Effect of estimated plasma volume status and left atrial diameter on prognosis of patients with acute heart failure

ObjectiveAcute heart failure (AHF) is a frequent cardiovascular emergency presenting with high mortality as well as readmission rates. The aim was to investigate the predictive value of estimated plasma volume status (ePVs) and left atrial diameter (LAD) for the prognosis of patients with AHF.MethodsClinical profiles were collected from 259 cases of AHF patients at the Affiliated Hospital of Putian University between September 2019 and October 2021.ResultsSix patients lost follow-up, resulting in 253 patients enrolled. Cardiogenic death and heart failure readmission during follow-up were defined as major cardiovascular events (MACE) group, other patients were defined as Non-MACE group. Apart from age, no significant differences were found between the two groups in demographics and comorbidities. The comparison between the two groups was statistically significant in terms of ePVs, LAD, and N-terminal-pro B-type natriuretic peptide (Nt-pro-BNP). On binary logistic regression analysis, ePVs (OR = 2.061, 95% CI 1.322∼3.214, P = 0.001), LAD (OR = 1.054, 95% CI 1.012∼1.098, P = 0.011), and Nt-pro-bnp (OR = 1.006, 95% CI 1.003∼1.010, P = 0.036) as predicting factors for MACE. Kaplan-Meier analysis indicated that the risk for cardiogenic death increasing with ePVs (p < 0.05).ConclusionEstimated plasma volume status and LADs have some predictive value in assessing cardiogenic death and heart failure readmission in patients with AHF

Semen CD4+ T cells and macrophages are productively infected at all stages of SIV infection in macaques.

International audienceThe mucosal events of HIV transmission have been extensively studied, but the role of infected cells present in the genital and rectal secretions, and in the semen, in particular, remains a matter of debate. As a prerequisite to a thorough in vivo investigation of the early transmission events through infected cells, we characterized in detail by multi-parameter flow cytometry the changes in macaque seminal leukocytes during SIVmac251 infection, focusing on T cells, macrophages and dendritic cells. Using immunocytofluorescence targeting SIV proteins and real-time quantitative PCR targeting SIV DNA, we investigated the nature of the infected cells on sorted semen leukocytes from macaques at different stages of infection. Finally, we cocultured semen CD4(+) T cells and macrophages with a cell line permissive to SIV infection to assess their infectivity in vitro. We found that primary infection induced strong local inflammation, which was associated with an increase in the number of leukocytes in semen, both factors having the potential to favor cell-associated virus transmission. Semen CD4(+) T cells and macrophages were productively infected at all stages of infection and were infectious in vitro. Lymphocytes had a mucosal phenotype and expressed activation (CD69 & HLA-DR) and migration (CCR5, CXCR4, LFA-1) markers. CD69 expression was increased in semen T cells by SIV infection, at all stages of infection. Macrophages predominated at all stages and expressed CD4, CCR5, MAC-1 and LFA-1. Altogether, we demonstrated that semen contains the two major SIV-target cells (CD4+ T cells and macrophages). Both cell types can be productively infected at all stages of SIV infection and are endowed with markers that may facilitate transmission of infection during sexual exposure

Experimental detection of short regulatory motifs in eukaryotic proteins: tips for good practice as well as for bad

It has become clear in outline though not yet in detail how cellular regulatory and signalling systems are constructed. The essential machines are protein complexes that effect regulatory decisions by undergoing internal changes of state. Subcomponents of these cellular complexes are assembled into molecular switches. Many of these switches employ one or more short peptide motifs as toggles that can move between one or more sites within the switch system, the simplest being on-off switches. Paradoxically, these motif modules (termed short linear motifs or SLiMs) are both hugely abundant but difficult to research. So despite the many successes in identifying short regulatory protein motifs, it is thought that only the “tip of the iceberg” has been exposed. Experimental and bioinformatic motif discovery remain challenging and error prone. The advice presented in this article is aimed at helping researchers to uncover genuine protein motifs, whilst avoiding the pitfalls that lead to reports of false discovery. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12964-015-0121-y) contains supplementary material, which is available to authorized users

Effects of body mass index and gender on left atrial size in Chinese hypertensive patients

Background Left atrial enlargement (LAE) is a common cardiac structural change in patients with hypertension, and obesity could further promote LAE. However, little is known about the effect of overweight on left atrial size, and if there is a gender difference of the effect. The aim of this study was to analyze the effects of different body mass index (BMI) grades (normal weight, overweight, and obesity) on left atrial size in both male and female patients with hypertension. Methods A total of 710 patients with hypertension were divided into 3 study groups: normal weight group (BMI  .05). For each additional unit of BMI, LAD increased by 0.034 mm and LADI increased by 0.305 mm/m. Multiple linear regression analysis showed that BMI, left ventricular mass index (LVMI), age and female gender were independently correlated with LADI (P < .05). And BMI was the most significant influencing factor of LADI in male patients (β = 0.350, P < .001), followed by LVMI (β = 0.343, P < .001). While in female patients, LVMI was the most significant (β = 0.353, P < .001), followed by BMI (β = 0.302, P < .001). Conclusion Overweight and obesity were significantly associated with LAE in hypertensive patients, with obesity more significant than overweight. While BMI had the greatest correlation with LAE in male, LVMI was the most important determinant of LAE in female. Therefore, in addition to weight loss, more attention should be paid to early inhibition of left ventricular remodeling in female with hypertension

Liraglutide ameliorates oxidized LDL-induced endothelial dysfunction by GLP-1R-dependent downregulation of LOX-1-mediated oxidative stress and inflammation

ABSTRACTObjective To investigate the effects of glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide on endothelial dysfunction in LDL receptor-deficient (LDLR-KO) mice and ox-LDL-challenged human umbilical vein endothelial cells (HUVECs) and its possible mechanism.Methods LDLR-KO mice were randomly treated with normal saline, liraglutide, or liraglutide plus a GLP-1R antagonist exendin-9 for four weeks. In parallel, HUVECs were cultured with ox-LDL alone or combined with liraglutide, in the presence or absence of lectin-like ox-LDL receptor-1(LOX-1) overexpression or GLP-1R knockdown. Endothelial-dependent relaxation and LOX-1 protein expression of thoracic aorta, circulating levels of oxidative and inflammatory markers in mice, and cell survival, reactive oxygen species production, and expression of adhesion molecules and signal regulators in ox-LDL cultured endothelial cells were measured.Results liraglutide effectively enhanced acetylcholine-induced vasodilation, reduced LOX-1 expression in aortas, and decreased circulatory oxidative and inflammatory levels in LDLR-KO mice, which were abolished by cotreatment with exendin-9. HUVECs exposed to ox-LDL exhibited reduced cell viability, increased reactive oxygen species production and apoptosis, and elevated protein expression of ICAM-1, VCAM-1, LOX-1, NOX4, and NF-κB, which were markedly ameliorated by liraglutide treatment. The protective effects of liraglutide against ox-LDL-induced cell injury were abrogated in HUVECs overexpressing LOX-1 or silencing GLP-1R.Conclusions Liraglutide improved oxidized LDL-induced endothelial dysfunction via GLP-1R-dependent downregulation of LOX-1-mediated oxidative stress and inflammation