Relevant bibliographies by topics / Psychoneuroimmunology; stress; the oxidative model

Academic literature on the topic 'Psychoneuroimmunology; stress; the oxidative model'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Antoni, Michael H. "Stress Management and Psychoneuroimmunology in HIV Infection." CNS Spectrums 8, no. 1 (January 2003): 40–51. http://dx.doi.org/10.1017/s1092852900023440.

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AbstractDoes stress management affect psychological and immune functioning in persons with human immunodeficiency virus infections? Stress-management techniques, such as relaxation training and imagery, cognitive restructuring, coping-skills training, and interpersonal-skills training, may reduce anxiety, depression, and social isolation in HIV-infected persons by lowering physical tension and increasing a sense of control and self-efficacy. A psychoneuroimmunologic model is proposed wherein these psychological changes are hypothesized to be accompanied by an improved ability to regulate neuroendocrine functioning, which in turn may be associated with a partial normalization of immune system functions such as lymphocyte proliferation and cytotoxicity, providing more efficient surveillance of latent viruses that may contribute directly to increased HIV replication and generate opportunistic infections or cancer if left unchecked. Such a normalization of stress-associated immune system decrements are hypothesized to forestall or minimize increases in viral load and expression of clinical symptoms. This model is useful for testing the factors contributing to the health effects of stress-management interventions in HIV-infected persons. In this context, one general research strategy for testing the effects of stress-management interventions is to target them toward the more prevalent psychosocial challenges that HIV-infected people face at various points in the disease process; enroll an HIV-infected population (eg, HIV-positive homosexual and bisexual men) into a randomized trial; and monitor changes in cognitive, affective, behavioral, and social factors in parallel with hormonal, immunologic, viral, and clinical changes over the course of time. This article will review the major psychoneuroimmunologic findings that have emerged using this paradigm and suggest future research directions and clinical applications.
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Koenig, Harold G. "Religion and Medicine III: Developing a Theoretical Model." International Journal of Psychiatry in Medicine 31, no. 2 (June 2001): 199–216. http://dx.doi.org/10.2190/2ybg-nl9t-ek7y-f6a3.

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In this third of a four-article series on religion and medicine, I describe a theoretical model to illustrate the complex pathways by which religion may influence physical health. Genetic factors, childhood training, psychological and social influences, health behaviors, and healthcare practices are discussed as part of this model. Considerable space is given to recent advances in psychoneuroimmunology and to stress-induced cardiovascular changes that demonstrate physiological pathways by which cognitive, emotional, and behavioral processes may influence susceptibility to disease and disease course. I also discuss research illustrating the important role that social support plays in moderating the physiological effects of stress and improving health outcomes. If religious beliefs and practices improve coping, reduce stress, prevent or facilitate the resolution of depression, improve social support, promote healthy behaviors, and prevent alcohol and drug abuse, then a plausible mechanism exists by which physical health may be affected.
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de la Torre-Ruiz, Maria, Nuria Pujol, and Venkatraghavan Sundaran. "Coping With Oxidative Stress. The Yeast Model." Current Drug Targets 16, no. 1 (January 19, 2015): 2–12. http://dx.doi.org/10.2174/1389450115666141020160105.

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Ercal, Nuran, Nukhet Aykin-Burns, Hande Gurer-Orhan, and J. David McDonald. "Oxidative stress in a phenylketonuria animal model." Free Radical Biology and Medicine 32, no. 9 (May 2002): 906–11. http://dx.doi.org/10.1016/s0891-5849(02)00781-5.

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Panayi, Adriana C., Yori Endo, Mehran Karvar, Prerana Sensharma, Valentin Haug, Siqi Fu, Bobin Mi, Yang An, and Dennis P. Orgill. "Low mortality oxidative stress murine chronic wound model." BMJ Open Diabetes Research & Care 8, no. 1 (September 2020): e001221. http://dx.doi.org/10.1136/bmjdrc-2020-001221.

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IntroductionInvestigators have struggled to produce a reliable chronic wound model. Recent progress with antioxidant enzyme inhibitors shows promise, but mortality rates are high. We modified the dosage and administration of an antioxidant enzyme inhibitor regimen to reduce mortality while inducing a chronic wound environment.Research design and methodsTo chemically induce a chronic wound environment, we applied modified doses of catalase (3-amino-1,2,4-triazole; intraperitoneal 0.5 g/kg) and glutathione peroxidase (mercaptosuccinic acid; topical 300 mg/kg) inhibitors to the dorsal wounds of 11-week-old db/db mice. A cohort of these mice was treated with a collagen-glycosaminoglycan scaffold. Both groups were compared with Diabetic control mice.ResultsThis study successfully induced a chronic wound in 11-week-old db/db mice, with no animal deaths. The antioxidant enzyme treated groups showed delayed wound contraction and significantly higher levels of inflammatory tissue, collagen deposition, cellular proliferation and leukocyte infiltration than the Diabetic control group. Angiogenesis was significantly higher in the antioxidant enzyme treated groups, but the vessels were immature and friable. Scaffold engraftment was poor but appeared to promote blood vessel maturation.ConclusionsOverall, the two in vivo groups treated with the antioxidant enzyme inhibitors appeared to be arrested in the inflammatory stage of wound healing, while the Diabetic control group progressed to the maturation phase and ultimately remodeling. This model may be instrumental for the development of new wound therapeutics.
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Adams, James D., Lori K. Klaidman, Carl P. LeBel, and Ifeoma N. Odunze. "Oxidative stress in the brain: A new model." Free Radical Biology and Medicine 9 (January 1990): 92. http://dx.doi.org/10.1016/0891-5849(90)90499-9.

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Breitenbach, Michael. "Oxidative stress and neurodegeneration: the yeast model system." Frontiers in Bioscience 18, no. 3 (2013): 1174. http://dx.doi.org/10.2741/4171.

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Tomás‐Zapico, Cristina, Beatriz Caballero, Verónica Sierra, Ignacio Vega‐Naredo, Óscar Álvarez‐García, Delio Tolivia, María Josefa Rodríguez‐Colunga, and Ana Coto‐Montes. "Survival mechanisms in a physiological oxidative stress model." FASEB Journal 19, no. 14 (September 26, 2005): 2066–68. http://dx.doi.org/10.1096/fj.04-3595fje.

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Oliveira, Renato B., Lázaro Alessandro Soares Nunes, Rodrigo Perroni Ferraresso, René Brenzikofer, Denise Vaz Macedo, and Rodrigo Hohl. "Oxidative Stress of an Endurance Overtraining Animal Model." Medicine & Science in Sports & Exercise 42 (May 2010): 786–87. http://dx.doi.org/10.1249/01.mss.0000386281.00666.6d.

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Fumoto, Toshio, Shouhei Kinoshita, Takao Sasaki, Norihito Shimamura, and Hiroki Ohkuma. "Oxidative Stress Mediates Vascular Tortuosity." Antioxidants 10, no. 6 (June 7, 2021): 926. http://dx.doi.org/10.3390/antiox10060926.

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Vascular tortuosity is associated with various disorders and is being increasingly detected through advances in imaging techniques. The underlying mechanisms for vascular tortuosity, however, remain unclear. Here, we tested the hypothesis that oxidative stress mediates the generation of tortuous vessels. We used the bilateral common carotid artery (CCA) ligation model to induce vascular tortuosity. Both young and adult rats showed basilar artery tortuous morphological changes one month after bilateral CCA ligation. These tortuous changes were permanent but more pronounced in the adult rats. Microarray and real-time PCR analysis revealed that these tortuous changes were accompanied by the induction of oxidative stress-related genes. Moreover, the indicated model in rabbits showed that tortuous morphological changes to the basilar artery were suppressed by antioxidant treatment. These results are highly suggestive of the significance of oxidative stress in the development of vascular tortuosity. Although further studies will be needed to elucidate the possible mechanisms by which oxidative stress enhances vascular tortuosity, our study also points toward possible prophylaxis and treatment for vascular tortuosity.
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Dissertations / Theses on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Vallis, Katherine Anne. "Menadione resistance : a model for cellular defences against oxidative stress." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20853.

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To study the genetic changes which confer resistance to oxidants, cell lines that are resistant to the redox-cycling agent, menadione, have been isolated from Chinese hamster ovary (CHO) and human transitional carcinoma (EJ) parental cell lines. They exhibit cross-resistance to chemical oxidants (hydrogen peroxide and sodium arsenite) but not to ionising radiation (in oxic conditions). The concentrations of the major sources of intracellular thiol groups, glutathione and cysteine, are two-fold greater in menadione-resistant than in the corresponding parental cell lines. Exposure to menadione results in depletion of both glutathione and cysteine but the subsequent recovery of thiols is more rapid and of greater magnitude in menadione-resistant than sensitive cell lines. 1H spin echo nuclear magnetic resonance (NMR) spectroscopy was used to study intact cells. Using this technique the removal of menadione from suspensions of resistant and sensitive cells was observed. However, only in menadione-sensitive cells was concomitant depletion of the NMR-visible pool of glutathione observed. The acquisition of resistance to menadione was associated with significant changes in the expression of several enzymes that are implicated in the oxygen-induced stress response and in protection from redox-cycling agents. The transcription of genes encoding heme oxygenase and the glutathione-related enzymes, GST-Pi and glutathione peroxidase, increases in CHO parental cells after transient oxidative stress. These genes are constitutively induced in CHO menadione-resistant cell lines. This suggests that resistance results from perpetuation of a response that normally occurs only transiently.
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Hälldin, Jonas. "Oxidative stress and alterations in the mammalian iron metabolism : a study on iron, inflammation, oxidative stress and neurodegeneration in cellular model systems /." Stockholm : Department of Neurochemistry, Stockholm University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7037.

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Crisóstomo, Luís Daniel Machado. "Pilot-model for oxidative post-competition recovery in swimmers." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1340.

