LES of Vertical Buoyant Jets in Jonswap Waves

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Human beta defensin 2 selectively inhibits HIV-1 in highly permissive CCR6+CD4+ T cells

Chemokine receptor type 6 (CCR6)+CD4+ T cells are preferentially infected and depleted during HIV disease progression, but are preserved in non-progressors. CCR6 is expressed on a heterogeneous population of memory CD4+ T cells that are critical to mucosal immunity. Preferential infection of these cells is associated, in part, with high surface expression of CCR5, CXCR4, and α4β7. In addition, CCR6+CD4+ T cells harbor elevated levels of integrated viral DNA and high levels of proliferation markers. We have previously shown that the CCR6 ligands MIP-3α and human beta defensins inhibit HIV replication. The inhibition required CCR6 and the induction of APOBEC3G. Here, we further characterize the induction of apolipoprotein B mRNA editing enzyme (APOBEC3G) by human beta defensin 2. Human beta defensin 2 rapidly induces transcriptional induction of APOBEC3G that involves extracellular signal-regulated kinases 1/2 (ERK1/2) activation and the transcription factors NFATc2, NFATc1, and IRF4. We demonstrate that human beta defensin 2 selectively protects primary CCR6+CD4+ T cells infected with HIV-1. The selective protection of CCR6+CD4+ T cell subsets may be critical in maintaining mucosal immune function and preventing disease progression

Association between Insurance Status and Hospital Outcomes among Acute Kidney Failure Patients

Objectives: To investigate the relationship between insurance status and the risk of acute kidney failure (AKF) and consequential hospitalization outcomes. Methods: A cross-sectional regression analysis was conducted for inpatients ages 18-64 in South Carolina 2012–2013. One dichotomous dependent variable - diagnosed with AKF at hospital admission, and two continuous dependent variables of hospital outcomes - total charge and length of stay, were examined. The key explanatory variable was the patient’s insurance status. Other covariates included patient’s age, gender, and race as well as AKF risk factors - Type 2 diabetic mellitus (T2DM), chronic kidney disease (CKD), hypertension, and proteinuria. Results: No insurance was significantly associated with an increased risk of AKF. The odds of having AKF with concurrent CKD diagnosed among the uninsured patients (OR 10.00) is about 1.5 times as high as that among Medicaid (OR 6.40) or private insurance patients (OR 6.91). Patients without insurance coverage incurred lower charges and were discharged earlier than those with Medicaid or private insurance. However, the presence of T2DM reversed this trend. Self-pay AKF patients with T2DM were charged 6% more and stayed in hospital 25% longer than similar patients with Medicaid. Likewise, their charges and hospital stay were 9% more than patients with private insurance. Discussion: Insurance coverage could play a role in determining the risk of AKF and hospital outcomes. Insurance coverage could reduce underlying risk factors for AKF and its adverse consequences. Hospital investment to treat diabetes among the uninsured people in the catchment area might reduce uncompensated care and improve community health