockdown facilitates gemcitabine-induced DNA damage and cell apoptosis. • Ku70 overexpression deceases gemcitabine's sensitivity in pancreatic cancer cells. • Ku70 knockdown sensitizes gemcitabine-induced anti-tumor activity in vivo.

Protective Effect of HSP25 on Radiation Induced Tissue Damage

International Nuclear Information System (INIS)

Lee, Hae-June; Lee, Yoon-Jin; Kwon, Hee-Choong; Bae, Sang-Woo; Lee, Yun-Sil; Kim, Sung Ho

2007-01-01

Control of cancer by irradiation therapy alone or in conjunction with combination chemotherapy is often limited by organ specific toxicity. Ionizing irradiation toxicity is initiated by damage to normal tissue near the tumor target and within the transit volume of radiotherapy beams. Irradiation-induced cellular, tissue, and organ damage is mediated by acute effects, which can be dose limiting. A latent period follows recovery from the acute reaction, then chronic irradiation fibrosis (late effects) pose a second cause of organ failure. HSP25/27 has been suggested to protect cells against apoptotic cell death triggered by hyperthermia, ionizing radiation, oxidative stress, Fas ligand, and cytotoxic drugs. And several mechanisms have been proposed to account for HSP27-mediated apoptotic protection. However radioprotective effect of HSP25/27 in vivo system has not yet been evaluated. The aim of this study was to evaluate the potential of exogenous HSP25 expression, as delivered by adenoviral vectors, to protect animal from radiation induced tissue damage

Muscle damage and repeated bout effect induced by enhanced eccentric squats.

Science.gov (United States)

Coratella, Giuseppe; Chemello, Alessandro; Schena, Federico

2016-12-01

Muscle damage and repeated bout effect have been studied after pure eccentric-only exercise. The aim of this study was to evaluate muscle damage and repeated bout effect induced by enhanced eccentric squat exercise using flywheel device. Thirteen healthy males volunteered for this study. Creatine kinase blood activity (CK), quadriceps isometric peak torque and muscle soreness were used as markers of muscle damage. The dependent parameters were measured at baseline, immediately after and each day up to 96 hours after the exercise session. The intervention consisted of 100 repetitions of enhanced eccentric squat exercise using flywheel device. The same protocol was repeated after 4 weeks. After the first bout, CK and muscle soreness were significantly greater (P0.05), while isometric peak torque and muscle soreness returned to values similar to baseline after respectively 48 and 72 hours. All muscle damage markers were significantly lower after second compared to first bout. The enhanced eccentric exercise induced symptoms of muscle damage up to 96 hours. However, it provided muscle protection after the second bout, performed four weeks later. Although it was not eccentric-only exercise, the enhancement of eccentric phase provided muscle protection.

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

Directory of Open Access Journals (Sweden)

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.

Repair of ultraviolet-light-induced DNA damage in Vibrio cholerae

International Nuclear Information System (INIS)

Das, G.; Sil, K.; Das, J.

1981-01-01

Repair of ultraviolet-light-induced DNA damage in a highly pathogenic Gram-negative bacterium, Vibrio cholerae, has been examined. All three strains of V. cholerae belonging to two serotypes, Inaba and Ogawa, are very sensitive to ultraviolet irradiation, having inactivation cross-sections ranging from 0.18 to 0.24 m 2 /J. Although these cells are proficient in repairing the DNA damage by a photoreactivation mechanism, they do not possess efficient dark repair systems. The mild toxinogenic strain 154 of classical Vibrios presumably lacks any excision repair mechanism and studies of irradiated cell DNA indicate that the ultraviolet-induced pyrimidine dimers may not be excised. Ultraviolet-irradiated cells after saturation of dark repair can be further photoreactivated. (Auth.)

Involvement of inducible nitric oxide synthase in radiation-induced vascular endothelial damage

International Nuclear Information System (INIS)

Hong, Chang-Won; Lee, Joon-Ho; Kim, Suwan; Noh, Jae Myoung; Kim, Young-Mee; Pyo, Hongryull; Lee, Sunyoung

2013-01-01

The use of radiation therapy has been linked to an increased risk of cardiovascular disease. To understand the mechanisms underlying radiation-induced vascular dysfunction, we employed two models. First, we examined the effect of X-ray irradiation on vasodilation in rabbit carotid arteries. Carotid arterial rings were irradiated with 8 or 16 Gy using in vivo and ex vivo methods. We measured the effect of acetylcholine-induced relaxation after phenylephrine-induced contraction on the rings. In irradiated carotid arteries, vasodilation was significantly attenuated by both irradiation methods. The relaxation response was completely blocked by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a potent inhibitor of soluble guanylate cyclase. Residual relaxation persisted after treatment with L-N ω -nitroarginine (L-NA), a non-specific inhibitor of nitric oxide synthase (NOS), but disappeared following the addition of aminoguanidine (AG), a selective inhibitor of inducible NOS (iNOS). The relaxation response was also affected by tetraethylammonium, an inhibitor of endothelium-derived hyperpolarizing factor activity. In the second model, we investigated the biochemical events of nitrosative stress in human umbilical-vein endothelial cells (HUVECs). We measured iNOS and nitrotyrosine expression in HUVECs exposed to a dose of 4 Gy. The expression of iNOS and nitrotyrosine was greater in irradiated HUVECs than in untreated controls. Pretreatment with AG, L-N 6 -(1-iminoethyl) lysine hydrochloride (a selective inhibitor of iNOS), and L-NA attenuated nitrosative stress. While a selective target of radiation-induced vascular endothelial damage was not definitely determined, these results suggest that NO generated from iNOS could contribute to vasorelaxation. These studies highlight a potential role of iNOS inhibitors in ameliorating radiation-induced vascular endothelial damage. (author)

The effect of dithiothreitol on radiation-induced genetic damage in Arabidopsis thaliana (L) Heynh

International Nuclear Information System (INIS)

Dellaert, L.M.W.

1980-01-01

A study was made on the effect of dithiothreitol (DTT; present during irradiation) on M 1 ovule sterility, M 2 embryonic lethals, M 2 chlorophyll mutants and M 2 viable mutants induced with fast neutrons or X-rays in Arabidopsis thaliana. DTT provides considerable protection against both fast-neutron and X-ray induced genetic damage. However, a higher protection was observed against M 1 ovule sterility, than against embryonic lethals, chlorophylls and viable mutants. This implies a significant DTT-induced spectral shift (0.01 < p < 0.05), i.e. a shift in the relative frequencies of the different genetic parameters. This spectral shift is explained on the basis of a specific DTT protection against radiation-induced strand breaks, and by differences in the ratio strand breaks/base damage for the genetic parameters concerned, i.e. a higher ratio for ovule sterility than for the other parameters. The induction of the genetic damage by ionizing radiation, either with or without DTT, is described by a mathematical model, which includes both strand breaks and base damage. The model shows that the resolving power of a test for a 'mutation'spectral shift depends on the relative values of the strandbreak reduction factor of -SH compounds and on the ratio strand breaks/base damage of the genetic parameters. For each genetic parameter the DTT damage reduction factor (DRF) is calculated per irradiation dose, and in addition the average (over-all doses) ratio strand breaks/base damage. (orig.)

Radiation damage in nonmetallic solids under dense electronic excitation

International Nuclear Information System (INIS)

Itoh, Noriaki; Tanimura, Katsumi; Nakai, Yasuo

1992-01-01

Basic processes of radiation damage of insulators by dense electronic excitation are reviewed. First it is pointed out that electronic excitation of nonmetallic solids produces the self-trapped excitons and defect-related metastable states having relatively long lifetimes, and that the excitation of these metastable states, produces stable defects. The effects of irradiation with heavy ions, including track registration, are surveyed on the basis of the microscopic studies. It is pointed out also that the excitation of the metastable states plays a role in laser-induced damage at relatively low fluences, while the laser damage has been reported to be governed by heating of free electrons produced by multiphoton excitation. Difference in the contributions of the excitation of metastable defects to laser-induced damage of surfaces, or laser ablation, and laser-induced bulk damage is stressed. (orig.)

Molecular dynamics simulation of temperature effects on low energy near-surface cascades and surface damage in Cu

Science.gov (United States)

Zhu, Guo; Sun, Jiangping; Guo, Xiongxiong; Zou, Xixi; Zhang, Libin; Gan, Zhiyin

2017-06-01

The temperature effects on near-surface cascades and surface damage in Cu(0 0 1) surface under 500 eV argon ion bombardment were studied using molecular dynamics (MD) method. In present MD model, substrate system was fully relaxed for 1 ns and a read-restart scheme was introduced to save total computation time. The temperature dependence of damage production was calculated. The evolution of near-surface cascades and spatial distribution of adatoms at varying temperature were analyzed and compared. It was found that near-surface vacancies increased with temperature, which was mainly due to the fact that more atoms initially located in top two layers became adatoms with the decrease of surface binding energy. Moreover, with the increase of temperature, displacement cascades altered from channeling-like structure to branching structure, and the length of collision sequence decreased gradually, because a larger portion of energy of primary knock-on atom (PKA) was scattered out of focused chain. Furthermore, increasing temperature reduced the anisotropy of distribution of adatoms, which can be ascribed to that regular registry of surface lattice atoms was changed with the increase of thermal vibration amplitude of surface atoms.

Molecular dynamics simulation of temperature effects on low energy near-surface cascades and surface damage in Cu

Energy Technology Data Exchange (ETDEWEB)

Zhu, Guo; Sun, Jiangping; Guo, Xiongxiong; Zou, Xixi; Zhang, Libin; Gan, Zhiyin, E-mail: ganzhiyin@126.com

2017-06-15

The temperature effects on near-surface cascades and surface damage in Cu(0 0 1) surface under 500 eV argon ion bombardment were studied using molecular dynamics (MD) method. In present MD model, substrate system was fully relaxed for 1 ns and a read-restart scheme was introduced to save total computation time. The temperature dependence of damage production was calculated. The evolution of near-surface cascades and spatial distribution of adatoms at varying temperature were analyzed and compared. It was found that near-surface vacancies increased with temperature, which was mainly due to the fact that more atoms initially located in top two layers became adatoms with the decrease of surface binding energy. Moreover, with the increase of temperature, displacement cascades altered from channeling-like structure to branching structure, and the length of collision sequence decreased gradually, because a larger portion of energy of primary knock-on atom (PKA) was scattered out of focused chain. Furthermore, increasing temperature reduced the anisotropy of distribution of adatoms, which can be ascribed to that regular registry of surface lattice atoms was changed with the increase of thermal vibration amplitude of surface atoms.

Damage-induced ectopic recombination in the yeast Saccharomyces cerevisiae.

Science.gov (United States)

Kupiec, M; Steinlauf, R

1997-06-09

Mitotic recombination in the yeast Saccharomyces cerevisiae is induced when cells are irradiated with UV or X-rays, reflecting the efficient repair of damage by recombinational repair mechanisms. We have used multiply marked haploid strains that allow the simultaneous detection of several types of ectopic recombination events. We show that inter-chromosomal ectopic conversion of lys2 heteroalleles and, to a lesser extent, direct repeat recombination (DRR) between non-tandem repeats, are increased by DNA-damaging agents; in contrast, ectopic recombination of the naturally occurring Ty element is not induced. We have tested several hypotheses that could explain the preferential lack of induction of Ty recombination by DNA-damaging agents. We have found that the lack of induction cannot be explained by a cell cycle control or by an effect of the mating-type genes. We also found no role for the flanking long terminal repeats (LTRs) of the Ty in preventing the induction. Ectopic conversion, DRR, and forward mutation of artificial repeats show different kinetics of induction at various positions of the cell cycle, reflecting different mechanisms of recombination. We discuss the mechanistic and evolutionary aspects of these results.

Automated 3D Damaged Cavity Model Builder for Lower Surface Acreage Tile on Orbiter

Science.gov (United States)

Belknap, Shannon; Zhang, Michael

2013-01-01

The 3D Automated Thermal Tool for Damaged Acreage Tile Math Model builder was developed to perform quickly and accurately 3D thermal analyses on damaged lower surface acreage tiles and structures beneath the damaged locations on a Space Shuttle Orbiter. The 3D model builder created both TRASYS geometric math models (GMMs) and SINDA thermal math models (TMMs) to simulate an idealized damaged cavity in the damaged tile(s). The GMMs are processed in TRASYS to generate radiation conductors between the surfaces in the cavity. The radiation conductors are inserted into the TMMs, which are processed in SINDA to generate temperature histories for all of the nodes on each layer of the TMM. The invention allows a thermal analyst to create quickly and accurately a 3D model of a damaged lower surface tile on the orbiter. The 3D model builder can generate a GMM and the correspond ing TMM in one or two minutes, with the damaged cavity included in the tile material. A separate program creates a configuration file, which would take a couple of minutes to edit. This configuration file is read by the model builder program to determine the location of the damage, the correct tile type, tile thickness, structure thickness, and SIP thickness of the damage, so that the model builder program can build an accurate model at the specified location. Once the models are built, they are processed by the TRASYS and SINDA.

Determination of ultra-short laser induced damage threshold of KH{sub 2}PO{sub 4} crystal: Numerical calculation and experimental verification

Energy Technology Data Exchange (ETDEWEB)

Cheng, Jian [Center for Precision Engineering, School of Mechatronics Engineering, Harbin Institute of Technology, Harbin 150001 (China); Department of Physics, The Ohio State University, 191 W. Woodruff Ave, Columbus, OH 43210 (United States); Chen, Mingjun, E-mail: chenmj@hit.edu.cn, E-mail: chowdhury.24@osu.edu; Wang, Jinghe; Xiao, Yong [Center for Precision Engineering, School of Mechatronics Engineering, Harbin Institute of Technology, Harbin 150001 (China); Kafka, Kyle; Austin, Drake; Chowdhury, Enam, E-mail: chenmj@hit.edu.cn, E-mail: chowdhury.24@osu.edu [Department of Physics, The Ohio State University, 191 W. Woodruff Ave, Columbus, OH 43210 (United States)

2016-03-15

Rapid growth and ultra-precision machining of large-size KDP (KH{sub 2}PO{sub 4}) crystals with high laser damage resistance are tough challenges in the development of large laser systems. It is of high interest and practical significance to have theoretical models for scientists and manufacturers to determine the laser-induced damage threshold (LIDT) of actually prepared KDP optics. Here, we numerically and experimentally investigate the laser-induced damage on KDP crystals in ultra-short pulse laser regime. On basis of the rate equation for free electron generation, a model dedicated to predicting the LIDT is developed by considering the synergistic effect of photoionization, impact ionization and decay of electrons. Laser damage tests are performed to measure the single-pulse LIDT with several testing protocols. The testing results combined with previously reported experimental data agree well with those calculated by the model. By taking the light intensification into consideration, the model is successfully applied to quantitatively evaluate the effect of surface flaws inevitably introduced in the preparation processes on the laser damage resistance of KDP crystals. This work can not only contribute to further understanding of the laser damage mechanisms of optical materials, but also provide available models for evaluating the laser damage resistance of exquisitely prepared optical components used in high power laser systems.

Furfural induces reactive oxygen species accumulation and cellular damage in Saccharomyces cerevisiae

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Slininger Patricia J

2010-01-01

Full Text Available Abstract Background Biofuels offer a viable alternative to petroleum-based fuel. However, current methods are not sufficient and the technology required in order to use lignocellulosic biomass as a fermentation substrate faces several challenges. One challenge is the need for a robust fermentative microorganism that can tolerate the inhibitors present during lignocellulosic fermentation. These inhibitors include the furan aldehyde, furfural, which is released as a byproduct of pentose dehydration during the weak acid pretreatment of lignocellulose. In order to survive in the presence of furfural, yeast cells need not only to reduce furfural to the less toxic furan methanol, but also to protect themselves and repair any damage caused by the furfural. Since furfural tolerance in yeast requires a functional pentose phosphate pathway (PPP, and the PPP is associated with reactive oxygen species (ROS tolerance, we decided to investigate whether or not furfural induces ROS and its related cellular damage in yeast. Results We demonstrated that furfural induces the accumulation of ROS in Saccharomyces cerevisiae. In addition, furfural was shown to cause cellular damage that is consistent with ROS accumulation in cells which includes damage to mitochondria and vacuole membranes, the actin cytoskeleton and nuclear chromatin. The furfural-induced damage is less severe when yeast are grown in a furfural concentration (25 mM that allows for eventual growth after an extended lag compared to a concentration of furfural (50 mM that prevents growth. Conclusion These data suggest that when yeast cells encounter the inhibitor furfural, they not only need to reduce furfural into furan methanol but also to protect themselves from the cellular effects of furfural and repair any damage caused. The reduced cellular damage seen at 25 mM furfural compared to 50 mM furfural may be linked to the observation that at 25 mM furfural yeast were able to exit the furfural-induced

ATM-activated autotaxin (ATX) propagates inflammation and DNA damage in lung epithelial cells: a new mode of action for silica-induced DNA damage?

Science.gov (United States)

Zheng, Huiyuan; Högberg, Johan; Stenius, Ulla

2017-12-07

Silica exposure is a common risk factor for lung cancer. It has been claimed that key elements in cancer development are activation of inflammatory cells that indirectly induce DNA damage and proliferative stimuli in respiratory epithelial cells. We studied DNA damage induced by silica particles in respiratory epithelial cells and focused the role of the signaling enzyme autotaxin (ATX). A549 and 16 bronchial epithelial cells (16HBE) lung epithelial cells were exposed to silica particles. Reactive oxygen species (ROS), NOD-like receptor family pyrin domain containing-3 (NLRP3) inflammasome activation, ATX, ataxia telangiectasia mutated (ATM), and DNA damage (γH2AX, pCHK1, pCHK2, comet assay) were end points. Low doses of silica induced NLRP3 activation, DNA damage accumulation, and ATM phosphorylation. A novel finding was that ATM induced ATX generation and secretion. Not only silica but also rotenone, camptothecin and H2O2 activated ATX via ATM, suggesting that ATX is part of a generalized ATM response to double-strand breaks (DSBs). Surprisingly, ATX inhibition mitigated DNA damage accumulation at later time points (6-16 h), and ATX transfection caused NLRP3 activation and DNA damage. Furthermore, the product of ATX enzymatic activity, lysophosphatidic acid, recapitulated the effects of ATX transfection. These data indicate an ATM-ATX-dependent loop that propagates inflammation and DSB accumulation, making low doses of silica effective inducers of DSBs in epithelial cells. We conclude that an ATM-ATX axis interconnects DSBs with silica-induced inflammation and propagates these effects in epithelial cells. Further studies of this adverse outcome pathway may give an accurate assessment of the lowest doses of silica that causes cancer. © The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

STING-IRF3 Triggers Endothelial Inflammation in Response to Free Fatty Acid-Induced Mitochondrial Damage in Diet-Induced Obesity

Science.gov (United States)

Mao, Yun; Luo, Wei; Zhang, Lin; Wu, Weiwei; Yuan, Liangshuai; Xu, Hao; Song, Juhee; Fujiwara, Keigi; Abe, Jun-ichi; LeMaire, Scott A.; Wang, Xing Li; Shen, Ying. H.

2017-01-01

Objective Metabolic stress in obesity induces endothelial inflammation and activation, which initiates adipose tissue inflammation, insulin resistance, and cardiovascular diseases. However, the mechanisms underlying endothelial inflammation induction are not completely understood. Stimulator of interferon genes (STING) is an important molecule in immunity and inflammation. In the present study, we sought to determine the role of STING in palmitic acid (PA)-induced endothelial activation/inflammation. Approach and Results In cultured endothelial cells, PA treatment activated STING, as indicated by its perinuclear translocation and binding to interferon regulatory factor 3 (IRF3), leading to IRF3 phosphorylation and nuclear translocation. The activated IRF3 bound to the promoter of intercellular adhesion molecule 1 (ICAM-1) and induced ICAM-1 expression and monocyte–endothelial cell adhesion. When analyzing the upstream signaling, we found that PA activated STING by inducing mitochondrial damage. PA treatment caused mitochondrial damage and leakage of mitochondrial DNA (mtDNA) into the cytosol. Through the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS), the mitochondrial damage and leaked cytosolic mtDNA activated the STING-IRF3 pathway and increased ICAM-1 expression. In mice with diet-induced obesity, the STING-IRF3 pathway was activated in adipose tissue. However, STING deficiency (Stinggt/gt) partially prevented diet-induced adipose tissue inflammation, obesity, insulin resistance, and glucose intolerance. Conclusions The mitochondrial damage-cGAS-STING-IRF3 pathway is critically involved in metabolic stress-induced endothelial inflammation. STING may be a potential therapeutic target for preventing cardiovascular diseases and insulin resistance in obese individuals. PMID:28302626

Studies of cellular damage induced by X-rays and visible light

International Nuclear Information System (INIS)

Christensen, T.; Kinn, G.; Reitan, J.B.

1989-01-01

DNA-damage in cells has been studied by use of spectrophotometry and fluorometry. The method is based on the differential fluorescence quantum yield of the fluorochrome Hoechst 33258 when bound to single and double stranded DNA, respectively. DNA-damage by doses of X-rays below 2 Gy was clearly detectable. Blue light from phototherapy lamps induced DNA-damage in human TMG-1 glioblastoma, but no significant effect could be observed after irradiation with green lamps. In the presence of bilirubin the amount of DNA-damage was increased, notably at high bilirubin concentration and by blue light. 9 refs; 12 figs

Clustered DNA damages induced in isolated DNA and in human cells by low doses of ionizing radiation

Science.gov (United States)

Sutherland, B. M.; Bennett, P. V.; Sidorkina, O.; Laval, J.; Lowenstein, D. I. (Principal Investigator)

2000-01-01

Clustered DNA damages-two or more closely spaced damages (strand breaks, abasic sites, or oxidized bases) on opposing strands-are suspects as critical lesions producing lethal and mutagenic effects of ionizing radiation. However, as a result of the lack of methods for measuring damage clusters induced by ionizing radiation in genomic DNA, neither the frequencies of their production by physiological doses of radiation, nor their repairability, nor their biological effects are known. On the basis of methods that we developed for quantitating damages in large DNAs, we have devised and validated a way of measuring ionizing radiation-induced clustered lesions in genomic DNA, including DNA from human cells. DNA is treated with an endonuclease that induces a single-strand cleavage at an oxidized base or abasic site. If there are two closely spaced damages on opposing strands, such cleavage will reduce the size of the DNA on a nondenaturing gel. We show that ionizing radiation does induce clustered DNA damages containing abasic sites, oxidized purines, or oxidized pyrimidines. Further, the frequency of each of these cluster classes is comparable to that of frank double-strand breaks; among all complex damages induced by ionizing radiation, double-strand breaks are only about 20%, with other clustered damage constituting some 80%. We also show that even low doses (0.1-1 Gy) of high linear energy transfer ionizing radiation induce clustered damages in human cells.

Carcinogen-induced damage to DNA

International Nuclear Information System (INIS)

Strauss, B.; Altamirano, M.; Bose, K.; Sklar, R.; Tatsumi, K.

1979-01-01

Human cells respond to carcinogen-induced damage in their DNA in at least two ways. The first response, excision repair, proceeds by at least three variations, depending on the nature of the damage. Nucleotide excision results in relatively large repair patches but few free DNA breaks, since the endonuclease step is limiting. Apurinic repair is characterized by the appearance of numerous breaks in the DNA and by short repair patches. The pathways behave as though they function independently. Lymphoic cells derived from a xeroderma pigmentosum complementation group C patient are deficient in their ability to perform nucleotide excision and also to excise 6 methoxyguanine adducts, but they are apurinic repair competent. Organisms may bypass damage in their DNA. Lymphoblastoid cells, including those derived from xeroderma pigmentosum treated with 3 H-anti-BPDE, can replicate their DNA at low doses of carcinogen. Unexcised 3 H is found in the light or parental strand of the resulting hybrid DNA when replication occurs in medium with BrdUrd. This observation indicates a bypass reaction occurring by a mechanism involving branch migration at DNA growing points. Branch migration in DNA preparations have been observed, but the evidence is that most occurs in BrdUrd-containing DNA during cell lysis. The measurement of the bifilarly substituted DNA resulting from branch migration is a convenient method of estimating the proportion of new synthesis remaining in the vicinity of the DNA growing point. Treatment with carcinogens or caffeine results in accumulation of DNA growing points accompanied by the synthesis of shortened pieces of daughter DNA

Feasibility of OCT to detect radiation-induced esophageal damage in small animal models (Conference Presentation)

Science.gov (United States)

Jelvehgaran, Pouya; Alderliesten, Tanja; Salguero, Javier; Borst, Gerben; Song, Ji-Ying; van Leeuwen, Ton G.; de Boer, Johannes F.; de Bruin, Daniel M.; van Herk, Marcel B.

2016-03-01

Lung cancer survival is poor and radiotherapy patients often suffer serious treatment side effects. The esophagus is particularly sensitive leading to reduced food intake or even fistula formation. Only few direct techniques exist to measure radiation-induced esophageal damage, for which knowledge is needed to improve the balance between risk of tumor recurrence and complications. Optical coherence tomography (OCT) is a minimally-invasive imaging technique that obtains cross-sectional, high-resolution (1-10µm) images and is capable of scanning the esophageal wall up to 2-3mm depth. In this study we investigated the feasibility of OCT to detect esophageal radiation damage in mice. In total 30 mice were included in 4 study groups (1 main and 3 control groups). Mice underwent cone-beam CT imaging for initial setup assessment and dose planning followed by single-fraction dose delivery of 4, 10, 16, and 20Gy on 5mm spots, spaced 10mm apart. Mice were repeatedly imaged using OCT: pre-irradiation and up to 3 months post-irradiation. The control groups received either OCT only, irradiation only, or were sham-operated. We used histopathology as gold standard for radiation-induced damage diagnosis. The study showed edema in both the main and OCT-only groups. Furthermore, radiation-induced damage was primarily found in the highest dose region (distal esophagus). Based on the histopathology reports we were able to identify the radiation-induced damage in the OCT images as a change in tissue scattering related to the type of induced damage. This finding indicates the feasibility and thereby the potentially promising role of OCT in radiation-induced esophageal damage assessment.

Aag DNA glycosylase promotes alkylation-induced tissue damage mediated by Parp1.

Science.gov (United States)

Calvo, Jennifer A; Moroski-Erkul, Catherine A; Lake, Annabelle; Eichinger, Lindsey W; Shah, Dharini; Jhun, Iny; Limsirichai, Prajit; Bronson, Roderick T; Christiani, David C; Meira, Lisiane B; Samson, Leona D

2013-04-01

Alkylating agents comprise a major class of front-line cancer chemotherapeutic compounds, and while these agents effectively kill tumor cells, they also damage healthy tissues. Although base excision repair (BER) is essential in repairing DNA alkylation damage, under certain conditions, initiation of BER can be detrimental. Here we illustrate that the alkyladenine DNA glycosylase (AAG) mediates alkylation-induced tissue damage and whole-animal lethality following exposure to alkylating agents. Aag-dependent tissue damage, as observed in cerebellar granule cells, splenocytes, thymocytes, bone marrow cells, pancreatic β-cells, and retinal photoreceptor cells, was detected in wild-type mice, exacerbated in Aag transgenic mice, and completely suppressed in Aag⁻/⁻ mice. Additional genetic experiments dissected the effects of modulating both BER and Parp1 on alkylation sensitivity in mice and determined that Aag acts upstream of Parp1 in alkylation-induced tissue damage; in fact, cytotoxicity in WT and Aag transgenic mice was abrogated in the absence of Parp1. These results provide in vivo evidence that Aag-initiated BER may play a critical role in determining the side-effects of alkylating agent chemotherapies and that Parp1 plays a crucial role in Aag-mediated tissue damage.

Aag DNA glycosylase promotes alkylation-induced tissue damage mediated by Parp1.

Directory of Open Access Journals (Sweden)

Jennifer A Calvo

2013-04-01

Full Text Available Alkylating agents comprise a major class of front-line cancer chemotherapeutic compounds, and while these agents effectively kill tumor cells, they also damage healthy tissues. Although base excision repair (BER is essential in repairing DNA alkylation damage, under certain conditions, initiation of BER can be detrimental. Here we illustrate that the alkyladenine DNA glycosylase (AAG mediates alkylation-induced tissue damage and whole-animal lethality following exposure to alkylating agents. Aag-dependent tissue damage, as observed in cerebellar granule cells, splenocytes, thymocytes, bone marrow cells, pancreatic β-cells, and retinal photoreceptor cells, was detected in wild-type mice, exacerbated in Aag transgenic mice, and completely suppressed in Aag⁻/⁻ mice. Additional genetic experiments dissected the effects of modulating both BER and Parp1 on alkylation sensitivity in mice and determined that Aag acts upstream of Parp1 in alkylation-induced tissue damage; in fact, cytotoxicity in WT and Aag transgenic mice was abrogated in the absence of Parp1. These results provide in vivo evidence that Aag-initiated BER may play a critical role in determining the side-effects of alkylating agent chemotherapies and that Parp1 plays a crucial role in Aag-mediated tissue damage.

The sequence specificity of UV-induced DNA damage in a systematically altered DNA sequence.

Science.gov (United States)

Khoe, Clairine V; Chung, Long H; Murray, Vincent

2018-06-01

The sequence specificity of UV-induced DNA damage was investigated in a specifically designed DNA plasmid using two procedures: end-labelling and linear amplification. Absorption of UV photons by DNA leads to dimerisation of pyrimidine bases and produces two major photoproducts, cyclobutane pyrimidine dimers (CPDs) and pyrimidine(6-4)pyrimidone photoproducts (6-4PPs). A previous study had determined that two hexanucleotide sequences, 5'-GCTC*AC and 5'-TATT*AA, were high intensity UV-induced DNA damage sites. The UV clone plasmid was constructed by systematically altering each nucleotide of these two hexanucleotide sequences. One of the main goals of this study was to determine the influence of single nucleotide alterations on the intensity of UV-induced DNA damage. The sequence 5'-GCTC*AC was designed to examine the sequence specificity of 6-4PPs and the highest intensity 6-4PP damage sites were found at 5'-GTTC*CC nucleotides. The sequence 5'-TATT*AA was devised to investigate the sequence specificity of CPDs and the highest intensity CPD damage sites were found at 5'-TTTT*CG nucleotides. It was proposed that the tetranucleotide DNA sequence, 5'-YTC*Y (where Y is T or C), was the consensus sequence for the highest intensity UV-induced 6-4PP adduct sites; while it was 5'-YTT*C for the highest intensity UV-induced CPD damage sites. These consensus tetranucleotides are composed entirely of consecutive pyrimidines and must have a DNA conformation that is highly productive for the absorption of UV photons. Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.

Effects of fatigue induced damage on the longitudinal fracture resistance of cortical bone.

Science.gov (United States)

Fletcher, Lloyd; Codrington, John; Parkinson, Ian

2014-07-01

As a composite material, cortical bone accumulates fatigue microdamage through the repetitive loading of everyday activity (e.g. walking). The accumulation of fatigue microdamage is thought to contribute to the occurrence of fragility fractures in older people. Therefore it is beneficial to understand the relationship between microcrack accumulation and the fracture resistance of cortical bone. Twenty longitudinally orientated compact tension fracture specimens were machined from a single bovine femur, ten specimens were assigned to both the control and fatigue damaged groups. The damaged group underwent a fatigue loading protocol to induce microdamage which was assessed via fluorescent microscopy. Following fatigue loading, non-linear fracture resistance tests were undertaken on both the control and damaged groups using the J-integral method. The interaction of the crack path with the fatigue induced damage and inherent toughening mechanisms were then observed using fluorescent microscopy. The results of this study show that fatigue induced damage reduces the initiation toughness of cortical bone and the growth toughness within the damage zone by three distinct mechanisms of fatigue-fracture interaction. Further analysis of the J-integral fracture resistance showed both the elastic and plastic component were reduced in the damaged group. For the elastic component this was attributed to a decreased number of ligament bridges in the crack wake while for the plastic component this was attributed to the presence of pre-existing fatigue microcracks preventing energy absorption by the formation of new microcracks.