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Physical exercise have several health benefits, but it can also be a source of cellular damage. The energetic demands of physical exercise and training promote an increase on metabolic rate, and its pathways may produce secondary harmful compounds that will cause cellular damage. Some of those compounds are the free radicals and Reactive Oxygen species, which are highly instable molecules that react quickly, oxidizing important functional molecules such as proteins, membrane lipids and DNA, in a condition known as oxidative stress. To dampen the action of these molecules, the cells express antioxidant defence proteins. One of the most ubiquitous and polymorphic of those is the family of Gluthatione STransferases (GSTs). The great physical load of competitive training creates serious oxidative stress on athletes so, it is expected that their expression of GSTs will vary throughout the season to overcome such aggression, quickly recovering from one training session and preparing the antioxidant defence for the next one. Our main objective was to verify if the expression of a GST (GSTT1) varies throughout the season, as expected theoretically, and how it fluctuates after a competition. We also check if the distribution of the GSTM1 and GSTT1 Null/Present genotypes had some influence in the preparation and performance of our sample, consisting in 20 national level swimmers. A control group of 52 random individuals was also used to compare genotype distribution. We collected blood samples in analytic filter paper, at 5 different moments throughout the winter season. DNA was isolated from a sample of each individual, amplified by PCR for our interest genes, and ran in agarose gel by electrophoresis to genotype our 20 swimmers. RNA was isolated from all the samples of a swimmer and converted in cDNA by reverse transcriptase. The relative expression of GSTT1 was done using β-actin (a housekeeping gene) as a control gene and the first collected sample of the swimmer as control condition, by the RT-PCR technic. Three swimmers were accessed for the whole 5 moments, while eight were only evaluated their expression at 48h and 72h after competition. The results showed little influence in the distribution of genotype from swimmers to controls. The expression results show influence of the GSTT1 expression profile throughout the season and after an intense exercise with sport performance and as a fitness check tool.
O treino desportivo com o objetivo de performance competitiva coloca os atletas sob um forte risco de desequilíbrio oxidativo, conhecido por stress oxidativo. A produção de radicais livres e espécies electrofílicas, como as Espécies Reativas de Oxigénio (ROS), são uma constante no metabolismo normal do organismo, no entanto, a maior taxa metabólica exigida pela demanda energética do exercício físico intenso, provocam uma produção de tais espécies a um nível superior às defesas antioxidantes disponíveis. Nesta situação de stress oxidativo, os radicais livres e ROS provocam danos a fulcrais estruturas e macromoléculas celulares, reagindo forte e rapidamente com estas, ameaçando a homeostasia celular. Para controlar a ação nefasta dessas agressões oxidativas, os organismos possuem mecanismos de defesas antioxidantes, podendo estas ser de origem endógena ou exógena. Entre as defesas antioxidantes endógenas encontram-se proteínas expressas pelas células, e cuja expressão pode ser influenciada pelo ambiente oxidativo celular, como é o caso das Glutationa S-Transferases (GST). Desta forma, situações que criem stress oxidativo, como no treino desportivo, ativam a expressão das defesas antioxidantes. Assim sendo, o treino desportivo regular e bem planeado, de forma a evitar danos constantes ao organismo, deve ativar uma resposta deste de forma a protege-lo dessa agressão, preparando-o previamente para essa agressão. Essa preparação pode ser verificada através da expressão génica de fatores antioxidantes endógenos. Além disso, certos genótipos podem revelar-se vantajosos nesta proteção, nomeadamente os genótipos associados às várias isoformas das GSTs. Nestes, constam vários e frequentes genótipos Null (ausência do gene), o que permite uma grande variabilidade entre indivíduos para a disponibilidade de isoformas de GSTs. O objetivo deste trabalho foi precisamente verificar a distribuição de genótipos Null/Present para duas isoformas de GSTs, a GSTM1 e a GSTT1, numa amostra de 20 nadadores portugueses de nível nacional. Para comparação de genótipos, foi recolhida semelhante informação a partir de um grupo de controlo constituído por 52 indivíduos aleatórios. Além disso, observou-se a expressão relativa de GSTT1 ao longo de 5 momentos distintos ao longo da época de Inverno (preparação geral, preparação específica, fase taper e dois momentos pós-competição) em 3 desses atletas, e a expressão relativa, também de GSTT1, 48h e 72h após uma competição, para 8 desses atletas. Para conseguir alcançar isto, foi necessário montar uma técnica totalmente nova para recolher as amostras de forma rápida, fiável e praticável nas condições de treino, e otimizar todos os procedimentos laboratoriais para conseguir processar essas amostras de forma eficiente e rigorosa. As amostras foram recolhidas em papel de filtro de análises clínica, através de uma picada no dedo dos nadadores, antes do início do treino do dia definido previamente para recolha de amostras. As amostras foram ainda conservadas em invólucros individuais para cada recolha a cada momento e de cada atleta, numa câmara-fria 4°C, no Centro de Investigação em Ciências da Saúde (CICS) da Faculdade de Ciências da Saúde (FCS) da Universidade da Beira Interior (UBI). Para genotipagem dos nadadores em amostra, DNA foi extraído da amostra de sangue em papel utilizando o método do Chelex 100. Após extração, o DNA foi usado para amplificação enzimática da sequência específica dos genes da GSTM1 e GSTT1, pela técnica de PCR. Por fim, os resultados foram corridos por electroforese em gel de agarose, usando Green-safe como fator de marcação de DNA, e os resultados foram visualizados à luz ultravioleta num transiluminador. A presença de GSTM1 foi identificada pela presença de uma banda com cerca de 215bp, enquanto a presença de GSTT1 foi identificada pela presença de banda aos 473bp. Para análise da expressão génica, RNA foi isolado a partir das amostras de sangue em papel, pelo método do Trizol. O RNA era correspondente a cada um dos momentos de recolha. De seguida o RNA foi convertido a cDNA através da técnica de transcriptase reversa, utilizando a enzima M-MLV. Por fim, o cDNA foi amplificado pela técnica de RT-PCR, para o gene GSTT1, tendo ainda como controlo a amplificação da β-Actin, também para cada um dos momentos de recolha e fazendo duplicados por uma questão de rigor. A expressão foi calculada através das curvas de amplificação de RT-PCR e utilizando o método ΔΔCT. Não foram encontradas distribuições de genótipos GSTM1 e GSTT1 Null/Present estatisticamente significativas entre a nossa amostra de teste e o grupo de controlo. No contexto da expressão relativa de GSTT1, verificou-se que variações muito acentuadas ao longo da época desportiva ou após um exercício foram prejudiciais à performance física dos nadadores. Encontramos também algumas diferenças na recuperação das nadadoras, mantendo uma expressão mais alta e por um maior período de tempo após o exercício físico intenso que os homens. Além disso, verificou-se uma tendência para os indivíduos GSTM1 Null manterem os níveis de expressão relativa de GSTT1, ao longo da época e após um exercício intenso, mais estáveis, o que parece favorecer o seu rendimento. Conclui-se ainda que a análise da evolução da expressão relativa de GSTT1 em vários treinos, após uma competição ou outro exercício de elevada intensidade, pode ajudar a perceber qual a forma atual de um nadador.
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Hung, T. H. "In vitro hypoxia-reoxygenation as a model for placental oxidative stress in preeclampsia." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604788.

