Notes

Human being coagulation element IX: an organized review of the characteristics.
There is limited data about the prognosis and impact of COVID-19 pneumonia on patients with diabetes mellitus (DM). We aimed to assess blood indices, ECG markers of sudden death and malignant arrhythmias on admission, and diabetes lowering drugs as possible predictors of adverse in-hospital outcome and COVID-19 pneumonia recovery status.

A retrospective study included patients with newly diagnosed COVID-19 pneumonia from August 20, to October 5, 2020.

A total of 192 patients with COVID-19 pneumonia were included in the present study, of whom 67 patients had DM. Low lymphocytes % [0.4(0.1-0.9), P=.011] and QTc interval prolongation [0.4(0.1-0.8), P=.022] were associated with increased length of ICU stay. On the other hand, metformin use [0.3(0.2-4), P=.032] and DPP-4 inhibitors use [0.3(0.2-3), P=.040] were associated with decreased length of ICU stay. QTc interval prolongation [0.4(0.1-0.9), P=.017] was associated with increased length of hospital stay, while using metformin [0.4(0.2-3), P=.022] was associated with decreased length of hospital stay. Low lymphocytes % [0.5(0.4-1.6), P=.001], insulin use [0.4(0.3-5), P=.003], and old age [0.5(0.1-2.3), P=.025] were associated with extensive lung injury. The risk for in-hospital death was associated with high neutrophil% [1(1-1.4), P=.045], while metformin use was associated with decreased risk for in-hospital death [0.1(0.1-0.6), P=.025]. Insulin use [0.3(0.2-4), P=.013] was associated with partial recovery following acute COVID pneumonia.

Metformin and DPP-4 inhibitors use were associated with favorable in-hospital outcomes, while insulin use was associated with extensive lung injury and post-acute COVID-19 pneumonia partial recovery.
Metformin and DPP-4 inhibitors use were associated with favorable in-hospital outcomes, while insulin use was associated with extensive lung injury and post-acute COVID-19 pneumonia partial recovery.
To compare the effect of sedation protocols with and without dexmedetomidine on delirium risk and duration in adult patients in intensive care units (ICUs).

A meta-analysis of randomized controlled trials.

We searched the Cochrane Central Register of Controlled Trials, PubMed, EMBASE, and ISI Web of Science from inception to September 3, 2020. We included studies comparing the effect of dexmedetomidine-based sedation on delirium risk with non-dexmedetomidine-based sedation in adult patients in ICUs. We pooled the data using a random-effects model using Review Manager 5.2, and assessed publication bias using Stata 11.0. The quality of evidence was rated using the Grading of Recommendations, Assessment, Development and Evaluation system.

We included 36 studies involving 9623 participants. The use of dexmedetomidine was associated with reduced risk of delirium (risk ratio [RR], 0.63; 95% confidence interval [CI], 0.54-0.75; very low-quality evidence), but higher incidences of hypotension and bradycardia tomidine include hypotension and bradycardia. PROSPERO registration number CRD42018095358.
Low- or very low-quality evidence suggests that dexmedetomidine was associated with a clinically-small reduction of delirium risk, ICU/hospital stay and mechanical ventilation duration, but were not associated with improved mortality or shorter delirium duration in ICU patients. These findings were inconclusive because of publication bias, heterogeneity, and limited sample size. Significant adverse effects of dexmedetomidine include hypotension and bradycardia. PROSPERO registration number CRD42018095358.The erector spinae plane block is an emerging analgesic technique, which is gaining popularity for a large number of procedures. The majority of publications are at the thoracic level and almost all indicate some benefit to patients. However, there have been relatively few randomized controlled trials and even fewer studies at the lumbar level. The aim of this study was to assess whether the erector spinae plane block at the lumbar level would confer early analgesic benefits and improve the quality of recovery in patients undergoing elective unilateral primary hip arthroplasty. Sixty-four patients were randomized to receive an erector spinae plane block at the third lumbar vertebra with either 30milliliters (ml) of 0.2% ropivacaine or 30 ml of 0.9% saline. The patient, anesthetist and assessor were blinded to allocation. The primary outcome was pain on movement at 6 h (numeric rating scale 0-10) with a reduction of 2 points considered clinically significant. Secondary outcomes included quality of recovery (QoR-15 score), mobilization and length of stay. In this study there was no appreciable analgesic benefit to adding an erector spinae plane block to patients who already receive neuraxial blocks, local anesthetic infiltration and oral multimodal analgesia for elective primary total hip arthroplasty. Both groups were found to have relatively low pain scores and a high quality of recovery with no significant difference in mobilization or length of stay.
To develop and validate a delirium risk prediction preoperative model for patients undergoing cardiac surgery.

Observational prospective multicentre study.

Six intensive care units in Spain.

689 patients undergoing cardiac surgery consecutively, aged ≥18 years.

The primary outcome measure was the development of delirium, diagnosed using the Confusion Assessment Method in Intensive Care Units (CAM-ICU), during the stay in the intensive care unit after cardiac surgery.