Surface Irregularity Factor as a Parameter to Evaluate the Fatigue Damage State of CFRP

Directory of Open Access Journals (Sweden)

Pablo Zuluaga-Ramírez

2015-11-01

Full Text Available This work presents an optical non-contact technique to evaluate the fatigue damage state of CFRP structures measuring the irregularity factor of the surface. This factor includes information about surface topology and can be measured easily on field, by techniques such as optical perfilometers. The surface irregularity factor has been correlated with stiffness degradation, which is a well-accepted parameter for the evaluation of the fatigue damage state of composite materials. Constant amplitude fatigue loads (CAL and realistic variable amplitude loads (VAL, representative of real in- flight conditions, have been applied to “dog bone” shaped tensile specimens. It has been shown that the measurement of the surface irregularity parameters can be applied to evaluate the damage state of a structure, and that it is independent of the type of fatigue load that has caused the damage. As a result, this measurement technique is applicable for a wide range of inspections of composite material structures, from pressurized tanks with constant amplitude loads, to variable amplitude loaded aeronautical structures such as wings and empennages, up to automotive and other industrial applications.

Surface Irregularity Factor as a Parameter to Evaluate the Fatigue Damage State of CFRP

Science.gov (United States)

Zuluaga-Ramírez, Pablo; Frövel, Malte; Belenguer, Tomás; Salazar, Félix

2015-01-01

This work presents an optical non-contact technique to evaluate the fatigue damage state of CFRP structures measuring the irregularity factor of the surface. This factor includes information about surface topology and can be measured easily on field, by techniques such as optical perfilometers. The surface irregularity factor has been correlated with stiffness degradation, which is a well-accepted parameter for the evaluation of the fatigue damage state of composite materials. Constant amplitude fatigue loads (CAL) and realistic variable amplitude loads (VAL), representative of real in- flight conditions, have been applied to “dog bone” shaped tensile specimens. It has been shown that the measurement of the surface irregularity parameters can be applied to evaluate the damage state of a structure, and that it is independent of the type of fatigue load that has caused the damage. As a result, this measurement technique is applicable for a wide range of inspections of composite material structures, from pressurized tanks with constant amplitude loads, to variable amplitude loaded aeronautical structures such as wings and empennages, up to automotive and other industrial applications. PMID:28793655

Reconstruction of radical prostatectomy-induced urethral damage using skeletal muscle-derived multipotent stem cells.

Science.gov (United States)

Hoshi, Akio; Tamaki, Tetsuro; Tono, Kayoko; Okada, Yoshinori; Akatsuka, Akira; Usui, Yukio; Terachi, Toshiro

2008-06-15

Postoperative damage of the urethral rhabdosphincter (URS) and neurovascular bundle (NVB) is a major operative complication of radical prostatectomy. It is generally recognized to be caused by unavoidable surgical damage to the muscle-nerve-blood vessel units around the urethra. We attempted to treat this damage using skeletal muscle-derived stem cells, which are able to reconstitute muscle-nerve-blood vessel units. Cells were enzymatically extracted and sorted by flow cytometry as CD34/45 (Sk-34) and CD34/45 (Sk-DN) cells from green fluorescent protein transgenic mice and rats. URS-NVB damage was induced by manually removing one-third of the total URS and unilateral invasion of NVB in wild-type Sprague-Dawley and node rats. Freshly isolated Sk-34, Sk-34+Sk-DN cells, and cultured Sk-DN cells were directly transplanted into the damaged portion. At 4 and 12 weeks after transplantation, urethral pressure profile by electrical stimulation through the sacral surface (L6-S1) was evaluated as functional recovery. The recovery ratio in the control and transplanted groups was 37.6% and 72.9%, at 4 weeks, and 41.6% and 78.4% at 12 weeks, respectively (Pcells differentiated into numerous skeletal muscle fibers having neuromuscular junctions (innervation) and nerve bundle-related Schwann cells and perineurium, and blood vessel-related endothelial cells and pericyte around the urethra. Thus, we conclude that transplantation of skeletal muscle-derived multipotent Sk-34 and Sk-DN cells is potentially useful for the reconstitution of postoperative damage of URS and NVB after radical prostatectomy.

Sleep loss and acute drug abuse can induce DNA damage in multiple organs of mice.

Science.gov (United States)

Alvarenga, T A; Ribeiro, D A; Araujo, P; Hirotsu, C; Mazaro-Costa, R; Costa, J L; Battisti, M C; Tufik, S; Andersen, M L

2011-09-01

The purpose of the present study was to characterize the genetic damage induced by paradoxical sleep deprivation (PSD) in combination with cocaine or ecstasy (3,4-methylenedioxymethamphetamine; MDMA) in multiple organs of male mice using the single cell gel (comet) assay. C57BL/6J mice were submitted to PSD by the platform technique for 72 hours, followed by drug administration and evaluation of DNA damage in peripheral blood, liver and brain tissues. Cocaine was able to induce genetic damage in the blood, brain and liver cells of sleep-deprived mice at the majority of the doses evaluated. Ecstasy also induced increased DNA migration in peripheral blood cells for all concentrations tested. Analysis of damaged cells by the tail moment data suggests that ecstasy is a genotoxic chemical at the highest concentrations tested, inducing damage in liver or brain cells after sleep deprivation in mice. Taken together, our results suggest that cocaine and ecstasy/MDMA act as potent genotoxins in multiple organs of mice when associated with sleep loss.

Heavy ion induced damage to plasmid DNA : plateau region vs. spread out Bragg-peak

NARCIS (Netherlands)

Dang, H.M.; van Goethem, M.J.; van der Graaf, E.R.; Brandenburg, S.; Hoekstra, R.A.; Schlathölter, T.A.

We have investigated the damage of synthetic plasmid pBR322 DNA in dilute aqueous solutions induced by fast carbon ions. The relative contribution of indirect damage and direct damage to the DNA itself is expected to vary with linear energy transfer along the ion track, with the direct damage

The yield, processing, and biological consequences of clustered DNA damage induced by ionizing radiation

International Nuclear Information System (INIS)

Shikazono, Naoya; Noguchi, Miho; Fujii, Kentaro; Urushibara, Ayumi; Yokoya, Akinari

2009-01-01

After living cells are exposed to ionizing radiation, a variety of chemical modifications of DNA are induced either directly by ionization of DNA or indirectly through interactions with water-derived radicals. The DNA lesions include single strand breaks (SSB), base lesions, sugar damage, and apurinic/apyrimidinic sites (AP sites). Clustered DNA damage, which is defined as two or more of such lesions within one to two helical turns of DNA induced by a single radiation track, is considered to be a unique feature of ionizing radiation. A double strand break (DSB) is a type of clustered DNA damage, in which single strand breaks are formed on opposite strands in close proximity. Formation and repair of DSBs have been studied in great detail over the years as they have been linked to important biological endpoints, such as cell death, loss of genetic material, chromosome aberration. Although non-DSB clustered DNA damage has received less attention, there is growing evidence of its biological significance. This review focuses on the current understanding of (1) the yield of non-DSB clustered damage induced by ionizing radiation (2) the processing, and (3) biological consequences of non-DSB clustered DNA damage. (author)

Accumulated surface damage on ZnS crystals produced by closely spaced pairs of picosecond laser pulses

International Nuclear Information System (INIS)

Chase, L.L.; Lee, H.W.H.

1988-12-01

Excitation of a transparent ZnS crystal by repetitive picosecond dye laser pulses causes an accumulated surface modification leading to optical damage. The onset of the damage is detected by an abrupt increase in the emission of neutral Zn (and possibly S 2 ) from the surface. Comparison of the neutral emission thresholds with pulse-pair and single-pulse excitation shows that linear absorption is the dominant laser-surface interaction. In general, this measurement technique shows considerable promise for investigating the possible influence of nonlinear absorption or excitation processes on damage mechanisms. The data suggest that heating of small absorbing regions produces the surface modification that leads to the observed surface ablation. The nature of the damage observed at fluences above the threshold suggests that it is caused by heating of a relatively large (/approximately/10 - 100 μm) surface region that has been modified by the accumulation pulses. 3 refs., 5 figs

Effect of electrical discharge machining on surface characteristics and machining damage of AISI D2 tool steel

International Nuclear Information System (INIS)

Guu, Y.H.; Hocheng, H.; Chou, C.Y.; Deng, C.S.

2003-01-01

In this work the electrical discharge machining (EDM) of AISI D2 tool steel was investigated. The surface characteristics and machining damage caused by EDM were studied in terms of machining parameters. Based on the experimental data, an empirical model of the tool steel was also proposed. A new damage variable was used to study the EDM damage. The workpiece surface and re-solidified layers were examined by a scanning electron microscopy. Surface roughness was determined with a surface profilometer. The residual stress acting on the EDM specimen was measured by the X-ray diffraction technique. Experimental results indicate that the thickness of the recast layer, and surface roughness are proportional to the power input. The EDM process introduces tensile residual stress on the machined surface. The EDM damage leads to strength degradation

Laser Induced Damage of Potassium Dihydrogen Phosphate (KDP Optical Crystal Machined by Water Dissolution Ultra-Precision Polishing Method

Directory of Open Access Journals (Sweden)

Yuchuan Chen

2018-03-01

Full Text Available Laser induced damage threshold (LIDT is an important optical indicator for nonlinear Potassium Dihydrogen Phosphate (KDP crystal used in high power laser systems. In this study, KDP optical crystals are initially machined with single point diamond turning (SPDT, followed by water dissolution ultra-precision polishing (WDUP and then tested with 355 nm nanosecond pulsed-lasers. Power spectral density (PSD analysis shows that WDUP process eliminates the laser-detrimental spatial frequencies band of micro-waviness on SPDT machined surface and consequently decreases its modulation effect on the laser beams. The laser test results show that LIDT of WDUP machined crystal improves and its stability has a significant increase by 72.1% compared with that of SPDT. Moreover, a subsequent ultrasonic assisted solvent cleaning process is suggested to have a positive effect on the laser performance of machined KDP crystal. Damage crater investigation indicates that the damage morphologies exhibit highly thermal explosion features of melted cores and brittle fractures of periphery material, which can be described with the classic thermal explosion model. The comparison result demonstrates that damage mechanisms for SPDT and WDUP machined crystal are the same and WDUP process reveals the real bulk laser resistance of KDP optical crystal by removing the micro-waviness and subsurface damage on SPDT machined surface. This improvement of WDUP method makes the LIDT more accurate and will be beneficial to the laser performance of KDP crystal.

Theoretical research of multi-pulses laser induced damage in dielectrics

International Nuclear Information System (INIS)

Luo Jin; Liu Zhichao; Chen Songlin; Ma Ping

2013-01-01

The pulse width is different, the mechanism of the laser-matter interaction is different. Damage results from plasma formation and ablation forτ≤10 ps and from heat depositing and conventional melting for τ>100 ps. Two theoretical models of transparent dielectrics irradiated by multi-pulses laser are respectively developed based on the above-mentioned different mechanism. One is the dielectric breakdown model based on electron density evolution equation for femtosecond multi-pluses laser, the other is the dielectric heat-damage model based on Fourier's heat exchange equation for nanosecond multi-pluses laser. Using these models, the effects of laser parameters and material parameters on the laser-induced damage threshold of dielectrics are analyzed. The analysis results show that different parameters have different influence on the damage threshold. The effect of parameters on the multi -pulses damage threshold is not entirely the same to the single-pulse damage threshold. The multi-pulses damage mechanism of dielectrics is discussed in detail, considering the effect of different parameters. The discussion provides more information for understanding its damage process and more knowledge to improve its damage thresholds. And the relationship between damage threshold and pulse number is illustrated, it is in good agreement with experimental results. The illustration can help us to predict the multi-pulses damage threshold and the lifetime of optical components. (authors)

Detection of UVR-induced DNA damage in mouse epidermis in vivo using alkaline elution

International Nuclear Information System (INIS)

Kinley, J.S.; Moan, J.; Brunborg, G.

1995-01-01

Alkaline elution has been used to detect ultraviolet radiation (UVR)-induced DNA damage in the epidermis of C3H/Tif hr/hr mice. This technique detects DNA damage in the form of single-strand breaks and alkali-labile sites (SSB) formed directly by UVA (320-400 nm) or indirectly by UVB (280-320 nm). The latter induces DNA damage such as cyclobutane pyrimidine dimers and pyrimidine-pyrimidone (6-4)-photoproducts, which are then converted into transient SSB by cellular endonucleases, during nucleotide excision repair (NER). (Author)

Hypoxic pretreatment protects against neuronal damage of the rat hippocampus induced by severe hypoxia.

Science.gov (United States)

Gorgias, N; Maidatsi, P; Tsolaki, M; Alvanou, A; Kiriazis, G; Kaidoglou, K; Giala, M

1996-04-01

The present study investigates whether under conditions of successive hypoxic exposures pretreatment with mild (15% O(2)) or moderate (10% O(2)) hypoxia, protects hippocampal neurones against damage induced by severe (3% O(2)) hypoxia. The ultrastructural findings were also correlated with regional superoxide dismutase (SOD) activity changes. In unpretreated rats severe hypoxia induced ultrastructural changes consistent with the aspects of delayed neuronal death (DND). However, in preexposed animals hippocampal damage was attenuated in an inversely proportional way with the severity of the hypoxic pretreatment. The ultrastructural hypoxic tolerance findings were also closely related to increased regional SOD activity levels. Thus the activation of the endogenous antioxidant defense by hypoxic preconditioning, protects against hippocampal damage induced by severe hypoxia. The eventual contribution of increased endogenous adenosine and/or reduced excitotoxicity to induce hypoxic tolerance is discussed.

Antagonist effects of veratric acid against UVB-induced cell damages.

Science.gov (United States)

Shin, Seoung Woo; Jung, Eunsun; Kim, Seungbeom; Lee, Kyung-Eun; Youm, Jong-Kyung; Park, Deokhoon

2013-05-10

Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in human epidermis, resulting in inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effect of UV irradiation is essential. In recent years naturally occurring herbal compounds such as phenolic acids, flavonoids, and high molecular weight polyphenols have gained considerable attention as beneficial protective agents. The simple phenolic veratric acid (VA, 3,4-dimethoxybenzoic acid) is one of the major benzoic acid derivatives from vegetables and fruits and it also occurs naturally in medicinal mushrooms which have been reported to have anti-inflammatory and anti-oxidant activities. However, it has rarely been applied in skin care. This study, therefore, aimed to explore the possible roles of veratric acid in protection against UVB-induced damage in HaCaT cells. Results showed that veratric acid can attenuate cyclobutane pyrimidine dimers (CPDs) formation, glutathione (GSH) depletion and apoptosis induced by UVB. Furthermore, veratric acid had inhibitory effects on the UVB-induced release of the inflammatory mediators such as IL-6 and prostaglandin-E2. We also confirmed the safety and clinical efficacy of veratric acid on human skin. Overall, results demonstrated significant benefits of veratric acid on the protection of keratinocyte against UVB-induced injuries and suggested its potential use in skin photoprotection.

Neutron induced permanent damage in Josephson junctions

International Nuclear Information System (INIS)

Mueller, G.P.; Rosen, M.

1982-01-01

14 MeV neutron induced permanent changes in the critical current density of Josephson junctions due to displacement damage in the junction barrier are estimated using a worst case model and the binary collision simulation code MARLOWE. No likelihood of single event hard upsets is found in this model. It is estimated that a fluence of 10 18 -10 19 neutrons/cm 2 are required to change the critical current density by 5%

Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis

Directory of Open Access Journals (Sweden)

Ifigeneia V. Mavragani

2017-07-01

Full Text Available Cellular effects of ionizing radiation (IR are of great variety and level, but they are mainly damaging since radiation can perturb all important components of the cell, from the membrane to the nucleus, due to alteration of different biological molecules ranging from lipids to proteins or DNA. Regarding DNA damage, which is the main focus of this review, as well as its repair, all current knowledge indicates that IR-induced DNA damage is always more complex than the corresponding endogenous damage resulting from endogenous oxidative stress. Specifically, it is expected that IR will create clusters of damage comprised of a diversity of DNA lesions like double strand breaks (DSBs, single strand breaks (SSBs and base lesions within a short DNA region of up to 15–20 bp. Recent data from our groups and others support two main notions, that these damaged clusters are: (1 repair resistant, increasing genomic instability (GI and malignant transformation and (2 can be considered as persistent “danger” signals promoting chronic inflammation and immune response, causing detrimental effects to the organism (like radiation toxicity. Last but not least, the paradigm shift for the role of radiation-induced systemic effects is also incorporated in this picture of IR-effects and consequences of complex DNA damage induction and its erroneous repair.

Damage resistance of AR-coated germanium surfaces for nanosecond CO2 laser pulses

International Nuclear Information System (INIS)

Newnam, B.E.; Gill, D.H.

1977-01-01

An evaluation of the state-of-the-art of AR coatings on gallium-doped germanium, used as a saturable absorber at 10.6 μm, has been conducted. Both 1-on-1 and N-on-1 laser damage thresholds were measured with 1.2 ns pulses on bare and coated surfaces. Only front surface damage was observed. With few exceptions, the thresholds for coated surfaces were centered at 0.49 +- 0.3 J/cm 2 . Bare Ge had a threshold ranging from 0.65 to 0.70 J/cm 2 . No significant differences due to substrate polish, crystallinity or doping level were evident and multiple-shot conditioning resulted in the same threshold as for single shot tests. From an analysis of standing-wave electric fields, damage for AR-coated Ge appeared to be limited by the surface properties of Ge. Measurements at both 1.2 and 70 ns indicated that the threshold (J/cm 2 ) of both coated and uncoated Ge increases as the square root of the pulse-width

Laser-induced cartilage damage: an ex-vivo model using confocal microscopy

Science.gov (United States)

Frenz, Martin; Zueger, Benno J.; Monin, D.; Weiler, C.; Mainil-Varlet, P. M.; Weber, Heinz P.; Schaffner, Thomas

1999-06-01

Although there is an increasing popularity of lasers in orthopedic surgery, there is a growing concern about negative side effects of this therapy e.g. prolonged restitution time, radiation damage to adjacent cartilage or depth effects like bone necrosis. Despite case reports and experimental investigations over the last few years little is known about the extent of acute cartilage damage induced by different lasers types and energies. Histological examination offers only limited insights in cell viability and metabolism. Ho:YAG and Er:YAG lasers emitting at 2.1 micrometer and 2.94 micrometer, respectively, are ideally suited for tissue treatment because these wavelengths are strongly absorbed in water. The Purpose of the present study is to evaluate the effect of laser type and energy on chondrocyte viability in an ex vivo model. Free running Er:YAG (E equals 100 and 150 mJ) and Ho:YAG (E equals 500 and 800 mJ) lasers were used at different energy levels using a fixed pulse length of 400 microseconds. The energy was delivered at 8 Hz through optical fibers. Fresh bovine hyaline cartilage samples were mounted in a water bath at room temperature and the fiber was positioned at 30 degree and 180 degree angles relative to the tissue surface. After laser irradiation the samples were assessed by a life-dead cell viability test using a confocal microscope and by standard histology. Thermal damage was much deeper with Ho:YAG (up to 1800 micrometer) than with the Er:YAG laser (up to 70 micrometer). The cell viability test revealed a damage zone about twice the one determined by standard histology. Confocal microscopy is a powerful tool for assessing changes in tissue structure after laser treatment. In addition this technique allows to quantify these alterations without necessitating time consuming and expensive animal experiments.

Multiple repair pathways mediate cellular tolerance to resveratrol-induced DNA damage.

Science.gov (United States)

Liu, Ying; Wu, Xiaohua; Hu, Xiaoqing; Chen, Ziyuan; Liu, Hao; Takeda, Shunichi; Qing, Yong

2017-08-01

Resveratrol (RSV) has been reported to exert health benefits for the prevention and treatment of many diseases, including cancer. The anticancer mechanisms of RSV seem to be complex and may be associated with genotoxic potential. To better understand the genotoxic mechanisms, we used wild-type (WT) and a panel of isogenic DNA-repair deficient DT40 cell lines to identify the DNA damage effects and molecular mechanisms of cellular tolerance to RSV. Our results showed that RSV induced significant formation of γ-H2AX foci and chromosome aberrations (CAs) in WT cells, suggesting direct DNA damage effects. Comparing the survival of WT with isogenic DNA-repair deficient DT40 cell lines demonstrated that single strand break repair (SSBR) deficient cell lines of Parp1 -/- , base excision repair (BER) deficient cell lines of Polβ -/- , homologous recombination (HR) mutants of Brca1 -/- and Brca2 -/- and translesion DNA synthesis (TLS) mutants of Rev3 -/- and Rad18 -/- were more sensitive to RSV. The sensitivities of cells were associated with enhanced DNA damage comparing the accumulation of γ-H2AX foci and number of CAs of isogenic DNA-repair deficient DT40 cell lines with WT cells. These results clearly demonstrated that RSV-induced DNA damage in DT40 cells, and multiple repair pathways including BER, SSBR, HR and TLS, play critical roles in response to RSV- induced genotoxicity. Copyright © 2017. Published by Elsevier Ltd.

Nuclear magnetic resonance-based metabolomics for prediction of gastric damage induced by indomethacin in rats

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Um, So Young [Department of Pharmacology, National Institute of Toxicological Research, Korea Food and Drug Administration, 643 Yeonje-ri, Gangoe-myeon, Cheongwon-gun, Chungbuk (Korea, Republic of); Division of Life and Pharmaceutical Science and College of Pharmacy, Ewha Womans University, 52 Ewahyeodae-gil, Seodaemun-gu, Seoul (Korea, Republic of); Park, Jung Hyun [Division of Life and Pharmaceutical Science and College of Pharmacy, Ewha Womans University, 52 Ewahyeodae-gil, Seodaemun-gu, Seoul (Korea, Republic of); Chung, Myeon Woo [Department of Pharmacology, National Institute of Toxicological Research, Korea Food and Drug Administration, 643 Yeonje-ri, Gangoe-myeon, Cheongwon-gun, Chungbuk (Korea, Republic of); Kim, Kyu-Bong [College of Pharmacy, Dankook University, Dandae-ro, Cheonan, Chungnam (Korea, Republic of); Kim, Seon Hwa [Department of Pharmacology, National Institute of Toxicological Research, Korea Food and Drug Administration, 643 Yeonje-ri, Gangoe-myeon, Cheongwon-gun, Chungbuk (Korea, Republic of); Division of Life and Pharmaceutical Science and College of Pharmacy, Ewha Womans University, 52 Ewahyeodae-gil, Seodaemun-gu, Seoul (Korea, Republic of); College of Pharmacy, Dankook University, Dandae-ro, Cheonan, Chungnam (Korea, Republic of); Choi, Ki Hwan, E-mail: hyokwa11@korea.kr [Department of Pharmacology, National Institute of Toxicological Research, Korea Food and Drug Administration, 643 Yeonje-ri, Gangoe-myeon, Cheongwon-gun, Chungbuk (Korea, Republic of); Lee, Hwa Jeong, E-mail: hwalee@ewha.ac.kr [Division of Life and Pharmaceutical Science and College of Pharmacy, Ewha Womans University, 52 Ewahyeodae-gil, Seodaemun-gu, Seoul (Korea, Republic of)

2012-04-13

Highlights: Black-Right-Pointing-Pointer NMR based metabolomics - gastric damage by indomethacin. Black-Right-Pointing-Pointer Pattern recognition analysis was performed to biomarkers of gastric damage. Black-Right-Pointing-Pointer 2-Oxoglutarate, acetate, taurine and hippurate were selected as putative biomarkers. Black-Right-Pointing-Pointer The gastric damage induced by NSAIDs can be screened in the preclinical step of drug. - Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) have side effects including gastric erosions, ulceration and bleeding. In this study, pattern recognition analysis of the {sup 1}H-nuclear magnetic resonance (NMR) spectra of urine was performed to develop surrogate biomarkers related to the gastrointestinal (GI) damage induced by indomethacin in rats. Urine was collected for 5 h after oral administration of indomethacin (25 mg kg{sup -1}) or co-administration with cimetidine (100 mg kg{sup -1}), which protects against GI damage. The {sup 1}H-NMR urine spectra were divided into spectral bins (0.04 ppm) for global profiling, and 36 endogenous metabolites were assigned for targeted profiling. The level of gastric damage in each animal was also determined. Indomethacin caused severe gastric damage; however, indomethacin administered with cimetidine did not. Simultaneously, the patterns of changes in their endogenous metabolites were different. Multivariate data analyses were carried out to recognize the spectral pattern of endogenous metabolites related to indomethacin using partial least square-discrimination analysis. In targeted profiling, a few endogenous metabolites, 2-oxoglutarate, acetate, taurine and hippurate, were selected as putative biomarkers for the gastric damage induced by indomethacin. These metabolites changed depending on the degree of GI damage, although the same dose of indomethacin (10 mg kg{sup -1}) was administered to rats. The results of global and targeted profiling suggest that the gastric damage induced by

Nuclear magnetic resonance-based metabolomics for prediction of gastric damage induced by indomethacin in rats

International Nuclear Information System (INIS)

Um, So Young; Park, Jung Hyun; Chung, Myeon Woo; Kim, Kyu-Bong; Kim, Seon Hwa; Choi, Ki Hwan; Lee, Hwa Jeong

2012-01-01

Highlights: ► NMR based metabolomics – gastric damage by indomethacin. ► Pattern recognition analysis was performed to biomarkers of gastric damage. ► 2-Oxoglutarate, acetate, taurine and hippurate were selected as putative biomarkers. ► The gastric damage induced by NSAIDs can be screened in the preclinical step of drug. - Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) have side effects including gastric erosions, ulceration and bleeding. In this study, pattern recognition analysis of the 1 H-nuclear magnetic resonance (NMR) spectra of urine was performed to develop surrogate biomarkers related to the gastrointestinal (GI) damage induced by indomethacin in rats. Urine was collected for 5 h after oral administration of indomethacin (25 mg kg −1 ) or co-administration with cimetidine (100 mg kg −1 ), which protects against GI damage. The 1 H-NMR urine spectra were divided into spectral bins (0.04 ppm) for global profiling, and 36 endogenous metabolites were assigned for targeted profiling. The level of gastric damage in each animal was also determined. Indomethacin caused severe gastric damage; however, indomethacin administered with cimetidine did not. Simultaneously, the patterns of changes in their endogenous metabolites were different. Multivariate data analyses were carried out to recognize the spectral pattern of endogenous metabolites related to indomethacin using partial least square-discrimination analysis. In targeted profiling, a few endogenous metabolites, 2-oxoglutarate, acetate, taurine and hippurate, were selected as putative biomarkers for the gastric damage induced by indomethacin. These metabolites changed depending on the degree of GI damage, although the same dose of indomethacin (10 mg kg −1 ) was administered to rats. The results of global and targeted profiling suggest that the gastric damage induced by NSAIDs can be screened in the preclinical stage of drug development using a NMR based metabolomics approach.

Enhancement of laser induced damage threshold of fused silica by acid etching combined with UV laser conditioning

International Nuclear Information System (INIS)

Chen Meng; Xiang Xia; Jiang Yong; Zu Xiaotao; Yuan Xiaodong; Zheng Wanguo; Wang Haijun; Li Xibin; Lu Haibing; Jiang Xiaodong; Wang Chengcheng

2010-01-01

Acid etching combined with UV laser conditioning is developed to enhance the laser induced damage threshold (LIDT) of fused silica. Firstly, the fused silica is etched for 1 ∼ 100 min with a buffered 1% HF solution. After acid etching, its transmittance, surface roughness and LIDT are measured. The results reveal that the fused silica has the highest LIDT and transmittance after etching for 10 min. Then UV laser (355 nm) conditioning is adopted to process the 10-min-etched fused silica. When the laser fluence is below 60% of fused silica's zero probability damage threshold, the LIDT increases gradually with the increase of laser conditioning fluence. However, the LIDT rapidly decreases to be lower than the threshold of the 10-min-etched fused silica when the conditioning fluence is up to 80% of the threshold. Proper acid etching and laser conditioning parameters will effectively enhance the laser damage resistance of fused silica. (authors)

Photodynamic DNA damage induced by phycocyanin and its repair in Saccharomyces cerevisiae

Directory of Open Access Journals (Sweden)

M. Pádula

1999-09-01

Full Text Available In the present study, we analyzed DNA damage induced by phycocyanin (PHY in the presence of visible light (VL using a set of repair endonucleases purified from Escherichia coli. We demonstrated that the profile of DNA damage induced by PHY is clearly different from that induced by molecules that exert deleterious effects on DNA involving solely singlet oxygen as reactive species. Most of PHY-induced lesions are single strand breaks and, to a lesser extent, base oxidized sites, which are recognized by Nth, Nfo and Fpg enzymes. High pressure liquid chromatography coupled to electrochemical detection revealed that PHY photosensitization did not induce 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo at detectable levels. DNA repair after PHY photosensitization was also investigated. Plasmid DNA damaged by PHY photosensitization was used to transform a series of Saccharomyces cerevisiae DNA repair mutants. The results revealed that plasmid survival was greatly reduced in rad14 mutants, while the ogg1 mutation did not modify the plasmid survival when compared to that in the wild type. Furthermore, plasmid survival in the ogg1 rad14 double mutant was not different from that in the rad14 single mutant. The results reported here indicate that lethal lesions induced by PHY plus VL are repaired differently by prokaryotic and eukaryotic cells. Morever, nucleotide excision repair seems to play a major role in the recognition and repair of these lesions in Saccharomyces cerevisiae.

Quantification of gravity-induced skin strain across the breast surface.

Science.gov (United States)

Sanchez, Amy; Mills, Chris; Haake, Steve; Norris, Michelle; Scurr, Joanna

2017-12-01

Quantification of the magnitude of skin strain in different regions of the breast may help to estimate possible gravity-induced damage whilst also being able to inform the selection of incision locations during breast surgery. The aim of this study was to quantify static skin strain over the breast surface and to estimate the risk of skin damage caused by gravitational loading. Fourteen participants had 21 markers applied to their torso and left breast. The non-gravity breast position was estimated as the mid-point of the breast positions in water and soybean oil (higher and lower density than breast respectively). The static gravity-loaded breast position was also measured. Skin strain was calculated as the percentage extension between adjacent breast markers in the gravity and non-gravity loaded conditions. Gravity induced breast deformation caused peak strains ranging from 14 to 75% across participants, with potentially damaging skin strain (>60%) in one participant and skin strains above 30% (skin resistance zone) in a further four participants. These peak strain values all occurred in the longitudinal direction in the upper region of the breast skin. In the latitudinal direction, smaller-breasted participants experienced greater strain on the outer (lateral) breast regions and less strain on the inner (medial) breast regions, a trend which was reversed in the larger breasted participants (above size 34D). To reduce tension on surgical incisions it is suggested that preference should be given to medial latitudinal locations for smaller breasted women and lateral latitudinal locations for larger breasted women. Copyright © 2017 Elsevier Ltd. All rights reserved.

Visualization of DNA clustered damage induced by heavy ion exposure

International Nuclear Information System (INIS)

Tomita, M.; Yatagai, F.

