Distributions of parvalbumin, calbindin-D28k, and calretinin in the cerebrum of Chinese tree shrews ( ): A high-resolution neuroanatomical resource.

The Chinese tree shrew has gained prominence as a model organism due to its phylogenetic proximity to primates, offering distinct advantages over traditional rodent models in biomedical research. However, the neuroanatomy of this species remains insufficiently defined, limiting its utility in neurophysiological and neuropathological studies. In this study, immunofluorescence microscopy was employed to comprehensively map the distribution of three calcium-binding proteins, parvalbumin, calbindin D-28k, and calretinin, across the tree shrew cerebrum.

The relationship between processing speed and remodeling spatial patterns of intrinsic brain activity in the elderly with different sleep duration.

Objective: Brain neuroplasticity in which sleep affects the speed of information processing in the elderly population has not been reported. Therefore, this study was conducted to explore the effects of sleep on information processing speed and its central plasticity mechanism in the elderly.

Methods: A total of 50 individuals aged 60 and older were enrolled in this case control study.

Development of Two Loop-Mediated Isothermal Amplification Assays for Rapid Detection of and Genes in .

is an important zoonotic pathogen that poses a serious threat to the pig industry and human health. The massive use of macrolides has led to the emergence of resistance in , and is suspected to be a reservoir of antimicrobial resistance genes. The mechanism to macrolide resistance in is mainly due to and .

[Concentration, Source, and Health Risk Assessment of PM Heavy Metals in Typical Pollution Processes in Zhengzhou].

Heavy metal elements in particulate matter can cause adverse effects on human health, and the smaller the particle size, the greater the harm. A total of 16 heavy metal elements (Al, Si, K, Ca, V, Cr, Mn, Fe, Ni, Cu, Zn, As, Se, Ba, Pb, and Cd) in PM were continuously determined by an online heavy metal observation instrument in Zhengzhou city from January 7 to 25, 2021. The results showed that (K) concentration was the highest during the observation period (0.

[Chemical Components and Sources of PM and Their Evolutive Characteristics in Zhengzhou].

To explore the main sources of PM and the characteristics of seasonal differences in Zhengzhou, PM sampling was conducted in 2019 and the concentrations of inorganic water-soluble ions, carbon components, and various elements were analyzed. Results showed that the average mass concentration of PM in 2019 was (67.0±37.

[Characteristics and Sources of PM Pollution in Typical Cities of the Central Plains Urban Agglomeration in Autumn and Winter].

To study the characteristics of PM pollution and the potential sources of its main components in the central plain urban agglomeration in autumn and winter, PM samples were collected continually in the four typical cities of Zhengzhou, Luoyang, Anyang, and Xinxiang from October 2018 to January 2019. X-ray fluorescence spectrometry, carbon analysis methods, and ion chromatography were used to determine 18 kinds of inorganic elements, organic carbon (OC)/elemental carbon (EC), and 9 kinds of water-soluble inorganic ions. According to the daily PM concentration, three pollution levels were divided, and the comparative analysis for the spatial and temporal variation of PM and its main components, i.

M1 Macrophage-Derived Exosomal MicroRNA-326 Suppresses Hepatocellular Carcinoma Cell Progression Via Mediating NF-κB Signaling Pathway.

Accumulating evidence has shown that microRNA (miR) derived from M1 macrophage-derived exosomes can regulate the progression of hepatocellular carcinoma (HCC). However, the effect of miR-326 derived from M1 macrophage-derived exosomes on HCC has not been reported. Therefore, the objective of the present study was to explore the mechanism of exosomal miR-326 from M1 macrophages in regulating HCC cell progression.

Whole-genome sequencing reveals origin and evolution of influenza A(H1N1)pdm09 viruses in Lincang, China, from 2014 to 2018.

