Evolution in anti-myelin oligodendrocyte glycoprotein antibody detection and its clinical significance: a narrative review.

Myelin oligodendrocyte glycoprotein (MOG) is a protein exclusively expressing on the surface of myelin sheaths and oligodendrocyte plasma membrane in the central nervous system of mammals, and it has a highly conserved nucleotide and amino acid structure between species. Evidence from animal research support that anti-MOG antibodies (MOG-Abs) are pathogenic antibodies rather than a bystander secondary to myelin destruction. Similarly, immunoglobulin-G against myelin oligodendrocyte glycoprotein (MOG-IgG) is considered a demyelinating disease-associated autoantibody in human beings.

SOX10 ablation severely impairs the generation of postmigratory neural crest from human pluripotent stem cells.

Animal studies have indicated that SOX10 is one of the key transcription factors regulating the proliferation, migration and differentiation of multipotent neural crest (NC), and mutation of SOX10 in humans may lead to type 4 Waardenburg syndrome (WS). However, the exact role of SOX10 in human NC development and the underlying molecular mechanisms of SOX10-related human diseases remain poorly understood due to the lack of appropriate human model systems. In this study, we successfully generated SOX10-knockout human induced pluripotent stem cells (SOX10 hiPSCs) by the CRISPR-Cas9 gene editing tool.

Adoptive transfer of -disrupted hematopoietic cells to wild-type mice exacerbates diet-induced hepatic steatosis and inflammation.

Background And Objectives: Hepatic steatosis and inflammation are key characteristics of non-alcoholic fatty liver disease (NAFLD). However, whether and how hepatic steatosis and liver inflammation are differentially regulated remains to be elucidated. Considering that disruption of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (iPfk2) dissociates fat deposition and inflammation, the present study examined a role for iPfk2 in hematopoietic cells in regulating hepatic steatosis and inflammation in mice.

Adipocyte inducible 6-phosphofructo-2-kinase suppresses adipose tissue inflammation and promotes macrophage anti-inflammatory activation.

Obesity-associated inflammation in white adipose tissue (WAT) is a causal factor of systemic insulin resistance. To better understand how adipocytes regulate WAT inflammation, the present study generated chimeric mice in which inducible 6-phosphofructo-2-kinase was low, normal, or high in WAT while the expression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (Pfkfb3) was normal in hematopoietic cells, and analyzed changes in high-fat diet (HFD)-induced WAT inflammation and systemic insulin resistance in the mice. Indicated by proinflammatory signaling and cytokine expression, the severity of HFD-induced WAT inflammation in WT → Pfkfb3 mice, whose Pfkfb3 was disrupted in WAT adipocytes but not hematopoietic cells, was comparable with that in WT → WT mice, whose Pfkfb3 was normal in all cells.

Age-Specific Imbalance of Circulating Tfh Cell Subsets and Its Association With Gout-Targeted Kidney Impairment.

Objective: Gout is a chronic disease characterized by the deposition of monosodium urate (MSU) crystals in tissue. Study with a focus on adaptive immune response remains to be understood although innate immune response has been reported extensively in gout etiology. Our study attempted to investigate the association of gout-related immune cell imbalance with clinical features and comorbidity with renal impairment and the implicated pathogenesis the assessment of T and B cell subsets in different activity phases or with immune effects combined with the analyses of clinical parameters.

Adipose tissue inflammation and systemic insulin resistance in mice with diet-induced obesity is possibly associated with disruption of PFKFB3 in hematopoietic cells.

Obesity-associated inflammation in white adipose tissue (WAT) is a causal factor of systemic insulin resistance; however, precisely how immune cells regulate WAT inflammation in relation to systemic insulin resistance remains to be elucidated. The present study examined a role for 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in hematopoietic cells in regulating WAT inflammation and systemic insulin sensitivity. Male C57BL/6J mice were fed a high-fat diet (HFD) or low-fat diet (LFD) for 12 weeks and examined for WAT inducible 6-phosphofructo-2-kinase (iPFK2) content, while additional HFD-fed mice were treated with rosiglitazone and examined for PFKFB3 mRNAs in WAT stromal vascular cells (SVC).

Generation of an induced pluripotent stem cell line (SYSUi002-A) from a patient with coronary slow flow phenomenon.

The coronary slow flow phenomenon (CSFP) is characterized by delayed progression of the injected contrast medium through the coronary tree during coronary angiography due to unknown mechanisms. Here, a human induced pluripotent stem cell (iPSC) line (SYSUi002-A) was established using the Sendai-virus delivery system from dermal fibroblasts of a CSFP patient. This cell line may represent a valuable tool for investigating the pathogenesis and therapeutic strategies of CSFP.

Prediction and Analysis of Hub Genes in Renal Cell Carcinoma based on CFS Gene Selection Method Combined with Adaboost Algorithm.

Background: Renal cell carcinoma (RCC) is the most common malignant tumor of the adult kidney.

Objective: The aim of this study was to identify key genes signatures during RCC and uncover their potential mechanisms.

Methods: Firstly, the gene expression profiles of GSE53757 which contained 144 samples, including 72 kidney cancer samples and 72 controls, were downloaded from the GEO database.

Visit-to-visit fasting plasma glucose variability is an important risk factor for long-term changes in left cardiac structure and function in patients with type 2 diabetes.

Background: To investigate the effect of visit-to-visit fasting plasma glucose (FPG) variability on the left cardiac structure and function in patients with type 2 diabetes mellitus (T2DM).

Methods: In this prospective cohort study, 455 T2DM patients were included and follow-up for a median of 4.7 years.