Hmgcs2 is the hub gene in diabetic cardiomyopathy and is negatively regulated by Hmgcs2, promoting high glucose-induced cardiomyocyte injury.

BACKGROUND: Diabetic cardiomyopathy (DCM) represents a major cause of heart failure and a large medical burden worldwide. This study screened the potentially regulatory targets of DCM and analyzed their roles in high glucose (HG)-induced cardiomyocyte injury. METHODS: Through GEO database, we obtained rat DCM expression chips and screened differentially expressed genes. Rat cardiomyocytes (H9C2) were induced with HG. 3-hydroxy-3-methylglutarylcoenzyme A synthase 2 (Hmgcs2) and microRNA (miR)-363-5p expression patterns in cells were measured by real-time quantitative polymerase chain reaction or Western blot assay, with the dual-luciferase assay to analyze their binding relationship. Then, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, lactate dehydrogenase assay, terminal deoxynucleotidyl transferase dUTP nick end labeling assay, enzyme-linked immunosorbent assay, and various assay kits were applied to evaluate cell viability, cytotoxicity, apoptosis, inflammation responses, and oxidative burden. RESULTS: Hmgcs2 was the vital hub gene in DCM. Hmgcs2 was upregulated in HG-induced cardiomyocytes. Hmgcs2 downregulation increased cell viability, decreased TUNEL-positive cell number, reduced HG-induced inflammation and oxidative stress. miR-363-5p is the upstream miRNA of Hmgcs2. miR-363-5p overexpression attenuated HG-induced cell injury. CONCLUSIONS: Hmgcs2 had the most critical regulatory role in DCM. We for the first time reported that miR-363-5p inhibited Hmgcs2 expression, thereby alleviating HG-induced cardiomyocyte injury.

Changes of Plasma Tumor Necrosis Factor α and C-Reactive Protein Levels in Patients with Hypertension Accompanied by Impaired Glucose Tolerance and their Clinical Significance.

BACKGROUND: Chronic inflammation could affect the occurrence and development of malignant tumors. To explore the levels of tumor necrosis factor α (TNF-α) and C-reactive protein (CRP) in patients accompanied by impaired glucose tolerance (IGT) and their clinical significance. MATERIALS AND METHODS: A total of 210 patients hospitalized in Affiliated Hospital of Taishan Medical University from Jun., 2013 to Dec., 2014 were selected, in which 92 cases were accompanied by IGT. Meanwhile, 80 randomly-selected healthy people by physical examination were as the control. The levels of routine biochemical indexes, plasma TNF-α and CRP in all subjects were measured. RESULTS: Both systolic and diastolic pressures in hypertension group and hypertension plus IGT group were significantly higher than in control group (p<0.01), but there was no statistical significance between these two groups (p>0.05). The levels of fasting plasma glucose (FPG) and blood glucose 2 h after taking glucose in hypertension plus IGT group were markedly higher than other groups (p<0.01). Homeostasis model assessment-insulin resistance (HOMA-IR), TNF-α and CRP contents were on the progressive increase in control, hypertension and hypertension plus IGT groups, but significant differences were presented among each group (P<0.01). Hypertension accompanied by IGT had a significantly-positive association with CRP, TNF-α, FPG and blood glucose 2h after taking glucose. CONCLUSIONS: The levels of plasma TNF-α and CPR in patients with hypertension accompanied by IGT increase significantly, indicating that inflammatory reaction in these patient increases, thus suggesting that these patients should be focused regarding cancer prevention.

A 3-D open-framework material with intrinsic chiral topology used as a stationary phase in gas chromatography.

Compared with liquid chromatography and capillary electrophoresis, the diversity of gas chromatography chiral stationary phases is rather limited. Here, we report the fabrication of Co(D-Cam)1/2(bdc)1/2(tmdpy) (D-Cam = D-camphoric acid; bdc = 1,4-benzenedicarboxylate; tmdpy = 4,4'-trimethylenedipyridine)-coated open tubular columns for high-resolution gas chromatographic separation of compounds. The Co(D-Cam)1/2(bdc)1/2(tmdpy) compound possesses a 3-D framework containing enantiopure building blocks embedded in intrinsically chiral topological nets. In this study, two fused-silica open tubular columns with different inner diameters and lengths, including column A (30 m × 530 µm i.d.) and column B (2 m × 75 µm i.d.), were prepared by a dynamic coating method using Co-(D-Cam)1/2(bdc)1/2(tmdpy) as the stationary phase. The chromatographic properties of the two columns were investigated using n-dodecane as the test compound at 120 °C. The number of theoretical plates (plates/m) of the two metal-organic framework columns was 1,450 and 3,100, respectively. The separation properties were evaluated using racemates, isomers, alkanes, alcohols, and Grob's test mixture. The limit of detection and limit of quantification were found to be 0.125 and 0.417 ng for citronellal enantiomers, respectively. Repeatability (n = 6) showed lower than 0.25 % relative standard deviation (RSD) for retention times and lower than 2.2 % RSD for corrected peak areas. The experimental results showed that the stationary phase has excellent selectivity and also possesses good recognition ability toward these organic compounds, especially chiral compounds.

Refractory platelet transfusion in a patient with CD36 deficiency due to pseudothrombocytopenia.

Type I CD36 deficiency is defined by the absence of CD36 on both platelets and monocytes. Pseudothrombocytopenia (PTCP) is characterized by a false reduction in the number of platelets in ethylenediaminetetraacetic acid (EDTA)-anticoagulated blood. Here we report a rare case of concomitant CD36 deficiency and PTCP. The patient was a 7-year-old boy who suffered comminuted fractures of the left humeral condyle. In the pre-operative examination, he was found to have thrombopenia and assumed to have idiopathic thrombocytopenic purpura. After immunotherapy and platelet transfusion, the platelet count remained low, suggesting that the patient was refractory to platelet transfusion. Serum was collected for the detection of platelet antibodies, and antibodies against CD36 were found. Flow cytometry verified the absence of CD36 on both the platelets and monocytes of this patient. However, the platelet count was normal when capillary blood smears were analysed; in addition, platelet coagulation was noted under the microscope when EDTA-anticoagulated peripheral blood was used. The patient underwent surgery without platelet transfusion and recovered uneventfully.