Дисертації з теми "Stress modulation"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 дисертацій для дослідження на тему "Stress modulation".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Переглядайте дисертації для різних дисциплін та оформлюйте правильно вашу бібліографію.
Chung, K. K. K. "Modulation of the response to stress by serotonin." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597687.
Повний текст джерелаLunga, Precious. "Modulation of the adaptation to stress by oestrogen." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619878.
Повний текст джерелаMoore, Anthony Norman. "Selenium modulation of gut epithelial cell stress responses." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3679.
Повний текст джерелаRodrigues, Maria Carolina Costa e. Santos Baptista. "Modulation of mitochondrial stress response by sestrin 2." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15410.
Повний текст джерелаAs mitocôndrias são organelos altamente dinâmicos com um papel crucial na homeostase celular. Uma rede de mitocôndrias funcionais é mantida por processos de biogénese e mitofagia, regulando desta forma o conteúdo e o metabolismo mitocondriais. Espécies reactivas de oxigénio (ROS) são formadas como consequência do processo normal de fosforilação oxidativa mitocondrial, desempenhando um papel importante na sinalização redox e regulação da função celular. Um aumento ligeiro na formação de ROS mitocondrial desencadeia o fenómeno de hormese mitocondrial, uma resposta adaptativa ao estado metabólico celular, ao stress e outros sinais intracelulares ou ambientais. Este mecanismo induz maior resistência a um stress posterior, tendo por isso efeitos benéficos para a saúde. Compostos que são tóxicos em doses maiores são conhecidos por induzir adaptações mitocondriais em doses mais baixas. O excesso de equivalentes redutores fornecidos à cadeia transportadora de electrões (ETC) em condições de sobrenutrição/inactividade física ou danos acumulados/defesas antioxidantes mais baixas associadas com o envelhecimento, causam um aumento nas taxas de produção de ROS, provocando stresse oxidativo e danos irreversíveis em proteínas, lípidios e DNA. A disfunção mitocondrial resultante é permanente e compromete o estado energético de todo o organismo, aumentando a susceptibilidade a lesões, provocando a aceleração do envelhecimento e desenvolvimento de doenças metabólicas, tais como a resistência à insulina e fígado gordo. Um dos principais reguladores do sistema de defesa antioxidante celular é a Sestrina 2 (SESN2), induzida em condições de stress. A diminuição da actividade da SESN2 está associada a um aumento de danos oxidativos, disfunção mitocondrial, degeneração muscular e acumulação de gordura, resultando num envelhecimento mais rápido dos tecido. No entanto, os mecanismos pelos quais a SESN2 afecta as funções mitocondriais não estão definidos. A compreensão dos mecanismos moleculares e de como a SESN2 afecta a mitocôndria, pode fornecer novas pistas para alvos terapêuticos, a fim de atenuar e prevenir o envelhecimento e as patologias relacionadas com a obesidade. Tendo em conta isto, este trabalho teve como objectivo avaliar se a SESN2 medeia uma resposta mitocondrial adaptativa protectora, desencadeada pela exposição de células C2C12 a menadiona, um estimulador da formação de aniões superóxido. Adicionalmente, e tendo em conta que a Sirtuina 1 (SIRT1) é um conhecido sensor metabólico e regulador da função mitocondrial, este estudo avaliou de que forma a modulação de SIRT1 afecta a SESN2 no contexto de fígado gordo induzido por uma dieta rica em gordura. Os resultados obtidos mostram um efeito da menadiona, dependente da dose, na viabilidade celular e a função mitocondrial. O tratamento com 10 μM de menadiona durante 1 h não alterou a formação de ROS, redução do MTT e o potencial de membrana mitocondrial, como avaliado 24 e 48 horas após a remoção de menadiona. No entanto, a exposição de células C2C12 a 30 μM menadiona durante 1 h, resultou no aumento da formação de ROS, diminuiu a redução do MTT e o potencial de membrana mitocondrial. Um aumento no conteúdo de SESN2 foi observado após 10 h de exposição a 10 μM de menadiona durante 1 h, enquanto 30 μM de menadiona resultou na diminuição do conteúdo em SESN2. Estes resultados sugerem que a indução de SESN2 por stress moderado, induzido pela menadiona, pode activar uma resposta mitocondrial protetora que preserva a viabilidade celular. O silenciamento da SESN2 com siRNA resultou num aumento da morte celular, bem como numa diminuição no potencial de membrana mitocondrial induzida por ambas as concentrações de menadiona, sendo mais drásticas as alterações induzidas por 30 μM. Na presença de SESN2, a exposição a menadiona causou um aumento no padrão pontuado de distribuição de LC3, indicando a indução de autofagia. Contrariamente, a depleção de SESN2 com siRNA resultou numa diminuição da pontuação de LC3, quer em condições controlo quer após a exposição a menadiona. Colectivamente estes resultados sugerem que o stress moderado provocado pela menadiona induz a SESN2 e activa autofagia/mitofagia como uma estratégia de sobrevivência celular. A ausência de SESN2 resultou na acumulação de dano mitocondrial induzido por ROS e consequente diminuição da viabilidade celular. Em relação ao impacto da modulação da SIRT1 na SESN2, os resultados obtidos mostram que a expressão hepática do factor de transcrição c/EBPα (proteína alfa potenciadora de ligação CCAAT) foi estimulada pela dieta rica em gordura (HFD) e reduzida pelo tratamento com resveratrol, um activador da SIRT1. Em ratinhos sem SIRT1 (SIRT1 - KO) a expressão c/EBPα estava diminuída comparativamente ao controlo. A expressão hepática de SESN2 apresentou-se reduzida em animais HFD e SIRT1 - KO. O tratamento com resveratrol, em animais controlo, preveniu a diminuição da SESN2 induzida por HFD. A expressão de KEAP1 (proteína kelch 1 associada a ECH) também se verificou dependente de SIRT1, sendo que, em ratinhos SIRT1-KO, o tratamento com resveratrol não induziu nenhuma alteração em KEAP1. A degradação de KEAP1 é promovida pela SESN2, permitindo a translocação de Nrf2 (factor nuclear derivado de eritróide 2) para o núcleo e, consequentemente, a indução de genes antioxidantes. A expressão hepática de Nrf2 não foi afetada pela modulação de SIRT1. O envelhecimento diminuiu a expressão de todos os genes estudados. Em conclusão, este trabalho demonstrou que a indução de SESN2 por stress ou compostos promotores de homeostase mitocondrial, como o resveratrol, aumenta a tolerância mitocondrial ao dano, através da modulação da autofagia/mitofagia. A estimulação da eliminação de mitocôndrias lesadas pela SESN2, pode ser uma via para evitar a acumulação de danos e, portanto, resultar num aumento da tolerância à sobrenutrição e ao envelhecimento.
Mitochondria are highly dynamic organelles with a crucial role in cellular homeostasis, with processes of biogenesis and mitophagy regulating mitochondrial content and metabolism and maintaining functional mitochondrial networks. Reactive oxygen species (ROS) are formed as a consequence of normal mitochondrial oxidative phosphorylation and are involved in redox signalling and regulation of cellular function. A mild increase in mitochondrial ROS triggers mitochondrial hormesis, an adaptive retrograde response to cellular metabolic state, stress and other intracellular or environmental signals that culminate in subsequently increased stress resistance with health promoting effects. Compounds that are toxic at higher doses are known to induce mitochondrial adaptations at lower doses. Overflow of reducing equivalents to the electron transport chain (ETC) under conditions of overnutrition/physical inactivity or accumulated damage/lower antioxidant defenses associated with aging, causes higher rates of ROS formation, resulting in oxidative stress and irreversible damage to proteins, lipids, and DNA. As a result, permanent mitochondrial dysfunction compromises whole-body energetic status and increases susceptibility to injuries, resulting in accelerated aging and development of metabolic diseases such as insulin resistance and fatty liver. One of the main regulators of the cellular antioxidant defense system is Sestrin 2 (SESN2), which is induced by several stress conditions. Decreased SESN2 activity is associated with increased oxidative damage, mitochondrial dysfunction, muscle degeneration and fat accumulation. However, the mechanisms by which SESN2 affects mitochondrial functions are not defined. Understanding the molecular mechanisms and how SESN2 affects mitochondria may provide new insights for novel therapeutic targets for attenuation and prevention of aging and obesity-related pathologies. In view of this, this work aimed to evaluate if SESN2 mediates an adaptive protective mitochondrial response in C2C12 cells triggered by menadione, a stimulator of superoxide anion formation. Additionally, and since Sirtuin 1 (SIRT1) is a known metabolic sensor and regulator of mitochondrial function, this work evaluated how modulation of SIRT1 affects SESN2 in the context of fatty liver induced by a high-fat diet. Results showed a dose-dependent effect of menadione on cellular viability and mitochondrial function. Treatment with 10 μM menadione for 1 h did not alter ROS formation, MTT reduction and mitochondrial membrane potential, as evaluated 24 and 48 h after menadione removal. However, exposure of C2C12 cells to 30 μM menadione for 1 h resulted in increased ROS generation, reduced MTT reduction and mitochondrial membrane potential. An increase in SESN2 content was observed 10 h after exposure to 10 μM menadione for 1 h, while 30 μM menadione resulted in SESN2 depletion. These results suggest that induction of SESN2 by mild stress induced by menadione may be involved in a mitochondrial protective response that preserves cell viability. SESN2 silencing with siRNA resulted in increased cellular death as well as a decrease in mitochondrial membrane potential induced by both concentrations of menadione, being more potent the alterations induced by 30 μM menadione. In presence of SESN2, exposure to menadione caused an increase in the punctuated pattern of LC3 (microtubule-associated protein 1A/1B-light chain 3 - PE phosphatidylethanolamine) distribution, showing induction of autophagy. However, depletion of SESN2 with siRNA resulted in a decrease in LC3 punctuation, both in control and menadione conditions. Altogether these results suggest that mild stress induced by menadione induces SESN2 and activates autophagy/mitophagy as a cell survival strategy. Absence of SESN2 results in accumulation of mitochondrial damage induced by ROS and consequent decrease in cell viability. Regarding the impact of SIRT1 modulation on SESN2, results showed that hepatic expression of transcription factor c/EBPα (CCAAT-enhancer-binding protein - α) was up-regulated by high-fat diet (HFD) and down-regulated by resveratrol treatment, a SIRT1 activator. In SIRT1-knock-out (SIRT1 - KO) mice c/EBPα expression was decreased when compared to control. SESN2 expression was reduced by HFD and SIRT1-KO. Resveratrol treatment in wild-type animals prevented the decrease in SESN2 induced by HFD. KEAP1 (Kelch-like ECH-associated protein 1) expression was also dependent on SIRT1 and resveratrol treatment showed no effect on KEAP1 in SiRT1-KO mice. KEAP1 degradation is promoted by SESN2 and when degraded, induces Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) translocation to the nucleus and consequently induction of antioxidant genes. Hepatic Nrf2 expression was not affected by SIRT1 modulation. Aging decreased the expression of all of the evaluated genes. The current work shows that SESN2 induction by mild stress or promotors of mitochondrial homeostasis, such as resveratrol acting on SIRT1, increase mitochondrial tolerance to damage, through modulation of autophagy/mitophagy. Elimination of damaged mitochondria is stimulated by SESN2 and may be the pathway to prevent accumulation of damage and thus result in increased tolerance to overnutrition and extend lifespan.
Lockwood, Donovan Blair. "TDP-43 Modulation of PABP Positive, RNA Stress Granule Formation during Oxidative Stress." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579304.
Повний текст джерелаNsiah, Barbara Akua. "Fluid shear stress modulation of embryonic stem cell differentiation." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/47552.
Повний текст джерелаVentura, Emilie. "Stress oxydant et vieillissement : modulation de la NADPH oxydase." Montpellier 2, 2008. http://www.theses.fr/2008MON20128.
