Vaccination against highly pathogenic avian influenza (HPAI) viruses, along with other measures, was successful in eradicating AI in very few countries where the competence of national veterinary services or the geography and bird density have contributed favorably to the outcome. The main constraints to an effective AI vaccination are vaccine composition matching field strains, reliable cold chain and logistics to target all poultry smallholders, constraints related to the availability of sufficient financial and human resources. When not conducted properly, vaccination can also contribute to the emergence of new field viral strains, through genetic drifts of HPAI viruses. While new technologies have improved the possibility to produce high quality vaccines matching field strains, recurrent issues like post-vaccination field surveillance and vaccination coverage continue to limit the relevance of AI vaccination in smallholder settings. A "game-changer" vaccine targeting smallholders should be universal to protect against all field viral strains and reduce significantly, if not totally eliminate, the need for costly post-vaccination surveillance. The ease of administration of this vaccine (eye drop or one single injection) would further contribute to its relevance in the field. These characteristics are considered essential for the product profile of an AI vaccine that can contribute in a meaningful way to the livelihoods of poultry smallholders.There remains a high risk of thrombosis in patients affected by the SARS-CoV-2 virus and recent reports have shown pulmonary embolism (PE) as a cause of sudden death in these patients. However, the pooled rate of this deadly and frequently underdiagnosed condition among COVID-19 patients remains largely unknown. Given the frequency with which pulmonary embolism has been reported as a fatal complication of severe coronavirus disease, we sought to ascertain the actual prevalence of this event in COVID-19 patients. Using PubMed/Medline, EMBASE, and SCOPUS, a thorough literature search was performed to identify the studies reporting rate of PE among COVID-19. Random effects models were obtained to perform a meta-analysis, and I2 statistics were used to measure inter-study heterogeneity. Among 3066 COVID-19 patients included from 9 studies, the pooled prevalence of PE was 15.8% (95% CI (6.0-28.8%), I2 = 98%). The pooled rate in younger cohort (age  65 years) showing 14.3% (95% CI (2.9-30.1%)) (p  less then  0.05). Single-center studies showed a prevalence of 12.9% (95% CI 1.0-30.2%), while that of multicenter studies was 19.5% (95% CI 14.9-25.2%) (p  less then  0.05). Pulmonary embolism is a common complication of severe coronavirus disease and a high degree of clinical suspicion for its diagnosis should be maintained in critically ill patients.Background  Extended duration thromboprophylaxis (ET) for approximately 30 days can effectively and safely reduce venous thromboembolism (VTE) risk in appropriately selected medically ill patients. https://www.selleckchem.com/products/zeocin.html We sought to estimate the proportion of hospitalized medically ill patients potentially qualifying for ET and assess their post-discharge clinical and economic outcomes using a large claims database. Methods  Using MarketScan claims from January 2012 to September 2018, we identified medically ill patients hospitalized with a primary diagnosis of heart failure, respiratory insufficiency, ischemic stroke, infection, or inflammatory disease and ≥1-additional risk factor for VTE. Patients 30 days, receiving oral anticoagulation prior to index hospitalization or having an indication for full-dose anticoagulation were excluded, as were patients deemed high-risk for bleeding due to active, in-hospital treated cancer, gastroduodenal ulcer or bleeding within the prior 3 months, bronchiectasis, pulmonary cavitation or hemorrhage, or dual antiplatelet therapy use. Results  We identified 2,782,988 patients ≥40 years of age and admitted for a high-risk medical illness. Of these, 724,531 patients (26.0%) were identified as ET candidates. Patients' VTE risk appeared highest in the first 30 days post-discharge (1,532/724,531, 0.2%). Adjusted post-index hospitalization costs (2018 US$) for patients with a VTE within 30 days were higher than those without VTE (Δ = $32,623 at 30 days, Δ = $43,325 at 90 days, Δ = $53,668 at 365 days; p   less then  0.001 for all). Conclusion  Post-discharge VTE in high-risk patients with medical illness is associated with substantially increased costs.Genome-wide association studies (GWASs) have identified genes that affect plasma von Willebrand factor (VWF) levels. ABO showed a strong effect, whereas smaller effects were seen for VWF , STXBP5 , STAB2 , SCARA5 , STX2 , TC2N , and CLEC4M . This study screened comprehensively for both common and rare variants in these eight genes by resequencing their coding sequences in 104 Swedish von Willebrand disease (VWD) patients. The common variants previously associated with the VWF level were all accumulated in the VWD patients compared to three control populations. The strongest effect was detected for blood group O coded for by the ABO gene (71 vs. 38% of genotypes). The other seven VWF level associated alleles were enriched in the VWD population compared to control populations, but the differences were small and not significant. The sequencing detected a total of 146 variants in the eight genes. Excluding 70 variants in VWF , 76 variants remained. Of the 76 variants, 54 had allele frequencies > 0.5% and have therefore been investigated for their association with the VWF level in previous GWAS. The remaining 22 variants with frequencies  less then  0.5% are less likely to have been evaluated previously. PolyPhen2 classified 3 out of the 22 variants as probably or possibly damaging (two in STAB2 and one in STX2 ); the others were either synonymous or benign. No accumulation of low frequency (0.05-0.5%) or rare variants ( less then 0.05%) in the VWD population compared to the gnomAD (Genome Aggregation Database) population was detected. Thus, rare variants in these genes do not contribute to the low VWF levels observed in VWD patients.