Clinical application of traditional Chinese medicine powder in the treatment of acute and chronic wounds.

This study aimed to explore the clinical application and efficacy of traditional Chinese medicine (TCM) powder in the treatment of acute and chronic wounds. Eighty patients with a wound infection were randomly and equally divided into a control group and an observation group. Gauze padding containing furacilin was used to dress the infected wounds of the control group. TCM powder was used to treat the wounds of the observation group. The total response rate of the observation group was significantly higher than the control group (P = .017). The colour and exudate volume scores in the observation group were lower than the control group, and the differences between the two groups were statistically significant (P < .05). The time to the appearance of new epithelium and time to the wound healing of the burns in the observation group were shorter than the control group, and the differences were statistically significant (P < .05). The TCM powder absorbed a large amount of necrotic tissue and exudate from the wound surface, cleared heat and toxins, and activated blood circulation. It also resolved blood stasis, eliminated pus, and allowed for new skin growth, as well as regenerating muscle.

Chronic exposure to microcystin-leucine-arginine induces epithelial hyperplasia and inflammation in the mouse bladder.

Microcystin-leucine-arginine (MC-LR) is a cyclic heptapeptide compound produced by cyanobacteria with strong cytotoxicity. Previous studies have confirmed that MC-LR could exert toxic effects on the genitourinary system, but there are few reports about its toxicity to the bladder. In this study, we investigated the effects of MC-LR on mouse bladder and human bladder epithelial cells (SV-HUC-1 cells). We observed that the bladder weight and the number of bladder epithelial cells were markedly increased in mice following chronic low-dose exposure to MC-LR. Further investigation showed that MC-LR activates AKT/NF-kB signaling pathway to induce the production of proinflammatory cytokines TNF-α and IL-6. In addition, the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in bladder tissue was increased and the relative migration and invasion capacities of SV-HUC-1 cells were enhanced upon exposure to MC-LR. In conclusion, these results suggest that chronic exposure to MC-LR induced epithelial hyperplasia and inflammation, upregulated the expression of matrix metalloproteinases (MMPs) and promoted the migration and invasion of bladder epithelial cells, which provides a basis for further exploring the potential mechanism by which environmental factors increasing the risk of bladder cancer.

Correlations Between mRNA Levels of Centrosomal Protein 55 (CEP55) and Clinical Features of Patients with Lung Cancer.

BACKGROUND The aim of this study was to investigate the prognostic relevance of CEP55 in lung cancer (LC). MATERIAL AND METHODS LC microarray profile GSE30219 was obtained from the GEO database. The 2-sample t test was performed to clarify the difference in CEP55 expression between LC and normal lung tissue. The chi-square test and logistic regression analysis were preformed to investigate the relationship between CEP55 expression and the clinical features of LC patients. Log-rank test and Cox proportional hazards regression analysis were conducted to evaluate the disease-free survival (DFS) and overall survival (OS) of LC patients. Gene set enrichment analysis was conducted to investigate the related mechanisms. RESULTS CEP55 was significantly increased in LC cells relative to normal lung tissues (P<0.0001). Univariate and multivariate correlation analyses demonstrated that CEP55 expression was associated with advanced T and N staging of LC (P<0.0001). Survival analyses indicated that CEP55 expression was an independent risk factor for DFS (HR: 1.515, 95% CI: 1.277-1.797, P<0.0001) and OS (HR: 1.436, 95% CI: 1.278-1.615). CEP55 might affect the proliferation of LC cells through Myc signaling, DNA repair, and G2M checkpoint. CONCLUSIONS Our results indicated that CEP55 was increased in LC cells and was associated with poor clinical outcomes of LC patients, and could be a prognostic biomarker for LC.

Association between the CYP1A1 A2455G polymorphism and risk of cancer: evidence from 272 case-control studies.

A2455G is a common polymorphism in CYP1A1, showing differences in its biological functions. Case-control studies have been performed to elucidate the role of A2455G in cancer; however, the results are conflicting and heterogeneous. Hence, we performed a meta-analysis to investigate the association between cancer susceptibility and A2455G (64,593 cases and 91,056 controls from 272 studies) polymorphism in different inheritance models. We used odds ratios with 95% confidence intervals to assess the strength of the association. Overall, significantly increased cancer risk was observed in any genetic model (dominant model, odds ration [OR] = 1.19, 95% confidence interval [CI] = 1.13-1.25; recessive model: OR = 1.41, 95% CI = 1.29-1.54; additive model: OR = 1.49, 95% CI = 1.35-1.65) when all eligible studies were pooled into the meta-analysis. In further stratified and sensitivity analyses, the elevated risk remained for subgroups of breast cancer, colorectal cancer, esophageal cancer, hepatocellular cancer, head and neck cancer, leukemia, lung cancer, and prostate cancer, but these associations vary in different ethnic populations. In summary, this meta-analysis suggests the participation of A2455G in the susceptibility for some cancers, such as breast cancer, colorectal cancer, lung cancer, and so on. Moreover, ethnicity, histological type of cancer, and smokers seem to contribute to varying expressions of the A2455G on some cancers risk. In addition, our work also points out the importance of new studies for A2455G polymorphism in some cancer types, such as gallbladder cancer, Indians of breast cancer, and Caucasians of ovarians, because these cancer types had high heterogeneity in this meta-analysis (I(2) > 75%).

Primary thyroid smooth muscle tumour.

Not required for Clinical Vignette.

Comparative analysis of antigen coding genes in 15 red cell blood group systems of Yunnan Yi nationality in China: A cross-sectional study.

Introduction: There are few analyses of the 15 red blood group system antigen coding genes found in the Yunnan Yi nationality. This has caused many poteintial dangers relating to clinical blood transfusion. In this report, the coding genes and distribution of 15 blood group antigens system in the Yi nationality were tested and compared with those of Han nationality and other ethnic minorities. Methods: The samples came from the healthy subjects in the first people's Hospital of Qujing, Yunnan Province. Two hundred and three Yunnan Yi and 197 Han nationality individuals were included. Thirty-three blood group antigens with a low frequency from the 15 blood group systems of Yunnan Yi blood donors were genotyped and analyzed by PCR-SSP. Sanger sequencing was used to detect A4GALT from the Yunnan Yi nationality. The χ 2 test was used to analyze observed and expected values of gene distribution to verify conformation to the Hardy-Weinberg equilibrium law. Fisher's exact test was used to analyze gene frequency distribution, and the statistical significance was set at p < 0.05. Results: The ABO blood group examination results for the Yi nationality and the local Han nationality in Qujing City, Yunnan Province, showed the majority were type A and type O, while the least prevalent was type AB. RhD+ accounts for more than 98% of the Yi and Han populations. There was a significant difference in ABO blood group antigen distribution between these two nationalities (p < 0.05), but there was no significant difference in the composition ratio of D antigen in the Rh blood group system (p > 0.05). Compared with Tibetan (Tibet), Zhuang (Nanning), and Dong (Guangxi), the gene distribution frequencies of Rh blood group system phenotype CC were significantly lower in the Yunnan Yi nationality (p < 0.05). There were significant differences in six erythrocyte phenotypic antigens in the Yi nationality in Yunnan compared with Han nationality, such as LW(a-b-), JK(a-b+), MMSs, Di(a-b+), Wr(a-b-), and Kp(a-b+) (p < 0.05). There were gene phenotypes with a low frequency in the four rare blood group systems: LW, MNS, Wright, and Colton. Several different mutation types occurred in the P1PK blood group system's A4GALT gene. Conclusion: Yunnan Yi nationality has a unique genetic background. There are some significantly different distributions of blood group system genes with a low frequency in different regions and groups in China. Multiple mutations in the A4GALT gene of the P1PK blood group system may be related to their environment and ethnic evolution.

[Expression of RhoC and ROCK-1 and their effects on MAPK and Akt proteins in prostate carcinoma].

OBJECTIVE: To detect the expression of RhoC and Rho kinase 1 (ROCK-1) in prostate carcinoma, and explore the possible mechanism of RhoC/ROCK-1 in the pathogenesis of prostate carcinoma. METHODS: Tissue specimens from 73 patients with prostate carcinoma and corresponding paracancerous tissues were obtained by prostate cancer biopsy or radical prostatectomy. The expression of RhoC/ROCK-1 mRNA was detected by RT-PCR. Western blot and immunohistochemistry were performed to dertect the expression of RhoC/ROCK-1 protein. Eukaryotic expression plasmids of RhoC were constructed and transfected into PC-3M-2B4 cells. p-MAPK and p-Akt were detected by Western bolt. RESULTS: The expression levels of RhoC and ROCK-1 mRNA in the prostate carcinomas were significantly higher than those in corresponding paracancerous tissues [72.6% (53/73) vs. 34.2% (25/73); 68.5% (50/73) vs. 38.4% (28/73), P < 0.01], respectively. The results indicated that RhoC/ROCK-1 mRNA expression had no significant correlation with Gleason grade. However, the expression of RhoC/ROCK-1 mRNA showed a significant positive correlation with distant metastasis. The RhoC/ROCK-1 protein expression in prostate cancer was also higher than corresponding paracancerous tissues, and showed a significant positive correlation with p-MAPK and p-Akt expression levels. In addition, p-MAPK and p-Akt expression levels were up-regulated in the transcripts. CONCLUSION: Expression levels of RhoC and ROCK-1 in prostate carcinoma are higher than those in corresponding paracancerous tissues, showing a significant positive correlation with distant metastasis. RhoC/ROCK-1 may be involved in the development, invasion and metastasis of prostate carcinoma.

