Relevant bibliographies by topics / Stress response

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Stress response'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 May 2024

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Journal articles on the topic "Stress response"

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Pingitore, Alessandro, Francesca Mastorci, and Giorgio Iervasi. "Heart Failure and Stress Response." Biomed Data Journal 1, no. 3 (2015): 33–35. http://dx.doi.org/10.11610/bmdj.01300.

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Arsić-Komljenović, Gordana, Dragan Mikić, and Jelena Kenić. "Stress and response to stress." Zdravstvena zastita 39, no. 6 (2010): 9–15. http://dx.doi.org/10.5937/zz1002009a.

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Jawwad, Ghazala, Humaira Fayyaz Khan, and Amanat Ali. "STRESS RESPONSE;." Professional Medical Journal 24, no. 09 (September 8, 2017): 1398–402. http://dx.doi.org/10.29309/tpmj/2017.24.09.822.

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Introduction: Psychological stress activate two axes: Hypothalamic- Pituitary-Adrenal axis and Sympathoadrenal axis leading to production of cortisol and catecholamines.Autonomic disturbances in the body can be evaluated by estimating heart rate variability.Study Design: Cross sectional study. Setting: Islamic International Medical College. Period:June 2014 to December 2014. Materials and Methods: Subjects were labeled as stress andcontrol on basis of DASS questionnaire proforma. Morning Cortisol level of all the subjectswas measured by quantitative ELISA method. Heart rate variability recording of all the subjectswas done. Results: Low frequency in absolute and normalized unit and low to high frequencyratio was significantly higher in stressed group, compared to control (p≤ .05, p ≤ .001, pp ≤.001 respectively). High frequency in normalized was significantly lower in stressed subjects,compared to control (p ≤ .001). Cortisol level was significantly higher in the stressed group incomparison with control (p ≤ .05). Conclusion: Stress can lead to increase morning cortisollevel and can cause autonomic disturbances which can be evaluated by measuring heart ratevariability.
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Rapport, David J. "Stress response." Trends in Ecology & Evolution 13, no. 1 (January 1998): 36–37. http://dx.doi.org/10.1016/s0169-5347(97)01249-4.

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Cummins, Nadia, and Rebecca C. Taylor. "A stress-free stress response." Nature Chemical Biology 16, no. 10 (July 23, 2020): 1038–39. http://dx.doi.org/10.1038/s41589-020-0616-8.

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Motzer, Sandra Adams, and Vicky Hertig. "Stress, stress response, and health." Nursing Clinics of North America 39, no. 1 (March 2004): 1–17. http://dx.doi.org/10.1016/j.cnur.2003.11.001.

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Milutinovic, Snezana, Qianli Zhuang, Alain Niveleau, and Moshe Szyf. "Epigenomic Stress Response." Journal of Biological Chemistry 278, no. 17 (February 7, 2003): 14985–95. http://dx.doi.org/10.1074/jbc.m213219200.

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Brown, I. R. "The stress response." Neuropathology and Applied Neurobiology 21, no. 6 (December 1995): 473–75. http://dx.doi.org/10.1111/j.1365-2990.1995.tb01088.x.

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Boerner, T. F., R. R. Bartkowski, M. Torjman, E. Frank, and H. Schieren. "SYMPATHOADRENAL STRESS RESPONSE." Anesthesiology 77, Supplement (September 1992): A888. http://dx.doi.org/10.1097/00000542-199209001-00888.

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Seelye, Edward E. "Stress Response Syndromes." American Journal of Psychotherapy 41, no. 2 (April 1987): 310–11. http://dx.doi.org/10.1176/appi.psychotherapy.1987.41.2.310.

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Dissertations / Theses on the topic "Stress response"

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Silva, Sara Maria Cunha Oliveira. "Stress response of Listeria monocytogenes." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/12617.

