Burgesshelms6204

To investigate the effects of 8-weeks of CT on specific domains of cognitive function, metabolic and cardiovascular parameters of subjects with Type 2 Diabetes Mellitus (T2DM).

31 sedentary T2DM adults and older divided into CT (3x/week, during 8-week, n=16) or Control group (CONT, n=15). Before and after the intervention, a cognitive task battery, blood samples, and functional tests were assessed.

CT improved inhibitory control (d=0.89), working memory (d=0.88), cognitive flexibility (d=0.67) and attention/concentration (d=0.64) in T2DM subjects. However, memory, verbal fluency, and processing speed (d<0.1, p>0.05 for all) were not changed. The CT-induced improvements on global cognitive z-score (r=-0.51; p<0.001) were inversely correlated to cognitive screening scores. Moreover, CT improved functional performance (p<0.05) and reduced insulin levels (p=0.04). Although there was no statistical significance, there were a clinically relevant reduction of peripheral insulin sensitivity (d=0.51, p=0.09), resistin levels (d=0.53, p=0.08), diastolic (d=0.63, p=0.09) and mean blood pressure (d=0.50, p=0.09). Conversely, no changes were observed for glucose, fructosamine and blood lipids (d<0.2 for all).

CT partially reversed the negative effects of T2DM on specific cognitive domains possibly by amelioration of metabolic regulation. Moreover, lower cognitive scores may modulate the responsivity of cognitive function to CT.

CT partially reversed the negative effects of T2DM on specific cognitive domains possibly by amelioration of metabolic regulation. Moreover, lower cognitive scores may modulate the responsivity of cognitive function to CT.

Minimally invasive glaucoma surgery (MIGS) is increasingly performed at the time of cataract extraction. Understanding the demographic and clinical characteristics of patients undergoing MIGS procedures may provide insight into patient selection. This study evaluates racial-ethnic and other differences in the use of MIGS in persons with cataract and open-angle glaucoma (OAG).

Retrospective cohort study using Intelligent Research in Sight (IRIS) Registry data.

Patients aged ≥ 40 years with a diagnosis of OAG and no history of MIGS or cataract surgery who were undergoing cataract extraction, with or without MIGS, during 2013 to 2017 in the United States.

Multivariable logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).

Variables assessed include age, sex, race-ethnicity, disease severity, insurance type, census region, comorbidity, and cup-to-disc ratio (CDR).

The odds of MIGS use was greater among patients who were aged ≥ 60 years (OR, 1.10 [95% Cher procedures in various patient populations.

This analysis highlights the importance of capturing race-ethnicity data and other pertinent patient characteristics in electronic health records to provide insight into practice patterns. Such data can be used to assess the long-term performance of MIGS and other procedures in various patient populations.

Diabetic retinopathy (DR) is the most common complication of type 2 diabetes mellitus, which could result in visual impairment. Accumulating studies have shown the implication of long non-coding RNAs (lncRNAs) in the pathogenesis of DR. Our aims are to investigate whether lncRNA SNHG7 plays a role during DR pathogenesis.

Human retinal microvascular endothelial cells (HRMECs) were treated with high glucose (HG) to build cell model. Relative expression of RNAs were examined using qPCR, and western blot or immunofluorescence analysis was adopted to detect the protein expression. Cell viability, migration and angiogenic capacity of HRMECs were estimated through CCK-8, transwell and tube formation experiments, respectively. Dual-luciferase reporter and RNA pull down assays were employed to verify the interplay between miR-34a-5p and SNHG7 or XBP1. Mesenchymal stem cells (MSCs) were identified by examining typical surface makers using flow cytometry and the differentiation abilities via Alizarin red, Oil red O and Alcian blue staining. MSC-derived exosomes were verified by transmission electron microscopy and western blot.

LncRNA SNHG7 sponged to and negatively regulated miR-34a-5p. SNHG7 overexpression repressed HG induced endothelial-mesenchymal transition (EndMT) and tube formation of HRMECs, while miR-34a-5p overexpression could reverse this effect. miR-34a-5p targeted and negative regulated XBP1. Knockdown of miR-34a-5p repressed HG induced EndMT and tube formation, which were partially blocked by XBP1 inhibition. MSC-derived exosomes could transfer SNHG7 to HRMECs and modulated EndMT and tube formation.

The MSC-derived exosomal lncRNA SNHG7 suppresses EndMT and tube formation in HRMECs via miR-34a-5p/XBP1 axis.

The MSC-derived exosomal lncRNA SNHG7 suppresses EndMT and tube formation in HRMECs via miR-34a-5p/XBP1 axis.

The aim of this study is to evaluate acute pancreatitis (AP)-associated NET activation mediated by a novel inflammatory mediator (high-mobility group box protein-1 [HMGB1]) and proinflammatory cytokine responses.

In this study, primary neutrophils, monocytes, and monocytic cell line Thp-1-derived macrophages were isolated and treated with HMGB1, lipopolysaccharide (LPS), adenosine triphosphate (ATP), and ATP+ATP inhibitor. The effects of HMGB1, ATP, and deoxyribonuclease (DNAse) were then examined for their in vivo effects using a newly established AP mouse model.

The mRNA and protein levels of inflammasome and interleukin IL-1β in cells, blood, and pancreatic tissues were examined. Within-cell nuclear DNA signal, cell-free DNA concentration, and pancreatic tissue damage were investigated. Our study showed that HMGB1 triggers NET formation in neutrophils and promotes the activation of inflammasome complexes (the NLR family, pyrin domain containing 3, and NLRP3; ASC; and caspase-1); therefore, the production of IL-1β is induced in human monocytes/macrophages. HMGB1 and NET cooperatively stimulate IL-1β processing in macrophages. Furthermore, the AP mouse model confirmed these HMGB1-mediated molecular mechanisms in vivo and indicated that HMGB1 is required for NET activation.

We found that NET inhibition reverses HMGB1-stimulated inflammasome activation and IL-1β production. HMGB1 thus leads to pancreatic injury through the activation of NET and subsequently induces IL-1β processing from neutrophils to pancreatic tissues. check details These findings demonstrate that HMGB1 and NET are new therapeutic targets for inflammation suppression in severe AP.

We found that NET inhibition reverses HMGB1-stimulated inflammasome activation and IL-1β production. HMGB1 thus leads to pancreatic injury through the activation of NET and subsequently induces IL-1β processing from neutrophils to pancreatic tissues. These findings demonstrate that HMGB1 and NET are new therapeutic targets for inflammation suppression in severe AP.