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Persistent inflammation disrupts functional recovery after spinal cord injury (SCI). Peroxisome proliferator-activated receptor gamma (PPAR-γ) activation promotes functional recovery in SCI rats by inhibiting inflammatory cascades and increasing neuronal survival. We sought to clarify the relationship between PPAR-γ activation and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome suppression, and the role of NF-κB in activating the NLRP3 inflammasome in neurons. In SCI rats, we found that rosiglitazone (PPAR-γ agonist) inhibited the expression of caspase-1. In in vitro neurons, G3335 (PPAR-γ antagonist) reversed the rosiglitazone-induced inhibition of caspase-1, interleukin 1 (IL-1β), and interleukin 6 (IL-6). Rosiglitazone inhibited the expression of NLRP3, caspase-1, IL-1β, and IL-6. However, the activator of NLRP3 could counteract this inhibition induced by PPAR-γ activation. NF-κB did not participate in the process of rosiglitazone-induced inhibition of NLRP3. Consistent with our in vitro results, we verified that locomotor recovery of SCI rats in vivo was regulated via PPAR-γ, NLRP3, and NF-κB. These results suggest that PPAR-γ activation exerts an anti-inflammatory effect by suppressing the NLRP3 inflammasome—but not NF-κB—in neurons and that PPAR-γ activation is a promising therapeutic target for SCI.

The peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone inhibits NF-κB expression and endogenous neural stem cell differentiation into neurons and reduces the inflammatory cascade after spinal cord injury (SCI). The aim of this study was to explore the mechanisms underlying rosiglitazone-mediated neuroprotective effects and regulation of the balance between the inflammatory cascade and generation of endogenous spinal cord neurons by using a spinal cord-derived neural stem cell culture system as well as SD rat SCI model. Activation of PPAR-γ could promote neural stem cell proliferation and inhibit PKA expression and neuronal formation in vitro. In the SD rat SCI model, the rosiglitazone + forskolin group showed better locomotor recovery compared to the rosiglitazone and forskolin groups. MAP2 expression was higher in the rosiglitazone + forskolin group than in the rosiglitazone group, NF-κB expression was lower in the rosiglitazone + forskolin group than in the forskolin group, and NeuN expression was higher in the rosiglitazone + forskolin group than in the forskolin group. PPAR-γ activation likely inhibits NF-κB, thereby reducing the inflammatory cascade, and PKA activation likely promotes neuronal cell regeneration.

Persistent inflammation disrupts functional recovery after spinal cord injury (SCI). Peroxisome proliferator-activated receptor gamma (PPAR-[gamma]) activation promotes functional recovery in SCI rats by inhibiting inflammatory cascades and increasing neuronal survival. We sought to clarify the relationship between PPAR-[gamma] activation and NACHT, LRR and PYD domaincontaining protein 3 (NLRP3) inflammasome suppression, and the role of NF-[kappa]B in activating the NLRP3 inflammasome in neurons. In SCI rats, we found that rosiglitazone (PPAR-[gamma] agonist) inhibited the expression of caspase-1. In in vitro neurons, G3335 (PPAR-[gamma] antagonist) reversed the rosiglitazone-induced inhibition of caspase-1, interleukin 1 (IL-1[beta]), and interleukin 6 (IL-6). Rosiglitazone inhibited the expression of NLRP3, caspase-1, IL-1[beta], and IL-6. However, the activator of NLRP3 could counteract this inhibition induced by PPAR-[gamma] activation. NF-[kappa]B did not participate in the process of rosiglitazone-induced inhibition of NLRP3. Consistent with our in vitro results, we verified that locomotor recovery of SCI rats in vivo was regulated via PPAR-[gamma], NLRP3, and NF-[kappa]B. These results suggest that PPAR-[gamma] activation exerts an anti-inflammatory effect by suppressing the NLRP3 inflammasome--but not NF-[kappa]B--in neurons and that PPAR-[gamma] activation is a promising therapeutic target for SCI.

Cubital tunnel syndrome is often accompanied by paresthesia in ulnar nerve sites and hand muscle atrophy. When muscle weakness occurs, or after failure of more conservative treatments, anterior transposition is used. In the present study, the ulnar nerve and its blood vessels were examined in the elbows of 18 adult cadavers, and the external diameter of the nutrient vessels of the ulnar nerve at the point of origin, the distances between the origin of the vessels and the medial epicondyle of the humerus, and the length of the vessels accompanying the ulnar nerve in the superior ulnar collateral artery, the inferior ulnar collateral artery, and the posterior ulnar recurrent artery were measured. Anterior transposition of the vascularized ulnar nerve was per- formed to treat cubital tunnel syndrome. The most appropriate distance that the vascularized ulnar nerve can be moved to the subcutaneous tissue under tension-free conditions was 1.8 ± 0.6 cm （1.1-2.5 cm）, which can be used as a reference value during the treatment of cubital tunnel syndrome with anterior transposition of the vascularized ulnar nerve.

