Cell-specific Nav1.6 knockdown reduced astrocyte-derived Aβ by reverse Na-Ca transporter-mediated autophagy in alzheimer-like mice.

Introduction: Nav1.6 is closely related to the pathology of Alzheimer's Disease (AD), and astrocytes have recently been identified as a significant source of β-amyloid (Aβ). However, little is known about the connection between Nav1.

Corrigendum: Scorpion Venom Heat-Resistant Peptide Attenuates Microglia Activation and Neuroinflammation.

[This corrects the article DOI: 10.3389/fphar.2021.

Scorpion Venom Heat-Resistant Peptide Attenuates Microglia Activation and Neuroinflammation.

Intervention of neuroinflammation in central nervous system (CNS) represents a potential therapeutic strategy for a host of brain disorders. The scorpion Buthus martensii Karsch (BmK) and its venom have long been used in the Orient to treat inflammation-related diseases such as rhumatoid arthritis and chronic pain. Scorpion venom heat-resistant peptide (SVHRP), a component from BmK venom, has been shown to reduce seizure susceptibility in a rat epileptic model and protect against cerebral ischemia-reperfusion injury.

SRC-1 Deficiency Increases Susceptibility of Mice to Depressive-Like Behavior After Exposure to CUMS.

Steroid receptor coactivator 1 (SRC-1) is one of the coactivators recruited by the nuclear receptors (NRs) when NRs are activated by steroid hormones, such as glucocorticoid. SRC-1 is abundant in hippocampus and hypothalamus and is also related to some major risk factors for depression, implicated by its reduced expression after stress and its effect on hypothalamus-pituitary-adrenal gland axis function. However, whether SRC-1 is involved in the formation of depression remains unclear.

GPR50 Distribution in the Mouse Cortex and Hippocampus.

G protein-coupled receptor 50 (GPR50) belongs to the G protein-coupled receptor which is highly homologous with the sequence of melatonin receptor MT1 and MT2. GPR50 expression has previously been reported in many brain regions, like cortex, midbrain, pons, amygdala. But, the distribution of GPR50 in the hippocampus and cortex and the cell types expressing GPR50 is not yet clear.

SRC-1 Knockout Exerts No Effect on Amyloid β Deposition in APP/PS1 Mice.

Steroid receptor coactivator 1 (SRC-1) is the key coactivator because of its transcriptional activity. Previous studies have shown that SRC-1 is abundant in the hippocampus and has been implicated in cognition. SRC-1 is also related to some major risk factors for Alzheimer's disease (AD), such as a decline in estrogen and aging, however, whether SRC-1 is involved in the pathogenesis of AD remains unclear.

Reduction of NgR in perforant path decreases amyloid-β peptide production and ameliorates synaptic and cognitive deficits in APP/PS1 mice.

Background: Amyloid beta (Aβ) which is recognized as a main feature of Alzheimer's disease (AD) has been proposed to "spread" through anatomically and functionally connected brain regions. The entorhinal cortex and perforant path are the earliest affected brain regions in AD. The perforant path is the most vulnerable circuit in the cortex with respect to both aging and AD.

TRIM32 Deficiency Impairs Synaptic Plasticity by Excitatory-Inhibitory Imbalance via Notch Pathway.

Synaptic plasticity is the neural basis of physiological processes involved in learning and memory. Tripartite motif-containing 32 (TRIM32) has been found to play many important roles in the brain such as neural stem cell proliferation, neurogenesis, inhibition of nerve proliferation, and apoptosis. TRIM32 has been linked to several nervous system diseases including autism spectrum disorder, depression, anxiety, and Alzheimer's disease.

Anti-infective biomaterials with surface-decorated tachyplesin I.

Implants decorated with antimicrobial peptides (AMPs) can prevent infection and reduce the risk of creating antibiotic resistance. Yet the restricted mobility of surficial AMP often compromises its activity. Here, we report a simple but effective strategy to allow a more flexible display of AMP on the biomaterial surface and demonstrate its efficacy for wound healing.

Scorpion Venom Heat-Resistant Peptide Protects Transgenic Caenorhabditis elegans from β-Amyloid Toxicity.

Scorpion venom heat-resistant peptide (SVHRP) is a component purified from Buthus martensii Karsch scorpion venom. Our previous studies found SVHRP could enhance neurogenesis and inhibit microglia-mediated neuroinflammation in vivo. Here, we use the transgenic CL4176, CL2006, and CL2355 strains of Caenorhabditis elegans which express the human Aβ1-42 to investigate the effects and the possible mechanisms of SVHRP mediated protection against Aβ toxicity in vivo.

