Gut microbiome changes in mouse, Mongolian gerbil, and hamster models following challenge.

Introduction: infection (CDI), as well as its etiology and pathogenesis, have been extensively investigated. However, the absence of suitable CDI animal models that reflect CDI symptoms and the associated gut microbiome changes in humans has limited research progress in this field. Thus, we aimed to investigate whether Mongolian gerbils, which present a range of human pathological conditions, can been used in studies on CDI.

Intestine epithelial cell-derived extracellular vesicles alleviate inflammation induced by TcdB through the activity of TGF-β1.

Background: infection (CDI) has been primarily associated with the toxin B (TcdB), one of the three known protein toxins secreted by , which can activate the intestinal immune system and lead to pathological damage. Even though the biological functions of intestine epithelial cell-derived extracellular vesicles (I-Evs) have been well documented, the role of I-Evs in the process of CDI is still unknown.

Objectives: The protective effect of I-Evs against TcdB was investigated both in cultured murine colon carcinoma MC38 cells and a mouse model used in this study.

Alanine scanning mutagenesis of SP70 epitope in characterizing species‑specific antibodies induced by enterovirus 71‑based antigens.

The enterovirus 71 (EV71) SP70 epitope, derived from amino acids 208‑222 of VP1, is a neutralizing epitope. The present study aimed to assess the inter‑species differences of the antibodies induced by EV71‑based antigens in responses to SP70 mutant peptides. BALB/c mice and Lou/C rats were immunized with EV71 SP70.

[Prediction and Identification of Immunodominant Linear B Cell Epitopes in the Nucleocapsid Protein of SFTSV].

In order to identify immunodominant linear B cell epitopes in the nucleocapsid protein N of severe fever with thrombocytopenia syndrome virus(SFTSV),bioinformatics programs were used to analyze antigenicity, hydrophilicity and surface probability of the amino acid sequence and predict possible linear B cell epitopes. PyMOL software was used to analyze the distribution of linear B cell epitopes in nucleocapsid protein N based on its crystal structure. Corresponding peptides were synthesized and examined in peptide enzyme-linked immunosorbent assay(Peptide-ELISA)individually to check whether they reacted with sera from SFTSV-infected patients.

Regulation of brain-derived neurotrophic factor exon IV transcription through calcium responsive elements in cortical neurons.

Activity-dependent transcription of brain-derived neurotrophic factor (BDNF) has been studied as an important model to elucidate the mechanisms underlying numerous aspects of neuroplasticity. It has been extensively emphasized that Ca(2+) influx through different routes may have significantly different effects on BDNF transcription. Here, we examined the regulatory property of the major calcium responsive elements (CaRE) in BDNF promoter IV in cultured rat cortical neurons.

N-methyl-D-aspartate-stimulated ERK1/2 signaling and the transcriptional up-regulation of plasticity-related genes are developmentally regulated following in vitro neuronal maturation.

The general features of neuroplasticity are developmentally regulated. Although it has been hypothesized that the loss of plasticity in mature neurons may be due to synaptic saturation and functional reduction of N-methyl-D-aspartate receptors (NMDAR), the molecular mechanisms remain largely unknown. We examined the effects of NMDAR activation and KCl-mediated membrane depolarization on ERK1/2 signaling following in vitro maturation of cultured cortical neurons.

Regulation of brain-derived neurotrophic factor-mediated transcription of the immediate early gene Arc by intracellular calcium and calmodulin.

The induction of the immediate early gene Arc is strongly implicated in synaptic plasticity. Although the role of ERK has been demonstrated, the regulation of Arc expression is largely unknown. In this study, we investigated the major signaling pathways underlying brain-derived neurotrophic factor (BDNF)-mediated Arc transcription in cultured cortical neurons.

Serine phosphorylation differentially affects RhoA binding to effectors: implications to NGF-induced neurite outgrowth.

Activation of RhoA prevents NGF-induced outgrowth and causes retraction of neurites in neuronal cells, including PC12 cells. Despite its inhibitory effect on neurite outgrowth, NGF activates GTP loading of and effector binding to RhoA, setting up an apparent contradiction. According to the molecular switch hypothesis of GTPase function GTP-loading of RhoA should be sufficient to activate its effectors uniformly.

A novel strategy for specifically down-regulating individual Rho GTPase activity in tumor cells.

The Rho family GTPases RhoA, RhoB, and RhoC regulate the actin cytoskeleton, cell movement, and cell growth. Unlike Ras, up-regulation or overexpression of these GDP/GTP binding molecular switches, but not activating point mutations, has been associated with human cancer. Although they share over 85% sequence identity, RhoA, RhoB, and RhoC appear to play distinct roles in cell transformation and metastasis.

Pseudomurein endoisopeptidases PeiW and PeiP, two moderately related members of a novel family of proteases produced in Methanothermobacter strains.

Sequence comparison of pseudomurein endoisopeptidases PeiW encoded by the defective prophage PsiM100 of Methanothermobacter wolfeii, and PeiP encoded by phage PsiM2 of Methanothermobacter marburgensis, revealed that the two enzymes share only limited similarity. Their amino acid sequences comprise an N-terminal domain characterized by the presence of direct repeats and a C-terminal domain with a catalytic triad C-H-D as in thiol proteases and animal transglutaminases. Both PeiW and PeiP catalyze the in vitro lysis of M.