The model was developed with 345 consecutive patients undergoing cardiac surgery at six hospitals and validated with another 344 patients from the same hospitals. The prediction model contained four preoperative risk factors age over 65 years, Mini-Mental State Examination (MMSE) score of 25-26 points (possible impairment of cognitive function) or < 25 (impairment of cognitive function), insomnia needing medical treatment and low physical activity (walk less than 30 min a day). The model had an area under the receiver operating chardiac surgery. An automatic version of the risk calculator is available.The activation of hepatic stellate cells (HSCs) has been considered one of the major events in hepatic fibrosis. Amygdalin has been used to treat cancers and alleviate pain; however, its role and mechanism in HSC activation and hepatic fibrosis remain unclear. In the present study, transforming growth factor-beta 1 (TGF-β1) stimulated the activation of HSCs, as indicated by significantly increased alpha-smooth muscle actin (α-SMA), desmin, collagen I, and tissue inhibitor of metalloproteinase-1 (TIMP-1) protein levels. Amygdalin treatment dramatically suppressed TGF-β1-induced HSC proliferation and activation. Moreover, amygdalin treatment also reduced the TGF-β1-induced secretion of cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), platelet-derived growth factor (PDGF), and chemokine (C-C motif) ligand 2 (CCL2), as well as the phosphorylation of Smad2, Smad3, and p65. In the CCl4-stimulated liver fibrosis rat model, amygdalin treatment improved liver fibrosis and liver damage by reducing focal necrosis, collagen fiber accumulation, and the protein levels of α-SMA, desmin, collagen I, and TIMP-1 in hepatic tissue samples and reducing serum alanine transaminase (ALT) and aspartate transaminase (AST) levels. In conclusion, we demonstrated the suppressive effects of amygdalin in TGF-β1-induced HSC activation through modulating proliferation, fibrogenesis, and inflammation signaling in vitro and the antifibrotic effects of amygdalin in CCl4-stimulated hepatic fibrosis in rats in vivo.
As a common joint disease, osteoarthritis (OA) is the main cause of limited joint mobility and disability. The role of lncRNAs in the regulation of OA is increasingly discovered. Therefore, further exploring the function of SNHG7 in OA is of great significance for understanding its occurrence and development.

We used interleukin-1β (IL-1β) to treat to establish an OA model primary on chondrocytes in vitro, and gain- and loss of function assays of SNHG7 and miR-214-5p were conducted. The cell viability and apoptosis of chondrocytes were detected by CCK8 assay, BrdU assay and flow cytometry. The inflammatory cytokines (IL-1β, IL-6 and TNF-α), NLRP3 inflammasome, protein level of PPARGC1B, PPARγ, P38 and NF-κB were determined by RT-PCR and/or western blot.

The results showed that SNHG7 was distinctly downregulated, while miR-214-5p was significantly upregulated in OA patients and primary chondrocytes treated with IL-1β. In addition, SNHG7 enhanced cell viability, inhibited apoptosis and inflammation of IL-1β-mediated chondrocytes. In contrast, miR-214-5p upregulation reduced viability, promoted apoptosis and inflammation of chondrocytes. Mechanistically, SNHG7 served as a competitive endogenous RNA by sponging miR-214-5p, which targeted PPARGC1B. Besides, the results of the compensation experiment affirmed that miR-214-5p attenuates SNHG7-mediated protective effects on IL-1β-mediated chondrocytes against apoptosis and inflammation, and activating PPARγ pathway markedly dampened the cytotoxic effects of miR-214-5p.

Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.
Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.MicroRNA-155 (miR-155) is implicated in the pathological processes of sepsis. However, the function and regulatory mechanism of miR-155 in sepsis-induced inflammation and intestinal barrier dysfunction remain unknown. In this study, mouse models of sepsis were established by caecal ligation and puncture (CLP). To reduce miR-155 expression, the mice were injected for three consecutive days with an miR-155 inhibitor (80 mg/kg) before CLP. The serum DAO concentration was measured by ELISA, and histological changes in the intestine were identified by H&E staining 24 h after CLP. FITC-dextran assays were used to evaluate intestinal permeability. MiR-155 gene expression was evaluated with RT-PCR, and relative protein expression was assessed by Western blotting. NCM460 cells were transfected with an miR-155 mimic/miR-155 inhibitor or pretreated with an NF-κB inhibitor before LPS treatment, and the cytokines levels, miR-155 gene expression and relative protein expression were measured. Selleck CWI1-2 Sepsis increased miR-155, DAO and FITC-dextran levels and reduced Occludin and ZO-1 expression. Mice injected with the miR-155 inhibitor recovered from the damages. Transfection of NCM460 cells with the miR-155 mimic elevated the NF-κB (P65) and p-NF-κB (p-P65) localization and expression in the nucleus, which was reversed by the miR-155 inhibitor. Pretreatment with an NF-κB inhibitor suppressed inflammation, improved cell permeability to FITC-dextran and increased Occludin and ZO-1 levels. Transfection with the miR-155 inhibitor decreased TNF-α and IL-6 levels, reduced cell permeability to FITC-dextran and increased ZO-1 and Occludin expression. The effects induced by transfection with the miR-155 mimic, including elevated TNF-α and IL-6 levels, hyperpermeability to FITC-dextran and reduced ZO-1 and Occludin expression, were partly rescued by pretreatment with the NF-κB inhibitor. These findings reveal that the miR-155 inhibitor alleviates inflammation and intestinal barrier dysfunction by inactivating NF-κB signaling during sepsis.
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