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Articles by S Parashar
Total Records ( 2 ) for S Parashar
  S Pryshchep , J. J Goronzy , S Parashar and C. M. Weyand
 

Rationale: In the vulnerable atherosclerotic plaque, T cells may destabilize the tissue structure through direct cell-injurious effector functions. T cells transmit environmental signals, such as recognition of antigen, into cellular responses through regulated phosphorylation of cytoplasmic proteins, with the Src family kinase Lck (lymphocyte-specific protein tyrosine kinase) in critical membrane-proximal position of the T-cell receptor (TCR) signaling cascade. The balance between protein phosphorylation and dephosphorylation defines the signal transduction threshold and determines appropriate T-cell responses.

Objective: We have examined whether abnormal calibration of intracellular signaling pathways renders acute coronary syndrome (ACS) patients susceptible to disproportionate T-cell responses.

Methods and Results: Intracellular signaling cascades were quantified in CD4 T cells from ACS patients and control individuals after stimulation with major histocompatibility complex class II–superantigen complexes. ACS T cells mobilized more intracellular calcium and accumulated higher levels of phosphotyrosine than control T cells. Proximal steps in TCR signaling, such as recruitment of ZAP-70 and clustering of TCR complexes in the immune synapse, were abnormally enhanced in ACS T cells. Acceleration of the signaling cascade derived from a proximal defect in ACS T cells, which failed to phosphorylate Lck at Tyr505, extending activation of the Src kinase. Abnormalities in TCR signaling did not correlate with systemic inflammation as measured by C-reactive protein.

Conclusions: An intrinsic abnormality in the signaling machinery of ACS T cells resulting in the accumulation of active Lck lowers the TCR threshold and renders lymphocytes hyperreactive and capable of unwanted immune responses.

  E. C Leifheit Limson , K. J Reid , S. V Kasl , H Lin , P. G Jones , D. M Buchanan , S Parashar , P. N Peterson , J. A Spertus and J. H. Lichtman
 

Background— Prior studies have associated low social support (SS) with increased rehospitalization and mortality after acute myocardial infarction. However, relatively little is known about whether similar patterns exist for other outcomes, such as health status and depressive symptoms, and whether these patterns vary by sex.

Methods and Results— Using data from 2411 English- or Spanish-speaking patients with acute myocardial infarction enrolled in a 19-center prospective study, we examined the association of SS (low, moderate, high) with health status (angina, disease-specific quality of life, general physical and mental functioning) and depressive symptoms over the first year of recovery. Overall and sex-stratified associations were evaluated using mixed-effects Poisson and linear regression, adjusting for site, baseline health status, baseline depressive symptoms, and demographic and clinical factors. Patients with the lowest SS (relative to those with the highest) had increased risk of angina (relative risk, 1.27; 95% confidence interval [CI], 1.10, 1.48); lower disease-specific quality of life (mean difference [β]=–3.33; 95% CI, –5.25, –1.41), lower mental functioning (β=–1.72; 95% CI, –2.65, –0.79), and more depressive symptoms (β=0.94; 95% CI, 0.51, 1.38). A nonsignificant trend toward lower physical functioning (β=–0.87; 95% CI, –1.95, 0.20) was observed. In sex-stratified analyses, the relationship between SS and outcomes was stronger for women than for men, with a significant SS-by-sex interaction for disease-specific quality of life, physical functioning, and depressive symptoms (all P<0.02).

Conclusions— Lower SS is associated with worse health status and more depressive symptoms over the first year of acute myocardial infarction recovery, particularly for women.

 
 
 
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