Role of automated functional imaging and myocardial work in assessment of cardiac function in children with obstructive sleep apnea.

Background: Early identification of abnormal left ventricular function in children with obstructive sleep apnea (OSA) is difficult using conventional echocardiographic indices and commonly used clinical markers of myocardial damage. We sought to investigate the value of automatic function imaging and myocardial work parameters in predicting early cardiac impairment in children having OSA with preserved left heart function and thereby identifying an optimal index for assessment.

Patients And Methods: Fifty-two children who presented with symptoms of nocturnal sleep snoring and open-mouth breathing and 34 healthy controls were enrolled in this study.

An investigation of a self-assembled cell-extracellular complex and its potentials in improving wound healing.

Background: To maintain and enhance the wound healing effects of mesenchymal stem cells (MSCs), a scaffold for hosting MSCs is needed, which ought to be completely biocompatible, durable, producible, and of human source.

Objective: To build a cell-extracellular matrix (ECM) complex assembled by human umbilical cord mesenchymal stem cells (HuMSCs) and to investigate its clinical potentials in promoting wound healing.

Method: HuMSCs were isolated and expanded.

PAX5 activates telomerase activity and proliferation in keloid fibroblasts by transcriptional regulation of SND1, thus promoting keloid growth in burn-injured skin.

Objective: Staphylococcal nuclease domain-containing 1 (SND1) that functioned as an oncogene in a variety of tumors was upregulated in burn-injured skin tissues, and this study aims to investigate the effect of SND1 on keloid and elucidate the underlying mechanism.

Methods: Keloid fibroblasts (KFs) and normal skin fibroblasts (NFs) were isolated from the keloid tissues and adjacent normal skin tissues of keloid patients. The SND1 expression was assessed in keloid tissues and KFs with Western blot assay.

LincRNA TINCR facilitates excessive proliferation and inflammation in post-burn skin fibroblasts by directly binding with SND1 protein and inducing SND1-mediated TGF-β1 expression.

In this study, we found that lincRNA-TINCR was significantly upregulated in burn-injured skin tissues in vivo and heat-stimulated dermal fibroblasts in vitro, accompanied by an increase in TGF-β1 expression. TINCR overexpression promoted cell proliferation, colony formation, release of pro-inflammatory factors and expression of TGF-β1 protein in human primary fibroblasts under normal condition. Moreover, silencing TINCR reduced expression of TGF-β1, cell proliferation, colony formation and inflammation in heat-stressed fibroblasts.

Effects of triclosan on hormones and reproductive axis in female Yellow River carp (Cyprinus carpio): Potential mechanisms underlying estrogen effect.

Triclosan (TCS), a member of the class of compounds called pharmaceutical and personal care products (PPCPs), is a broad antibacterial and antifungal agent found in a lot of consumer products. However, TCS hormone effect mechanism in teleost female fish is not clear. Female Yellow River carp (Cyprinus carpio) were exposed to 1/20, 1/10 and 1/5 LC TCS (96h LC of TCS to carp) under semi-static conditions for 42days.

CTRP6 inhibits fibrogenesis in TGF-β1-stimulated human dermal fibroblasts.

Skin fibrosis is characterized by excessive proliferation of fibroblasts and overproduction of extracellular matrix (ECM). C1q/tumor necrosis factor-related protein 6 (CTRP6), a member of CTRPs, has been involved in the development of cardiac fibrosis. However, the function and detailed regulatory mechanism of CTRP6 in skin fibrosis remain unclear.

NF-YA promotes invasion and angiogenesis by upregulating EZH2-STAT3 signaling in human melanoma cells.

The process of angiogenesis is essential for tumor development and metastasis. Vascular endothelial growth factor (VEGF), which is overexpressed in most human cancers, has been demonstrated to be a major modulator of angiogenesis. Thus, inhibition of VEGF signaling has the potential for tumor anti-angiogenic therapy.

MicroRNA-143-3p inhibits hyperplastic scar formation by targeting connective tissue growth factor CTGF/CCN2 via the Akt/mTOR pathway.

Post-traumatic hypertrophic scar (HS) is a fibrotic disease with excessive extracellular matrix (ECM) production, which is a response to tissue injury by fibroblasts. Although emerging evidence has indicated that miRNA contributes to hypertrophic scarring, the role of miRNA in HS formation remains unclear. In this study, we found that miR-143-3p was markedly downregulated in HS tissues and fibroblasts (HSFs) using qRT-PCR.

[The application of delayed skin grafting combined traction in severe joint cicatricial contracture].

Objective: To investigate the effect of delayed skin grafting combined traction in severe joint cicatricial contracture.

Methods: At the first stage, the joint cicatricial contracture was released completely with protection of vessels, nerves and tendons. The wound was covered with allogenetic skin or biomaterials.

Tanshinone IIA pretreatment renders free flaps against hypoxic injury through activating Wnt signaling and upregulating stem cell-related biomarkers.

Partial or total flap necrosis after flap transplantation is sometimes clinically encountered in reconstructive surgery, often as a result of a period of hypoxia that exceeds the tolerance of the flap tissue. In this study, we determine whether tanshinone IIA (TSA) pretreatment can protect flap tissue against hypoxic injury and improve its viability. Primary epithelial cells isolated from the dorsal skin of mice were pretreated with TSA for two weeks.

Tanshinone IIA pretreatment protects free flaps against hypoxic injury by upregulating stem cell-related biomarkers in epithelial skin cells.

Background: Partial or total flap necrosis after flap transplantation is sometimes encountered in reconstructive surgery, often as a result of a period of hypoxia that exceeds the tolerance of the flap tissue. The purpose of this study was to determine whether Tanshinone IIA (TSA) pretreatment can protect flap tissue against hypoxic injury and improve its viability.

Methods: Primary epithelial cells isolated from the dorsal skin of mice were pretreated with TSA for 2 weeks.