Purification of a factor from human peritoneal fluid that is able to immobilize spermatozoa

Human peritoneal fluid has been claimed to influence sperm motility. This report gives evidence for the presence in mid-cycle peritoneal fluid of a protein-bound, lipidic (hydrophobic) component able to immobilize spermatozoa as a function of time. This component was extracted from molecular weight-sieving and ion-exchange/high pressure liquid chromatography (HPLC)-purified peritoneal fluid fractions by either chloroform/methanol or charcoal treatments; resuspension of the chloroform/methanol extract with BWW-buffer and subsequent testing on spermatozoa resulted in sperm immobilization. Sequential or step-down chromatographic procedures (molecular weight-sieving→cation-exchange→anion-exchange HPLC separations of native peritoneal fluid) and extensive dialysis against double distilled water allowed the purification of the sperm immobilizing factor, as evidenced by the shorter incubation times necessary for sperm immobilization. Furthermore, the active fraction was found to immobilize spermatozoa without affecting its viability. Separation of the chloroform/methanol extracted immobilizing fraction on thin layer chromatography under conditions for phospholipid detection allowed the identification of a characteristic band which, after re-extraction, was found to be the sperm immobilizing substance. This factor does not contain choline, ethanolamine or serine. These results suggest that some lipidic peritoneal fluid components may influence sperm motilit

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Joint effect of obesity and TNFA variability on asthma: two international cohort studies

Obesity is a risk factor for asthma. Adipose tissue expresses pro-inflammatory molecules including tumour necrosis factor (TNF), and levels of TNF are also related to polymorphisms in the TNF-a (TNFA) gene. The current authors examined the joint effect of obesity and TNFA variability on asthma in adults by combining two population-based studies. The European Community Respiratory Health Survey and the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-a (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7–3.2; OR for TNFA -308 polymorphism 1.3, 95% CI 1.1–1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5–14.4; OR for G/G genotype 1.7, 95% CI 0.8–3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma