AIMTo investigate the liver X receptors agonists T0901317's effect on expression of FAT/CD36 gene mRNA in adult human skeletal muscle cell.

METHODSMyotubes from humans were exposed to different T0901317 concentrations (0, 0.5, and 1.0 micromol/L) for 24 hours before experiments were performed. Then the expression of FAT/CD36 mRNA in skeletal muscle cell of each experimental group was detected by SYBR Green I real-time quantitative polymerase chain reaction. The relative data were compared among groups by 2-delta delta Ct method.

RESULTS(1) The Ct mean of control group, T0901317 (0.5 micromol/L) group, T0901317 (1 micromol/L) group were analyzed and there was significant difference (P < 0.01). (2) The expression of FAT/CD36 mRNA with liver X receptors agonists T0901317 in human skeletal muscle cell in the T0901317 (0.5 micromol/L) group and T0901317 (1 micromol/L) group were 2.91 times and 3.03 times than the control group.

CONCLUSIONThe expression of FAT/CD36 mRNA in human skeletal muscle cell afer the treatment of liver X receptors agonists T0901317 is increased, so we may propose that T0901317 may increase the risk of resistance in adult human skeletal muscle.

Adult ; CD36 Antigens ; genetics ; metabolism ; Cells, Cultured ; Female ; Humans ; Hydrocarbons, Fluorinated ; pharmacology ; Liver X Receptors ; Male ; Muscle, Skeletal ; cytology ; metabolism ; Orphan Nuclear Receptors ; agonists ; RNA, Messenger ; genetics ; metabolism ; Sulfonamides ; pharmacology

Objective To investigate the gene mutations of calcium-and integrin-binding protein 2 (CIB2) 196C＞T, 272T ＞ C and 297C ＞ G carried by students with non-syndromic hearing impairment from special educational schools in Yunnan Province. Methods The experimental group included 337 students with non-syndromic hearing impairment who failed to carry deafness gene with GJB2 (35 del G, 176_191 del 16,235delC, 299_300 del AT), GJB3 (C538T,G547A), mtDNA 12S rRNA (A1555G, C1494T), and SLC26A4 (IVS7_2A＞G, A2168G) . The control group consisted with 150 healthy people. Genomic DNA was isolated from peripheral blood with EDTA anti-coagulate. The subject's DNA fragments including CIB2 196C＞T, 272T ＞ C and 297C＞ G were amplified by polymerase chain reaction (PCR), and subsequently analyzed by direct sequencing to identify deafness-associated mutations. Results Both in the experimental group and control group, we failed to find the mutation of CIB2 196C＞T, 272T＞C and 297C＞G in all individuals. Conclusion Mutations in CIB2 gene 196C＞T, 272T＞C and 297C＞G are not a frequent cause of non-syndromic hearing loss among deaf people in Yunnan province. It provided important information for deafness with formulating landscape of gene screening in this region.

Exosomes are bilayer-lipid membrane nanovesicle from almost all living cell types which are in-volved in intercellular substance transporting and signaling communication .Exosomes are 30 ~120 nm in diameter , can transfer bioactive molecules including DNA , RNA, microRNA, protein as well as lipids derived from parents ' cells to re-cipient cells by body fluids , and specifically influence their physiological or pathological conditions .Leukemia is due to malignant proliferation of hematopoietic stem and progenitor cells .It was reported that leukemia cells derived exosomes play a key role in disease progression , drug resistance , and predict prognosis .This paper will outline the role of exosomes de-rived from leukemia cells and provide important information to help explore the molecular pathogenesis , biomarker as well as therapeutic target of leukemia .

