Nervonic acid protects against oligodendrocytes injury following chronic cerebral hypoperfusion in mice.

Chronic cerebral hypoperfusion (CCH) has been acknowledged as a potential contributor to cognitive dysfunction and brain injury, causing progressive demyelination of white matter, oligodendrocytes apoptosis and microglia activation. Nervonic acid (NA), a naturally occurring fatty acid with various pharmacological effects, has been found to alleviate neurodegeneration. Nonetheless, evidence is still lacking on whether NA can protect against neurological dysfunction resulting from CCH.

Role of Histamine H Receptor Antagonist Pitolisant in Early Neural Differentiation of Mouse Embryonic Stem Cells.

The histamine H receptor, prominently expressed in neurons with a minor presence in glial cells, acts as both an autoreceptor and an alloreceptor, controlling the release of histamine and other neurotransmitters. The receptor impacts various essential physiological processes. Our team's initial investigations had demonstrated that the histamine H receptor antagonists could facilitate nerve regeneration by promoting the histamine H receptors on primary neural stem cells (NSCs) in the traumatic brain injury mouse, which suggested the potential of histamine H receptor as a promising target for treating neurological disorders and promoting nerve regeneration.

Non-intubated deep paralysis: a new anaesthesia strategy for vocal cord polypectomy.

Background: Vocal cord polyp is common otorhinolaryngological disease, traditionally treated by vocal cord polypectomy under a supporting laryngoscope with general anaesthesia. Although it is safe and controllable, it would cause some anaesthesia complications. Moreover, the complex process of general anaesthesia may significantly reduce surgical efficiency.

Lysosomal dysfunction in Schwann cells is involved in bortezomib-induced peripheral neurotoxicity.

Bortezomib (BTZ) is a proteasome inhibitor serves as a first-line drug for multiple myeloma treatment. BTZ-induced peripheral neuropathy (BIPN) is the most common adverse effect of BTZ with an incidence as high as 40-60%. However, the pathological mechanisms underlying BIPN remain largely unclear.

Association of different central venous pressure levels with outcome of living-donor liver transplantation in children under 12 years.

Background: Pediatric liver transplantation is an important modality for treating biliary atresia. The overall survival (OS) rate of pediatric liver transplantation has significantly improved compared with that of 20 years ago, but it is still unsatisfactory. The anesthesia strategy of maintaining low central venous pressure (CVP) has shown a positive effect on prognosis in adult liver transplantation.

Peripheral Iron Metabolism is Associated with Leg Movements on Polysomnography but Not with the Severity of Restless Legs Syndrome or Its Impact on Patients.

Purpose: This study investigated the associations of peripheral iron status with different manifestations of restless legs syndrome (RLS), including leg movements (LMs) on polysomnography (PSG), disease severity, and impact on patients.

Patients And Methods: In this cross-sectional study, 108 patients with RLS were enrolled at Sir Run Run Shaw Hospital's Center for Sleep Medicine. Demographic information, disease characteristics, RLS severity, and impact on patients were assessed through a semi-structured questionnaire.

Augmentation in patients with restless legs syndrome receiving pramipexole therapy: a retrospective study in a single center from China.

Purpose: Augmentation is a major complication of long-term pramipexole treatment of restless legs syndrome (RLS). However, there have been no studies on augmentation in Chinese patients with RLS. We therefore investigated the clinical characteristics of augmentation in RLS patients treated with pramipexole in a real-world Chinese setting.

Discovery of novel antagonists targeting the DNA binding domain of androgen receptor by integrated docking-based virtual screening and bioassays.

Androgen receptor (AR), a ligand-activated transcription factor, is a master regulator in the development and progress of prostate cancer (PCa). A major challenge for the clinically used AR antagonists is the rapid emergence of resistance induced by the mutations at AR ligand binding domain (LBD), and therefore the discovery of novel anti-AR therapeutics that can combat mutation-induced resistance is quite demanding. Therein, blocking the interaction between AR and DNA represents an innovative strategy.

