Carbon nanotubes (CNTs) provide an essential 2-D microenvironment for cardiomyocyte growth and function. However, it remains to be elucidated whether CNT nanostructures can promote cell–cell integrity and facilitate the formation of functional tissues in 3-D hydrogels. Here, single-walled CNTs were incorporated into collagen hydrogels to fabricate (CNT/Col) hydrogels, which improved mechanical and electrical properties. The incorporation of CNTs (up to 1 wt%) exhibited no toxicity to cardiomyocytes and enhanced cell adhesion and elongation. Through the use of immunohistochemical staining, transmission electron microscopy, and intracellular calcium-transient measurement, the incorporation of CNTs was found to improve cell alignment and assembly remarkably, which led to the formation of engineered cardiac tissues with stronger contraction potential. Importantly, cardiac tissues based on CNT/Col hydrogels were noted to have better functionality. Collectively, the incorporation of CNTs into the Col hydrogels improved cell alignment and the performance of cardiac constructs. Our study suggests that CNT/Col hydrogels offer a promising tissue scaffold for cardiac constructs, and might serve as injectable biomaterials to deliver cell or drug molecules for cardiac regeneration following myocardial infarction in the near future.

Thirty-eight patients with histologically proven pancreatic adenocarcinoma were investigated to establish the utility of serum CA 19-9 as a prognostic indicator. CA 19-9 assays were performed serially during the course of the disease. In four patients with negative Lewis blood type, the CA 19-9 levels remained essentially normal throughout the disease course. In the remaining 34 patients, (1) CA 19-9 levels were significantly lower in patients with tumor size no larger than 5 cm in diameter, and in patients with resectable tumors than in those with tumor size larger than 5 cm or with unresectable tumors (p less than 0.01). 2) CA 19-9 levels dropped sharply after resection in all 11 resectable patients, whereas no significant change was found after laparotomy without resection. (3) The average survival time in seven patients whose CA 19-9 levels returned to normal after resection was significantly longer than in those four patients with postoperative CA 19-9 levels that decreased but did not return to normal (21.9 versus 8.7 months, p less than 0.05). (4) In 6 of 11 patients who underwent resection, recurrent elevation of CA 19-9 preceded changes detectable by computed tomography or clinical examination by 2 to 9 months. (5) In 23 patients who died of pancreatic carcinoma, 15 (65%) had an obvious rise in CA 19-9 level before death. There was a correlation between the doubling time of the CA 19-9 serum level and survival time (r = 0.5, p less than 0.05). Because it can be demonstrated that the reduction of tumor burden by resection lowers serum CA 19-9 levels, serum CA 19-9 levels may be a useful indicator of whether other forms of treatment such as radiation therapy or chemotherapy also reduce the tumor burden.

Treatment with H2 S prevented NASH induced by MCD diet in rats possibly through abating oxidative stress and suppressing inflammation.

Long noncoding RNAs (lncRNAs) are known to play important roles in cancers. However, little is known about lncRNAs in cholangiocarcinoma (CCA), a cholangiocyte malignancy with poor prognosis. We investigated the role of nuclear paraspeckle assembly transcript 1 (NEAT1) lncRNA in promoting CCA. qRT-PCR analysis of patient samples showed that NEAT1 expression was higher in CCA tumors than in matched adjacent nontumor tissue. NEAT1 levels were also higher in CCA cell lines than in a normal biliary epithelium cell line (HIBEpic). NEAT1 knockdown in CCA cell lines using shNEAT1 reduced cell proliferation and colony formation in CCK-8 and colony formation assays, respectively. CCA cells transfected with shNEAT1 also exhibited reduced metastasis and invasiveness in Transwell assays. NEAT1 knockdown cells produced smaller tumors, demonstrating that NEAT1 promotes tumor growth in vivo. Silencing of NEAT1 increased E-cadherin expression in vitro, and E-cadherin expression was inversely correlated with NEAT1 expression in CCA tissue samples. RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA. We postulate that NEAT1 is a potentially useful diagnostic and therapeutic target for CCA.