2003-01-01

Full text: DNA double-strand breaks (DSBs) are the most lethal damage induced by ionizing radiations. Accelerated heavy-ions have been shown to induce DNA clustered damage, which is two or more DNA lesions induced within a few helical turns. Higher biological effectiveness of heavy-ions could be provided predominantly by induction of complex DNA clustered damage, which leads to non-repairable DSBs. DNA-dependent protein kinase (DNA-PK) is composed of catalytic subunit (DNA-PKcs) and DNA-binding heterodimer (Ku70 and Ku86). DNA-PK acts as a sensor of DSB during non-homologous end-joining (NHEJ), since DNA-PK is activated to bind to the ends of double-stranded DNA. On the other hand, NBS1 and histone H2AX are essential for DSB repair by homologous recombination (HR) in higher vertebrate cells. Here we report that phosphorylated H2AX at Ser139 (named γ-H2AX) and NBS1 form large undissolvable foci after exposure to accelerated Fe ions, while DNA-PKcs does not recognize DNA clustered damage. NBS1 and γ-H2AX colocalized with forming discrete foci after exposure to X-rays. At 0.5 h after Fe ion irradiation, NBS1 and γ-H2AX also formed discrete foci. However, at 3-8 h after Fe ion irradiation, highly localized large foci turned up, while small discrete foci disappeared. Large NBS1 and γ-H2AX foci were remained even 16 h after irradiation. DNA-PKcs recognized Ku-binding DSB and formed foci shortly after exposure to X-rays. DNA-PKcs foci were observed 0.5 h after 5 Gy of Fe ion irradiation and were almost completely disappeared up to 8 h. These results suggest that NBS1 and γ-H2AX can be utilized as molecular marker of DNA clustered damage, while DNA-PK selectively recognizes repairable DSBs by NHEJ

DNA damage and mutagenesis of lambda phage induced by gamma-rays

International Nuclear Information System (INIS)

Bertram, Heidi

1988-01-01

Lambda phage DNA was gamma irradiated in aqueous solution and strand breakage determined. Twice as much minor structural damage per lethal hit was found in this DNA compared with DNA from irradiated phage suspensions. The in vitro irradiated DNA was repackaged into infectious particles. Induction of mutations in the cI or cII cistron was scored using SOS-induced host cells. In vitro prepared particles were found to have second-order kinetics for mutagenesis induced by gamma rays indicating two pre-mutational events were necessary to produce a mutation, but bacteria-free phage suspensions ('lys-phage') showed single hit kinetics for mutagenesis after irradiation. Increase in the mutation rate in the phage particles was mainly due to minor lesions, i.e. ssb, als and unidentified base damage. In lys-phage, mutagenesis might be enhanced by clustered DNA damage - configuration not existing in pack-phage. Loss of infectivity was analysed in comparison with structural damage. All lesions contributed to biological inactivation. Minor lesions were tolerated by lambda phage to a limited extent. Major lesions (e.g. dsb) contributed most to infectivity loss and were considered lethal events. (U.K.)

Multiphysics model of thermomechanical and helium-induced damage of tungsten during plasma heat transients

Energy Technology Data Exchange (ETDEWEB)

Crosby, Tamer, E-mail: tcrosby@ucla.edu; Ghoniem, Nasr M., E-mail: ghoniem@ucla.edu

2013-11-15

A combination of transient heating and bombardment by helium and hydrogen atoms has been experimentally proven to lead to severe surface and sub-surface damage. We developed a computational model to determine the relationship between the thermomechanical loading conditions and the onset of damage and failure of tungsten surfaces. The model is based on a thermoelasticity fracture damage approach that was developed using the phase field method. The model simulates the distribution of helium bubbles inside the grains and on grain boundaries using space-dependent rate theory. In addition, the model is coupled with a transient heat conduction analysis for temperature distributions inside the material. The results show the effects of helium bubbles on reducing tungsten surface energy. Further, a temperature gradient in the material equals to 10 K/μm, resulted in deep cracks propagating from the tungsten surface.

A study of oxidative stress induced by non-thermal plasma-activated water for bacterial damage

Energy Technology Data Exchange (ETDEWEB)

Zhang, Qian; Ma, Ruonan; Tian, Ying [Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871 (China); Liang, Yongdong; Feng, Hongqing [College of Engineering, Peking University, Beijing 100871 (China); Zhang, Jue; Fang, Jing [Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871 (China); College of Engineering, Peking University, Beijing 100871 (China)

2013-05-20

Ar/O{sub 2} (2%) cold plasma microjet was used to create plasma-activated water (PAW). The disinfection efficacy of PAW against Staphylococcus aureus showed that PAW can effectively disinfect bacteria. Optical emission spectra and oxidation reduction potential results demonstrated the inactivation is attributed to oxidative stress induced by reactive oxygen species in PAW. Moreover, the results of X-ray photoelectron spectroscopy, atomic absorption spectrometry, and transmission electron microscopy suggested that the chemical state of cell surface, the integrity of cell membrane, as well as the cell internal components and structure were damaged by the oxidative stress.

A study of oxidative stress induced by non-thermal plasma-activated water for bacterial damage

International Nuclear Information System (INIS)

Zhang, Qian; Ma, Ruonan; Tian, Ying; Liang, Yongdong; Feng, Hongqing; Zhang, Jue; Fang, Jing

2013-01-01

Ar/O 2 (2%) cold plasma microjet was used to create plasma-activated water (PAW). The disinfection efficacy of PAW against Staphylococcus aureus showed that PAW can effectively disinfect bacteria. Optical emission spectra and oxidation reduction potential results demonstrated the inactivation is attributed to oxidative stress induced by reactive oxygen species in PAW. Moreover, the results of X-ray photoelectron spectroscopy, atomic absorption spectrometry, and transmission electron microscopy suggested that the chemical state of cell surface, the integrity of cell membrane, as well as the cell internal components and structure were damaged by the oxidative stress.

Reduction of damage initiation density in fused silica optics via UV laser conditioning

Science.gov (United States)

Peterson, John E.; Maricle, Stephen M.; Brusasco, Raymond M.; Penetrante, Bernardino M.

2004-03-16

The present invention provides a method for reducing the density of sites on the surface of fused silica optics that are prone to the initiation of laser-induced damage, resulting in optics which have far fewer catastrophic defects and are better capable of resisting optical deterioration upon exposure for a long period of time to a high-power laser beam having a wavelength of about 360 nm or less. The initiation of laser-induced damage is reduced by conditioning the optic at low fluences below levels that normally lead to catastrophic growth of damage. When the optic is then irradiated at its high fluence design limit, the concentration of catastrophic damage sites that form on the surface of the optic is greatly reduced.

Repair of endogenous and ionizing radiation-induced DNA damages: mechanisms and biological functions

International Nuclear Information System (INIS)

Boiteux, S.

2002-01-01

The cellular DNA is continuously exposed to endogenous and exogenous stress. Oxidative stress due to cellular metabolism is the major cause of endogenous DNA damage. On the other hand, ionizing radiation (IR) is an important exogenous stress. Both induce similar DNA damages: damaged bases, abasic sites and strand breakage. Most of these lesions are lethal and/or mutagenic. The survival of the cell is managed by efficient and accurate DNA repair mechanisms that remove lesions before their replication or transcription. DNA repair pathways involved in the removal of IR-induced lesions are briefly described. Base excision repair (BER) is mostly involved in the removal of base damage, abasic sites and single strand breaks. In contrast, DNA double strand breaks are mostly repaired by non-homologous end joining (NHEJ) or homologous recombination (HR). How DNA repair pathways prevent cancer process is also discussed. (author)

Simulation study of radiation damage induced by energetic helium nuclei

CERN Document Server

Hoang Dac Luc; Hoang Dac Dat

2003-01-01

High energy alpha particles produced by neutron-induced nuclear reactions can damage severely reactor materials. Simulation of this process is described using theoretical calculation and ion irradiation experiments at different displacement doses and Helium doses.

The thyroid hormone receptor β induces DNA damage and premature senescence.

Science.gov (United States)

Zambrano, Alberto; García-Carpizo, Verónica; Gallardo, María Esther; Villamuera, Raquel; Gómez-Ferrería, Maria Ana; Pascual, Angel; Buisine, Nicolas; Sachs, Laurent M; Garesse, Rafael; Aranda, Ana

2014-01-06

There is increasing evidence that the thyroid hormone (TH) receptors (THRs) can play a role in aging, cancer and degenerative diseases. In this paper, we demonstrate that binding of TH T3 (triiodothyronine) to THRB induces senescence and deoxyribonucleic acid (DNA) damage in cultured cells and in tissues of young hyperthyroid mice. T3 induces a rapid activation of ATM (ataxia telangiectasia mutated)/PRKAA (adenosine monophosphate-activated protein kinase) signal transduction and recruitment of the NRF1 (nuclear respiratory factor 1) and THRB to the promoters of genes with a key role on mitochondrial respiration. Increased respiration leads to production of mitochondrial reactive oxygen species, which in turn causes oxidative stress and DNA double-strand breaks and triggers a DNA damage response that ultimately leads to premature senescence of susceptible cells. Our findings provide a mechanism for integrating metabolic effects of THs with the tumor suppressor activity of THRB, the effect of thyroidal status on longevity, and the occurrence of tissue damage in hyperthyroidism.

Damages of surface ozone: evidence from agricultural sector in China

Science.gov (United States)

Yi, Fujin; McCarl, Bruce A.; Zhou, Xun; Jiang, Fei

2018-03-01

This study measures the damages that surface ozone pollution causes within the Chinese agricultural sector under 2014 conditions. It also analyzes the agricultural benefits of ozone reductions. The analysis is done using a partial equilibrium model of China’s agricultural sector. Results indicate that there are substantial, spatially differentiated damages that are greatest in ozone-sensitive crop growing areas with higher ozone concentrations. The estimated damage to China’s agricultural sector range is between CNY 1.6 trillion and 2.2 trillion, which for comparison is about one fifth of 2014 agricultural revenue. When considering concentration reduction we find a 30% ozone reduction yields CNY 678 billion in sectoral benefits. These benefits largely fall to consumers with producers losing as the production gains lead to lower prices.

Simulation study of radiation damage induced by energetic helium nuclei

International Nuclear Information System (INIS)

Hoang Dac Luc; Vo Tuong Hanh; Hoang Dac Dat

2003-01-01

High energy alpha particles produced by neutron-induced nuclear reactions can damage severely reactor materials. Simulation of this process is described using theoretical calculation and ion irradiation experiments at different displacement doses and Helium doses. (author)

Plasma induced DNA damage: Comparison with the effects of ionizing radiation

Energy Technology Data Exchange (ETDEWEB)

Lazović, S.; Maletić, D.; Puač, N.; Malović, G.; Petrović, Z. Lj. [Institute of Physics, University of Belgrade, Pregrevica 118, 11080 Belgrade (Serbia); Leskovac, A.; Filipović, J.; Joksić, G. [Department of Physical Chemistry, Vinča Institute of Nuclear Sciences, University of Belgrade, 11001 Belgrade (Serbia)

2014-09-22

We use human primary fibroblasts for comparing plasma and gamma rays induced DNA damage. In both cases, DNA strand breaks occur, but of fundamentally different nature. Unlike gamma exposure, contact with plasma predominantly leads to single strand breaks and base-damages, while double strand breaks are mainly consequence of the cell repair mechanisms. Different cell signaling mechanisms are detected confirming this (ataxia telangiectasia mutated - ATM and ataxia telangiectasia and Rad3 related - ATR, respectively). The effective plasma doses can be tuned to match the typical therapeutic doses of 2 Gy. Tailoring the effective dose through plasma power and duration of the treatment enables safety precautions mainly by inducing apoptosis and consequently reduced frequency of micronuclei.

Surfactant Protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage

DEFF Research Database (Denmark)

Lock Johansson, Sofie; Tan, Qihua; Holst, Rene

2014-01-01

Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The associat......Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage...... or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 second and forced vital capacity in the presence of current tobacco smoking but not in non...... with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive...

Protective effect of hemin against cadmium-induced testicular damage in rats

International Nuclear Information System (INIS)

Fouad, Amr A.; Qureshi, Habib A.; Al-Sultan, Ali Ibrahim; Yacoubi, Mohamed T.; Ali, Abdellah Abusrie

2009-01-01

The protective effect of hemin, the heme oxygenase-1 inducer, was investigated in rats with cadmium induced-testicular injury, in which oxidative stress and inflammation play a major role. Testicular damage was induced by a single i.p. injection of cadmium chloride (2 mg/kg). Hemin was given for three consecutive days (40 μmol/kg/day, s.c.), starting 1 day before cadmium administration. Hemin treatment significantly increased serum testosterone level that was reduced by cadmium. Hemin compensated deficits in the antioxidant defense mechanisms (reduced glutathione, and catalase and superoxide dismutase activities), and suppressed lipid peroxidation in testicular tissue resulted from cadmium administration. Also, hemin attenuated the cadmium-induced elevations in testicular tumor necrosis factor-α and nitric oxide levels, and caspase-3 activity. Additionally, hemin ameliorated cadmium-induced testicular tissue damage observed by light and electron microscopic examinations. The protective effect afforded by hemin was abolished by prior administration of zinc protoporphyrin-IX, the heme oxygenase-1 inhibitor. It was concluded that hemin, through its antioxidant, anti-inflammatory and antiapoptotic effects, represents a potential therapeutic option to protect the testicular tissue from the detrimental effects of cadmium

Measurements and TCAD Simulations of Bulk and Surface Radiation Damage Effects

CERN Document Server

F. Moscatelli; G. M. Bilei; A. Morozzi; G.-F. Dalla Betta; R. Mendicino; M. Boscardin; N. Zorzi; L. Servoli; P. Maccagnani

2016-01-01

In this work we propose the application of a radiation damage model based on the introduction of deep level traps/recombination centers suitable for device level numerical simulation of radiation detectors at very high fluences (e.g. 1÷2×1016 1-MeV equivalent neutrons per square centimeter) combined with a surface damage model developed by using experimental parameters extracted from measurements from gamma irradiated p-type dedicated test structures.

Multi-Dimensional Damage Detection for Surfaces and Structures

Science.gov (United States)

Williams, Martha; Lewis, Mark; Roberson, Luke; Medelius, Pedro; Gibson, Tracy; Parks, Steen; Snyder, Sarah

2013-01-01

Current designs for inflatable or semi-rigidized structures for habitats and space applications use a multiple-layer construction, alternating thin layers with thicker, stronger layers, which produces a layered composite structure that is much better at resisting damage. Even though such composite structures or layered systems are robust, they can still be susceptible to penetration damage. The ability to detect damage to surfaces of inflatable or semi-rigid habitat structures is of great interest to NASA. Damage caused by impacts of foreign objects such as micrometeorites can rupture the shell of these structures, causing loss of critical hardware and/or the life of the crew. While not all impacts will have a catastrophic result, it will be very important to identify and locate areas of the exterior shell that have been damaged by impacts so that repairs (or other provisions) can be made to reduce the probability of shell wall rupture. This disclosure describes a system that will provide real-time data regarding the health of the inflatable shell or rigidized structures, and information related to the location and depth of impact damage. The innovation described here is a method of determining the size, location, and direction of damage in a multilayered structure. In the multi-dimensional damage detection system, layers of two-dimensional thin film detection layers are used to form a layered composite, with non-detection layers separating the detection layers. The non-detection layers may be either thicker or thinner than the detection layers. The thin-film damage detection layers are thin films of materials with a conductive grid or striped pattern. The conductive pattern may be applied by several methods, including printing, plating, sputtering, photolithography, and etching, and can include as many detection layers that are necessary for the structure construction or to afford the detection detail level required. The damage is detected using a detector or

Edaravone ameliorates compression-induced damage in rat nucleus pulposus cells.

Science.gov (United States)

Lin, Hui; Ma, Xuan; Wang, Bai-Chuan; Zhao, Lei; Liu, Jian-Xiang; Pu, Fei-Fei; Hu, Yi-Qiang; Hu, Hong-Zhi; Shao, Zeng-Wu

2017-11-15

Edaravone is a strong free radical scavenger most used for treating acute ischemic stroke. In this study we investigated the protective effects and underlying mechanisms of edaravone on compression-induced damage in rat nucleus pulposus (NP) cells. Cell viability was determined using MTT assay methods. NP cell apoptosis was measured by Hoechst 33,258 staining and Annexin V/PI double staining. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and intracellular calcium ([Ca 2+ ] i ) were determined by fluorescent probes DCFH-DA, JC-1 and Fluo-3/AM, respectively. Apoptosis-related proteins (cleaved caspase-3, cytosolic cytochrome c, Bax and Bcl-2) and extracellular matrix proteins (aggrecan and collagen II) were analyzed by western blot. Edaravone attenuated the compression-induced decrease in viability of NP cells in a dose-dependent manner. 33,258 and Annexin V/PI double staining showed that edaravone protected NP cells from compression-induced apoptosis. Further studies confirmed that edaravone protected NP cells against compression-induced mitochondrial pathway of apoptosis by inhibiting overproduction of ROS, collapse of MMP and overload of [Ca 2+ ] i . In addition, edaravone promoted the expression of aggrecan and collagen II in compression-treated NP cells. These results strongly indicate that edaravone ameliorates compression-induced damage in rat nucleus pulposus cells. Edaravone could be a potential new drug for treatment of IDD. Copyright © 2017 Elsevier Inc. All rights reserved.

Antagonist Effects of Veratric Acid against UVB-Induced Cell Damages

Directory of Open Access Journals (Sweden)

Deokhoon Park

2013-05-01

Full Text Available Ultraviolet (UV radiation induces DNA damage, oxidative stress, and inflammatory processes in human epidermis, resulting in inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effect of UV irradiation is essential. In recent years naturally occurring herbal compounds such as phenolic acids, flavonoids, and high molecular weight polyphenols have gained considerable attention as beneficial protective agents. The simple phenolic veratric acid (VA, 3,4-dimethoxybenzoic acid is one of the major benzoic acid derivatives from vegetables and fruits and it also occurs naturally in medicinal mushrooms which have been reported to have anti-inflammatory and anti-oxidant activities. However, it has rarely been applied in skin care. This study, therefore, aimed to explore the possible roles of veratric acid in protection against UVB-induced damage in HaCaT cells. Results showed that veratric acid can attenuate cyclobutane pyrimidine dimers (CPDs formation, glutathione (GSH depletion and apoptosis induced by UVB. Furthermore, veratric acid had inhibitory effects on the UVB-induced release of the inflammatory mediators such as IL-6 and prostaglandin-E2. We also confirmed the safety and clinical efficacy of veratric acid on human skin. Overall, results demonstrated significant benefits of veratric acid on the protection of keratinocyte against UVB-induced injuries and suggested its potential use in skin photoprotection.

Radiation induced crystallinity damage in poly(L-lactic acid)

CERN Document Server

Kantoglu, O

2002-01-01

The radiation-induced crystallinity damage in poly(L-lactic acid) (PLLA) in the presence of air and in vacuum, is studied. From the heat of fusion enthalpy values of gamma irradiated samples, some changes on the thermal properties were determined. To identify these changes, first the glass transition temperature (T sub g) of L-lactic acid polymers irradiated to various doses in air and vacuum have been investigated and it is found that it is independent of irradiation atmosphere and dose. The fraction of damaged units of PLLA per unit of absorbed energy has been measured. For this purpose, SAXS and differential scanning calorimetry methods were used, and the radiation yield of number of damaged units (G(-u)) is found to be 0.74 and 0.58 for PLLA samples irradiated in vacuum and air, respectively.

Effects of Resveratrol on Methotrexate-Induced Testicular Damage in Rats

Directory of Open Access Journals (Sweden)

Esin Yuluğ

2013-01-01

Full Text Available This study investigated the probable protective effects of resveratrol (RES, an antioxidant, against methotrexate- (MTX- induced testis damage. Twenty-four male Sprague Dawley rats were randomly divided into four groups: control, RES, MTX, and MTX + RES groups. Rats were sacrificed at the end of the experiment. Plasma and tissue malondialdehyde (MDA levels, superoxide dismutase (SOD and catalase (CAT activity in tissue, testicular histopathological damage scores, and testicular and epididymal epithelial apoptotic index (AI were evaluated. The MTX group had significantly higher plasma and tissue MDA levels and significantly lower SOD and CAT activity than those of the control group. In the MTX + RES group, plasma and tissue MDA levels decreased significantly and SOD activity rose significantly compared to the MTX group. The MTX group had significantly lower Johnsen’s testicular biopsy score (JTBS values than those of the control group. JTBS was significantly higher in the MTX + RES group than in the MTX group. AI increased in the testis and epididymis in the MTX group and significantly decreased in the MTX + RES group. Our results indicate that RES has protective effects against MTX-induced testis damage at the biochemical, histopathological, and apoptotic levels.

Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis

Energy Technology Data Exchange (ETDEWEB)

Halliday, Gary M. [Dermatology Research Laboratories, Division of Medicine, Melanoma and Skin Cancer Research Institute, Royal Prince Alfred Hospital at the University of Sydney, Sydney, NSW (Australia)]. E-mail: garyh@med.usyd.edu.au

2005-04-01

Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppression in the skin. These biological changes are responsible for photocarcinogenesis. UV radiation in sunlight is divided into two wavebands, UVB and UVA, both of which contribute to these biological changes, and therefore probably to skin cancer in humans and animal models. Oxidative damage caused by UV contributes to inflammation, gene mutation and immunosuppression. This article reviews evidence for the hypothesis that UV oxidative damage to these processes contributes to photocarcinogenesis. UVA makes a larger impact on oxidative stress in the skin than UVB by inducing reactive oxygen and nitrogen species which damage DNA, protein and lipids and which also lead to NAD+ depletion, and therefore energy loss from the cell. Lipid peroxidation induces prostaglandin production that in association with UV-induced nitric oxide production causes inflammation. Inflammation drives benign human solar keratosis (SK) to undergo malignant conversion into squamous cell carcinoma (SCC) probably because the inflammatory cells produce reactive oxygen species, thus increasing oxidative damage to DNA and the immune system. Reactive oxygen or nitrogen appears to cause the increase in mutational burden as SK progress into SCC in humans. UVA is particularly important in causing immunosuppression in both humans and mice, and UV lipid peroxidation induced prostaglandin production and UV activation of nitric oxide synthase is important mediators of this event. Other immunosuppressive events are likely to be initiated by UV oxidative stress. Antioxidants have also been shown to reduce photocarcinogenesis. While most of this evidence comes from studies in mice, there is supporting evidence in humans that UV-induced oxidative damage contributes to inflammation, gene mutation and immunosuppression. Available evidence implicates oxidative damage as an important contributor to sunlight-induced carcinogenesis in humans.

Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis

International Nuclear Information System (INIS)

Halliday, Gary M.

2005-01-01

Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppression in the skin. These biological changes are responsible for photocarcinogenesis. UV radiation in sunlight is divided into two wavebands, UVB and UVA, both of which contribute to these biological changes, and therefore probably to skin cancer in humans and animal models. Oxidative damage caused by UV contributes to inflammation, gene mutation and immunosuppression. This article reviews evidence for the hypothesis that UV oxidative damage to these processes contributes to photocarcinogenesis. UVA makes a larger impact on oxidative stress in the skin than UVB by inducing reactive oxygen and nitrogen species which damage DNA, protein and lipids and which also lead to NAD+ depletion, and therefore energy loss from the cell. Lipid peroxidation induces prostaglandin production that in association with UV-induced nitric oxide production causes inflammation. Inflammation drives benign human solar keratosis (SK) to undergo malignant conversion into squamous cell carcinoma (SCC) probably because the inflammatory cells produce reactive oxygen species, thus increasing oxidative damage to DNA and the immune system. Reactive oxygen or nitrogen appears to cause the increase in mutational burden as SK progress into SCC in humans. UVA is particularly important in causing immunosuppression in both humans and mice, and UV lipid peroxidation induced prostaglandin production and UV activation of nitric oxide synthase is important mediators of this event. Other immunosuppressive events are likely to be initiated by UV oxidative stress. Antioxidants have also been shown to reduce photocarcinogenesis. While most of this evidence comes from studies in mice, there is supporting evidence in humans that UV-induced oxidative damage contributes to inflammation, gene mutation and immunosuppression. Available evidence implicates oxidative damage as an important contributor to sunlight-induced carcinogenesis in humans

Nuclear DNA damage-triggered NLRP3 inflammasome activation promotes UVB-induced inflammatory responses in human keratinocytes

Energy Technology Data Exchange (ETDEWEB)

Hasegawa, Tatsuya, E-mail: tatsuya.hasegawa@to.shiseido.co.jp; Nakashima, Masaya; Suzuki, Yoshiharu

2016-08-26

Ultraviolet (UV) radiation in sunlight can result in DNA damage and an inflammatory reaction of the skin commonly known as sunburn, which in turn can lead to cutaneous tissue disorders. However, little has been known about how UV-induced DNA damage mediates the release of inflammatory mediators from keratinocytes. Here, we show that UVB radiation intensity-dependently increases NLRP3 gene expression and IL-1β production in human keratinocytes. Knockdown of NLRP3 with siRNA suppresses UVB-induced production of not only IL-1β, but also other inflammatory mediators, including IL-1α, IL-6, TNF-α, and PGE{sub 2}. In addition, inhibition of DNA damage repair by knockdown of XPA, which is a major component of the nucleotide excision repair system, causes accumulation of cyclobutane pyrimidine dimer (CPD) and activation of NLRP3 inflammasome. In vivo immunofluorescence analysis confirmed that NLRP3 expression is also elevated in UV-irradiated human epidermis. Overall, our findings indicate that UVB-induced DNA damage initiates NLRP3 inflammasome activation, leading to release of various inflammatory mediators from human keratinocytes. - Highlights: • UVB radiation induces NLRP3 inflammasome activation in human keratinocytes. • NLRP3 knockdown suppresses production of UVB-induced inflammatory mediators. • UVB-induced DNA damage triggers NLRP3 inflammasome activation. • NLRP3 expression in human epidermis is elevated in response to UV radiation.

Nuclear DNA damage-triggered NLRP3 inflammasome activation promotes UVB-induced inflammatory responses in human keratinocytes

International Nuclear Information System (INIS)

Hasegawa, Tatsuya; Nakashima, Masaya; Suzuki, Yoshiharu

2016-01-01

Ultraviolet (UV) radiation in sunlight can result in DNA damage and an inflammatory reaction of the skin commonly known as sunburn, which in turn can lead to cutaneous tissue disorders. However, little has been known about how UV-induced DNA damage mediates the release of inflammatory mediators from keratinocytes. Here, we show that UVB radiation intensity-dependently increases NLRP3 gene expression and IL-1β production in human keratinocytes. Knockdown of NLRP3 with siRNA suppresses UVB-induced production of not only IL-1β, but also other inflammatory mediators, including IL-1α, IL-6, TNF-α, and PGE_2. In addition, inhibition of DNA damage repair by knockdown of XPA, which is a major component of the nucleotide excision repair system, causes accumulation of cyclobutane pyrimidine dimer (CPD) and activation of NLRP3 inflammasome. In vivo immunofluorescence analysis confirmed that NLRP3 expression is also elevated in UV-irradiated human epidermis. Overall, our findings indicate that UVB-induced DNA damage initiates NLRP3 inflammasome activation, leading to release of various inflammatory mediators from human keratinocytes. - Highlights: • UVB radiation induces NLRP3 inflammasome activation in human keratinocytes. • NLRP3 knockdown suppresses production of UVB-induced inflammatory mediators. • UVB-induced DNA damage triggers NLRP3 inflammasome activation. • NLRP3 expression in human epidermis is elevated in response to UV radiation.

Clustered DNA damages induced in human hematopoietic cells by low doses of ionizing radiation

Science.gov (United States)

Sutherland, Betsy M.; Bennett, Paula V.; Cintron-Torres, Nela; Hada, Megumi; Trunk, John; Monteleone, Denise; Sutherland, John C.; Laval, Jacques; Stanislaus, Marisha; Gewirtz, Alan

2002-01-01

Ionizing radiation induces clusters of DNA damages--oxidized bases, abasic sites and strand breaks--on opposing strands within a few helical turns. Such damages have been postulated to be difficult to repair, as are double strand breaks (one type of cluster). We have shown that low doses of low and high linear energy transfer (LET) radiation induce such damage clusters in human cells. In human cells, DSB are about 30% of the total of complex damages, and the levels of DSBs and oxidized pyrimidine clusters are similar. The dose responses for cluster induction in cells can be described by a linear relationship, implying that even low doses of ionizing radiation can produce clustered damages. Studies are in progress to determine whether clusters can be produced by mechanisms other than ionizing radiation, as well as the levels of various cluster types formed by low and high LET radiation.

Cerium oxide nanoparticles, combining antioxidant and UV shielding properties, prevent UV-induced cell damage and mutagenesis

Science.gov (United States)

Caputo, Fanny; de Nicola, Milena; Sienkiewicz, Andrzej; Giovanetti, Anna; Bejarano, Ignacio; Licoccia, Silvia; Traversa, Enrico; Ghibelli, Lina

2015-09-01

Efficient inorganic UV shields, mostly based on refracting TiO2 particles, have dramatically changed the sun exposure habits. Unfortunately, health concerns have emerged from the pro-oxidant photocatalytic effect of UV-irradiated TiO2, which mediates toxic effects on cells. Therefore, improvements in cosmetic solar shield technology are a strong priority. CeO2 nanoparticles are not only UV refractors but also potent biological antioxidants due to the surface 3+/4+ valency switch, which confers anti-inflammatory, anti-ageing and therapeutic properties. Herein, UV irradiation protocols were set up, allowing selective study of the extra-shielding effects of CeO2vs. TiO2 nanoparticles on reporter cells. TiO2 irradiated with UV (especially UVA) exerted strong photocatalytic effects, superimposing their pro-oxidant, cell-damaging and mutagenic action when induced by UV, thereby worsening the UV toxicity. On the contrary, irradiated CeO2 nanoparticles, via their Ce3+/Ce4+ redox couple, exerted impressive protection on UV-treated cells, by buffering oxidation, preserving viability and proliferation, reducing DNA damage and accelerating repair; strikingly, they almost eliminated mutagenesis, thus acting as an important tool to prevent skin cancer. Interestingly, CeO2 nanoparticles also protect cells from the damage induced by irradiated TiO2, suggesting that these two particles may also complement their effects in solar lotions. CeO2 nanoparticles, which intrinsically couple UV shielding with biological and genetic protection, appear to be ideal candidates for next-generation sun shields.

Optimum inductively coupled plasma etching of fused silica to remove subsurface damage layer

Energy Technology Data Exchange (ETDEWEB)

Jiang, Xiaolong; Liu, Ying, E-mail: liuychch@ustc.edu.cn; Liu, Zhengkun; Qiu, Keqiang; Xu, Xiangdong; Hong, Yilin; Fu, Shaojun

2015-11-15

Highlights: • SSD layer of fused silica is removed by ICP etch with surface roughness of 0.23 nm. • Metal contamination is successfully avoided by employing an isolation device. • Unique low-density plasma induced pitting damage is discovered and eliminated. • Lateral etching of SSD is avoided due to the improvement of etching anisotropy. - Abstract: In this work, we introduce an optimum ICP etching technique that successfully removes the subsurface damage (SSD) layer of fused silica without causing plasma induced surface damage (PISD) or lateral etching of SSD. As one of the commonest PISD initiators, metal contamination from reactor chamber is prevented by employing a simple isolation device. Based on this device, a unique low-density pitting damage is discovered and subsequently eliminated by optimizing the etching parameters. Meanwhile etching anisotropy also improves a lot, thus preventing the lateral etching of SSD. Using this proposed technique, SSD layer of fused silica is successfully removed with a surface roughness of 0.23 nm.

