Recent studies indicate important roles for long noncoding RNAs (lncRNAs) as essential regulators of myogenesis and adult skeletal muscle regeneration. However, the specific roles of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells and myogenesis are still largely unknown. Here we identify a lncRNA that is specifically enriched in skeletal muscle (myogenesis-associated lncRNA, in short, lnc-mg). In mice, conditional knockout of lnc-mg in skeletal muscle results in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promotes muscle hypertrophy. In vitro analysis of primary skeletal muscle cells shows that lnc-mg increases gradually during myogenic differentiation and its overexpression improves cell differentiation. Mechanistically, lnc-mg promotes myogenesis, by functioning as a competing endogenous RNA (ceRNA) for microRNA-125b to control protein abundance of insulin-like growth factor 2. These findings identify lnc-mg as a novel noncoding regulator for muscle cell differentiation and skeletal muscle development.

Ischemia and reperfusion injury (IRI) is an inevitable event in conventional organ transplant procedure and is associated with significant mortality and morbidity post-transplantation. We hypothesize that IRI is avoidable if the blood supply for the organ is not stopped, thus resulting in optimal transplant outcomes. Here we described the first case of a novel procedure called ischemia-free organ transplantation (IFOT) for patients with end-stage liver disease. The liver graft with severe macrovesicular steatosis was donated from a 25-year-old man. The recipient was a 51-year-old man with decompensated liver cirrhosis and hepatocellular carcinoma. The graft was procured, preserved, and implanted under continuous normothermic machine perfusion. The recipient did not suffer post-reperfusion syndrome or vasoplegia after revascularization of the allograft. The liver function test and histological study revealed minimal hepatocyte, biliary epithelium and vascular endothelium injury during preservation and post-transplantation. The inflammatory cytokine levels were much lower in IFOT than those in conventional procedure. Key pathways involved in IRI were not activated after allograft revascularization. No rejection, or vascular or biliary complications occurred. The patient was discharged on day 18 post-transplantation. This marks the first case of IFOT in humans, offering opportunities to optimize transplant outcomes and maximize donor organ utilization.

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Carbohydrate structures on PRBC are different from those on PAEC. Healthy human sera contain anti-nonGal IgG antibodies to NeuGc expressed on PRBC, but not on PAEC. We speculate that anti-nonGal IgG antibodies to PRBC can recognize both NeuGc and protein, and this may be the reason why such antibodies have not been detected by ELISA. A definite conclusion about the immunogenicity of NeuGc has not been obtained. More sera from patients (not from non-human primates) sensitized with porcine cells or organs need to be studied.

This meta-analysis shows that DEB-TACE provides significantly better tumor response compared with conventional TACE. One-year and 2-year survival are better with DEB-TACE. In addition, DEB-TACE is as safe as conventional TACE. Therefore, DEB-TACE is a better choice for HCC patients for whom curative treatments like liver transplantation and liver resection are not suitable.

BackgroundPrevious studies have documented that heightened impulsivity likely contributes to the development and maintenance of alcohol use disorders. However, there is still a lack of studies that comprehensively detected the brain changes associated with abnormal impulsivity in alcohol addicts. This study was designed to investigate the alterations in brain structure and functional connectivity associated with abnormal impulsivity in alcohol dependent patients.MethodsBrain structural and functional magnetic resonance imaging data as well as impulsive behavior data were collected from 20 alcohol dependent patients and 20 age- and sex-matched healthy controls respectively. Voxel-based morphometry was used to investigate the differences of grey matter volume, and tract-based spatial statistics was used to detect abnormal white matter regions between alcohol dependent patients and healthy controls. The alterations in resting-state functional connectivity in alcohol dependent patients were examined using selected brain areas with gray matter deficits as seed regions.ResultsCompared with healthy controls, alcohol dependent patients had significantly reduced gray matter volume in the mesocorticolimbic system including the dorsal posterior cingulate cortex, the dorsal anterior cingulate cortex, the medial prefrontal cortex, the orbitofrontal cortex and the putamen, decreased fractional anisotropy in the regions connecting the damaged grey matter areas driven by higher radial diffusivity value in the same areas and decreased resting-state functional connectivity within the reward network. Moreover, the gray matter volume of the left medial prefrontal cortex exhibited negative correlations with various impulse indices.ConclusionsThese findings suggest that chronic alcohol dependence could cause a complex neural changes linked to abnormal impulsivity.

Previous studies have reported aberrant expression of the miR-183-96-182 cluster in a variety of tumors, which indicates its' diagnostic or prognostic value. However, a key characteristic of the miR-183-96-182 cluster is its varied expression levels, and pleomorphic functional roles in different tumors or under different conditions. In most tumor types, the cluster is highly expressed and promotes tumorigenesis, cancer progression and metastasis; yet tumor suppressive effects have also been reported in some tumors. In the present study, we discuss the upstream regulators and the downstream target genes of miR-183-96-182 cluster, and highlight the dysregulation and functional roles of this cluster in various tumor cells. Newer insights summarized in this review will help readers understand the different facets of the miR-183-96-182 cluster in cancer development and progression.

The purpose of the study was to detect the effect and possible mechanism of human umbilical cord mesenchymal stem cells (hUCMSCs) on the in vitro and in vivo growth of stem cells isolated from primary human breast cancer cells and cell lines MDA-MB-231 and MCF-7. Primary human breast cancer cells and MDA-MB-231 and MCF-7 cells were sorted in vitro using flow cytometry, and the ESA+, CD44+, CD24-/low cells were isolated as breast cancer stem cells (CSCs). The inhibitory effect of hUCMSCs on CSCs was examined using the Cell Counting Kit-8 cell proliferation and soft agar colony formation assay. In vivo tumor inhibition was studied using a severe combined immunodeficient xenograft mouse model transplanted with MDA-MB-231 breast CSCs. The expression of phosphoinositide 3-kinase (PI3K) and AKT was examined in the xenograft tumors using immunohistochemistry. The number of colonies formed by breast CSCs co-cultured with hUCMSCs at the bottom of soft agar was significantly lower than those formed by the control group (P < 0.01). Compared with the control group, the CSCs co-cultured with hUCMSCs showed a higher number of cells in the G2-M phase (P < 0.05) and an increased number of apoptotic cells (P < 0.01). The mice in the medium- and high-concentration hUCMSC treatment groups exhibited clearly reduced tumor volume and tumor weight, compared with the control group (P < 0.01). Compared with the saline group, the xenograft tumor tissues from the mice treated with different concentrations of hUCMSCs showed significantly reduced levels of PI3K and AKT proteins (P < 0.001). In conclusion, hUCMSC significantly inhibited the growth of breast CSCs in vitro and in vivo. The underlying mechanism is likely related to cell cycle arrest, induction of tumor cell apoptosis, and suppressed activities of PI3K and AKT protein kinases.