ObjectiveExosomes secreted by BMSC overexpressing GATA-4 gene (BMSCGATA-4-exosome) can promote the differentiation of BMSC into cardiomyocyte-like cells, thereby improve cardiac function after myocardial infarction. However, the molecular mechanism of BMSCGATA-4-exosome in cardiomyocyte-like cell differentiation is unknown. The effect of the secretion of BMSCGATA-4 exosome from bone marrow mesenchymal stem cells (BMSC) in the differentiation of stem cells into cardiomyocytes was determined in miRNA-673-5p/Tsc-1 axis dependent manner.MethodsMouse models of myocardial infarction were established and divided into seven groups. Simulation group (BMSCmiR-673-5p-mimic exosome), inhibition group (BMSCmiR-673-5p-inhibitor exosome), GATA-4 group (BMSCGATA-4 exosome), empty vector group (BMSCempty vector exosome）, and BMSC group (BMSC exosome) were injected into the tail vein for 48 h, and the untreated and normal mice were used as the control group. Cardiac ultrasound was used to detect cardiac function in each group. miRNA-673-5p expression in myocardial infarction was detected using real-time polymerase chain reaction (RT-PCR). The myocardial tissues were extracted from the same myocardial infarction site. Myocardial-specific molecules, such as α-actin, Desmin, cTnT, and Cx43, were detected using RT-PCR. Western blot was used to determine the expression of the corresponding target gene of miRNA-673-5p, Tsc-1, Erk1/2, and Mef2c proteins.ResultsThe simulation group wan shown the most significantly improved myocardial function (P<0.05) with an expression peak of miRNA-673-5p in cardiomyocytes (P<0.05). The highest content of myocardial-specific molecules including α-actin, Desmin, cTnT, and Cx43 was found in the simulation group. The simulation group had the lowest expression of Tsc-1 in cardiomyocytes (P<0.05).ConclusionOverexpressed BMSCGATA-4 exosomes inhibit Tsc-1 expression through miRNA-673-5p to improve cardiac function during myocardial infarction.

OBJECTIVE: To investigate the correlation of single nucleotide polymorphisms (SNP) in arachidonate 5-lipoxygenase gene (ALOX5) rs2029253, rs2228064 and rs2228065 sites, 5-lipoxygenase activating protein gene (ALOX5AP) rs10507391, rs4769874 sites with the risk for genesis of adult myeloid leukemia. METHODS: By the approval from the hospital ethics committee and the informed consent of participants. 150 patients with myeloid leukemia (ML) as ML group and 134 healthy people as the control group were selected. The genomic DNA was extracted from the samples. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) combined with directly sequencing, PCR-amplified products were applied to test the polymorphism of 5 sites in ALOX5 and ALOX5AP gene. RESULTS: A allele frequencies of ALOX5 gene rs2029253 site in the ML group and the control group were 43.0% and 34.3%, respectively. And the G allele frequencies in the ML group and the control group were 57.0% and 65.7%, respectively. The genotype distributions of AA, AG and GG in ALOX5 gene rs2029253 site in the ML group were 32.2%, 21.5% and 46.3% respectively. That in the control group were 15.7%, 37.3% and 47.0% respectively. The genotype AA and A allele frequency of ALOX5 gene rs2029253 site were linked with the increased risk of myeloid leukemia (OR=2.26, 95% CI: 1.43-4.56, P＜0.05; OR=1.44, 95% CI: 1.02-2.03, P＜0.05). And the genotype AG and allele G reduced the susceptibility to myeloid leukemia (OR=0.46, 95% CI: 0.27-0.78, P＜0.01; OR=0.69, 95% CI: 0.50-0.98, P＜0.05), however, the polymorphisms of ALOX5 gene rs2228064 and rs2228065 site not correlated with the risk of myeloid leukemia (P＞0.05). The A allele frequency of ALOX5AP gene rs10507391 site in the ML group and the control group were 30.7% and 36.2% respectirely. The genotype distribution rates of AA, AT and TT in ALOX5AP gene rs10507391 site in the ML group was 1.3%, 58.7% and 40.0% respectively, that in the control group were 9.7%, 53.0% and 37.3% respectively. The genotype AA of ALOX5AP gene rs10507391 site correlated with the decreased risk of myeloid leukemia (OR=0.13, 95% CI: 0.03-0.57, P＜0.05), but the polymorphism of ALOX5AP gene rs4769874 site not correlated with the risk of myeloid leukemia (P＞0.05). CONCLUSION The genotype AA, AG and allele A, G of ALOX5 rs2029253, as well as ALOX5AP rs10507391 may be correlate with the susceptibility to myeloid leukemia.