Home About us Contact
|
Home About us Contact | ||
|
|
||
Stress Agents (stress + agent)
Selected AbstractsVasodilator Stress Induces Infrequent Wall Thickening Abnormalities Compared to Perfusion Defects in Mild-to-Moderate Coronary Artery Disease: Implications for the Choice of Imaging Modality with Vasodilator StressECHOCARDIOGRAPHY, Issue 4 2004M.R.C.P., Ph.D., Prem Soman M.D. Background: Experimental evidence suggests that although vasodilator stress agents consistently induce regional flow disparity between stenosed and normal coronary vascular beds, the occurrence of functional myocardial ischemia is infrequent, especially in mild-to-moderate coronary artery stenosis. Thus, it is hypothesized that dipyridamole infusion, even at high doses, will result in a disproportionately higher frequency of perfusion defects compared to regional wall thickening abnormalities. Methods: We performed simultaneous high-dose (0.84 mg/kg) dipyridamole stress echocardiography (Echo) and Tc-99m sestamibi SPECT (MIBI, methoxyisobutyl isonitrile) in 46 patients with coronary artery diameter stenosis >50% and ,90% in one or two epicardial coronary arteries, and no previous myocardial infarction. Results: Of a total of 828 segments, MIBI showed 97 reversible defects while Echo showed only 23 reversible wall thickening abnormalities. Of the 97 segments with reversible MIBI defects, only 13 (13%) showed simultaneous reversible wall thickening abnormalities during dipyridamole infusion. There were 24 patients with MIBI defects, of whom 10 (41%) showed a corresponding wall thickening abnormality. The sensitivity of MIBI and Echo for the detection of coronary artery disease was 52% and 21%, respectively (P = 0.001). Conclusion: This suggests that vasodilator stress is not optimally suited for use with techniques that use regional wall thickening abnormality as a marker of ischemia for the diagnosis of coronary artery disease. (ECHOCARDIOGRAPHY, Volume 21, May 2004) [source] Cross-talk involving extracellular sensors and extracellular alarmones gives early warning to unstressed Escherichia coli of impending lethal chemical stress and leads to induction of tolerance responsesJOURNAL OF APPLIED MICROBIOLOGY, Issue 5 2001R.J. Rowbury 1. Summary, 678 2. Introduction 2.1. Chemical and biological stress agents affecting enterobacteria, 678 2.2. Sensing of chemical and biological stress stimuli, 678 2.3. Intracellular sensors detect intracellularly-produced chemical stressing agents, 679 2.4. Intracellular sensors and intracellular induction components could delay response induction by extracellular chemical or biological stress agents, 680 2.5. Extracellular sensors and EICs give early warning of stress, 681 2.6. Disadvantages of extracellular components being needed for stress response induction, 682 2.7. Extracellular sensors and EICs allow stressed cells to warn unstressed ones, 682 2.8. A second role for some extracellular stress sensors, 683 3. Responses switched on by extracellular sensors and EICs 3.1. Involvement of EICs and ESCs in acid tolerance induction at pH 5·0 and at other mildly acidic pH values, 683 3.2. Further evidence for the obligate involvement of extracellular sensors and EICs in acid tolerance induction at pH 5·0, 684 3.3. On the nature of the acid pH tolerance-inducing ESC and EIC, 686 3.4. The acid tolerance ECs and their relation to other extracellular response-inducing components, 686 3.5. Extracellular components are needed for other inducible acid tolerance responses, 687 3.6. Involvement of EICs and extracellular sensors in acid tolerance in E. coli O157, 687 3.7. EICs involved in acid tolerance induction are diffusible, 687 4. Acid sensitization at alkaline pH and the role of extracellular sensor and EIC(s), 688 5. Responses affecting tolerance to alkali 5.1. Alkali sensitization at acidic pH, 688 5.2. Induced alkali tolerance at pH 9·0 and role of extracellular components, 688 6. Inducible tolerance to alkylhydroperoxides, 689 7. Are extracellular sensors and extracellular induction components needed for all stress responses?, 689 8. Altered responsiveness of extracellular sensors depending on growth conditions, 691 9. Protection of living cells from chemical stress by dead cultures, 691 10. How can intracellular levels of stress be detected?, 692 11. Are Nikolaev's extracellular ,protectants' and similar components related to EICs?, 693 12. Conclusions, 693 13. References, 694 [source] Involvement of Gadd153 in the pathogenic action of presenilin-1 mutationsJOURNAL OF NEUROCHEMISTRY, Issue 3 2002Ollivier Milhavet Abstract Mutations in the presenilin-1 (PS1) gene cause early onset familial Alzheimer's disease (FAD) by a mechanism believed to involve perturbed endoplasmic reticulum (ER) function and altered proteolytic processing of the amyloid precursor protein. We investigated the molecular mechanisms underlying cell death and ER dysfunction in cultured cells and knock-in mice expressing FAD PS1 mutations. We report that PS1 mutations cause a marked increase in basal protein levels of the pro-apoptotic transcription factor Gadd153. PS1 mutations increase Gadd153 protein translation without affecting mRNA levels, while decreasing levels of the anti-apoptotic protein Bcl-2. Moreover, an exaggerated Gadd153 response to stress induced by ER stress agents was observed in PS1 mutant cells. Cell death in response to ER stress is enhanced by PS1 mutations, and this endangering effect is attenuated by anti-sense-mediated suppression of Gadd153 production. An abnormality in the translational regulation of Gadd153 may sensitize cells to the detrimental effects of ER stress and contribute to the pathogenic actions of PS1 mutations in FAD. [source] In Vivo and In Vitro Evidence of the Involvement of CXCL1, a Keratinocyte-Derived Chemokine, in Equine LaminitisJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2009R.R. Faleiros Background: C-X-C motif ligand 1 (CXCL1) is an important chemokine of epithelial origin in rodents and humans. Objectives: To assess in vivo and in vitro the regulation of CXCL1 in equine laminitis. Animals: Twenty adult horses. Methods: Real-time quantitative polymerase chain reaction (PCR) was used to assess expression of CXCL1 in samples of laminae, liver, skin, and lung from the black walnut extract (BWE) model of laminitis, and in cultured equine epithelial cells (EpCs). Tissue was obtained from control animals (CON, n = 5), and at 1.5 hours (early time point [ETP] group, n = 5), at the onset of leukopenia (developmental time point [DTP] group, n = 5), and at the onset of lameness (LAM group, n = 5) after BWE administration. EpCs were exposed to Toll-like/Nod receptor ligands, oxidative stress agents, and reduced atmospheric oxygen (3%). In situ PCR was used to localize the laminar cell types undergoing CXCL1 mRNA expression. Results: Increases in laminar CXCL1 mRNA concentrations occurred in the ETP (163-fold [P= .0001]) and DTP groups (21-fold [P= .005]). Smaller increases in CXCL1 expression occurred in other tissues and organs. In cultured EpCs, increases (P < .05) in CXCL1 mRNA concentration occurred after exposure to lipopolysaccharide (LPS [28-fold]), xanthine/xanthine oxidase (3.5-fold), and H2O2 (2-fold). Hypoxia enhanced the LPS-induced increase in CXCL1 mRNA (P= .007). CXCL1 gene expression was localized to laminar EpCs, endothelial cells, and emigrating leukocytes. Conclusion and Clinical Importance: These findings indicate that CXCL1 plays an early and possibly initiating role in neutrophil accumulation in the BWE laminitis model, and that laminar keratinocytes are an important source of this chemokine. New therapies using chemokine receptor antagonists may be indicated. [source] Susceptibility to insecticides in the Q biotype of Bemisia tabaci is correlated with bacterial symbiont densitiesPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 9 2009Murad Ghanim Abstract BACKGROUND: The presence of symbiotic microorganisms may influence an insect's ability to tolerate natural and artificial stress agents such as insecticides. The authors have previously shown that Rickettsia in the B biotype of the whitefly Bemisia tabaci (Gennadius) (Homoptera: Aleyrodidae) increases this insect's susceptibility to several insecticidal compounds. This communication reports a comparison of the susceptibilities of three isofemale strains of the Q biotype of B. tabaci harbouring different bacterial complements to major insecticides from different chemical groups: one strain harboured only Arsenophonus, one harboured Rickettsia and Arsenophonus and one harboured Arsenophonus and Wolbachia. RESULTS: The presence of different symbiont combinations in the three strains had a significant influence on their susceptibility to most of the insecticides tested. Thiamethoxam, imidacloprid, pyriproxyfen and spiromesifen had a significant influence on strains that had the double infections Rickettsia,Arsenophonus and Wolbachia,Arsenophonus, which also carried higher amounts of symbionts as assessed by quantitative real-time PCR. No significant differences in mortality rates were observed when the tested strains were treated with diafenthiuron. CONCLUSION: The results suggest a correlation between the presence of high bacterial densities in B. tabaci and the insect's ability to detoxify toxic compounds such as insecticides. Copyright © 2009 Society of Chemical Industry [source] | |||||||||||||