Study of the laser-induced damage of reflective components in the sub-picosecond regime

International Nuclear Information System (INIS)

Sozet, Martin

2016-01-01

In this thesis, laser-induced damage phenomenon of reflective components is investigated in the sub-picosecond regime. These components, made of stacks of dielectric materials, are widely used in powerful laser facilities such as PETAL laser. PETAL laser has been built at the CEA-CESTA in France to deliver multi-kJ/500 fs pulses at 1053 nm and reach a power higher than 6 PW. For this kind of laser systems, reflective components are commonly used instead of optics operating in transmission to limit the accumulation of non-linear phase along the beam propagation due to the high intensities. Optical components irradiated by the highest power densities are the pulse compression gratings, transport mirrors and the focusing parabola, located at the end of the laser chain. Nowadays, laser-induced damage is the main factor that limits the overall performances of powerful laser systems. This manuscript presents three study axes to better understand and control damage phenomenon. The first one concerns the conception of reflective optics for the peta-watt applications. The design of new structures has been investigated to reach high diffraction efficiencies in the case of pulse compression gratings and a high reflectivity in the case of mirrors, while reducing the Electric-field enhancement which is one of the causes of the laser-induced damage. The second axis deals with the development of a precise damage metrology with new testing tools which brings new perspectives and a new viewpoint for the assessment of the laser resistance of optical components. Finally, the third axis concerns the study the damage growth after several irradiations in the sub-picosecond regime. The evolution of the damage area during growth sequences is observed and compared to numerical simulations. It enables to improve the understanding in the growth phenomenon. In the end, these studies will allow to develop predictive models of the laser-induced damage and new tools for the conception of

Effects of ionizing radiation on laser-induced damage in SiO/sub 2/

Energy Technology Data Exchange (ETDEWEB)

Soileau, M J; Mansour, N; Canto, E; Griscom, D L

1988-05-01

The effects of radiation damage on bulk laser-induced damage in SiO/sub 2/ were investigated. Samples studied included Spectrasil A, B, and WF (water free). Measurements of laser-induced breakdown were conducted with 532 and 1064 nm laser pulses of approximately 20 ns duration. Reductions of up to 40% in the laser-induced breakdown threshold were observed at 532 nm for samples exposed to 10/sup 8/ rad of ..gamma..-radiation. The decrease in breakdown threshold for irradiated SiO/sub 2/ samples at 532 nm was found to be proportional to the linear absorption of the specimen at 266 nm. These results are in good agreement with a proposed model which suggests that two-photon absorption initiated avalanche process is responsible for laser-induced breakdown for these materials.

The impact of mechanical log surface damage on chip size ...

African Journals Online (AJOL)

Mechanised harvesting operations are becoming more prevalent in South Africa with the realisation that motormanual and manual harvesting operations pose significant health and safety risks to workers. The damage inflicted by single-grip harvester feed rollers and delimbing knives on log surfaces during debranching ...

Laser-induced damage thresholds of gold, silver and their alloys in air and water

Science.gov (United States)

Starinskiy, Sergey V.; Shukhov, Yuri G.; Bulgakov, Alexander V.

2017-02-01

The nanosecond-laser-induced damage thresholds of gold, silver and gold-silver alloys of various compositions in air and water have been measured for single-shot irradiation conditions. The experimental results are analyzed theoretically by solving the heat flow equation for the samples irradiated in air and in water taking into account vapor nucleation at the solid-water interface. The damage thresholds of Au-Ag alloys are systematically lower than those for pure metals, both in air and water that is explained by lower thermal conductivities of the alloys. The thresholds measured in air agree well with the calculated melting thresholds for all samples. The damage thresholds in water are found to be considerably higher, by a factor of ∼1.5, than the corresponding thresholds in air. This cannot be explained, in the framework of the used model, neither by the conductive heat transfer to water nor by the vapor pressure effect. Possible reasons for the high damage thresholds in water such as scattering of the incident laser light by the vapor-liquid interface and the critical opalescence in the superheated water are suggested. Optical pump-probe measurements have been performed to study the reflectance dynamics of the surface irradiated in air and water. Comparison of the transient reflectance signal with the calculated nucleation dynamics provides evidence that the both suggested scattering mechanisms are likely to occur during metal ablation in water.

Quantitative evaluation for small surface damage based on iterative difference and triangulation of 3D point cloud

Science.gov (United States)

Zhang, Yuyan; Guo, Quanli; Wang, Zhenchun; Yang, Degong

2018-03-01

This paper proposes a non-contact, non-destructive evaluation method for the surface damage of high-speed sliding electrical contact rails. The proposed method establishes a model of damage identification and calculation. A laser scanning system is built to obtain the 3D point cloud data of the rail surface. In order to extract the damage region of the rail surface, the 3D point cloud data are processed using iterative difference, nearest neighbours search and a data registration algorithm. The curvature of the point cloud data in the damage region is mapped to RGB color information, which can directly reflect the change trend of the curvature of the point cloud data in the damage region. The extracted damage region is divided into three prism elements by a method of triangulation. The volume and mass of a single element are calculated by the method of geometric segmentation. Finally, the total volume and mass of the damage region are obtained by the principle of superposition. The proposed method is applied to several typical injuries and the results are discussed. The experimental results show that the algorithm can identify damage shapes and calculate damage mass with milligram precision, which are useful for evaluating the damage in a further research stage.

Enhanced susceptibility of ovaries from obese mice to 7,12-dimethylbenz[a]anthracene-induced DNA damage

International Nuclear Information System (INIS)

Ganesan, Shanthi; Nteeba, Jackson; Keating, Aileen F.

2014-01-01

7,12-Dimethylbenz[a]anthracene (DMBA) depletes ovarian follicles and induces DNA damage in extra-ovarian tissues, thus, we investigated ovarian DMBA-induced DNA damage. Additionally, since obesity is associated with increased offspring birth defect incidence, we hypothesized that a DMBA-induced DNA damage response (DDR) is compromised in ovaries from obese females. Wild type (lean) non agouti (a/a) and KK.Cg-Ay/J heterozygote (obese) mice were dosed with sesame oil or DMBA (1 mg/kg; intraperitoneal injection) at 18 weeks of age, for 14 days. Total ovarian RNA and protein were isolated and abundance of Ataxia telangiectasia mutated (Atm), X-ray repair complementing defective repair in Chinese hamster cells 6 (Xrcc6), breast cancer type 1 (Brca1), Rad 51 homolog (Rad51), poly [ADP-ribose] polymerase 1 (Parp1) and protein kinase, DNA-activated, catalytic polypeptide (Prkdc) were quantified by RT-PCR or Western blot. Phosphorylated histone H2AX (γH2AX) level was determined by Western blotting. Obesity decreased (P < 0.05) basal protein abundance of PRKDC and BRCA1 proteins but increased (P < 0.05) γH2AX and PARP1 proteins. Ovarian ATM, XRCC6, PRKDC, RAD51 and PARP1 proteins were increased (P < 0.05) by DMBA exposure in lean mice. A blunted DMBA-induced increase (P < 0.05) in XRCC6, PRKDC, RAD51 and BRCA1 was observed in ovaries from obese mice, relative to lean counterparts. Taken together, DMBA exposure induced γH2AX as well as the ovarian DDR, supporting that DMBA causes ovarian DNA damage. Additionally, ovarian DDR was partially attenuated in obese females raising concern that obesity may be an additive factor during chemical-induced ovotoxicity. - Highlights: • DMBA induces markers of ovarian DNA damage. • Obesity induces low level ovarian DNA damage. • DMBA-induced DNA repair response is altered by obesity

Enhanced susceptibility of ovaries from obese mice to 7,12-dimethylbenz[a]anthracene-induced DNA damage

Energy Technology Data Exchange (ETDEWEB)

Ganesan, Shanthi, E-mail: shanthig@iastate.edu; Nteeba, Jackson, E-mail: nteeba@iastate.edu; Keating, Aileen F., E-mail: akeating@iastate.edu

2014-12-01

7,12-Dimethylbenz[a]anthracene (DMBA) depletes ovarian follicles and induces DNA damage in extra-ovarian tissues, thus, we investigated ovarian DMBA-induced DNA damage. Additionally, since obesity is associated with increased offspring birth defect incidence, we hypothesized that a DMBA-induced DNA damage response (DDR) is compromised in ovaries from obese females. Wild type (lean) non agouti (a/a) and KK.Cg-Ay/J heterozygote (obese) mice were dosed with sesame oil or DMBA (1 mg/kg; intraperitoneal injection) at 18 weeks of age, for 14 days. Total ovarian RNA and protein were isolated and abundance of Ataxia telangiectasia mutated (Atm), X-ray repair complementing defective repair in Chinese hamster cells 6 (Xrcc6), breast cancer type 1 (Brca1), Rad 51 homolog (Rad51), poly [ADP-ribose] polymerase 1 (Parp1) and protein kinase, DNA-activated, catalytic polypeptide (Prkdc) were quantified by RT-PCR or Western blot. Phosphorylated histone H2AX (γH2AX) level was determined by Western blotting. Obesity decreased (P < 0.05) basal protein abundance of PRKDC and BRCA1 proteins but increased (P < 0.05) γH2AX and PARP1 proteins. Ovarian ATM, XRCC6, PRKDC, RAD51 and PARP1 proteins were increased (P < 0.05) by DMBA exposure in lean mice. A blunted DMBA-induced increase (P < 0.05) in XRCC6, PRKDC, RAD51 and BRCA1 was observed in ovaries from obese mice, relative to lean counterparts. Taken together, DMBA exposure induced γH2AX as well as the ovarian DDR, supporting that DMBA causes ovarian DNA damage. Additionally, ovarian DDR was partially attenuated in obese females raising concern that obesity may be an additive factor during chemical-induced ovotoxicity. - Highlights: • DMBA induces markers of ovarian DNA damage. • Obesity induces low level ovarian DNA damage. • DMBA-induced DNA repair response is altered by obesity.

Laser induced damage and fracture in fused silica vacuum windows

International Nuclear Information System (INIS)

Campbell, J.H.; Hurst, P.A.; Heggins, D.D.; Steele, W.A.; Bumpas, S.E.

1996-11-01

Laser-induced damage, that initiates catastrophic fracture, has been observed in large (≤61 cm dia) fused silica lenses that also serve as vacuum barriers in Nova and Beamlet lasers. If the elastic stored energy in the lens is high enough, the lens will fracture into many pieces (implosion). Three parameters control the degree of fracture in the vacuum barrier window: elastic stored energy (tensile stress), ratio of window thickness to flaw depth, and secondary crack propagation. Fracture experiments were conducted on 15-cm dia fused silica windows that contain surface flaws caused by laser damage. Results, combined with window failure data on Beamlet and Nova, were used to develop design criteria for a ''fail-safe'' lens (that may catastrophically fracture but not implode). Specifically, the window must be made thick enough so that the peak tensile stress is less than 500 psi (3.4 MPa) and the thickness/critical flaw size is less than 6. The air leak through the window fracture and into the vacuum must be rapid enough to reduce the load on the window before secondary crack growth occurs. Finite element stress calculations of a window before and immediately following fracture into two pieces show that the elastic stored energy is redistributed if the fragments ''lock'' in place and thereby bridge the opening. In such cases, the peak stresses at the flaw site can increase, leading to further (i.e. secondary) crack growth

Lattice damage induced by Tb-implanted AlN crystalline films

International Nuclear Information System (INIS)

Lu Fei; Hu Hui; Rizzi, A.

2002-01-01

AlN films with thickness from 100 to 1000 nm were grown on SiC substrate by MBE. AlN crystalline films were doped by implantation with 160 keV Tb ions to fluences of 5x10 14 , 1.5x10 15 , 3x10 15 and 6x10 15 ions/cm 2 , respectively. The damage profiles in AlN films induced by Tb implantation were investigated using RBS/channeling technique. A procedure developed by Feldman and Rodgers was used to extract damage profile by considering the dechanneling mechanism of multiple. The comparison of the extracted profile with TRIM prediction shows a significant difference in the shape and in the position of damage profile. The damage profile in AlN film is similar as Tb distribution. The RBS/channeling of Tb-implanted AlN film before and after 950 deg. C annealing treatments show a good consistency, which indicate that high temperature annealing cannot result in a significant change in both crystal damage and in Tb distribution

Gender differences in alcohol-induced neurotoxicity and brain damage.

Science.gov (United States)

Alfonso-Loeches, Silvia; Pascual, María; Guerri, Consuelo

2013-09-06

Considerable evidence has demonstrated that women are more vulnerable than men to the toxic effects of alcohol, although the results as to whether gender differences exist in ethanol-induced brain damage are contradictory. We have reported that ethanol, by activating the neuroimmune system and Toll-like receptors 4 (TLR4), can cause neuroinflammation and brain injury. However, whether there are gender differences in alcohol-induced neuroinflammation and brain injury are currently controversial. Using the brains of TLR4(+/+) and TLR4(-/-) (TLR4-KO) mice, we report that chronic ethanol treatment induces inflammatory mediators (iNOS and COX-2), cytokines (IL-1β, TNF-α), gliosis processes, caspase-3 activation and neuronal loss in the cerebral cortex of both female and male mice. Conversely, the levels of these parameters tend to be higher in female than in male mice. Using an in vivo imaging technique, our results further evidence that ethanol treatment triggers higher GFAP levels and lower MAP-2 levels in female than in male mice, suggesting a greater effect of ethanol-induced astrogliosis and less MAP-2(+) neurons in female than in male mice. Our results further confirm the pivotal role of TLR4 in alcohol-induced neuroinflammation and brain damage since the elimination of TLR4 protects the brain of males and females against the deleterious effects of ethanol. In short, the present findings demonstrate that, during the same period of ethanol treatment, females are more vulnerable than males to the neurotoxic/neuroinflammatory effects of ethanol, thus supporting the view that women are more susceptible than men to the medical consequences of alcohol abuse. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Mild hyperthermia can induce adaptation to cytogenetic damage caused by subsequent X irradiation

International Nuclear Information System (INIS)

Cai, Lu.; Jiang, Jie.

1995-01-01

Many low-level environmental agents are able to induce an increased resistance to subsequent mutagenic effects induced by ionizing radiation. In this paper, an induced cytogenetic adaptation to radiation in human lymphocytes was studied with mild hyperthermia as the adaptive treatment and compared with that induced by low-dose radiation. We found that this adaptation could be induced not only in PHA-stimulated human lymphocytes (at 14, 38 and 42 h after addition of PHA), but also in unstimulated G 0 -phase cells (before addition of PHA) by mild hyperthermia (41 degrees C for 1 h) as well as 50 mGy X rays. When the two adaptive treatments were combined, no additive effects on the magnitude of the adaptation induced were observed, suggesting that low-dose radiation and hyperthermia may share one mechanism of induction of adaptation to cytogenetic damage. Some mechanisms which may be involved in the induction of adaptation to cytogenetic damage by low-dose radiation are discussed and compared with the effects of mild hyperthermia in inducing thermotolerance and radioresistance. 56 refs., 4 figs., 3 tabs

Surface/subsurface observation and removal mechanisms of ground reaction bonded silicon carbide

Science.gov (United States)

Yao, Wang; Zhang, Yu-Min; Han, Jie-cai; Zhang, Yun-long; Zhang, Jian-han; Zhou, Yu-feng; Han, Yuan-yuan

2006-01-01

Reaction Bonded Silicon Carbide (RBSiC) has long been recognized as a promising material for optical applications because of its unique combination of favorable properties and low-cost fabrication. Grinding of silicon carbide is difficult because of its high hardness and brittleness. Grinding often induces surface and subsurface damage, residual stress and other types of damage, which have great influence on the ceramic components for optical application. In this paper, surface integrity, subsurface damage and material removal mechanisms of RBSiC ground using diamond grinding wheel on creep-feed surface grinding machine are investigated. The surface and subsurface are studied with scanning electron microscopy (SEM) and optical microscopy. The effects of grinding conditions on surface and subsurface damage are discussed. This research links the surface roughness, surface and subsurface cracks to grinding parameters and provides valuable insights into the material removal mechanism and the dependence of grind induced damage on grinding conditions.

Laser-induced damage thresholds of gold, silver and their alloys in air and water

Energy Technology Data Exchange (ETDEWEB)

Starinskiy, Sergey V.; Shukhov, Yuri G.; Bulgakov, Alexander V., E-mail: bulgakov@itp.nsc.ru

2017-02-28

Highlights: • Laser damage thresholds of Ag, Au and Ag-Au alloys in air and water are measured. • Alloy thresholds are lower than those of Ag and Au due to low thermal conductivity. • Laser damage thresholds in water are ∼1.5 times higher than those in air. • Light scattering mechanisms responsible for high thresholds in water are suggested. • Light scattering mechanisms are supported by optical reflectance measurements. - Abstract: The nanosecond-laser-induced damage thresholds of gold, silver and gold-silver alloys of various compositions in air and water have been measured for single-shot irradiation conditions. The experimental results are analyzed theoretically by solving the heat flow equation for the samples irradiated in air and in water taking into account vapor nucleation at the solid-water interface. The damage thresholds of Au-Ag alloys are systematically lower than those for pure metals, both in air and water that is explained by lower thermal conductivities of the alloys. The thresholds measured in air agree well with the calculated melting thresholds for all samples. The damage thresholds in water are found to be considerably higher, by a factor of ∼1.5, than the corresponding thresholds in air. This cannot be explained, in the framework of the used model, neither by the conductive heat transfer to water nor by the vapor pressure effect. Possible reasons for the high damage thresholds in water such as scattering of the incident laser light by the vapor-liquid interface and the critical opalescence in the superheated water are suggested. Optical pump-probe measurements have been performed to study the reflectance dynamics of the surface irradiated in air and water. Comparison of the transient reflectance signal with the calculated nucleation dynamics provides evidence that the both suggested scattering mechanisms are likely to occur during metal ablation in water.

Tumor induced hepatic myeloid derived suppressor cells can cause moderate liver damage.

Science.gov (United States)

Eggert, Tobias; Medina-Echeverz, José; Kapanadze, Tamar; Kruhlak, Michael J; Korangy, Firouzeh; Greten, Tim F

2014-01-01

Subcutaneous tumors induce the accumulation of myeloid derived suppressor cells (MDSC) not only in blood and spleens, but also in livers of these animals. Unexpectedly, we observed a moderate increase in serum transaminases in mice with EL4 subcutaneous tumors, which prompted us to study the relationship of hepatic MDSC accumulation and liver injury. MDSC were the predominant immune cell population expanding in livers of all subcutaneous tumor models investigated (RIL175, B16, EL4, CT26 and BNL), while liver injury was only observed in EL4 and B16 tumor-bearing mice. Elimination of hepatic MDSC in EL4 tumor-bearing mice using low dose 5-fluorouracil (5-FU) treatment reversed transaminase elevation and adoptive transfer of hepatic MDSC from B16 tumor-bearing mice caused transaminase elevation indicating a direct MDSC mediated effect. Surprisingly, hepatic MDSC from B16 tumor-bearing mice partially lost their damage-inducing potency when transferred into mice bearing non damage-inducing RIL175 tumors. Furthermore, MDSC expansion and MDSC-mediated liver injury further increased with growing tumor burden and was associated with different cytokines including GM-CSF, VEGF, interleukin-6, CCL2 and KC, depending on the tumor model used. In contrast to previous findings, which have implicated MDSC only in protection from T cell-mediated hepatitis, we show that tumor-induced hepatic MDSC themselves can cause moderate liver damage.

Damage induced in semiconductors by swift heavy ion irradiation

International Nuclear Information System (INIS)

Levalois, M.; Marie, P.

1999-01-01

The behaviour of semiconductors under swift heavy ion irradiation is different from that of metals or insulators: no spectacular effect induced by the inelastic energy loss has been reported in these materials. We present here a review of irradiation effects in the usual semiconductors (silicon, germanium and gallium arsenide). The damage is investigated by means of electrical measurements. The usual mechanisms of point defect creation can account for the experimental results. Besides, some results obtained on the wide gap semiconductor silicon carbide are reported. Concerning the irradiation effects induced by heavy ions in particle detectors, based on silicon substrate, we show that the deterioration of the detector performances can be explained from the knowledge of the substrate properties which are strongly perturbed after high doses of irradiation. Finally, some future ways of investigation are proposed. The silicon substrate is a good example to compare the irradiation effects with different particles such as electrons, neutrons and heavy ions. It is then necessary to use parameters which account for the local energy deposition, in order to describe the damage in the material

Autophagy activation promotes removal of damaged mitochondria and protects against renal tubular injury induced by albumin overload.

Science.gov (United States)

Tan, Jin; Wang, Miaohong; Song, Shuling; Miao, Yuyang; Zhang, Qiang

2018-01-10

Proteinuria (albuminuria) is an important cause of aggravating tubulointerstitial injury. Previous studies have shown that autophagy activation can alleviate renal tubular epithelial cell injury caused by urinary protein, but the mechanism is not clear. Here, we investigated the role of clearance of damaged mitochondria in this protective effect. We found that albumin overload induces a significant increase in turnover of LC3-II and decrease in p62 protein level in renal proximal tubular (HK-2) cells in vitro. Albumin overload also induces an increase in mitochondrial damage. ALC, a mitochondrial torpent, alleviates mitochondrial damage induced by albumin overload and also decreases autophagy, while mitochondrial damage revulsant CCCP further increases autophagy. Furthermore, pretreatment of HK-2 cells with rapamycin reduced the amount of damaged mitochondria and the level of apoptosis induced by albumin overload. In contrast, blocking autophagy with chloroquine exerted an opposite effect. Taken together, our results indicated autophagy activation promotes removal of damaged mitochondria and protects against renal tubular injury caused by albumin overload. This further confirms previous research that autophagy activation is an adaptive response in renal tubular epithelial cells after urinary protein overload.

TDP1 repairs nuclear and mitochondrial DNA damage induced by chain-terminating anticancer and antiviral nucleoside analogs

Science.gov (United States)

Huang, Shar-yin N.; Murai, Junko; Dalla Rosa, Ilaria; Dexheimer, Thomas S.; Naumova, Alena; Gmeiner, William H.; Pommier, Yves

2013-01-01

Chain-terminating nucleoside analogs (CTNAs) that cause stalling or premature termination of DNA replication forks are widely used as anticancer and antiviral drugs. However, it is not well understood how cells repair the DNA damage induced by these drugs. Here, we reveal the importance of tyrosyl–DNA phosphodiesterase 1 (TDP1) in the repair of nuclear and mitochondrial DNA damage induced by CTNAs. On investigating the effects of four CTNAs—acyclovir (ACV), cytarabine (Ara-C), zidovudine (AZT) and zalcitabine (ddC)—we show that TDP1 is capable of removing the covalently linked corresponding CTNAs from DNA 3′-ends. We also show that Tdp1−/− cells are hypersensitive and accumulate more DNA damage when treated with ACV and Ara-C, implicating TDP1 in repairing CTNA-induced DNA damage. As AZT and ddC are known to cause mitochondrial dysfunction, we examined whether TDP1 repairs the mitochondrial DNA damage they induced. We find that AZT and ddC treatment leads to greater depletion of mitochondrial DNA in Tdp1−/− cells. Thus, TDP1 seems to be critical for repairing nuclear and mitochondrial DNA damage caused by CTNAs. PMID:23775789

Heavy Metal-Induced Oxidative DNA Damage in Earthworms: A Review

Directory of Open Access Journals (Sweden)

Takeshi Hirano

2010-01-01

Full Text Available Earthworms can be used as a bio-indicator of metal contamination in soil, Earlier reports claimed the bioaccumulation of heavy metals in earthworm tissues, while the metal-induced mutagenicity reared in contaminated soils for long duration. But we examined the metal-induced mutagenicity in earthworms reared in metal containing culture beddings. In this experiment we observed the generation of 8-oxoguanine (8-oxo-Gua in earthworms exposed to cadmium and nickel in soil. 8-oxo-Gua is a major premutagenic form of oxidative DNA damage that induces GC-to-TA point mutations, leading to carcinogenesis.

Applications of high order harmonic radiation to UVX-solids interaction: high excitation density in electronic relaxation dynamics and surface damaging

International Nuclear Information System (INIS)

De Grazia, M.

2007-12-01

The new sources of radiation in the extreme-UV (X-UV: 10-100 nm), which deliver spatially coherent, ultra-short and intense pulses, allow studying high flux processes and ultra-fast dynamics in various domains. The thesis work presents two applications of the high-order laser harmonics (HH) to solid state physics. In Part I, we describe the optimization of the harmonic for studies of X-UV/solids interaction. In Part II, we investigate effects of high excitation density in the dynamics of electron relaxation in dielectric scintillator crystals - tungstates and fluorides, using time-resolved luminescence spectroscopy. Quenching of luminescence at short time gives evidence of the competition between radiative and non-radiative recombination of self-trapped excitons (STE). The non-radiative channel is identified to mutual interaction of STE at high excitation density. In Part III, we study the X-UV induced damage mechanism in various materials, either conductor (amorphous carbon) or insulators (organic polymers, e.g., PMMA). In PMMA-Plexiglas, in the desorption regime (0.2 mJ/cm 2 , i.e., below damage threshold), the surface modifications reflect X-UV induced photochemical processes that are tentatively identified, as a function of dose: at low dose, polymer chain scission followed by the blow-up of the volatile, low-molecular fragments leads to crater formation; at high dose, cross-linking in the near-surface layer of remaining material leads to surface hardening. These promising results have great perspectives considering the performances already attained and planned in the next future in the development of the harmonic sources. (author)

Impact of environmental contamination on laser induced damage of silica optics in Laser MegaJoule; Impact de l'environnement sur l'endommagement laser des optiques de silice du Laser MegaJoule

Energy Technology Data Exchange (ETDEWEB)

Bien-Aime, K.

2009-11-15

Laser induced damage impact of molecular contamination on fused polished silica samples in a context of high power laser fusion facility, such as Laser MegaJoule (LMJ) has been studied. One of the possible causes of laser induced degradation of optical component is the adsorption of molecular or particular contamination on optical surfaces. In the peculiar case of LMJ, laser irradiation conditions are a fluence of 10 J/cm{sup 2}, a wavelength of 351 nm, a pulse duration of 3 ns for a single shot/days frequency. Critical compounds have been identified thanks to environmental measurements, analysis of material outgassing, and identification of surface contamination in the critical environments. Experiments of controlled contamination involving these compounds have been conducted in order to understand and model mechanisms of laser damage. Various hypotheses are proposed to explain the damage mechanism. (author)

Calculation on spectrum of direct DNA damage induced by low-energy electrons including dissociative electron attachment.

Science.gov (United States)

Liu, Wei; Tan, Zhenyu; Zhang, Liming; Champion, Christophe

2017-03-01

In this work, direct DNA damage induced by low-energy electrons (sub-keV) is simulated using a Monte Carlo method. The characteristics of the present simulation are to consider the new mechanism of DNA damage due to dissociative electron attachment (DEA) and to allow determining damage to specific bases (i.e., adenine, thymine, guanine, or cytosine). The electron track structure in liquid water is generated, based on the dielectric response model for describing electron inelastic scattering and on a free-parameter theoretical model and the NIST database for calculating electron elastic scattering. Ionization cross sections of DNA bases are used to generate base radicals, and available DEA cross sections of DNA components are applied for determining DNA-strand breaks and base damage induced by sub-ionization electrons. The electron elastic scattering from DNA components is simulated using cross sections from different theoretical calculations. The resulting yields of various strand breaks and base damage in cellular environment are given. Especially, the contributions of sub-ionization electrons to various strand breaks and base damage are quantitatively presented, and the correlation between complex clustered DNA damage and the corresponding damaged bases is explored. This work shows that the contribution of sub-ionization electrons to strand breaks is substantial, up to about 40-70%, and this contribution is mainly focused on single-strand break. In addition, the base damage induced by sub-ionization electrons contributes to about 20-40% of the total base damage, and there is an evident correlation between single-strand break and damaged base pair A-T.

Carnosine attenuates cyclophosphamide-induced bone marrow suppression by reducing oxidative DNA damage

Directory of Open Access Journals (Sweden)

Jie Deng

2018-04-01

Full Text Available Oxidative DNA damage in bone marrow cells is the main side effect of chemotherapy drugs including cyclophosphamide (CTX. However, not all antioxidants are effective in inhibiting oxidative DNA damage. In this study, we report the beneficial effect of carnosine (β-alanyl-l-histidine, a special antioxidant with acrolein-sequestering ability, on CTX-induced bone marrow cell suppression. Our results show that carnosine treatment (100 and 200 mg/kg, i.p. significantly inhibited the generation of reactive oxygen species (ROS and 8-hydroxy-2′-deoxyguanosine (8-oxo-dG, and decreased chromosomal abnormalities in the bone marrow cells of mice treated with CTX (20 mg/kg, i.v., 24 h. Furthermore, carnosine evidently mitigated CTX-induced G2/M arrest in murine bone marrow cells, accompanied by reduced ratios of p-Chk1/Chk1 and p-p53/p53 as well as decreased p21 expression. In addition, cell apoptosis caused by CTX was also suppressed by carnosine treatment, as assessed by decreased TUNEL-positive cell counts, down-regulated expressions of Bax and Cyt c, and reduced ratios of cleaved Caspase-3/Caspase-3. These results together suggest that carnosine can protect murine bone marrow cells from CTX-induced DNA damage via its antioxidant activity. Keywords: Carnosine, Cyclophosphamide, Oxidative DNA damage, Sister chromatid exchange, Apoptosis, Cell cycle arrest

Surface damage in TEM thick α-Fe samples by implantation with 150 keV Fe ions

International Nuclear Information System (INIS)

Aliaga, M.J.; Caturla, M.J.; Schäublin, R.

2015-01-01

We have performed molecular dynamics simulations of implantation of 150 keV Fe ions in pure bcc Fe. The thickness of the simulation box is of the same order of those used in in situ TEM analysis of irradiated materials. We assess the effect of the implantation angle and the presence of front and back surfaces. The number and type of defects, ion range, cluster distribution and primary damage morphology are studied. Results indicate that, for the very thin samples used in in situ TEM irradiation experiments the presence of surfaces affect dramatically the damage produced. At this particular energy, the ion has sufficient energy to damage both the top and the back surfaces and still leave the sample through the bottom. This provides new insights on the study of radiation damage using TEM in situ

Effects of tissue mechanical properties on susceptibility to histotripsy-induced tissue damage

Science.gov (United States)

Vlaisavljevich, Eli; Kim, Yohan; Owens, Gabe; Roberts, William; Cain, Charles; Xu, Zhen

2014-01-01

Histotripsy is a non-invasive tissue ablation method capable of fractionating tissue by controlling acoustic cavitation. To determine the fractionation susceptibility of various tissues, we investigated histotripsy-induced damage on tissue phantoms and ex vivo tissues with different mechanical strengths. A histotripsy bubble cloud was formed at tissue phantom surfaces using 5-cycle long ultrasound pulses with peak negative pressure of 18 MPa and PRFs of 10, 100, and 1000 Hz. Results showed significantly smaller lesions were generated in tissue phantoms of higher mechanical strength. Histotripsy was also applied to 43 different ex vivo porcine tissues with a wide range of mechanical properties. Gross morphology demonstrated stronger tissues with higher ultimate stress, higher density, and lower water content were more resistant to histotripsy damage in comparison to weaker tissues. Based on these results, a self-limiting vessel-sparing treatment strategy was developed in an attempt to preserve major vessels while fractionating the surrounding target tissue. This strategy was tested in porcine liver in vivo. After treatment, major hepatic blood vessels and bile ducts remained intact within a completely fractionated liver volume. These results identify varying susceptibilities of tissues to histotripsy therapy and provide a rational basis to optimize histotripsy parameters for treatment of specific tissues.

Preparation of high laser-induced damage threshold Ta{sub 2}O{sub 5} films

Energy Technology Data Exchange (ETDEWEB)

Xu, Cheng, E-mail: xucheng@cumt.edu.cn [School of Materials Science and Engineering, China University of Mining and Technology, Xuzhou 221116 (China); Yi, Peng; Fan, Heliang; Qi, Jianwei; Yang, Shuai; Qiang, Yinghuai; Liu, Jiongtian [School of Materials Science and Engineering, China University of Mining and Technology, Xuzhou 221116 (China); Li, Dawei [Key Laboratory of High Power Laser Materials, Shanghai Institute of Optics and Fine Mechanics, Chinese Academy of Sciences, Shanghai 201800 (China)

2014-08-01

High laser-induced damage threshold (LIDT) Ta{sub 2}O{sub 5} films were prepared by the sol–gel method using TaCl{sub 5} as a new precursor. The optical properties, surface morphologies, chemical composition, absorption and LIDT of the films were investigated. The results showed that the transparent and homogenous Ta{sub 2}O{sub 5} films had small surface roughness, low absorption and high LIDT even with large number of layers. The maximum LIDT at 1064 nm and 12 ns of the films was 24.8 J/cm{sup 2}. The ion chromatograph and Fourier transform infrared spectrum were used to reveal the functions of the addition of H{sub 2}O{sub 2} in the sol formation. It was shown that H{sub 2}O{sub 2} had two important functions, which were the decrease of Cl element content and the rapid generation of tantalum oxide. The high LIDT achieved was mainly due to the nearly free of defects in the films.

