Effect of Dexmedetomidine on Postoperative Plasma Neurofilament Light Chain in Elderly Patients Undergoing Thoracoscopic Surgery: A Prospective, Randomized Controlled Trial.

Purpose: Dexmedetomidine exerts a neuroprotective effect, however, the mechanism underlying this effect remains unclear. This study aimed to explore whether dexmedetomidine can reduce the increase in neurofilament light chain (NfL) protein concentration to play a neuroprotective role during thoracoscopic surgery.

Patients And Methods: Patients aged ≥60 years undergoing general anesthesia for thoracoscopic surgery were randomly assigned to receive dexmedetomidine (group D) or not receive dexmedetomidine (group C).

Effect of intravenous vs. inhaled penehyclidine on respiratory mechanics in patients during one-lung ventilation for thoracoscopic surgery: a prospective, double-blind, randomised controlled trial.

Background: Minimising postoperative pulmonary complications (PPCs) after thoracic surgery is of utmost importance. A major factor contributing to PPCs is the driving pressure, which is determined by the ratio of tidal volume to lung compliance. Inhalation and intravenous administration of penehyclidine can improve lung compliance during intraoperative mechanical ventilation.

Analysis of the impact of peritoneal dialysis catheter tail-end design on catheter-related complications.

Objective: Evaluate the impact of peritoneal dialysis catheter (PDC) tail-end design variations on PDC-related complications.

Method: Effective data were extracted from databases. The literature was evaluated according to the Cochrane Handbook for Systematic Reviews of Interventions, and a meta-analysis was conducted.

LncRNA NEAT1 accelerates renal fibrosis progression via targeting miR-31 and modulating RhoA/ROCK signal pathway.

Renal fibrosis is the final pathway for chronic kidney disease to end-stage renal failure. Noncoding RNAs have been reported to play a crucial role in renal fibrosis. Here, the effects of long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and miR-31 on renal fibrosis and their regulatory mechanism were evaluated.

LncRNA Dlx6os1 Accelerates Diabetic Nephropathy Progression by Epigenetically Repressing SOX6 via Recruiting EZH2.

Introduction: Diabetic nephropathy (DN) is the leading cause of kidney failure worldwide. To explore the pathogenesis and effective biological target of DN is beneficial to seeking novel treatment strategies.

Objective: This study aimed to investigate the role of the lncRNA Dlx6os1/SOX6/EZH2 axis in DN progression.

Overexpression of HOTAIR attenuates Pi-induced vascular calcification by inhibiting Wnt/β-catenin through regulating miR-126/Klotho/SIRT1 axis.

Vascular calcification is one of the most common effects of macrovascular complications in patients in aging with chronic kidney disease and diabetes. Previous studies showed that HOTAIR attenuated vascular calcification via the Wnt/β-catenin-signaling pathway, yet the molecular mechanism has not been fully elucidated. This study aimed to identify the explicit molecular mechanism underlying HOTAIR regulated vascular calcification.

The Clinical Value of Klotho and FGF23 in Cardiac Valve Calcification Among Patients with Chronic Kidney Disease.

Objective: This study aims to investigate the clinical value of serum Klotho and FGF23 in cardiac valve calcification in patients with chronic kidney disease (CKD).

Methods: In the present study, 180 patients with CKD, who were admitted to the department of nephrology of our hospital on April 1, 2016 (solstice, 2019), were selected as the main subjects. According to the CKD stage, these patients were divided into three groups: CKD2~3 group, CKD4 group, and CKD5 group.

Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

Background: Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown.

A Novel RFXANK Mutation in a Chinese Child With MHC II Deficiency: Case Report and Literature Review.

Major histocompatibility complex (MHC) II deficiency is a rare primary immunodeficiency disorder that is characterized by the deficiency of MHC class II molecules. The disease is caused by transcription factor mutations including class II transactivator (), regulatory factor X-5 (), RFX-associated protein (), and RFXAP-containing ankyrin repeat (), respectively. Mutations in the gene account for >70% of all known patients worldwide.

LncRNA-SNHG29 inhibits vascular smooth muscle cell calcification by downregulating miR-200b-3p to activate the α-Klotho/FGFR1/FGF23 axis.

Background: Vascular calcification (VC) is characterized by mineral accumulation on the walls of arteries and veins, which is a pathological process commonly found in elderly individuals and patients with atherosclerosis, hypertension, and diabetes. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play an important role in VC. However, the role of SNHG29 is less clear.

Long noncoding RNA NEAT1 sponges miR-129 to modulate renal fibrosis by regulation of collagen type I.

The long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to promote liver fibrosis progression. However, its molecular mechanism in renal fibrosis was not elucidated. In the present study, an in vitro model of renal fibrosis was established with HK-2 and HKC-8 cells treated with transforming growth factor-β1.

Klotho/FGF23 axis mediates high phosphate-induced vascular calcification in vascular smooth muscle cells via Wnt7b/β-catenin pathway.

Vascular calcification (VC) plays as a critical role on cardiovascular disease (CVD) and acts as a notable risk factor in cardiovascular system. Vascular smooth muscle cells (VSMCs) calcification can be triggered by high phosphate treatment; however, the explicit mechanism remains unclear. In the present study, we isolated VSMCs from primary rat artery, applied β-GP (β-glycerophosphate) for inducing VSMCs calcification in vitro to explore the mechanism of phosphate-induced calcification in VSMCs.