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Articles by S Rich
Total Records ( 3 ) for S Rich
  L Wise Faberowski , P. N Robinson , S Rich and D. S. Warner

BACKGROUND: Oganotypic hippocampal slices (OHS) are commonly used to screen for neuroprotective effects of pharmacological agents relevant to pediatric brain injury. The importance of donor rat pup age and N-methyl-d-aspartate (NMDA) receptor subunit composition have not been addressed. In this study, we evaluated the age-dependent effect of oxygen-glucose deprivation (OGD) in the developing rat brain and determined whether OGD modulates the NMDA receptor subunit composition.

METHODS: OHS were prepared from rat pups on postnatal days (PND) 4, 7, 14, and 21 and cultured 7 days in vitro. The slices were exposed to OGD for durations of 5–60 min. After 24 and 72 h, OHS survival and NMDA subunit composition were assessed.

RESULTS: Cell death was evident in OHS prepared from PND 14 and 21 rat pups (P < 0.001) with OGD durations of 5 and 10 min, respectively. In OHS prepared from PND7 rat pups, neurodegeneration was not evident until 20 min OGD (P < 0.001). Exposure to OGD in OHS prepared from PND4 and PND7 rat pups was associated with a transition in the NMDA receptor subunit composition from NR2B predominant to NR2A predominant subunit composition.

CONCLUSIONS: This in vitro neonatal rat pup investigation using OHS supports both an age and an NMDA receptor subunit composition-dependent relationship between OGD and neuronal cell death.

  M McGeachie , R. L. B Ramoni , J. C Mychaleckyj , K. L Furie , J. M Dreyfuss , Y Liu , D Herrington , X Guo , J. A Lima , W Post , J. I Rotter , S Rich , M Sale and M. F. Ramoni

Background— Many different genetic and clinical factors have been identified as causes or contributors to atherosclerosis. We present a model of preclinical atherosclerosis based on genetic and clinical data that predicts the presence of coronary artery calcification in healthy Americans of European descent 45 to 84 years of age in the Multi-Ethnic Study of Atherosclerosis (MESA).

Methods and Results— We assessed 712 individuals for the presence or absence of coronary artery calcification and assessed their genotypes for 2882 single-nucleotide polymorphisms. With the use of these single-nucleotide polymorphisms and relevant clinical data, a Bayesian network that predicts the presence of coronary calcification was constructed. The model contained 13 single-nucleotide polymorphisms (from genes AGTR1, ALOX15, INSR, PRKAB1, IL1R2, ESR2, KCNK1, FBLN5, PPARA, VEGFA, PON1, TDRD6, PLA2G7, and 1 ancestry informative marker) and 5 clinical variables (sex, age, weight, smoking, and diabetes mellitus) and achieved 85% predictive accuracy, as measured by area under the receiver operating characteristic curve. This is a significant (P<0.001) improvement on models that use just the single-nucleotide polymorphism data or just the clinical variables.

Conclusions— We present an investigation of joint genetic and clinical factors associated with atherosclerosis that shows predictive results for both cases, as well as enhanced performance for their combination.

  S. J Shah , T Thenappan , S Rich , J Sur , S. L Archer and M. Gomberg Maitland

Background— The ability of the Naughton-Balke exercise treadmill test, an objective indicator of exercise capacity, to predict abnormal hemodynamics and mortality in pulmonary hypertension is unknown.

Methods and Results— We performed a cohort study of 603 patients with pulmonary hypertension from 1982 to 2006, and studied the utility of exercise treadmill test as a predictor of abnormal hemodynamics and death. We used multivariable linear regression to determine whether exercise capacity, measured in metabolic equivalents, was associated with abnormal hemodynamics, and we used a Cox proportional hazards model to determine whether decreased exercise capacity predicted death. Mean age was 50±15 years, 76% were women, 63% had World Health Organization category I pulmonary arterial hypertension, and 23% were World Health Organization functional classes I and II. Mean exercise capacity was 3.7±2.2 metabolic equivalents. Decreased exercise capacity was independently associated with elevated right atrial and mean pulmonary artery pressure, decreased cardiac index, and increased pulmonary vascular resistance. During median follow-up of 4.6 years, 36% of the patients died. Decreased exercise capacity was associated with mortality (multivariable hazard ratio, 1.18; 95% CI, 1.01 to 1.37 for each 1-metabolic equivalent decrease in exercise capacity; P=0.031; P=0.052 after adjusting for invasive hemodynamic variables). Decreased exercise capacity also predicted mortality in functional classes I–II patients, 24% of whom died (hazard ratio, 1.53; 95% CI, 1.04 to 2.26 for each 1-metabolic equivalent decrease in exercise capacity; P=0.032), although this association did not persist after adjusting for invasive hemodynamic variables (P=0.63).

Conclusions— Reduced exercise capacity on exercise treadmill test is associated with worse hemodynamics and is a predictor of mortality in patients with pulmonary hypertension.

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