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Mestrado em Biologia Molecular e Celular
Thirty-five Listeria monocytogenes isolates previously collected from food (n=20) and human patients suffering from listeriosis (n=15), with different antibiotic resistance profiles were characterized and compared based on: (i) their ability to survive through sequential conditions that parallel the digestive tract; (ii) their capacity to survive extreme pH values; (iii) the potential relationship, between antibiotic resistance and the resistance of L. monocytogenes isolates to the stress conditions investigated. The response was shown to be strain- and stress-dependent and no relation between food and clinical isolates was observed (p > 0.05). The results showed that L. monocytogenes is able to survive under extreme acid and alkaline conditions and did not survive when submitted to simulated sequential gastro-intestinal transit, i.e. the activity of bile salts after combined action of hydrochloric acid and pepsin. No correlation was observed between antibiotic resistance and response to the stress conditions applied to the isolates investigated.
Trinta e cinco isolados de Listeria monocytogenes provenientes de alimentos (n=20) e pacientes humanos com listeriose (n=15) e com diferentes perfis de resistência a antibióticos foram caracterizados e comparados com base na: (i) sua capacidade de sobrevivência à passagem pelo trato gastrointestinal simulado, (ii) sua capacidade de sobrivência a condições extremas de pH, (iii) potencial relação entre a resistência a antibióticos e a resistência às condições de stresse investigadas. A resposta às várias condições de stresse demonstrou ser estirpe- e stresse-dependente e não foi observada nenhuma relação entre isolados alimentares e clínicos (p > 0.05). Os resultados mostraram que L. monocytogenes sobrevive em condições ácidas e alcalinas extremas e não sobrevive quando submetida à passagem pelo trato gastrointestinal simulado, ou seja, à atividade dos sais biliares após ação conjunta do ácido clorídrico e pepsina. Não foi observada qualquer correlação entre a resistência a antibióticos e a resposta às condições de stresse aplicadas para os isolados estudados.
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Di, Paolo Tiziano. "Stress response in Entamoeba histolytica." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68169.

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The heat shock response was studied in the intestinal parasitic protozoan Entamoeba histolytica. Temperature shifts from 37$ sp circ$C to 44$ sp circ$C enhanced the synthesis of five major heat shock (or stress) proteins (HSP) of 100, 50, 42, 37, and 28 kDa. Similarly, exposure of amebae to lymphokine activated macrophages and hydrogen peroxide caused HSP expression. Heat shock caused the reversible inhibition of amebic adherence to Chinese hamster ovary cells and human colonic mucin binding to trophozoites by ${>80 %}$. This was due to a decrease in the surface expression of the Gal/GalNAc adherence lectin and a marked reduction in the lectin mRNA expression. However, the presence of target Chinese hamster ovary cells during recovery at 37$ sp circ$C augmented amebic adherence. These results suggest that E. histolytica trophozoites produce a variety of HSP in response to different stimuli and can modulate the expression of the surface adherence lectin which maybe important in pathogenesis.
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Brorsson, Camilla. "Trauma - logistics and stress response." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-93324.