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Oxidative stress of the placenta is considered a key intermediary step in the pathogenesis of preeclampsia, but the cause for the stress remains unknown. Ischaemia-reperfusion injury, as a result of intermittent placental perfusion secondary to deficient trophoblast invasion of the endometrial arteries, is a possible mechanism. This thesis therefore tests whether hypoxia-reoxygenation (H/R) in vitro can induce placental oxidative stress, and cause increased apoptosis and production of tumour necrosis factor-α as seen in the preeclamptic placenta. The first aim was to examine the oxidative status of human placental tissues during periods of hypoxia and reoxygenation in vitro. Rapid generation of reactive oxygen species (ROS) was detected using a fluorescent marker when hypoxic villous samples were reoxygenated. The expression of oxidative stress markers including nitrotyrosine residues, 4-hydroxy-2-nonenal adducts, and inducible heat shock protein 72 was greatly increased in villous samples subjected to H/R compared to the controls maintained under constant hypoxia. Furthermore, preloading villous samples with ROS scavengers such as desferrioxamine and α-phenyl-N-tert-butylnitrone significantly reduced the levels of oxidative stress in H/R. Having demonstrated that in vitro H/R is capable of inducing oxidative stress in a reproducible and manipulable manner, investigations were next carried out to study the effects of resultant oxidative stress on apoptosis within the trophoblast. Compared to hypoxic and normoxic controls, there was a significant increase in the release of cytochrome c from mitochondria, activation of caspase , and cleavage of poly (ADP-ribose) polymerase in villous samples subjected to H/R. These events were associated with an increased number of syncytiotrophoblastic nuclei displaying apoptotic changes and increased lactate dehydrogenase release into the medium. The causal relationship between the generation of ROS and these apoptotic changes was revealed by the fact that pre-administration of desferrioxamine attenuated the insult.
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Millican, Stephanie A. "Human vascular endothelial cells in culture : a model system for studying oxidative stress." Thesis, University of Aberdeen, 1993. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU554288.

