Role of Cholesterol Metabolic Enzyme CYP46A1 and Its Metabolite 24S-Hydroxycholesterol in Ischemic Stroke.

Background: For several decades, it has been recognized that overactivation of the glutamate-gated N-methyl-D-aspartate receptors (NMDARs) and subsequent Ca toxicity play a critical role in ischemic brain injury. 24S-hydroxycholesterol (24S-HC) is a major cholesterol metabolite in the brain, which has been identified as a potent positive allosteric modulator of NMDAR in rat hippocampal neurons. We hypothesize that 24S-HC worsens ischemic brain injury via its potentiation of the NMDAR, and reducing the production of 24S-HC by targeting its synthetic enzyme CYP46A1 provides neuroprotection.

Cholestane-3β,5α,6β-Triol Inhibits Acid-Sensing Ion Channels and Reduces Acidosis-Mediated Ischemic Brain Injury.

Background: Activation of the acid-sensing ion channels (ASICs) by tissue acidosis, a common feature of brain ischemia, contributes to ischemic brain injury, while blockade of ASICs results in protection. Cholestane-3β,5α,6β-triol (Triol), a major cholesterol metabolite, has been demonstrated as an endogenous neuroprotectant; however, the mechanism underlying its neuroprotective activity remains elusive. In this study, we tested the hypothesis that inhibition of ASICs is a potential mechanism.

Free Radical and Viral Infection: A Review from the Perspective of Ferroptosis.

Free radicals, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), play critical roles in various physiological activities such as cell differentiation, apoptosis, and vascular tension when existing in cells at low levels. However, excessive amounts of free radicals are harmful, causing DNA damage, lipid peroxidation, protein degeneration, and abnormal cell death. Certain viral infections induce cells to produce excessive free radicals, which in multiple ways help the virus to replicate, mature, and exit.

Inhibition of Acid-Sensing Ion Channels by KB-R7943, a Reverse Na/Ca Exchanger Inhibitor.

KB-R7943, an isothiourea derivative, is widely used as a pharmacological inhibitor of reverse sodium-calcium exchanger (NCX). It has been shown to have neuroprotective and analgesic effects in animal models; however, the detailed molecular mechanisms remain elusive. In the current study, we investigated whether KB-R7943 modulates acid-sensing ion channels (ASICs), a group of proton-gated cation channels implicated in the pathophysiology of various neurological disorders, using the whole-cell patch clamp techniques.

Mycoplasma synoviae induces serum amyloid A upregulation and promotes chicken synovial fibroblast cell proliferation.

Mycoplasma synoviae (MS) infection causes infectious synovitis and arthritis with hyperplasia of synovial cells in the chicken joint. However, its mechanism is unknown. We used primary chicken synovial fibroblast (CSF) as the research object to study the role of MS in the proliferation of MS-infected CSF and determine the mechanisms involved.

Comparative Genomics of and New Targets for Molecular Diagnostics.

is an important pathogen of poultry, causing significant economic losses in this industry. Analysis of the unique genes and shared genes among different strains and among related species is helpful for studying the molecular pathogenesis of and provides valuable molecular diagnostic targets to facilitate the identification of species. We selected a total of 46 strains, including six strains, from 25 major animal (including avian) species/subspecies that had complete genome sequences and annotation information published in GenBank, and used them for comparative genomic analysis.

Interaction of Mycoplasma synoviae with chicken synovial sheath cells contributes to macrophage recruitment and inflammation.

Mycoplasma synoviae (MS) is an important avian pathogen causing considerable economic hardship in the poultry industry. A major inflammation caused by MS is synovitis that occurs in the synovial tendon sheath and joint synovium. However, the overall appearance of pathological changes in the tendon sheath and surrounding tissues caused by MS infection at the level of pathological tissue sections was poor.

LncRNA-NEF regulated the hyperoxia-induced injury of lung epithelial cells by FOXA2.

Introduction: Hyperoxia-induced injury is a common form of damage in lung tissues, which could lead to bronchopulmonary dysplasia (BPD) in newborns. Recent studies have discovered that FOXA2 played a substantial role in protecting lung tissues from various injuries and lncRNA-NEF could activate the expression of FOXA2. However, it is unclear whether lncRNA-NEF could alleviate hyperoxia-caused damage of lung tissues by activating FOXA2.

Development of a live attenuated duck hepatitis A virus type 3 vaccine (strain SD70).

Duck hepatitis A virus type 3 (DHAV-3) is an important pathogen that causes substantial losses in the Chinese duck industry. DHAV-3 is highly fatal to ducklings and there is no licensed vaccine in China available to reduce DHAV-3 infection. Our goal was to develop a live attenuated vaccine candidate against DHAV-3.

Integrated Transcriptomic and Proteomic Analyses of the Interaction Between Chicken Synovial Fibroblasts and .

(MS), which causes respiratory disease, eggshell apex abnormalities, infectious synovitis, and arthritis in avian species, has become an economically detrimental poultry pathogen in recent years. In China, the disease is characterized by infectious synovitis and arthritis. However, the mechanism by which MS causes infectious synovitis and arthritis remains unknown.

Complete Genome Sequencing of Mycoplasma synoviae Strain HN01, Isolated from Chicken in Henan Province, China.

Here, we report the complete genome sequence of HN01, a virulent epidemic strain isolated from a sick chicken with synovitis in Henan Province, China. HN01 is the Asian source of an strain that is completely sequenced, genome annotated, and published with relevant data.

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings.