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Background: Trauma is a major cause of death and disability. Adverse events, such as prolonged prehospital time, hypoxia, hypotension and/or hyperventilation have been reported to correlate to poor outcome. Adequate cortisol levels are essential for survival after major trauma. In hypotensive critically ill patients, lack of sufficient amount of cortisol can be suspected, and a concept of critical illness related corticosteroid insufficiency has been proposed. Corticosteroid therapy has many adverse effects in critically ill patients and should only be given if life-saving. Correct measurement of serum cortisol levels is important but difficult in critically ill patients with capillary leakage. Estimation of the free and biologically active cortisol is preferable. In serum less than 10% of cortisol is free and biologically active and not possible to measure with routine laboratory methods. Salivary cortisol can be used as a surrogate for free cortisol, but salivary production is reduced in critically ill patients. Liver resection could reduce cortisol levels due to substrate deficiency. Aims: 1. Evaluate the occurrence of early adverse events in patients with traumatic brain injury and relate them to outcome. 2. Assess cortisol levels over time after trauma and correlate to severity of trauma, sedative/analgesic drugs and cardiovascular function. 3. Evaluate if saliva stimulation could be performed without interfering with salivary cortisol levels. 4. Assess cortisol levels over time after liver resection in comparison to other major surgery. Results: There was no significant correlation between prehospital time ³60 minutes, hypoxia (saturation <95%), hypotension (systolic blood pressure <90 mmHg), or hyperventilation (ETCO2 <4.5 kPa) and a poor outcome (Glasgow Outcome Scale 1-3) in patients with traumatic brain injury. Cortisol levels decreased significantly over time after trauma, but there was no correlation between low (<200 nmol/L) serum cortisol levels and severity of trauma. Infusion of sedative/analgesic drugs was the strongest predictor for a low (<200 nmol/L) serum cortisol. The odds ratio for low serum cortisol levels (<200 nmol/L) was 8.0 for patients receiving continuous infusion of sedative/analgesic drugs. There was no significant difference between unstimulated and stimulated salivary cortisol levels (p=0.06) in healthy volunteers. Liver resection was not associated with significantly lower cortisol levels compared to other major surgery. Conclusion: There was no significant correlation between early adverse events and outcome in patients with traumatic brain injury. Cortisol levels decreased significantly over time in trauma patients. Low cortisol levels (<200 nmol/L) were significantly correlated to continuous infusion of sedative/analgesic drugs. Saliva stimulation could be performed without interfering with salivary cortisol levels. Liver resection was not associated with low cortisol levels compared to other major surgery.
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GUCCINI, ILARIA. "Frataxin and the stress response." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202279.