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Cell culture systems were used to investigate the mechanisms of oxidant-induced cellular damage. The Girardi heart cell line was used to investigate possible mechanisms of ischaemic cell damage whilst human endothelial cells derived from the umbilical vein (HUVEC) were used to study the direct cellular effects of hydrogen peroxide (H2O2). A number of parameters including cytosolic enzyme leakage, ATP content and DNA and protein synthesis were used to assess cell damage. Girardi cells were found to be resistant to the effects of oxygen deprivation. In contrast, HUVEC were sensitive to H2O2 and concentrations of H2O2 250M resulted in irreversible cell damage. Irreversible damage produced by H2O2 was dependent upon the initial exposure time of the cells to H2O2, the cellular metabolism of H2O2 and the possible conversion of H2O2 to the hydroxyl radical via the iron catalysed Fenton reaction. Catalase activity was not detectable in HUVEC. In contrast, HUVEC contained relatively high concentrations of reduced glutathione (GSH) which decreased, with growth, during culture and were also reduced by the experimental treatment conditions. Cell damage appeared to occur independently of cellular GSH, however depletion of GSH with butathione sulfoximine, to below 10&'37 of control values did potentiate cytotoxicity in response to H2O2. Depletion of ATP, alone, did not correlate with irreversible cell damage. However, cells could recover from oxidant damage as long as the capability to synthesise ATP was maintained. The main mechanism by which ATP was depleted was via the activation of poly (ADP-ribose)polymerase, as demonstrated by the ability of 3-Aminobenzamide to prevent ATP depletion and cell lysis. The mechanism for this activation is most likely to be a consequence of hydroxyl radical-induced damage to DNA. However, activation of poly(ADP-ribose)polymerase was not the only mechanism which accounted for the depletion of ATP and a H2O2-dependent pathway appeared to exist.
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Zhong, Wenwen. "Protection against oxidative stress in human endothelial cells in an in vitro diabetes model." Thesis, University of Hull, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431079.

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Duggan, Simon. "The role of mitochondria and oxidative stress in a model of coronary artery disease." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761669.

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Alinde, Olatogni Berenice Lidwine. "Effects of red palm oil-supplementation on oxidative stress biomarkers in an experimental rat model." Thesis, Cape Peninsula University of Technology, 2012. http://hdl.handle.net/20.500.11838/2257.

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Thesis (MTech (Biomedical Technology))--Cape Peninsula University of Technology, 2012.
Oxidative stress, in recent times appears to be a major underlying risk factor in the occurrence of various diseases such as cardiovascular disease (CVD) and ischemic heart disease (IHD). During oxidative stress, there is an imbalance between the production of reactive oxygen species (ROS) and antioxidant defence mechanisms in favour of ROS. This results in severe cellular damages in the heart, vascular membranes and other organs. Potential benefits of dietary supplements as one of the major quenching elements against oxidative stress have been highlighted. Thus, a growing interest has been stimulated in finding natural alternatives for the treatment and! or prevention of oxidative stress-mediated diseases. Red palm oil (RPO), refined from the tropical plant Elaeis guineensis was used in this study since it has captivated much attention in the health sector lately. The effects of RPO-supplementation on oxidative stress biomarkers as well as homocysteine, a cardiovascular disease risk factor in an oxidative stress-induced rat model were investigated in this in vivo study. All experiments were conducted for a period of six weeks. Male Wistar rats (120-150g) were randomly divided into six groups (n=5) where all the rats received a standard diet. Two groups (groups C, D) were supplemented with 0.175g RPO (7g RPO/kg chow) for four weeks whereas groups (groups E, F) were given 0.175g RPO (7g RPO/kg chow) supplementation for six weeks. Rats in control groups (groups A, B) were not given any RPO-supplementation. Groups B, 0, F were induced with oxidative stress by injection of 0.5ml (20IlM/100g of body weight) organic tertiary-butyl hydroperoxide. All parameters were determined using appropriate methods in plasma, serum and erythrocytes. Data were expressed as mean ± SEM. No significant differences were obtained between groups for total antioxidant capacity and glutathione peroxidase activity. Red palm oil supplementation significantly increased superoxide dismutase activity after 6 weeks consumption, total glutathione levels after 4 weeks consumption and homocysteine levels after four and six weeks consumption in rats not subjected to oxidative stress. Under oxidative stress conditions, malondialdehyde (MOA) level, a marker of oxidative stress related damage, significantly increased in rats receiving a standard diet. However, when RPO diet was supplemented for 4 and 6 weeks, MOA levels significantly decreased towards the value of normal controls. In conclusion, our findings suggest that RPO-supplementation could ameliorate antioxidant status in the body through its potential ability to increase some antioxidant enzymes activity. Similarly, it is suggested that RPO-supplementation could protect the rat against oxidative stress induced damage in diseased state.
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Miller, Rebecca Louise. "The mechanism for paraquat toxicity involves oxidative stress and inflammation a model for Parkinson's disease /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4764.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2007" Includes bibliographical references.
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Du, Plessis Michelle. "The role of carnitine in eukaryotic cells : Using yeast as a model." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97946.