The continuous variation of the seasonal influenza viruses, particularly A(H1N1)pdm09, persistently threatens human life and health around the world. In local areas of southwest china, the large time-scale genomic research on A(H1N1)pdm09 is still insufficient. Here, we sequenced 45 whole-genome sequences of influenza A(H1N1)pdm09 viruses in Lincang, China, from 2014 to 2018, by next-generation sequencing technology to characterize molecular mechanisms of their origin and evolution.

The NK-1R Antagonist Aprepitant Prevents LPS-Induced Oxidative Stress and Inflammation in RAW264.7 Macrophages.

Background: The macrophage is one of the most important types of immune cells that protect against harmful stimuli. Macrophage activation plays a pivotal role in the progression and development of various inflammatory diseases. The neurokinin 1 receptor (NK-1R) is a G protein-coupled receptor that plays an important role in inflammatory diseases.

Timing of Expansion of Fragile X Premutation Alleles During Intergenerational Transmission in a Mouse Model of the Fragile X-Related Disorders.

Fragile X syndrome (FXS) is caused by the maternal expansion of an unstable CGG-repeat tract located in the first exon of the gene. Further changes in repeat number occur during embryogenesis resulting in individuals sometimes being highly mosaic. Here we show in a mouse model that, in males, expansions are already present in primary spermatocytes with no additional expansions occurring in later stages of gametogenesis.

FAN1 protects against repeat expansions in a Fragile X mouse model.

The Fragile X-related disorders (FXDs) are members of a large group of human neurological or neurodevelopmental conditions known as the Repeat Expansion Diseases. The mutation responsible for all of these diseases is an expansion in the size of a disease-specific tandem repeat tract. However, the underlying cause of this unusual mutation is unknown.

Ups and Downs: Mechanisms of Repeat Instability in the Fragile X-Related Disorders.

The Fragile X-related disorders (FXDs) are a group of clinical conditions resulting from the expansion of a CGG/CCG-repeat tract in exon 1 of the Fragile X mental retardation 1 (FMR1) gene. While expansions of the repeat tract predominate, contractions are also seen with the net result being that individuals can show extensive repeat length heterogeneity in different tissues. The mechanisms responsible for expansion and contraction are still not well understood.

A MutSβ-Dependent Contribution of MutSα to Repeat Expansions in Fragile X Premutation Mice?

The fragile X-related disorders result from expansion of a CGG/CCG microsatellite in the 5' UTR of the FMR1 gene. We have previously demonstrated that the MSH2/MSH3 complex, MutSβ, that is important for mismatch repair, is essential for almost all expansions in a mouse model of these disorders. Here we show that the MSH2/MSH6 complex, MutSα also contributes to the production of both germ line and somatic expansions as evidenced by the reduction in the number of expansions observed in Msh6-/- mice.

Identification of key genes associated with cervical cancer by comprehensive analysis of transcriptome microarray and methylation microarray.

Cervical cancer is the second most commonly diagnosed type of cancer and the third leading cause of cancer-associated mortality in women. The current study aimed to determine the genes associated with cervical cancer development. Microarray data (GSE55940 and GSE46306) were downloaded from Gene Expression Omnibus.

Mutsβ generates both expansions and contractions in a mouse model of the Fragile X-associated disorders.

Fragile X-associated disorders are Repeat Expansion Diseases that result from expansion of a CGG/CCG-repeat in the FMR1 gene. Contractions of the repeat tract also occur, albeit at lower frequency. However, these contractions can potentially modulate disease symptoms or generate an allele with repeat numbers in the normal range.

The Repeat Expansion Diseases: The dark side of DNA repair.

DNA repair normally protects the genome against mutations that threaten genome integrity and thus cell viability. However, growing evidence suggests that in the case of the Repeat Expansion Diseases, disorders that result from an increase in the size of a disease-specific microsatellite, the disease-causing mutation is actually the result of aberrant DNA repair. A variety of proteins from different DNA repair pathways have thus far been implicated in this process.