Correlation of DT and DD fusion neutron damage in silicon surface barrier detector

International Nuclear Information System (INIS)

Iida, Toshiyuki; Sueyoshi, Yasuhiro; Sunarno; Takahashi, Akito

1994-01-01

In order to examine the correlation of DT and DD fusion neutron damage in Si, a silicon surface barrier detector (Si-SBD) was irradiation with neutrons from a deuteron accelerator. The leakage current increased proportionally with neutron fluence, which determined the neutron damage constant for the Si-SBD. The correlation factor of the DT and DD neutron damage in the Si-SBD was determined from the ratio of the DT and DD neutron damage constants and was found to be 2.3. We also calculated the rate of DT and DD neutron displacement damage for Si by using the TRIM-90 computer program and actual data on neutron reactions in the Si-SBD. The correlation factor of DT and DD neutron damage from the calculation agreed with that from the Si-SBD irradiation experiment. (author)

Low surface damage dry etched black silicon

DEFF Research Database (Denmark)

Plakhotnyuk, Maksym M.; Gaudig, Maria; Davidsen, Rasmus Schmidt

2017-01-01

Black silicon (bSi) is promising for integration into silicon solar cell fabrication flow due to its excellent light trapping and low reflectance, and a continuously improving passivation. However, intensive ion bombardment during the reactive ion etching used to fabricate bSi induces surface dam...

The basic chemistry of exercise-induced DNA oxidation: oxidative damage, redox signalling and their interplay

Directory of Open Access Journals (Sweden)

James Nathan Cobley

2015-06-01

Full Text Available Acute exercise increases reactive oxygen and nitrogen species generation. This phenomenon is associated with two major outcomes: (1 redox signalling and (2 macromolecule damage. Mechanistic knowledge of how exercise-induced redox signalling and macromolecule damage are interlinked is limited. This review focuses on the interplay between exercise-induced redox signalling and DNA damage, using hydroxyl radical (·OH and hydrogen peroxide (H2O2 as exemplars. It is postulated that the biological fate of H2O2 links the two processes and thus represents a bifurcation point between redox signalling and damage. Indeed, H2O2 can participate in two electron signalling reactions but its diffusion and chemical properties permit DNA oxidation following reaction with transition metals and ·OH generation. It is also considered that the sensing of DNA oxidation by repair proteins constitutes a non-canonical redox signalling mechanism. Further layers of interaction are provided by the redox regulation of DNA repair proteins and their capacity to modulate intracellular H2O2 levels. Overall, exercise-induced redox signalling and DNA damage may be interlinked to a greater extent than was previously thought but this requires further investigation.

Detection of laser damage by Raman microscopy

International Nuclear Information System (INIS)

Fauchet, P.M.; Campbell, I.H.; Adar, F.

1988-01-01

The authors demonstrate that Raman miroscopy is a sensitive and quantitative tool to detect and characterize laser-induced damage in solids. After damage is induced with single or multiple high power laser pulses, a Raman microprobe maps the surface of the sample with one micron spatial resolution. By performing accurate measurements of the Stokes line, the authors have been able to measure stress, strain and crystallinity in various samples which had been exposed to high intensity pulses. These results are compared to those obtained using conventional tools such as Nomarski microscopy. Major advantages of Raman microscopy include sensitivity to subtle structural modifications and the fact that it gives quantitative measurements

Effects of wearing bio-active material coated fabric against γ-irradiation-induced cellular damaged in Sprague-Dawley rats

International Nuclear Information System (INIS)

Kang, Jung Ae; Kim, Hye Rim; Yoon, Sun Hye; Nam, Sang Hyun; Park, Sang Hyun; Jang, Beom Su; Go, Kyung Chan; Yang, Gwang Wung; Rho, Young Hwan; Park, Hyo Suk

2016-01-01

Ionizing radiation causes cellular damage and death through the direct damage and/or indirectly the production of ROS, which induces oxidative stress. This study was designed to evaluate the in vivo radioprotective effects of a bio-active material coated fabric (BMCF) against γ-irradiation-induced cellular damage in Sprague-Dawley (SD) rats. Healthy male SD rats wore bio-active material coated (concentrations in 10% and 30%) fabric for 7 days after 3 Gy of γ-irradiation. Radioprotective effects were evaluated by performing various biochemical assays including spleen and thymus index, WBC count, hepatic damage marker enzymes [aspartate transaminase (AST) and alanine transaminase (ALT)] in plasma, liver antioxidant enzymes, and mitochondrial activity in muscle. Exposure to γ-irradiation resulted in hepatocellular and immune systemic damage. Gamma-irradiation induced decreases in antioxidant enzymes. However, wearing the BMCF-30% decreased significantly AST and ALT activities in plasma. Furthermore, wearing the BMCF-30% increased SOD (superoxide dismutase) and mitochondrial activity. These results suggest that wearing BMCF offers effective radioprotection against γ-irradiation-induced cellular damage in SD rats

Effects of wearing bio-active material coated fabric against γ-irradiation-induced cellular damaged in Sprague-Dawley rats

Energy Technology Data Exchange (ETDEWEB)

Kang, Jung Ae; Kim, Hye Rim; Yoon, Sun Hye; Nam, Sang Hyun; Park, Sang Hyun; Jang, Beom Su [Korea Atomic Energy Research Institute, Jeongeup (Korea, Republic of); Go, Kyung Chan; Yang, Gwang Wung; Rho, Young Hwan; Park, Hyo Suk [Research and Development Center, VENTEX Co. Ltd., Seoul (Korea, Republic of)

2016-09-15

Ionizing radiation causes cellular damage and death through the direct damage and/or indirectly the production of ROS, which induces oxidative stress. This study was designed to evaluate the in vivo radioprotective effects of a bio-active material coated fabric (BMCF) against γ-irradiation-induced cellular damage in Sprague-Dawley (SD) rats. Healthy male SD rats wore bio-active material coated (concentrations in 10% and 30%) fabric for 7 days after 3 Gy of γ-irradiation. Radioprotective effects were evaluated by performing various biochemical assays including spleen and thymus index, WBC count, hepatic damage marker enzymes [aspartate transaminase (AST) and alanine transaminase (ALT)] in plasma, liver antioxidant enzymes, and mitochondrial activity in muscle. Exposure to γ-irradiation resulted in hepatocellular and immune systemic damage. Gamma-irradiation induced decreases in antioxidant enzymes. However, wearing the BMCF-30% decreased significantly AST and ALT activities in plasma. Furthermore, wearing the BMCF-30% increased SOD (superoxide dismutase) and mitochondrial activity. These results suggest that wearing BMCF offers effective radioprotection against γ-irradiation-induced cellular damage in SD rats.

Spatiotemporal kinetics of γ-H2AX protein on charged particles induced DNA damage

Energy Technology Data Exchange (ETDEWEB)

Niu, H., E-mail: hniu@mx.nthu.edu.tw [Nuclear Science and Technology Development Center, National Tsing Hua University, Hsinchu, Taiwan (China); Chang, H.C. [Department of Biomedical Engineering and Environmental Sciences, National Tsing Hua University, Hsinchu, Taiwan (China); Cho, I.C. [Institute for Radiological Research, Chang Gung University and Chang Gung Memorial Hospital, Taoyuan, Taiwan (China); Chen, C.H. [Nuclear Science and Technology Development Center, National Tsing Hua University, Hsinchu, Taiwan (China); Liu, C.S. [Cancer Center of Taipei Veterans General Hospital, Taipei, Taiwan (China); Chou, W.T. [Department of Biomedical Engineering and Environmental Sciences, National Tsing Hua University, Hsinchu, Taiwan (China)

2014-08-15

Highlights: • Charged particles can induce more complex DNA damages, and these complex damages have higher ability to cause the cell death or cell carcinogenesis. • In this study, we used γ-H2AX protein to investigate the spatiotemporal kinetics of DNA double strand breaks in particle irradiated HeLa cells. • The HeLa cells were irradiated by 400 keV alpha-particles in four different dosages. • The result shows that a good linear relationship can be observed between foci number and radiation dose. • The data shows that the dissolution rate of γ-H2AX foci agree with the two components DNA repairing model, and it was decreasing as the radiation dose increased. • These results suggest that charged particles can induce more complex DNA damages and causing the retardation of DNA repair. - Abstract: In several researches, it has been demonstrated that charged particles can induce more complex DNA damages. These complex damages have higher ability to cause the cell death or cell carcinogenesis. For this reason, clarifying the DNA repair mechanism after charged particle irradiation plays an important role in the development of charged particle therapy and space exploration. Unfortunately, the detail spatiotemporal kinetic of DNA damage repair is still unclear. In this study, we used γ-H2AX protein to investigate the spatiotemporal kinetics of DNA double strand breaks in alpha-particle irradiated HeLa cells. The result shows that the intensity of γ-H2AX foci increased gradually, and reached to its maximum at 30 min after irradiation. A good linear relationship can be observed between foci intensity and radiation dose. After 30 min, the γ-H2AX foci intensity was decreased with time passed, but remained a large portion (∼50%) at 48 h passed. The data show that the dissolution rate of γ-H2AX foci agreed with two components DNA repairing model. These results suggest that charged particles can induce more complex DNA damages and causing the retardation of DNA

Quantification of acute vocal fold epithelial surface damage with increasing time and magnitude doses of vibration exposure.

Directory of Open Access Journals (Sweden)

Tsuyoshi Kojima

Full Text Available Because the vocal folds undergo repeated trauma during continuous cycles of vibration, the epithelium is routinely susceptible to damage during phonation. Excessive and prolonged vibration exposure is considered a significant predisposing factor in the development of vocal fold pathology. The purpose of the present study was to quantify the extent of epithelial surface damage following increased time and magnitude doses of vibration exposure using an in vivo rabbit phonation model. Forty-five New Zealand white breeder rabbits were randomized to nine groups and received varying phonation time-doses (30, 60, or 120 minutes and magnitude-doses (control, modal intensity phonation, or raised intensity phonation of vibration exposure. Scanning electron microscopy and transmission electron microscopy was used to quantify the degree of epithelial surface damage. Results revealed a significant reduction in microprojection density, microprojection height, and depth of the epithelial surface with increasing time and phonation magnitudes doses, signifying increased epithelial surface damage risk with excessive and prolonged vibration exposure. Destruction to the epithelial cell surface may provide significant insight into the disruption of cell function following prolonged vibration exposure. One important goal achieved in the present study was the quantification of epithelial surface damage using objective imaging criteria. These data provide an important foundation for future studies of long-term tissue recovery from excessive and prolonged vibration exposure.

p38-MK2 signaling axis regulates RNA metabolism after UV-light-induced DNA damage

DEFF Research Database (Denmark)

Borisova, Marina E; Voigt, Andrea; Tollenaere, Maxim A X

2018-01-01

quantitative phosphoproteomics and protein kinase inhibition to provide a systems view on protein phosphorylation patterns induced by UV light and uncover the dependencies of phosphorylation events on the canonical DNA damage signaling by ATM/ATR and the p38 MAP kinase pathway. We identify RNA-binding proteins......Ultraviolet (UV) light radiation induces the formation of bulky photoproducts in the DNA that globally affect transcription and splicing. However, the signaling pathways and mechanisms that link UV-light-induced DNA damage to changes in RNA metabolism remain poorly understood. Here we employ...

Surface damage in the small intestine of the mouse after X - or neutron irradiation

International Nuclear Information System (INIS)

Hamlet, R.; Carr, K.E.; Nias, A.H.; Watt, C.

1981-01-01

Damage after X-irradiation includes lateral villous collapse, progressing after 3 - 5 days to villi which sometimes show signs of vertical collapse. After neutron irradiation vertical villous collapse is established earlier, with less swelling of villous tips. It seems, therefore, that at radiobiologically equivalent doses, neutron and X-irradiation produce different levels of surface damage, with neutron irradiation being the more destructive. Early villous tip damage may perhaps be due to disruption of susceptible cells already at the extrusion zone, or to stromal damage

Free methionine supplementation limits alcohol-induced liver damage in rats

DEFF Research Database (Denmark)

Parlesak, Alexandr; Bode, C.; Bode, J.C.

1998-01-01

Alcohol feeding to rats that were submitted to a jejunoileal bypass operation has been shown to result in liver damage being comparable with alcohol-induced liver disease in man. In the present study, a striking effect of free methionine consumption on histological liver injury, triglyceride accu...

SHI induced damage in electrical properties of silicon NPN BJTs

Energy Technology Data Exchange (ETDEWEB)

Kumar, M. Vinay, E-mail: vkm288@gmail.com; Krishnaveni, S. [Department of studies in Physics, University of Mysore, Mysore (India); Kumar, Santhosh [Department of Physics, Regional Institute of Education, Mysore (India); Yashoda, T. [Department of Physics, AVK College for Women, Hassan (India)

2016-05-23

The investigation of radiation damage in Si microelectronic circuitry and devices are being carried out by various research groups globally. In particular the Si Bipolar junction transistors are very sensitive to high energetic radiation. In the present study, radiation response of NPN Bipolar junction transistor (2N3773) has been examined for 60 MeV B{sup 4+} ion. Key electrical properties like Gummel, dc current gain and capacitance – voltage (C-V) characteristics of 60 MeV B{sup 4+} ion irradiated transistor were studied before and after irradiation. Ion irradiation and subsequent electrical characterizations were performed at room temperature. Current voltage (I-V) measurements showed the increase in collector current for V{sub BE} ≤ 0.4 V as a function of fluence, which is due to B{sup 4+} ion induced surface leakage currents. Base current is observed to be more sensitive than collector current and gain appears to be degraded with ion fluence. Also, C-V measurements shows that both built in potential and doping concentration increased significantly after irradiation.

Can ebselen prevent cisplatin-induced ovarian damage?

Science.gov (United States)

Soyman, Zeynep; Uzun, Hafize; Bayindir, Nihan; Esrefoglu, Mukaddes; Boran, Birtan

2018-06-01

The occurrence of ovarian damage is a major shortcoming in treating tumors with cisplatin (CP). The present study investigates the beneficial effects of ebselen-a seleno-organic compound with antioxidant and antiinflammatory properties-vis-à-vis CP-induced ovarian damage. Twenty-eight adult female rats were divided into four study groups. Group 1 received no treatment. The rats in Groups 2, 3, and 4 were intraperitoneally administered CP (2 mg/kg/day) twice per week, for 5 weeks. Those in Group 2 received 0.3 ml saline (0.9% NaCl) intraperitoneally 60 min before each CP treatment, while those in Group 3 received 0.2 ml dimethyl sulfoxide (DMSO) and 0.3 ml saline intraperitoneally 60 min before each CP treatment. The rats in Group 4 were pretreated with an intraperitoneal injection of 15 mg/kg/day ebselen 60 min before each CP treatment. Ovarian tissue malondialdehyde (MDA), total nitric oxide (NOx), glutathione (GSH), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), and catalase levels, as well as histopathological damage scores (HDSs) and serum antimullerian hormone (AMH) levels, were assessed. Cu/Zn-SOD and GSH levels were significantly higher, and MDA and NOx levels significantly lower, in Group 4 than in Groups 2 and 3. Pretreatment with ebselen significantly improved serum AMH levels, relative to Groups 2 and 3. Additionally, HDS values were significantly lower in Group 4 than in Groups 2 and 3. Our results from using an experimental rat model of CP chemotherapy suggest that ebselen use may ameliorate ovarian damage by preventing oxidative injury.

A decrease in cyclin B1 levels leads to polyploidization in DNA damage-induced senescence.

Science.gov (United States)

Kikuchi, Ikue; Nakayama, Yuji; Morinaga, Takao; Fukumoto, Yasunori; Yamaguchi, Naoto

2010-05-04

Adriamycin, an anthracycline antibiotic, has been used for the treatment of various types of tumours. Adriamycin induces at least two distinct types of growth repression, such as senescence and apoptosis, in a concentration-dependent manner. Cellular senescence is a condition in which cells are unable to proliferate further, and senescent cells frequently show polyploidy. Although abrogation of cell division is thought to correlate with polyploidization, the mechanisms underlying induction of polyploidization in senescent cells are largely unclear. We wished, therefore, to explore the role of cyclin B1 level in polyploidization of Adriamycin-induced senescent cells. A subcytotoxic concentration of Adriamycin induced polyploid cells having the features of senescence, such as flattened and enlarged cell shape and activated beta-galactosidase activity. In DNA damage-induced senescent cells, the levels of cyclin B1 were transiently increased and subsequently decreased. The decrease in cyclin B1 levels occurred in G2 cells during polyploidization upon treatment with a subcytotoxic concentration of Adriamycin. In contrast, neither polyploidy nor a decrease in cyclin B1 levels was induced by treatment with a cytotoxic concentration of Adriamycin. These results suggest that a decrease in cyclin B1 levels is induced by DNA damage, resulting in polyploidization in DNA damage-induced senescence.

Spectroscopic study of site selective DNA damage induced by intense soft X-rays

CERN Document Server

Fujii, K

2003-01-01

To investigate the mechanisms of DNA damage induced by direct photon impact, we observed the near edge X-ray absorption fine structures (NEXAFS) of DNA nucleobases using monochromatic synchrotron soft X-rays around nitrogen and oxygen K-shell excitation regions. Each spectrum obtained has unique structure corresponding to pi* excitation of oxygen or nitrogen 1s electron. These aspects open a way of nucleobase-selective photo-excitation in a DNA molecule using high resolution monochromatized soft X-rays. From the analysis of polarization-dependent intensities of the pi* resonance peak, it is clarified that adenine, guanine an uracil form orientated surface structure. Furthermore from the direct measurement of positive ions desorbed from photon irradiated DNA components, it is revealed that the sugar moiety is a fragile site in a DNA molecule. (author)

Analytical studies into radiation-induced starch damage in black and white peppers

International Nuclear Information System (INIS)

Farkas, J.; Sharif, M.M.; Barabassy, S.

1990-01-01

In order to develop detection methods of radiation treatment, ground black pepper samples equilibrated to water activity levels of 0.25, 0.50 and 0.75 a w , respectively, were irradiated with gamma radiation doses of 0, 4, 8, 16 or 32 kGy, and their damaged starch content, reduced sugar content and alcohol induced turbidity of their aqueous extracts were investigated. The colorimetric method and the alcohol-induced turbidity showed statistically significant increase of starch damage at 4 kGy or higher dose levels. However, all investigated analytical indices of starch radio-depolymerization were changed less dramatically by irradiation than the apparent viscosity of the gelatinized suspensions of spices reported previously. (author) 15 refs.; 4 tabs

Cell surface damage and morphological changes in Oenococcus oeni after freeze-drying and incubation in synthetic wine.

Science.gov (United States)

Bravo-Ferrada, Bárbara Mercedes; Gonçalves, Sónia; Semorile, Liliana; Santos, Nuno C; Brizuela, Natalia; Elizabeth Tymczyszyn, E; Hollmann, Axel

2018-04-28

The aim of the present study was to evaluate the effects of freeze-drying in the presence of trehalose as a cryoprotectant, followed by incubation in synthetic wine, on surface damage, viability and l-malic acid consumption of the oenological strain Oenococcus oeni UNQOe 73.2. After freeze-drying, no significant differences were observed in the number of viable cells (for both acclimated and non-acclimated cultures) respect to the fresh culture. In contrast, loss of viability was observed after wine incubation for 24 h, being acclimated freeze-dried cells the best conditions for this. After the preservation process, small changes in cell morphology were observed by Atomic Force Microscopy (AFM). The Zeta potential and AFM showed that 24 h of wine incubation was enough to induce several cell surface modifications. Plate count data allowed us to establish that surface damage is an important factor for loss of viability, regardless of the acclimation treatment. Although the number of surviving O. oeni cells decreased dramatically after incubation in synthetic wine for 15 days, the consumption of l-malic acid was higher than 70%, with freeze-dried cells showing a better performance than fresh cultures. These results demonstrate that O. oeni freeze-dried cultures could be applied to direct wine inoculation, to conduct malolactic fermentation, maintaining its technological properties and reducing the time and costs of the winemaking process. Copyright © 2018. Published by Elsevier Inc.

Gum acacia mitigates genetic damage in adenine-induced chronic renal failure in rats.

Science.gov (United States)

Ali, B H; Al Balushi, K; Al-Husseini, I; Mandel, P; Nemmar, A; Schupp, N; Ribeiro, D A

2015-12-01

Subjects with chronic renal failure (CRF) exhibit oxidative genome damage, which may predispose to carcinogenesis, and Gum acacia (GumA) ameliorates this condition in humans and animals. We evaluated here renal DNA damage and urinary excretion of four nucleic acid oxidation adducts namely 8-oxoguanine (8-oxoGua), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), 8-oxoguanosine (8-oxoGuo) and 8-hydroxy-2-deoxyguanisone (8-OHdg) in rats with adenine (ADE)-induced CRF with and without GumA treatment. Twenty-four rats were divided into four equal groups and treated for 4 weeks. The first group was given normal food and water (control). The second group was given normal food and GumA (15% w/v) in drinking water. The third group was fed powder diet containing adenine (ADE) (0·75% w/w in feed). The fourth group was fed like in the third group, plus GumA in drinking water (15%, w/v). ADE feeding induced CRF (as measured by several physiological, biochemical and histological indices) and also caused a significant genetic damage and significant decreases in urinary 8-oxo Gua and 8-oxoGuo, but not in the other nucleic acids. However, concomitant GumA treatment reduced the level of genetic damage in kidney cells as detected by Comet assay and significantly reversed the effect of adenine on urinary 8-oxoGuo. Treatment with GumA is able to mitigate genetic damage in renal tissues of rats with ADE-induced CRF. © 2015 Stichting European Society for Clinical Investigation Journal Foundation.

Role of marble microstructure in near-infrared laser-induced damage during laser cleaning

International Nuclear Information System (INIS)

Rodriguez-Navarro, Carlos; Rodriguez-Navarro, Alejandro; Elert, Kerstin; Sebastian, Eduardo

2004-01-01

When marble is cleaned by nanosecond neodymium yttrium-aluminum-garnet lasers (1064 nm), strongly absorbing surface contaminants are removed at fluences substantially below the damage threshold for the much less absorptive marble substrate. Recent studies have shown, however, that unacceptable roughening of the marble surface also may occur at low fluences due to removal of individual grains. In order to elucidate this effect, we have compared the low-fluence response of marbles with two different grain sizes and single-crystal calcite, in the fluence range 0.12-1.25 J cm-2. Damage was greater in fine-grained than coarse-grained marble, and did not occur in the single-crystal calcite at these fluences. The temperature rise following defect-mediated absorption triggers thermal plasma emission and generates shock waves; the concomitant surface damage depends on the size and crystallographic orientation of the crystals. Laser irradiation anneals the defects and increases ''crystallite size.'' The implications for the laser-assisted cleaning of marble artworks are outlined

Autophagy and senescence, stress responses induced by the DNA-damaging mycotoxin alternariol

International Nuclear Information System (INIS)

Solhaug, A.; Torgersen, M.L.; Holme, J.A.; Lagadic-Gossmann, D.; Eriksen, G.S.

2014-01-01

Highlights: • AOH induces autophagy, lamellar bodies and senescence in RAW264.7 macrophages. • DNA damage is suggested as a triggering signal. • The Sestrin2-AMPK-mTOR-S6K pathway is proposed to link DNA damage to autophagy. - Abstract: The mycotoxin alternariol (AOH), a frequent contaminant in fruit and grain, is known to induce cellular stress responses such as reactive oxygen production, DNA damage and cell cycle arrest. Cellular stress is often connected to autophagy, and we employed the RAW264.7 macrophage model to test the hypothesis that AOH induces autophagy. Indeed, AOH treatment led to a massive increase in acidic vacuoles often observed upon autophagy induction. Moreover, expression of the autophagy marker LC3 was markedly increased and there was a strong accumulation of LC3-positive puncta. Increased autophagic activity was verified biochemically by measuring the degradation rate of long-lived proteins. Furthermore, AOH induced expression of Sestrin2 and phosphorylation of AMPK as well as reduced phosphorylation of mTOR and S6 kinase, common mediators of signaling pathways involved in autophagy. Transmission electron microscopy analyzes of AOH treated cells not only clearly displayed structures associated with autophagy such as autophagosomes and autolysosomes, but also the appearance of lamellar bodies. Prolonged AOH treatment resulted in changed cell morphology from round into more star-shaped as well as increased β-galactosidase activity. This suggests that the cells eventually entered senescence. In conclusion, our data identify here AOH as an inducer of both autophagy and senescence. These effects are suggested to be to be linked to AOH-induced DSB (via a reported effect on topoisomerase activity), resulting in an activation of p53 and the Sestrin2-AMPK-mTOR-S6K signaling pathway

Caryocar brasiliense camb protects against genomic and oxidative damage in urethane-induced lung carcinogenesis

Directory of Open Access Journals (Sweden)

N.B.R. Colombo

2015-01-01

Full Text Available The antioxidant effects of Caryocar brasiliense Camb, commonly known as the pequi fruit, have not been evaluated to determine their protective effects against oxidative damage in lung carcinogenesis. In the present study, we evaluated the role of pequi fruit against urethane-induced DNA damage and oxidative stress in forty 8-12 week old male BALB/C mice. An in vivo comet assay was performed to assess DNA damage in lung tissues and changes in lipid peroxidation and redox cycle antioxidants were monitored for oxidative stress. Prior supplementation with pequi oil or its extract (15 µL, 60 days significantly reduced urethane-induced oxidative stress. A protective effect against DNA damage was associated with the modulation of lipid peroxidation and low protein and gene expression of nitric oxide synthase. These findings suggest that the intake of pequi fruit might protect against in vivo genotoxicity and oxidative stress.

Cerium oxide nanoparticles, combining antioxidant and UV shielding properties, prevent UV-induced cell damage and mutagenesis

KAUST Repository

Caputo, Fanny

2015-08-20

Efficient inorganic UV shields, mostly based on refracting TiO2 particles, have dramatically changed the sun exposure habits. Unfortunately, health concerns have emerged from the pro-oxidant photocatalytic effect of UV-irradiated TiO2, which mediates toxic effects on cells. Therefore, improvements in cosmetic solar shield technology are a strong priority. CeO2 nanoparticles are not only UV refractors but also potent biological antioxidants due to the surface 3+/4+ valency switch, which confers anti-inflammatory, anti-ageing and therapeutic properties. Herein, UV irradiation protocols were set up, allowing selective study of the extra-shielding effects of CeO2vs. TiO2 nanoparticles on reporter cells. TiO2 irradiated with UV (especially UVA) exerted strong photocatalytic effects, superimposing their pro-oxidant, cell-damaging and mutagenic action when induced by UV, thereby worsening the UV toxicity. On the contrary, irradiated CeO2 nanoparticles, via their Ce3+/Ce4+ redox couple, exerted impressive protection on UV-treated cells, by buffering oxidation, preserving viability and proliferation, reducing DNA damage and accelerating repair; strikingly, they almost eliminated mutagenesis, thus acting as an important tool to prevent skin cancer. Interestingly, CeO2 nanoparticles also protect cells from the damage induced by irradiated TiO2, suggesting that these two particles may also complement their effects in solar lotions. CeO2 nanoparticles, which intrinsically couple UV shielding with biological and genetic protection, appear to be ideal candidates for next-generation sun shields. © The Royal Society of Chemistry 2015.

Tumor induced hepatic myeloid derived suppressor cells can cause moderate liver damage.

Directory of Open Access Journals (Sweden)

Tobias Eggert

Full Text Available Subcutaneous tumors induce the accumulation of myeloid derived suppressor cells (MDSC not only in blood and spleens, but also in livers of these animals. Unexpectedly, we observed a moderate increase in serum transaminases in mice with EL4 subcutaneous tumors, which prompted us to study the relationship of hepatic MDSC accumulation and liver injury. MDSC were the predominant immune cell population expanding in livers of all subcutaneous tumor models investigated (RIL175, B16, EL4, CT26 and BNL, while liver injury was only observed in EL4 and B16 tumor-bearing mice. Elimination of hepatic MDSC in EL4 tumor-bearing mice using low dose 5-fluorouracil (5-FU treatment reversed transaminase elevation and adoptive transfer of hepatic MDSC from B16 tumor-bearing mice caused transaminase elevation indicating a direct MDSC mediated effect. Surprisingly, hepatic MDSC from B16 tumor-bearing mice partially lost their damage-inducing potency when transferred into mice bearing non damage-inducing RIL175 tumors. Furthermore, MDSC expansion and MDSC-mediated liver injury further increased with growing tumor burden and was associated with different cytokines including GM-CSF, VEGF, interleukin-6, CCL2 and KC, depending on the tumor model used. In contrast to previous findings, which have implicated MDSC only in protection from T cell-mediated hepatitis, we show that tumor-induced hepatic MDSC themselves can cause moderate liver damage.

Edaravone protects human peripheral blood lymphocytes from γ-irradiation-induced apoptosis and DNA damage.

Science.gov (United States)

Chen, Liming; Liu, Yinghui; Dong, Liangliang; Chu, Xiaoxia

2015-03-01

Radiation-induced cellular injury is attributed primarily to the harmful effects of free radicals, which play a key role in irradiation-induced apoptosis. In this study, we investigated the radioprotective efficacy of edaravone, a licensed clinical drug and a powerful free radical scavenger that has been tested against γ-irradiation-induced cellular damage in cultured human peripheral blood lymphocytes in studies of various diseases. Edaravone was pre-incubated with lymphocytes for 2 h prior to γ-irradiation. It was found that pretreatment with edaravone increased cell viability and inhibited generation of γ-radiation-induced reactive oxygen species (ROS) in lymphocytes exposed to 3 Gy γ-radiation. In addition, γ-radiation decreased antioxidant enzymatic activity, such as superoxide dismutase and glutathione peroxidase, as well as the level of reduced glutathione. Conversely, treatment with 100 μM edaravone prior to irradiation improved antioxidant enzyme activity and increased reduced glutathione levels in irradiated lymphocytes. Importantly, we also report that edaravone reduced γ-irradiation-induced apoptosis through downregulation of Bax, upregulation of Bcl-2, and consequent reduction of the Bax:Bcl-2 ratio. The current study shows edaravone to be an effective radioprotector against γ-irradiation-induced cellular damage in lymphocytes in vitro. Finally, edaravone pretreatment significantly reduced DNA damage in γ-irradiated lymphocytes, as measured by comet assay (% tail DNA, tail length, tail moment, and olive tail moment) (p edaravone offers protection from radiation-induced cytogenetic alterations.

Summary of the mechanism of U-induced renal damage and its biochemical studies

International Nuclear Information System (INIS)

Chen Rusong

1994-05-01

In China studies on the toxicology of uranium were systematically conducted from the 1960's. Among them the studies of the change of biochemical indicators of U-induced renal damage were involved. On the basis of summarizing the relevant information of our country and the study progress of biochemical methods in recent years, the mechanism of U-induced renal damage and its biochemical basis, the behavior of uranium in kidney and the recent progress to detect renal damage with several biochemical indexes (such as α 1 -or β 2 -microglobulin, N-acetyl-β-D-glucosaminidase and alanine aminopeptidase etc.) are introduced respectively. Finally, the evaluation on the biochemical basis for acquired tolerance to U in kidney is performed. It should be noted that from the clinical viewpoint the tolerance cannot be considered as a practical measure of protection

Stem Cell Therapy to Reduce Radiation-Induced Normal Tissue Damage

NARCIS (Netherlands)

Coppes, Rob P.; van der Goot, Annemieke; Lombaert, Isabelle M. A.

