Acquisition Delays Affect Lymphocyte Subset Counts but not Markers of Exercise-induced Apoptosis

International Journal of Exercise Science 6(3) : 250-255, 2013. With the emergence of shared facilities, the possibility of a processing delay is increased as time on instrumentation becomes less available. The purpose of this investigation was the evaluate the effect of a 24h time delay on lymphocyte subset concentration, as well as for the apoptotic marker annexin V. Fourteen healthy individuals completed an incremental treadmill test to exhaustion, and blood samples were obtained before and after exercise. The samples were labeled in duplicate with mixtures consisting of flow cytometry staining buffer, the biomarker for early-phase cell death (annexin V), and antibodies for specific lymphocyte phenotypes (CD4, CD8, and CD19). Samples were labeled for 30-min, centrifuged, and decanted, before the addition of RBC Lysis Buffer. Upon the completion of processing, the first set of samples were immediately analyzed using flow cytometry and the remaining duplicate samples were acquired 24 h later. Data were analyzed using a paired sample t-test with significance accepted at the p \u3c 0.05 level. For blood draws obtained at rest, no differences between acquisition days were observed with regard to cell volume for any lymphocyte subfraction. However, blood samples obtained following an exhaustive exercise bout had significant decreases in CD4+ (p=0.002) and CD8+ (p= 0.021) concentration between acquisition days. Processing delays did not affect the number of apoptotic cells in any lymphocyte subset either at rest or following exercise. As the number of apoptotic cells was unaffected by processing, the reduction in cell concentration is likely due to mechanisms other than programmed cell death. It is possible that exercise makes lymphocytes more susceptible to necrosis during the post-activity period

Chromosome Xq23 is associated with lower atherogenic lipid concentrations and favorable cardiometabolic indices

Abstract Autosomal genetic analyses of blood lipids have yielded key insights for coronary heart disease (CHD). However, X chromosome genetic variation is understudied for blood lipids in large sample sizes. We now analyze genetic and blood lipid data in a high-coverage whole X chromosome sequencing study of 65,322 multi-ancestry participants and perform replication among 456,893 European participants. Common alleles on chromosome Xq23 are strongly associated with reduced total cholesterol, LDL cholesterol, and triglycerides (min P = 8.5 × 10−72), with similar effects for males and females. Chromosome Xq23 lipid-lowering alleles are associated with reduced odds for CHD among 42,545 cases and 591,247 controls (P = 1.7 × 10−4), and reduced odds for diabetes mellitus type 2 among 54,095 cases and 573,885 controls (P = 1.4 × 10−5). Although we observe an association with increased BMI, waist-to-hip ratio adjusted for BMI is reduced, bioimpedance analyses indicate increased gluteofemoral fat, and abdominal MRI analyses indicate reduced visceral adiposity. Co-localization analyses strongly correlate increased CHRDL1 gene expression, particularly in adipose tissue, with reduced concentrations of blood lipids