[Expression profile of microRNAs in the cardiomyocytes derived from mouse embryonic stem cells].

Embryonic stem cells (ESCs), derived from the inner cell mass of blastocysts, are self-renewing and pluripotent cells with the ability to differentiate into all derivatives of three primary germ layers, including cardiomyocytes. Recent studies have revealed that posttranscriptional regulations of lineage specific genes by microRNAs (miRNAs) emerge as a new class of cell fate and lineage determinants of ESCs. However, the miRNAs that control ESC differentiation are still largely unexplored.

Uncoupling protein 3 mediates H₂O₂ preconditioning-afforded cardioprotection through the inhibition of MPTP opening.

Aims: Uncoupling protein 3 (UCP3), located in the mitochondrial inner membrane, is cardioprotective, but its mechanisms of preserving mitochondrial function during ischaemia/reperfusion (I/R) are not fully understood. This study investigated whether UCP3 mediates/mimics the cardioprotection of H₂O₂ preconditioning (H₂O₂PC) against I/R injury and the downstream pathway that mediates H₂O₂PC- and UCP3-afforded cardioprotection.

Methods And Results: H₂O₂PC at 20 µM for 5 min significantly improved post-ischaemic functional recovery and reduced lactate dehydrogenase (LDH) release and infarct size with concurrently up-regulated UCP3 expressions in perfused rat hearts subjected to global no-flow I/R.

Lactate promotes resistance to glucose starvation via upregulation of Bcl-2 mediated by mTOR activation.

Solid tumors grow faster and need more glucose than normal tissue; however, due to poor angiogenesis and excessive growth, tumors remote from blood vessels are always under glucose starvation. Even so, cancer cells remain alive in vivo. Thus, making cancer cells sensitive to glucose depletion may potentially provide an effective strategy for cancer intervention.

Histone deacetylase1 promotes TGF-β1-mediated early chondrogenesis through down-regulating canonical Wnt signaling.

Cartilage formation during both embryonic development and bone repairing processes involves mesenchymal stem cells (MSCs) differentiation. Wnt/β-catenin signaling pathway inhibits early chondrogenesis and is down-regulated during Transforming growth factor-β1 (TGF-β1)-induced chondrogenesis. However, the regulatory molecules that participate in the process is unknown.

Bactericidal properties and biocompatibility of a gentamicin-loaded Fe3O4/carbonated hydroxyapatite coating.

Postoperative implant-associated infection remains a serious complication in total joint arthroplasty (TJA) surgery. The addition of antibiotics to bone cement is used as an antimicrobial prophylaxis in cemented joint arthroplasty; however, in cementless arthroplasty, there are no comparable measures for the local delivery of antibiotics. In this study, a gentamicin-loaded Fe3O4/carbonated hydroxyapatite coating (Gent-MCHC) was fabricated according to the following steps: (i) deposition of Fe3O4/CaCO3 particles on Ti6Al4V substrates by electrophoretic deposition; (ii) conversions of MCHC from Fe3O4/CaCO3 coatings by chemical treatment; and (iii) formation of Gent-MCHC by loading gentamicin into MCHC.

Analysis of tumor suppressor genes based on gene ontology and the KEGG pathway.

Cancer is a serious disease that causes many deaths every year. We urgently need to design effective treatments to cure this disease. Tumor suppressor genes (TSGs) are a type of gene that can protect cells from becoming cancerous.

Adenanthin targets peroxiredoxin I/II to kill hepatocellular carcinoma cells.

Adenanthin, a natural diterpenoid isolated from the leaves of Isodon adenanthus, has recently been reported to induce leukemic cell differentiation by targeting peroxiredoxins (Prx) I and II. On the other hand, increasing lines of evidence propose that these Prx proteins would become potential targets to screen drugs for the prevention and treatment of solid tumors. Therefore, it is of significance to explore the potential activities of adenanthin on solid tumor cells.

Combined analysis with copy number variation identifies risk loci in lung cancer.

Background: Lung cancer is the most important cause of cancer mortality worldwide, but the underlying mechanisms of this disease are not fully understood. Copy number variations (CNVs) are promising genetic variations to study because of their potential effects on cancer.