Homocysteine induced a calcium-mediated disruption of mitochondrial function and dynamics in endothelial cells.

Homocysteine (Hcy) is a sulfur-containing amino acid that originated in methionine metabolism and the elevated level of Hcy in plasma is considered to be an independent risk factor for cardiovascular diseases (CVD). Endothelial dysfunction plays a major role in the development of CVD, while the potential mechanism of Hcy-induced endothelial dysfunction is still unclear. Here, in Hcy-treated endothelial cells, we observed the destruction of mitochondrial morphology and the decline of mitochondrial membrane potential.

Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43.

Rictor is a key component of the mammalian target of rapamycin complex 2 (mTORC2) and is required for Akt phosphorylation (Ser473). Our previous study shows that knockdown of Rictor prevents cardiomyocyte differentiation from mouse embryonic stem (ES) cells and induces abnormal electrophysiology of ES cell-derived cardiomyocytes (ESC-CMs). Besides, knockdown of Rictor causes down-expression of connexin 43 (Cx43), the predominant gap junction protein, that is located in both the sarcolemma and mitochondria in cardiomyocytes.

Molecular modeling evaluation of the binding effect of five protease inhibitors to COVID-19 main protease.

Coronavirus disease 2019 (COVID-19) has caused more than 840,000 deaths as of 31 August 2020 in the whole world. The COVID-19 main protease (M) has been validated as an attractive target for drug design. In this work, the binding mechanisms of five protease inhibitors (e.

Establishment and characterization of a docetaxel-resistant human prostate cancer cell line.

The aim of the present study was to establish a novel docetaxel-resistant prostate cancer cell line and investigate its biological characteristics. The human prostate cell line, PC-3, was exposed to docetaxel, the concentrations of which were increased in a stepwise manner in the medium to select the drug-resistant cell line, PC-3/DTX. The morphological features were observed using inverted microscopy.

Perfluorooctane sulfonate induced toxicity in embryonic stem cell-derived cardiomyocytes via inhibiting autophagy-lysosome pathway.

Perfluorooctane sulfonate (PFOS), a classic environmental pollutant, is reported to cause cardiotoxicity in animals and humans. It has been demonstrated that PFOS exposure down-regulates expression of cardiac-development related genes and proteins. However, the related mechanism of PFOS has not been fully elucidated.

Cytochrome P450 Enzyme-Mediated Bioactivation as an Underlying Mechanism of Columbin-Induced Hepatotoxicity.

Columbin, a furanoid compound, is the major bioactive ingredient of (Oliv.) Gagnep, a traditional Chinese medicine that has been reported to cause liver injury in the clinic. The aim of this study was to investigate the hepatotoxicity caused by columbin and its underlying mechanism.

WITHDRAWN: LncRNA DSCAM-AS1 Promotes Proliferation, Migration and Invasion of Colorectal Cancer Cells via Modulating miR-144-5p/CDKL1.

This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.

The glymphatic system delivery enhances the transduction efficiency of AAV1 to brain endothelial cells in adult mice.

Background: Recombinant adeno-associated virus (rAAV) is increasingly applied in neuroscience research or gene therapy. However, there is no simple and efficient tool for specific transfection of rAAV into cerebrovascular tissues. It has been reported that fluorescent tracers or beta-amyloid protein can enter the brain through perivascular spaces, named as "glymphatic system".

[Rictor regulates mitochondrial calcium signaling in mouse embryo stem cell-derived cardiomyocytes].

Objective: To explore the expression, localization and regulatory effect on mitochondrial calcium signaling of Rictor in embryonic stem cell-derived cardiomyocytes (ESC-CMs).

Methods: Classical embryonic stem cell cardiomyogenesis model was used for differentiation of mouse embryonic stem cells into cardiomyocytes. The location of Rictor in ESC-CMs was investigated by immunofluorescence and Western blot.

MiR-218 regulated cardiomyocyte differentiation and migration in mouse embryonic stem cells by targeting PDGFRα.

