The HSS could be used to stratify patients via other possible modulators of haemophilia and discover other aetiologies of the disease. “
“Summary. Successful strategies by which to effectively recruit and retain academic subspecialists in benign haematology have not been established. To evaluate
the effectiveness of a grant-funded, mentored fellowship with respect to retention and early career goals in haemostasis/thrombosis, we sought to compare outcomes for graduates of a grant-funded, mentored fellowship training programme in haemostasis/thrombosis [the National Hemophilia Foundation (NHF)-Baxter Clinical Fellowship Award] TGF-beta inhibitor during conventional haematology/oncology fellowship training (cases), vs. their training peers who were graduates of conventional haematology/oncology fellowship training alone (controls), via a nested case-control survey study. Survey response rate was 85% (11/13) for cases and 90% (9/10) for controls. All respondents had pursued careers in academic haematology/oncology. Median (range) percent time spent in benign haematology postfellowship was 98% (70–100%) for cases vs. 0% (0–20%) for controls. Time spent in research was significantly greater among cases than controls (median 80% [range: 42–90%] vs. 55% [10–80%],
respectively; P = 0.01). By years 3–4 postfellowship, median annual number of peer-reviewed publications was HM781-36B mouse higher for cases than controls (3.5 vs. 1.0; P = 0.01). Cases were also more successful in grant funding Benzatropine (including K-awards). These data suggest that a grant-funded, mentored fellowship training programme in haemostasis/thrombosis
may be superior to conventional haematology/oncology fellowship training alone with respect to outcomes of retention in clinical care/research, early-career grant funding and publication productivity. “
“Coagulation factor XIII (FXIII) exists as heterotetramer (FXIII-A2B2) in the plasma and as dimer (FXIII-A2) in cells. Activated FXIII mechanically stabilizes fibrin and protects it from fibrinolysis by cross-linking fibrin chains and α2-plasmin inhibitor to fibrin. FXIII is essential to maintaining haemostasis, and its deficiency causes severe bleeding diathesis. Due to improper laboratory practices, FXIII deficiency is considered the most under-diagnosed bleeding disorder. The aim of this study was to demonstrate in two cases how FXIII deficiency is properly diagnosed and classified, and to compare results of laboratory analysis and clinical symptoms. FXIII activity from plasma and platelets was measured by a modified ammonia release assay, while FXIII-A2B2, FXIII-A and FXIII-B antigens were determined by ELISA. The exon–intron boundaries and the promoter region of F13A1 gene were amplified by PCR and the amplified products were analysed by direct fluorescent sequencing. FXIII-A mRNA in platelets was determined by RT-qPCR.