Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In different tissues alteration of protein synthesis has been observed during acute stress. In this review we characterise the modulation of pancreatic protein synthesis during inflammation. A sustained decrease of mRNA levels of secretory enzymes is accompanied by noncoordinated alterations of protein synthesis during the acute phase and the recovery from pancreatitis. For that regulation both translational and transcriptional alterations are of importance. The most prominent finding was the expression of pancreatitis-associated proteins (PAP) in humans or rats, which are absent in the normal gland but synthesised during acute pancreatitis. PAPs are pancreatic secretory proteins, their mRNA were cloned and sequenced and the sequence of encoded preproteins of 175 amino acids were deduced. The PAP expression increased as a function of the severity of pancreatitis. It can be assayed in serum and may be used as a marker of the disease. Due to its affinity to bacterial surfaces the PAP molecule could act as an endogenous antibiotic factor that prevents the bacterial infection of the inflamed pancreas.
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PMID:The acute phase reaction of the exocrine pancreas. Gene expression and synthesis of pancreatitis-associated proteins. 818 76

While postnatal bacterial infection is capable of inducing a variety of long lasting functional alterations in immune function, the specific physiological pathways responsible for this modification are largely unknown. In the current investigation we explore the hypothesis that early life exposure to endotoxin permanently modifies the function of T helper (Th) cell activity. Therefore we examined Th-cell regulated in vivo humoral and ex vivo cellular responses to keyhole limpet hemocyanin (KLH). Given that stress has been shown to exacerbate some of the immunological alterations exhibited by the neonatally endotoxin challenged adult, we examined the adult's Th1/Th2 responses to KLH under conditions of no stress, acute stress (2 daysx2 h), and chronic stress (7 daysx2 h). Our results demonstrate that adults neonatally challenged with endotoxin were found to produce significantly less IgG1 following KLH challenge following acute stress (p<0.05). Neonatally endotoxin treated animals exposed to acute stress were also found to produce less IgM than saline or endotoxin treated animals exposed to no-stress or chronic stress. No neonatal treatment group differences observed in the production of INF-gamma or IL-4 in adulthood. In summary, the results from the present study provide little evidence to directly support the hypothesis that neonatal endotoxin exposure significantly alters the Th1/Th2 balance in adulthood.
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PMID:Neonatal bacterial endotoxin challenge interacts with stress in the adult male rat to modify KLH specific antibody production but not KLH stimulated ex vivo cytokine release. 1911 14

The focus of the 2011 American Aging Association meeting was emerging concepts in the mechanisms of aging. Many of the usual topics in aging were covered, such as dietary restriction (DR), inflammation, stress resistance, homeostasis and proteasome activity, sarcopenia, and neural degeneration. There was also discussion of newer methods, such as microRNAs and genome sequencing, that have been employed to investigate gene expression variance with aging and genetic signatures of longevity. Aging as a field continues to mature, including the following areas: Using a systems approach to tracing conserved pathways across organisms; sharpening definitions of sarcopenia, frailty, and health span; and distinguishing interventions by age tier (early-onset versus late-onset). A preconference session on late-onset intervention concluded that there are numerous benefits to deriving such interventions. Conference talks applied the biology of aging in a translational manner to intervention development. Using an individual's own stem cells to regenerate organs for transplantation and as a cell source for cellular therapies could be a powerful near-term solution to disease. Several proposed interventions were pharmaceutical, myostatin inhibition, losartan, Janus kinase (JAK) pathway inhibitors, and enalapril for frailty and sarcopenia, and metformin to promote the Nrf2 antiinflammation response. In DR, protein restriction was found to be better than general calorie restriction. Short-term fasting may be helpful in chemotherapy, surgery, and acute stress, simultaneously increasing the killing of cancer cells by chemotherapy, while improving the survival of normal cells. Immune system interventions remain elusive, although statins may help to improve cellular senescence promoted bacterial infection. Engineered enzymes may be useful in lysosomal catabolism. Dietary restriction mimetics, most promisingly involving target of rapamycin (TOR; TORC1 inhibition and rapamycin), may be more feasible than dietary restriction.
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PMID:Meeting report: American Aging Association 40th Annual Meeting, Raleigh, North Carolina, June 3-6, 2011. 2185 Nov 78

The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathway is involved in the regulation of intestinal stem cell (ISC) activity to ensure a continuous renewal of the adult Drosophila midgut. Three ligands, Unpaired 1, Unpaired 2 and Unpaired 3 (Upd1, Upd2 and Upd3, respectively) are known to activate the JAK/STAT pathway in Drosophila. Using newly generated upd mutants and cell-specific RNAi, we showed that Upd1 is required throughout the fly life to maintain basal turnover of the midgut epithelium by controlling ISC maintenance in an autocrine manner. A role of Upd2 and Upd3 in basal conditions is discernible only in old gut, where they contribute to increased ISC abnormal division. Finally, upon an acute stress such as oral bacterial infection, we showed that Upd3 is released from enterocytes and has an additive effect with Upd2 to promote rapid epithelial regeneration. Taken together, our results show that Upd ligands are required to maintain the midgut homeostasis under both normal and pathological states.
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PMID:Autocrine and paracrine unpaired signaling regulate intestinal stem cell maintenance and division. 2303 75

Immobilization is an easy and convenient method to induce both psychological and physical stress resulting in restricted motility and aggression and is believed to be the most severe type of stress in rodent models. Although it has been generally accepted that chronic stress often results in immunosuppression while acute stress has been shown to enhance immune responses, the effects of IS on the host resistance to Escherichia coli (E. coli) infection and associated behavioral changes are still not clear. In a series of experiments aimed at determining the level of hypothalamic COX-2, HSP-90, HSP-70, SOD-1 and plasma level of corticosterone, cytokine, antibody titer and their association with behavioral activities, mice were infected with viable E. coli during acute and chronic IS by taping their paws. In this study we show that acute and chronic IS enhances the resistance of mice to E. coli infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and by improving the exploratory behavior. Altogether, our findings support the notion that cytokines released during immune activation and under the influence of corticosterone can modulate the open field behavior both in terms of locomotor activity as well as exploration. One of the features observed with chronic stressor was a lower ability to resist bacterial infection, although in case of acute stress, a better clearance of bacterial infection was observed in vivo with improvement of exploratory behavior and cognitive functions.
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PMID:Increased resistance of immobilized-stressed mice to infection: correlation with behavioral alterations. 2314 5