A polymorphism in the 3'-untranslated region of the matrix metallopeptidase 9 gene is associated with susceptibility to idiopathic calcium nephrolithiasis in the Chinese population.

OBJECTIVE: To investigate whether single nucleotide polymorphisms (SNPs) in the 3' untranslated region (UTR) of the matrix metallopeptidase 9 gene (MMP9) are associated with susceptibility to calcium oxalate stones. METHODS: A total of 428 patients with kidney stone disease (KSD) and 450 control individuals were enrolled. Three MMP9 SNPs (rs20544, rs9509, and rs1056628) were genotyped, and MMP9 mRNA and protein expression was determined in patients and controls. The dual luciferase reporter gene assay was conducted by transfecting HEK293 cells with miR-491-5p mimics and plasmids containing MMP9 with rs1056628 AA/CC genotypes. RESULTS: The rs1056628 CC genotype was significantly increased in KSD patients compared with controls (CC vs AA: odds ratio [OR] = 2.279, 95% confidence interval [CI] = 1.048-4.956). The rs1056628 C allele frequency was higher in KSD patients than controls. The increased KSD risks associated with rs1056628 were more evident in individuals aged <30 years (OR = 3.504, 95% CI = 1.102-11.139) and men (OR = 2.522, 95% CI = 1.004-6.334). mRNA and protein levels of MMP9 were significantly higher in KSD patients with the CC genotype than in those with the AA genotype. CONCLUSION: This study demonstrates that MMP9 SNP rs1056628 is associated with a significant KSD risk in Chinese Han individuals.

MicroRNA-93 promotes bladder cancer proliferation and invasion by targeting PEDF.

OBJECTIVE: MicroRNA-93 (miR-93) is upregulated in the urine of patients with bladder cancer (BC). Here, we investigated the role of miR-93 in BC progression and explored the underlying mechanism. METHODS: miR-93 expression in BC tissues and cells was detected by real time-polymerase chain reaction. The effects of miR-93 and pigment epithelium-derived factor (PEDF) on cell proliferation and invasion were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. The binding of miR-93 to the 3'-untranslated region of PEDF was identified by the luciferase reporter assay. RESULTS: miR-93 expression was higher in BC tissues than in normal controls, and its expression was associated with tumor stage and node stage. Inhibition of miR-93 suppressed the proliferation and invasion of BC cells. PEDF was identified as a target of miR-93 and shown to mediate the effect of miR-93 on cell proliferation and invasion. CONCLUSIONS: The present data suggested that miR-93 promoted BC cell proliferation and invasion by targeting PEDF, providing new biomarkers and targets for BC diagnosis and treatment.

Hypoxia-inducible factor-1α rs11549465 C>T and rs11549467 G>A gene polymorphisms are associated with an increased risk of digestive cancers in Asians.

OBJECTIVE: We used a meta-analysis framework to examine the correlation between HIF-1α gene polymorphisms and the susceptibility to digestive cancers. METHODS: Cochrane Library Database, EMBASE, MEDLINE, Pubmed, CINAHL, Chinese Biomedical Database and Web of Science were searched without language restrictions to identify relevant case-control studies reporting data on HIF-1α gene polymorphisms in digestive cancers. Data was extracted from the selected studies and meta-analysis was carried out using STATA 12.0 and Comprehensive Meta-analysis 2.0 softwares. Relative risk (RR) and its 95% confidence interval (95%CI) were calculated. A total of 8 eligible case-control studies were included. These 8 studies contained a combined total of 1,276 patients diagnosed with various digestive cancers and 3,392 healthy controls. Two functional HIF-1α polymorphisms (rs11549465 C>T and rs11549467 G>A) were examined in these 8 studies. RESULTS: Our findings demonstrated that both rs11549465 C>T and rs11549467 G>A HIF-1α polymorphisms conferred significantly increased risk of digestive cancers. However, ethnicity-stratified analysis revealed that HIF-1α rs11549465 C>T and rs11549467 G>A polymorphisms were associated with an elevated risk of digestive cancer in Asians, but not in Caucasians. These two polymorphisms also conferred different degrees of susceptibility to various digestive cancer types. CONCLUSION: Our meta-analysis suggests that HIF-1α rs11549465 C>T and rs11549467 G>A polymorphisms influence the pathogenesis of digestive cancers in Asians.

Protection of preconditioning, postconditioning and combined therapy against hepatic ischemia/reperfusion injury.

