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Stress Activation (stress + activation)

Distribution by Scientific Domains

Life Sciences	50%

Selected Abstracts

Stress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor , antagonists

ARTHRITIS & RHEUMATISM, Issue 2 2008
Sarosh J. Motivala
Objective Psychological stress is thought to aggravate disease activity in rheumatoid arthritis (RA), although the physiologic mechanisms are unclear. Tumor necrosis factor , (TNF,) is an inflammatory cytokine involved in the exacerbation of RA, and TNF, antagonists have emerged as efficacious treatments. The purpose of this study was to determine whether RA patients show increased monocyte production of TNF, following acute psychological stress and whether such responses are abrogated in RA patients taking TNF, antagonists. Methods A standardized stress task was administered to 3 groups of subjects: RA patients taking TNF, antagonists, RA patients not taking such medications, and healthy controls. Lipopolysaccharide-stimulated monocyte production of inflammatory cytokines was repeatedly measured using intracellular staining and flow cytometry. Subjective stress, cardiovascular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured. Results The stress task induced increases in subjective stress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 groups. In addition, the stress task induced a significant increase (P < 0.001) in monocyte production of TNF, among RA patients who were not taking TNF, antagonists. However, monocyte production of TNF, did not change following psychological stress in RA patients taking TNF, antagonists or in healthy controls. Conclusion Brief psychological stress can trigger increased stimulated monocyte production of TNF, in RA patients. The use of TNF, antagonists protects against stress activation of cellular markers of inflammation in RA patients. [source]

Indications for cell stress in response to adenoviral and baculoviral gene transfer observed by proteome profiling of human cancer cells

ELECTROPHORESIS, Issue 11 2010
Christopher Gerner
Abstract Gene transfer to cultured cells is an important tool for functional studies in many areas of biomedical research and vector systems derived from adenoviruses and baculoviruses are frequently used for this purpose. In order to characterize how viral gene transfer vectors affect the functional state of transduced cells, we applied 2-D PAGE allowing quantitative determination of protein amounts and synthesis rates of metabolically labeled cells and shotgun proteomics. Using HepG2 human hepatoma cells we show that both vector types can achieve efficient expression of green fluorescent protein, which accounted for about 0.1% of total cellular protein synthesis 72,h after transduction. No evidence in contrast was found for expression of proteins from the viral backbones. With respect to the host cell response, both vectors induced a general increase in protein synthesis of about 50%, which was independent of green fluorescent protein expression. 2-D PAGE autoradiographs identified a 3.6-fold increase of ,-actin synthesis in adenovirus transduced cells. In addition shotgun proteomics of cytoplasmic and nuclear extract fractions identified a slight induction of several proteins related to inflammatory activation, cell survival and chromatin function by both virus types. These data demonstrate that commonly used gene transfer vectors induce a response reminiscent of stress activation in host cells, which needs to be taken into account when performing functional assays with transduced cells. [source]

REVIEW: Stress, alcohol and drug interaction: an update of human research

ADDICTION BIOLOGY, Issue 1 2009
Magdalena Uhart
ABSTRACT A challenging question that continues unanswered in the field of addiction is why some individuals are more vulnerable to substance use disorders than others. Numerous risk factors for alcohol and other drugs of abuse, including exposure to various forms of stress, have been identified in clinical studies. However, the neurobiological mechanisms that underlie this relationship remain unclear. Critical neurotransmitters, hormones and neurobiological sites have been recognized, which may provide the substrates that convey individual differences in vulnerability to addiction. With the advent of more sophisticated measures of brain function in humans, such as functional imaging technology, the mechanisms and neural pathways involved in the interactions between drugs of abuse, the mesocorticolimbic dopamine system and stress systems are beginning to be characterized. This review provides a neuroadaptive perspective regarding the role of the hormonal and brain stress systems in drug addiction with a focus on the changes that occur during the transition from occasional drug use to drug dependence. We also review factors that contribute to different levels of hormonal/brain stress activation, which has implications for understanding individual vulnerability to drug dependence. Ultimately, these efforts may improve our chances of designing treatment strategies that target addiction at the core of the disorder. [source]