Red blood cell distribution width is an index reflecting the size heterogeneity of circulating red blood cells, which is usually used for diagnosis and treatment of blood system diseases.In recent years, more and more evidences show that the increase of red blood cell distribution width level is closely related to the occurrence, development and prognosis of cardiovascular diseases.We focused on the relationship between red blood cell distribution width and atrial fibrillation (AF) and its possible mechanism, in order to provide some reference value for the clinical treatment of AF.

10.3969/j.issn.1007-3969.2013.04.011

Objective:To explore the application of microvascular flow imaging (MVFI) combined with high-frequency ultrasonography in children with haemophilic arthropathy A (HAA).Methods:Retrospective study.A total of 82 children diagnosed with HAA in the First Affiliated Hospital of Zhengzhou University from October 2018 to October 2020 were recruited.The elbow, knee and ankle joints of each child were examined by high-frequency ultrasonography.The numbers of thickened synovial joints were recorded.Blood flow signals of the thickening of synovial joints was checked by the MVFI and power Doppler ultrasound (PDUS), respectively.Color flow signals were graded by the semi-quantitative scoring systems.The chi- square test and independent multi-group ordinal multi-category rank-sum test were used to compare the differences of MVFI and PDUS in the display of thickened synovial blood flow. Results:A total of 254 joints were involved in 82 children with HAA, including synovial hypertrophy in 188 joints, hydrops articuli in 146 joints, fibrotic septa in 66 joints, cartilage damage in 63 joints, haemosider indeposition in 45 joints, bone erosion in 25 joints, osteophytes in 15 joints and bone remodeling in 8 joints.Grade Ⅱ synovial thickened joints were the most common.The proportion of blood flow signals detected by PDUS in thickened synovial membranes was significantly higher than that detected MVFI (52.66% vs.70.21%, χ2=12.225, P<0.05). Numbers of grade 0 and Ⅰ joints with thickened synovial membranes detected by MVFI were less than those of PDUS, while the opposite result was obtained in detecting grade Ⅱ and Ⅲ joints ( H=21.158, P<0.05). Compared with PDUS, MVFI more sensitively visualized the blood flow of the thickened synovial membrane. Conclusions:MVFI can more prominently detect the thickened synovial blood flow in children with HAA.A combined application of MVFI and high-frequency ultrasonography contributes to the evaluation of children with HAA.

Cholestatic liver disease is a common disease that causes bile flow dysfunction due to various reasons. The etiology of cholestatic liver disease is complexed, and therapeutic drugs are extremely limited. To date, ursodeoxycholic acid is the only FDA-approved drug for treating primary biliary cirrhosis, whereas its efficacy is limited to early stage of the disease, therefore novel drugs are urgently needed. Nuclear receptors become therapeutic hotspot target in cholestasis since these receptors play a key role in regulating bile acid homeostasis. Peroxisome proliferator-activated receptor (PPAR) is an important nuclear receptor involved in regulating multiple mechanisms of cholestasis in vivo. It can improve intrahepatic cholestasis by inhibiting bile acid synthesis, reducing bile acid toxicity, affecting the expression of bile acid metabolic enzymes and transporters, and can play an anti-inflammatory, anti-oxidation and anti-fibrosis role. A number of studies have shown that PPAR agonists represented by fibrates alone or in combination can improve liver function indexes, inflammatory factors and fibrosis markers in patients with cholestasis. This review analyzes and summarizes the lastest advances in the molecular mechanism of PPAR as a therapeutic target for cholestasis and drug treatment in development or have been used in clinical.

In order to explore the mechanisms underlying the calcium alleviating fluorosis at protein level, we made an attempt to establish fluorosis and calcium supplementation rat models to isolate and identify bone differential proteins. The bone proteins of different groups were compared by two-dimensional electrophoresis (2-DE) and mass spectrometry (MALDI-TOF MS), and analyzed by gene ontology annotation, pathway enrichment and interaction networks. The 17 proteins were identified in the fluorosis group (F) and the fluorosis calcium supplement group (F+Ca), including type I collagen (Col1a1), actin (Actb), protein glutamine transferase 2 (Tgm2), compared with the control group (C). These differential proteins are enriched in 38 bone metabolic pathways such as focal adhesion, PI3K-Akt signaling pathway, and AMPK signaling pathway. And the functions of these proteins are mainly related to cytoskeleton, energy metabolism, substance transport, ion channel, and apoptosis. Therefore, it is speculated that calcium may alleviate the fluoride-induced bone damage by regulating the focal adhesion, PI3K-Akt, AMPK and other signaling pathway, but the specific mechanism needs further research.
Animals ; Calcium ; Dietary Supplements ; Fluoride Poisoning ; Fluorosis, Dental ; Phosphatidylinositol 3-Kinases ; Rats

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.