Objective To investigate the association of the TNFRSF11B gene polymorphism and the lean muscle mass in population of Chinese Han living in Jinan. Methods Lean muscle mass of 419 volunteers were measured with dual energy X-ray absorptiometry. 8 tagging single nucleotide polymorphism (tSNP) of TNFRSF11B gene were genotyped. Results Lean muscle mass of whole body increased with the copy of the G allele of TNFRSF11B-rs2875845 and the T allele of TNFRSF11B-rs1485288 (P<0.05). Conclusion The G allele of rs2875845 and the T allele of rs1485288 in TNFRSF11B gene increase the level of the lean muscle mass in Chinese Han population.

Objective To investigate the association of the polymorphism of rs3750344 and rs1435252 of G-protein family GABABR2 gene with obesity in population of Uygur and Han. Methods 785 Uygur subjects from Xinjiang and 425 Han subjects from Jinan Maternity and Child Care Hospital were recruited by epidemiology survey. Exposure indicators such as body mass index (BMI), total cholesterol (Tch), triglyceride (TG), fasting glucose (Glu) concentration were measured. Two single nucleotide polymorphisms (SNPs) of rs3750344 and rs1435252 of GABABR2 gene were typed with Taqman. Linkage disequilibrium and haplotype were analysed with Haploview software. Results The frequency of rs1435252 was significantly different in AA carries of Uygur subjects between overweight group (12.5%) and normal weight group (6.6%), the subject with AA genotype significantly increased risk of overweight (OR=1.43, 95% CI: 1.06~1.91). The frequency of rs1435252 was significantly different in A alleles carries of Han subjects between obesity group (80.0%) and normal weight group (65.2%), the subject with A alleles significantly increased risk of obesity (OR=2.13, 95%CI: 1.18~3.86). The C alleles of rs3750344 significantly decreased risk of obesity (OR=0.69, 95%CI: 0.49~0.97) in Uygur, but the significance disappeared after controlling for covariates of age and gender. Conclusion The rs1435252 A allele of GABABR2 gene is a risk factor for overweight or obesity in population of Uygur and Han.

PURPOSE: Studies have found that long noncoding RNA HEIH (lncRNA-HEIH) is upregulated and facilitates hepatocellular carcinoma tumor growth. However, its clinical significances, roles, and action mechanism in colorectal cancer (CRC) remains unidentified. MATERIALS AND METHODS: lncRNA-HEIH expression in CRC tissues and cell lines was measured by quantitative real-time polymerase chain reaction. Cell CountingKit-8, ethynyl deoxyuridine incorporation assay, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and nude mice xenografts assays were performed to investigate the roles of lncRNA-HEIH. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays were performed to investigate the action mechanisms of lncRNA-HEIH. RESULTS: In this study, we found that lncRNA-HEIH is significantly increased in CRC tissues and cell lines. lncRNA-HEIH expression is positively associated with tumor size, invasion depth, and poor prognosis of CRC patients. Enhanced expression of lncRNA-HEIH promotes CRC cell proliferation and decreases apoptosis in vitro, and promotes CRC tumor growth in vivo. Whereas knockdown of lncRNA-HEIH inhibits CRC cell proliferation and induces apoptosis in vitro, and suppresses CRC tumor growth in vivo. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor κB (NF-κB), increases the binding of NF-κB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL. Moreover, Bcl-xL expression is positively associatedwith lncRNA-HEIH in CRC tissues. Blocking the interaction between lncRNA-HEIH and miR-939 abolishes the effects of lncRNA-HEIH on CRC tumorigenesis. CONCLUSION: This study demonstrated that lncRNA-HEIH promotes CRC tumorigenesis through counteracting miR-939-mediated transcriptional repression of Bcl-xL, and suggested that lncRNA-HEIH may serve as a prognostic biomarker and therapeutic target for CRC.
Animals ; Apoptosis ; Carcinogenesis* ; Carcinoma, Hepatocellular ; Cell Line ; Cell Proliferation ; Chromatin Immunoprecipitation ; Colorectal Neoplasms* ; Deoxyuridine ; DNA Nucleotidylexotransferase ; Heterografts ; Humans ; Immunoprecipitation ; In Vitro Techniques ; Luciferases ; Mice ; Mice, Nude ; Prognosis ; Real-Time Polymerase Chain Reaction ; Repression, Psychology* ; RNA ; RNA, Long Noncoding*

Activation of the heart normally begins in the sinoatrial node (SAN). Electrical impulses spontaneously released by SAN pacemaker cells (SANPCs) trigger the contraction of the heart. However, the cellular nature of SANPCs remains controversial. Here, we report that SANPCs exhibit glutamatergic neuron-like properties. By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse, we found that SANPCs co-clustered with cortical neurons. Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system, expressing genes encoding glutamate synthesis pathway (Gls), ionotropic and metabotropic glutamate receptors (Grina, Gria3, Grm1 and Grm5), and glutamate transporters (Slc17a7). SANPCs highly expressed cell markers of glutamatergic neurons (Snap25 and Slc17a7), whereas Gad1, a marker of GABAergic neurons, was negative. Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca