Effect of Emodin on Coxsackievirus B3m-Mediated Encephalitis in Hand, Foot, and Mouth Disease by Inhibiting Toll-Like Receptor 3 Pathway In Vitro and In Vivo.

Background: Encephalitis in hand, foot, and mouth disease (HFMD) is a serious threat to children's health and life. Toll-like receptor 3 (TLR3) is an innate immune-recognition receptor that can recognize virus and initiate innate immune responses. Emodin has the effects of anti-inflammatory and regulating immune function, but the mechanism is not very clear.

New Dual-Spectroscopic Strategy for the Direct Detection of Aristolochic Acids in Blood and Tissue.

Aristolochic acids (AAs) contained in herbal plants are implicated in multiple organ injuries and have a high mutational burden in upper tract urothelial cancers. The currently available techniques for monitoring AAs include LC (liquid chromatography) and LC/MS (mass spectrometry), but the application of these approaches are limited due to the complex sample preparation and derivatization steps. Therefore, there is an urgent need to develop efficient methods for identifying and quantifying AAs.

Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis.

Herpes simplex encephalitis (HSE) is the most common infectious disease of the central nervous system worldwide. However, the pathogenesis of HSE is not clear. Research has shown that the immune response mediated by the toll-like receptor 3 (TLR3) signaling pathway is essential to protect the central nervous system against herpes simplex virus (HSV) infection.

Emodin Attenuates Lipopolysaccharide-Induced Acute Liver Injury via Inhibiting the TLR4 Signaling Pathway and .

Emodin is an anthraquinone with potential anti-inflammatory properties. However, the possible molecular mechanisms and protective effects of emodin are not clear. The objective of this study was to investigate the possible molecular mechanisms and protective effects of emodin on lipopolysaccharide (LPS)-induced acute liver injury (ALI) via the Toll-like receptor 4 (TLR4) signaling pathway in the Raw264.

[Analysis of deafness gene mutations by gene chip and its clinical significance].

Objective: To analyze deafness gene mutations by genechip.

Method: The peripheral blood samples were obtained and DNA templates were extracted by extraction kits. The deafness gene mutations were distinguished by genechip.

Loss-of-function mutations in the PRPS1 gene cause a type of nonsyndromic X-linked sensorineural deafness, DFN2.

We report a large Chinese family with X-linked postlingual nonsyndromic hearing impairment in which the critical linkage interval spans a genetic distance of 5.41 cM and a physical distance of 15.1 Mb that overlaps the DFN2 locus.

GJB2 mutation spectrum in 2,063 Chinese patients with nonsyndromic hearing impairment.

Background: Mutations in GJB2 are the most common molecular defects responsible for autosomal recessive nonsyndromic hearing impairment (NSHI). The mutation spectra of this gene vary among different ethnic groups.

Methods: In order to understand the spectrum and frequency of GJB2 mutations in the Chinese population, the coding region of the GJB2 gene from 2063 unrelated patients with NSHI was PCR amplified and sequenced.

[Report on the study of who ear and hearing disorders survey protocol in Guizhou province].

Objective: To undertake a population-based survey on the prevalence, pathogenic factors and medical requirements of ear and hearing impairment.

Method: Using the probability proportion to size (PPS) method, 6626 residents were investigated in 30 clusters with the WHO protocol.

Result: The prevalence of hearing impairment was 17.

[Screening for mitochondrial DNA mutation in two pedigrees with nonsyndromic inherited sensorineural hearing loss].

Objective: To investigate the genetic mechanism of maternal nonsyndromic inherited sensorineural hearing loss(SNHL), to identify the incidence of the 7445(G) mutation in such pedigrees and sporadic patients with SNHL, and to provide the theoretical evidence for the diagnosis of this disease.

Methods: Blood samples were obtained from 2 pedigrees and 14 sporadic patients with SNHL. DNA was extracted from the isolated leukocytes.