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Статті в журналах з теми "Stress modulation"
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.
Повний текст джерелаSameena, 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.
Повний текст джерелаValiente-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.
Повний текст джерелаColzato, 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.
Повний текст джерелаDeVries, 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.
Повний текст джерелаZhai, 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.
Повний текст джерелаPiterková, 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.
Повний текст джерелаCarlesi, 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.
Повний текст джерелаBeltran, 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.
Повний текст джерелаZima, 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.
Повний текст джерелаДисертації з теми "Stress modulation"
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 джерелаКниги з теми "Stress modulation"
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.
Повний текст джерелаChakraborti, 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.
Повний текст джерелаOHOLO Conference (40th 1996 Zikhron Ya'akov, Israel). New frontiers in stress research: Modulation of brain function. Australia: Harwood Academic Publishers, 1998.
Знайти повний текст джерелаBezaire, Jake. Lead stress and modulation of TCA cycle enzymes in "Pseudomonas fluorescens". Sudbury, Ont: Laurentian University, 2001.
Знайти повний текст джерелаSingh, 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.
Знайти повний текст джерелаRainville, Nathalie-Sylvie. Modulation des voies métaboliques impliquant glutamate déhydrogénase chez Pseudomonas fluorescens stressé par l'aluminium. Sudbury, Ont: Université Laurentienne, 2005.
Знайти повний текст джерелаSaso, Luciano, Alessandro Giuffrè, Giuseppe Valacchi, and Mauro Maccarrone. Pharmacological Modulation of Oxidative Stress. Elsevier Science & Technology Books, 2023.
Знайти повний текст джерелаBansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer (India) Private Limited, 2014.
Знайти повний текст джерелаBansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2014.
Знайти повний текст джерелаBansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2016.
Знайти повний текст джерелаЧастини книг з теми "Stress modulation"
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.
Повний текст джерелаBansal, 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.
Повний текст джерелаBansal, 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.
Повний текст джерелаBansal, 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.
Повний текст джерелаBalitsky, 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.
Повний текст джерелаBansal, 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.
Повний текст джерелаRana, 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.
Повний текст джерелаBansal, 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.
Повний текст джерелаJugdutt, 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.
Повний текст джерелаBansal, 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.
Повний текст джерелаТези доповідей конференцій з теми "Stress modulation"
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.
Повний текст джерелаVan 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.
Повний текст джерелаLuo, 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.
Повний текст джерелаGong, 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.
Повний текст джерелаMoy, 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.
Повний текст джерелаMa, 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.
Повний текст джерелаAvila, 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.
Повний текст джерелаXu, 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.
Повний текст джерелаTiwari, 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.
Повний текст джерелаDizaji, 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.
Повний текст джерелаЗвіти організацій з теми "Stress modulation"
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.
Повний текст джерелаLocy, 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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