OBJECTIVES: To investigate the ethnic origin of Chuanqing people, one of the largest unidentified ethnic groups in Guizhou, China, and analyze its genetic relationships with surrounding populations. METHODS: Based on a self-developed microhaplotype system, we conducted genotyping and analyzed the genetic distribution of microhaplotype loci and their forensic applicability in Chuanqing population in Guizhou Province. Using the microhaplotype data from different intercontinental populations and previously reported data from Han population living in Guizhou Province, we systematically investigated the genetic background of Chuanqing people through population genetic approaches, including genetic distance estimation, principal component analysis, and phylogenetic tree construction. RESULTS: Among the studied population, the number of haplotype per microhaplotype ranged from 6 to 25. The average expected heterozygosity (He), observed heterozygosity (Ho), power of discrimination (PD), and probability of exclusion (PE) were 0.8291, 0.8301, 0.9387, and 0.6593, respectively. The cumulative power of discrimination (CPD) and cumulative probability of exclusion (CPE) for these 33 loci were 1-2.62×10^-41 and 1-7.64×10^-17, respectively. Population genetic analyses revealed that the Chuanqing population had close genetic relationships with the East Asian populations, especially the local Guizhou Han population, Beijing Han population and the Han populations living in southern China. CONCLUSIONS The 33 microhaplotypes exhibit high levels of genetic diversity in the Guizhou Chuanqing population, highlighting their potentials for both forensic identification and parentage testing. The Han populations might have contributed a significant amount of genetic material to the Chuanqing population during the formation and development of the latter.
Humans ; China/ethnology* ; Ethnicity/genetics* ; Forensic Genetics/methods* ; Genetics, Population ; Genotype ; Haplotypes ; Phylogeny ; East Asian People/genetics*

Objective:To analyze the expression of hsa-microRNA-6832-5p (hsa-miR-6832-5p) in bladder tumor tissues and bladder tumor cells, and to explore its interference on the expression of proline-rich protein 11 (PRR11) gene in bladder tumor cells and its effect on cell proliferation and migration.Methods:Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression level of hsa-miR-6832-5p in bladder tumor tissues, paratumorous tissues, bladder tumor cell lines and normal bladder epithelial cells. Bioinformatics predicts and the dual luciferase reporter gene validates the downstream target gene of hsa-miR-6832-5p. hsa-miR-6832-5p or miR-NC were transfected to the bladder tumor cell lines with the lowest expression level of hsa-miR-6832-5p, respectively, and named as miR-6832-5p group and miR-NC group. qPCR was used to detect the expression levels of hsa-miR-6832-5p and target gene mRNA in the transfected cells. Western blot was used to detect the expression level of target gene protein. Methyl thiazolyl tetrazolium (MTT) assay and transwell assay were used to detect cell proliferation and migration, respectively.Results:The expression of hsa-miR-6832-5p was lower in bladder tumor tissues than in adjacent tissues ( P<0.01). The expression of hsa-miR-6832-5p in bladder tumor cells was lower than that in normal bladder epithelial cells ( P<0.05), and T24 cells had the lowest hsa-miR-6832-5p expression level ( P<0.01). Bioinformatics and dual luciferase reporter genes showed that hsa-miR-6832-5p can directly act on the 3′-untranslated region of the PRR11 gene ( P<0.01). The expression of hsa-miR-6832-5p in the miR-6832-5p group was significantly higher than that in the miR-NC group ( P<0.01). The expression of PRR11 in the miR-6832-5p group was significantly lower than that in the miR-NC group ( P<0.01). Western blot results were consistent with qPCR results. Compared with the miR-NC group, the proliferation of bladder tumor cells was significantly decreased after transfection with hsa-miR-6832-5p ( P<0.05), and the migration ability of cells was significantly decreased ( P<0.01). Conclusions:The expression of hsa-miR-6832-5p was significantly decreased in bladder tumor tissues and cell lines. hsa-miR-6832-5p inhibited the proliferation and migration of bladder tumor cells by down-regulating the expression of PRR11 gene.