Повний текст джерелаOxidative stress is the result of an imbalance between production of oxidants and antioxidant defense mechanisms. The NADPH oxidase is a key enzyme for excessive production of oxidants, strengthening the interest of its modulation. NADPH oxidase is involved in the initiation and progression of age-related diseases such as cardiovascular diseases and dementia. Through an epidemiological study consisted of 517 subjects (79. 5 ± 7. 1 years), we determined NADPH oxidase activation and its main determinants with age. Among the factors tested, homocysteine and inflammation were significantly associated with NADPH oxidase activity in a multivariate analysis. These data are confirmed in vitro because homocysteine thiolactone and lipopolysaccharide induce a dose-dependent activation and expression of NADPH oxidase in cell line THP-1. In an in vitro on THP-1 and animal studies, we studied the negative modulation of the NADPH oxidase by natural antioxidants (polyphenols) and enzymatic antioxidants (melon extract rich in SOD and catalase). These nutritional antioxidants negatively modulate the activity but also the expression of NADPH oxidase. In conclusion, NADPH oxidase activity is associated with age and is positively regulated by inflammation and homocysteine. The superoxide anion production is associated with cardiovascular and neurodegenerative diseases. NADPH oxidase may be modulated in vitro by natural antioxidants. Links with dementia, cardiovascular disease or mortality must be further study. The antioxidant supplements efficiency must be clarified in animal models and then on a clinical study
Javadi, Hamed H. "Stress induced modulation of edema during cutaneous wound healing." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1413364771.
Повний текст джерелаQiu, Ye. "Modulation and roles of stress-responsive proteins in coxsackievirus infection." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62935.
Повний текст джерелаMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Wainberg, Zev Aryeh. "Stress protein modulation in HIV-1 infected CD4-expressing cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29807.pdf.
Повний текст джерелаWainberg, Zev. "Stress protein modulation in HIV-1 infected CD4-expressing cells." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27432.
Повний текст джерелаHarris, Jessica Lynn. "INVESTIGATIONS INTO MODULATION OF BRAIN OXIDATIVE STRESS BY VARIOUS INTERVENTIONS." UKnowledge, 2012. http://uknowledge.uky.edu/chemistry_etds/12.
Повний текст джерелаBunyard, Peter Robert. "Modulation of dendritic cell maturation by ribotoxic and oxidative stress." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271744.
Повний текст джерелаPerez, Emilie. "Communicating about stress : modulation of vocalisations in the zebra finch." Thesis, Saint-Etienne, 2013. http://www.theses.fr/2013STET4026/document.
Повний текст джерелаIn social species, vocalisations convey information that participates in the maintenance and the survival of the group. While many studies were interested in stable information carried by vocal signals, like identity, fewer studies dealt with their potential role in informing about labile information such as the senders’ emotional state. Stress is a good candidate for the study of the expression of emotions in animals, as it is directly measurable by the plasma levels of glucocorticoïds. Stress is known to modify acoustic parameters of vocalisations in mammals, but few studies studied the process in birds, that also show complex social networks. The aim of this thesis is thus to determine how birds can vocally express their stress and to what extent corticosterone, the main stress hormone in birds, is implicated in this expression. I focused my research on the zebra finch (Taenopygia guttata), a gregarious Australian songbird that form lifelong pairbond and provides biparental care to its young. Using oral administration of exogenous corticosterone but also social stressful events, we show that both adult males and nestlings can express their stress through modulations of their calls’ structure, suggesting that flexibility in birds’ vocalisations is higher than previously expected. With a complete analysis of temporal and spectral parameters of calls, we show for the first time that stress evokes the emission of vocalisations with up-shifted frequency spectrum via a direct effect of corticosterone. Moreover, we show that females and parents are able to decode the information carried by stressed-induced calls of respectively their male partner and their young, as they exhibit modifications of behaviour in accordance with the context. The physical processes leading to the emission of stressed-induced vocalisations are discussed by applying the source-filter theory usually used in mammals. Adaptive values are also proposed, in regards with the zebra finch social network and predation risks for the caller. This work gives new evidences about the expression of stress in birds, and proposes a comprehensive study, from the physiological signals involved in stress to the resulting modifications of communication behaviour for the sender, that leads to an adaptive response from the receivers
Bouzidi, Mohamed Salah. "Stress cellulaire et modulation de l'activité des cytidines désaminases APOBEC3." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066597/document.
Повний текст джерелаAPOBEC3 proteins (A3A-A3H) catalyse the deamination of cytosine (C) to thymidine (T) on single stranded DNA. This activity, called cytidine deaminase, has initially been described as a mechanism involved in restriction against retroviruses and DNA viruses by massively inducing C->T mutations on viral genome : this phenomenon is called "hypermutations". Nevertheless, this activity is not virus-specific and some A3 can induce mutations on mitochondrial DNA (A3A, C, F, G, H) and nuclear DNA (A3A and A3B). Thus, the impact of those proteins on cancer formation is now established in cancers where mutations mostly show an APOBEC3 signature. In view of those considerations, we decided to study how those enzymes are regulated in the context of a viral cellular stress or an endogenous cellular stress. The first part of our work is focused on A3DE, the only APOBEC3 lacking a cytidine deaminase activity. Interestingly, A3DE is upregulated in cirrhotic livers infected by HBV, HCV or coinfected with HBV & HCV. We show that A3DE inhibits A3F & A3G activity by interacting with those HBV restriction involved A3. Then, we studied the attributes of the genotoxicity potential of A3B. This protein, by his strictly nuclear localization, constitutes the only double domain A3 which is not regulated by A3DE. Unlike A3A, A3B is weakly active on nuclear DNA and does not induce double strand breaks. We determine by directed mutagenesis the clusters of A3B involved in genotoxicity attenuation compared with A3A. We also show that this attenuation is conserved among primates. Finally, we investigated the role and regulation of A3A in the context of DNA catabolism. We proved that mitochondrial cytoplasmic DNA (mtcyDNA) triggers the RIG-I/DNA polymerase III pathway, which induces IFN production leading to A3A expression. So A3A will be involved in mtcyDNA catabolism and contribute to the clearance of this stress signal, but will also induce double strand breaks on nuclear DNA. A3 are major enzymes of the innate immune response and DNA catabolism. We show that A3DE modulates A3F and A3G activity while A3B is attenuated among primates and is less genotoxic than A3A. A3A participates to cytoplasmic DNA catabolism and limits inflammation. Nevertheless, A3A could be dangerous for the genomic integrity and contributes to cancer, especially in cases of chronic inflammation
Qiao, Shuxi. "Pharmacological Modulation of Oxidative and Proteotoxic Stress for Antimelanoma Intervention." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/311348.