Scorpion Venom Heat-Resistant Peptide Attenuates Glial Fibrillary Acidic Protein Expression via c-Jun/AP-1.

Scorpion venom has been used in the Orient to treat central nervous system diseases for many years, and the protein/peptide toxins in Buthus martensii Karsch (BmK) venom are believed to be the effective components. Scorpion venom heat-resistant peptide (SVHRP) is an active component of the scorpion venom extracted from BmK. In a previous study, we found that SVHRP could inhibit the formation of a glial scar, which is characterized by enhanced glial fibrillary acidic protein (GFAP) expression, in the epileptic hippocampus.

Scorpion venom heat-resistant peptide (SVHRP) enhances neurogenesis and neurite outgrowth of immature neurons in adult mice by up-regulating brain-derived neurotrophic factor (BDNF).

Scorpion venom heat-resistant peptide (SVHRP) is a component purified from Buthus martensii Karsch scorpion venom. Although scorpions and their venom have been used in Traditional Chinese Medicine (TCM) to treat chronic neurological disorders, the underlying mechanisms of these treatments remain unknown. We applied SVHRP in vitro and in vivo to understand its effects on the neurogenesis and maturation of adult immature neurons and explore associated molecular mechanisms.

Bromate oxidized from bromide during sonolytic ozonation.

Sonolytic ozonation (US/O3) is an effective way to degrade many pollutants in drinking water as the elevated mass transfer rate of ozone gas and the enhanced forming of hydroxyl radicals (OH). This work investigated the formation of bromate (BrO3(-)) from bromide (Br(-)) in sonolytic ozonation. At neutral pH, the bromate conversion rate ([BrO3(-)]/[Br(-)]0) was increased to 60% by ultrasound at continuous ozone flow (0-0.

Frequency and predictors of normalization of left ventricular ejection fraction in recent-onset nonischemic cardiomyopathy.

Emerging evidence has shown the potential of marked improvement in left ventricular ejection fraction (LVEF) in patients with recent-onset cardiomyopathy (ROCM) on medical therapy. This study was designed to determine the frequency and to identify predictors of normalization of LVEF in a cohort of Chinese patients with ROCM receiving contemporary medication. A consecutive series of patients admitted from October 2008 to November 2012 with the clinical diagnosis of ROCM and LVEF ≤ 40% by echocardiography at presentation were followed up at least 12 months to identify those with normalization of LVEF, defined as an increase in LVEF to a final level of ≥ 50%.

[Spectral analysis of formation of trihalomethanes during reaction of tryptophan with disinfectants].

UV and fluorescence spectra were applied to analyze the characteristics of reaction of disinfectants (free chlorine, free bromine) with tryptophan, as well as the formation of disinfection byproduct-trihalomethanes (THMs). The results show that disinfecting reaction decrease both the intensity and FRI (fluorescence region integration) of tryptophan. A linear relationship was found between the two indexes.

[Effects of scorpion venom heat-resistant protein on kainic acid induced-damage of cultured primitive rat hippocampal neuropeptide Y-nergic neurons].

Aim: To investigate the effects of scorpion venom heat-resistant protein (SVHRP) on kainic acid induced-damage of cultured primitive rat hippocampal neuropeptide Y-nergic neurons.

Methods: We observed morphological changes, celluar vigor, NPY-immunoreactivity and NPY mRNA expression by means of Thionine staining, MTT assay, immunocytochemistry and RT-PCR, respectively, on the primitively cultured Sprague-Dawley rat hippocampal neuron treated with KA and SVHRP for 24 h.

Results: MTT assay and morphologic analysis showed that SVHRP markedly increased neuron survival-rate, and protected them from kA-induced damage.

[Study on differentially expressed genes of ulcerative colitis in the rat treated by herbs-partitioned moxibustion].

Objective: To probe the mechanism of herbs-partitioned moxibustion for treatment of ulcerative colitis.

Methods: The rats with ulcerative colitis were randomly divided into 3 groups, normal control group, model group, and herbs-partitioned moxibustion group. The rats in the herbs-partitioned moxibustion group were treated by herbs-partitioned moxibustion at bilateral Tianshu (ST 25).

The role of microglia in paraquat-induced dopaminergic neurotoxicity.

The herbicide paraquat (PQ) has been implicated as a potential risk factor for the development of Parkinson's disease. In this study, PQ (0.5-1 microM) was shown to be selectively toxic to dopaminergic (DA) neurons through the activation of microglial NADPH oxidase and the generation of superoxide.