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La frataxina è una proteina mitocondriale, la cui ridotta espressione è responsabile di una malattia neurodegenerativa ereditaria, l’atassia di Friedreich (FRDA). La frataxina è una proteina che lega il ferro ed è coinvolta nella biogenesi dei gruppi ferro-zolfo (ISC), gruppi prostetici che svolgono funzioni cellulari essenziali come la fosforilazione ossidativa, la catalisi enzimatica e regolazione dei geni. La frataxina è richiesta per lo sviluppo, poiché la sua assenza è letale in embrioni di topo e provoca l’arresto nello sviluppo del nematode C. elegans. Una parziale espressione della frataxina permette lo sviluppo e la sopravvivenza dell’organismo, e determina una progressiva degenerazione di tessuti specifici. Sebbene molte evidenze suggeriscano che la frataxina agisca da chaperone nel compartimento mitocondriale, è stato recentemente dimostrato l'esistenza di un pool funzionale di frataxina extramitocondriale in vari tipi di cellule umane. Lo scopo del mio lavoro nella prima parte è stato di indagare sul possibile ruolo fisiologico della frataxina extramitocondriale nel compartimento citoplasmatico studiando l’interazione della proteina con un possibile patner ISC-dipendente. E' stato dimostrato che la forma extramitocondriale della frataxina interagisce direttamente con l’aconitasi citosolica/ proteina regolatoria del ferro-1 (IRP1), una proteina bifunzionale che alterna la funzione enzimatica di aconitasi e la funzione di “RNA-binding” attraverso il meccanismo dello “switch” del cluster ferro-zolfo. Inoltre il difetto dell’aconitasi citosolica e la conseguente attivazione di IRP1 come proteina che lega l’RNA, che si verifica nelle cellule dei pazienti affetti da atassia di Friedreich, viene revertito con l'azione della frataxina extramitocondriale. La frataxina, inoltre, protegge le cellule tumorali dallo stress ossidativo e dall’apoptosi, ma agisce anche da soppressore tumorale. Le basi molecolari di questo apparente paradosso non sono ad oggi note. Nella seconda parte del mio lavoro ho osservato che l'espressione della frataxina è aumentata in diverse linee cellulari tumorali in risposta allo stress ipossico, una condizione spesso associata alla progressione del tumore. Inoltre, l'aumento della frataxina in risposta all'ipossia dipende dai Fattori di espressione Ipossia-Inducibili (HIF) e modula l’attivazione del soppressore tumorale p53. E’ stato mostrato per la prima volta in vivo l’ aumento di frataxina in campioni chirurgici di glioblastoma umano e campioni umani di carcinoma di colon. Questi risultati mostrano che la frataxina partecipa alla risposta allo stress indotto da ipossia nei tumori, ciò implica che la modulazione della sua espressione potrebbe svolgere un ruolo determinante nella sopravvivenza e/o nella progressione delle cellule tumorali.
Defective expression of frataxin is responsible for the degenerative disease Friedreich’s ataxia (FRDA). Frataxin is an iron-binding protein involved in the biogenesis of iron–sulfur clusters (ISC), prosthetic groups allowing essential cellular functions such as oxidative phosphorylation, enzyme catalysis and gene regulation. Frataxin is a protein required for cell survival since complete knock-out is lethal. Partial expression of the frataxin allows the development and survival of the organism, yet results in progressive degeneration of specific tissues. Although several evidence suggest that frataxin acts as an iron-chaperone within the mitochondrial compartment, it was recently demonstrated the existence of a functional extramitochondrial pool of mature frataxin in various human cell types. The aim of my work in the first part was to investigate for a physiological role of extramitochondrial frataxin in the cytoplasmic compartment searching for ISCdependent interaction. The extramitochondrial form of frataxin was demonstrated to directly interact with cytosolic aconitase/iron regulatory protein-1 (IRP1), a bifunctional protein that alternates between an enzymatic and a RNA-binding function through the “iron–sulfur switch” mechanism. Importantly, the cytosolic aconitase defect and consequent IRP1 activation occurring in FRDA cells was found to be reversed by the action of extramitochondrial frataxin. Frataxin protects tumor cells against oxidative stress and apoptosis but also acts as a tumor suppressor. The molecular bases of this apparent paradox are missing. The aim of my work in the second part was to investigate the pathways through which frataxin enhances stress resistance in tumor cells. Frataxin expression was found to be upregulated in several tumor cell lines in response to hypoxic stress, a condition often associated with tumor progression. Moreover, frataxin upregulation in response to hypoxia is dependent on HypoxiaInducible-Factors (HIFs) expression and modulates tumor suppressor p53 activation. Importantly, this work shows for the first time an in vivo increase of frataxin in human glioblastoma and colon carcinoma tumor samples. These results show that frataxin participates to the hypoxia-induced stress response in tumors, thus implying that modulation of its expression could play a critical role in tumor cell survival and/or progression.
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Chen, Chun-Chun. "Response to social stress : sensory input, stress response and the neural substrates of reproductive suppression /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Lindahl, Andreas. "Neuroendocrine Stress Response after Burn Trauma." Doctoral thesis, Uppsala universitet, Plastikkirurgi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198466.

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Some aspects of the stress response during acute intensive care for severe burns are described and quantified by measuring hormonal and neuroendocrine patterns and relating these to organ function in the short term. This includes an assessment of whether there are markers for the severity of stress that are better than conventional descriptors of the severity of a burn in predicting failing organ function. P-CgA after a major burn injury is an independent and better predictor of organ dysfunction assessed as SOFA score than the traditionally used TBSA% burned. The results also suggest that the extent of neuroendocrine activation is related to organ dysfunction, and this motivates a more extensive effort to evaluate P-CgA as a prognostic marker with respect to mortality and long-term outcome. P-NT-proBNP exhibited a complex pattern with considerable inter-individual and day-to-day variations. Values of P-NT-proBNP were related to size of burn, water accumulation and systemic inflammatory response. A considerable covariation with trauma response and SOFA scores was observed in day by day analyses, but with weight change only on day 2. Maximum P-NT-proBNP showed a stronger correlation with SOFA score on day 14, with mortality, and with LOS, than did age and TBSA% burned. High values were also independent predictors of all subsequent SOFA scores up to two weeks after injury. P-NT-proBNP and NT-proANP reflect and predict organ function after burn injury similarly, notwithstanding a significantly larger intra-individual variability for P-NT-proBNP. P-NT-proBNP, but not NT-proANP, reflects the systemic inflammatory trauma response. Free cortisol concentration was related to the size of burns, as was the circadian cortisol rhythm. This effect of burn size was, at least in part, related to its effect on organ function. This thesis points to the fact that the stress response is richly interwoven, and cannot be adequately assessed by one biomarker only. All biomarkers studied here can be viewed as representing efferent limbs of the stress reaction, and they would need to be supplemented by biomarkers representing individual physiologic responses that follow the stress signaling.
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Löw, Christian Frank. "Regulation of the cytosolic stress response." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168322.

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The cytosolic stress response, also known as the heat-shock response (HSR), is one of the major defense mechanisms activated by cells to maintain the integrity of the cellular proteome under proteotoxic environmental conditions. It is characterized by the increased synthesis of heat-shock proteins (Hsps), mainly molecular chaperones and proteases which prevent the aggregation of misfolded proteins and mediate their refolding or degradation. It is generally accepted that the induction of the HSR is coordinated by the heat-shock transcription factor 1 (HSF1). However, many mechanistic aspects of the HSF1 regulation remain unclear. In the present study, a genome-wide RNA interference screen was combined with an extensive biochemical analysis and quantitative proteomics to better understand the regulation of the HSR upon thermal stress. In the screening experiments novel positive and negative modulators of the stress response were identified, including proteins involved in chromatin remodeling, transcription, mRNA splicing, DNA damage repair, and proteolytic degradation. The diversity of the identified regulators suggests that induction and attenuation of the HSR integrate signals from different cellular pathways and are rather multi-factorial processes than single gene/protein events. The modulator proteins are localized in multiple cellular compartments with the majority having their primary location in the nucleus. A protein-protein interaction analysis revealed a HSR regulatory network, with chromatin modifiers and nuclear protein quality control components occupying hub positions. These observations are supported by quantitative proteomics experiments, which showed specific stress-induced reorganizations of the nuclear proteome, including the transient accumulation of chaperones and proteasomal subunits. The histone acetyltransferase EP300 was shown to specifically control the cellular level of HSF1 by stabilizing it against proteasomal turnover under normal conditions. Moreover, the ubiquitin-proteasome system (UPS) was found to participate in the attenuation of the HSR by degrading stress-activated, hyperphosphorylated HSF1. Since HSF1 competes with stress-denatured proteins for access to the proteasome, the extent of cellular protein damage modulates the rate of HSR attenuation. In addition to thermal stress, various other proteotoxic stresses are known to induce the HSR such as the proteasome inhibitor MG132 and the triterpenoid celastrol, which activates HSF1 by an unknown mechanism. Therefore, the networks regulating HSF1 activation upon thermal stress, proteasome inhibition and celastrol treatment were compared in this study. Whereas there is a large overlap between the sets of regulatory factors activated after heat stress and proteasomal impairment, HSF1 activation after celastrol treatment seems to bypass the HSR regulatory network to a large extent. Nevertheless, comparison of the regulatory networks under different proteotoxic conditions revealed a set of HSR core components, including factors involved in chromatin remodeling, DNA damage repair, RNA transport, transcription, and ion transport. The various cellular functions and localizations of these core components reinforce the multifaceted nature of the HSR regulation. The results obtained in this study can help to identify potential targets for the pharmacologic manipulation of the HSR in the treatment of aggregate deposition diseases and cancer.
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Ibrahim, Yasser Musa. "Stress response proteins in Streptococcus pneumoniae." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412962.

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Vine, Claire Elizabeth. "Escherichia coli response to nitrosative stress." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3544/.

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Previous transcriptomic experiments have revealed that various Escherichia coli K-12 genes encoding proteins of unknown function are highly expressed during anaerobic growth in the presence of nitrate, or especially nitrite. Products of some of these genes, especially YeaR-YoaG, YgbA, YibIH and the hybrid cluster protein, Hcp, have been implicated in the response to nitrosative stress. The aims of this study were to investigate sources of nitrosative stress, and the possible roles of some of these proteins in protection against nitric oxide. The YtfE protein has been implicated in the repair of iron centres, especially in iron-sulphur proteins. The previously unexplained anaerobic growth defect of the ytfE strain LMS 4209 was shown to be due to a secondary 126-gene deletion rather than to the deletion of ytfE. At the start of the project, the transcription factor, NsrR, was known to respond to low concentrations of intracellular NO, and to repress expression of ytfE, hcp-hcr encoding the hybrid cluster protein and its reductase, and hmp that encodes the flavohaemoglobin, Hmp. In this work, a biochemical assay of hcp promoter activity was developed as a reporter of intracellular NO generation. This assay was used in combination with a range of mutants to show that the major source of intracellular NO is the reduction of nitrite by the cytoplasmic nitrate reductase, NarG. Although the periplasmic cytochrome c nitrite reductase, NrfAB, and the cytoplasmic nitrite reductase, NirBD, decrease nitrosative stress by reducing nitrite to ammonia, at least one additional source of NO production from nitrite remains unidentified. An assay for NO reduction using a Clark-Type electrode was validated. Rates of NO reduction were induced 2-fold in the presence of nitrate. Lowest rates of NO reduction were found in a mutant defective in nsrR. A quadruple mutant defective in Hmp, the flavorubredoxin, NorV, NrfAB and NirBD still reduced NO at more than half the rate of the parent. This residual activity was not due to YibIH, YeaR-YoaG or YgbA. Various hcp-hcr derivatives of strains defective in NO reductases revealed a severe growth defect under conditions of nitrosative stress, but Hcp was eliminated as a possible additional NO reductase. This growth defect was substantially suppressed by a further mutation in ytfE. Growth experiments with isogenic sets of mutant defective in all combinations of hcp and ytfE in addition to deletions in hmp, norVW and nrfAB implicated both YtfE and Hcp in repair of nitrosative damage. However, weaker phenotypes of these strains in absence of nitrate or nitrite are consistent with more general roles for these proteins in the repair of damage to protein iron centres.
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Branco, Ricardo Garcia. "Stress response in critically ill children." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609718.

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Books on the topic "Stress response"

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Keyse, Stephen M. Stress Response. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590543.

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Stress response syndromes. 2nd ed. Northvale, N.J: J. Aronson, 1986.

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Stress response syndromes. 2nd ed. Northvale, NJ: J. Aronson, 1986.

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Horowitz, Mardi Jon. Stress response syndromes. Northvale, N.J: J. Aronson, 1992.

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Matějů, Daniel, and Jeffrey A. Chao, eds. The Integrated Stress Response. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1975-9.

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Egamberdieva, Dilfuza, and Parvaiz Ahmad, eds. Plant Microbiome: Stress Response. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-5514-0.

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Wondrak, Georg T., ed. Skin Stress Response Pathways. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43157-4.

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Tenhunen, John D., Fernando M. Catarino, Otto L. Lange, and Walter C. Oechel, eds. Plant Response to Stress. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-70868-8.

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Requena, Jose M. Stress response in microbiology. Norfolk, UK: Caister Academic Press, 2012.

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Kidd, S. P., ed. Stress response in pathogenic bacteria. Wallingford: CABI, 2011. http://dx.doi.org/10.1079/9781845937607.0093.

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Book chapters on the topic "Stress response"

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Ronai, Ze’ev. "Stress Response." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_5528-2.

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Morgan, Michael M., MacDonald J. Christie, Luis De Lecea, Jason C. G. Halford, Josee E. Leysen, Warren H. Meck, Catalin V. Buhusi, et al. "Stress-Response." In Encyclopedia of Psychopharmacology, 1289. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1704.

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Ronai, Ze’ev. "Stress Response." In Encyclopedia of Cancer, 4372–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_5528.

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Ronai, Ze’ev. "Stress Response." In Encyclopedia of Cancer, 3539–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5528.

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Ciampi, Quirino, Ayana Arystan, and Eugenio Picano. "Grading of Ischemic Response." In Stress Echocardiography, 291–302. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20958-6_18.

