Effectiveness of rotavirus vaccination in prevention of hospital admissions for rotavirus gastroenteritis among young children in Belgium : case-control study

Objective : To evaluate the effectiveness of rotavirus vaccination among young children in Belgium. Design : Prospective case-control study. Setting : Random sample of 39 Belgian hospitals, February 2008 to June 2010. Participants : 215 children admitted to hospital with rotavirus gastroenteritis confirmed by polymerase chain reaction and 276 age and hospital matched controls. All children were of an eligible age to have received rotavirus vaccination (that is, born after 1 October 2006 and aged >= 14 weeks). Main outcome measure : Vaccination status of children admitted to hospital with rotavirus gastroenteritis and matched controls. Results : 99 children (48%) admitted with rotavirus gastroenteritis and 244 (91%) controls had received at least one dose of any rotavirus vaccine (P= 12 months. The G2P[4] genotype accounted for 52% of cases confirmed by polymerase chain reaction with eligible matched controls. Vaccine effectiveness was 85% (64% to 94%) against G2P[4] and 95% (78% to 99%) against G1P[8]. In 25% of cases confirmed by polymerase chain reaction with eligible matched controls, there was reported co-infection with adenovirus, astrovirus and/or norovirus. Vaccine effectiveness against co-infected cases was 86% (52% to 96%). Effectiveness of at least one dose of any rotavirus vaccine (intention to vaccinate analysis) was 91% (82% to 95%). Conclusions : Rotavirus vaccination is effective for the prevention of admission to hospital for rotavirus gastroenteritis among young children in Belgium, despite the high prevalence of G2P[4] and viral co-infection

Asymétrie d’information et marchés financiers : une synthèse de la littérature récente

Cet article est une synthèse des recherches récentes en matière d’asymétrie d’informations sur les marchés financiers. L’impact de différentes hypothèses sur l’existence et l’efficience informationnelle des équilibres est étudié. Le cas de la concurrence parfaite est d’abord analysé (Grossman et Stiglitz, 1980). Puis la concurrence imparfaite est analysée. On distingue deux cas, selon que le bruit qui empêche le prix d’être parfaitement révélateur provient d’une offre exogène (KyIe, 1985, 1989), ou d’une dotation aléatoire des agents informés (Glosten, 1989; Bhattacharya et Spiegel, 1990; Bossaerts et Hughson, 1991). Dans le premier cas, l’équilibre existe toujours. Dans le second cas, il n’existe que si le bruit est assez élevé ou si le support de sa distribution est borné.The impact of different hypotheses on the existence and informativeness of rational expectations equilibria is analyzed within a simple synthetic model. The case of perfect competition is first analyzed (Grossman and Stiglitz, 1980). Second imperfect competition with exogenous noise trading is studied (KyIe 1985, 1989). Informational efficiency is lower than in the previous case, because of the strategic behaviour of the insider. Third, imperfect competition without noise trader, but with unknown random endowments of the informed agent is analyzed (Glosten, 1989; Bhattacharya and Spiegel, 1990; Bossaerts and Hughson, 1991). In contrast with the previous case, equilibrium exists only if there is enough noise

Heterozygous Loss-of-Function SEC61A1 Mutations Cause Autosomal-Dominant Tubulo-Interstitial and Glomerulocystic Kidney Disease with Anemia

Autosomal-dominant tubulo-interstitial kidney disease (ADTKD) encompasses a group of disorders characterized by renal tubular and interstitial abnormalities, leading to slow progressive loss of kidney function requiring dialysis and kidney transplantation. Mutations in UMOD, MUC1, and REN are responsible for many, but not all, cases of ADTKD. We report on two families with ADTKD and congenital anemia accompanied by either intrauterine growth retardation or neutropenia. Ultrasound and kidney biopsy revealed small dysplastic kidneys with cysts and tubular atrophy with secondary glomerular sclerosis, respectively. Exclusion of known ADTKD genes coupled with linkage analysis, whole-exome sequencing, and targeted re-sequencing identified heterozygous missense variants in SEC61A1—c.553A>G (p.Thr185Ala) and c.200T>G (p.Val67Gly)—both affecting functionally important and conserved residues in SEC61. Both transiently expressed SEC6A1A variants are delocalized to the Golgi, a finding confirmed in a renal biopsy from an affected individual. Suppression or CRISPR-mediated deletions of sec61al2 in zebrafish embryos induced convolution defects of the pronephric tubules but not the pronephric ducts, consistent with the tubular atrophy observed in the affected individuals. Human mRNA encoding either of the two pathogenic alleles failed to rescue this phenotype as opposed to a complete rescue by human wild-type mRNA. Taken together, these findings provide a mechanism by which mutations in SEC61A1 lead to an autosomal-dominant syndromic form of progressive chronic kidney disease. We highlight protein translocation defects across the endoplasmic reticulum membrane, the principal role of the SEC61 complex, as a contributory pathogenic mechanism for ADTKD