Supercritical carbon dioxide decellularized porcine cartilage graft with PRP attenuated OA progression and regenerated articular cartilage in ACLT-induced OA rats.

Knee osteoarthritis (OA) is a common degenerative articular disorder and considered one of the primary causes of pain and functional disability. Knee OA is prevalent in 10% of men and 13% of women aged 60 years above. The study aims to use cartilage tissue engineering that combines the triads of decellularized porcine cartilage graft as "scaffold," plasma rich platelet (PRP) as "signal" and chondrocytes from rat as "cell" to attenuate ACLT-induced OA progression and regenerate the knee cartilage in rats.

A novel 3D histotypic cartilage construct engineered by supercritical carbon dioxide decellularized porcine nasal cartilage graft and chondrocytes exhibited chondrogenic capability .

Augmentative and reconstructive rhinoplasty surgical procedures use autologous tissue grafts or synthetic grafts to repair the nasal defect and aesthetic reconstruction. Donor site trauma and morbidity are common in autologous grafts. The desperate need for the production of grafted 3D cartilage tissues as rhinoplasty grafts without the adverse effect is the need of the hour.

3D composite engineered using supercritical CO decellularized porcine cartilage scaffold, chondrocytes, and PRP: Role in articular cartilage regeneration.

At present, no definitive treatment for articular cartilage defects has been perfected. Most of the previous treatments involved multiple drilling and microfracture over defect sites with repair-related substances, which poses a limited therapeutic effect. End-stage therapy includes artificial knee joint replacement.

Improve blood compatibility of bioresorbable magnesium stents coated with functionalized anti-CD34 antibody and heparin-collagen multiplayers.

Instentrestenosis and late stent thrombosis continue to be the greatest limitations of drug-eluting stents. In this study, an anti-CD34 antibody functionalized multilayer of heparin/collagen type I is developed by layer-by-layer assemble to enhance biocompatibility and recruit endothelial progenitor cells. The SEM results demonstrate that (Hep/Col)5-coated samples have a rougher surface compared to (Hep/Col)2-coated samples and untreated samples.

Hypoxia suppresses myocardial survival pathway through HIF-1α-IGFBP-3-dependent signaling and enhances cardiomyocyte autophagic and apoptotic effects mainly via FoxO3a-induced BNIP3 expression.

The HIF-1α transcriptional factor and the BH-3 only protein BNIP3 are known to play fundamental roles in response to hypoxia. The objective of this research is to investigate the molecular mechanisms and the correlation of HIF-1α, BNIP3 and IGFBP-3 in hypoxia-induced cardiomyocytes injuries. Heart-derived H9c2 cells and neonatal rat ventricular myocytes (NRVMs) were incubated in normoxic or hypoxic conditions.

17β-Estradiol and/or Estrogen Receptor β Attenuate the Autophagic and Apoptotic Effects Induced by Prolonged Hypoxia Through HIF-1α-Mediated BNIP3 and IGFBP-3 Signaling Blockage.

Background/aims: The risk of heart disease is higher in males than in females. However, this advantage of females declines with increasing age, presumably a consequence of decreased estrogen secretion and malfunctioning of the estrogen receptor. We previously demonstrated that 17β-estradiol (E2) prevents cardiomyocyte hypertrophy, autophagy and apoptosis via estrogen receptor α (ERα), but the effects of ERβ on myocardial injury remained elusive.

[An experience applying the transtheoretical model to assist a highly educated case to quit smoking].

Although smokers who are highly educated understand the risks involved in smoking, they tend to be highly influenced by the opinions of others and thus subject to severe social pressures. This is a case report on the application of the transtheoretical model of behavioral change to a an individual with a PhD in biotechnology who had been smoking for 20 years. The effects of the developed smoking cessation intervention were investigated and data were collected through personal meetings, telephone interviews, and e-mail during a smoking cessation counseling program that lasted from October 18th, 2012, to April 15th, 2013.

Up-regulation of connective tissue growth factor in hyperoxia-induced lung fibrosis.

Pulmonary oxygen toxicity plays an important role in the lung injury process that leads to the development of bronchopulmonary dysplasia. Connective tissue growth factor (CTGF) is a fibroblast mitogen and promoter of collagen deposition. We investigated the effects of postnatal hyperoxia on lung collagen and CTGF expression in rats.