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Thesis (MSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: Previous studies in yeast in this laboratory have found carnitine to be both protective against oxidative stress induced by hydrogen peroxide and to increase the detrimental effect of dithiothreitol. These phenotypes were found to be independent of the role of carnitine within the carnitine shuttle. A screen for suppressor mutations for these carnitine-dependent phenotypes identified, among others, Δcho2 and Δopi3. Cho2p and Opi3p catalyse the sequential methylation reactions in the formation of phosphatidylcholine from phosphatidylethanolamine. Therefore, this study aimed to investigate the relationship between choline, phosphatidylcholine and the carnitine phenotypes. Liquid growth assays of Δcho2 and Δopi3 cultures revealed that addition of choline can restore the protective effects of carnitine against hydrogen peroxide. The connection between the cellular phospholipid composition and the carnitine-dependent shuttleindependent phenotypes was also investigated. Analysis of the lipid composition of cells by LCMS showed that Δcho2 and Δopi3 had a largely different lipid composition compared with the wild type, most notably, a reduction in phosphatidylcholine and an increase in triacylglycerol content were observed for both mutants. These changes were reversed by supplementation with choline. However, no effects on the lipid composition of cells in response to carnitine treatment were observed, either when supplemented alone or in combination with DTT and hydrogen peroxide. Carnitine has also been investigated in mammalian systems for its potential to protect cells from oxidative stress, an effect which would be of benefit in various neurodegenerative disorders. Several studies have documented the positive effects of carnitine against oxidative stress in mammalian cells however the mechanism behind this action remains unknown. It is therefore thought that, provided similar effects for carnitine can be shown in mammalian cells as was observed in yeast, it would be beneficial to use yeast as a model system for the study of the molecular changes induced by carnitine. In view of this, the effects of carnitine on toxicity induced by oxidative stress in mammalian neural cells were compared to that which has been observed in yeast. For this purpose the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, a measure of reductive capacity of cells, was used. However, no effects for carnitine were observed in the MTT assay in combination with either dithiothreitol or paraquat.
AFRIKAANSE OPSOMMING: Vorige studies op gis in hierdie laboratorium het bevind dat karnitien beskermend is teenoor oksidatiewe stres wat deur waterstofperoksied geïnduseer word en ook die nadelige effek van ditiotreitol verhoog. Hierdie fenotipes is gevind om onafhanklik te wees van die rol van karnitien binne die karnitien-pendel. Die sifting vir onderdrukker-mutasies van hierdie karnitienafhanklike fenotipes het onder andere Δcho2 en Δopi3 geïdentifiseer. Cho2p en Opi3p kataliseer die opvolgende metileringsreaksies tydens die vorming van fosfatidielcholien vanaf fosfatidieletanolamien. Hierdie studie het dus gepoog om die verhouding tussen cholien, fosfatidielcholien en die karnitienfenotipes te ondersoek. Vloeistofanalises van Δcho2- en Δopi3-kulture het aangedui dat die byvoeging van cholien die beskermende effekte van karnitien teenoor waterstofperoksied kan herstel. Die verband tussen die sellulêre fosfolipiedsamestelling en die karnitienafhanklike pendel-onafhanklike fenotipes is ook ondersoek. Die analise van die lipiedsamestelling van selle deur middel van LCMS het getoon dat Δcho2 en Δopi3 ‘n grootliks verskillende samestelling het in vergelyking met die wilde tipe, en daar is veral ‘n afname in fosfatidielcholien en ‘n verhoging in triasielgliserol-inhoud vir beide mutante waargeneem. Hierdie veranderinge is omgekeer deur aanvulling met cholien. Geen effekte op die lipiedsamestelling van die selle is egter in reaksie op die karnitienbehandelings waargeneem nie, hetsy toe dit alleen aangevul is of in kombinasie met ditiotreitol en waterstofperoksied. Karnitien is ook in soogdierstelsels ondersoek vir sy potensiaal om selle teen oksidatiewe stres te beskerm, ‘n effek wat groot voordeel sal inhou vir verskeie neurodegeneratiewe steurings. Verskeie studies het reeds die positiewe effekte van karnitien teen oksidatiewe stres in soogdierselle opgeteken, hoewel die meganisme agter hierdie werking nog onbekend is. Daar word dus vermoed dat, gegewe dat soortgelyke effekte vir karnitien in soogdierselle getoon kan word as wat in gis waargeneem is, dit voordelig sou wees om gis as ‘n modelsisteem vir die studie van die molekulêre veranderinge wat deur karnitien geïnduseer word, te gebruik. In die lig hiervan is die effekte van karnitien op giftigheid wat deur oksidatiewe stres in soogdiersenuselle geïnduseer is, vergelyk met dít wat in gis waargeneem is. Om hierdie rede is die 3-[4,5-dimetieltiasool-2-iel]-2,5-difeniel tetrasoliumbromied (MTT) essaiëring, ‘n meting van die verminderende kapasiteit van selle, gebruik. Geen effekte vir karnitien is egter met die MTT essaiëring in kombinasie met óf ditiotreitol óf parakwat waargeneem nie.
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Books on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Miwa, Satomi, Kenneth Bruce Beckman, and Florian Muller. Oxidative Stress in Aging: From Model Systems to Human Diseases. Humana, 2010.

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Miwa, Satomi, Kenneth Bruce Beckman, and Florian Muller. Oxidative Stress in Aging: From Model Systems to Human Diseases. Humana Press, 2008.

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Satomi, Miwa, Beckman Kenneth B, and Muller Florian L, eds. Oxidative stress in aging: From model systems to human diseases. New York: Springer, 2008.

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Freitas, Rivelilson Mendes de. Antioxidant Treatments: Effect on Behaviour, Histopathological and Oxidative Stress in Epilepsy Model. INTECH Open Access Publisher, 2012.

