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041). Our results suggested that miR-182 polymorphism rs4541843 may contribute to the susceptibility to HCC. Tasquinimod nmr Our findings require validation in further studies with larger sample sizes.

Diabetes is associated with the dysfunction of endothelial progenitor cells (EPCs), characterized as impaired angiogenesis, a phenomenon thought to be involved in the development of diabetic foot. lncRNA plays an essential role in microvascular dysfunction and signaling pathways in patients with diabetes. lncRNA taurine upregulated gene 1 (TUG1) participates in angiogenesis in various cells. However, the mechanisms of TUG1 activity in EPCs have not been elucidated.

We isolated and then characterized EPCs from the peripheral blood of mice using immunofluorescence and flow cytometry. Western blot detected the wnt/β-catenin pathway in high glucose-treated EPCs. Bioinformatics analysis predicted a putative binding site for TUG1 on miR-29c-3p. The interactions among TUG1, platelet-derived growth factor-BB (PDGF-BB), and miR-29c-3p were analyzed by luciferase assays. In vivo, diabetic mouse ischemic limb was treated with normal saline or TUG1 overexpression lentiviruses.

We found that EPC migration, invasion, and tube formation declined after treatment with high glucose, but improved with TUG1 overexpression. Mechanically, wnt/β-catenin pathway and autophagy were involved in the function of TUG1 overexpression in high glucose-treated EPCs. Moreover, TUG1 regulates the PDGF-BB/wnt pathway and function of high glucose-treated EPCs via miR-29c-3p. In vivo, injection of TUG1 lentivirus in a diabetic mouse ischemic limb model stimulated angiogenesis.

Our findings suggest that TUG1 restores high glucose-treated EPC function by regulating miR-29c-3p/PDGF-BB/Wnt signaling.

Our findings suggest that TUG1 restores high glucose-treated EPC function by regulating miR-29c-3p/PDGF-BB/Wnt signaling.

Clinical frailty among older adults admitted to intensive care has been proposed as an important determinant of patient outcomes. Among this group of patients, an acute episode of delirium is also common, but its relationship to frailty and increased risk of mortality has not been extensively explored. Therefore, the aim of this study was to explore the relationship between clinical frailty, delirium and hospital mortality of older adults admitted to intensive care.

This study is part of a Delirium in Intensive Care (Deli) Study. During the initial 6-month baseline period, clinical frailty status on admission to intensive care, among adults aged 50years or more; acute episodes of delirium; and the outcomes of intensive care and hospital stay were explored.

During the 6-month baseline period, 997 patients, aged 50years or more, were included in this study. The average age was 71 years (IQR, 63-79); 55% were male (n = 537). Among these patients, 39.2% (95% CI 36.1-42.3%, n = 396) had a Clinical Frailty Scum significantly increase the risk of hospital mortality. Therefore, it is important to identify patients who are frail and institute measures to reduce the risk of adverse events in the ICU such as delirium and, importantly, to discuss these issues in an open and empathetic way with the patient and their families.

Research has the potential to influence US social policy; however, existing research in this area lacks a coherent message. The Model for Dissemination of Research provides a framework through which to synthesize lessons learned from research to date on the process of translating research to US policymakers.

The peer-reviewed and grey literature was systematically reviewed to understand common strategies for disseminating social policy research to policymakers in the United States. We searched Academic Search Premier, PolicyFile, SocINDEX, Social Work Abstracts, and Web of Science from January 1980 through December 2019. Articles were independently reviewed and thematically analyzed by two investigators and organized using the Model for Dissemination of Research.

The search resulted in 5225 titles and abstracts for inclusion consideration. 303 full-text articles were reviewed with 27 meeting inclusion criteria. Common sources of research dissemination included government, academic researchers, the peer reviewed literature, and independent organizations. The most frequently disseminated research topics were health-related, and legislators and executive branch administrators were the most common target audience. Print materials and personal communication were the most common channels for disseminating research to policymakers. There was variation in dissemination channels by level of government (e.g., a more formal legislative process at the federal level compared with other levesl). Findings from this work suggest that dissemination is most effective when it starts early, galvanizes support, uses champions and brokers, considers contextual factors, is timely, relevant, and accessible, and knows the players and process.

Effective dissemination of research to US policymakers exists; yet, rigorous quantitative evaluation is rare. A number of cross-cutting strategies appear to enhance the translation of research evidence into policy.

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While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelial barrier. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems.

16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 μg/cm

SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 μg/m

 ; 2 h per day for 5 days) and changes in the tight junction protein Tricellulin were assessed 2 weeks post exposure.

A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran.