Relevant bibliographies by topics / Stress modulation

Academic literature on the topic 'Stress modulation'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Stress modulation"

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Akirav, Irit, and Mouna Maroun. "Stress modulation of reconsolidation." Psychopharmacology 226, no. 4 (October 6, 2012): 747–61. http://dx.doi.org/10.1007/s00213-012-2887-6.

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Sameena, T., and S. Pranesh. "Synchronous and Asynchronous Boundary Temperature Modulations on Triple-Diffusive Convection in Couple Stress Liquid Using Ginzburg-Landau Model." International Journal of Engineering & Technology 7, no. 4.10 (October 2, 2018): 645. http://dx.doi.org/10.14419/ijet.v7i4.10.21304.

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A nonlinear study of synchronous and asynchronous boundary temperature modulations on the onset of triple-diffusive convection in couple stress liquid is examined. Two cases of temperature modulations are studied: (a) Synchronous temperature modulation ( ) and (b) Asynchronous temperature modulation ( ). It is done to examine the influence of mass and heat transfer by deriving Ginzburg-Landau equation. The resultant Ginzburg-Landau equation is Bernoulli equation and it is solved numerically by means of Mathematica. The influence of solute Rayleigh numbers and couple stress parameter is studied. It is observed that couple stress parameter increases the mass and heat transfer whereas solute Rayleigh numbers decreases the mass and heat transfer.
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Valiente-Echeverría, Fernando, Luca Melnychuk, and Andrew J. Mouland. "Viral modulation of stress granules." Virus Research 169, no. 2 (November 2012): 430–37. http://dx.doi.org/10.1016/j.virusres.2012.06.004.

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Colzato, Lorenza S., Wouter Kool, and Bernhard Hommel. "Stress modulation of visuomotor binding." Neuropsychologia 46, no. 5 (2008): 1542–48. http://dx.doi.org/10.1016/j.neuropsychologia.2008.01.006.

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DeVries, A. Courtney, Erica R. Glasper, and Courtney E. Detillion. "Social modulation of stress responses." Physiology & Behavior 79, no. 3 (August 2003): 399–407. http://dx.doi.org/10.1016/s0031-9384(03)00152-5.

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Zhai, Xiaojing, Dongyu Zhou, Yi Han, Ming-Hu Han, and Hongxing Zhang. "Noradrenergic modulation of stress resilience." Pharmacological Research 187 (January 2023): 106598. http://dx.doi.org/10.1016/j.phrs.2022.106598.

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Piterková, J., L. Luhová, L. Zajoncová, M. Šebela, and M. Petřivalský. "Modulation of polyamine catabolism in pea seedlings by calcium during salinity stress." Plant Protection Science 48, No. 2 (May 3, 2012): 53–64. http://dx.doi.org/10.17221/62/2011-pps.

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The relation of polyamine catabolism in the response of Pisum sativum to salinity stress was investigated. Pea seedlings were grown in increasing concentrations of Na<sup>+</sup> or K<sup>+</sup> or at different concentration ratios of these ions. We studied the effect of Ca<sup>2+</sup> supplementation on plants exposed to salinity stress. The parameters measured in the roots and shoots of pea seedlings included biomass production, levels of Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup> and polyamines and activity of enzymes of polyamine catabolism: diamine oxidase, aminoaldehyde dehydrogenase and peroxidases. Salinity induced increased polyamine levels and higher activity of enzymes participating in polyamine degradation. Supplementation of Ca<sup>2+</sup> had a positive effect on biomass production and in most cases it stabilised both the polyamine level and the activity of the studied enzymes. Our results confirm the role of aminoaldehyde dehydrogenase and polyamine catabolism in defence mechanisms of pea plants under salinity stress.
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Carlesi, C., E. Caldarazzo Ienco, S. Piazza, A. Lo Gerfo, R. Alessi, L. Pasquali, and Gabriele Siciliano. "Oxidative stress modulation in neurodegenerative diseases." Mediterranean Journal of Nutrition and Metabolism 4, no. 3 (February 5, 2011): 219–25. http://dx.doi.org/10.3233/s12349-011-0053-z.

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Beltran, Michael J., Cory A. Collinge, and Michael J. Gardner. "Stress Modulation of Fracture Fixation Implants." Journal of the American Academy of Orthopaedic Surgeons 24, no. 10 (October 2016): 711–19. http://dx.doi.org/10.5435/jaaos-d-15-00175.

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Zima, Tom??&OV0165;, Emanuele Albano, Magnus Ingelman-Sundberg, Gavin E. Arteel, Geoffrey M. Thiele, Lynell W. Klassen, and Albert Y. Sun. "Modulation of Oxidative Stress by Alcohol." Alcoholism: Clinical & Experimental Research 29, no. 6 (June 2005): 1060–65. http://dx.doi.org/10.1097/01.alc.0000168168.43419.54.