MicroRNAs (miRNAs) have been identified as key players in cardiogenesis and heart pathophysiological processes. However, many miRNAs are still not recognized for their roles in cardiomyocytes differentiation. In this study, we evaluated the effects of microRNA-218 (miR-218) in cardiomyocyte differentiation of the mouse embryonic stem cells (ESCs) in vitro.

Efficacy and safety of Sofosbuvir-containing regimens in patients co-infected with chronic hepatitis C virus and human immunodeficiency virus: a meta-analysis.

Background: The treatment of hepatitis C virus (HCV) in HCV/human immunodeficiency virus (HIV) co-infected patients remains complex. This present meta-analysis evaluated the efficacy and safety of Sofosbuvir (SOF) for treatment in HCV/HIV co-infected patients using the most recent and available data.

Methods: A systematic search of the published data was conducted in PubMed Medline, EMBASE and Cochrane databases.

Mitochondrial toxicity of perfluorooctane sulfonate in mouse embryonic stem cell-derived cardiomyocytes.

Perfluorooctane sulfonate (PFOS) is a persistent organic contaminant that may cause cardiotoxicity in animals and humans. However, little is known about the underlying mechanism by which it affects the organelle toxicity in cardiomyocytes during the cardiogenesis. Our previous proteomic study showed that differences of protein expression mainly existed in mitochondria of cardiomyocytes differentiated from embryonic stem (ES) cells after exposure to PFOS.

mTORC1 and mTORC2 play different roles in regulating cardiomyocyte differentiation from embryonic stem cells.

Mammalian target of rapamycin (mTOR) is a serine/threonine kinase and functions through two distinct complexes, mTOR complex 1 (mTORC1) and complex 2 (mTORC2), with their key components Raptor and Rictor, to play crucial roles in cellular survival and growth. However, the roles of mTORC1 and mTORC2 in regulating cardiomyocyte differentiation from mouse embryonic stem (mES) cells are not clear. In this study, we performed Raptor or Rictor knockdown experiments to investigate the roles of mTORC1 and mTORC2 in cardiomyocyte differentiation.

Involvement of Rictor/mTORC2 in cardiomyocyte differentiation of mouse embryonic stem cells .

Rictor is a key regulatory/structural subunit of the mammalian target of rapamycin complex 2 (mTORC2) and is required for phosphorylation of Akt at serine 473. It plays an important role in cell survival, actin cytoskeleton organization and other processes in embryogenesis. However, the role of Rictor/mTORC2 in the embryonic cardiac differentiation has been uncovered.

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells.

S-nitrosoglutathione (GSNO)-induced apoptosis is associated with reactive oxygen species and loss of mitochondrial Omi/HtrA2 in human endothelial cells (ECs). But its upstream regulation is still not elucidated. Here, we demonstrate that hypoxia induced factor-1α (HIF-1α)-linked aerobic glycolysis is associated with mitochondrial abnormality by treatment of human EC-derived EA.

Premalignant alteration assessment in liver-like tissue derived from embryonic stem cells by aristolochic acid I exposure.

The in vitro predictive evaluation of chemical carcinogenicity based on hepatic premalignance has so far not been established. Here, we report a novel approach to investigate the premalignant events triggered by human carcinogen aristolochic acid I (AAI) in the liver-like tissue derived from mouse embryonic stem cells. By AAI exposure, the liver-like tissue exhibited the paracrine interleukin-6 phenotypic characteristics.

A Flavonoid Compound Promotes Neuronal Differentiation of Embryonic Stem Cells via PPAR-β Modulating Mitochondrial Energy Metabolism.

Relatively little is known regarding mitochondrial metabolism in neuronal differentiation of embryonic stem (ES) cells. By using a small molecule, present research has investigated the pattern of cellular energy metabolism in neural progenitor cells derived from mouse ES cells. Flavonoid compound 4a faithfully facilitated ES cells to differentiate into neurons morphologically and functionally.