Objective:To explore the expression of Bcl related anti-apoptotic protein 3 (BAG3 protein)in colon cancer and its clinical significance,and to clarify the relationship between its expression and the occurrence and development of colon cancer.Methods:A total of 90 cases of colon cancer tissue and paracancerous tissue were selected, the expressions of BAG3 protein in different tissues were detected by tissue microarray and immunohistochemical SP method;Kaplan-Meier method,univariate analysis and multivariate analysis were used to investigate the relationship between the clinicopathological parameters and the prognosis of the patients with colon cancer.Results:The expression of BAG3 protein in the colon cancer tissue was high,and the positive expression rates of BAG3 protein in the colon cancer tissue and paracancerous tissue were 37.8% and 0.01%,respectively, and the difference was significant (P < 0.05).The expression of BAG3 protein was associated with gender and tumor size (P <0.05),but there was no correlation between the expression of BAG3 protein in the colon cancer tissue and age,pathologic grade,TNM stage,and lymph node metastasis (P >0.05).The Kaplan-Meier results showed that the expression of BAG3 protein in the colon cancer tissue was not related with the prognosis of the patients and the survival rates of the younger patients and the higher TNM staging patients were high. Conclusion:The expression of BAG3 protein in the colon cancer tissue is high,and its expression is associated with the tumor size;BAG3 protein may act as a tumor marker and therapeutic target for colon cancer.

Objective To explore the role of hydrogen sulfide (H 2S ) in acute liver injury induced by crush-ing hind lim bs of rats. Methods The rats w ere random ly divided into the follow ing groups:control, crush-ing, H 2S donor sodium hydrosulfide (NaHS) + crushing, H 2S inhibitor propargylglycine (PAG ) + crush-ing group. The acute liver injury m odel w as established by crushing the hind lim bs of rats w ith standard w eight. R ats w ere sacrificed at 30 m in and 120 m in after the crush. The activities of serum aspartate am inotransferase (AST) and alanine am inotransferase (ALT) w ere m easured by colorim etric m ethod, and the content of H 2S in plasm a and the contents of m alondialdehyde (MDA), protein carbonyl, glutathione (GSH) in the liver and the activity of H 2S generating enzym e (cystathionine γ-lyase, CSE) w ere deter-m ined by chem ical m ethod. The expression of CSEm R N Ain liver w as detected by R T-PCR . Results For crush injury group, the levels of ASTand ALTin serum , MDAand protein carbonyl in liver in-creased. The levels of GSH, CSE, CSEm R N Ain liver and H 2S in serum decreased. The adm inistration of NaHS before lim bs crush could attenuate the changes of liver injury, but the pre-treatm ent w ith PAG could exacerbate the changes. Conclusion The decrease of H 2S production could involve in m ediating the acute liver injury induced by traum atic stress in rats.

Objective To investigate effects of antioxidant stress protein hem e oxygenase-1 (HO-1) on lipopolysaccharide (LPS)-induced endoplasm ic reticulum stress (ERS) of rat hepatocytes. Methods The BRL cells (rat hepatocyte cell line) were cultured. The hepatocytes were treated with LPS, LPS+HO-1 si RNA , HO-1 siRNA and PB S solution, respectively. The cell viability was m easured by trypan blue ex-clusion test. The apoptosis cells were detected by the fluorescent dye Hoechst 33258. E xpressions of GR P78, C HO P, caspase-12 and HO-1 were detected by Western blotting. Results LPS caused an in-crease of HO-1 protein expression of rat hepatocytes in a dose-dependent and tim e-dependent m anner, a up-regulation of GRP78, CHO P and caspase-12, a decrease in cellviability,and an increase in apopto-sis rate of hepatocytes. Pretreatm ent of HO-1 siRNA inhibited the up-regulation of LPS-induced HO-1, however, aggravated ERS and cellular injury. Conclusion HO-1 inhibites ERS-m ediated cellular injury of rat hepatocytes induced by LPS.