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Book chapters on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Minami, M., N. Hamaue, M. Hirafuji, H. Saito, T. Hiroshige, A. Ogata, K. Tashiro, and S. H. Parvez. "Isatin, an endogenous MAO inhibitor, and a rat model of Parkinson’s disease induced by the Japanese encephalitis virus." In Oxidative Stress and Neuroprotection, 87–95. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-33328-0_10.

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Gomez-Cabrera, Mari Carmen, Fabian Sanchis-Gomar, Vladimir Essau Martinez-Bello, Sandra Ibanez-Sania, Ana Lucia Nascimento, Li Li Ji, and Jose Vina. "Exercise as a Model to Study Oxidative Stress." In Studies on Experimental Models, 531–42. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-956-7_26.

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del Carmen Baez, María, Mariana Tarán, Mónica Moya, and María de la Paz Scribano Parada. "Oxidative Stress in Metabolic Syndrome: Experimental Model of Biomarkers." In Modulation of Oxidative Stress in Heart Disease, 313–38. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7_12.

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Farooqui, Tahira. "Molecular Basis of Iron-induced Oxidative Stress in the Honeybee Brain: A Potential Model System of Olfactory Dysfunction in Neurological Diseases." In Oxidative Stress in Vertebrates and Invertebrates, 295–307. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118148143.ch21.

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Furnari, Melody, Constance L. L. Saw, Ah-Ng T. Kong, and George C. Wagner. "Animal Model of Autistic Regression: Link to Toxicant-Induced Oxidative Stress." In Oxidative Stress in Applied Basic Research and Clinical Practice, 393–416. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0440-2_19.

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Morita, Manabu, Daisuke Ekuni, and Takaaki Tomofuji. "Association Between Oxidative Stress and Periodontal Diseases in Animal Model Studies." In Studies on Periodontal Disease, 33–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9557-4_3.

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Conway, Brian, and Harout Tossonian. "HIV/AIDS – A Model of Chronic Oxidative Stress and Immune Activation." In Systems Biology of Free Radicals and Antioxidants, 3217–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_149.

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Carail, Michel, Pascale Goupy, Eric Reynaud, Olivier Dangles, and Catherine Caris-Veyrat. "Oxidative Cleavage Products of Lycopene: Production and Reactivity in a Biomimetic Experimental Model of Oxidative Stress." In ACS Symposium Series, 191–205. Washington, DC: American Chemical Society, 2013. http://dx.doi.org/10.1021/bk-2013-1134.ch016.

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Yfanti, Christina, Søren Nielsen, Camilla Scheele, and Bente Klarlund Pedersen. "Exercise as a Model to Study Interactions Between Oxidative Stress and Inflammation." In Studies on Experimental Models, 521–29. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-956-7_25.

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Hastings, Teresa G., and Michael J. Zigmond. "Neurodegenerative Disease and Oxidative Stress: Insights from an Animal Model of Parkinsonism." In Neurodegenerative Diseases, 37–46. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0209-2_6.

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Conference papers on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Sridharan, S., R. Layek, A. Datta, and J. Venkatraj. "Boolean network model of oxidative stress response pathways." In 2012 American Control Conference - ACC 2012. IEEE, 2012. http://dx.doi.org/10.1109/acc.2012.6315168.

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Umriukhin, Pavel, Natalia Veiko, Elizaveta Ershova, Galina Shmarina, Andrey Martynov, Anton Filev, Anastasia Poletkina, et al. "OXIDATIVE DNA MODIFICATION IN EXPERIMENTAL STRESS MODEL IN VIVO." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m588.sudak.ns2019-15/418-419.

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Mizutani, T., A. Sato, A. Watanabe, Y. Hamakawa, K. Uemasu, N. Tanabe, S. Sato, and T. Hirai. "Susceptibility to Oxidative Stress Characterizes Phenotypes in Murine Model of BPD." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5488.

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Ghanian, Zahra, Sepideh Maleki, Sandeep Gopalakrishnan, Reyhaneh Sepehr, Janis T. Eells, and Mahsa Ranji. "Optical imaging of oxidative stress in retinitis pigmentosa (RP) in rodent model." In SPIE BiOS, edited by Gerard L. Coté. SPIE, 2013. http://dx.doi.org/10.1117/12.2004843.

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Tai, Wan-Yu, Yi-Cyun Yang, Ian Liau, P. M. Champion, and L. D. Ziegler. "Raman Spectroscopy Reveals the Structure-Fluidity Interplay of Model Lipid Membranes under Oxidative Stress." In XXII INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY. AIP, 2010. http://dx.doi.org/10.1063/1.3482736.

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ONUFRIEV, MIKHAIL, MIKHAIL STEPANICHEV, LYUDMILA CHERNYAVSKAYA, NATALIA LAZAREVA, YULIA MOISEEVA, and NATALIA GULYAEVA. "CORRELATIONS BETWEEN OXIDATIVE STRESS, APOPTOSIS AND SEIZURES: STUDIES USING KAINIC ACID MODEL IN RAT." In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0026.

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Pannu, N., and A. Bhatnagar. "102 Inhibitory effect of resveratrol on oxidative stress in murine model of systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.102.