Normal tissue damage after radiotherapy is still a major problem in cancer treatment. Stem cell therapy may provide a means to reduce radiation-induced side effects and improve the quality of life of patients. This review discusses the current status in stem cell research with respect to their

Ellipticine induces apoptosis in T-cell lymphoma via oxidative DNA damage

DEFF Research Database (Denmark)

Savorani, Cecilia; Manfé, Valentina; Biskup, Edyta

2015-01-01

(CTCL), a disease that is progressive, chemoresistant and refractory to treatment. We tested the effect of ellipticine in three cell lines with different p53 status: MyLa2000 (p53(wt/wt)), SeAx ((G245S)p53) and Hut-78 ((R196Stop)p53). Ellipticine caused apoptosis in MyLa2000 and SeAx and restored...... the transcriptional activity of (G245S)p53 in SeAx. However, p53 siRNA knockdown experiments revealed that p53 was not required for ellipticine-induced apoptosis in CTCL. The lipophilic antioxidant α-tocopherol inhibited ellipticine-dependent apoptosis and we linked the apoptotic response to the oxidative DNA damage....... Our results provide evidence that ellipticine-induced apoptosis is exerted through DNA damage and does not require p53 activation in T-cell lymphoma....

The apparent effect of sample surface damage on the dielectric parameters of GaAs

Energy Technology Data Exchange (ETDEWEB)

Engelbrecht, J.A.A. [Physics Department, Nelson Mandela Metropolitan University, P.O. Box 77000, Port Elizabeth 6031 (South Africa)], E-mail: Japie.Engelbrecht@nmmu.ac.za; Hashe, N.G. [Physics Department, Nelson Mandela Metropolitan University, P.O. Box 77000, Port Elizabeth 6031 (South Africa); Hillie, K.T. [CSIR-NML Laboratory, P.O. Box 395, Pretoria 0001 (South Africa); Claassens, C.H. [Physics Department, University of the Free State, Bloemfontein 9300 (South Africa)

2007-12-15

The dielectric and optical parameters determined by infrared reflectance spectroscopy and computer simulation of a set of GaAs substrates of various surface topologies are reported. The influence of surface damage on the parameters is noted.

The apparent effect of sample surface damage on the dielectric parameters of GaAs

International Nuclear Information System (INIS)

Engelbrecht, J.A.A.; Hashe, N.G.; Hillie, K.T.; Claassens, C.H.

2007-01-01

The dielectric and optical parameters determined by infrared reflectance spectroscopy and computer simulation of a set of GaAs substrates of various surface topologies are reported. The influence of surface damage on the parameters is noted

Correlation of simulated TEM images with irradiation induced damage

International Nuclear Information System (INIS)

Schaeublin, R.; Almeida, P. de; Almazouzi, A.; Victoria, M.

2000-01-01

Crystal damage induced by irradiation is investigated using transmission electron microscopy (TEM) coupled to molecular dynamics (MD) calculations. The displacement cascades are simulated for energies ranging from 10 to 50 keV in Al, Ni and Cu and for times of up to a few tens of picoseconds. Samples are then used to perform simulations of the TEM images that one could observe experimentally. Diffraction contrast is simulated using a method based on the multislice technique. It appears that the cascade induced damage in Al imaged in weak beam exhibits little contrast, which is too low to be experimentally visible, while in Ni and Cu a good contrast is observed. The number of visible clusters is always lower than the actual one. Conversely, high resolution TEM (HRTEM) imaging allows most of the defects contained in the sample to be observed, although experimental difficulties arise due to the low contrast intensity of the smallest defects. Single point defects give rise in HTREM to a contrast that is similar to that of cavities. TEM imaging of the defects is discussed in relation to the actual size of the defects and to the number of clusters deduced from MD simulations

Longitudinal diffusion tensor magnetic resonance imaging study of radiation-induced white matter damage in a rat model.

Science.gov (United States)

Wang, Silun; Wu, Ed X; Qiu, Deqiang; Leung, Lucullus H T; Lau, Ho-Fai; Khong, Pek-Lan

2009-02-01

Radiation-induced white matter (WM) damage is a major side effect of whole brain irradiation among childhood cancer survivors. We evaluate longitudinally the diffusion characteristics of the late radiation-induced WM damage in a rat model after 25 and 30 Gy irradiation to the hemibrain at 8 time points from 2 to 48 weeks postradiation. We hypothesize that diffusion tensor magnetic resonance imaging (DTI) indices including fractional anisotropy (FA), trace, axial diffusivity (lambda(//)), and radial diffusivity (lambda( perpendicular)) can accurately detect and monitor the histopathologic changes of radiation-induced WM damage, measured at the EC, and that these changes are dose and time dependent. Results showed a progressive reduction of FA, which was driven by reduction in lambda(//) from 4 to 40 weeks postradiation, and an increase in lambda( perpendicular) with return to baseline in lambda(//) at 48 weeks postradiation. Histologic evaluation of irradiated WM showed reactive astrogliosis from 4 weeks postradiation with reversal at 36 weeks, and demyelination, axonal degeneration, and necrosis at 48 weeks postradiation. Moreover, changes in lambda(//) correlated with reactive astrogliosis (P histopathologic changes of WM damage and our results support the use of DTI as a biomarker to noninvasively monitor radiation-induced WM damage.

Reduction of DNA damage induced by titanium dioxide nanoparticles through Nrf2 in vitro and in vivo

Energy Technology Data Exchange (ETDEWEB)

Shi, Zhiqin [Department of Toxicology, Hebei Medical University, Shijiazhuang (China); Department of Laboratory Diagnosis, Hebei Medical University, Shijiazhuang (China); Niu, Yujie [Department of Occupational Health and Environmental Health, Hebei Medical University, Shijiazhuang (China); Wang, Qian [Department of Toxicology, Hebei Medical University, Shijiazhuang (China); Shi, Lei [Department of Occupational Health and Environmental Health, Hebei Medical University, Shijiazhuang (China); Guo, Huicai; Liu, Yi; Zhu, Yue [Department of Toxicology, Hebei Medical University, Shijiazhuang (China); Liu, Shufeng; Liu, Chao [Hebei Keylab of Laboratory Animal Science, Shijiazhuang (China); Chen, Xin [Xiumen Community Health Service Centre, Shijiazhuang (China); Zhang, Rong, E-mail: rongzhang@hebmu.edu.cn [Department of Toxicology, Hebei Medical University, Shijiazhuang (China); Hebei Keylab of Laboratory Animal Science, Shijiazhuang (China)

2015-11-15

Highlights: • Nrf2 signals were partly responsible for the DNA damage induced by Nano-TiO{sub 2}. • Nrf2 loss could aggravate the DNA damage induced by Nano-TiO{sub 2}. • Acquired Nrf2 decreased the susceptibility to DNA damage induced by Nano-TiO{sub 2}. - Abstract: Titanium dioxide nanoparticles (Nano-TiO{sub 2}) are widely used to additives in cosmetics, pharmaceutical, paints and foods. Recent studies have demonstrated that Nano-TiO{sub 2} induces DNA damage and increased the risk of cancer and the mechanism might relate with oxidative stress. The aim of this study was to evaluate the effects of Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), an anti-oxidative mediator, on DNA damage induced by Nano-TiO{sub 2}. Wildtype, Nrf2 knockout (Nrf2(-/-)) and tert-butylhydroquinone (tBHQ) pre-treated HepG2 cells and mice were treated with Nano-TiO{sub 2}. And then the oxidative stress and DNA damage were evaluated. Our data showed that DNA damage, reactive oxygen species (ROS) generation and MDA content in Nano-TiO{sub 2} exposed cells were significantly increased than those of control in dose dependent manners. Nrf2/ARE droved the downstream genes including NAD(P)H dehydrogenase [quinine] 1(NQO1), heme oxygenase 1 (HO-1) and glutamate-cysteine ligase catalytic subunit (GCLC) expression were significantly higher in wildtype HepG2 cells after Nano-TiO{sub 2} treatment. After treatment with Nano-TiO{sub 2}, the DNA damages were significantly increased in Nrf(-/-) cells and mice whereas significantly decreased in tBHQ pre-treatment cells and mice, compared with the wildtype HepG2 cells and mice, respectively. Our results indicated that the acquired of Nrf2 leads to a decreased susceptibility to DNA damages induction by Nano-TiO{sub 2} and decreasing of risk of cancer which would provide a strategy for a more efficacious sensitization of against of Nano-TiO{sub 2} toxication.

Plastic Strain Induced Damage Evolution and Martensitic Transformation in Ductile Materials at Cryogenic Temperatures

CERN Document Server

Garion, C

2002-01-01

The Fe-Cr-Ni stainless steels are well known for their ductile behaviour at cryogenic temperatures. This implies development and evolution of plastic strain fields in the stainless steel components subjected to thermo-mechanical loads at low temperatures. The evolution of plastic strain fields is usually associated with two phenomena: ductile damage and strain induced martensitic transformation. Ductile damage is described by the kinetic law of damage evolution. Here, the assumption of isotropic distribution of damage (microcracks and microvoids) in the Representative Volume Element (RVE) is made. Formation of the plastic strain induced martensite (irreversible process) leads to the presence of quasi-rigid inclusions of martensite in the austenitic matrix. The amount of martensite platelets in the RVE depends on the intensity of the plastic strain fields and on the temperature. The evolution of the volume fraction of martensite is governed by a kinetic law based on the accumulated plastic strain. Both of thes...

DNA damages induced by Ar F laser

Energy Technology Data Exchange (ETDEWEB)

Chapel, C.; Rose, S.; Chevrier, L.; Cordier, E.; Courant, D. [CEA Fontenay-aux-Roses, 92 (France). Dept. de Radiobiologie et de Radiopathologie

2006-07-01

The photo ablation process used in corneal refractive surgery by the Argon Fluoride (Ar F) laser emitting in ultraviolet C at 193 nm, exposes viable cells round the irradiated zone to sub ablative doses (< 400 joules.m -2). Despite that DNA absorption is higher at 193 nm than 254 nm, cytotoxicity of 193 nm laser radiation is lower than radiation emitted by 254 nm UV-C lamps. In situ, DNA could be protected of laser radiation by cellular components. Consequently, some authors consider that this radiation does not induce genotoxic effect whereas others suspect it to be mutagenic. These lasers are used for fifteen years but many questions remain concerning the long term effects on adjacent cells to irradiated area. The purpose of this study is to describe the effect of 193 nm laser radiation on DNA of stromal keratocytes which are responsible of the corneal structure. The 193 nm laser irradiation induces directly DNA breakage in keratocytes as it has been shown by the comet assay under alkaline conditions. Two hours post irradiation, damages caused by the highest exposure (150 J.m-2) are not repaired as it has been measured with the Olive Tail Moment (product of tail length and tail DNA content). They give partly evidence of induction of an apoptotic process in cells where DNA could be too damaged. In order to characterize specifically double strand breaks, a comparative analysis by immunofluorescence of the H2 Ax histone phosphorylation (H2 Ax) has been performed on irradiated keratocytes and unirradiated keratocytes. Results show a dose dependent increase of the number of H2 Ax positive cells. Consequences of unrepaired DNA lesions could be observed by the generation of micronuclei in cells. Results show again an increase of micronuclei in laser irradiated cells. Chromosomal aberrations have been pointed out by cytogenetic methods 30 mn after irradiation. These aberrations are dose dependent (from 10 to 150 J.m-2). The number of breakage decreases in the long run

Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo

International Nuclear Information System (INIS)

Ostrau, Christian; Huelsenbeck, Johannes; Herzog, Melanie; Schad, Arno; Torzewski, Michael; Lackner, Karl J.; Fritz, Gerhard

2009-01-01

Background and purpose: HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro. Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo. Materials and methods: Four hours to 24 h after total body irradiation (6 Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5 Gy and analyses were performed 3 weeks after the first radiation treatment. Molecular markers of inflammation and fibrosis as well as organ toxicities were measured. Results: Lovastatin attenuated IR-induced activation of NF-κB, mRNA expression of cell adhesion molecules and mRNA expression of pro-inflammatory and pro-fibrotic marker genes (i.e. TNFα, IL-6, TGFβ, CTGF, and type I and type III collagen) in a tissue- and time-dependent manner. γH2AX phosphorylation stimulated by IR was not affected by lovastatin, indicating that the statin has no major impact on the induction of DNA damage in vivo. Radiation-induced thrombopenia was significantly alleviated by lovastatin. Conclusions: Lovastatin inhibits both acute and subchronic IR-induced pro-inflammatory and pro-fibrotic responses and cell death in normal tissue in vivo. Therefore, lovastatin might be useful for selectively attenuating acute and subchronic normal tissue damage caused by radiotherapy.

A comparison of atom and ion induced SSIMS - evidence for a charge induced damage effect in insulator materials

International Nuclear Information System (INIS)

Brown, A.; Berg, J.A. van den; Vickerman, J.C.

1985-01-01

A static secondary ion mass spectrometry (SSIMS) study of two very low conductivity materials, polystyrene and niobium pentoxide, using on the one hand a primary ion beam with electron neutralisation, and on the other, atom bombardment, shows that whilst the initial spectra obtained were quite similar, subsequent damage effects were much greater under ion impact conditions. For an equivalent flux density the half-life of the polystyrene surface structure was four times longer under atom bombardment. Significant reduction of the niobium surface was observed under ion bombardment whereas an equivalent atom flux had little apparent effect on the surface oxidation state. These data suggest that the requirement to dissipate the charge delivered to the sample by the primary ion beam contributes significantly to the damage mechanisms in electrically insulating materials. (author)

Oral Polypodium leucotomos extract decreases ultraviolet-induced damage of human skin

NARCIS (Netherlands)

Middelkamp-Hup, Maritza A.; Pathak, Madhu A.; Parrado, Concepcion; Goukassian, David; Rius-Díaz, Francisca; Mihm, Martín C.; Fitzpatrick, Thomas B.; González, Salvador

2004-01-01

BACKGROUND: UV radiation induces damage to human skin. Protection of skin by an oral photoprotective agent would have substantial benefits. Objective We investigated the photoprotective effect of oral administration of an extract of the natural antioxidant Polypodium leucotomos (PL). METHODS: A

Condition Assessment for Wastewater Pipes: Method for Assessing Cracking and Surface Damage of Concrete Pipes

OpenAIRE

Hauge, Petter

2013-01-01

The objective of the Master Thesis has been to provide an improved method for condition assessment, which will give a better correlation between Condition class and actual Condition of concrete pipes with cracking and/or surface damages. Additionally improvement of the characterization of cracking (SR) and surface (KO) damages was a sub goal.Based on the findings described in my Thesis and my Specialization Project (Hauge 2012), I recommend that the Norwegian condition assessment method based...

Trophic complexity and the adaptive value of damage-induced plant volatiles.

Directory of Open Access Journals (Sweden)

Ian Kaplan

Full Text Available Indirect plant defenses are those facilitating the action of carnivores in ridding plants of their herbivorous consumers, as opposed to directly poisoning or repelling them. Of the numerous and diverse indirect defensive strategies employed by plants, inducible volatile production has garnered the most fascination among plant-insect ecologists. These volatile chemicals are emitted in response to feeding by herbivorous arthropods and serve to guide predators and parasitic wasps to their prey. Implicit in virtually all discussions of plant volatile-carnivore interactions is the premise that plants "call for help" to bodyguards that serve to boost plant fitness by limiting herbivore damage. This, by necessity, assumes a three-trophic level food chain where carnivores benefit plants, a theoretical framework that is conceptually tractable and convenient, but poorly depicts the complexity of food-web dynamics occurring in real communities. Recent work suggests that hyperparasitoids, top consumers acting from the fourth trophic level, exploit the same plant volatile cues used by third trophic level carnivores. Further, hyperparasitoids shift their foraging preferences, specifically cueing in to the odor profile of a plant being damaged by a parasitized herbivore that contains their host compared with damage from an unparasitized herbivore. If this outcome is broadly representative of plant-insect food webs at large, it suggests that damage-induced volatiles may not always be beneficial to plants with major implications for the evolution of anti-herbivore defense and manipulating plant traits to improve biological control in agricultural crops.

Genetic Damage Induced by Accidental Environmental Pollutants

Directory of Open Access Journals (Sweden)

Beatriz Pérez-Cadahía

2006-01-01

Full Text Available Petroleum is one of the main energy sources worldwide. Its transport is performed by big tankers following some established marine routes. In the last 50 years a total amount of 37 oil tankers have given rise to great spills in different parts of the world, Prestige being the last one. After the accident, a big human mobilisation took place in order to clean beaches, rocks and fauna, trying to reduce the environmental consequences of this serious catastrophe. These people were exposed to the complex mixture of compounds contained in the oil. This study aimed at determine the level of environmental exposure to volatile organic compounds (VOC, and the possible damage induced on the population involved in the different cleaning tasks by applying the genotoxicity tests sister chromatid exchanges (SCE, micronucleus (MN test, and comet assay. Four groups of individuals were included: volunteers (V, hired manual workers (MW, hired high-pressure cleaner workers (HPW and controls. The higher VOC levels were associated with V environment, followed by MW and lastly by HPW, probably due to the use of high-pressure cleaners. Oil exposure during the cleaning tasks has caused an increase in the genotoxic damage in individuals, the comet assay being the most sensitive biomarker to detect it. Sex, age and tobacco consumption have shown to influence the level of genetic damage, while the effect of using protective devices was less noticeable than expected, perhaps because the kind used was not the most adequate.

Surface damage of TFTR protective plate candidate materials by energetic D+ irradiation

International Nuclear Information System (INIS)

Kaminsky, M.; Das, S.K.

1979-01-01

Experiments were conducted to determine the surface damage of ATJ graphite, V, Cu, and Type 316 stainless steel under 60-keV D + irradiation. The irradiations were conducted in the pulsed mode. For a total accumulated dose of 8.1 x 10 18 ions/cm 2 , blisters were readily seen for Cu surfaces, but no blisters were observed on Type 316 stainless steel and vanadium surfaces. For the case of ATJ graphite, the surface damage was observed in the form of ridges and grooves. In the case of copper, many large blisters with diameters ranging from 3.5 μm to 46 μm are observed in addition to some small ones (average diameter approx. 2 μm. The blister density of the large blisters is the highest in the case of copper (1.1 x 10 5 blisters/cm 2 ). These observations of blister formation are related to the differences in the premeability of deuterium in these materials. An examination of the cross section of the ridges in fractured samples of graphite indicates that they are not hollow. The mechanisms of formation of these ridges is not clear at present. 1 figure

Oxidative stress and DNA damage induced by imidacloprid in zebrafish (Danio rerio).

Science.gov (United States)

Ge, Weili; Yan, Saihong; Wang, Jinhua; Zhu, Lusheng; Chen, Aimei; Wang, Jun

2015-02-18

Imidacloprid is a neonicotinoid insecticide that can have negative effects on nontarget animals. The present study was conducted to assess the toxicity of various imidacloprid doses (0.3, 1.25, and 5 mg/mL) on zebrafish sampled after 7, 14, 21, and 28 days of exposure. The levels of catalase (CAT), superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione-S-transferase (GST), and malondialdehyde (MDA) and the extent of DNA damage were measured to evaluate the toxicity of imidacloprid on zebrafish. SOD and GST activities were noticeably increased during early exposure but were inhibited toward the end of the exposure period. In addition, the CAT levels decreased to the control level following their elevation during early exposure. High concentrations of imidacloprid (1.25 and 5 mg/L) induced excessive ROS production and markedly increased MDA content on the 21st day of exposure. DNA damage was dose- and time-dependent. In conclusion, the present study showed that imidacloprid can induce oxidative stress and DNA damage in zebrafish.

Numerical Analyses of the Influence of Blast-Induced Damaged Rock Around Shallow Tunnels in Brittle Rock

Science.gov (United States)

Saiang, David; Nordlund, Erling

2009-06-01

Most of the railway tunnels in Sweden are shallow-seated (rock cover) and are located in hard brittle rock masses. The majority of these tunnels are excavated by drilling and blasting, which, consequently, result in the development of a blast-induced damaged zone around the tunnel boundary. Theoretically, the presence of this zone, with its reduced strength and stiffness, will affect the overall performance of the tunnel, as well as its construction and maintenance. The Swedish Railroad Administration, therefore, uses a set of guidelines based on peak particle velocity models and perimeter blasting to regulate the extent of damage due to blasting. However, the real effects of the damage caused by blasting around a shallow tunnel and their criticality to the overall performance of the tunnel are yet to be quantified and, therefore, remain the subject of research and investigation. This paper presents a numerical parametric study of blast-induced damage in rock. By varying the strength and stiffness of the blast-induced damaged zone and other relevant parameters, the near-field rock mass response was evaluated in terms of the effects on induced boundary stresses and ground deformation. The continuum method of numerical analysis was used. The input parameters, particularly those relating to strength and stiffness, were estimated using a systematic approach related to the fact that, at shallow depths, the stress and geologic conditions may be highly anisotropic. Due to the lack of data on the post-failure characteristics of the rock mass, the traditional Mohr-Coulomb yield criterion was assumed and used. The results clearly indicate that, as expected, the presence of the blast-induced damage zone does affect the behaviour of the boundary stresses and ground deformation. Potential failure types occurring around the tunnel boundary and their mechanisms have also been identified.

Effects of laser radiation on surfaces and coatings

International Nuclear Information System (INIS)

Lowdermilk, W.H.

1985-01-01

A summary is given of the principal aspects of laser-induced damage to polished optical surfaces and dielectric, thin-film, high-reflectivity and antireflective coatings. Methods for producing porous antireflective surfaces and coatings and their damage properties are also reviewed. Finally, new areas of basic research to solve current and future problems are addressed

Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats

International Nuclear Information System (INIS)

Gultekin, Fatma Ayca; Bakkal, Bekir Hakan; Guven, Berrak; Tasdoven, Ilhan; Bektas, Sibel; Can, Murat; Comert, Mustafa

2013-01-01

Because radiation-induced cellular damage is attributed primarily to harmful effects of free radicals, molecules with direct free radical scavenging properties are particularly promising as radioprotectors. It has been demonstrated that controlled ozone administration may promote an adaptation to oxidative stress, preventing the damage induced by reactive oxygen species. Thus, we hypothesized that ozone would ameliorate oxidative damage caused by total body irradiation (TBI) with a single dose of 6 Gy in rat liver and ileum tissues. Rats were randomly divided into groups as follows: control group; saline-treated and irradiated (IR) groups; and ozone oxidative preconditioning (OOP) and IR groups. Animals were exposed to TBI after a 5-day intraperitoneal pretreatment with either saline or ozone (1 mg/kg/day). They were decapitated at either 6 h or 72 h after TBI. Plasma, liver and ileum samples were obtained. Serum AST, ALT and TNF-α levels were elevated in the IR groups compared with the control group and were decreased after treatment with OOP. TBI resulted in a significant increase in the levels of MDA in the liver and ileal tissues and a decrease of SOD activities. The results demonstrated that the levels of MDA liver and ileal tissues in irradiated rats that were pretreated with ozone were significantly decreased, while SOD activities were significantly increased. OOP reversed all histopathological alterations induced by irradiation. In conclusion, data obtained from this study indicated that ozone could increase the endogenous antioxidant defense mechanism in rats and there by protect the animals from radiation-induced organ toxicity. (author)

The AID-induced DNA damage response in chromatin

DEFF Research Database (Denmark)

Daniel, Jeremy A; Nussenzweig, André

2013-01-01

Chemical modifications to the DNA and histone protein components of chromatin can modulate gene expression and genome stability. Understanding the physiological impact of changes in chromatin structure remains an important question in biology. As one example, in order to generate antibody diversity...... with somatic hypermutation and class switch recombination, chromatin must be made accessible for activation-induced cytidine deaminase (AID)-mediated deamination of cytosines in DNA. These lesions are recognized and removed by various DNA repair pathways but, if not handled properly, can lead to formation...... of oncogenic chromosomal translocations. In this review, we focus the discussion on how chromatin-modifying activities and -binding proteins contribute to the native chromatin environment in which AID-induced DNA damage is targeted and repaired. Outstanding questions remain regarding the direct roles...

Surface damage characterization of FBK devices for High Luminosity LHC (HL-LHC) operations

Science.gov (United States)

Moscatelli, F.; Passeri, D.; Morozzi, A.; Dalla Betta, G.-F.; Mattiazzo, S.; Bomben, M.; Bilei, G. M.

2017-12-01

The very high fluences (e.g. up to 2×1016 1 MeV neq/cm2) and total ionising doses (TID) of the order of 1 Grad, expected at the High Luminosity LHC (HL-LHC), impose new challenges for the design of effective, radiation resistant detectors. Ionising energy loss is the dominant effect for what concerns SiO2 and SiO2/Si interface radiation damage. In particular, surface damage can create a positive charge layer near the SiO2/Si interface and interface traps along the SiO2/Si interface, which strongly influence the breakdown voltage, the inter-electrode isolation and capacitance, and might also impact the charge collection properties of silicon sensors. To better understand in a comprehensive framework the complex and articulated phenomena related to surface damage at these very high doses, measurements on test structures have been carried out in this work (e.g. C-V and I-V). In particular, we have studied the properties of the SiO2 layer and of the SiO2/Si interface, using MOS capacitors, gated diodes (GD) and MOSFETs manufactured by FBK on high-resistivity n-type and p-type silicon, before and after irradiation with X-rays in the range from 50 krad(SiO2) to 20 Mrad(SiO2). Relevant parameters have been determined for all the tested devices, converging in the oxide charge density NOX, the surface generation velocity s0 and the integrated interface-trap density NIT dose-dependent values. These parameters have been extracted to both characterize the technology as a function of the dose and to be used in TCAD simulations for the surface damage effect modeling and the analysis and optimization of different classes of detectors for the next HEP experiments.

Terbium fluorescence as a sensitive, inexpensive probe for UV-induced damage in nucleic acids

International Nuclear Information System (INIS)

El-Yazbi, Amira F.; Loppnow, Glen R.

2013-01-01

Graphical abstract: -- Highlights: •Simple, inexpensive, mix-and-read assay for positive detection of DNA damage. •Recognition of undamaged DNA via hybridization to a hairpin probe. •Terbium(III) fluorescence reports the amount of damage by binding to ssDNA. •Tb/hairpin is a highly selective and sensitive fluorescent probe for DNA damage. -- Abstract: Much effort has been focused on developing methods for detecting damaged nucleic acids. However, almost all of the proposed methods consist of multi-step procedures, are limited, require expensive instruments, or suffer from a high level of interferences. In this paper, we present a novel simple, inexpensive, mix-and-read assay that is generally applicable to nucleic acid damage and uses the enhanced luminescence due to energy transfer from nucleic acids to terbium(III) (Tb 3+ ). Single-stranded oligonucleotides greatly enhance the Tb 3+ emission, but duplex DNA does not. With the use of a DNA hairpin probe complementary to the oligonucleotide of interest, the Tb 3+ /hairpin probe is applied to detect ultraviolet (UV)-induced DNA damage. The hairpin probe hybridizes only with the undamaged DNA. However, the damaged DNA remains single-stranded and enhances the intrinsic fluorescence of Tb 3+ , producing a detectable signal directly proportional to the amount of DNA damage. This allows the Tb 3+ /hairpin probe to be used for sensitive quantification of UV-induced DNA damage. The Tb 3+ /hairpin probe showed superior selectivity to DNA damage compared to conventional molecular beacons probes (MBs) and its sensitivity is more than 2.5 times higher than MBs with a limit of detection of 4.36 ± 1.2 nM. In addition, this probe is easier to synthesize and more than eight times cheaper than MBs, which makes its use recommended for high-throughput, quantitative analysis of DNA damage

Flow cytometric determination of radiation-induced chromosome damage and its correlation with cell survival

International Nuclear Information System (INIS)

Welleweerd, J.; Wilder, M.E.; Carpenter, S.G.; Raju, M.R.

1984-01-01

Chinese hamster M3-1 cells were irradiated with several doses of x rays or α particles from 238 Pu. Propidium iodide-stained chromosome suspensions were prepared at different times after irradiation; cells were also assayed for survival. The DNA histograms of these chromosomes showed increased background counts with increased doses of radiation. This increase in background was cell-cycle dependent and was correlated with cell survival. The correlation between radiation-induced chromosome damage and cell survival was the same for X rays and α particles. Data are presented which indicate that flow cytometric analysis of chromosomes of irradiated cell populations can be a useful adjunct to classical cytogenic analysis of irradiation-induced chromosomal damage by virtue of its ability to express and measure chromosomal damage not seen by classical cytogenic methods

Renal tissue damage induced by focused shock waves

Science.gov (United States)

Ioritani, N.; Kuwahara, M.; Kambe, K.; Taguchi, K.; Saitoh, T.; Shirai, S.; Orikasa, S.; Takayama, K.; Lush, P. A.

1990-07-01

Biological evidence of renal arterial wall damage induced by the microjet due to shock wave-cavitation bubble interaction was demonstrated in living dog kidneys. We also intended to clarify the mechanism of renal tissue damage and the effects of different conditions of shock wave exposure (peak pressure of focused area, number of shots, exposure rate) on the renal tissue damage in comparison to stone disintegration. Disruption of arterial wall was the most remarkable histological change in the focused area of the kidneys. This lesion appeared as if the wall had been punctured by a needle. Large hematoma formation in the renal parenchym, and interstitial hemorrhage seemed to be the results of the arterial lesion. This arterial disorder also led to ischemic necrosis of the tubules surrounding the hematoma. Micro-angiographic examination of extracted kidneys also proved such arterial puncture lesions and ischemic lesions. The number of shots required for model stone disintegration was not inversely proportional to peak pressure. It decreased markedly when peak pressure was above 700 bar. Similarly thenumber of shots for hematoma formation was not inversely proportional to peak pressure, however, this decreased markedly above 500 bar. These results suggested that a hematoma could be formed under a lower peak pressure than that required for stone disintegration.

Effects of carotenoids on damage of biological lipids induced by gamma irradiation

International Nuclear Information System (INIS)

Saito, Takeshi; Fujii, Noriko

2014-01-01

Carotenoids are considered to be involved in the radioresistant mechanisms of radioresistant bacteria. In these bacterial cells, carotenoids are present in biological lipids, and therefore may be related to the radiation-induced damage of lipids. However, only limited data are available for the role of carotenoids in such damage. In this study, we irradiated an α-linolenic acid–benzene solution with gamma rays and analyzed the resulting oxidative degradation and peroxidation damage in the presence or absence of two typical carotenoids: β-carotene and astaxanthin. The analyses revealed that oxidative degradation and peroxidation of α-linolenic acid, as evaluated by the amount of malondialdehyde and conjugated diene formed, respectively, increased in a dose-dependent manner. Moreover, 8.5×10 −3 M β-carotene inhibited gamma radiation-induced oxidative degradation of α-linolenic acid, whereas 5.0×10 −5 and 5.0×10 −6 M β-carotene, and 5.0×10 −7 and 5.0×10 −8 M astaxanthin promoted degradation. In contrast, neither β-carotene nor astaxanthin affected peroxidation of α-linolenic acid. These results suggest that an optimum concentration of carotenoids in radioresistant bacteria protects biological lipid structures from radiation-induced damage. - Highlights: • Gamma radiation dose-dependently increases degradation levels of α-linolenic acid. • Gamma radiation dose-dependently increases peroxidation levels of α-linolenic acid. • An optimum concentration of carotenoids inhibits degradation of α-linolenic acid. • Relatively low concentrations of carotenoids promote degradation of α-linolenic acid. • Carotenoids do not affect the peroxidation level of α-linolenic acid

Functional analysis of molecular mechanisms of radiation induced apoptosis, that are not mediated by DNA damages

International Nuclear Information System (INIS)

Angermeier, Marita; Moertl, Simone

2012-01-01

The effects of low-dose irradiation pose new challenges on the radiation protection efforts. Enhanced cellular radiation sensitivity is displayed by disturbed cellular reactions and resulting damage like cell cycle arrest, DNA repair and apoptosis. Apoptosis serves as genetically determinate parameter for the individual radiation sensitivity. In the frame of the project the radiation-induced apoptosis was mechanistically investigated. Since ionizing radiation induced direct DNA damage and generates a reactive oxygen species, the main focus of the research was the differentiation and weighting of DNA damage mediated apoptosis and apoptosis caused by the reactive oxygen species (ROS).

