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Background Many hospitals experience a reduction in the number of available physicians on days when national scientific meetings are conducted. This study investigates the relationship between in-hospital mortality in acute myocardial infarction (AMI) patients and admission during national cardiology meeting dates. Methods Using an administrative database, we analyzed patients with AMI admitted to acute care hospitals in Japan from 2011 to 2013. There were 3 major national cardiology meetings held each year. A hierarchical logistic regression model was used to compare in-hospital mortality and treatment patterns between patients admitted on meeting dates and those admitted on identical days during the week before and after the meeting dates. Results We identified 6,332 eligible patients, with 1,985 patients admitted during 26 meeting days and 4,347 patients admitted during 52 non-meeting days. No significant differences between meeting and non-meeting dates were observed for in-hospital mortality (7.4% vs. 8.5%, respectively; p = 0.151, unadjusted odds ratio: 0.861, 95% confidence interval: 0.704-1.054) and the proportion of percutaneous coronary intervention (PCI) performed on the day of admission (75.9% vs. 76.2%, respectively; p = 0.824). We also found that some low-staffed hospitals did not treat AMI patients during meeting dates. Conclusion Little or no “national meeting effect” was observed on in-hospital mortality in AMI patients, and PCI rates were similar for both meeting and non-meeting dates. Our findings also indicated that during meeting dates, AMI patients may have been consolidated to high-performance and sufficiently staffed hospitals [ABSTRACT FROM AUTHOR]

The COVID-19 vaccine will be safe and effective in solid organ transplant recipients (SOTs). However, the blunted antibody responses were also of concern. Few studies have reported prolonged serologic follow-up after 2 doses of BNT162b2 vaccine in SOTs. We performed a single-center, prospective observational study of 78 SOTs who received 2 doses of BNT162b2 vaccine. We identified the trajectory of antibody titers after vaccination among SOTs with or without mycophenolate mofetil (MMF) or withdrawn from MMF. We found low seroconversion rates (29/42: 69%) and low antibody titers in SOTs treated with MMF. An inverse linear relationship between neutralizing antibody titers and MMF concentration was confirmed in restricted cubic spline plots (P for effect <.01, P for nonlinearity =.08). For the trajectory of antibody responses, seroconversion and improved antibody titers were observed after withdrawal from MMF in SOTs who showed seronegative or low antibody titers at the first visit after 2 doses of vaccine (P for effect <.01, P for nonlinearity <.05, and P for interaction <.01). We identified increased B-cell counts after withdrawal from MMF (P <.01). The recovery of antibody responses was seen in SOTs withdrawn from MMF. The trajectories of antibody responses were modified by MMF administration. [ABSTRACT FROM AUTHOR]

Abstract: Major depression is a complex disorder characterized by genetic and environmental interactions. Selective serotonin reuptake inhibitors (SSRIs) effectively treat depression. Neurogenesis following chronic antidepressant treatment activates brain derived neurotrophic factor (BDNF) signaling. In this study, we analyzed the effects of the SSRI fluvoxamine (Flu) on locomotor activity and forced-swim behavior using chronic dexamethasone (cDEX) infusions in mice, which engenders depression-like behavior. Infusion of cDEX decreased body weight and produced a trend towards lower locomotor activity during darkness. In the forced-swim test, cDEX-mice exhibited increased immobility times compared with mice administered saline. Flu treatment reversed decreased locomotor activity and mitigated forced-swim test immobility. Real-time polymerase chain reactions using brain RNA samples yielded significantly lower BDNF mRNA levels in cDEX-mice compared with the saline group. Endoplasmic reticulum stress-associated X-box binding protein-1 (XBP1) gene expression was lower in cDEX-mice compared with the saline group. However, marked expression of the XBP1 gene was observed in cDEX-mice treated with Flu compared with mice given saline and untreated cDEX-mice. Expression of 5-HT2A and Sigma-1 receptors decreased after cDEX infusion compared with the saline group, and these decreases normalized to control levels upon Flu treatment. Our results indicate that the Flu moderates reductions in voluntary activity following chronic dexamethasone infusions in mice via recovery of BDNF signal cascades. [Copyright &y& Elsevier]

Abstract: Genetic factors are important for the development of osteoporosis. During the search for novel markers of single-nucleotide polymorphisms (SNPs) associated with bone mineral density (BMD) by performing a large-scale SNP screen with 251 Japanese postmenopausal women utilizing 50K SNP array, we here focused on the rs1370005 in the WD repeats and SOF1 domain-containing (WDSOF1) gene because we could found common non-synonymous variants in this WDSOF1 gene. The analysis of linkage disequilibrium (LD) in the WDSOF1 gene revealed that rs1370005 and 3 other non-synonymous SNPs (Arg47Ser, Pro108Leu and Ile194Val) lie in a 30-kb region of high LD. Quantitative real-time PCR (qRT-PCR) analysis showed that WDSOF1 mRNA was expressed in mouse primary osteoblasts and osteoclasts, suggesting that WDSOF1 plays some roles in the bone metabolism. We examined the 3 non-synonymous SNPs in WDSOF1 gene in 750 Japanese postmenopausal women. A trend test showed that Arg47Ser, Pro108Leu, and Ile194Val genotypes were significant associated with total body BMD (Arg47Ser; P =0.021, Pro108Leu; P =0.022 and Ile194Val; P =0.009). We also compared Z scores for total body BMD between the subjects bearing at least one minor allele and those lacking the minor allele using unpaired t test. Subjects with the one or two minor alleles had significantly lower Z scores for total body BMD (Arg47Ser; P =0.010, Pro108Leu; P =0.019 and Ile194Val; P =0.003). The present study suggests that these non-synonymous WDSOF1 polymorphisms play a role in the genetic susceptibility to osteoporosis. [ABSTRACT FROM AUTHOR]