Relevant bibliographies by topics / Stress suppression

Academic literature on the topic 'Stress suppression'

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

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Journal articles on the topic "Stress suppression"

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Beury, Daniel, Phillip Fitzgerald, Minu Srivastava, and Suzanne Ostrand-Rosenberg. "Do stress response genes play a role in maintaining MDSC survival and suppression? (100.17)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 100.17. http://dx.doi.org/10.4049/jimmunol.184.supp.100.17.

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Abstract Myeloid- derived suppressor cells (MDSC) contribute to immune suppression in tumor bearing individuals. Their suppression and survival are increased by inflammation. MDSC production of toxic radicals is the primary mechanism of suppression but the toxic mediators do not affect the MDSC themselves. We are investigating stress response genes that may maintain MDSC survival and facilitate suppression. BALB/c mice were injected with BALB/c derived mammary carcinoma 4T1 or 4T1 constitutively expressing the pro-inflammatory cytokine IL-1β (4T1/IL-1β). Primary tumors were surgically removed after 25 days. At 35 days, spleens were harvested and assayed for the percentage of Gr1+ CD11b+ MDSC. Surgical removal of 4T1 results in a regression of the MDSC population, however MDSC do not regress in mice bearing 4T1/IL-1β tumors, confirming that inflammation increases MDSC survival. Western blots and confocal microscopy of MDSC induced by 4T1 and 4T1/IL-1β tumors localize Nrf2 in the nucleus, demonstrating that Nrf2 is activated in MDSC. Catalase, a protein transcriptionally regulated by Nrf2, when added to a T cell activation assay eliminates MDSC suppressive activity. Addition of catalase to T cells co-cultured with MDSC and peptide causes a synergistic effect, activating T cells to a greater level than peptide alone. Collectively these data suggest that stress genes may play a role in maintaining MDSC survival and suppressive activity.
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Pollock, R. E., E. Lotzová, S. D. Stanford, and M. M. Romsdahl. "Effect of surgical stress on murine natural killer cell cytotoxicity." Journal of Immunology 138, no. 1 (January 1, 1987): 171–78. http://dx.doi.org/10.4049/jimmunol.138.1.171.

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Abstract Natural killer cell cytotoxicity (NKCC) against tumors may be important in preventing in vivo solid tumor dissemination. Multiple animal models demonstrate increased rates of tumor dissemination after surgical stress; previously, we have observed that surgical stress impairs murine NKCC. Because of the importance of surgery in the control of solid tumors, it appeared valuable to examine the mechanism underlying surgical stress impairment of NKCC. The results of this study demonstrate that postsurgical suppression of NKCC begins as early as 2 hr after murine hind limb amputation, reaches nadir at 4 days, and does not recover to control level until postoperative day 12. Anesthetic treatment alone does not cause comparable NKCC suppression. The suppression of NKCC accompanied changes in both splenic size and morphology. The immune suppression was observed in multiple compartments including peripheral blood, bone marrow, and spleen. Mixing experiments demonstrated that surgical stress per se generated a suppressor cell population affecting NKCC. The observed suppression apparently required cell-to-cell contact, because supernatants from 4 and 18 hr cultures of suppressor cells did not cause suppression. The observed suppression was prevented by perioperative treatment with the pyrimidinone analog 2-amino-5-bromo-6-phenyl-4-pyrimidinol. These preclinical observations point to the future prospect of NK-specific perioperative immunotherapy that may help prevent possible tumor dissemination from occurring at the time of surgery.
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Guigueno, Agnès, Janie Dassa, Pascal Belin, and Paul Louis Boquet. "Oversynthesis of a New Escherichia coliSmall RNA Suppresses Export Toxicity of DsbA′-PhoA Unfoldable Periplasmic Proteins." Journal of Bacteriology 183, no. 4 (February 15, 2001): 1147–58. http://dx.doi.org/10.1128/jb.183.4.1147-1158.2001.

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ABSTRACT In Escherichia coli, the DsbA′-PhoA hybrid proteins carrying an unfoldable DsbA′ fragment can be targeted to the envelope, where they exert their toxicity. Hybrid proteins stick to the periplasmic face of the inner membrane and paralyze the export mechanism, becoming lethal if sufficiently overproduced and if not degraded by the DegP protease (A. Guigueno, P. Belin, and P. L. Boquet, J. Bacteriol. 179:3260–3269, 1997). We isolated a multicopy suppressor that restores viability to a degP strain without modifying the expression level of the toxic fusion. Suppression does not involve activation of the known envelope stress-combative pathways, the Cpx pathway and the ςE regulon. Subclone analysis of the suppressor revealed a 195-bp DNA fragment that is responsible for toxicity suppression. The cloned gene, called uptR, is ≈130 bp long (including the promoter and a transcription termination signal) and is transcribed into a small RNA (92 nucleotides). Using site-directed mutagenesis, we found that UptR RNA does not require translation for toxicity suppression. UptR-mediated action reduces the amount of membrane-bound toxic hybrid protein. UptR RNA is the first example of a small RNA implicated in extracytoplasmic toxicity suppression. It appears to offer a new way of suppressing toxicity, and its possible modes of action are discussed.
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Amit, Z., and Z. H. Galina. "Stress-induced analgesia: adaptive pain suppression." Physiological Reviews 66, no. 4 (October 1, 1986): 1091–120. http://dx.doi.org/10.1152/physrev.1986.66.4.1091.

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In this paper we have examined the phenomenon of stress-induced analgesia. We have described the procedures used to measure analgesia and have suggested that the tests can be designed not only to indicate changes in pain threshold but also to allow for the determination of the capacity to execute adaptive behavior. Aside from enabling the analysis of responses, tests that induce reflexive as well as nonreflexive behavior may have the capacity to separate the more complex aspects of pain such as the possible presence of two components of pain, sensory/discriminative and motivational/affective. These components may be of fundamental importance for any attempt to understand the biological significance of SIA. Our examination of the neurotransmitter and neuropeptide systems has revealed that they are affected by the same manipulations that induce SIA. These amines and perhaps peptides play an integral role in learning, motivation, and performance. We conclude that the functional advantage of a reduction of pain during stressful situations is significant because it allows the animal to react in threatening and perhaps critical situations as if there were no pain. Once the pain system is inhibited, other systems modulate and mediate adaptive responses that expedite the survival of the animal.
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Glaser, Ronald, John Rice, John Sheridan, Richard Fertel, Julie Stout, Carl Speicher, David Pinsky, et al. "Stress-related immune suppression: Health implications." Brain, Behavior, and Immunity 1, no. 1 (March 1987): 7–20. http://dx.doi.org/10.1016/0889-1591(87)90002-x.

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Grachev, P., X. F. Li, M. H. Hu, S. Y. Li, R. P. Millar, S. L. Lightman, and K. T. O’Byrne. "Neurokinin B Signaling in the Female Rat: a Novel Link Between Stress and Reproduction." Endocrinology 155, no. 7 (July 1, 2014): 2589–601. http://dx.doi.org/10.1210/en.2013-2038.

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Acute systemic stress disrupts reproductive function by inhibiting pulsatile gonadotropin secretion. The underlying mechanism involves stress-induced suppression of the GnRH pulse generator, the functional unit of which is considered to be the hypothalamic arcuate nucleus kisspeptin/neurokinin B/dynorphin A neurons. Agonists of the neurokinin B (NKB) receptor (NK3R) have been shown to suppress the GnRH pulse generator, in a dynorphin A (Dyn)-dependent fashion, under hypoestrogenic conditions, and Dyn has been well documented to mediate several stress-related central regulatory functions. We hypothesized that the NKB/Dyn signaling cascade is required for stress-induced suppression of the GnRH pulse generator. To investigate this ovariectomized rats, iv administered with Escherichia coli lipopolysaccharide (LPS) following intracerebroventricular pretreatment with NK3R or κ-opioid receptor (Dyn receptor) antagonists, were subjected to frequent blood sampling for hormone analysis. Antagonism of NK3R, but not κ-opioid receptor, blocked the suppressive effect of LPS challenge on LH pulse frequency. Neither antagonist affected LPS-induced corticosterone secretion. Hypothalamic arcuate nucleus NKB neurons project to the paraventricular nucleus, the major hypothalamic source of the stress-related neuropeptides CRH and arginine vasopressin (AVP), which have been implicated in the stress-induced suppression of the hypothalamic-pituitary-gonadal axis. A separate group of ovariectomized rats was, therefore, used to address the potential involvement of central CRH and/or AVP signaling in the suppression of LH pulsatility induced by intracerebroventricular administration of a selective NK3R agonist, senktide. Neither AVP nor CRH receptor antagonists affected the senktide-induced suppression of the LH pulse; however, antagonism of type 2 CRH receptors attenuated the accompanying elevation of corticosterone levels. These data indicate that the suppression of the GnRH pulse generator by acute systemic stress requires hypothalamic NKB/NK3R signaling and that any involvement of CRH therewith is functionally upstream of NKB.
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Lin, Yuanshao, Xiaofeng Li, Micol Lupi, James S. Kinsey-Jones, Bei Shao, Strafford L. Lightman, and Kevin T. O'Byrne. "The Role of the Medial and Central Amygdala in Stress-Induced Suppression of Pulsatile LH Secretion in Female Rats." Endocrinology 152, no. 2 (February 1, 2011): 545–55. http://dx.doi.org/10.1210/en.2010-1003.

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Abstract Stress exerts profound inhibitory effects on reproductive function by suppressing the pulsatile release of GnRH and therefore LH. Although the mechanisms by which stressors disrupt the hypothalamic GnRH pulse generator remain to be fully elucidated, numerous studies have implicated the amygdala, especially its medial (MeA) and central nuclei (CeA), as key modulators of the neuroendocrine response to stress. In the present study, we investigated the roles of the MeA and CeA in stress-induced suppression of LH pulses. Ovariectomized rats received bilateral ibotenic acid or sham lesions targeting the MeA or CeA; blood samples (25 μl) were taken via chronically implanted cardiac catheters every 5 min for 6 h for the measurement of LH pulses. After 2 h of baseline sampling, the rats were exposed to either: restraint (1 h), insulin-induced hypoglycemia (IIH) (0.3 U/kg, iv), or lipopolysaccharide (LPS) (25 μg/kg, iv) stress. The restraint but not IIH or LPS stress–induced suppression of LH pulses was markedly attenuated by the MeA lesions. In contrast, CeA lesioning attenuated LPS, but not restraint or IIH stress–induced suppression of LH pulses. Moreover, after restraint stress, the number of Fos-positive neurons and the percentage of glutamic acid decarboxylase67 neurons expressing Fos was significantly greater in the GnRH-rich medial preoptic area (mPOA) of rats with intact, rather than lesioned, MeA. These data indicate that the MeA and CeA play key roles in psychogenic and immunological stress-induced suppression of the GnRH pulse generator, respectively, and the MeA-mediated effect may involve γ-aminobutyric acid ergic signaling within the mPOA.
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Tolbert, Dawn, Xiangdong Lu, Chaoying Yin, Mathew Tantama, and Terry Van Dyke. "p19ARF Is Dispensable for Oncogenic Stress-Induced p53-Mediated Apoptosis and Tumor Suppression In Vivo." Molecular and Cellular Biology 22, no. 1 (January 1, 2002): 370–77. http://dx.doi.org/10.1128/mcb.22.1.370-377.2002.

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ABSTRACT Recent studies have shown the p19ARF tumor suppressor to be involved in the response to oncogenic stress by regulating the activity of p53. This response is mediated by antagonizing the function of Mdm2, a negative regulator of p53, indicating a pathway for tumor suppression that involves numerous genes altered in human tumors. We previously described a transgenic mouse brain tumor model in which oncogenic stress, provided by cell-specific inactivation of the pRb pathway, triggers a p53-dependent apoptotic response. This response suppresses the growth of developing tumors and thus represents a bona fide in vivo tumor suppressor activity. We further showed that E2F1, a transcription factor known to induce p19ARF expression, was required for the response. Here, we use a genetic approach to test whether p19ARF functions to transduce the signal from E2F1 to p53 in this tumor suppression pathway. Contrary to the currently accepted hypothesis, we show that a deficiency in p19ARF has no impact on p53-mediated apoptosis or tumor suppression in this system. All measures of p53 function, including the level of apoptosis induced by pRb inactivation, the expression of p21 (a p53-responsive gene), and the rate of tumor growth, were comparable in mice with and without a functional p19ARF gene. Thus, although p19ARF is required in some cell types to transmit an oncogenic response signal to p53, it is dispensable for this function in an in vivo epithelial system. These results underscore the complexity of p53 tumor suppression and further indicate the existence of distinct cell-specific pathways that respond to similar stimuli.
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Wiest, David L. "Gadd45 stress sensors in suppression of leukemia." Oncotarget 9, no. 76 (September 28, 2018): 34191–92. http://dx.doi.org/10.18632/oncotarget.26154.

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Ogawa, Kenji, Masanori Hirai, Takao Katsube, Minoru Murayama, Kanako Hamaguchi, Takeshi Shimakawa, Yoshihiko Naritake, Toshihiko Hosokawa, and Tetsuro Kajiwara. "Suppression of cellular immunity by surgical stress." Surgery 127, no. 3 (March 2000): 329–36. http://dx.doi.org/10.1067/msy.2000.103498.

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Dissertations / Theses on the topic "Stress suppression"

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Bridgett, Stephen John. "Detail suppression of stress analysis models." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387980.

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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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N'Guessan, Prudence. "Décryptage du rôle de TP53INP1 dans la suppression de tumeur." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22070.

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Notre laboratoire a caractérisé TP53INP1 comme un gène clé de réponse au stress cellulaire. Cible de p53, TP53INP1 est ubiquitairement exprimé et fortement induit lors de différents stress in vivo et in vitro. Sa surexpression ectopique induit un arrêt du cycle cellulaire et la mort cellulaire. Nous avons montré que l’expression de TP53INP1 est perdue dans plusieurs cancers chez l’homme et que sa réexpression dans les cellules cancéreuses inhibe la croissance tumorale. De plus, les souris TP53INP1-déficientes sont très susceptibles au développement de tumeurs induites et présentent un stress oxydatif permanent caractérisé par une augmentation du taux de ROS. L’ensemble de ces résultats indique que TP53INP1 possède une fonction suppressive de tumeur probablement en lien avec son implication dans la régulation du statut redox cellulaire. Le but de mon travail de thèse est de décrypter cette fonction an niveau cellulaire et moléculaire en exploitant le modèle des souris déficientes. Mes travaux montrent que l’absence de TP53INP1 affecte tous les processus biologiques dérégulés lors de la tumorigenèse. En effet, la perte de TP53INP1 se caractérise par une augmentation de la prolifération cellulaire, de la migration cellulaire, de l’angiogenèse et de l’instabilité génétique. De façon paradoxale, les cellules déficientes pour TP53INP1 présentent une sensibilité accrue à l’apoptose induite par un stress indépendant ou non de p53. Cette sensibilité se base probablement sur un fort défaut de l’autophagie dans ces cellules. Nous observons également une diminution du taux des petites molécules antioxydantes liée au stress oxydatif constitutif observé dans ces souris. Les défauts observés en absence de TP53INP1 sont corrigés par un traitement avec un antioxydant, le N-Acetylcystéine, ce qui démontre le lien entre le rôle suppresseur de tumeur de TP53INP1 et son implication dans le contrôle du stress oxydatif. Ce travail a permis de mieux comprendre le rôle antioxydant TP53INP1 en lien avec sa fonction de suppresseur de tumeur
Our laboratory has characterized TP53INP1 as a key gene in cell stress response. Target of p53, TP53INP1 is ubiquitously expressed and strongly induced during various stress-inducing treatments in vivo and in vitro. Its ectopic overexpression induces cell cycle arrest and cell death. We have shown that the expression of TP53INP1 is lost in many human cancers and that its re-expression in cancer cells inhibits tumor growth. In addition, TP53INP1-deficient mice are highly susceptible to induced tumors and show a permanent oxidative stress characterized by increased ROS levels. Taken together, these results indicate that TP53INP1 has a tumor suppressor function likely related to its involvement in the regulation of cellular redox status. The purpose of my PhD is to decipher the cellular and molecular function of TP53INP1 by exploiting the model of deficient mice. My work shows that the absence of TP53INP1 affects all biological processes deregulated in tumorigenesis. Indeed, the loss of TP53INP1 is characterized by an increase in cell proliferation, cell migration, angiogenesis and genetic instability. Paradoxically, TP53INP1-deficient cells have increased susceptibility to stress-induced apoptosis, independently or not of p53. This sensitivity is probably based on a strong impairment of autophagy in these cells. We also observed a decrease in the rate of small antioxidant molecules related to constitutive oxidative stress in these mice. The defects observed in the absence of TP53INP1 are corrected by treatment with an antioxidant, N-acetylcysteine, demonstrating the link between the role of TP53INP1 in tumor suppression and its involvement in redox control. This work has led to a better understanding of the antioxidant role of TP53INP1 linked to its function as a tumor suppressor
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Blake-Mortimer, Jane. "Lymphocytic 5'-ectonucleotidase : a marker of psychological stress-induced immune suppression /." Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phb6364.pdf.

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Amstadter, Ananda Beth Laura L. Vernon Laura L. Burkhart Barry R. "Physiological effects of suppression of neutral and traumatic thoughts in posttraumatic stress disorder." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SUMMER/Psychology/Dissertation/AMSTADTER_ANA_20.pdf.

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Kennedy, Sarah L. "Stress-induced suppression of an antibody response: A role for splenic norepinephrine." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/dissertations/fullcit/3165815.

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Drysdale, Shara D. "Posttraumatic stress disorder, thought suppression and the self-regulatory executive function model." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368151.

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Stoeser, Casey J. "Expressive suppression : relation to post-traumatic stress disorder symptoms and emotional experience /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456295331&sid=7&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Davies, Mark Ian. "Vulnerability to analogue post-traumatic intrusions and experimental investigations of thought suppression." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308667.

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Arensdorf, Angela Marie. "The Mechanisms and Consequences of Gene Suppression During the Unfolded Protein Response." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/4816.

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The endoplasmic reticulum (ER) facilitates the synthesis, assembly and quality control of all secretory, transmembrane, and resident proteins of the endomembrane system. An accumulation of unfolded proteins or a disruption in the specialized folding environment within the organelle causes ER stress, thus impairing the folding capacity of the ER. In response to this stress, the ER initiates a signaling cascade called the unfolded protein response (UPR) in an attempt to restore ER homeostasis. The vertebrate UPR is propagated by three ER-resident transmembrane proteins (i.e., PERK, IRE1α, and ATF6α), each initiating a signaling cascade that ultimately culminates in production of a transcriptional activator. The UPR was originally characterized as a pathway for the upregulation of ER chaperones, and a comprehensive body of subsequent work has shown that protein synthesis, folding, oxidation, trafficking, and degradation are all transcriptionally enhanced by the UPR. However, UPR activation is also accompanied by extensive mRNA suppression. The mechanisms responsible for this suppression and its consequences for physiological processes beyond the realm of ER protein folding and processing are only now beginning to be described. The overall goal of my thesis work was to explore this process of UPR-mediated gene suppression by identifying the mechanisms involved and the cellular processes affected. As a result, I characterized a novel mechanism of UPR-mediated transcriptional repression involving the translational regulation of the transcription factor C/EBPβ resulting in the suppression of the gene Il4ra, encoding an essential subunit of the IL-4/IL-13 receptor. As a consequence of this suppression, a novel effect of ER stress was identified in the impairment of IL-4/IL-13 signaling, a finding of potential significance in the study of inflammatory disease. In addition to this mechanism, I validated a novel approach to the identification of UPR-regulated transcription factors using publically available bioinformatic software. Through this analysis, I identified the transcription factor HNF4α as a novel post-translational UPR-regulated transcription factor, the regulation of which, resulted in the suppression of a number of lipid metabolic genes. This analysis not only identified a novel UPR-regulated transcription factor, but also presented a new tool for the characterization of UPR-mediated gene suppression. My work represents an independent and original investigation into the process of UPR-mediated gene suppression; and reveals that the UPR facilitates transcriptional suppression through the transcriptional, translational, and post-translational regulation of multiple transcription factors, resulting in the coordinated attenuation of physiological pathways. This function of the UPR is likely to contribute to metabolic, inflammatory, and other chronic disease states.
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Books on the topic "Stress suppression"

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Jacobi, William R. Environmental effects of magnesium chloride-based dust suppression products on roadside soils, vegetation and stream water chemistry. Fort Collins, Colo: College of Agricultural Sciences, Dept. of Bioagricultural Sciences and Pest Management, Colorado State University, 2009.