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Dissertations / Theses on the topic "Stress modulation"

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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.

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This thesis investigates the role of central 5-hydroxytryptamine (5-HT) in the process of adaptation to chronic stress. Central 5-HT of male rats was depleted by bilateral intraventricular (i.c.v.) infusion of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) with the use of specific re-uptake blockers to protect the dopamine (DA) and noradrenaline (NA) system. They were then exposed to different chronic stress paradigms. The effect of 5-HT depletion on social defeat was studied. Lesioned or sham-operated rats were either exposed daily for 10 days to a second larger aggressive male in the latter's home cage, or simply transferred to an empty cage (control procedure). Lesioned rats failed to show the increased freezing behaviour during the pre-defeat phase of the social interaction test characteristics of sham-operated animals. Core temperature increased during aggressive interaction in sham-operated rats, and this did not adapt with repeated stress. By contrast, stress-induced hyperthermia was accentuated in 5-HT-reduced rats as the number of defeat sessions increased. Basal core temperature was unaffected by 5-HT depletion. Heart rate increased during social defeat, but this did not adapt with repeated stress: 5-HT depletion had no effect on this cardiovascular response. Basal corticosterone was increased in lesioned rats, but the progressive reduction in stress response over days was not altered. C-fos expression patterns in lateral preoptic area (LPOA) and medial amygdala (Me-AMY) in rats with repeated defeat were altered by 5-HT depletion. These results suggest that 5-HT is important in the modulation of overall adaptation process in exposure to chronic stress.
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Lunga, 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.

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Moore, Anthony Norman. "Selenium modulation of gut epithelial cell stress responses." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3679.

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Selenium (Se) is an essential micronutrient necessary for human health. In humans, Se de ciency has been associated with in ammatory bowel disease (IBD) and increased risk of certain cancers, including colorectal cancer. Se has well established antioxidant and anti-in ammatory properties which are medi- ated, in part, though the actions of the selenoproteins, in which Se is present in the form of the amino acid selenocysteine (Sec). The cells of the gastrointestinal tract are exposed to stresses from pro-oxidative and hypoxic conditions, which have been suggested to be involved in the pathogenesis and pathology of IBD. Further characteristics of IBD are inappropriate immune responses of the gut epithelial cells to the gut microbiota. Thus, to help explain the roles of Se in IBD, it is important to understand the modulatory e ects of Se on the cell innate immune responses following challenge of intestinal epithelial cells with pathogen-associated molecular patterns (PAMPs), as well as oxidative and hypoxic stresses. The present work aimed to assess the roles of Se and the selenoproteins, SelH and TR1, in the responses of Caco-2 cell, modelling the gut epithelium, to hypoxia and infection, the latter replicated by challenge with S. typhimurium agellin. To investigate the responses of gut cells to low Se and PAMPs, undi erentiated Caco-2 cells with either supplemented with Se (40 nM selenite) or depleted of Se for 72 h before challenging with agellin (F) (500 ng/mL). The gene expression of the pro-in ammatory cytokines IL-8 and TNF- were measured in addition to the genes encoding the antimicrobial peptides (AMPs) hBD1 and hBD2. Data showed that Se depletion signi cantly a ected hBD1 expression (0.88-fold increase, P < 0.05), but that Se depletion plus F signi cantly increased the induced expression of all genes (IL-8: 1.68-fold, P < 0.001; TNF- : 0.71-fold, P < 0.001; hBD2: 1.74-fold, P < 0.001) compared with the Se supplemented cells. F and Se depletion were also associated with a signi cant increase in expression of TR1 (F: 1.68-fold, P < 0.001; Se depletion: 0.33-fold, P < 0.01) and GPX2 (F: 3-fold, P < 0.001; Se depletion: 11-fold, P < 0.001), but a signi cant decrease due to Se depletion in SelH (62 %, P < 0.001) and GPX1 (47 %, P < 0.001). The selenoprotein TR1 is an antioxidant enzyme and the primary regulator of the thioredoxin system (TXN), which has previously been shown to regulate immune responses. Knockdown of TR1 expression resulted in the reduced agellin-induced expression of IL-8 (40 %, P < 0.001), TNF-a (45 %, P < 0.01), hBD1 (40 %, P < 0.01) and hBD2 (45 %, P < 0.001). These data suggested that Se, through TR1, is involved in regulating the expression of agellin-induced immune e ectors. The selenoprotein SelH has also been suggested to have antioxidant functions. Knockdown of SelH was associated with the increased expression of the oxidative stress-associated genes NQO1 (0.41-fold, P < 0.001), and HMOX1 (1.78-fold, P < 0.001), supporting a role for SelH in the expression of oxidative stress-associated genes. The role of Se, through SelH and oxidative stress, in regulating the gut responses to agellin, has been discussed. The Caco-2 cell model is more representative of intestinal epithelial cells in vivo, when the cells are di erentiated and placed in a gaseous environment re ecting the oxygen gradient of the gut. Thus the F challenge experiments using di erentiated Caco-2 cells were repeated using a dualoxic environment. Interestingly, no potentiation of gene expression relating to the pro-in ammatory agents IL-8 and TNF- , and the defensins hBD1 and hBD2 was observed. These data suggested that the dualoxic environment completely diminished the e ects of Se depletion on the expression of immune e ectors IL-8, TNF- , hBD2 and hBD1, following agellin challenge. These data suggested the e ects of Se in more physiologically relevant intestinal epithelial cell models, more representative of the in vivo state, are required.
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Rodrigues, 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.