Повний текст джерелаKurz, Michael Wayne. "Nutritional modulation of immunity and physiological responses in beef calves." Thesis, Texas A&M University, 2004. http://hdl.handle.net/1969.1/1096.
Повний текст джерелаThomas, Audrey. "Effet sur le microenvironnement tumoral d’une modulation pharmacologique du stress oxydant." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T086/document.
Повний текст джерелаSeveral reports have demonstrated the involvement of reactive oxygen species (ROS) in carcinogenesis, through promotion of cancer cell proliferation and invasion. But ROS could also have consequences on non cancerous cells which are part of the tumor microenvironment, such as immune cells. Therefore, a pharmacological modulation of oxidative stress can induce a cytotoxic effect on tumor cells but its consequences on microenvironment are unknown. The aim of our studies was to evaluate the effects of a pharmacological modulation of oxidative stress on immune cells from the tumor microenvironment. At low dose, Arsenic trioxide (As203), an oxidative stress modulator, was shown to exert antitumor effects in colon tumor-bearing mice. We observed that this effect was related to As203-induced regulatory T cells (Tregs) -selective depletion in vitro and in vivo and was mediated by oxidative and nitrosative bursts. The differential effect of As203 on Tregs versus other CD4 cells was related to difference in the cells’redox status. We also observed that vinorelbine, an anticancer agent, could interfere with the antitumor immune response. We showed that vinorelbine could alter the function of immune cells surrounding tumor cells by a bystander toxic effect against tumor effector cells. In vivo experiment in A549 tumor bearing nude mice showed that adoptive transfer of A549 immune splenocytes was not able to delay tumor growth when vinorelbine-pretreated A549 cells were used for immunization. This effect was mediated by ROS and was inhibited by an oxidative stress modulator, mangafodipir, which restored antitumor immune function. Therefore, our work showed that oxidative stress modulators can influence tumor microenvironment and more specifically, immune cells. They could be used to restore antitumor immune response
Khaper, Neelam. "Modulation of oxidative stress and antioxidants by losartan in heart failure." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ62645.pdf.
Повний текст джерелаDe, Haaij Yolanda. "Modulation of oxidative stress parameters in healthy volunteers by strenuous exercise." Diss., Pretoria : [s.n.], 2006. http://upetd.up.ac.za/thesis/available/etd-07312007-153855.
Повний текст джерелаSarna, Lindsei. "Regulation of oxidative stress and its modulation by natural health products." NRC Research Press, 2010. http://hdl.handle.net/1993/30624.
Повний текст джерелаOctober 2015
Nagam, Satya Mohan Babu. "Effect of Thyroid Modulation on Arsenic-Induced Oxidative Stress in Zebrafish." Thesis, Southern Illinois University at Edwardsville, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1549814.
Повний текст джерелаIt is well known that environmental contaminants such as arsenic can induce oxidative stress in fish. It is also known that thyroid hormone status affects susceptibility to oxidative stress. However, the effect of thyroid hormone status on pollutant- induced oxidative stress is unknown. This is significant, because such knowledge would help to assess the risk of xenobiotics such as arsenate, a prevalent contaminant in the environment. The interaction between arsenate- induced oxidative stress and altered thyroid hormones has not been elucidated thoroughly in previous studies. In order to address this, we used zebrafish (Danio rerio). There are many advantages of using this as a research model over rodents such as rats. For example, it is often used to study the effects of xenobiotic compounds such as arsenic. This xenobiotic is widespread in the environment due to human activities such as agricultural, industrial and military activities. For this purpose, it is more appropriate to use this fish as a research model. The reason for using the chemicals perchlorate and arsenic is that they occur together in the environment. Oxidative stress can be caused by environmental pollutants such as arsenic. One of the key defenses against oxidative stress is glutathione (GSH). GSH concentrations, GSSG/GSH ratios, and lipid peroxidation (TBARS) were used to assess the affect of arsenic, perchlorate and thyroxine (T4) on zebrafish (Danio rerio) liver, gills, and muscle tissue. Our results support the hypothesis that thyroid hormones modulates the toxicity of arsenic. Moreover, arsenite was found to cause oxidative stress as reflected by GSH levels, GSSG/GSH levels, and lipid peroxidation (TBARS). Although hypothyroidism caused by perchlorate did not cause any major difference on oxidative stress, but hyperthyroidism caused by treating the fish with T4 enhanced GSH levels. This shows that thyroxine is involved in response to oxidative stress. In addition, perchlorate abrogated or reversed the affects of arsenite on oxidative stress parameters. These results support the hypotheses that thyroid hormones modulate oxidative stress in general, and arsenite-mediated oxidative stress in particular.
Lopardo-Spehner, Véronique. "Stress et immunomodulation : modulation de l'activation des macrophages murins apres stress experimental et role de l'immunomodulation therapeutique." Besançon, 1996. http://www.theses.fr/1996BESA3703.
Повний текст джерелаGriffon, Céline. "Modulation et rôle des paramètres hémorhéologiques dans la physiopathologie de la drépanocytose." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1278/document.