Purine receptor P2Y_6 mediates cellular response to γ-ray-induced DNA damage

International Nuclear Information System (INIS)

Ide, Shunta; Nishimaki, Naoko; Tsukimoto, Mitsutoshi; Kojima, Shuji

2014-01-01

We previously showed that nucleotide P2 receptor agonists such as ATP and UTP amplify γ-ray-induced focus formation of phosphorylated histone H2A variant H2AX (γH2AX), which is considered to be an indicator of DNA damage so far, by activating purine P2Y_6 and P2Y_1_2 receptors. Therefore, we hypothesized that these P2 receptors play a role in inducing the repair response to γ-ray-induced DNA damage. In the present study, we tested this idea by using human lung cancer A549 cells. First, reverse-transcription polymerase chain reaction (RT-PCR) showed that P2Y_6 receptor is highly expressed in A549 cells, but P2Y_1_2 receptor is only weakly expressed. Next, colony formation assay revealed that P2Y_6 receptor antagonist MRS2578 markedly reduced the survival rate of γ-ray-exposed A549 cells. The survival rate was also significantly reduced in P2Y_6-knock-down cells, compared with scramble siRNA-transfected cells. Since it has reported that phosphorylation of ERK1/2 after activation of EGFR via P2Y_6 and P2Y_1_2 receptors is involved in the repair response to γ-ray-induced DNA damage, we next examined whether γ-ray-induced phosphorylation of ERK1/2 was also inhibited by MRS2578 in A549 cells. We found that it was. Taken together, these findings indicate that purinergic signaling through P2Y_6 receptor, followed by ERK1/2 activation, promotes the cellular repair response to γ-ray-induced DNA damage. (author)

Skin protection against UVA-induced iron damage by multiantioxidants and iron chelating drugs/prodrugs.

Science.gov (United States)

Reelfs, Olivier; Eggleston, Ian M; Pourzand, Charareh

2010-03-01

In humans, prolonged sunlight exposure is associated with various pathological states. The continuing drive to develop improved skin protection involves not only approaches to reduce DNA damage by solar ultraviolet B (UVB) but also the development of methodologies to provide protection against ultraviolet A (UVA), the oxidising component of sunlight. Furthermore identification of specific cellular events following ultraviolet (UV) irradiation is likely to provide clues as to the mechanism of the development of resulting pathologies and therefore strategies for protection. Our discovery that UVA radiation, leads to an immediate measurable increase in 'labile' iron in human skin fibroblasts and keratinocytes provides a new insight into UVA-induced skin damage, since iron is a catalyst of biological oxidations. The main purpose of this overview is to bring together some of the new findings related to mechanisms underlying UVA-induced iron release and to discuss novel approaches based on the use of multiantioxidants and light-activated caged-iron chelators for efficient protection of skin cells against UVA-induced iron damage.

Comparison of laser-induced surface damage density measurements with small and large beams: toward representativeness

International Nuclear Information System (INIS)

Lamaignere, Laurent; Dupuy, Gabriel; Donval, Thierry; Grua, Pierre; Bercegol, Herve

2011-01-01

Pulsed laser damage density measurements obtained with diverse facilities are difficult to compare, due to the interplay of numerous parameters, such as beam area and pulse geometry, which, in operational large beam conditions, are very different from laboratory measurements. This discrepancy could have a significant impact; if so, one could not even pretend that laser damage density control is a real measurement process. In this paper, this concern is addressed. Tests with large beams of centimeter size on a high-power laser facility have beam performed according to a parametric study and are compared to small beam laboratory tests. It is shown that laser damage densities obtained with large and small beams are equal, within calculated error bars.

Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma

Energy Technology Data Exchange (ETDEWEB)

Dasgupta, Amrita [Hampton University Skin of Color Research Institute, Hampton, VA 23668 (United States); Katdare, Meena, E-mail: mkatdare@gmail.com [Hampton University Skin of Color Research Institute, Hampton, VA 23668 (United States); Department of Dermatology, Eastern Virginia Medical School, Norfolk, VA 23507 (United States)

2015-08-14

Cutaneous Melanoma (CM) is a leading cause of cancer deaths, with reports indicating a rising trend in the incidence rate of melanoma among Hispanics in certain U.S. states. The level of melanin pigmentation in the skin is suggested to render photoprotection from the DNA-damaging effects of Ultraviolet Radiation (UVR). UVR-induced DNA damage leads to cytogenetic defects visualized as the formation of micronuclei, multinuclei and polymorphic nuclei in cells, and a hallmark of cancer risk. The causative relationship between Sun exposure and CM is controversial, especially in Hispanics and needs further evaluation. This study was initiated with melanocytes from White, Hispanic and Black neonatal foreskins which were exposed to UVR to assess their susceptibility to UVR-induced modulation of cellular growth, cytogenetic damage, intracellular and released melanin. Our results show that White and Hispanic skin melanocytes with similar levels of constitutive melanin are susceptible to UVR-induced cytogenetic damage, whereas Black skin melanocytes are not. Our data suggest that the risk of developing UVR-induced CM in a skin type is correlated with the level of cutaneous pigmentation and its ethnic background. This study provides a benchmark for further investigation on the damaging effects of UVR as risk for CM in Hispanics.

Ultraviolet Radiation-Induced Cytogenetic Damage in White, Hispanic and Black Skin Melanocytes: A Risk for Cutaneous Melanoma

International Nuclear Information System (INIS)

Dasgupta, Amrita; Katdare, Meena

2015-01-01

Cutaneous Melanoma (CM) is a leading cause of cancer deaths, with reports indicating a rising trend in the incidence rate of melanoma among Hispanics in certain U.S. states. The level of melanin pigmentation in the skin is suggested to render photoprotection from the DNA-damaging effects of Ultraviolet Radiation (UVR). UVR-induced DNA damage leads to cytogenetic defects visualized as the formation of micronuclei, multinuclei and polymorphic nuclei in cells, and a hallmark of cancer risk. The causative relationship between Sun exposure and CM is controversial, especially in Hispanics and needs further evaluation. This study was initiated with melanocytes from White, Hispanic and Black neonatal foreskins which were exposed to UVR to assess their susceptibility to UVR-induced modulation of cellular growth, cytogenetic damage, intracellular and released melanin. Our results show that White and Hispanic skin melanocytes with similar levels of constitutive melanin are susceptible to UVR-induced cytogenetic damage, whereas Black skin melanocytes are not. Our data suggest that the risk of developing UVR-induced CM in a skin type is correlated with the level of cutaneous pigmentation and its ethnic background. This study provides a benchmark for further investigation on the damaging effects of UVR as risk for CM in Hispanics

Ultraviolet B (UVB) induced DNA damage affects alternative splicing in skin cells

International Nuclear Information System (INIS)

Munoz, M.J.; Nieto Moreno, N.; Kornblihtt, A.R.

2010-01-01

The ultraviolet (UV) radiation from the Sun that reaches the Earth's surface is a combination of low (UVA, 320-400 nm) and high (UVB, 290-320 nm) energy light. UVB light causes two types of mutagenic DNA lesions: thymine dimers and (6-4) photo-products. UVB mutagenesis is a critical step in the generation of different forms of skin cancer, which develops almost exclusively in sun exposed areas. We have previously shown that RNA polymerase II (pol II) hyperphosphorylation induced by UVC (254 nm) irradiation of non-skin cells inhibits pol II elongation rates which in turn affects alternative splicing (AS) patterns, altering the synthesis of pro- and anti-apoptotic isoforms of key proteins like Bcl-x or Caspase 9 (C9). Since the UVC radiation is fully filtered by the ozone layer and AS regulation in skin pathologies has been poorly studied, we decided to extend our studies to human keratinocytes in culture treated with UVB (302 nm) light. We observed that pol II hyperphosphorylation is increased upon UVB irradiation, being this modification necessary for the observed change in AS of a model cassette exon. Moreover, UVB irradiation induces the proapoptotic mRNA isoforms of Bcl-x and C9 consistently with a key role of AS in skin response to DNA damage. (authors)

Gc-protein-derived macrophage activating factor counteracts the neuronal damage induced by oxaliplatin.

Science.gov (United States)

Morucci, Gabriele; Branca, Jacopo J V; Gulisano, Massimo; Ruggiero, Marco; Paternostro, Ferdinando; Pacini, Alessandra; Di Cesare Mannelli, Lorenzo; Pacini, Stefania

2015-02-01

Oxaliplatin-based regimens are effective in metastasized advanced cancers. However, a major limitation to their widespread use is represented by neurotoxicity that leads to peripheral neuropathy. In this study we evaluated the roles of a proven immunotherapeutic agent [Gc-protein-derived macrophage activating factor (GcMAF)] in preventing or decreasing oxaliplatin-induced neuronal damage and in modulating microglia activation following oxaliplatin-induced damage. The effects of oxaliplatin and of a commercially available formula of GcMAF [oleic acid-GcMAF (OA-GcMAF)] were studied in human neurons (SH-SY5Y cells) and in human microglial cells (C13NJ). Cell density, morphology and viability, as well as production of cAMP and expression of vascular endothelial growth factor (VEGF), markers of neuron regeneration [neuromodulin or growth associated protein-43 (Gap-43)] and markers of microglia activation [ionized calcium binding adaptor molecule 1 (Iba1) and B7-2], were determined. OA-GcMAF reverted the damage inflicted by oxaliplatin on human neurons and preserved their viability. The neuroprotective effect was accompanied by increased intracellular cAMP production, as well as by increased expression of VEGF and neuromodulin. OA-GcMAF did not revert the effects of oxaliplatin on microglial cell viability. However, it increased microglial activation following oxaliplatin-induced damage, resulting in an increased expression of the markers Iba1 and B7-2 without any concomitant increase in cell number. When neurons and microglial cells were co-cultured, the presence of OA-GcMAF significantly counteracted the toxic effects of oxaliplatin. Our results demonstrate that OA-GcMAF, already used in the immunotherapy of advanced cancers, may significantly contribute to neutralizing the neurotoxicity induced by oxaliplatin, at the same time possibly concurring to an integrated anticancer effect. The association between these two powerful anticancer molecules would probably produce

Nrf2 deficiency potentiates methamphetamine-induced dopaminergic axonal damage and gliosis in the striatum.

Science.gov (United States)

Granado, Noelia; Lastres-Becker, Isabel; Ares-Santos, Sara; Oliva, Idaira; Martin, Eduardo; Cuadrado, Antonio; Moratalla, Rosario

2011-12-01

Oxidative stress that correlates with damage to nigrostriatal dopaminergic neurons and reactive gliosis in the basal ganglia is a hallmark of methamphetamine (METH) toxicity. In this study, we analyzed the protective role of the transcription factor Nrf2 (nuclear factor-erythroid 2-related factor 2), a master regulator of redox homeostasis, in METH-induced neurotoxicity. We found that Nrf2 deficiency exacerbated METH-induced damage to dopamine neurons, shown by an increase in loss of tyrosine hydroxylase (TH)- and dopamine transporter (DAT)-containing fibers in striatum. Consistent with these effects, Nrf2 deficiency potentiated glial activation, indicated by increased striatal expression of markers for microglia (Mac-1 and Iba-1) and astroglia (GFAP) one day after METH administration. At the same time, Nrf2 inactivation dramatically potentiated the increase in TNFα mRNA and IL-15 protein expression in GFAP+ cells in the striatum. In sharp contrast to the potentiation of striatal damage, Nrf2 deficiency did not affect METH-induced dopaminergic neuron death or expression of glial markers or proinflammatory molecules in the substantia nigra. This study uncovers a new role for Nrf2 in protection against METH-induced inflammatory and oxidative stress and striatal degeneration. Copyright © 2011 Wiley‐Liss, Inc.

Consequences of PAI-1 specific deletion in endothelium on radiation-induced intestinal damage

International Nuclear Information System (INIS)

Rannou, Emilie

2015-01-01

Radiation-induced injury to healthy tissues is a real public health problem, since they are one of the most limiting factors that restrict efficiency of radiation therapy. This problematic is also part of the French Cancer Plan 2014-2017, and involves clinical research. Concepts surrounding the development of radiation-induced damage have gradually evolved into a contemporary and integrated view of the pathogenesis, involving all compartments of target tissue. Among them, endothelium seems to be central in the sequence of interrelated events that lead to the development of radiation-induced damage, although there are rare concrete elements that support this concept. By using new transgenic mouse models, this PhD project provides a direct demonstration of an endothelium-dependent continuum in evolution of radiation-induced intestinal damage. Indeed, changes in the endothelial phenotype through targeted deletion of the gene SERPINE1, chosen because of its key role in the development of radiation enteritis, influences various parameters of the development of the disease. Thus, lack of PAI-1 secretion by endothelial cells significantly improves survival of the animals, and limits severity of early and late tissue damage after a localized small bowel irradiation. Furthermore, these mice partially KO for PAI-1 showed a decrease in the number of apoptotic intestinal stem cells in the hours following irradiation, a decrease in the macrophages infiltrate density one week after irradiation, and a change in the polarization of macrophages throughout the pathophysiological process. In an effort to protect healthy tissues from radiation therapy side effects, without hindering the cancer treatment, PAI-1 seems to be an obvious therapeutic target. Conceptually, this work represents the direct demonstration of the link between endothelium phenotype and radiation enteritis pathogenesis. (author)

Radiation-induced liver damage

International Nuclear Information System (INIS)

Marcial, V.A.; Santiago-Delpin, E.A.; Lanaro, A.E.; Castro-Vita, H.; Arroyo, G.; Moscol, J.A.; Gomez, C.; Velazquez, J.; Prado, K.

1977-01-01

Due to the recent increase in the use of radiation therapy in the treatment of cancer with or without chemotherapy, the risk of liver radiation damage has become a significant concern for the radiotherapist when the treated tumour is located in the upper abdomen or lower thorax. Clinically evident radiation liver damage may result in significant mortality, but at times patients recover without sequelae. The dose of 3000 rads in 3 weeks to the entire liver with 5 fractions per week of 200 rads each, seems to be tolerated well clinically by adult humans. Lower doses may lead to damage when used in children, when chemotherapy is added, as in recent hepatectomy cases, and in the presence of pre-existent liver damage. Reduced fractionation may lead to increased damage. Increased fractionation, limitation of the dose delivered to the entire liver, and restriction of the high dose irradiation volume may afford protection. With the aim of studying the problems of hepatic radiation injury in humans, a project of liver irradiation in the dog is being conducted. Mongrel dogs are being conditioned, submitted to pre-irradiation studies (haemogram, blood chemistry, liver scan and biopsy), irradiated under conditions resembling human cancer therapy, and submitted to post-irradiation evaluation of the liver. Twenty-two dogs have been entered in the study but only four qualify for the evaluation of all the study parameters. It has been found that dogs are susceptible to liver irradiation damage similar to humans. The initial mortality has been high mainly due to non-radiation factors which are being kept under control at the present phase of the study. After the initial experiences, the study will involve variations in total dose and fractionation, and the addition of anticoagulant therapy for possible prevention of radiation liver injury. (author)

Photoelectrochemical Sensors for the Rapid Detection of DNA Damage Induced by Some Nanoparticles

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M. Jamaluddin Ahmed

2010-06-01

Full Text Available Photoelectrochemcal sensors were developed for the rapid detection of oxidative DNA damage induced by titanium dioxide and polystyrene nanoparticles. Each sensor is a multilayer film prepared on a tin oxide nanoparticle electrode using layer- by-layer self assembly and is composed of separate layer of a photoelectrochemical indicator, DNA. The organic compound and heavy metals represent genotoxic chemicals leading two major damaging mechanisms, DNA adduct formation and DNA oxidation. The DNA damage is detected by monitoring the change of photocurrent of the indicator. In one sensor configuration, a DNA intercalator, Ru(bpy2 (dppz2+ [bpy=2, 2′ -bipyridine, dppz=dipyrido( 3, 2-a: 2′ 3′-c phenazine], was employed as the photoelectrochemical indicator. The damaged DNA on the sensor bound lesser Ru(bpy2 (dppz2+ than the intact DNA, resulting in a drop in photocurrent. In another configuration, ruthenium tris(bipyridine was used as the indicator and was immobilized on the electrode underneath the DNA layer. After oxidative damage, the DNA bases became more accessible to photoelectrochemical oxidation than the intact DNA, producing a rise in photocurrent. Both sensors displayed substantial photocurrent change after incubation in titanium dioxide / polystyrene solution in a time – dependent manner. According to the data, damage of the DNA film was completed in 1h in titanium dioxide / polystyrene solution. In addition, the titanium dioxide induced much more sever damage than polysterene. The results were verified independently by gel electrophoresis and UV-Vis absorbance experiments. The photoelectrochemical reaction can be employed as a new and inexpensive screening tool for the rapid assessment of the genotoxicity of existing and new chemicals.

Photoelectrochemical sensors for the rapid detection of DNA damage Induced by some nanoparticles

International Nuclear Information System (INIS)

Ahmed, M.J.; Zhang, B.T.; Guo, L.H.

2010-01-01

Photoelectrochemical sensors were developed for the rapid detection of oxidative DNA damage induced by titanium dioxide and polystyrene nanoparticles. Each sensor is a multilayer film prepared on a tin oxide nanoparticle electrode using layer- by-layer self assembly and is composed of separate layer of a photoelectrochemical indicator, DNA. The organic compound and heavy metals represent genotoxic chemicals leading two major damaging mechanisms, DNA adduct formation and DNA oxidation. The DNA damage is detected by monitoring the change of photocurrent of the indicator. In one sensor configuration, a DNA intercalator, Ru(bpy)2 (dppz)2+ [bpy=2, 2' -bipyridine, dppz=dipyrido (3, 2-a: 2' 3'-c) phenazine], was employed as the photoelectrochemical indicator. The damaged DNA on the sensor bound lesser Ru(bpy)2 (dppz)2+ than the intact DNA, resulting in a drop in photocurrent. In another configuration, ruthenium tris(bipyridine) was used as the indicator and was immobilized on the electrode underneath the DNA layer. After oxidative damage, the DNA bases became more accessible to photoelectrochemical oxidation than the intact DNA, producing a rise in photocurrent. Both sensors displayed substantial photocurrent change after incubation in titanium dioxide / polystyrene solution in a time . dependent manner. According to the data, damage of the DNA film was completed in 1h in titanium dioxide / polystyrene solution. In addition, the titanium dioxide induced much more sever damage than polystyrene. The results were verified independently by gel electrophoresis and UV-Vis absorbance experiments. The photoelectrochemical reaction can be employed as a new and inexpensive screening tool for the rapid assessment of the genotoxicity of existing and new chemicals. (author)

Surface damages of polycrystalline W and La2O3-doped W induced by high-flux He plasma irradiation

Science.gov (United States)

Liu, Lu; Li, Shouzhe; Liu, Dongping; Benstetter, Günther; Zhang, Yang; Hong, Yi; Fan, Hongyu; Ni, Weiyuan; Yang, Qi; Wu, Yunfeng; Bi, Zhenhua

2018-04-01

In this study, polycrystalline tungsten (W) and three oxide dispersed strengthened W with 0.1 vol %, 1.0 vol % and 5.0 vol % lanthanum trioxide (La2O3) were irradiated with low-energy (200 eV) and high-flux (5.8 × 1021 or 1.4 × 1022 ions/m2ṡs) He+ ions at elevated temperature. After He+ irradiation at a fluence of 3.0 × 1025/m2, their surface damages were observed by scanning electron microscopy, energy dispersive spectroscopy, scanning electron microscopy-electron backscatter diffraction, and conductive atomic force microscopy. Micron-sized holes were formed on the surface of W alloys after He+ irradiation at 1100 K. Analysis shows that the La2O3 grains doped in W were sputtered preferentially by the high-flux He+ ions when compared with the W grains. For irradiation at 1550 K, W nano-fuzz was formed at the surfaces of both polycrystalline W and La2O3-doped W. The thickness of the fuzz layers formed at the surface of La2O3-doped W is 40% lower than the one of polycrystalline W. The presence of La2O3 could suppress the diffusion and coalescence of He atoms inside W, which plays an important role in the growth of nanostructures fuzz.

Alpha-phellandrene-induced DNA damage and affect DNA repair protein expression in WEHI-3 murine leukemia cells in vitro.

Science.gov (United States)

Lin, Jen-Jyh; Wu, Chih-Chung; Hsu, Shu-Chun; Weng, Shu-Wen; Ma, Yi-Shih; Huang, Yi-Ping; Lin, Jaung-Geng; Chung, Jing-Gung

2015-11-01

Although there are few reports regarding α-phellandrene (α-PA), a natural compound from Schinus molle L. essential oil, there is no report to show that α-PA induced DNA damage and affected DNA repair associated protein expression. Herein, we investigated the effects of α-PA on DNA damage and repair associated protein expression in murine leukemia cells. Flow cytometric assay was used to measure the effects of α-PA on total cell viability and the results indicated that α-PA induced cell death. Comet assay and 4,6-diamidino-2-phenylindole dihydrochloride staining were used for measuring DNA damage and condensation, respectively, and the results indicated that α-PA induced DNA damage and condensation in a concentration-dependent manner. DNA gel electrophoresis was used to examine the DNA damage and the results showed that α-PA induced DNA damage in WEHI-3 cells. Western blotting assay was used to measure the changes of DNA damage and repair associated protein expression and the results indicated that α-PA increased p-p53, p-H2A.X, 14-3-3-σ, and MDC1 protein expression but inhibited the protein of p53, MGMT, DNA-PK, and BRCA-1. © 2014 Wiley Periodicals, Inc.

A detailed physical model for ion implant induced damage in silicon

International Nuclear Information System (INIS)

Tian, S.; Morris, M.F.; Morris, S.J.; Obradovic, B.; Wang, G.; Tasch, A.F.

1998-01-01

A unified physically based ion implantation damage model has been developed which successfully predicts both the impurity profiles and the damage profiles for a wide range of implant conditions for arsenic, phosphorus, BF 2 , and boron implants into single-crystal silicon. In addition, the amorphous layer thicknesses predicted by this new damage model are also in excellent agreement with experimental measurements. This damage model is based on the physics of point defects in silicon, and explicitly simulates the defect production, diffusion, and their interactions which include interstitial-vacancy recombination, clustering of same type of defects, defect-impurity complex formation, emission of mobile defects from clusters, and surface effects for the first time. New computationally efficient algorithms have been developed to overcome the barrier of the excessive computational requirements. In addition, the new model has been incorporated in the UT-MARLOWE ion implantation simulator, and has been developed primarily for use in engineering workstations. This damage model is the most physical model in the literature to date within the framework of the binary collision approximation (BCA), and provides the required, accurate as-implanted impurity profiles and damage profiles for transient enhanced diffusion (TED) simulation

DNA damage responses in human induced pluripotent stem cells and embryonic stem cells.

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Olga Momcilovic

2010-10-01

Full Text Available Induced pluripotent stem (iPS cells have the capability to undergo self-renewal and differentiation into all somatic cell types. Since they can be produced through somatic cell reprogramming, which uses a defined set of transcription factors, iPS cells represent important sources of patient-specific cells for clinical applications. However, before these cells can be used in therapeutic designs, it is essential to understand their genetic stability.Here, we describe DNA damage responses in human iPS cells. We observe hypersensitivity to DNA damaging agents resulting in rapid induction of apoptosis after γ-irradiation. Expression of pluripotency factors does not appear to be diminished after irradiation in iPS cells. Following irradiation, iPS cells activate checkpoint signaling, evidenced by phosphorylation of ATM, NBS1, CHEK2, and TP53, localization of ATM to the double strand breaks (DSB, and localization of TP53 to the nucleus of NANOG-positive cells. We demonstrate that iPS cells temporary arrest cell cycle progression in the G(2 phase of the cell cycle, displaying a lack of the G(1/S cell cycle arrest similar to human embryonic stem (ES cells. Furthermore, both cell types remove DSB within six hours of γ-irradiation, form RAD51 foci and exhibit sister chromatid exchanges suggesting homologous recombination repair. Finally, we report elevated expression of genes involved in DNA damage signaling, checkpoint function, and repair of various types of DNA lesions in ES and iPS cells relative to their differentiated counterparts.High degrees of similarity in DNA damage responses between ES and iPS cells were found. Even though reprogramming did not alter checkpoint signaling following DNA damage, dramatic changes in cell cycle structure, including a high percentage of cells in the S phase, increased radiosensitivity and loss of DNA damage-induced G(1/S cell cycle arrest, were observed in stem cells generated by induced pluripotency.

Delayed repair of radiation induced clustered DNA damage: Friend or foe?

International Nuclear Information System (INIS)

Eccles, Laura J.; O'Neill, Peter; Lomax, Martine E.

2011-01-01

A signature of ionizing radiation exposure is the induction of DNA clustered damaged sites, defined as two or more lesions within one to two helical turns of DNA by passage of a single radiation track. Clustered damage is made up of double strand breaks (DSB) with associated base lesions or abasic (AP) sites, and non-DSB clusters comprised of base lesions, AP sites and single strand breaks. This review will concentrate on the experimental findings of the processing of non-DSB clustered damaged sites. It has been shown that non-DSB clustered damaged sites compromise the base excision repair pathway leading to the lifetime extension of the lesions within the cluster, compared to isolated lesions, thus the likelihood that the lesions persist to replication and induce mutation is increased. In addition certain non-DSB clustered damaged sites are processed within the cell to form additional DSB. The use of E. coli to demonstrate that clustering of DNA lesions is the major cause of the detrimental consequences of ionizing radiation is also discussed. The delayed repair of non-DSB clustered damaged sites in humans can be seen as a 'friend', leading to cell killing in tumour cells or as a 'foe', resulting in the formation of mutations and genetic instability in normal tissue.

Investigation on the effect of developed product and new food for radiation-induced skin damage

Energy Technology Data Exchange (ETDEWEB)

Kim, Sung Ho; Kim, Jong Chun; Bae, Chun Sik; Kim, Se Ra; Lee, Hae Jun; Bang, Dae Won; Lee, Jin Hee; Kim, Joong Sun; Ki, Sun Ah; Song, Myung Seop [Chonnam National University, Gwangju (Korea, Republic of)

2007-07-15

In vivo evaluation of the developed pilot product on the skin protection against UV irradiation and screening of new candidate materials. Project Results are Establishment of experimental methods for 3 morphological indices of UV-induced skin damages -Establishment of experimental methods for whitening effect evaluation -Evaluation of HemoHIM administration on the skin damage indices -Evaluation of HemoHIM skin application on the skin damage indices -Evaluation of HemoTonic administration on the skin damage indices -Evaluation of HemoTonic skin application on the skin damage indices -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 1 -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 2 -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 3 -Evaluation of HemoHIM on the antiinflamatory effects in the TNBS-induced colitis -Evaluation of HemoHIM on the anti-wrinkle effects in the skin -Evaluation of HemoHIM on the protective effects on the skin tissue (epidermal thickening, dermal cellularity, dermal cyst) -Evaluation of HemoHIM on the protective effects on the skin tumor development

Investigation on the effect of developed product and new food for radiation-induced skin damage

International Nuclear Information System (INIS)

Kim, Sung Ho; Kim, Jong Chun; Bae, Chun Sik; Kim, Se Ra; Lee, Hae Jun; Bang, Dae Won; Lee, Jin Hee; Kim, Joong Sun; Ki, Sun Ah; Song, Myung Seop

2007-07-01

In vivo evaluation of the developed pilot product on the skin protection against UV irradiation and screening of new candidate materials. Project Results are Establishment of experimental methods for 3 morphological indices of UV-induced skin damages -Establishment of experimental methods for whitening effect evaluation -Evaluation of HemoHIM administration on the skin damage indices -Evaluation of HemoHIM skin application on the skin damage indices -Evaluation of HemoTonic administration on the skin damage indices -Evaluation of HemoTonic skin application on the skin damage indices -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 1 -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 2 -Evaluation of HemoHIM on the antiinflamatory effects in the inflammation stage 3 -Evaluation of HemoHIM on the antiinflamatory effects in the TNBS-induced colitis -Evaluation of HemoHIM on the anti-wrinkle effects in the skin -Evaluation of HemoHIM on the protective effects on the skin tissue (epidermal thickening, dermal cellularity, dermal cyst) -Evaluation of HemoHIM on the protective effects on the skin tumor development

Protection of vanillin derivative VND3207 on plasmid DNA damage induced by different LET ionizing radiation

International Nuclear Information System (INIS)

Xu Huihui; Wang Li; Sui Li; Guan Hua; Wang Yu; Liu Xiaodan; Zhang Shimeng; Xu Qinzhi; Wang Xiao; Zhou Pingkun

2011-01-01

Objective: To evaluate the radioprotective effect of vanillin derivative VND3207 on DNA damage induced by different LET ionizing radiation. Methods: The plasmid DNA in liquid was irradiated by 60 Co γ-rays, proton or 7 Li heavy ion with or without VND3207. The conformation changes of plasmid DNA were assessed by agarose gel electrophoresis and the quantification was done using gel imaging system. Results: The DNA damage induced by proton and 7 Li heavy ion was much more serious as compared with that by 60 Co γ-rays, and the vanillin derivative VND3207 could efficiently decrease the DNA damage induced by all three types of irradiation sources, which was expressed as a significantly reduced ratio of open circular form (OC) of plasmid DNA. The radioprotective effect of VND3207 increased with the increasing of drug concentration. The protective efficiencies of 200 μmol/L VND3207 were 85.3% (t =3.70, P=0.033), 73.3% (t=10.58, P=0.017) and 80.4% (t=8.57, P=0.008) on DNA damage induction by 50 Gy of γ-rays, proton and 7 Li heavy ion, respectively. It seemed that the radioprotection of VND3207 was more effective on DNA damage induced by high LET heavy ion than that by proton. Conclusions: VND3207 has a protective effect against the genotoxicity of different LET ionizing radiation, especially for γ-rays and 7 Li heavy ion. (authors)

Cellular characterization of compression induced-damage in live biological samples

Science.gov (United States)

Bo, Chiara; Balzer, Jens; Hahnel, Mark; Rankin, Sara M.; Brown, Katherine A.; Proud, William G.

2011-06-01

Understanding the dysfunctions that high-intensity compression waves induce in human tissues is critical to impact on acute-phase treatments and requires the development of experimental models of traumatic damage in biological samples. In this study we have developed an experimental system to directly assess the impact of dynamic loading conditions on cellular function at the molecular level. Here we present a confinement chamber designed to subject live cell cultures in liquid environment to compression waves in the range of tens of MPa using a split Hopkinson pressure bars system. Recording the loading history and collecting the samples post-impact without external contamination allow the definition of parameters such as pressure and duration of the stimulus that can be related to the cellular damage. The compression experiments are conducted on Mesenchymal Stem Cells from BALB/c mice and the damage analysis are compared to two control groups. Changes in Stem cell viability, phenotype and function are assessed flow cytometry and with in vitro bioassays at two different time points. Identifying the cellular and molecular mechanisms underlying the damage caused by dynamic loading in live biological samples could enable the development of new treatments for traumatic injuries.

Oxidative damage and cell-programmed death induced in Zea mays L. by allelochemical stress.