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Mestrado em Biologia Aplicada
As 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.
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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.

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RNA dysregulation is a recently recognized disease mechanism in amyotrophic lateral sclerosis (ALS). ALS is a neurodegenerative disease characterized by muscle atrophy and death of both upper and lower motor neurons. A key feature of the disease is the mislocalization of the RNA binding protein TDP-43 and formation of TDP-43 containing cytoplasmic aggregates in motor neurons and surrounding glia. TDP-43 is known to associate with stress granules, and recent studies in mammalian cell culture have indicated that pathological TDP-43 aggregates may arise from RNA stress granules following prolonged stress. We set out to test this hypothesis by investigating the interaction between PolyA Binding Protein (PABP), a known core RNA stress granule component, and TDP-43. Here we show that PABP colocalizes with TDP-43 in a variant dependent manner. Given that the highest risk factor for ALS is aging, an attractive model is that age-related oxidative stress triggers formation of toxic cytoplasmic aggregates from TDP-43 containing stress granules. We have therefore begun investigations using a time course, and live imaging of RNA stress granules under oxidative stress to determine if this leads to an altered RNA stress granule dynamics in cultured motor neurons. These studies will yield a better understanding of the mechanisms that lead to the toxic cytoplasmic aggregates in cases of ALS.
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Nsiah, Barbara Akua. "Fluid shear stress modulation of embryonic stem cell differentiation." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/47552.

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Vascularization of tissue-engineered substitutes is imperative for successful implantation into sites of injury. Strategies to promote vascularization within tissue-engineered constructs have focused on incorporating endothelial or endothelial progenitor cells within the construct. However, since endothelial and endothelial progenitor cells are adult cell types and limited in number, acquiring quantities needed for regenerative medicine applications is not feasible. Pluriopotent stem cells have been explored as a cell source for tissue-engineered substitutes because of their inherent ability to differentiate into all somatic cell types, including endothelial cells (ECs). Current EC differentiation strategies require laborious and extensive culture periods, utilize large quantities of expensive growth factors and extracellular matrix, and generally yield heterogenous populations for which only a small percentage of the differentiated cells are ECs. In order to recapitulate in vivo embryonic stem cell (ESC) differentiation, 3D stem cell aggregates or embryoid bodies (EBs) have been employed in vitro. In the developing embryo, fluid shear stress, VEGF, and oxygen are instructive cues for endothelial differentiation and vasculogenesis. Thus, the objective of this work was to study the effects of fluid shear stress pre-conditioning of ESCs on EB endothelial differentiation and vasculogensis. The overall hypothesis is that exposing ESCs to fluid shear stress prior to EB differentiation will promote EB endothelial differentiation and vasculogenesis. Pre-conditioning ESCs with fluid shear stress modulated EB differentiation as well as endothelial cell-like cellular organization and EB morphogenesis. To further promote endothelial differentiation, ESCs pre-conditioned with shear were treated with VEGF. Exposing EBs formed from ESCs pre-conditioned with shear to low oxygen resulted in increased production of VEGF and formation of endothelial networks. The results of this work demonstrate the role that physical forces play in modulating stem cell fate and morphogenesis.
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Ventura, Emilie. "Stress oxydant et vieillissement : modulation de la NADPH oxydase." Montpellier 2, 2008. http://www.theses.fr/2008MON20128.

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Le stress oxydant est la conséquence d'un déséquilibre au sein d'un organisme entre la production d'oxydants et les mécanismes de défenses antioxydants. La NADPH oxydase est l'enzyme clé d'une production excessive d'oxydants renforçant l'intérêt de sa modulation. Elle participe à l'initiation et à la progression des maladies associées au vieillissement comme les maladies cardiovasculaires et les démences. Au moyen d'une étude épidémiologique composée de 517 sujets (79,5 ± 7,1 ans), nous avons déterminé l'activation de la NADPH oxydase et de ses principaux déterminants en fonction de l'âge. Parmi les facteurs testés, l'homocystéine et l'inflammation sont significativement associés à l'activité de la NADPH oxydase en analyse multivariée. Ces données sont confirmées in vitro puisque l'homocystéine thiolactone et le lipopolysaccharide induisent de façon dose-dépendante l'activation et l'expression de la NADPH oxydase sur le modèle cellulaire THP-1. Dans une étape in vitro sur les THP-1, nous avons étudié la modulation négative de la NADPH oxydase par des antioxydants naturels (polyphénols) et enzymatiques (extrait de melon riche en SOD et catalase). Ces antioxydants nutritionnels modulent négativement l'activité mais aussi l'expression de la NADPH oxydase monocytaire. En conclusion, l'activité de la NADPH oxydase est associée à l'âge et est positivement régulée par l'inflammation et l'homocystéine. La production d'anion superoxyde est associée aux pathologies neurodégénératives et cardiovasculaires. La NADPH oxydase peut être modulée in vitro par des antioxydants naturels. Les liens avec la démence, les maladies cardiovasculaires ou la mortalité doivent faire l'objet d'études ultérieures. L'efficacité de manœuvres de supplémentation en antioxydants doit être précisée sur des modèles animaux puis sur une étude clinique
Oxidative 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
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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.

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Qiu, Ye. "Modulation and roles of stress-responsive proteins in coxsackievirus infection." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62935.

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Viral myocarditis is an inflammatory heart disease caused by viral infection, which is a major cause of sudden death in children and young adults. Among the various viruses, coxsackievirus B3 (CVB3) is a predominant pathogen of viral myocarditis. As CVB3 replication is tightly tangled with signaling pathways in host cells, an in-depth study of CVB3-host interactions would promote the understanding of the pathogenesis of viral myocarditis and provide critical drug targets for the development of therapeutics. CVB3 infection induces different types of stress in host cells, and in turn, the cells respond to the stress via expressing certain stress-responsive proteins (SRPs) to counteract the stress for cell survival. During the co-evolution of virus and host, CVB3 has developed sophisticated strategies to modulate and utilize SRPs to benefit its own replication. The main objective of this dissertation is to investigate the modulation and functional roles of SRPs in CVB3 infection and CVB3-induced myocardium damage. I hypothesize that 1) CVB3 infection differentially regulates the expression and activity of SRPs at transcription, translation or post-translation level; 2) the dysregulation of SRPs benefits CVB3 replication and promotes CVB3-induced cell damage. This dissertation mainly focuses on two SRPs, the inducible heat shock 70 kDa protein (Hsp70) and nuclear factor of activated T-cell 5 (NFAT5), during CVB3 infection. Using in vitro (cell culture) and in vivo (mouse) models, I demonstrated an increase of Hsp70 but a decrease of NFAT5 during CVB3 infection. Further studies elucidated the mechanism underlying such changes as well as the feedback effects on CVB3 replication. Hsp70 was upregulated via CaMKII-HSF1 signaling cascade activated in CVB3 infection and in turn promoted CVB3 infectivity via stabilizing viral genome and benefiting viral translation. NFAT5 was cleaved by CVB3 proteases 2A and 3C, generating a 70 kDa dominant negative truncate, which inhibited the iNOS-mediated anti-viral activity of NFAT5. Together, my findings have uncovered the new roles of SRPs in CVB3 infection and potential novel drug targets for CVB3-induced myocarditis.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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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.

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Books on the topic "Stress modulation"

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Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and their Modulation. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9.

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Chakraborti, Sajal, Naranjan S. Dhalla, Madhu Dikshit, and Nirmal K. Ganguly, eds. Modulation of Oxidative Stress in Heart Disease. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7.

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OHOLO Conference (40th 1996 Zikhron Ya'akov, Israel). New frontiers in stress research: Modulation of brain function. Australia: Harwood Academic Publishers, 1998.

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Bezaire, Jake. Lead stress and modulation of TCA cycle enzymes in "Pseudomonas fluorescens". Sudbury, Ont: Laurentian University, 2001.

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Singh, Ranji. The modulation of NADPH, NADH, and a-ketoglutarate in Pseudomonas fluorescens exposed to oxidative stress. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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Rainville, Nathalie-Sylvie. Modulation des voies métaboliques impliquant glutamate déhydrogénase chez Pseudomonas fluorescens stressé par l'aluminium. Sudbury, Ont: Université Laurentienne, 2005.

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Saso, Luciano, Alessandro Giuffrè, Giuseppe Valacchi, and Mauro Maccarrone. Pharmacological Modulation of Oxidative Stress. Elsevier Science & Technology Books, 2023.

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Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer (India) Private Limited, 2014.

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Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2014.

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Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2016.

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Book chapters on the topic "Stress modulation"

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Misbah, C., P. Berger, and K. Kassner. "Stress-Induced Surface Modulation." In Atomistic Aspects of Epitaxial Growth, 383–96. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-010-0391-9_29.

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Bansal, Mohinder, and Naveen Kaushal. "Introduction to Oxidative Stress." In Oxidative Stress Mechanisms and their Modulation, 1–18. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_1.

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Bansal, Mohinder, and Naveen Kaushal. "Oxidative Stress in Pathogenesis." In Oxidative Stress Mechanisms and their Modulation, 19–53. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_2.

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Bansal, Mohinder, and Naveen Kaushal. "Oxidative Stress and Carcinogenesis." In Oxidative Stress Mechanisms and their Modulation, 85–103. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_4.

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Balitsky, K. P., Yu P. Shmalko, and V. G. Pinchuk. "Stress, Cancer: Stress Modulation of the Metastatic Process." In Cancer, Stress, and Death, 113–32. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-9573-8_10.

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Bansal, Mohinder, and Naveen Kaushal. "Managing Oxidative Stress/Targeting ROS." In Oxidative Stress Mechanisms and their Modulation, 127–46. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_6.

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Rana, Rashid Mehmood, Azhar Iqbal, Fahad Masoud Wattoo, Muhammad Azam Khan, and Hongsheng Zhang. "HSP70 Mediated Stress Modulation in Plants." In Heat Shock Proteins and Stress, 281–90. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90725-3_13.

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Bansal, Mohinder, and Naveen Kaushal. "Oxidative Stress in Metabolic Disorders/Diseases." In Oxidative Stress Mechanisms and their Modulation, 55–83. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_3.

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Jugdutt, Bodh I., and Bernadine A. Jugdutt. "Oxidative Stress and Heart Failure." In Modulation of Oxidative Stress in Heart Disease, 257–311. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7_11.

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Bansal, Mohinder, and Naveen Kaushal. "Cell Signaling and Gene Regulation by Oxidative Stress." In Oxidative Stress Mechanisms and their Modulation, 105–26. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9_5.

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Conference papers on the topic "Stress modulation"

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Wu, Hwai-Chung. "Active Wave Modulation for Bond Evaluation." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33487.

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Many recent studies have indicated that externally bonded Fiber Reinforced Plastic (FRP) composite sheets can be used effectively to strengthen concrete structures. Composite action suggests that the individual parts of a composite work together as one. Stresses must be transferred from one constituent to the other through some interface. If there is little or no bond at the interface then there is little or no transfer of stress and therefore poor composite action. In this study, we intend to develop a NDE tool for evaluating such interfacial bond conditions. Attention is placed on an innovative active modulation approach, Nonlinear Wave Modulation Spectroscopy. In this procedure, a probe wave will be passed through the system. Simultaneously, a second, modulating wave will be applied to the system to agitate the state of damage in the materials. The resulting frequency modulations will be analyzed, and will be correlated to the presence of the interfacial flaws between a FRP thin sheet and concrete substrate.
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Van Nguyen, Nghiem. "GPS Sensor Electronics Unit Environmental Stress Screening Test Technique." In NCSL International Workshop & Symposium. NCSL International, 2014. http://dx.doi.org/10.51843/wsproceedings.2014.16.

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The Environmental Stress Screening test objective is to validate proper manufacturing and find any manufacturing defects in a flight unit before delivery by using temperature modulation and vibration simulations. The ESS test performs temperature cycling and employs random vibrations to test the reliability of the unit. Temperature regulation is also provided via the poly-alpha-olefin (PAO) coolant flowing through the unit under test (UUT), which is controlled by a cooling system.
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Luo, Qian, Changgui Tan, Xiangzhan Wang, and Bin Liu. "Trench based stress modulation structure for 90nm-gate CESL strained N MOSFET." In 2017 2nd International Conference on Automation, Mechanical Control and Computational Engineering (AMCCE 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/amcce-17.2017.143.

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Gong, Jian, Zhao Liu, Yiyan Lu, Jiawei Ji, Jie Yu, Deping Tang, and Sibin Lu. "A Current-stress-optimized Control Strategy for DAB Converter Using Hybrid Modulation." In IECON 2020 - 46th Annual Conference of the IEEE Industrial Electronics Society. IEEE, 2020. http://dx.doi.org/10.1109/iecon43393.2020.9254461.

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Moy, G., and R. S. Fearing. "Effects of Shear Stress in Teletaction and Human Perception." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0264.