Background： There are more than 300 genetic loci that have been found to be related to hereditary hearing impairment （HHI）, including 92 causative genes for nonsyndromic hearing loss, among which 34 genes are related to autosomal dominant nonsyndromic HHI （ADNSHH 1）. Traditional linkage analysis and candidate gene sequencing are not effective at detecting the ADNSHHI, especially for the unconditional families that may have more than one pathogenic cause. This study identified two disease-causing genes TJP2 and GJB2 in a Chinese family with unconditional ADNSHHI. Methods： To decipher the genetic code of a Chinese family （family 686） with ADNSHHI, different gene screening techniques have been performed, including linkage analysis, candidate genes screening, high-throughput sequencing and Sanger sequencing. These techniques were done on samples obtained from this family over a period of 10 years. Results： We identified a pathogenic missense mutation, c. 2081G〉A （p.G694E）, in TJP2, a gene that plays a crucial role in apoptosis and age-related hearing loss （ARHL）. The mutation was co-segregated in this pedigree in all, but not in the two patients who presented with different phenotypes from the other affected family members. In one of the two patients, we confirmed that the compound heterozygosity for p.Y136^＊ and p.G45E in the GJB2 gene may account for the phenotype shown in this patient. Conclusions： We identified the co-occurrence of two genetic causes in family 686. The possible disease-causing missense mutation of TJP2 in family 686 presents an opportunity for further investigation into ARHL. It is necessary to combine various genes screening methods, especially for some unconventional cases.

Aim： Aldosterone is elevated in many diseases such as hypertension, diabetic nephropathy and chronic kidney disease, etc. The aim of this study was to investigate the effects of aldosterone on intracellular ROS production and autophagy in podocytes in vitro, and to explore the possibility of ginsenoside Rg1 （Rg1） being used for protecting podocytes from aldosterone-induced injury. Methods： MPC5 mouse podocyte cells were tested. Autophagosome and autophagic vacuole formation were examined under confocal microscopy with MDC and acridine orange staining, respectively. ROS were detected with flow cytometry. Malondialdehyde content and superoxide dismutase （T-SOD） activity were measured using commercial kits. The expression of LC3-II, beclin-1, SOD2 and catalase was measured by Western blotting. Results： Treatment with aldosterone （10 nmol/L） significantly increased ROS generation and the expression of SOD2 and catalase in MPC5 cells. Furthermore, treatment with aldosterone significantly increased the conversion of LC3-I to LC3-II, beclin-1 expression and autophagosome formation. Co-treatment with rapamycin （1 ng/mL） or chloroquine （10 μmol/L） further increased aldosterone-induced autophagosome formation. Co-treatment with Rg1 （80 ng/mL） effectively relieved oxidative stress and increased T-SOD activity at the early stage and subsequently decreased autophagy in aldosterone-treated podocytes. Co-treatment with 3-MA （4 mmol/L） or NAC （50 mmol/L） exerted similar effects against aldosterone-induced autophagy in podocytes. Conclusion： Aldosterone enhances ROS generation and promotes autophagy in podocytes in vitro. Ginsenoside-Rg1 effectively relieves aldosterone-induced oxidative stress, thereby indirectly inhibiting aldosterone-induced podocyte autophagy.

Aim： To construct an eukaryotic expression vector containing the aldehyde dehydrogenase-2 （ALDH2） gene, and determine whether transfection with the ALDH2 gene can provide protection against hydrogen peroxide-induced oxidative damage, as well as attenuate apoptosis or cell death in human peripheral blood mononuclear cells （PBMCs）. Methods： The ALDH2 gene was cloned from human hepatocytes by RT-PCR. The eukaryotic expression vector containing the gene was constructed and then transfected into PBMCs via liposomes. RT-PCR, indirect immunofluorescence assay, and Western blot were used to evaluate the expression of the transgene in target cells. MTT assay and flow cytometry were used to detect the effects of ALDH2 on PBMCs damaged by hydrogen peroxide （H2O2）. The level of intracellular reactive oxygen species （ROS） was determined by fluorescence spectrophotometry. Results： The eukaryotic expression vector pcDNA3.1/myc-His-ALDH2 was successfully constructed and transfected into PBMCs. RTPCR results showed higher mRNA expression of ALDH2 in the gene-transfected group than in the two control groups （empty vector- transfected group and negative control）. Indirect immunofluorescence assay and Western blot indicated distinct higher protein expression of ALDH2 in the gene-transfected group. The cell survival rate against H2O2-Jnduced oxidative damage was higher in the ALDH2 gene-transfected group. Moreover, apoptosis rates in gene-transfected PBMCs incubated with 50 and 75 pmol/L H2O2 decreased by 7% and 6%, respectively. The generation of intracellular ROS was also markedly downregulated. Conclusion： ALDH2 gene transfection can protect PBMCs against H2O2-induced damage and attenuate apoptosis, accompanied with a downregulation of intracellular ROS. ALDH2 functions as a protector against oxidative stress.

Studies have explored the relationship between social class and health for decades. However, the underlying mechanism between the two remains not fully understood. This study aimed to explore whether health self-management had a mediating role between social class and health under the framework of Socio-cultural Self Model. 663 adults, randomly sampled from six communities in Southwest China, completed the survey for this study. Social class was assessed using individuals' income, education, occupation. Health self-management was assessed through evaluation of the health self-management behavior, health self-management cognition, health self-management environment. Physical health and mental health were measured by the Chinese version of Short-Form (36-item) Health Survey, which contains Physical Functioning, Role-Physical, Role-Emotional, Vitality, Mental Health, Social Function, Bodily Pain and General Health. Pearson's correlation was used to examine the associations between major variables. Mediation analyses were performed to explore the mediating role of health self-management. Social class positively predicted self-rated health. The lower the social class, the lower the self-reported physical and mental health. Health self-management partially mediated the relationship between social class and self-rated health. That is, the health self-management ability of the lower class, such as access to healthy and nutritious food and evaluate their own health status, is worse than that of the higher class, which leads to physical and mental health inequality between the high and the low classes. Health self-management mediated the relationship between social class and health. Promoting health self-management abilities are conducive to improving both physical and mental health.

Background DNA methylation plays important biological roles in plants and animals. To examine the rice genomic methylation landscape and assess its functional significance, we generated single-base resolution DNA methylome maps for Asian cultivated rice Oryza sativa ssp . japonica , indica and their wild relatives, Oryza rufipogon and Oryza nivara . Results The overall methylation level of rice genomes is four times higher than that of Arabidopsis . Consistent with the results reported for Arabidopsis , methylation in promoters represses gene expression while gene-body methylation generally appears to be positively associated with gene expression . Interestingly, we discovered that methylation in gene transcriptional termination regions (TTRs) can significantly repress gene expression, and the effect is even stronger than that of promoter methylation. Through integrated analysis of genomic, DNA methylomic and transcriptomic differences between cultivated and wild rice, we found that primary DNA sequence divergence is the major determinant of methylational differences at the whole genome level, but DNA methylational difference alone can only account for limited gene expression variation between the cultivated and wild rice. Furthermore, we identified a number of genes with significant difference in methylation level between the wild and cultivated rice. Conclusions The single-base resolution methylomes of rice obtained in this study have not only broadened our understanding of the mechanism and function of DNA methylation in plant genomes, but also provided valuable data for future studies of rice epigenetics and the epigenetic differentiation between wild and cultivated rice.

Community-acquired pneumonia is primarily caused by , and , leading to severe illness and death in developing countries. A rapid, straightforward, sensitive, high-throughput, and precise multiplex PCR-dipstick DNA chromatography assay was devised. This innovative technique was specifically engineered for the immediate and efficient detection of the aforementioned eight respiratory pathogens, with particular emphasis on scenarios involving co-infections. Custom-designed specific primers were employed, wherein the 5' end of the forward primers was tagged with oligonucleotide tags (Tag) and the 5' end of the reverse primers was conjugated with biotin. A C3 spacer was incorporated to bridge the Tag and the forward primer. Complementary oligonucleotides (cTag) corresponding to each of the eight pathogens were immobilized within the test area of the test strip. Meanwhile, biotin was strategically utilized to create an internal control line at the distal end of the test strip. The biotin moiety at the 5' end of the reverse primer was engineered to interact with blue latex microspheres coated with streptavidin, thereby triggering a detectable signal. Following the PCR amplification of the target DNA fragments, during the membrane strip chromatography hybridization process, the Tag- and biotin-labeled target DNA engaged in a dual interaction. First, it bound to the blue latex microspheres via streptavidin-biotin binding, and second, it hybridized with the cTag on the membrane strip. This led to the accumulation of captured blue latex microspheres at both the test line and the internal control line, manifesting as visible blue bands. A total of 186 respiratory sputum or bronchoalveolar lavage fluid specimens were collected and analyzed. The multiplex PCR-dipstick DNA chromatography assay was deployed for detection, while traditional bacterial culture was also carried out in parallel for comparative purposes. To rigorously validate the accuracy of the multiplex PCR-dipstick DNA chromatography assay in identifying PCR products, DNA sequencing was performed on all PCR products derived from the clinical samples. The multiplex PCR-dipstick DNA chromatography assay demonstrated remarkable efficacy, being capable of specifically discriminating among the eight pathogens within a remarkably short timeframe of 40 minutes. The detection limit for individual bacterial species ranged from 10 to 10 CFU/mL. Notably, no cross-reactions were observed among the eight target bacteria, nor with other representative respiratory bacteria, including , , , , , , and . The concordance between the results obtained from the multiplex PCR-dipstick DNA chromatography assay and those from DNA sequencing was absolute, with a kappa value of 1.00. A successful multiplex PCR-dipstick DNA chromatography assay was established for the simultaneous detection of eight respiratory bacterial pathogens and was effectively applied in clinical sample analysis. This indicates that this single-use device has promising potential for analyzing the microbial composition related to respiratory infections and is also suitable for small laboratories and field diagnostics.