Science.gov (United States)

Ciniglia, Claudia; Mastrobuoni, Francesco; Scortichini, Marco; Petriccione, Milena

2015-05-01

The allelochemical stress on Zea mays was analyzed by using walnut husk washing waters (WHWW), a by-product of Juglans regia post-harvest process, which possesses strong allelopathic potential and phytotoxic effects. Oxidative damage and cell-programmed death were induced by WHWW in roots of maize seedlings. Treatment induced ROS burst, with excess of H2O2 content. Enzymatic activities of catalase were strongly increased during the first hours of exposure. The excess in malonildialdehyde following exposure to WHWW confirmed that oxidative stress severely damaged maize roots. Membrane alteration caused a decrease in NADPH oxidase activity along with DNA damage as confirmed by DNA laddering. The DNA instability was also assessed through sequence-related amplified polymorphism assay, thus suggesting the danger of walnut processing by-product and focusing the attention on the necessity of an efficient treatment of WHWW.

Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C

Directory of Open Access Journals (Sweden)

Roy Siddhartha

2008-11-01

Full Text Available Abstract Background Cigarette smoke-induced cellular and molecular mechanisms of lung injury are not clear. Cigarette smoke is a complex mixture containing long-lived radicals, including p-benzosemiquinone that causes oxidative damage. Earlier we had reported that oxidative protein damage is an initial event in smoke-induced lung injury. Considering that p-benzosemiquinone may be a causative factor of lung injury, we have isolated p-benzosemiquinone and compared its pathophysiological effects with cigarette smoke. Since vitamin C is a strong antioxidant, we have also determined the modulatory effect of vitamin C for preventing the pathophysiological events. Methods Vitamin C-restricted guinea pigs were exposed to cigarette smoke (5 cigarettes/day; 2 puffs/cigarette for 21 days with and without supplementation of 15 mg vitamin C/guinea pig/day. Oxidative damage, apoptosis and lung injury were assessed in vitro, ex vivo in A549 cells as well as in vivo in guinea pigs. Inflammation was measured by neutrophilia in BALF. p-Benzosemiquinone was isolated from freshly prepared aqueous extract of cigarette smoke and characterized by various physico-chemical methods, including mass, NMR and ESR spectroscopy. p-Benzosemiquinone-induced lung damage was examined by intratracheal instillation in guinea pigs. Lung damage was measured by increased air spaces, as evidenced by histology and morphometric analysis. Oxidative protein damage, MMPs, VEGF and VEGFR2 were measured by western blot analysis, and formation of Michael adducts using MALDI-TOF-MS. Apoptosis was evidenced by TUNEL assay, activation of caspase 3, degradation of PARP and increased Bax/Bcl-2 ratio using immunoblot analysis and confocal microscopy. Results Exposure of guinea pigs to cigarette smoke resulted in progressive protein damage, inflammation, apoptosis and lung injury up to 21 days of the experimental period. Administration of 15 mg of vitamin C/guinea pig/day prevented all these

Modeling of combined physical-mechanical moisture induced damage in asphaltic mixes

NARCIS (Netherlands)

Kringos, N.

2007-01-01

Moisture induced damage in asphaltic mixes is recognized as a major issue, resulting to the need for frequent maintenance operations. This does not only imply high maintenance costs, but also temporary closure of traffic and hence increased road congestion. Given the high costs for the road

Temporal scaling law and intrinsic characteristic of laser induced damage on the dielectric coating

Science.gov (United States)

Zhou, Li; Jiang, Youen; Wang, Chao; Wei, Hui; Zhang, Peng; Fan, Wei; Li, Xuechun

2018-01-01

High power laser is essential for optical manipulation and fabrication. When the laser travels through optics and to the target finally, irreversible damage on the dielectric coating is always accompanied without knowing the law and principle of laser induced damage. Here, an experimental study of laser induced damage threshold (LIDT) Fth of the dielectric coating under different pulse duration t is implemented. We observe that the temporal scaling law of square pulse for high-reflectivity (HR) coating and anti-reflectivity (AR) coating are Fth = 9.53t0.47 and Fth = 6.43t0.28 at 1064 nm, respectively. Moreover, the intrinsic LIDT of HR coating is 62.7 J/cm2 where the coating is just 100% damaged by gradually increasing the fluence densities of a 5ns-duration pulse, which is much higher than the actual LIDT of 18.6 J/cm2. Thus, a more robust and reliable high power laser system will be a reality, even working at very high fluence, if measures are taken to improve the actual LIDT to a considerable level near the intrinsic value.

REC-2006-A Fractionated Extract of Podophyllum hexandrum Protects Cellular DNA from Radiation-Induced Damage by Reducing the Initial Damage and Enhancing Its Repair In Vivo.

Science.gov (United States)

Chaudhary, Pankaj; Shukla, Sandeep Kumar; Sharma, Rakesh Kumar

2011-01-01

Podophyllum hexandrum, a perennial herb commonly known as the Himalayan May Apple, is well known in Indian and Chinese traditional systems of medicine. P. hexandrum has been widely used for the treatment of venereal warts, skin infections, bacterial and viral infections, and different cancers of the brain, lung and bladder. This study aimed at elucidating the effect of REC-2006, a bioactive fractionated extract from the rhizome of P. hexandrum, on the kinetics of induction and repair of radiation-induced DNA damage in murine thymocytes in vivo. We evaluated its effect on non-specific radiation-induced DNA damage by the alkaline halo assay in terms of relative nuclear spreading factor (RNSF) and gene-specific radiation-induced DNA damage via semi-quantitative polymerase chain reaction. Whole body exposure of animals with gamma rays (10 Gy) caused a significant amount of DNA damage in thymocytes (RNSF values 17.7 ± 0.47, 12.96 ± 1.64 and 3.3 ± 0.014) and a reduction in the amplification of β-globin gene to 0, 28 and 43% at 0, 15 and 60 min, respectively. Administrating REC-2006 at a radioprotective concentration (15 mg kg(-1) body weight) 1 h before irradiation resulted in time-dependent reduction of DNA damage evident as a decrease in RNSF values 6.156 ± 0.576, 1.647 ± 0.534 and 0.496 ± 0.012, and an increase in β-globin gene amplification 36, 95 and 99%, at 0, 15 and 60 min, respectively. REC-2006 scavenged radiation-induced hydroxyl radicals in a dose-dependent manner stabilized DPPH free radicals and also inhibited superoxide anions. Various polyphenols and flavonoides present in REC-2006 might contribute to scavenging of radiation-induced free radicals, thereby preventing DNA damage and stimulating its repair.

Adherence to abiotic surface induces SOS response in Escherichia coli K-12 strains under aerobic and anaerobic conditions.

Science.gov (United States)

Costa, Suelen B; Campos, Ana Carolina C; Pereira, Ana Claudia M; de Mattos-Guaraldi, Ana Luiza; Júnior, Raphael Hirata; Rosa, Ana Cláudia P; Asad, Lídia M B O

2014-09-01

During the colonization of surfaces, Escherichia coli bacteria often encounter DNA-damaging agents and these agents can induce several defence mechanisms. Base excision repair (BER) is dedicated to the repair of oxidative DNA damage caused by reactive oxygen species (ROS) generated by chemical and physical agents or by metabolism. In this work, we have evaluated whether the interaction with an abiotic surface by mutants derived from E. coli K-12 deficient in some enzymes that are part of BER causes DNA damage and associated filamentation. Moreover, we studied the role of endonuclease V (nfi gene; 1506 mutant strain) in biofilm formation. Endonuclease V is an enzyme that is involved in DNA repair of nitrosative lesions. We verified that endonuclease V is involved in biofilm formation. Our results showed more filamentation in the xthA mutant (BW9091) and triple xthA nfo nth mutant (BW535) than in the wild-type strain (AB1157). By contrast, the mutant nfi did not present filamentation in biofilm, although its wild-type strain (1466) showed rare filaments in biofilm. The filamentation of bacterial cells attaching to a surface was a consequence of SOS induction measured by the SOS chromotest. However, biofilm formation depended on the ability of the bacteria to induce the SOS response since the mutant lexA Ind(-) did not induce the SOS response and did not form any biofilm. Oxygen tension was an important factor for the interaction of the BER mutants, since these mutants exhibited decreased quantitative adherence under anaerobic conditions. However, our results showed that the presence or absence of oxygen did not affect the viability of BW9091 and BW535 strains. The nfi mutant and its wild-type did not exhibit decreased biofilm formation under anaerobic conditions. Scanning electron microscopy was also performed on the E. coli K-12 strains that had adhered to the glass, and we observed the presence of a structure similar to an extracellular matrix that depended on the

[Oxidative damage effects induced by CdTe quantum dots in mice].

Science.gov (United States)

Xie, G Y; Chen, W; Wang, Q K; Cheng, X R; Xu, J N; Huang, P L

2017-07-20

Objective: To investigate Oxidative damage effects induced by CdTe Quantum Dots (QDs) in mice. Methods: 40 ICR mice were randomly divided into 5 groups: one control group (normal saline) ; four CdTe QDs (exposed by intravenous injection of 0.2 ml of CdTe QDs at the concentration of 0、0.5、5.0、50.0 and 500.0 nmol/ml respectively) . After 24 h, the mice were decapitated and the blood was collected for serum biochemically indexes、hematology indexes, the activities of SOD、GSH-Px and the concentration of MDA were all detected. Results: The results showed in the four CdTe QDs exposure groups, the level of CRE、PLT and the concentration of MDA were all significantly lower than those of the control group ( P control group ( P <0.01) . Conclusion: It was suggested that CdTe QDs at 0.5 nmol/ml could induce Oxidative damage effects in mice.

The protective effect of hypoxia and dithiothreitol on X-ray-induced genetic damage in Arabidopsis

International Nuclear Information System (INIS)

Sree Ramulu, K.; Veen, J.H. van der

1987-01-01

A study was made on the protective effect of hypoxia and dithiothreitol (DTT) on X-ray-induced ovule sterility and embryonic lethality in Arabidopsis. Both hypoxia and DTT gave a pronounced and additive reduction of radiation-induced genetic damage. The reduction was significantly higher for ovule sterility than for embryonic lethals. It is suggested that non-fertilized ovules contain a higher ratio of strand breaks/other damage than embryonic lethals do, for hypoxia and DTT are known specifically to give a reduction of strand breaks. (Auth.)

Induction of the Wnt antagonist Dickkopf-1 is involved in stress-induced hippocampal damage.

Directory of Open Access Journals (Sweden)

Francesco Matrisciano

Full Text Available The identification of mechanisms that mediate stress-induced hippocampal damage may shed new light into the pathophysiology of depressive disorders and provide new targets for therapeutic intervention. We focused on the secreted glycoprotein Dickkopf-1 (Dkk-1, an inhibitor of the canonical Wnt pathway, involved in neurodegeneration. Mice exposed to mild restraint stress showed increased hippocampal levels of Dkk-1 and reduced expression of β-catenin, an intracellular protein positively regulated by the canonical Wnt signalling pathway. In adrenalectomized mice, Dkk-1 was induced by corticosterone injection, but not by exposure to stress. Corticosterone also induced Dkk-1 in mouse organotypic hippocampal cultures and primary cultures of hippocampal neurons and, at least in the latter model, the action of corticosterone was reversed by the type-2 glucocorticoid receptor antagonist mifepristone. To examine whether induction of Dkk-1 was causally related to stress-induced hippocampal damage, we used doubleridge mice, which are characterized by a defective induction of Dkk-1. As compared to control mice, doubleridge mice showed a paradoxical increase in basal hippocampal Dkk-1 levels, but no Dkk-1 induction in response to stress. In contrast, stress reduced Dkk-1 levels in doubleridge mice. In control mice, chronic stress induced a reduction in hippocampal volume associated with neuronal loss and dendritic atrophy in the CA1 region, and a reduced neurogenesis in the dentate gyrus. Doubleridge mice were resistant to the detrimental effect of chronic stress and, instead, responded to stress with increases in dendritic arborisation and neurogenesis. Thus, the outcome of chronic stress was tightly related to changes in Dkk-1 expression in the hippocampus. These data indicate that induction of Dkk-1 is causally related to stress-induced hippocampal damage and provide the first evidence that Dkk-1 expression is regulated by corticosteroids in the central

Surface damage versus defect microstructures in He and H ion co-implanted Si{sub 3}N{sub 4}/Si

Energy Technology Data Exchange (ETDEWEB)

Zhu, F. [School of Science, Tianjin University, Tianjin 300072 (China); Liu, C.L., E-mail: liuchanglong@tju.edu.cn [School of Science, Tianjin University, Tianjin 300072 (China); Tianjin Key Laboratory of Low Dimensional Materials Physics and Preparing Technology, Institute of Advanced Materials Physics Faculty of Science, Tianjin 300072 (China); Gao, Y.J.; Wang, Z.; Wang, J. [School of Science, Tianjin University, Tianjin 300072 (China)

2012-09-01

Cz n-type Si (1 0 0) wafers with a top Si{sub 3}N{sub 4} layer of about 170 nm in thickness were sequentially implanted with 40 keV He ions at a fluence of 5 Multiplication-Sign 10{sup 16}/cm{sup 2} and 35 keV H ions at fluences of 1 Multiplication-Sign 10{sup 15}, 5 Multiplication-Sign 10{sup 15} and 1 Multiplication-Sign 10{sup 16}/cm{sup 2}, respectively. Creation and evolution of surface damage as well as micro-defects have been studied. Our results clearly show that production of surface damage depends strongly on both the H implant fluence and annealing temperature. Only blistering or localized exfoliation of the top Si{sub 3}N{sub 4} layer has been observed for post H implantation at fluences of 1 Multiplication-Sign 10{sup 15} and 5 Multiplication-Sign 10{sup 15}/cm{sup 2} upon 800 Degree-Sign C annealing. However, serious surface exfoliation has been found for the 1 Multiplication-Sign 10{sup 16}/cm{sup 2} H co-implanted samples after annealing at 450 Degree-Sign C and above. The exfoliation occurs at a depth of about 360 nm from the surface, which is obviously larger than the He or H ion range. Moreover, the exfoliated craters show clear two-step structures. Cross-sectional transmission electron microscopy (XTEM) observations reveal formation of micro-cracks in Si bulk and along the original interface, which is mainly responsible for the observed surface phenomena. The formation mechanism of micro-cracks has been discussed in combination of He and H implant-induced defects, impurities as well as their interactions upon annealing.

Umbelliferone suppresses radiation induced DNA damage and apoptosis in hematopoietic cells of mice

International Nuclear Information System (INIS)

Jayakumar, S.; Bhilwade, H.N.; Chaubey, R.C.

2012-01-01

Radiotherapy is one of the major modes of treatment for different types of cancers. But the success of radiotherapy is limited by injury to the normal cells. Protection of the normal cells from radiation damage by radioprotectors can increase therapeutic efficiency. These radioprotectors can also be used during nuclear emergency situations. Umbelliferone (UMB) is a wide spread natural product of the coumarin family. It occurs in many plants from the Apiaceae family. In the present study radioprotective effect of UMB was investigated in vitro and in vivo. Anti genotoxic effect of Umbelliferone was tested by treating the splenic lymphocytes with various doses of UMB (6.5 μM - 50 μM) prior to radiation (6Gy) exposure. After the radiation exposure, extent of DNA damage was assessed by comet assay at 5 mm and two hours after radiation exposure. At both the time points, it was observed that the pretreatment of UMB reduced the radiation induced DNA damage to a significant extent in comparison to radiation control. UMB pretreatment also significantly reduced the radiation induced apoptosis enumerated by propidium iodide staining assay. Results of clonogenic survival assay using intestinal cell line showed that pretreatment with UMB significantly protected against radiation induced loss of colony forming units. To assess the anti genotoxic role of umbelliferone in vivo two different doses of UMB (20 mg/Kg and 40 mg/Kg of body weight) were injected into Swiss mice or with vehicle and exposed to radiation. Thirty minutes after the radiation comet assay was performed in peripheral leukocytes. Frequency of micro nucleated erythrocytes was scored in bone marrow cells. It was observed that UMB alone did not cause any significant increase in DNA damage in comparison to control. Animals which are exposed to radiation alone showed significant increase in DNA damage and micronuclei frequency. But animals treated with UMB prior to the radiation exposure showed significant decrease

Self-induced free surface oscillations caused by water jet

International Nuclear Information System (INIS)

Fukaya, M.; Madarame, H.; Okamoto, K.; Iida, M.; Someya, S.

1995-01-01

The interaction between the high speed flow and the free surfaces could induced surface oscillations. Recently, some kinds of self-induced free surface oscillations caused by water jet were discovered, e.g., a self-induced sloshing, 'Jet-Flutter' and a self-induced manometer oscillation. These oscillations have many different characteristics with each other. In this study, the similarities and differences of these oscillations are examined, and the geometrical effects on the phenomena are experimentally investigated. The self-induced sloshing and the Jet-Flutter have different dimensionless traveling times, which suggests a difference in the energy supply mechanism. When the distance between the inlet and the outlet is small in a vessel, the self-induced manometer oscillation could occur in the multi-free-surface system. (author)

Protective effects of rosmarinic acid on sepsis-induced DNA damage in the liver of Wistar albino rats

Directory of Open Access Journals (Sweden)

Hatice Gul Goktas

2015-06-01

Full Text Available Sepsis is an imbalance between pro and anti-inflammatory responses. Sepsis induced multiple organ failure that is associated with mortality is characterized by liver, renal, cardiovascular and pulmonary dysfunction and reactive oxygen species (ROS are believed to be involved in the development of sepsis. Plant polyphenols may act as antioxidants by different mechanisms such as free radical scavenging, metal chelation and protein binding. Data indicates possible beneficial effects of plant derived phenolic compounds against sepsis. Rosmarinic acid (RA (α-O-caffeoyl-3,4-dihydroxyphenyllactic acid is a phenolic compound commonly found in various plants such as Rosmarinus officinalis (rosemary, Origanum vulgare (oregano, Thymus vulgaris (thyme, Mentha spicata (spearmint, Perilla frutescens (perilla, Ocimum basilicum (sweet basil and several other medicinal plants. It has been shown that RA has many biological activities including antioxidant, anti-inflammatory, antiallergic, anticancer and actimicrobial and is widely used in cosmetic and food industry. In the present study, we aimed to determine the protective effects of RA against the oxidative DNA damage induced by sepsis in Wistar albino rats. The rats were divided into four groups; sham, sepsis induced, RA-treated, RA treated and sepsis induced groups. Wistar rats were subjected to sepsis by cecal ligation puncture. The liver tissues were carefully dissected from their attachments and totally excised. The concentrations of the hepatic tissue cells were adjusted to approximately 2 x 106 cells/ml. Standard and formamidopyrimidine-DNA glycosylase (Fpg modified comet assay described by Singh et al were used. There were no statistically significant differences in terms of tail length, tail intensity and tail moment between the sham group and the RA-treated groups (p>0.05. The DNA damage was found significantly higher in the sepsis-induced group compared to the sham group (p0.05, and the DNA damage

Testosterone Depletion by Castration May Protect Mice from Heat-Induced Multiple Organ Damage and Lethality

Directory of Open Access Journals (Sweden)

Ruei-Tang Cheng

2010-01-01

Full Text Available When the vehicle-treated, sham-operated mice underwent heat stress, the fraction survival and core temperature at +4 h of body heating were found to be 5 of 15 and 34.4∘C±0.3∘C, respectively. Castration 2 weeks before the start of heat stress decreased the plasma levels of testosterone almost to zero, protected the mice from heat-induced death (fraction survival, 13/15 and reduced the hypothermia (core temperature, 37.3∘C. The beneficial effects of castration in ameliorating lethality and hypothermia can be significantly reduced by testosterone replacement. Heat-induced apoptosis, as indicated by terminal deoxynucleotidyl- transferase- mediatedαUDP-biotin nick end-labeling staining, were significantly prevented by castration. In addition, heat-induced neuronal damage, as indicated by cell shrinkage and pyknosis of nucleus, to the hypothalamus was also castration-prevented. Again, the beneficial effects of castration in reducing neuronal damage to the hypothalamus as well as apoptosis in multiple organs during heatstroke, were significantly reversed by testosterone replacement. The data indicate that testosterone depletion by castration may protect mice from heatstroke-induced multiple organ damage and lethality.

The possible DNA damage induced by environmental organic compounds: The case of Nonylphenol.

Science.gov (United States)

Noorimotlagh, Zahra; Mirzaee, Seyyed Abbas; Ahmadi, Mehdi; Jaafarzadeh, Neemat; Rahim, Fakher

2018-08-30

Human impact on the environment leads to the release of many pollutants that produce artificial compounds, which can have harmful effects on the body's endocrine system; these are known as endocrine disruptors (EDs). Nonylphenol (NP) is a chemical compound with a nonyl group that is attached to a phenol ring. NP-induced H 2 AX is a sensitive genotoxic biomarker for detecting possible DNA damage; it also causes male infertility and carcinogenesis. We attempt to comprehensively review all the available evidence about the different ways with descriptive mechanisms for explaining the possible DNA damage that is induced by NP. We systematically searched several databases, including PubMed, Scopus, Web of Science, and gray literature, such as Google Scholar by using medical subheading (MeSH) terms and various combinations of selected keywords from January 1970 to August 2017. The initial search identified 62,737 potentially eligible studies; of these studies, 33 were included according to the established inclusion criteria. Thirty-three selected studies, include the topics of animal model (n = 21), cell line (n = 6), human model (n = 4), microorganisms (n = 1), solid DNA (n = 1), infertility (n = 4), apoptosis (n = 6), and carcinogenesis (n = 3). This review highlighted the possible deleterious effects of NP on DNA damage through the ability to produce ROS/RNS. Finally, it is significant to observe caution at this stage with the continued use of environmental pollutants such as NP, which may induce DNA damage and apoptosis. Copyright © 2018 Elsevier Inc. All rights reserved.

Ganoderma extract prevents albumin-induced oxidative damage and chemokines synthesis in cultured human proximal tubular epithelial cells.

Science.gov (United States)

Lai, Kar Neng; Chan, Loretta Y Y; Tang, Sydney C W; Leung, Joseph C K

2006-05-01

Ganoderma lucidum (Ganoderma or lingzhi) is widely used as an alternative medicine remedy to promote health and longevity. Recent studies have indicated that components extracted from Ganoderma have a wide range of pharmacological actions including suppressing inflammation and scavenging free radicals. We recently reported that tubular secretion of interleukin-8 (IL-8) induced by albumin is important in the pathogenesis of tubulointerstitial injury in the proteinuric state. In this study, we explored the protective effect of Ganoderma extract (LZ) on albumin-induced kidney epithelial injury. Growth arrested human proximal tubular epithelial cells (PTECs) were incubated with 0.625 to 10 mg/ml human serum albumin (HSA) for up to 72 h. HSA induced DNA damage and apoptosis in PTEC in a dose- and time-dependent manner. Co-incubation of PTEC with 4-64 microg/ml LZ significantly reduced the oxidative damage and cytotoxic effect of HSA in a dose-dependent manner (PGanoderma (16 microg/ml). To explore the components of LZ that exhibited most protective effect in HSA-induced PTEC damages, LZ was further separated into two sub-fractions, LZF1 (MW effective in reducing sICAM-1 released from HSA-activated PTEC whereas the high molecular weight LZ (unfractionated LZ) was more effective in diminishing IL-8 production. Our results suggest that Ganoderma significantly reduces oxidative damages and apoptosis in PTEC induced by HSA. The differential reduction of IL-8 or sICAM-1 released from HSA-activated PTEC by different components of the LZ implicates that components of Ganoderma with different molecular weights could play different roles and operate different mechanisms in preventing HSA-induced PTEC damage.

A protective effect of anthocyanins and xanthophylls on UVB-induced damage in retinal pigment epithelial cells.

Science.gov (United States)

Silván, Jose Manuel; Reguero, Marina; de Pascual-Teresa, Sonia

2016-02-01

Increased exposure to solar ultraviolet B (UVB) radiation causes oxidative damage that may promote age related macular degeneration (AMD) and other ocular pathologies. This study is aimed to demonstrate the protective effects of some anthocyanins and xanthophylls against the UVB-induced oxidative damage to retinal pigment epithelial (RPE) cells. ARPE-19 cells were treated with 5 μM cyanidin-3-O-glucoside, delphinidin-3-O-glucoside, lutein, zeaxanthin or a mixture of cyanidin-3-O-glucoside:zeaxanthin prior to UVB exposure (500 J m(-2)). Cell viability and mitogen-activated protein kinase (MAPK) phosphorylation were determined by MTT assay and western blot analysis, respectively. Oxidative damage was evaluated by measuring the intracellular reactive oxygen species (ROS). The data showed that UVB irradiation reduces the cell viability to 46% with increasing of intracellular ROS levels and phosphorylation of MAPKs. However, pre-treatment (60 min) with 5 μM cyanidin-3-O-glucoside, lutein or zeaxanthin significantly reduced cellular ROS levels and phosphorylation of MAPKs (JNK1/2 and p38) mediated by UVB irradiation and subsequently increased cell viability. Thus, results show that UVB irradiation is able to induce apoptosis in ARPE-19 cells through oxidative stress; however anthocyanins and xanthophylls pre-treatment can attenuate this damage. This suggests that cyanidin-3-O-glucoside, lutein and zeaxanthin are effective in preventing UVB-induced damage in RPE cells and may be suitable as chemoprotective factors for the prevention of ocular damage. The use of natural dietary antioxidants might reduce ocular oxidative damage caused by UVB radiation.

Membrane damage induced in cultured human skin fibroblasts by UVA irradiation

International Nuclear Information System (INIS)

Gaboriau, F.; Morliere, P.; Marquis, I.; Moysan, A.; Geze, M.; Dubertret, L.

1993-01-01

Irradiation of cultured human skin fibroblasts with ultraviolet light from 320 to 400 nm (UVA) leads to a decrease in the membrane fluidity exemplified by an enhanced fluorescence anisotropy of the lipophilic fluorescent probe 1-[4-trimethylamino)-phenyl]-6-phenylhexa-1,3,5-triene. This UVA-induced decrease in fluidity is associated with lactate dehydrogenase leakage in the supernatant. Vitamin E, an inhibitor of lipid peroxidation, exerts a protective effect on both phenomena. Therefore, this UVA-induced damage in membrane properties may be related to lipid peroxidation processes. Moreover, exponentially growing cells are more sensitive to these UVA-induced alterations than confluent cells. (Author)

Application of Laser Pulse Heating to Simulate Thermomechanical Damage at Gun Bore Surfaces

National Research Council Canada - National Science Library

Cote, Paul

2003-01-01

Laser pulse heating experiments were performed to provide insights into the thermomechanical damage effects that occur at the surface of coated and uncoated gun steel under cyclic rapid heating and cooling...

Experimental Protoporphyria: Effect of Bile Acids on Liver Damage Induced by Griseofulvin

Directory of Open Access Journals (Sweden)

María del Carmen Martinez

2015-01-01

Full Text Available The effect of bile acids administration to an experimental mice model of Protoporphyria produced by griseofulvin (Gris was investigated. The aim was to assess whether porphyrin excretion could be accelerated by bile acids treatment in an attempt to diminish liver damage induced by Gris. Liver damage markers, heme metabolism, and oxidative stress parameters were analyzed in mice treated with Gris and deoxycholic (DXA, dehydrocholic (DHA, chenodeoxycholic, or ursodeoxycholic (URSO. The administration of Gris alone increased the activities of glutathione reductase (GRed, superoxide dismutase (SOD, alkaline phosphatase (AP, gamma glutamyl transpeptidase (GGT, and glutathione-S-transferase (GST, as well as total porphyrins, glutathione (GSH, and cytochrome P450 (CYP levels in liver. Among the bile acids studied, DXA and DHA increased PROTO IX excretion, DXA also abolished the action of Gris, reducing lipid peroxidation and hepatic GSH and CYP levels, and the activities of GGT, AP, SOD, and GST returned to control values. However, porphyrin accumulation was not prevented by URSO; instead this bile acid reduced ALA-S and the antioxidant defense enzymes system activities. In conclusion, we postulate that DXA acid would be more effective to prevent liver damage induced by Gris.

Impact of helium implantation and ion-induced damage on reflectivity of molybdenum mirrors

Energy Technology Data Exchange (ETDEWEB)

Garcia-Carrasco, A., E-mail: alvarogc@kth.se [Department of Fusion Plasma Physics, Royal Institute of Technology (KTH), Teknikringen 31, 100 44 Stockholm (Sweden); Petersson, P.; Hallén, A. [Department of Fusion Plasma Physics, Royal Institute of Technology (KTH), Teknikringen 31, 100 44 Stockholm (Sweden); Grzonka, J. [Faculty of Materials Science and Engineering, Warsaw University of Technology, 02-507 Warsaw (Poland); Institute of Electronic Materials Technology, 133 Wolczynska Str., 01-919 Warsaw (Poland); Gilbert, M.R. [Culham Centre for Fusion Energy, Culham Science Centre, Abingdon, Oxon OX14 3DB (United Kingdom); Fortuna-Zalesna, E. [Faculty of Materials Science and Engineering, Warsaw University of Technology, 02-507 Warsaw (Poland); Rubel, M. [Department of Fusion Plasma Physics, Royal Institute of Technology (KTH), Teknikringen 31, 100 44 Stockholm (Sweden)

2016-09-01

Molybdenum mirrors were irradiated with Mo and He ions to simulate the effect of neutron irradiation on diagnostic first mirrors in next-generation fusion devices. Up to 30 dpa were produced under molybdenum irradiation leading to a slight decrease of reflectivity in the near infrared range. After 3 × 10{sup 17} cm{sup −2} of helium irradiation, reflectivity decreased by up to 20%. Combined irradiation by helium and molybdenum led to similar effects on reflectivity as irradiation with helium alone. Ion beam analysis showed that only 7% of the implanted helium was retained in the first 40 nm layer of the mirror. The structure of the near-surface layer after irradiation was studied with scanning transmission electron microscopy and the extent and size distribution of helium bubbles was documented. The consequences of ion-induced damage on the performance of diagnostic components are discussed.

Grinding damage assessment for CAD-CAM restorative materials.

Science.gov (United States)

Curran, Philippe; Cattani-Lorente, Maria; Anselm Wiskott, H W; Durual, Stéphane; Scherrer, Susanne S

2017-03-01

To assess surface/subsurface damage after grinding with diamond discs on five CAD-CAM restorative materials and to estimate potential losses in strength based on crack size measurements of the generated damage. The materials tested were: Lithium disilicate (LIT) glass-ceramic (e.max CAD), leucite glass-ceramic (LEU) (Empress CAD), feldspar ceramic (VM2) (Vita Mark II), feldspar ceramic-resin infiltrated (EN) (Enamic) and a composite reinforced with nano ceramics (LU) (Lava Ultimate). Specimens were cut from CAD-CAM blocs and pair-wise mirror polished for the bonded interface technique. Top surfaces were ground with diamond discs of respectively 75, 54 and 18μm. Chip damage was measured on the bonded interface using SEM. Fracture mechanics relationships were used to estimate fracture stresses based on average and maximum chip depths assuming these to represent strength limiting flaws subjected to tension and to calculate potential losses in strength compared to manufacturer's data. Grinding with a 75μm diamond disc induced on a bonded interface critical chips averaging 100μm with a potential strength loss estimated between 33% and 54% for all three glass-ceramics (LIT, LEU, VM2). The softer materials EN and LU were little damage susceptible with chips averaging respectively 26μm and 17μm with no loss in strength. Grinding with 18μm diamond discs was still quite detrimental for LIT with average chip sizes of 43μm and a potential strength loss of 42%. It is essential to understand that when grinding glass-ceramics or feldspar ceramics with diamond discs surface and subsurface damage are induced which have the potential of lowering the strength of the ceramic. Careful polishing steps should be carried out after grinding especially when dealing with glass-ceramics. Copyright © 2017 The Academy of Dental Materials. Published by Elsevier Ltd. All rights reserved.

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage.