Elevated hematocrit enhances platelet accumulation following vascular injury

Red blood cells (RBCs) demonstrate procoagulant properties in vitro, and elevated hematocrit is associated with reduced bleeding and increased thrombosis risk in humans. These observations suggest RBCs contribute to thrombus formation. However, effects of RBCs on thrombosis are difficult to assess because humans and mice with elevated hematocrit typically have coexisting pathologies. Using an experimental model of elevated hematocrit in healthy mice, we measured effects of hematocrit in 2 in vivo clot formation models. We also assessed thrombin generation, platelet-thrombus interactions, and platelet accumulation in thrombi ex vivo, in vitro, and in silico. Compared with controls, mice with elevated hematocrit (RBCHIGH) formed thrombi at a faster rate and had a shortened vessel occlusion time. Thrombi in control and RBCHIGH mice did not differ in size or fibrin content, and there was no difference in levels of circulating thrombin-antithrombin complexes. In vitro, increasing the hematocrit increased thrombin generation in the absence of platelets; however, this effect was reduced in the presence of platelets. In silico, direct numerical simulations of whole blood predicted elevated hematocrit increases the frequency and duration of interactions between platelets and a thrombus.Whenhumanwhole blood was perfused over collagen at arterial shear rates, elevating the hematocrit increased the rate of platelet deposition and thrombus growth. These data suggest RBCs promote arterial thrombosis by enhancing platelet accumulation at the site of vessel injury. Maintaining a normal hematocrit may reduce arterial thrombosis risk in humans

Differential enzymatic activity of common haplotypic versions of the human acidic Mammalian chitinase protein

FWN – Publicaties zonder aanstelling Universiteit Leide

Do Nurses Use Discourse Markers Differently when Using Their Second Language as Opposed to Their First while Interviewing Patients?

This study examined whether discourse-marker use changes in nurse-patient interactions as a function of nurses using their first (L1) or second (L2) language. Discourse markers were analyzed as turn-maintenance markers that indicate acknowledgement and discourse-shift markers that signal shifts of a topic or speaker in the conversation. These two categories differ in terms of degree of discourse management and interactional control. Sixteen nurses conducted a pain-assessment interview with a patient native speaker of English and with a patient native speaker of French, where the nurses used their own L1 in one case and their own weaker L2 in the other. The first hypothesis, that nurses would generally use discourse markers more frequently in the L1 than in the L2, was not supported. The second hypothesis, that nurses would use discourse-shift markers less frequently in their L2 compared to the L1, relative to their (baseline) use of turn-maintenance markers, was supported. The findings, especially the support for the second hypothesis, could have implications for the development of L2 training for health practitioners.</p

The hypersensitive response and resistance to Solanum tuberosum L. to Phytophthora infestans (Mont.) de Bary

SIGLEAvailable from British Library Document Supply Centre- DSC:D061253 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

A novel association between a SNP in CYBRD1 and serum ferritin levels in a cohort study of HFE hereditary haemochromatosis

There is emerging evidence that there are genetic modifiers of iron indices for HFE gene mutation carriers at risk of hereditary hemochromatosis. A random sample, stratified by HFE genotype, of 863 from a cohort of 31 192 people of northern European descent provided blood samples for genotyping of 476 single nucleotide polymorphisms (SNPs) in 44 genes involved in iron metabolism. Single SNP association testing, using linear regression models adjusted for sex, menopause and HFE genotype, was conducted for four continuously distributed outcomes: serum ferritin (log transformed), transferrin saturation, serum transferrin, and serum iron. The SNP rs884409 in CYBRD1 is a novel modifier specific to HFE C282Y homozygotes. Median unadjusted serum ferritin concentration decreased from 1194 microg/l (N = 27) to 387 microg/l (N = 16) for male C282Y homozygotes and from 357 microg/l (N = 42) to 69 microg/l (N = 12) for females, comparing those with no copies to those with one copy of rs884409. Functional testing of this CYBRD1 promoter polymorphism using a heterologous expression assay resulted in a 30% decrease in basal promoter activity relative to the common genotype (P = 0.004). This putative genetic modifier of iron overload expression accounts for 11% (95% CI 0.4%, 22.6%) of the variance in serum ferritin levels of C282Y homozygotes