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Abstract Ideally, a tactile stimulator presents information through control of surface normal stress and surface shear stresses. Psychophysical experiments measured the effect of shear stress information on the perception of static stimuli applied normal to the surface. Wax gratings in two different orientations and various spatial frequencies were used as stimuli. Elastic layers, representing the anti-aliasing filter on a tactile display, were placed over the stimuli. Using an elastic layer which reduces shear stress transmission improved perception compared to standard elastic layers. Spatial resolution differences due to different elastic layers are explained by modulation indices determined from the predicted sub-surface strain using an elastic half-plane model.
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Ma, Hong Y., Q. Xu, J. R. Bellesteros, Vasilis Ntziachristos, Qingqi Zhang, and Britton Chance. "Quantitative study of hypoxia stress in piglet brain by IQ phase modulation oximetry." In BiOS '99 International Biomedical Optics Symposium, edited by Britton Chance, Robert R. Alfano, and Bruce J. Tromberg. SPIE, 1999. http://dx.doi.org/10.1117/12.356793.

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Avila, Anderson R., Shruti R. Kshirsagar, Abhishek Tiwari, Daniel Lafond, Douglas O'Shaughnessy, and Tiago H. Falk. "Speech-Based Stress Classification based on Modulation Spectral Features and Convolutional Neural Networks." In 2019 27th European Signal Processing Conference (EUSIPCO). IEEE, 2019. http://dx.doi.org/10.23919/eusipco.2019.8903014.

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Xu, Shuang, Riming Shao, and Liuchen Chang. "Single-Phase Voltage Source Inverter with Power Decoupling and Minimal Voltage Stress Modulation." In 2018 9th IEEE International Symposium on Power Electronics for Distributed Generation Systems (PEDG). IEEE, 2018. http://dx.doi.org/10.1109/pedg.2018.8447614.

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Tiwari, Shipra, and Saumendra Sarangi. "Comparison of Current Stress For Different Modulation Techniques In Dual Active Bridge Converter." In 2019 International Conference on Electrical, Electronics and Computer Engineering (UPCON). IEEE, 2019. http://dx.doi.org/10.1109/upcon47278.2019.8980050.

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Dizaji, Mohammad Rezagholipour, Clemens J. Krückel, Attila Fülöp, Peter A. Andrekson, Victor Torres-Company, and Lawrence R. Chen. "Cross-Phase-Modulation-Based Wavelength Conversion in Low-Stress Silicon-Rich Nitride Waveguide." In Optical Fiber Communication Conference. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/ofc.2016.tu2k.4.

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Reports on the topic "Stress modulation"

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Tzvetkova, Mimoza, Zafer Sabit, Christina Vidinova, Roman Tashev, and Hristina Nocheva. Cannabinoid and Serotonergic Systems in Modulation of Stress induced Analgesia. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, April 2021. http://dx.doi.org/10.7546/crabs.2021.04.17.

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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker, and Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.
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Fromm, Hillel, and Joe Poovaiah. Calcium- and Calmodulin-Mediated Regulation of Plant Responses to Stress. United States Department of Agriculture, September 1993. http://dx.doi.org/10.32747/1993.7568096.bard.

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We have taken a molecular approach to clone cellular targets of calcium/calmodulin (Ca2+/CaM). A 35S-labeled recombinant CaM was used as a probe to screen various cDNA expression libraries. One of the isolated clones from petunia codes for the enzyme glutamate decarboxylase (GAD) which catalyzes the conversion of glutamate to g-aminobutyric acid (GABA). The activity of plant GAD has been shown to be dramatically enhanced in response to cold and heat shock, anoxia, drought, mechanical manipulations and by exogenous application of the stress phytohormone ABA in wheat roots. We have purified the recombinant GAD by CaM-affinity chromatography and studied its regulation by Ca2+/CaM. At a physiological pH range (7.0-7.5), the purified enzyme was inactive in the absence of Ca2+ and CaM but could be stimulated to high levels of activity by the addition of exogenous CaM (K0.5 = 15 nM) in the presence of Ca2+ (K 0.5 = 0.8 mM). Neither Ca2+ nor CaM alone had any effect on GAD activity. Transgenic tobacco plants expressing a mutant petunia GAD lacking the CaM-binding domain, or transgenic plants expressing the intact GAD were prepared and studied in detail. We have shown that the CaM-binding domain is necessary for the regulation of glutamate and GABA metabolism and for normal plant development. Moreover, we found that CaM is tightly associated with a 500 kDa GAD complex. The tight association of CaM with its target may be important for the rapid modulation of GAD activity by Ca2+ signaling in response to stresses.
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Paran, Ilan, and Allen Van Deynze. Regulation of pepper fruit color, chloroplasts development and their importance in fruit quality. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598173.bard.

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Pepper exhibits large natural variation in chlorophyll content in the immature fruit. To dissect the genetic and molecular basis of this variation, we conducted QTL mapping for chlorophyll content in a cross between light and dark green-fruited parents, PI 152225 and 1154. Two major QTLs, pc1 and pc10, that control chlorophyll content by modulation of chloroplast compartment size in a fruit-specific manner were detected in chromosomes 1 and 10, respectively. The pepper homolog of GOLDEN2- LIKE transcription factor (CaGLK2) was found as underlying pc10, similar to its effect on tomato fruit chloroplast development. A candidate gene for pc1was found as controlling chlorophyll content in pepper by the modulation of chloroplast size and number. Fine mapping of pc1 aided by bulked DNA and RNA-seq analyses enabled the identification of a zinc finger transcription factor LOL1 (LSD-One-Like 1) as a candidate gene underlying pc1. LOL1 is a positive regulator of oxidative stress- induced cell death in Arabidopsis. However, over expression of the rice ortholog resulted in an increase of chlorophyll content. Interestingly, CaAPRR2 that is linked to the QTL and was found to affect immature pepper fruit color in a previous study, did not have a significant effect on chlorophyll content in the present study. Verification of the candidate's function was done by generating CRISPR/Cas9 knockout mutants of the orthologues tomato gene, while its knockout experiment in pepper by genome editing is under progress. Phenotypic similarity as a consequence of disrupting the transcription factor in both pepper and tomato indicated its functional conservation in controlling chlorophyll content in the Solanaceae. A limited sequence diversity study indicated that null mutations in CaLOL1 and its putative interactorCaMIP1 are present in C. chinensebut not in C. annuum. Combinations of mutations in CaLOL1, CaMIP1, CaGLK2 and CaAPRR2 are required for the creation of the extreme variation in chlorophyll content in Capsicum.
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Dickman, Martin B., and Oded Yarden. Modulation of the Redox Climate and Phosphatase Signaling in a Necrotroph: an Axis for Inter- and Intra-cellular Communication that Regulates Development and Pathogenicity. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697112.bard.

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The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotiorum. The focus in this project is on the elucidation of the signaling events and environmental cues that contribute to broad pathogenic success of S. sclerotiorum. In this proposal, we have taken advantage of the recent conceptual (ROS/PPs signaling) and technical (genome sequence availability and gene inactivation possibilities) developments to address the following questions, as appear in our research goals stated below, specifically concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum. Our stated specific objectives were to progress our understanding of the following questions: (i) Which ROS species affect S. sclerotiorum development and pathogenicity? (ii) In what manner do PPs affect S. sclerotiorum development and pathogenicity? (iii) Are PPs affected by ROS production and does PP activity affect ROS production and SMK1? (iv) How does Sclerotinia modulate the redox environment in both host and pathogen? While addressing these questions, our main findings include the identification and characterization the NADPH oxidase (NOX) family in S. sclerotiorum. Silencing of Ssnox1 indicated a central role for this enzyme in both virulence and pathogenic (sclerotial) development, while inactivation of Ssnox2 resulted in limited sclerotial development but remained fully pathogenic. Interestingly, we found a consistent correlation with Ssnox1(involved with pathogenicity) and oxalate levels. This same observation was also noted with Sssod1. Thus, fungal enzymes involved in oxidative stress tolerance,when inactivated, also exhibit reduced OA levels. We have also shown that protein phosphatases (specifically PP2A and PTP1) are involved in morphogenesis and pathogenesis of S. sclerotiorum, demonstrating the regulatory role of these key proteins in the mentioned processes. While probing the redox environment and host-pathogen interactions we determined that oxalic acid is an elicitor of plant programmed cell death during S. sclerotiorum disease development and that oxalic acid suppresses host defense via manipulation of the host redox environment. During the course of this project we also contributed to the progress of understanding S. sclerotiorum function and the manipulation of this fungus by establishing an efficient gene replacement and direct hyphal transformation protocols in S. sclerotiorum. Lastly, both PIs were involved in thegenomic analysis of this necrotrophic fungal pathogen (along with Botrytis cinerea). Our results have been published in 11 papers (including joint papers and refereed reviews) and have set the basis for a continuum towards a better understanding and eventual control of this important pathogen (with implications to other fungal-host systems as well).
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Dahl, Geoffrey E., Sameer Mabjeesh, Thomas B. McFadden, and Avi Shamay. Environmental manipulation during the dry period of ruminants: strategies to enhance subsequent lactation. United States Department of Agriculture, February 2006. http://dx.doi.org/10.32747/2006.7586544.bard.

