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Articles by C Hutchinson
Total Records ( 5 ) for C Hutchinson
  D. S De Silva , R. M Wilson , C Hutchinson , P. C Ip , A. G Garcia , S Lancel , M Ito , D. R Pimentel and F. Sam
 

Aldosterone induces extracellular signal-regulated kinase (ERK)-dependent cardiac remodeling. Fenofibrate improves cardiac remodeling in adult rat ventricular myocytes (ARVM) partly via inhibition of aldosterone-induced ERK1/2 phosphorylation and inhibition of matrix metalloproteinases. We sought to determine whether aldosterone caused apoptosis in cultured ARVM and whether fenofibrate ameliorated the apoptosis. Aldosterone (1 µM) induced apoptosis by increasing terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL)-positive nuclei in ARVM. Spironolactone (100 nM), an aldosterone receptor antagonist, but not RU-486, a glucocorticoid receptor, inhibited aldosterone-mediated apoptosis, indicating that the mineralocorticoid receptor (MR) plays a role. SP-600125 (3 µM)—a selective inhibitor of c-Jun NH2-terminal kinase (JNK)—inhibited aldosterone-induced apoptosis in ARVM. Although aldosterone increased the expression of both stress-activated protein kinases, pretreatment with fenofibrate (10 µM) decreased aldosterone-mediated apoptosis by inhibiting only JNK phosphorylation and the aldosterone-induced increases in Bax, p53, and cleaved caspase-3 and decreases in Bcl-2 protein expression in ARVM. In vivo studies demonstrated that chronic fenofibrate (100 mg·kg body wt–1·day–1) inhibited myocardial Bax and increased Bcl-2 expression in aldosterone-induced cardiac hypertrophy. Similarly, eplerenone, a selective MR inhibitor, used in chronic pressure-overload ascending aortic constriction inhibited myocardial Bax expression but had no effect on Bcl-2 expression. Therefore, involvement of JNK MAPK-dependent mitochondrial death pathway mediates ARVM aldosterone-induced apoptosis and is inhibited by fenofibrate, a peroxisome proliferator-activated receptor (PPAR) ligand. Fenofibrate mediates beneficial effects in cardiac remodeling by inhibiting programmed cell death and the stress-activated kinases.

  M Misra , N Greenberg , C Hutchinson , A Brain and N. Glozier
 

Background This study was conducted following the London bombings of 7 July 2005.

Aims To assess the psychological impact of the 2005 London bombings on London Ambulance Service (LAS) personnel, risk factors for the development of psychological ill-health and employee awareness of post incident support.

Methods A total of 525 LAS personnel involved in the bombings, and a control group of uninvolved staff, were sent a questionnaire 2 months after the bombings. Main outcome measures were the presence of probable post-traumatic stress disorder (PTSD) measured using the Trauma Screening Questionnaire and substantial psychological distress using a tool identical to that used to assess the impact of these bombings on the population of London.

Results Fifty-six per cent of those who responded were involved in the bombings. Overall, including controls, the response rate was 32% (341). Four per cent of respondents reported probable PTSD and 13% reported substantial distress. Probable PTSD was more common in those involved in the bombings (6% overall), those working at the disaster scene and, in particular, at one of the incident locations (where 50% of all probable PTSD cases worked). The majority of staff were aware of the post incident support available and how to access this, particularly if personnel were involved in the bombings.

Conclusions The LAS did not report higher levels of probable PTSD and psychological distress than the rest of the London population; however, those more proximal to the incident were more likely to have been affected in spite of being aware of various staff support measures put in place.

 
 
 
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