The transcription-coupled repair protein ERCC6/CSB also protects against repeat expansion in a mouse model of the fragile X premutation.

The fragile X-related disorders (FXDs) are members of the group of diseases known as the repeat expansion diseases. The FXDs result from expansion of an unstable CGG/CCG repeat tract in the 5' UTR of the FMR1 gene. Contractions are also seen, albeit at lower frequency.

Repeat-mediated genetic and epigenetic changes at the FMR1 locus in the Fragile X-related disorders.

The Fragile X-related disorders are a group of genetic conditions that include the neurodegenerative disorder, Fragile X-associated tremor/ataxia syndrome (FXTAS), the fertility disorder, Fragile X-associated primary ovarian insufficiency (FXPOI) and the intellectual disability, Fragile X syndrome (FXS). The pathology in all these diseases is related to the number of CGG/CCG-repeats in the 5' UTR of the Fragile X mental retardation 1 (FMR1) gene. The repeats are prone to continuous expansion and the increase in repeat number has paradoxical effects on gene expression increasing transcription on mid-sized alleles and decreasing it on longer ones.

Intrathecal baclofen, a GABAB receptor agonist, inhibits the expression of p-CREB and NR2B in the spinal dorsal horn in rats with diabetic neuropathic pain.

This study aimed to investigate the effect of baclofen, a γ-aminobutyric acid B (GABAB) receptor agonist, on the expression of p-CREB and NR2B in the spinal dorsal horn of rats with diabetic neuropathic pain (DNP). The DNP rats, which were successfully induced with streptozocin, were distributed among 3 groups that were treated with saline (D1 group), baclofen (D2 group), or CGP55845 + baclofen (D3 group) continuously for 4 days. The rats induced with saline and subsequently treated with saline were used as controls (C group).

X inactivation plays a major role in the gender bias in somatic expansion in a mouse model of the fragile X-related disorders: implications for the mechanism of repeat expansion.

The Fragile X-related disorders are X-linked disorders resulting from the inheritance of FMR1 alleles with >54 CGG/CCG repeats in their 5' UTR. The repeats expand both somatically and on intergenerational transmission and increased repeat numbers are associated with increased risk of disease and increased risk of further expansion. The mechanism responsible for expansion is unknown.

Gender and cell-type-specific effects of the transcription-coupled repair protein, ERCC6/CSB, on repeat expansion in a mouse model of the fragile X-related disorders.

The repeat expansion diseases are human genetic disorders that arise from the expansion of a tandem-repeat tract. The Fragile X-related disorders are members of this disease group in which the repeat unit is CGG/CCG and is located in the 5′ untranslated region of the FMR1 gene. Affected individuals often show mosaicism with respect to repeat number resulting from both expansion and contraction of the repeat tract; however, the mechanism responsible for these changes in repeat number is unknown.

A specific cholesterol metabolic pathway is established in a subset of HCCs for tumor growth.

The liver plays a central role in cholesterol homeostasis. It exclusively receives and metabolizes oxysterols, which are important metabolites of cholesterol and are more cytotoxic than free cholesterol, from all extrahepatic tissues. Hepatocellular carcinomas (HCCs) impair certain liver functions and cause pathological alterations in many processes including cholesterol metabolism.

The mismatch repair protein MSH2 is rate limiting for repeat expansion in a fragile X premutation mouse model.

Fragile X-associated tremor and ataxia syndrome, Fragile X-associated primary ovarian insufficiency, and Fragile X syndrome are Repeat Expansion Diseases caused by expansion of a CGG•CCG-repeat microsatellite in the 5 UTR of the FMR1 gene. To help understand the expansion mechanism responsible for these disorders, we have crossed mice containing∼147 CGG•CCG repeats in the endogenous murine Fmr1 gene with mice containing a null mutation in the gene encoding the mismatch repair protein MSH2. MSH2 mutations are associated with elevated levels of generalized microsatellite instability.