Background: Duck hepatitis A virus type 3 (DHAV-3) is one of the most harmful pathogens in the duck industry. However, the molecular mechanism underlying DHAV-3 infection in ducklings remains poorly understood. To study the genetic regulatory network for miRNA-mRNA and the signaling pathways involved in DHAV-3 infection in ducklings, we conducted global miRNA and mRNA expression profiling of duckling liver tissues infected with lethal DHAV-3 by high-throughput sequencing.

Efficacy of fluoxetine for anorexia nervosa caused by chemotherapy in patients with cholangiocarcinoma.

Background: Fluoxetine has been reported to treat anorexia nervosa (AN) caused by chemotherapy in patients with cholangiocarcinoma effectively. However, no study systematically investigated its efficacy and safety. Thus, this study will systematically assess its efficacy and safety for AN caused by chemotherapy in patients with cholangiocarcinoma.

CXCR5 CD8 T cells displayed higher activation potential despite high PD-1 expression, in tumor-involved lymph nodes from patients with thyroid cancer.

Thyroid cancer is one of the malignancies with better clinical outcomes. However, a minority of patients develops an aggressive anaplastic thyroid carcinoma. Development of innovative and multimodal therapeutic strategies is urgently needed.

LncRNA ASAP1-IT1 positively modulates the development of cholangiocarcinoma via hedgehog signaling pathway.

Over the past decades, lncRNAs have attracted more and more attentions of researchers. It has been verified that lncRNAs can modulate multiple biological behaviors in various human cancers. LncRNA ASAP1-IT1 has been certified to be a tumor facilitator in several malignant tumors.

TRPM7 channel inhibition mediates midazolam-induced proliferation loss in human malignant glioma.

The melastatin-like transient receptor potential 7 (TRPM7) has been implicated in proliferation or apoptosis of some cancers, indicating the potential of TRPM7 as an anti-anaplastic target. Here, we identified the characteristic TRPM7 channel currents in human malignant glioma MGR2 cells, which could be blocked by a pharmacologic inhibitor Gd. We mined the clinical sample data from Oncomine Database and found that human malignant glioma tissues expressed higher TRPM7 mRNA than normal brain ones.

Silencing TRPM7 in mouse cortical astrocytes impairs cell proliferation and migration via ERK and JNK signaling pathways.

Transient receptor potential melastatin 7 (TRPM7), a non-selective cation channel, is highly expressed expressed in the brain and plays a critical role in ischemic neuronal death. Astrocyte, the most abundant cell type in central nervous system (CNS), exerts many essential functions in the physiological and pathological conditions. Here we investigated the expression and functions of the TRPM7 channel in mouse cortical astrocytes.

TRPM7 regulates vascular endothelial cell adhesion and tube formation.

Transient receptor potential melastatin 7 (TRPM7) is a nonselective cation channel with an α-kinase domain in its COOH terminal, known to play a role in diverse physiological and pathological processes such as Mg2+ homeostasis, cell proliferation, and hypoxic neuronal injury. Increasing evidence suggests that TRPM7 contributes to the physiology/pathology of vascular systems. For example, we recently demonstrated that silencing TRPM7 promotes growth and proliferation and protects against hyperglycemia-induced injury in human umbilical vein endothelial cells (HUVECs).

Suppression of TRPM7 inhibits proliferation, migration, and invasion of malignant human glioma cells.

Background: Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor with a dismal prognosis. Despite intensive study on tumor biology, the underlying mechanisms of the unlimited proliferation and progressive local invasion are still poorly understood, and no effective treatment has been developed for GBM patients.

Aims: We determine the role of TRPM7 channels in the growth, migration, and infiltration of malignant glioma cells.

Local anesthetic lidocaine inhibits TRPM7 current and TRPM7-mediated zinc toxicity.

Background: Previous study demonstrated that overstimulation of TRPM7 substantially contributes to zinc-mediated neuronal toxicity. Inhibition of TRPM7 activity and TRPM7-mediated intracellular Zn(2+) accumulation may represent a promising strategy in the treatment of stroke.

Aims: To investigate whether local anesthetics lidocaine could inhibit TRPM7 channel and TRPM7-mediated zinc toxicity.

Role of TRPM7 channels in hyperglycemia-mediated injury of vascular endothelial cells.

This study investigated the change of transient receptor potential melastatin 7 (TRPM7) expression by high glucose and its role in hyperglycemia induced injury of vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were incubated in the presence or absence of high concentrations of D-glucose (HG) for 72 h. RT-PCR, Real-time PCR, Western blotting, Immunofluorescence staining and whole-cell patch-clamp recordings showed that TRPM7 mRNA, TRPM7 protein expression and TRPM7-like currents were increased in HUVECs following exposure to HG.

Alphaxalone inhibits growth, migration and invasion of rat C6 malignant glioma cells.

Malignant gliomas are the most devastating and aggressive brain tumors affecting the central nervous system. The insidious growth and infiltration are the most prominent characteristics of malignant gliomas, which render the current therapies for malignant gliomas including surgery, radiation and chemotherapy unsuccessful. Inhibition of infiltration as well as proliferation in combination with surgery might be more effective in the treatment of malignant gliomas.

Effects of hydrochlorothiazide on cardiac remodeling in a rat model of myocardial infarction-induced congestive heart failure.

Heart failure is a major cause of morbidity and mortality worldwide. Diuretics are regarded as the first-line treatment for patients with heart failure because they provide symptomatic relief. However, the specific benefits of diuretics and their effects on heart failure survival remain unclear.

Alcohol, volatile fatty acid, phenol, and methane emissions from dairy cows and fresh manure.

There are approximately 2.5 million dairy cows in California. Emission inventories list dairy cows and their manure as the major source of regional air pollutants, but data on their actual emissions remain sparse, particularly for smog-forming volatile organic compounds (VOCs) and greenhouse gases (GHGs).