Methodology/principal Findings: Here we conducted a pilot study in which we systematically analyzed the association of CNVs in two lung cancer datasets: the Environment And Genetics in Lung cancer Etiology (EAGLE) and the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial datasets.

Formation of electrophilic oxidation products from mitochondrial cardiolipin in vitro and in vivo in the context of apoptosis and atherosclerosis.

Emerging evidence indicates that mitochondrial cardiolipins (CL) are prone to free radical oxidation and this process appears to be intimately associated with multiple biological functions of mitochondria. Our previous work demonstrated that a significant amount of potent lipid electrophiles including 4-hydroxy-nonenal (4-HNE) was generated from CL oxidation through a novel chemical mechanism. Here we provide further evidence that a characteristic class of CL oxidation products, epoxyalcohol-aldehyde-CL (EAA-CL), is formed through this novel mechanism in isolated mice liver mitochondria when treated with the pro-apoptotic protein t-Bid to induce cyt c release.

Interleukin-17 enhances immunosuppression by mesenchymal stem cells.

IL-17 is one of the most potent and most actively investigated proinflammatory cytokines. In this study, we examined the effect of IL-17 on mesenchymal stem cells (MSCs) under the influence of inflammatory cytokines. Ironically, IL-17 dramatically enhanced the immunosuppressive effect of MSCs induced by IFNγ and TNFα, revealing a novel role of IL-17 in immunosuppression.

High extracellular magnesium inhibits mineralized matrix deposition and modulates intracellular calcium signaling in human bone marrow-derived mesenchymal stem cells.

Mesenchymal stem cells (MSCs) have the potential to differentiate into several cell types and provide an attractive source of autologous cells for regenerative medicine. However, their cellular biology is not fully understood. Similar to Ca(2+), extracellular Mg(2+) plays an important role in the functions of the skeletal system.

The lysosomal v-ATPase-Ragulator complex is a common activator for AMPK and mTORC1, acting as a switch between catabolism and anabolism.

AMPK and mTOR play principal roles in governing metabolic programs; however, mechanisms underlying the coordination of the two inversely regulated kinases remain unclear. In this study we found, most surprisingly, that the late endosomal/lysosomal protein complex v-ATPase-Ragulator, essential for activation of mTORC1, is also required for AMPK activation. We also uncovered that AMPK is a residential protein of late endosome/lysosome.

Autophagy protects end plate chondrocytes from intermittent cyclic mechanical tension induced calcification.

Calcification of end plate chondrocytes is a major cause of intervertebral disc (IVD) degeneration. However, the underlying molecular mechanism of end plate chondrocyte calcification is still unclear. The aim of this study was to clarify whether autophagy in end plate chondrocytes could protect the calcification of end plate chondrocytes.

Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF-β1 generation.

Chronic psychological stress has been demonstrated to play an important role in several severe diseases, but whether it affects disease therapy or not remains unclear. Mesenchymal stem cells (MSCs) have been demonstrated to have therapeutic potentials in treating tissue injury based on their multidifferentiation potential toward various cell types. We investigated the effect of chronic restraint stress on therapeutic potential of MSCs on carbon tetrachloride (CCl4)-induced liver injury in mice.

Regulation of flowering time by the miR156-mediated age pathway.

Precise flowering time is critical to reproductive success. In response to diverse exogenous and endogenous cues including age, hormones, photoperiod, and temperature, the floral transition is controlled by a complex regulatory network, which involves extensive crosstalks, feedback, or feedforward loops between the components within flowering time pathways. The newly identified age pathway, which is controlled by microRNA156 (miR156) and its target SQUAMOSA PROMOTER BINDING-LIKE (SPL) transcription factors, ensures plants flower under non-inductive conditions.

Concentration-dependent wrestling between detrimental and protective effects of H2O2 during myocardial ischemia/reperfusion.

Reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress are paradoxically implicated in myocardial ischemia/reperfusion (I/R) injury and cardioprotection. However, the precise interpretation for the dual roles of ROS and its relationship with the ER stress during I/R remain elusive. Here we investigated the concentration-dependent effects of hydrogen peroxide (H2O2) preconditioning (PC) and postconditioning (PoC) on the ER stress and prosurvival reperfusion injury salvage kinase (RISK) activation using an ex vivo rat myocardial I/R model.