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The project resulted from earlier observations that environmental factors, especially photoperiod and temperature, had profound effects on milk yield in dairy cattle during lactation. More recently we had determined that photoperiod manipulation during the dry period altered milk yield in the next lactation, and this was associated with shifts in circulating concentrations of prolactin; specifically exposure to short days during the dry period decreases prolactin but increases milk yield. Because prolactin is also affected by temperature, with heat stress causing an increase in prolactin similar to that of long day exposure, we focused our efforts on determining prolactin signaling provides a common pathway for generation of environmental effects on mammary growth, development and subsequent function during the dry period of dairy ruminants. Over the project period we made significant progress toward testing our hypotheses that (I): In cows, there is a discrete duration of time during the dry period in which exposure to short days will result in optimal enhancement of mammary development and milk yield in the following lactation, and that this effect is mediated through demonstrable changes in mammary gland development, prolactin signaling, and mammary gene expression; and (II): Modulation of photoperiod and temperature during the dry period will affect milk yield in goats in the subsequent lactation via shifts in nutrient and endocrine partitioning, and mammary gene expression, during the dry period and into lactation. Cows exposed to short days for only the final 21 days of the dry period did not produce more milk that those on long day or natural photoperiod when dry. However, cows on short days for the entire 60 days dry did produce more milk than the other 3 groups. This indicates that there is a duration effect of short day exposure on subsequent milk yield. Results of the second study in cows indicate that mammary growth increases differentially during the dry period under long vs. short days, and that short days drive more extensive growth which is associated with altered prolactin signaling via decreases in an suppressors of cytokine signaling that represent an inhibitory pathway to mammary growth. Evidence from the studies in Israel confirms that goats respond to short days during the dry period in a similar manner to cows. In addition, heat stress effects on during the dry period can be limited by exposure to short days. Here again, shifts in prolactin signaling, along with changes in IGF-I secretion, are associated with the observed changes in mammary function in goats. These results have a number of biological and practical implications. For dairy producers, it is clear that we can recommend that cows and goats should be on reduced light exposure during the dry period, and further, cows and goats should be cooled to avoid heat stress during that time. Environmental influences on mammary growth are apparent during the dry period, and those effects have persistent impact in the subsequent lactation. Prolactin signaling is a consistent mechanism whereby extended light exposure and heat stress may depress mammary growth and development during the dry period. Thus, the prolactin signaling system offers an opportunity for further manipulation to improve production efficiency in dairy ruminants.
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Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
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9

Harris, Gregory, Brooke Hatchell, Davelin Woodard, and Dwayne Accardo. Intraoperative Dexmedetomidine for Reduction of Postoperative Delirium in the Elderly: A Scoping Review. University of Tennessee Health Science Center, July 2021. http://dx.doi.org/10.21007/con.dnp.2021.0010.

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Background/Purpose: Post-operative delirium leads to significant morbidity in elderly patients, yet there is no regimen to prevent POD. Opioid use in the elderly surgical population is of the most significant risk factors for developing POD. The purpose of this scoping review is to recognize that Dexmedetomidine mitigates cognitive dysfunction secondary to acute pain and the use of narcotic analgesia by decreasing the amount of norepinephrine (an excitatory neurotransmitter) released during times of stress. This mechanism of action also provides analgesia through decreased perception and modulation of pain. Methods: The authors developed eligibility criteria for inclusion of articles and performed a systematic search of several databases. Each of the authors initially selected five articles for inclusion in the scoping review. We created annotated literature tables for easy screening by co-authors. After reviewing the annotated literature table four articles were excluded, leaving 11 articles for inclusion in the scoping review. There were six level I meta-analysis/systematic reviews, four level II randomized clinical trials, and one level IV qualitative research article. Next, we created a data-charting form on Microsoft Word for extraction of data items and synthesis of results. Results: Two of the studies found no significant difference in POD between dexmedetomidine groups and control groups. The nine remaining studies noted decreases in the rate, duration, and risk of POD in the groups receiving dexmedetomidine either intraoperatively or postoperatively. Multiple studies found secondary benefits in addition to decreased POD, such as a reduction of tachycardia, hypertension, stroke, hypoxemia, and narcotic use. One study, however, found that the incidence of hypotension and bradycardia were increased among the elderly population. Implications for Nursing Practice: Surgery is a tremendous stressor in any age group, but especially the elderly population. It has been shown postoperative delirium occurs in 17-61% of major surgery procedures with 30-40% of the cases assumed to be preventable. Opioid administration in the elderly surgical population is one of the most significant risk factors for developing POD. With anesthesia practice already leaning towards opioid-free and opioid-limited anesthetic, the incorporation of dexmedetomidine could prove to be a valuable resource in both reducing opioid use and POD in the elderly surgical population. Although more research is needed, the current evidence is promising.
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Li, Guangyao, Xueqin Hong, Qin Wen, Min Li, Jinghu Li, and Qi Wang. Acupuncture improves cognitive function in animals with vascular dementia by modulating oxidative stress, inflammation and apoptosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0022.

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