Повний текст джерелаThe first goal of this thesis (Study 1 and 2) was to improve the use and the comprehension of tools for red blood cell (RBC) deformability measurements in sickle cell disease (SCD). The first study showed the importance of standardization of RBC deformability measurements by ektacytometry in SCD children. In the study 2, the RBC proprieties was modified and the variation of « classic » RBC deformability curve (elongation index as a function of the shear stress in isotonic medium) was compared to osmoscan results (elongation index in hyperosmolar gradient and constant shear stress), the gold standard for RBC membrane defect studies. Thus, the modifications of RBC deformability curve above 3 Pa were affected by RBC internal viscosity and cellular surface modification (and thus surface/volume ratio) while membran elasticity modifications affected RBC deformability whatever the shear stress (low, moderate or high). The second goal of this thesis was to study the effects of genetic modifiers, hemorheological parameters and oxidative stress level on vaso-occlusive complications (VOC) in SCD (Study 3 to 6). Hemorheological parameters were measured on 165 patients from Lyon and 240 patients from Gwada and the results showed that blood viscosity increased until the age of 30 and RBC deformability decreased with age (Study 3). This modifications probably play role in the chronic complications of SCD adult patients. The studies 4 and 5 were conducted on SCD children. We studied the effects of genetic modifiers (alpha-thalassemia, glucose-6-phospho-deshydrogenase deficiency and S haplotypes ; study 3) and nitro-oxidative stress level (study 5). Alpha-thalassemia increase RBC deformability and RBC aggregation. This phenomenon could contribute to increase VOC. Moreover, alpha-thalassemia decreased hemolysis and thus oxidative stress, a major component of SCD physiopathology. Then the study 6 showed that Sbeta+ patient hemorheology was quite the same of AA ubjects but the more severe patients could have a defect in circulating nitric oxide. To conclude, my thesis contribute to a better understanding of SCD physiopathology
Qin, Yongjun. "Gene expression in identified rat hippocampal neurons modulation by corticosteroids and stress /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/73991.
Повний текст джерелаTroakes, Claire. "The neurobiology of anxiety : pharmacological modulation and programming by early life stress." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423721.
Повний текст джерелаElizalde, Violeta Serra. "Modulation of telomere length by oxidative stress in vitro and in vivo." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366579.
Повний текст джерелаHanlon, Amy. "Stress and release : chemical modulation of secondary metabolite production in Aspergillus sp." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37692.
Повний текст джерелаIncludes bibliographical references (leaf 18).
Cyclosporin A induced biosynthesis of colored compounds in three species of Aspergillus. Diode array HPLC MS analysis of culture extracts revealed Aspergillus terreus demonstrated the most profound response, with upregulation of more then twelve compounds from three distinct chemical families; butyrolactones, aspulvinones, and asterriquinones. Compounds from these three families are prenylated, and biosynthetically derived from homodimers of amino acids. The majority of the upregulated compounds were the aspulvinones, a class of butenolides. Structural elucidation of four isolated aspulvinones revealed both known and novel structures. Inducer concentration had a significant impact on aspulvinone profile. Bioassay revealed previously unreported antibacterial activity for the aspulvinones. A high-throughput colorimetric screen was designed to probe the response. The screen of 2480 known bioactives revealed multiple compounds capable of inducing aspulvinone production, and one compound, rapamycin, capable of inhibiting the response. Additionally, the increase in aspulvinone production was correlated with a decrease in culture density, indicating aspulvinone production is a general stress response.
by Amy Hanlon.
S.M.
Francisco, Ngiambudulu Mbandu. "Modulation of postprandial oxidative stress by rooibos (aspalathus linearis) in normolipidaemic individuals." Thesis, Cape Peninsula University of Technology, 2010. http://hdl.handle.net/20.500.11838/1469.
Повний текст джерелаConsumption of sucrose with a meal containing oxidised and oxidisable lipids cause an increase in oxidative stress which is referred to as postprandial oxidative stress. The modulating effect on postprandial oxidative stress by an antioxidant-rich beverage, fermented rooibos (Aspalathus linearis) was compared to that of a commercial soft drink (soda). Both study beverages contained sucrose and were consumed with a standardised fat meal. The study consisted of two parts, a pilot study (Phase One) where participants consumed either a standardised fat meal with water (control group n = 5) or a standardised fat meal with a sucrose-containing commercial soda (treatment group n = 8) using a parallel design, and the experimental study (Phase Two) where participants (n = 14) consumed the standardised fat meal with the commercial soda (control group) or the rooibos beverage (treatment group) using a crossover design. Specific analytical techniques and methods for determination of plasma glucose, serum insulin, lipid profile, an inflammatory indicator (high sensitive C-reactive protein), plasma antioxidant capacity, whole blood redox status and plasma lipid oxidation biomarkers were used. Results from the pilot study indicated significantly (P<0.05) higher postprandial levels of glucose in the control group at 4 hr and 6hr postprandially. The inflammatory biomarker and triglyceride levels were significantly (P<0.05) elevated in both groups when compared to their respective baselines. Results also showed the total antioxidant capacity and total glutathione levels in the plasma of both groups to be significantly (P<0.05) lowered when compared to the baseline values. The level of lipid oxidation biomarkers in the plasma was significantly (P<0.05) higher at 2 hr, 4 hr and 6 hr post time intervals for thiobarbituric acid reactive substances and 4 hr post time interval for conjugated dienes in the participants consuming the standardised fat meal with soda when compared to the baseline value, while this was reflected only at 2 hr post time interval for thiobarbituric acid reactive substances, with the conjugated dienes levels being significantly (P<0.05) lowered at 6 hr post time interval in the control group. No differences were shown on inter group level for the pilot study. On inter group level, results from Phase Two showed significant (P<0.05) lower levels of plasma glucose at 6 hr post time interval in the treatment group when compared to the control group, with insulin levels being significantly (P<0.05) higher in the control group at 4 hr post time interval.
Chu, Xiaohong. "Restraint Stress Modulation of The Murine Humoral Response to Influenza A Virus /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487933648648752.
Повний текст джерелаPayet, Olivier. "Modulation des transporteurs rétiniens du glutamate par l'ischémie et le stress oxydant." Montpellier 2, 2003. http://www.theses.fr/2003MON20129.