A heterocyclic molecule kartogenin induces collagen synthesis of human dermal fibroblasts by activating the smad4/smad5 pathway.

Declined production of collagen by fibroblasts is one of the major causes of aging appearance. However, only few of compounds found in cosmetic products are able to directly increase collagen synthesis. A novel small heterocyclic compound called kartogenin (KGN) was found to stimulate collagen synthesis of mesenchymal stem cells (MSCs).

Dichloroacetate enhances adriamycin-induced hepatoma cell toxicity in vitro and in vivo by increasing reactive oxygen species levels.

A unique bioenergetic feature of cancer, aerobic glycolysis is considered an attractive therapeutic target for cancer therapy. Recently, dichloroacetate (DCA), a small-molecule metabolic modulator, was shown to reverse the glycolytic phenotype, induce reactive oxygen species (ROS) generation, and trigger apoptosis in various tumor cells. In this work, the capacity of DCA to enhance Adriamycin (ADM) efficacy in hepatoma cells by modulating glucose metabolism and redox status was evaluated.

Activating hotspot L205R mutation in PRKACA and adrenal Cushing's syndrome.

Adrenal Cushing's syndrome is caused by excess production of glucocorticoid from adrenocortical tumors and hyperplasias, which leads to metabolic disorders. We performed whole-exome sequencing of 49 blood-tumor pairs and RNA sequencing of 44 tumors from cortisol-producing adrenocortical adenomas (ACAs), adrenocorticotropic hormone-independent macronodular adrenocortical hyperplasias (AIMAHs), and adrenocortical oncocytomas (ADOs). We identified a hotspot in the PRKACA gene with a L205R mutation in 69.

Using a yeast two-hybrid system to identify FTCD as a new regulator for HIF-1α in HepG2 cells.

HIF-1α is implicated in hepatocellular carcinoma (HCC) pathologies. Here, we screened a human liver cDNA library for HIF-1α-interacting partners using a yeast two-hybrid system. We identified 53 genes, including formiminotransferase cyclodeaminase (FTCD), which was confirmed by co-immunoprecipitation.

HSP40 interacts with pyruvate kinase M2 and regulates glycolysis and cell proliferation in tumor cells.

Pyruvate kinase M2 (PKM2) is predominantly expressed in cancers, which is considered as a key regulator of the Warburg effect. In this study, HSP40 was identified as a novel binding partner of PKM2. HSP40-PKM2 association destabilized PKM2 protein through HSC70.

China's growing contribution to global intracranial aneurysm research (1991-2012): a bibliometric study.

Background: We sought to analyze the growing worldwide trends of intracranial aneurysm research, investigate China's recent contribution, and compare the contributions of mainland China, Taiwan, and Hong Kong.

Methods: Global and China intracranial aneurysm-related publications were retrieved from the Web of Science database from 1991 to 2012. Excel 2007, Matlab, and Thomson Data Analyzer (TDA) software were used to analyze the search results for number of publications, cited frequency, h-index, and organization contributions.

Uncovering the rare variants of DLC1 isoform 1 and their functional effects in a Chinese sporadic congenital heart disease cohort.

Congenital heart disease (CHD) is the most common birth defect affecting the structure and function of fetal hearts. Despite decades of extensive studies, the genetic mechanism of sporadic CHD remains obscure. Deleted in liver cancer 1 (DLC1) gene, encoding a GTPase-activating protein, is highly expressed in heart and essential for heart development according to the knowledge of Dlc1-deficient mice.

Lens culinaris agglutinin-reactive α-fetoprotein decline after transcatheter arterial chemoembolization in patients with hepatocellular carcinoma predicts survival.

Background: Lens culinaris agglutinin-reactive α-fetoprotein (AFP-L3) is a fucosylated fraction of AFP that is highly specific for hepatocellular carcinoma (HCC). We studied the relationship between AFP-L3 response and treatment outcome in terms of radiologic response and overall survival in patients undergoing transcatheter arterial chemoembolization (TACE).

Methods: We retrospectively analyzed 152 patients with advanced HCC undergoing TACE.