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Lowe, Jack, Ian Adcock, and Coen Wiegman. "Oxidative stress and mitochondrial dysfunction in a novel in vivo exacerbation model of severe asthma." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4083.

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"A Plant Model for Assessing Arsenic Phytotoxicity: Effect on Growth and Oxidative Stress Response Molecules." In 5th International Conference on Agriculture, Environment and Biological Sciences. International Academy of Arts, Science & Technology, 2016. http://dx.doi.org/10.17758/iaast.a0416001.

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Thacher, Tyler, Rafaela da Silva, Paolo Silacci, and Nikos Stergiopulos. "Autonomous Effects of Shear Stress and Cyclic Circumferential Stretch Regarding Endothelial Dysfunction and Oxidative Stress: An Ex Vivo Arterial Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205503.

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Within the vasculature endothelial cells are constantly exposed to dynamic mechanical forces generated by pulsatile blood flow. Two stimuli known to modulate endothelial function are shear stress and cyclic circumferential strain. Yet, in most studies these two stimuli are simultaneously coupled in-vivo, making it very difficult to understand their individual contributions to vascular disease. Some attempts have been made to de-couple stretch and shear stress in-vitro by using different cell lines in a variety of stretch systems and flow chambers, straying from reality and making it hard to draw definitive conclusions. In this study we wish to find a compromise between the in-vivo and in-vitro work of the past by studying the independent effects of shear stress and cyclic stretch and how they contribute to endothelial dysfunction.
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Reports on the topic "Psychoneuroimmunology; stress; the oxidative model"

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Handa, Avtar K., Yuval Eshdat, Avichai Perl, Bruce A. Watkins, Doron Holland, and David Levy. Enhancing Quality Attributes of Potato and Tomato by Modifying and Controlling their Oxidative Stress Outcome. United States Department of Agriculture, May 2004. http://dx.doi.org/10.32747/2004.7586532.bard.

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General The final goal and overall objective of the current research has been to modify lipid hydroperoxidation in order to create desirable phenotypes in two important crops, potato and tomato, which normally are exposed to abiotic stress associated with such oxidation. The specific original objectives were: (i) the roles of lipoxygenase (LOX) and phospholipids hydroperoxide glutathione peroxidase (PHGPx) in regulating endogenous levels of lipid peroxidation in plant tissues; (ii) the effect of modified lipid peroxidation on fruit ripening, tuber quality, crop productivity and abiotic stress tolerance; (iii) the effect of simultaneous reduction of LOX and increase of PHGPx activities on fruit ripening and tuber quality; and (iv) the role of lipid peroxidation on expression of specific genes. We proposed to accomplish the research goal by genetic engineering of the metabolic activities of LOX and PHGPx using regulatable and tissue specific promoters, and study of the relationships between these two consecutive enzymes in the metabolism and catabolism of phospholipids hydroperoxides. USA Significant progress was made in accomplishing all objectives of proposed research. Due to inability to regenerate tomato plants after transforming with 35S-PHGPx chimeric gene construct, the role of low catalase induced oxidative stress instead of PHGPx was evaluated on agronomical performance of tomato plant and fruit quality attributes. Effects of polyamine, that protects DNA from oxidative stress, were also evaluated. The transgenic plants under expressing lipoxygenase (LOX-sup) were crossed with catalase antisense (CAT-anti) plants or polyamine over producing plants (SAM-over) and the lines homozygous for the two transgenes were selected. Agronomical performance of these line showed that low catalase induced oxidative stress negatively affected growth and development of tomato plants and resulted in a massive change in fruit gene expression. These effects of low catalase activity induced oxidative stress, including the massive shift in gene expression, were greatly overcome by the low lipoxygenase activity. Collectively results show that oxidative stress plays significant role in plant growth including the fruit growth. These results also for the first time indicated that a crosstalk between oxidative stress and lipoxygenase regulated processes determine the outcome during plant growth and development. Israel Regarding PHGPx, most of the study has concentrated on the first and the last specific objectives, since it became evident that plant transformation with this gene is not obvious. Following inability to achieve efficient transformation of potato and tomato using a variety of promoters, model plant systems (tobacco and potato cell cultures, tobacco calli and plantlets, and Arabidopsis) were used to establish the factors and to study the obstacles which prohibited the regeneration of plants carrying the genetic machinery for overproduction of PHGPx. Our results clearly demonstrate that while genetic transformation and over-expression of PHGPx occurs in pre-developmental tissue stage (cell culture, calli clusters) or in completed plant (Arabidopsis), it is likely that over-expression of this enzyme before tissue differentiation is leading to a halt of the regeneration process. To support this assumption, experiments, in which genetic engineering of a point-mutated PHGPx gene enable transformation and over-expression in plants of PhSPY modified in its catalytic site and thus inactive enzymatically, were successfully carried out. These combined results strongly suggest, that if in fact, like in animals and as we established in vitro, the plant PHGPx exhibits PH peroxidase activity, these peroxides are vital for the organisms developmental process.
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Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.

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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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