Повний текст джерелаKirkland, Scott, and University of Lethbridge Faculty of Arts and Science. "Modulation of recovery and compensation after stroke." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2007, 2007. http://hdl.handle.net/10133/387.
Повний текст джерелаxii, 122 leaves : ill. ; 29 cm.
Mason, Kathryn. "Modulation of central noradrenaline efflux by pharmacological and novel environmental stimuli : a microdialysis study." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264181.
Повний текст джерелаMerlot, Elodie. "Modulation de la production de cytokines par l'environnement social et susceptibilité aux infections." Paris, Institut national d'agronomie de Paris Grignon, 2003. https://pastel.archives-ouvertes.fr/pastel-00000790.
Повний текст джерелаIn social species, social environment contributes to the development and expression of diseases. Indeed, the social position in a group modulates susceptibility to infections. However, the endocrine and immune mechanisms involved in these differences are not known. Furthermore, instability in the social organisation generates a severe stress of which immune consequences are still controversial. The purposes of this thesis are (1) to describe the influence of social status on the endocrine and immune systems, (2) to specify the effects of social stress on cytokine production and susceptibility to infections and (3) to look for possible sources of variability in the immune consequences of social stress. Excepted a single study on piglets, experiments were performed in mice. Results show an influence of social status. In the absence of stress, dominants show higher basal corticosterone levels and specific response to tuberculin than subordinates. After social defeat, dominants are more affected. Social defeat increases inflammatory reactivity but does not clearly modify the balance between Th1 and Th2 cytokines production and does not affect the development of specific immunity against a mycobacterial infection. Immune effects of social defeat can be observed only when the stress involves significant fights and injuries. Our work also shows that the response to stress depends on individual social experience, in particular on social status, and on the recent immune experience of the individual
Nephew, Benjamin Charles. "Simultaneous modulation of behavioral, cardiovascular, and corticosterone responses to acute stress, with an emphasis on arginine vasotocin /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2003.
Знайти повний текст джерелаAdviser: L. Michael Romero. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 158-180). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
Bless, Yo-Neal. "Modulation of brassica rapa L. antioxidant activities by exogenous methylglyoxal under zirconium stress." University of the Western Cape, 2016. http://hdl.handle.net/11394/4961.
Повний текст джерелаWith a decrease in water availability and arable land, and the ever-increasing reports of toxic chemical pollutants, it is crucial to elucidate plants’ mechanisms of adaptability to these abiotic stressors. South Africa alone accounts for approximately 30% of global Zirconium (Zr) production. However, reports on Zr-induced stress in plants are sparse. Increased mining activity leads to soil contamination which subsequently has harmful effects on crop plants. Under normal conditions B. rapa crop plants flourish, they are rapid in their cycling and circumvent the seed dormancy stage which enables them to have high yields over relatively short periods. However, when unfavourable conditions arise, such as exposure to toxic chemicals and metal ions like Zirconium, the development and growth of B. rapa L., much like other crop plants is affected. More specifically, the damaging effects of Zr is not only attributed directly; as with substitutions of biometals [like Iron (Fe)] in various biomolecules rendering them inactive, but more as a consequence of the production of toxic molecules such as reactive oxygen species (ROS) and methylglyoxal (MG). ROS such as superoxide anion (O₂⁻) and hydrogen peroxide (H₂O₂ ) are known to have signalling roles in plants with reports on their involvement in alleviating seed dormancy and seedling development. However, the signalling roles of MG are not known with regards to plant cells and have been reported more so in animal cells; playing vital roles in fat signalling in diseases such as diabetes. Furthermore MG, in plant and animal cells, directly converts oxygen (O₂) to O₂⁻ and thus increases the cell’s oxidative imbalance, leading to cell damage if O₂⁻ is not rapidly dismutated to H₂O₂ and H₂O by superoxide dismutase (SOD). In turn, H₂O₂ is more stable than O₂⁻ and consequently is more toxic to cells over time. Therefore, H O must be removed as well by a collection of enzymes, such as ascorbate peroxidase (APX) and catalases (CAT). In this study, possible stress-signalling of MG in seedlings under normal conditions and Zr-stress were investigated to establish whether MG at a low dose (6 μM) would benefit seedling growth and development, via a proposed preinduction of the B. rapa L. antioxidant system. Therefore, it was proposed that ROS accumulation due to the exogenous application of MG, would incite the activation of antioxidants and thus mitigate the effects of Zr stress. Physiological tests to determine dry weights (figure 3.2.3) and germination percentage (figure 3.2.2) revealed that MG-treated seedlings yielded an improved biomass and early development compared to Zr-treated seedlings and the control. Membrane damage as assessed by lipid peroxidation viz. Malondialdehyde [MDA] (figure 3.2.4) and conjugated dienes [CD] (figure 3.2.5) also indicated less damage in MG-treated seedlings compared to the Zr-treated set. The chlorophyll content observed was prominent (table 3.1). MG-treated seedlings exhibited a 40% and 15.5% increase compared to Zr-treated seedlings and the control respectively. Moreover cell viability had improved in MG-treated seedlings compared to the control, and in MG+Zr-treated seedlings only a slight increase in cell death occurred despite Zr being present. O₂⁻, H₂O₂ and •OH (figure 4.2.1 – 4.2.3) were investigated in B. rapa L. seedlings in response to Zr and MG by spectrophotometric biochemical assays, as well as their scavenging enzymes, MG accumulation and Gly-I activity. Furthermore, BrGLY1 gene expression and Zr-uptake by ICP-OES were performed. Seedlings treated with MG and Zr respectively showed an increase in ROS. However, all of the ROS observed in MG+Zr-treated seedlings were markedly lower compared to Zr-treated seedlings. SOD and CAT activity observed in MG+Zr-treated seedlings had decreased compared to Zr-treated seedlings, whereas APX activity had increased. Gly-I activity and BrGlyI gene expression had increased across all treatments, showing an elicited response to oxidative stress, due to the observed upregulation, as a result of the accumulated MG. The observed Zr-uptake in MG+Zr-treated seedlings was inhibited by 5-fold compared to Zr-treated seedlings. Clear signs of stress were evident in seedlings treated with Zr compared to the control and MG- treated seedlings, the MG-supplemented (MG and MG+Zr) seedlings displayed a vast improvement comparatively. Modulation of antioxidant activity observed in this study is indicative of an incited response to oxidative stress (figure 4.2.4 – 4.2.6). MG revealed distinct involvement in stress-signalling, ROS levels had increased, although not as severely as with Zr-treated seedlings, but seemingly enough to activate antioxidants without eliciting damage. Furthermore, the proposed early-onset activation of antioxidants has been observed in B. rapa L. seedlings of this study, and as such has resulted in improved growth, development and seed germination. The results of this study has therefore negated the previous reports on MG-toxicity (at high concentrations), and has shed light on further properties of this ubiquitous and inevitably-occurring metabolite at low levels.
National Research Foundation (NRF)
Sinal, Christopher J. "Isozyme-selective modulation of cytochrome P450 by mechanism-based inactivation and pathobiological stress." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ31118.pdf.
Повний текст джерелаAlexandre, Jérôme. "Applications thérapeutiques d'une modulation pharmacologique du stress oxydatif intracellulaire au cours du cancer." Paris 5, 2006. http://www.theses.fr/2006PA05D038.
Повний текст джерелаHydrogen peroxyde is necessary to cellular proliferation but is toxic at high concentrations. Tumor cells are submitted to severe oxidative, close to toxic threshold, increasing their sensitivity to pharmacologic compounds able to increase intracellular concentration of hydrogen peroxide. Placlitaxel induces an early hydrogen peroxide accumulation which is significantly involved in its antitumoral effect, in vitro and in vivo. Mangafodipir, a superoxide dismutase (SOD) mimic, increases the hydrogen peroxide production in tumor cells and enhances the antitumoral effect of paclitaxel. Moreover, it is able the hematologic toxicity of paclitaxel in vivo. This differential effect of mangafodipir seems to be related to its dual activity, SOD and glutathione reductase, responsible for an antioxidant effect in non-tumoral cells
MERLOT, Élodie. "Modulation de la production de cytokines par l'environnement." Phd thesis, Institut national agronomique paris-grignon - INA P-G, 2003. http://tel.archives-ouvertes.fr/tel-00007518.
Повний текст джерелаcontribue largement au développement et à l'expression de maladies. Dans les espèces sociales, la position sociale occupée dans le groupe module la susceptibilité aux infections mais les supports endocriniens et immunitaires de ces différences de susceptibilité sont ignorés. La remise en cause de l'organisation sociale engendre un stress important dont les conséquences immunitaires sont encore sujettes à controverse.
Ce travail de thèse a pour objectifs (1) de décrire l'influence du statut social sur le fonctionnement des systèmes endocrinien et immunitaire, (2) de préciser les effets du stress
social sur la production de cytokines et la susceptibilité aux infections et (3) de rechercher des facteurs à l'origine de la variabilité des conséquences immunitaires du stress social.
Chez le porcelet, un regroupement après le sevrage élève transitoirement le cortisol salivaire et altère le comportement mais n'affecte pas la réactivité des lymphocytes sanguins.
La suite des travaux a utilisé une procédure de défaite sociale chronique chez la souris. Les résultats obtenus mettent en évidence une influence du statut social. En absence de stress, les
dominants présentent des niveaux de base de corticostérone et une réponse spécifique à la tuberculine supérieurs aux dominés. Suite à une défaite sociale, les dominants sont plus affectés que les dominés. La défaite sociale augmente la réactivité inflammatoire mais ne modifie pas de façon nette l'équilibre de la production de cytokines de type Th1 et Th2 et n'affecte pas l'immunité spécifique développée contre une infection mycobactérienne. Les conséquences immunitaires de la défaite sociale ne sont observées que lorsque le stress est associé à des combats et à des blessures. Ces travaux montrent que la réponse au stress dépend de l'histoire sociale de l'individu, en particulier de son statut social. De plus, les
répercussions immunitaires du stress dépendent aussi de l'histoire immunitaire récente. En effet, une réaction inflammatoire systémique inhibe la libération plasmatique de cytokines
inflammatoires en réponse à un stress psychologique ultérieur.
Feairheller, Deborah Lynn. "Race-Dependent Modulation of Endothelial Cell Responses to Shear Stress: Implications for Vascular Health in African Americans." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/121935.
Повний текст джерелаPh.D.
It is known that African American ethnicity is an independent risk factor for exaggerated oxidative stress which is intricately intertwined with inflammation, hypertension (HT), and cardiovascular disease (CVD). The purpose of this dissertation study was to examine the racial differences that exist between African Americans and Caucasians in oxidative stress levels at the molecular level using an in vitro model of Human Umbilical Vein Endothelial Cells (HUVECs). African American HUVECs were found to have significantly higher baseline levels of oxidative stress in vitro compared to Caucasian HUVECs. In order to establish proof of concept, three preliminary studies were conducted. The first preliminary study, an acute exercise protocol was conducted in young healthy adults in order to measure plasma oxidative stress markers in response to a single moderate intensity treadmill exercise bout. In this study, it was found that the treadmill exercise did not elicit a race-dependent responses, but that African American adults had higher level of oxidative stress at all sample times when compared to the Caucasians. A second preliminary study was conducted using a parallel cell culture design to measure basal oxidative stress levels in African American and Caucasian HUVECs without stimulation. These data were shown in relation to the plasma levels of oxidative stress in resting African American and Caucasian adults. This was done in order to show that the common oxidative stress markers measured in human plasma can also be measured in cell culture supernatant and lysate. It was found that both African American adults and HUVECs had heightened oxidative stress and inflammatory markers when compared to their Caucasian counterparts. The third preliminary study was conducted using tumor Necrosis Factor-#945; (TNF-#945;) as an inflammatory stimulant and measuring the oxidative stress response in both African American and Caucasian HUVECs. This was done in order to show that cells of different race respond differently to stimuli. It was found that the response to TNF-α was blunted in African American HUVECs. The final step was to use laminar shear stress (LSS) as an exercise mimetic in order to examine whether HUVECs from different race respond differently. HUVECs from both race were harvested under static condition (no LSS), with low LSS at 5 dyne/cm2, and with a moderate level of LSS at 20 dyne/cm2. It was found that despite the fact that African American HUVECs had higher levels of oxidative stress under static conditions, when LSS was applied, protein expressions and oxidative stress biomarkers adjusted to levels that were similar to the Caucasian HUVEC adaptations to LSS. From this, it appears that African American HUVECs have a larger response to LSS stimulus indicating that aerobic exercise prescriptions may be valuable for this population since the potential exists for large improvements in oxidative stress levels for this population.