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Kim, Raymond H. DJ-1 regulates tumour suppression by PTEN and cellular responses to oxidative stress in Parkinson's disease. 2006.

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Rutkowski, Krzysztof, and Michael Linden. Hurting Memories and Beneficial Forgetting: Posttraumatic Stress Disorders, Biographical Developments, and Social Conflicts. Elsevier Science & Technology Books, 2013.

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Rutkowski, Krzysztof, and Michael Linden. Hurting Memories and Beneficial Forgetting: Posttraumatic Stress Disorders, Biographical Developments, and Social Conflicts. Elsevier, 2013.

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Alhazzani, Waleed, and Deborah J. Cook. Stress ulcer prophylaxis and treatment drugs in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0041.

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Many changes have occurred over the last three decades in the field of stress ulcer gastrointestinal bleeding and its prevention. The topic is controversial, fuelled by disparate data, studies at risk of bias, and the impression that the problem is not as serious as it once was. Indeed, compared with over four decades ago when mucosal ulceration of the stomach causing serious bleeding was first described, a relatively small proportion of critically-ill patients now develop clinically important bleeding. Acid suppression is commonly prescribed for stress ulcer prophylaxis (SUP), targeting subgroups of patients at high risk in the intensive care unit (ICU), rather than universal prevention. The randomized clinical trials to date suggest a significant reduction in CIB with use of histamine-2-receptor antagonists (H2RAs) compared with no SUP, with no impact on pneumonia, ICU mortality, or length of stay. However, these trials are of moderate quality. More recent RCTs suggest proton pump inhibitors compared with H2RAs may significantly reduce the risk of CIB without influencing the risk of pneumonia, ICU mortality, or length of stay. These trials are also of moderate quality. Today, the decision whether to use SUP, and which agent to use, is complex. Clinical considerations include local epidemiological data (for centres documenting these outcomes), and patient-specific risks of gastrointestinal bleeding and infection, indexed to case mix.
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Luginbühl, Martin, and Arvi Yli-Hankala. Assessment of the components of anaesthesia. Edited by Antony R. Wilkes and Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0026.

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In modern anaesthesia practice, hypnotic drugs, opioids, and neuromuscular blocking agents (NMBAs) are combined. The introduction of NMBAs in particular substantially increased the risk of awareness and recall during general anaesthesia. Hypnotic drugs such as propofol and volatile anaesthetics act through GABAA receptors and have typical effects on the electroencephalogram (EEG). During increasing concentrations of these pharmaceuticals, the EEG desynchronization is followed by gradual synchronization, slowing frequency, and increasing amplitude of EEG, thereafter EEG suppressions (burst suppression), and, finally, isoelectric EEG. Hypnotic depth monitors such as the Bispectral Index™, Entropy™, and Narcotrend® are based on quantitative EEG analysis and translate these changes into numbers between 100 and 0. Although they are good predictors of wakefulness and deep anaesthesia, their usefulness in prevention of awareness and recall has been challenged, especially when inhalation anaesthetics are used. External and patient-related artifacts such as epileptiform discharges and frontal electromyography (EMG) affect the signal so their readings need careful interpretation. Their use is recommended in patients at increased risk of awareness and recall and in patients under total intravenous anaesthesia. Monitors of analgesia and nociception are not established in clinical practice but mostly remain experimental although some are commercially available. Some use EEG changes induced by noxious stimulation (EEG arousal) or quantify the frontal EMG in relation to EEG, while others are based on the sympathoadrenergic stress response. Various other devices are also discussed in this chapter.
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Bittner, Edward A., and Shawn P. Fagan. The host response to trauma and burns in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0304.

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Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.
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McGonagle, Dennis, and Iris Eshed. MRI. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0018.

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The features of psoriatic arthritis (PsA) are disparate—from peripheral synovitis to axial inflammation, from bone destruction to bone formation or both, and nail disease. Fat suppression magnetic resonance imaging (MRI) has had a major impact on understanding PsA. MRI suggests a unifying anatomical basis for PsA with the common denominator of disease localization to entheses and adjacent bone and other sites of high biomechanical stress. MRI has also shown that entheseal changes are not uncommon in generalized osteoarthritis and occasionally in normals, making careful clinical correlation essential for imaging interpretation. MRI is useful in predicting the course of axial spondyloarthritis but there are no specific studies in axial PsA; most data comes from ankylosing spondylitis. Additionally MRI has been used for monitoring therapeutic response in PsA where good resolution of enthesitis/osteitis has been reported. Further studies are needed to define the role of MRI in measuring biological remission of PsA.
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Lane, Jeffrey. Going to Jail Because of the Internet. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199381265.003.0005.

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Chapter 5 shows how the law works on the digital street. It reveals a new approach to gang suppression based on the editorial control of suspects’ online content. This chapter addresses a series of gang indictments in which police and prosecutors utilized social media to define and prosecute youth crews under conspiracy law, a practice that emerged as a stop-and-frisk method on the physical street lost legitimacy. The author shows how prosecutors learned to marshal social media as criminal evidence. This chapter explores also the pushback by teenagers whose code-switching strategies evolved to manage police suspicion. It considers gains in public safety and the collateral costs of the indictments.
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Pollock, Linda. The Affective Life in Shakespearean England. Edited by Malcolm Smuts. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199660841.013.25.

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Critiquing the amount of scholarly attention paid to the body and to intense, overwhelming feelings, this chapter examines how individuals, mainly the landed ranks, experienced and dealt with affect in daily life and relationships. While scholarship emphasizes suppression and disapproval of passion, this chapter views the management of affect as not only the repression of feelings but also as the encouragement and elicitation of them. It examines the available coping strategies for dealing with strong feelings such as anger or grief. It stresses the interconnections between affect and morality. Affect, judgment and conduct constituted a dynamic interchange in Shakespearean England. Feelings involve judgement and evaluation and are intimately connected to thoughts, norms, and culture. Finally, it points to the importance of the performative nature of affect in this period, concluding that culturally mandated or sanctioned emotions were not necessarily less authentic than spontaneous feelings.
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Book chapters on the topic "Stress suppression"

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Hornsby, Peter J. "Stress-Induced Senescence." In Cellular Senescence and Tumor Suppression, 85–106. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1075-2_4.

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Carcillo, J. A. "Critical Illness Stress-induced Immune Suppression." In Yearbook of Intensive Care and Emergency Medicine, 217–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-49433-1_20.

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Carcillo, J. A. "Critical Illness Stress-induced Immune Suppression." In Intensive Care Medicine, 217–28. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-49518-7_20.

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Sileshi, Gudeta W., and Taye Tessema. "Weed Suppression in Legume Crops for Stress Management." In Climate Change and Management of Cool Season Grain Legume Crops, 243–81. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3709-1_14.

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Dbaibo, Ghassan, and Yusuf A. Hannun. "Ceramide: A Stress Response Mediator Involved in Growth Suppression." In Sphingolipid-Mediated Signal Transduction, 19–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-22425-0_2.

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Schieman, Scott. "Suppression Effects in Social Stress Research and Their Implications for the Stress Process Model." In Advances in the Conceptualization of the Stress Process, 53–68. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1021-9_4.

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Peal, Lila, Michael Puckette, and Ramamurthy Mahalingam. "Identification of Stress-Responsive Genes in Plants Using Suppression Subtraction Hybridization: Ozone Stress as an Example." In Methods in Molecular Biology, 157–70. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-702-0_9.

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Zhang, Canhui, Dongdong Wang, and Jianlin Zhang. "Suppression of Zero-Energy Modes in Hybrid Finite Elements via Assumed Stress Fields." In Computational Methods in Engineering & Science, 254. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-48260-4_100.

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White, E. "Role of the Metabolic Stress Responses of Apoptosis and Autophagy in Tumor Suppression." In Oncogenes Meet Metabolism, 23–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/2789_2008_087.

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Ohtaki, Hirokazu, A. Takaki, L. Yin, K. Dohi, T. Nakamachi, M. Matsunaga, R. Horai, M. Asano, Y. Iwakura, and S. Shioda. "Suppression of oxidative stress after transient focal ischemia in interleukin-1 knock out mice." In Brain Edema XII, 191–94. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_41.

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Conference papers on the topic "Stress suppression"

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Onishi, Takashi, Eiji Iwamura, and Katsutoshi Takagi. "A study of hillock suppression in Al alloy interconnections for liquid crystal displays." In STRESS INDUCED PHENOMENA IN METALLIZATION. ASCE, 1998. http://dx.doi.org/10.1063/1.54658.

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Blackwell, Brendan, Athrey Nadhan, Alex Wu, and Randy Ewoldt. "Video: Fire suppression with yield-stress fluids." In 68th Annual Meeting of the APS Division of Fluid Dynamics. American Physical Society, 2015. http://dx.doi.org/10.1103/aps.dfd.2015.gfm.v0007.

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Koyama, H., Y. Mashiko, and T. Nishioka. "Suppression of Stress Induced Aluminum Void Formation." In 24th International Reliability Physics Symposium. IEEE, 1986. http://dx.doi.org/10.1109/irps.1986.362107.

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Likhite, Rugved, Aishwaryadev Banerjee, Chayanjit Ghosh, Apratim Majumder, Mohit Karkhanis, Hanseup Kim, and Carlos H. Mastrangelo. "Mems Stiction Suppression Using Low-Stress Camphor Sublimation." In 2020 IEEE 33rd International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2020. http://dx.doi.org/10.1109/mems46641.2020.9056436.

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Okuno, Masaki, Takayuki Aoyama, Satoshi Nakamura, Hiroshi Arimoto, and Kei Horiuchi. "Suppression of Transient Enhanced Diffusion by LOCOS Induced Stress." In 1998 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 1998. http://dx.doi.org/10.7567/ssdm.1998.a-8-3.

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Aziz, Imran, Wasim Tarar, Imran Akhtar, and M. Nadeem Azam. "Vibratory Stress Suppression in Turbine Blades Subjected to Aerodynamic Loading." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-63724.

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Vibratory stresses are the main cause of failure in gas turbine engines and other rotating machinery components. These stresses must be attenuated to an acceptable level through an efficient process in order to prevent failures in turbine blades. Research [8] has shown that a thin magneto mechanical coating layer can make a significant contribution to the damping and reduction of these vibratory stresses. Previous studies on analyzing the damping characteristics of these coatings for various applications, such as beams and turbine blades, employed general solid mechanics loads. In this study, we numerically compute aerodynamic loads on one and a half stage axial turbine in order to bring more reality to the problem. We employ a three-dimensional finite-volume based solver to simulate the flow in the turbine using SST model to account for turbulence effects. Sliding mesh technique is used to allow the transfer of flow parameters across the sliding rotor/stator interfaces. In order to model a single passage configuration, profile transformation method is used. A free vibration analysis has been performed to obtain natural frequencies and corresponding mode shapes to analyze resonance conditions. The computed CFD loads are then applied to an uncoated and coated turbine blade through a finite-element analysis (FEA) package. A forced response analysis is performed at the critical frequencies to obtain vibratory stresses. Numerical results show suppression of vibratory stresses at various low and high frequency vibration modes. The results are benchmarked against published data and closely match the expected outcome. The research presents an effective procedure for suppression of vibratory stresses in gas turbine engine component subjected to real world aerodynamic loading. The new procedure is a significant improvement towards more realistic simulation based solutions for vibration suppression problems.
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Baucom, J. N., M. A. Qidwai, W. R. Pogue, and J. P. Thomas. "Suppression of Edge Delamination Through Meso-Scale Structuring." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-81534.

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We are developing a new class of fiber-reinforced polymer composite materials to facilitate imbedding multifunctional features and devices in material systems, and to manage interlaminar stresses at free edges and cut-outs. The idea is centered on introducing one more level of design space by composing plies with individual tiles possessing the same degrees of design freedom that are associated with individual plies. In this work, we have focused on tiling schemes that will allow blending of laminates (lay-ups), where a lay-up suitable for suppressing interlaminar stresses could be placed at necessary locations whereas another lay-up could be used for the main objective. This results in the introduction of matrix-rich tile-to-tile interface pockets in the blending region. Preliminary mechanical testing shows that uniaxially reinforced tiled composites attain stiffness levels near those of their traditional counterparts, yet with a potential degradation of strength. We used the finite element method to investigate the effects of resin-rich pocket size, the use of supporting continuous layers, tile size, and tile overlapping (interface stacking) schemes on stress distribution around interfaces in uniaxially reinforced tiled composites, with the aim to identify parameters controlling overall strength. We discovered that alignment of the resin-rich pockets through the thickness exacerbates stress-concentration and that outer continuous layers on the composite may help in better load transfer. As a first step in the application of this technique for the suppression of delamination at the free edges of holes in laminates, a bilaminate material was modeled, and the concept was shown to be effective in the suppression of edge delamination.
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Hayes, D. B. "Precursor Suppression by Shear Stress Relaxation in U-Nb(6-wt%)." In SHOCK COMPRESSION OF CONDENSED MATTER - 2003: Proceedings of the Conference of the American Physical Society Topical Group on Shock Compression of Condensed Matter. AIP, 2004. http://dx.doi.org/10.1063/1.1780304.

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Miyata, Shohei, Terukazu Sato, Kimihiro Nishijima, and Takashi Nabeshima. "Voltage stress suppression method using coupled transformer for phase shift controlled converter." In 2013 International Conference on Renewable Energy Research and Applications (ICRERA). IEEE, 2013. http://dx.doi.org/10.1109/icrera.2013.6749842.

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Iwamoto, Hiroyuki, Katsuji Nakamura, Kaichi Tsuruta, and Osamu Munekata. "Study on Suppression of External Stress Type Tin Whisker by PR Current Method." In 2021 International Conference on Electronics Packaging (ICEP). IEEE, 2021. http://dx.doi.org/10.23919/icep51988.2021.9451952.

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Reports on the topic "Stress suppression"

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Sugama, H., and W. Horton. Shear flow generation by Reynolds stress and suppression of resistive g-modes. Office of Scientific and Technical Information (OSTI), August 1993. http://dx.doi.org/10.2172/10184529.

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Granot, David, and Noel Michelle Holbrook. Role of Fructokinases in the Development and Function of the Vascular System. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592125.bard.

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Plant vascular tissues are superhighways whose development and function have profound implications for productivity, yield and stress response. Preliminary studies by the PI indicated that sugar metabolism mediated by fructokinases (FRKs) has a pronounced effect on the transport properties of the xylem. The goal of this research was to determine how the main fructokinase gene, FRK2, and the only plastidic fructokinase, FRK3, influence vascular development and physiology, emphasizing processes that occur at both the cellular and organismic level. We found that both genes are expressed in vascular tissues, but FRK3 is expressed primarily in vascular tissues of mature petioles. Vascular anatomy of plants with antisense suppression of FRK2 uncovered that FRK2 is necessary for xylem and phloem development, most likely due to its role in vascular cell-wall synthesis, and affects vascular development all over the plant. As a result, suppression of FRK2 reduced hydraulic conductivity of roots, stem and leaves and restricted sugar phloem transport. Vascular anatomy of plants with RNAi suppression of FRK3 uncovered that FRK3 is required for vascular development in mature petiole but its role is partially complemented by FRK2. Suppression of FRK3 combined with partial suppression of FRK2 had effects completely different from that of FRK2 suppression, resulting in wilting of mature leaves rather than young leaves of FRK2 suppressed plants, and decreased export of photoassimilates. This primary effect of FRK2 suppression on mature petioles had a secondary effect, reducing the hydraulic conductivity in roots and stem. The very fact that a plastidic fructokinase plays a role in vascular development is quite surprising and we are still seeking to uncover its metabolic mode-of-action. Yet, it is clear that these two fructokinases have different roles in the coordination between photosynthetic capacity and vascular development. We have started analyzing the role of the last third FRK, FRK1, and discovered that it is also expressed exclusively in vascular tissues. It appears therefore, that all FRKs studied here are involved in vascular development. An interesting unexpected outcome of this study was the connection of FRK2 with hormonal regulation of vascular development, most likely auxin. This observation together with the yet to be solved questions on the exact roles of FRK3 are the subjects of our current efforts.
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Wolfenson, David, William W. Thatcher, Rina Meidan, Charles R. Staples, and Israel Flamenbaum. Hormonal and Nutritional Stretegies to Optimize Reproductive Function and Improve Fertility of Dairy Cattle during Heat Stress in Summer. United States Department of Agriculture, August 1994. http://dx.doi.org/10.32747/1994.7568773.bard.

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The BARD program includes two main parts. In the first, experiments were conducted to complete our understanding of the mechanisms responsible for the impairment of reproductive functions under heat stress. Experiments focused on follicular development and function, since results obtained in our previous BARD project indicate that the preovulatory follicle is susceptible to heat stress. The theca cells, sensitive to thermal stress, produced less androgen during the summer, as well as during the autumn. Similarly, luteinized theca cells obtained from cows in summer produced much less progesterone than in winter. Granulosa cells and luteinized granulosa cells were less susceptible to heat stress. A delayed effect of heat stress on follicular development, on suppression of dominance and on steroid production by theca and granulosa cells was noted. This may be related to the low fertility of cows during the cool months of autumn. In the second part, experiments were conducted aiming to improve fertility in summer. The timed AI program was developed using two injections of GnRH coupled with PGF2a. It was found effective in improving reproductive performance in lactating cows. Limitations induced by heat stress on estrus detection were eliminated with the timed AI management program. Replacing the second injection of GnRH with hCG instead of GnRH agonist increased plasma progesterone levels post ovulation but did not improve fertility. Use of the timed AI program in summer, shortened days open and increased the net revenue per cow, however, it did not protect the embryo fiom temperature-induced embryonic mortality. Incorporation of a GnRH-agonist implant into the timed AJ program was examined. The implant increased plasma progesterone and LH concentrations and altered follicular dynamics. The use of a GnRH-implant enhanced pregnancy rate in cows with low body conditions. In a timed embryo transfer experiment, the use of fresh or frozen in vitro produced embryos was compared in the summer to improve fertility. The use of flesh embryos (but not frozen ones) improved pregnancy rate, however, substantial embryonic death occurred between 21 and 45 days. The timed AI program, which is now being used commercially, shortened days open, and increased pregnancy rate during summer. Other approaches which were found to improve fertility in small-scale studies, need to be tested again in large-scale field trials.
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Crowley, David E., Dror Minz, and Yitzhak Hadar. Shaping Plant Beneficial Rhizosphere Communities. United States Department of Agriculture, July 2013. http://dx.doi.org/10.32747/2013.7594387.bard.

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PGPR bacteria include taxonomically diverse bacterial species that function for improving plant mineral nutrition, stress tolerance, and disease suppression. A number of PGPR are being developed and commercialized as soil and seed inoculants, but to date, their interactions with resident bacterial populations are still poorly understood, and-almost nothing is known about the effects of soil management practices on their population size and activities. To this end, the original objectives of this research project were: 1) To examine microbial community interactions with plant-growth-promoting rhizobacteria (PGPR) and their plant hosts. 2) To explore the factors that affect PGPR population size and activity on plant root surfaces. In our original proposal, we initially prqposed the use oflow-resolution methods mainly involving the use of PCR-DGGE and PLFA profiles of community structure. However, early in the project we recognized that the methods for studying soil microbial communities were undergoing an exponential leap forward to much more high resolution methods using high-throughput sequencing. The application of these methods for studies on rhizosphere ecology thus became a central theme in these research project. Other related research by the US team focused on identifying PGPR bacterial strains and examining their effective population si~es that are required to enhance plant growth and on developing a simulation model that examines the process of root colonization. As summarized in the following report, we characterized the rhizosphere microbiome of four host plant species to determine the impact of the host (host signature effect) on resident versus active communities. Results of our studies showed a distinct plant host specific signature among wheat, maize, tomato and cucumber, based on the following three parameters: (I) each plant promoted the activity of a unique suite of soil bacterial populations; (2) significant variations were observed in the number and the degree of dominance of active populations; and (3)the level of contribution of active (rRNA-based) populations to the resident (DNA-based) community profiles. In the rhizoplane of all four plants a significant reduction of diversity was observed, relative to the bulk soil. Moreover, an increase in DNA-RNA correspondence indicated higher representation of active bacterial populations in the residing rhizoplane community. This research demonstrates that the host plant determines the bacterial community composition in its immediate vicinity, especially with respect to the active populations. Based on the studies from the US team, we suggest that the effective population size PGPR should be maintained at approximately 105 cells per gram of rhizosphere soil in the zone of elongation to obtain plant growth promotion effects, but emphasize that it is critical to also consider differences in the activity based on DNA-RNA correspondence. The results ofthis research provide fundamental new insight into the composition ofthe bacterial communities associated with plant roots, and the factors that affect their abundance and activity on root surfaces. Virtually all PGPR are multifunctional and may be expected to have diverse levels of activity with respect to production of plant growth hormones (regulation of root growth and architecture), suppression of stress ethylene (increased tolerance to drought and salinity), production of siderophores and antibiotics (disease suppression), and solubilization of phosphorus. The application of transcriptome methods pioneered in our research will ultimately lead to better understanding of how management practices such as use of compost and soil inoculants can be used to improve plant yields, stress tolerance, and disease resistance. As we look to the future, the use of metagenomic techniques combined with quantitative methods including microarrays, and quantitative peR methods that target specific genes should allow us to better classify, monitor, and manage the plant rhizosphere to improve crop yields in agricultural ecosystems. In addition, expression of several genes in rhizospheres of both cucumber and whet roots were identified, including mostly housekeeping genes. Denitrification, chemotaxis and motility genes were preferentially expressed in wheat while in cucumber roots bacterial genes involved in catalase, a large set of polysaccharide degradation and assimilatory sulfate reduction genes were preferentially expressed.
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Droby, Samir, Michael Wisniewski, Ron Porat, and Dumitru Macarisin. Role of Reactive Oxygen Species (ROS) in Tritrophic Interactions in Postharvest Biocontrol Systems. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7594390.bard.

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To elucidate the role of ROS in the tri-trophic interactions in postharvest biocontrol systems a detailed molecular and biochemical investigation was undertaken. The application of the yeast biocontrol agent Metschnikowia fructicola, microarray analysis was performed on grapefruit surface wounds using an Affymetrix Citrus GeneChip. the data indicated that 1007 putative unigenes showed significant expression changes following wounding and yeast application relative to wounded controls. The expression of the genes encoding Respiratory burst oxidase (Rbo), mitogen-activated protein kinase (MAPK) and mitogen-activated protein kinase kinase (MAPKK), G-proteins, chitinase (CHI), phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS) and 4-coumarate-CoA ligase (4CL). In contrast, three genes, peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT), were down-regulated in grapefruit peel tissue treated with yeast cells. The yeast antagonists, Metschnikowia fructicola (strain 277) and Candida oleophila (strain 182) generate relatively high levels of super oxide anion (O2−) following its interaction with wounded fruit surface. Using laser scanning confocal microscopy we observed that the application of M. fructicola and C. oleophila into citrus and apple fruit wounds correlated with an increase in H2O2 accumulation in host tissue. The present data, together with our earlier discovery of the importance of H₂O₂ production in the defense response of citrus flavedo to postharvest pathogens, indicate that the yeast-induced oxidative response in fruit exocarp may be associated with the ability of specific yeast species to serve as biocontrol agents for the management of postharvest diseases. Effect of ROS on yeast cells was also studied. Pretreatment of the yeast, Candida oleophila, with 5 mM H₂O₂ for 30 min (sublethal) increased yeast tolerance to subsequent lethal levels of oxidative stress (50 mM H₂O₂), high temperature (40 °C), and low pH (pH 4). Suppression subtractive hybridization analysis was used to identify genes expressed in yeast in response to sublethal oxidative stress. Transcript levels were confirmed using semi quantitative reverse transcription-PCR. Seven antioxidant genes were up regulated. Pretreatment of the yeast antagonist Candida oleophila with glycine betaine (GB) increases oxidative stress tolerance in the microenvironment of apple wounds. ROS production is greater when yeast antagonists used as biocontrol agents are applied in the wounds. Compared to untreated control yeast cells, GB-treated cells recovered from the oxidative stress environment of apple wounds exhibited less accumulation of ROS and lower levels of oxidative damage to cellular proteins and lipids. Additionally, GB-treated yeast exhibited greater biocontrol activity against Penicillium expansum and Botrytis cinerea, and faster growth in wounds of apple fruits compared to untreated yeast. The expression of major antioxidant genes, including peroxisomal catalase, peroxiredoxin TSA1, and glutathione peroxidase was elevated in the yeast by GB treatment. A mild heat shock (HS) pretreatment (30 min at 40 1C) improved the tolerance of M. fructicola to subsequent high temperature (45 1C, 20–30 min) and oxidative stress (0.4 mol-¹) hydrogen peroxide, 20–60 min). HS-treated yeast cells showed less accumulation of reactive oxygen species (ROS) than non-treated cells in response to both stresses. Additionally, HS-treated yeast exhibited significantly greater (P≥0.0001) biocontrol activity against Penicillium expansum and a significantly faster (Po0.0001) growth rate in wounds of apple fruits stored at 25 1C compared with the performance of untreated yeast cells. Transcription of a trehalose-6-phosphate synthase gene (TPS1) was up regulated in response to HS and trehalose content also increased.
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Weinschenk, Craig, Keith Stakes, and Robin Zevotek. Impact of Fire Attack Utilizing Interior and Exterior Streams on Firefighter Safety and Occupant Survival: Air Entrainment. UL Firefighter Safety Research Institute, December 2017. http://dx.doi.org/10.54206/102376/gmax3657.

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As research continues into how fire department interventions affect fire dynamics in the modern fire environment, questions continue to arise on the impact and implications of interior versus exterior fire attack on both firefighter safety and occupant survivability. Previous research into various types of fire ground ventilation, flow paths, and exterior fire streams has provided the fire service with an increased understanding of fire dynamics. However, in some instances, the information from the studies did not support current, experience-based practices. This gap between the research to date and the fire ground suppression experience has driven the need for further study. This study will build upon the fire research conducted to date by analyzing how firefighting tactics, specifically different fire suppression tools and tactics, affect the thermal exposure and survivability of both firefighters and building occupants and affect fire behavior in structures. The purpose of this study is to improve firefighter safety, fire ground tactics, and the knowledge of fire dynamics by providing the fire service with scientific information, developed from water flow and full-scale fire testing, in representative single-family homes. This study will build and expand upon the fire research conducted to date by analyzing how firefighting tactics, specifically suppression methods, affect the thermal exposure and survivability of both firefighters and building occupants in addition to impacting fire behavior in structures. The purpose of this study is to improve firefighter safety, fireground tactics, and the knowledge of fire dynamics by providing the fire service with credible scientific information, developed from both water flow and full-scale fire testing, in representative single family homes. The project is comprised of 3 parts: • Part I: Water Distribution • Part II: Air Entrainment • Part III: Full-Scale Residential Fire Experiments This report details the results and analysis from the air entrainment testing. These tests were conducted without the presence of fire to gain a fundamental understanding of how hose streams entrain air. Each set of experiments was intended to add to the understanding of air entrainment and pressure from fire service hose streams by evaluating the differences caused by various application methods, hose stream types, nozzle movements, pressures/flow rates, manufacturers, and ventilation configurations.
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Regan, Jack, Julie Bryant, and Craig Weinschenk. Analysis of the Coordination of Suppression and Ventilation in Single-Family Homes. UL Firefighter Safety Research Institute, March 2020. http://dx.doi.org/10.54206/102376/slzh7498.

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Prior full-scale research with the fire service was primarily designed to isolate specific tactics, most often either ventilation or suppression, which allowed researchers to develop science-based recommendations related to the specific components of fireground operations studied in relatively controlled conditions. The current project went beyond earlier research by conducting twenty experiments in eight acquired, single-family residential structures and that combined fireground tactics to quantify the impact of coordination between ventilation and suppression actions. This experimental series included second-story bedroom fires (14 experiments) and first-floor kitchen fires (6 experiments). The main control variables studied included the position of initial application of water, the ventilation method, and the timing of ventilation relative to water application. The ventilation tactics examined in these experiments included horizontal, vertical, positive pressure, and hydraulic ventilation, while the suppression tactics included both interior water application and initial exterior water application followed by interior water application. While some elements of the experiments (e.g. structure floor plan and weather) resulted in increased variability, the lessons learned highlighted the importance of having a systematic approach to the implementation of tactics. Most importantly, there was no meaningful increase in temperature outside of fire rooms when ventilation tactics were executed in coordination with (shortly after or shortly before) the onset of suppression. The effectiveness of suppression actions in extinguishing the fire were dependent on the ability of those actions to 1) cool surfaces in the fire room and 2) wet unburned fuel. Exterior suppression actions on second-floor bedroom fires resulted in a decrease in temperatures throughout the second floor, followed by regrowth prior to final suppression through interior streams. When exterior suppression was performed on first-floor kitchen fires, where more complete fuel wetting was possible, regrowth was not observed prior to interior suppression. When surface cooling or fuel wetting are not possible due to the elevation of the fire room, missing ceiling, or obstacles, firefighters should consider alternative means of water distribution to improve the effectiveness of suppression actions from outside the fire room. Suppression actions, whether interior or exterior, generally resulted in a decrease in temperatures and gas concentrations at locations where occupants may potentially be located. Conditions improved most quickly at locations closest in proximity to the inlet of the flow path established between the front door and the fire room. For this reason, opening an exterior door to gain access should be thought of as an important ventilation action, both in terms of its potential to cause fire growth and its potential to improve conditions for potentially trapped occupants. After effective suppression, structure ventilation operations should similarly be cognizant of gas flows, with the aim of establishing flow throughout all areas where occupants may be located.
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Menefee, Maia Catherine, and Michael W. Salmon. Allowable Stresses For Use in Dynamic Analysis of PF-4 Fire Suppression System Piping. Office of Scientific and Technical Information (OSTI), May 2017. http://dx.doi.org/10.2172/1360690.

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Weinschenk, Craig, Keith Stakes, and Robin Zevotek. Impact of Fire Attack Utilizing Interior and Exterior Streams on Firefighter Safety and Occupant Survival: Water Mapping. UL Firefighter Safety Research Institute, December 2017. http://dx.doi.org/10.54206/102376/nevx1787.

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As research continues into how fire department interventions affect fire dynamics in the modern fire environment; questions continue to arise on the impact and implications of interior versus exterior fire attack on both firefighter safety and occupant survivability. Previous research into various types of fire ground ventilation, flow paths, and exterior fire streams has provided the fire service with an increased understanding of fire dynamics. However, in some instances, the information from the studies may not support current, experienced-based practices. This gap between the research to date and the fire ground suppression experience has driven the need for further study. Therefore, research into the various methods of fire attack will allow a broader understanding of how firefighter interventions on the fire ground can impact the outcome of both life safety and property protection. This study will build upon the fire research conducted to date by analyzing how firefighting tactics, specifically different fire suppression tools and tactics, affect the thermal exposure and survivability of both firefighters and building occupants and affect fire behavior in structures. The purpose of this study is to improve firefighter safety, fireground tactics, and the knowledge of fire dynamics by providing the fire service with scientific information, developed from water flow and full-scale fire testing, in representative single-family homes. The project will be comprised of 3 parts: • Part I: Water Distribution • Part II: Air Entrainment • Part III: Full-Scale Residential Fire Experiments This report details the results and analysis from the water distribution experiments. These tests were conducted without the presence of fire to gain a fundamental understanding of water flows into compartments. Each test was designed to quantify water distribution within a compartment by evaluating the differences caused by various application methods, hose stream types, nozzle movements, pressures/flow rates, stream locations and elevation angles.
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Zevotek, Robin, Keith Stakes, and Joseph Willi. Impact of Fire Attack Utilizing Interior and Exterior Streams on Firefighter Safety and Occupant Survival: Full-Scale Experiments. UL Firefighter Safety Research Institute, January 2018. http://dx.doi.org/10.54206/102376/dnyq2164.

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As research continues into how fire department interventions affect fire dynamics in the modern fire environment, questions continue to arise on the impact and implications of interior versus exterior fire attack on both occupant survivability and firefighter safety. This knowledge gap and lack of previous research into the impact of fire streams has driven the need for further research into fire department interventions at structure fires with a focus on hose streams and suppression tactics. As the third report in the project “Impact of Fire Attack Utilizing Interior and Exterior Streams on Firefighter Safety and Occupant Survival”, this report expands upon the fire research conducted to date by analyzing how firefighting tactics, specifically suppression methods, affect the thermal exposure and survivability of both building occupants and firefighters in residential structures. • Part I: Water Distribution • Part II: Air Entrainment • Part III: Full-Scale Residential Fire Experiments. This report evaluates fire attack in residential structures through twenty-six full-scale structure fire experiments. Two fire attack methods, interior and transitional, were preformed at UL’s large fire lab in Northbrook, IL, in a single-story 1,600 ft2 ranch test structure utilizing three different ventilation configurations. To determine conditions within the test structure it was instrumented for temperature, pressure, gas velocity, heat flux, gas concentration, and moisture content. Ad- ditionally, to provide information on occupant burn injuries, five sets of instrumented pig skin were located in pre-determined locations in the structure. The results were analyzed to determine consistent themes in the data. These themes were evaluated in conjunction with a panel of fire service experts to develop 18 tactical considerations for fire ground operations. As you review the following tactical considerations it is important to utilize both these research results and your per- sonal experience to develop your department’s polices and implement these considerations during structural firefighting.
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