Health-related quality of life in children after surgical repair of esophageal atresia: a cross-sectional study in China.

Objective: To investigate health-related quality of life (HRQOL) in patients after surgical repair for esophageal atresia (EA) and identify its potential influencing factors.

Methods: A total of 102 EA children who had previously visited our hospital participated in this cross-sectional study. Basic data and disease data of the patients were collected.

MicroRNA-454 modulates the oxidative stress and neuronal apoptosis after cerebral ischemia/reperfusion injury via targeting NADPH oxidase 4 (NOX4).

To investigate the function of miR-454 in ischemic stroke, this study was carried out. Cerebral ischemia/reperfusion (I/R) injury animal model and a SHSY5Y cell culture model of oxygen-glucose deprivation/reoxygenation (OGD/R) were constructed. The effects of miR-454 were detected by evaluating the levels of biochemical markers, gene expression, and pathophysiological markers.

Sanghuang Tongxie Formula Ameliorates Insulin Resistance in Through Regulating PI3K/Akt Signaling.

Insulin resistance (IR) is a pivotal pathological characteristic that affects the occurrence and development of type 2 diabetes mellitus (T2DM). Thus, the effective control of IR is of great significance for diabetes prevention and treatment. Traditional Chinese medicine (TCM) represents a valuable tool handed down to the world by the Chinese nation and has a long history of use for diabetes clinical therapy.

Identification and Validation of Autophagy-Related Genes in Necrotizing Enterocolitis.

Background: Autophagy plays an essential role in the occurrence and progression of necrotizing enterocolitis (NEC). We intend to carry out the identification and validation of the probable autophagy-related genes of NEC bioinformatics methods and experiment trials.

Methods: The autophagy-related differentially expressed genes (arDEGs) of NEC were identified by analyzing the RNA sequencing data of the experiment neonatal mouse model and dataset GSE46619.

Artificial intelligence in clinical research of cancers.

Several factors, including advances in computational algorithms, the availability of high-performance computing hardware, and the assembly of large community-based databases, have led to the extensive application of Artificial Intelligence (AI) in the biomedical domain for nearly 20 years. AI algorithms have attained expert-level performance in cancer research. However, only a few AI-based applications have been approved for use in the real world.

Circular RNA circ_0070441 regulates MPP-triggered neurotoxic effect in SH-SY5Y cells via miR-626/IRS2 axis.

Circular RNAs (circRNAs) was suggested to play crucial regulatory roles in various human diseases, including Parkinson's disease (PD). This research aimed to investigate the function and potential mechanism of circ_0070441 in PD. MPP (1-methyl-4-phenylpyridinium)-treated SH-SY5Y cells was used as an in vitro cellular PD model.

MicroRNA-449 targets histone deacetylase 1 to regulate the proliferation, invasion, and apoptosis of synovial fibroblasts in rheumatoid arthritis.

Background: Rheumatoid arthritis (RA) is a chronic joint disease. The study aimed to explore the effects of microRNA (miR)-449 and histone deacetylase 1 (HDAC1) on the proliferation, invasion, and apoptosis of synovial fibroblasts in rheumatoid arthritis.

Methods: Synovial tissue was collected from 20 patients with RA and 20 patients with osteoarthritis (OA) who underwent joint replacement surgery.

Tumor necrosis factor receptor-associated factor 6 (TRAF6) inhibition modulates bone loss and matrix metalloproteinase expression levels in collagen-induced rheumatoid arthritis rat.

Background: Rheumatoid arthritis (RA) is a main characterized by persistent synovitis, systemic inflammation, and autoantibodies. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is an E3 ubiquitin ligase and is a crucial cytoplasm signal adaptor that can regulate critical biological processes. This research aims to explore the function of TRAF6 on bone loss and matrix metalloproteinase (MMP) expression in collagen-induced RA rats.

SIRT1 promotes tumor-like invasion of fibroblast-like synoviocytes in rheumatoid arthritis via targeting TIMP1.

Suppression of tissue inhibitor of matrix metalloproteinase (TIMP) is associated with the tumor-like invasion of fibroblast-like synoviocytes (FLSs) that occurs during rheumatoid arthritis-related cartilage destruction. Silent information regulator 2 homolog1 (SIRT1), a histone deacetylase, is widely involved in transcriptional regulation, genomic stability, metabolism and DNA repair. Recent studies suggest that SIRT1 may also impact inflammatory response and the proliferation of FLSs in rheumatoid arthritis (RA).

[Expression and purification ficolin 3 and its role for RAW264.7 macrophage activation in vitro].

Objective: To establish a prokaryotic expression plasmid of ficolin-3, express and purify the fusion protein His-ficolin 3 in E.coli, and explore the role of ficolin-3 in the activation of RAW264.7 macrophages.

Effects of UCH-L1 on alpha-synuclein over-expression mouse model of Parkinson's disease.

The rare inherited form of Parkinson's disease (PD), PARK5, is caused by a missense mutation in ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) gene, resulting in Ile93Met substitution in its gene product (UCH-L1(Ile93Met)). PARK5 is inherited in an autosomal-dominant mode, but whether the Ile93Met mutation gives rise to a gain-of-toxic-function or loss-of-function of UCH-L1 protein remains controversial. Here, we investigated the selective vulnerabilities of dopaminergic (DA) neurons in UCH-L1-transgenic (Tg) and spontaneous UCH-L1-null gracile axonal dystrophy mice to an important PD-causing insult, abnormal accumulation of alpha-synuclein (alphaSyn).

Recombinant human granulocyte colony-stimulating factor protects against MPTP-induced dopaminergic cell death in mice by altering Bcl-2/Bax expression levels.

Granulocyte colony-stimulating factor (G-CSF) has been used for the treatment of neutropenia in hematologic disorders. The neuroprotective effects of G-CSF were reported in neurological disease models. In the present study, we examined whether G-CSF can protect dopaminergic neurons against MPTP-induced cell death in a mouse model of Parkinson's disease.