Temple University--Theses
Strömberg, Jessica. "Sex and stress steroid modulation of GABA mediated chloride ion flux in rat CNS." Doctoral thesis, Umeå universitet, Obstetrik och gynekologi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1056.
Повний текст джерелаBrown, Erin. "Modulation of intracellular GSH in THP-1 cells during oxidative stress induced by AAPH." Thesis, University of Canterbury. School of Biological Sciences, 2006. http://hdl.handle.net/10092/2629.
Повний текст джерелаAzoulay, Nelson. "Epigenetic modulation of glucocorticoid receptors in posttraumatic stress disorder: examining child vs. adult trauma." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104876.
Повний текст джерелаLe TSPT est un syndrome dévastateur qui touche entre 7 et 12% de gens qui vivent un événement traumatique. Les personnes qui souffrent du syndrome ont un axe HPA dysfonctionnel avec moins de cortisol salivaire et une augmentation de sensitivité des récepteurs glucocorticoïdes. Il y a récemment eu des études épigénétiques qui ont montré une association entre les traumas et les effets sur l'axe HPA chez des patients abusés qui ont commis un suicide. De plus, les résultats indiquent qu'un trauma durant l'enfance est un facteur significatif pour la méthylation d'ADN dans la région promoteur 1F de l'hippocampe. Cette thèse présente le possible rôle modulateur de l'épigénétique des récepteurs glucocorticoïdes chez les personnes touchées du TSPT tout en examinant les effets du temps du trauma. Les résultats montrent que les individus qui souffrent du TSPT ont moins de cortisol salivaire le matin, une augmentation des récepteurs glucocorticoïdes et une augmentation de niveaux de méthylation totale dans la région promoteur 1C du sang. Il semblerait aussi qu'un trauma vécu durant l'âge adulte soit plus significatif pour l'axe HPA, alors qu'un trauma durant l'enfance semblerait prendre le dessus pour les modifications épigénétiques. Ces résultats montrent que 1) les personnes souffrant du TSPT ont une activité HPA atténuée, 2) l'épigénétique joue un rôle différent chez les TSPT comparés aux patients abusés qui ont commis un suicide et 3) le temps du trauma a des effets significatifs pour l'axe HPA et les modifications épigénétiques.
Adams, Julye Marie. "MODULATION OF THE ADRENAL MEDULLARY RESPONSE TO STRESS BY ESTRADIOL IN THE FEMALE RAT." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/419.
Повний текст джерелаMaudling, Stuart. "Modulation of the health status of ornamental fish by stress and dietary immuno-stimulants." Thesis, University of Plymouth, 2006. http://hdl.handle.net/10026.1/2761.
Повний текст джерелаAndrews, Janice M. "The modulation of htlv-1 gene expression following induction of the cellular stress response /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487935573771058.
Повний текст джерелаBialik, Robert J. (Robert Joseph) Carleton University Dissertation Psychology. "Mediation and modulation of blood glucose responses to stress by adrenal hormones and brain norepinephrine; implications for behavioral responses to stress." Ottawa, 1987.
Знайти повний текст джерелаBourdonnay, Emilie. "Modulation de l'expression génique par l'arsenic inorganique dans le monocyte/macrophage humain." Rennes 1, 2009. http://www.theses.fr/2009REN1B076.
Повний текст джерелаGaignier, Fanny. "Modulation de l'immunité adaptative murine par la micropesanteur simulée, l'hypergravité ou les stress chroniques ultra légers." Thesis, Université de Lorraine, 2014. http://www.theses.fr/2014LORR0171/document.
Повний текст джерелаSpaceflight weaken the immune system. The aims of this thesis were to determine the effects of exposure to simulated microgravity, hypergravity or chronic ultra-Mild stress on murine humoral immunity, using ground-Based models. We were able to show that the anti-Orthostatic suspension, that mimics some of the effects of microgravity, caused a 59% decrease of the number of splenic B cells and an inversion of the ratio between B and T lymphocytes. A decrease in B lymphopoiesis, as evidenced by the decrease of lymphoid progenitors and pre-B cells is likely the cause. Furthermore, we showed that the anti-Orthostatic position, in the absence of stress, leads to a decreased in vitro response of B cells to LPS, more important than the one of T cells to ConA, as did hypergravity exposure. To determine the mechanisms responsible of the decreased response of B cells from hypergravity mice, transcripts encoding genes involved in the TLR-4 signaling pathway, the LPS receptor on B cells, have been quantified. The expression of several genes of the MyD88-Dependent pathway was increased after 21 days of hypergravity, but no change was observed in B cells stimulated with LPS. Finally, the contribution of chronic ultra-Mild stresses was evaluated. The proportions of splenic lymphocytes were not affected by these stresses. However, the levels of serum IgA were increased and those of Th1 pro-Inflammatory cytokines were decreased, as in astronauts. Thus, these stresses do not fully explain the negative impact of spaceflight conditions on humoral immunity. These researches are important to identify the cause(s) of spaceflight-Associated impaired immunity in order to test/develop effective countermeasures to strengthen the immune system of astronauts, but also of stressed or elderly people
Monroy, Carlos Aaron. "Endogenous and exogenous modulation of regulator of G-protein signaling 4." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/1366.
Повний текст джерела