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Picano, Eugenio. "Grading of Ischemic Response." In Stress Echocardiography, 247–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-76466-3_18.

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Picano, Eugenio. "Grading of Ischemic Response." In Stress Echocardiography, 139–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-10090-5_18.

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Picano, Eugenio. "Grading of Ischemic Response." In Stress Echocardiography, 189–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05096-5_17.

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Bouveret, Emmanuelle, and Aurélia Battesti. "The Stringent Response." In Bacterial Stress Responses, 229–50. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816841.ch14.

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Miller, Dana L., Joseph Horsman, and Frazer I. Heinis. "Stress Response Pathways." In Healthy Ageing and Longevity, 191–217. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44703-2_9.

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Conference papers on the topic "Stress response"

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McKelvie, J,. "Consideration Of The Surface Temperature Response To Cyclic Thermoelastic Heat Generation." In Stress Analysis by Thermoelastic Techniques, edited by B. C. Gasper. SPIE, 1987. http://dx.doi.org/10.1117/12.937886.

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Sridharan, Sriram, Ritwik Layek, Aniruddha Datta, and Jijayanagaram Venkatraj. "Modelling oxidative stress response pathways." In 2011 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2011. http://dx.doi.org/10.1109/gensips.2011.6169471.

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Varghese, Rajani, Sriram Sridharan, Aniruddha Datta, and Jijayanagaram Venkatraj. "Modeling hypoxia stress response pathways." In 2013 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2013. http://dx.doi.org/10.1109/gensips.2013.6735939.

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Worthington, Paul F. "The Stress Response of Permeability." In SPE Annual Technical Conference and Exhibition. Society of Petroleum Engineers, 2004. http://dx.doi.org/10.2118/90106-ms.

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Reed, R. P., J. I. Greenwoll, F. Bauer, L. M. Lee, F. W. Davies, and D. J. Johnson. "Pulsed radiation response of stressed PVDF shock stress gauges." In High-pressure science and technology—1993. AIP, 1994. http://dx.doi.org/10.1063/1.46165.

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Laub, Michael. "2022 Microbial Stress Response GRC/GRS." In 2022 Microbial Stress Response GRC/GRS, Mount Holyoke College, South Hadley, Massachusetts, July 16-22, 2022. US DOE, 2022. http://dx.doi.org/10.2172/1898884.

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Beghi, M. G., C. E. Bottani, G. Caglioti, and A. Fazzi. "A Spectral Analyzer for the Thermoelastic and Thermoplastic Response of Solids to Low Frequency Dynamic Loads." In Stress Analysis by Thermoelastic Techniques, edited by B. C. Gasper. SPIE, 1987. http://dx.doi.org/10.1117/12.937887.

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Al-Ramahi, N., R. Joffe, and J. Varna. "Numerical Stress Analysis for Prediction of Crack Propagation Direction in Adhesive Layer." In VIII Conference on Mechanical Response of Composites. CIMNE, 2021. http://dx.doi.org/10.23967/composites.2021.060.

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Addis, M. A. "The Stress-Depletion Response Of Reservoirs." In SPE Annual Technical Conference and Exhibition. Society of Petroleum Engineers, 1997. http://dx.doi.org/10.2118/38720-ms.

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Zhou, Lang, Jinzi Deng, Jinzi Deng, Reinaldo E. Alcalde, Reinaldo E. Alcalde, Robert A. Sanford, Robert A. Sanford, et al. "BACTERIAL RESPONSE TO MICROFLUIDIC STRESS GRADIENTS." In 50th Annual GSA North-Central Section Meeting. Geological Society of America, 2016. http://dx.doi.org/10.1130/abs/2016nc-275646.

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Reports on the topic "Stress response"

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Dorsey, Achsah, Elissa M. Scherer, Randy Eckhoff, and Robert Furberg. Measurement of Human Stress: A Multidimensional Approach. RTI Press, June 2022. http://dx.doi.org/10.3768/rtipress.2022.op.0073.2206.

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Stress is a multidimensional construct that comprises exposure to events, perceptions of stress, and physiological responses to stress. Research consistently demonstrates a strong association between stress and a myriad of physical and mental health concerns, resulting in a pervasive and interdisciplinary agreement on the importance of investigating the relationship between stress and health. Developing a holistic understanding of stress requires assessment of the three domains vital to the study of stress: (1) the presence of environmental stressors, (2) psychological and biological reactions to stressors, and (3) the length of time over which the stressor or stress response occurs. Research into all three domains requires multiple methods. Self-reports allow for subjective evaluations of stress that illuminate the duration and severity of the psychological response to stressors. Biomarkers, in turn, capture a more-objective measure of stress and create a deeper understanding of the biological response to chronic and acute stress. Finally, the use of digital biomarkers allows for further exploration of the physiological fluctuations caused by stress by measuring the changes occurring at the same time as the stressor. Future research on stress and health should favor a multidimensional approach that creates a triangulated picture of stress, drawing from each of the three aforementioned method groups.
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Yu, David. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599228.

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Yu, Davis S. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada621841.

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Murray, Steven A., Matthew Yanagi, Wayne Ensign, and Burcu Darst. Stress Response as a Function of Task Relevance. Fort Belvoir, VA: Defense Technical Information Center, December 2010. http://dx.doi.org/10.21236/ada535519.

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Johnson, Jay, Rebecca Boddicker, Maria Victoria Sanz Fernandez, Jason W. Ross, Lance H. Baumgard, and Joshua T. Selsby. Gestational Thermal Environment Alters Postnatal Response to Heat Stress. Ames (Iowa): Iowa State University, January 2012. http://dx.doi.org/10.31274/ans_air-180814-690.

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Bray, Elizabeth, Zvi Lerner, and Alexander Poljakoff-Mayber. The Role of Phytohormones in the Response of Plants to Salinity Stress. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7613007.bard.

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Salinity is an increasing problem in many irrigated areas of crop production and is a significant factor in reducing crop productivity. Developmental, physiological, and molecular responses to salinity were studied in order to improve our understanding of these responses. Improvements in our understanding of plant responses to salinity are necessary in order to develop crops with improved salt tolerance. Previously, in Israel, it was shown that Sorghum biccolor can adapt to an otherwise lethal concentration of NaCl. These experiments were refined and it was shown that there is a specific window of development in which this adaption can occur. Past the window of development, Sorghum plants can not be adapted. In addition, the ability to adapt is not present in all genotypes of Sorghum. Cultivars that adapt have an increased coefficient of variation for many of the physiological parameters measured during the mid-phase of adaptation. Therefore, it is possible that the adaptation process does not occur identically in the entire population. A novel gene was identified, isolated and characterized from Sorghum that is induced in roots in response to salinity. This gene is expressed in roots in response to salt treatments, but it is not salt-induced in leaves. In leaves, the gene is expressed without a salt treatment. The gene encodes a proline-rich protein with a novel proline repeat, PEPK, repeated more than 50 times. An antibody produced to the PEPK repeat was used to show that the PEPK protein is present in the endodermal cell wall of the root during salt treatments. In the leaves, the protein is also found predominantly in the cell wall and is present mainly in the mesophyll cells. It is proposed that this protein is involved in the maintenance of solute concentration.
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Carey, Hannah V. The Adaptive Response to Intestinal Oxidative Stress in Mammalian Hibernation. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada442363.

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Clauw, Daniel. Dysregulation of the Stress Response in the Persian Gulf Syndrome. Fort Belvoir, VA: Defense Technical Information Center, November 1999. http://dx.doi.org/10.21236/ada393957.

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Lin, Shiaw-Yih, Chun-Jen Lin, Lili Gong, Hui Dai, and Ju-Seog Lee. Characterizing and Targeting Replication Stress Response Defects in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada611097.

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Clauw, Daniel J. Dysregulation of the Stress Response in the Persian Gulf Syndrome. Fort Belvoir, VA: Defense Technical Information Center, June 1997. http://dx.doi.org/10.21236/ada329210.

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