Infections Combined With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: A Case Report and Systematic Review of the Literature.

Myelinating oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an immune-mediated inflammatory demyelinating disease of the central nervous system. Its specific etiology and pathogenesis remain unclear. In recent years, there have been increasing reports of MOGAD occurring after infections.

Coexistence of Guillain-Barré Syndrome and Subacute Combined Degeneration of the Spinal Cord Due to Autoimmune Gastritis: A Case Report and Literature Review.

Guillain-Barré syndrome (GBS) and autoimmune gastritis (AIG) are both autoimmune diseases (ADs) that have a low prevalence in China. Both conditions involve the immune system mistakenly attacking the body's own tissues. GBS primarily affects the peripheral nervous system, leading to muscle weakness and paralysis, while AIG targets the stomach lining, causing inflammation and reduced absorption of vital nutrients.

Manifestations of Myelinating Oligodendrocyte Glycoprotein Antibody-Associated Disease: A Rare Case of Suppurative Meningoencephalitis.

Myelinating oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disease of the central nervous system (CNS) mediated by MOG antibodies (MOG-IgG). It is associated with autoimmunity and encompasses various syndromes. However, manifestations presenting with symptoms of suppurative meningoencephalitis are rare.

Clinical value of chemiluminescence method for detection of antinuclear antibody profiles.

Background: Antinuclear antibodies (ANAs) are crucial in diagnosing autoimmune diseases, mainly systemic lupus erythematosus (SLE). This study aimed to compare the performance of chemiluminescence assay (CLIA) and line immunoassay (LIA) in detecting ANAs in patients with autoimmune diseases, evaluate their diagnostic accuracy for SLE, and develop a novel diagnostic model using CLIA-detected antibodies for SLE. Specimens from patients with autoimmune diseases and physical examination specimens were collected to parallel detect specific antibodies.

The correlation between the methylation of PTEN gene and the apoptosis of osteosarcoma cells mediated by SeHA nanoparticles.

The invasive spreading of residual osteosarcoma cells becomes a serious threat to human health, urgently needing new bone regenerative biomaterials for orthopedic therapy. Thus, in this work, selenite-substituted hydroxyapatite (SeHA) nanoparticles were prepared for both inhibiting the recurrence of the tumor and accelerating the regenerative repair of bone defect. Physicochemical characterization showed these synthetic nanoparticles were spherical poly-crystals with the shape of snowflakes.

ECSM2, an endothelial specific VE-cadherin binding protein, has a tyrosine phosphorylation site essential to cell migration.

Endothelial cell-specific molecule 2 (ECSM2) is a transmembrane protein located in cell-cell junction of endothelial cells (EC). ECSM2 was determined to play an important role in vascular development, EC migration, apoptosis and proliferation, however, no functional domains were determined in intracellular and extracellular region of ECSM2. In current work, functional domains of ECSM2, the relationship of ECSM2 with other endothelial specific protein such as VE-cadherin and the role of ECSM2 in neovascular diseases were determined.

RY10-4 Inhibits the Proliferation of Human Hepatocellular Cancer HepG2 Cells by Inducing Apoptosis In Vitro and In Vivo.

This study aimed to investigate the anti-tumor activity of RY10-4, a small molecular that was designed and synthesized based on the structure of protoapigenone. A previous screening study showed that RY10-4 possessed anti-proliferative effects against HepG2 human hepatocellular carcinoma cells. However, the full range of RY10-4 anti-cancer effects on liver tumors and the underlying mechanisms have not been identified.

MicroRNA involvement in mechanism of endogenous protection induced by fastigial nucleus stimulation based on deep sequencing and bioinformatics.

Background: Neurogenic neuroprotection is a promising approach for treating patients with ischemic brain lesions. Fastigial nucleus stimulation (FNS) has been shown to reduce the tissue damage resulting from focal cerebral ischemia in the earlier studies. However, the mechanisms of neuroprotection induced by FNS remain unclear.

Fastigial nucleus stimulation regulates neuroprotection via induction of a novel microRNA, rno-miR-676-1, in middle cerebral artery occlusion rats.

Previous studies have shown that fastigial nucleus stimulation (FNS) reduces tissue damage resulting from focal cerebral ischemia. Although the mechanisms of neuroprotection induced by FNS are not entirely understood, important data have been presented in the past two decades. MicroRNAs (miRNAs) are a newly discovered group of non-coding small RNA molecules that negatively regulate target gene expression and are involved in the regulation of cell proliferation and cell apoptosis.

MicroRNA-29c Correlates with Neuroprotection Induced by FNS by Targeting Both Birc2 and Bak1 in Rat Brain after Stroke.

Aims: Studies showed fastigial nucleus stimulation (FNS) reduced brain damage, but the mechanisms of neuroprotection induced by FNS were not entirely understood; MicroRNAs are noncoding RNA molecules that regulate gene expression in a posttranscriptional manner, but their functional consequence in response to ischemia-reperfusion (IR) remains unknown. We investigated the role of microRNA-29c in the neuroprotection induced by FNS in rat.

Methods: The IR rat models were conducted 1 day after FNS.