OBJECTIVE: To study the protective effect of ischemic preconditioning (I-pre) and ischemic postconditioning (I-post) against ischemia/reperfusion (I/R) injury in rat's liver. METHODS: Using rat model of hepatic segmental I/R injury, rats were divided into 5 groups: Group A (sham group), Group B (I/R injury), Group C (I-pre group), Group D (I-post group) and Group E (combined treatment of I-pre and I-post). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) in hepatic tissues were determined, respectively. In addition, 7 days'survival of Groups B, C, D and E were evaluated. RESULTS: Compared with Group B, Groups C, D and E exhibited significantly decreased ALT and AST release, minimized tissue injury, suppressed values of MDA and MPO, increased activities of SOD, GSH-Px and GSH (P less than 0.05), as well as improved animal survival. The differences among Groups C, D and E were not statistically significant. CONCLUSIONS: I-pre, I-post and combined therapy of I-pre and I-post have protective effect against hepatic I/R injury, which is correlated with its function of reducing the production of reactive oxygen species, maintaining the activities of antioxidant systems and suppressing neutrophils recruitment. No additive effect can be obtained in Group E.

Do mutations in DNMT3A/3B affect global DNA hypomethylation among benzene-exposed workers in Southeast China?: Effects of mutations in DNMT3A/3B on global DNA hypomethylation.

Global DNA hypomethylation is commonly observed in benzene-exposed workers, but the underlying mechanisms remain unclear. We sought to discover the relationships among reduced white blood cell (WBC) counts, micronuclear (MN) frequency, and global DNA methylation to determine whether there were associations with mutations in DNMT3A/3B. Therefore, we recruited 410 shoe factory workers and 102 controls from Wenzhou in Zhenjiang Province. A Methylated DNA Quantification Kit was used to quantify global DNA methylation, and single nucleotide polymorphisms (SNPs) in DNMT3A (rs36012910, rs1550117, and R882) and DNMT3B (rs1569686, rs2424909, and rs2424913) were identified using the restriction fragment length polymorphism method. A multilinear regression analysis demonstrated that the benzene-exposed workers experienced significant global DNA hypomethylation compared with the controls (ß = -0.51, 95% CI: -0.69 to -0.32, P < 0.001). The DNMT3A R882 mutant allele (R882H and R882C) (ß = -0.25, 95% CI: -0.54 to 0.04, P = 0.094) and the DNMT3B rs2424909 GG allele (ß = -0.37, 95% CI: -0.70 to -0.03, P = 0.031) were significantly associated with global DNA hypomethylation compared with the wild-type genotype after adjusting for confounding factors. Furthermore, the MN frequency in the R882 mutant allele (R882H and R882C) (FR = 1.18, 95% CI: 0.99 to 1.40, P = 0.054) was higher than that of the wild-type. The results imply that hypomethylation occurs due to benzene exposure and that mutations in DNMTs are significantly associated with global DNA methylation, which might have influenced the induction of MN following exposure to benzene. Environ. Mol. Mutagen. 58:678-687, 2017. © 2017 Wiley Periodicals, Inc.

Benchmark Doses Based on Abnormality of WBC or Micronucleus Frequency in Benzene-Exposed Chinese Workers.

OBJECTIVES: The aim of the study was to calculate benchmark dose for chromosomal damage and reduced white blood cell (WBC) associated with exposure to benzene (BZ). METHODS: A group of 317 exposed workers and 102 controls were examined for WBC count and genotoxicity by micronucleus (MN) frequency. The cumulative exposure concentration of BZ was calculated by ambient air BZ concentration at worksites in conjunction with job type and associated service duration. RESULTS: MN frequency (P < 0.01) was higher and WBC count was lower (P < 0.01) in exposed workers on average than in the controls. MN frequency was a more sensitive than WBC; workers older than 30 were more susceptible to abnormal MN frequency and WBC count reduction than those younger than 30. CONCLUSIONS: Benchmark dose estimates indicated that BZ exposure at levels below the current occupational exposure standard can induce genotoxicity and hematotoxicity.

Duodenal-jejunal exclusion improves insulin resistance in type 2 diabetic rats by upregulating the hepatic insulin signaling pathway.

OBJECTIVES: Previous studies have shown duodenal-jejunal exclusion (DJE) results in the rapid resolution of type 2 diabetes; however, the underlying mechanism is unknown. This study aimed to measure the hepatic expression of insulin receptor substrate-2 (IRS-2) and glucose transporter-2 (GLUT-2) in type 2 diabetic rats post-DJE, and to investigate their roles in improved hepatic insulin resistance and glucose intolerance. METHODS: Type 2 diabetic Sprague-Dawley (SD) rats were randomly divided into DJE operation (DO) and control (DC) groups. Normal SD rats were also divided into DJE operation and control groups. Fasting plasma glucose and insulin concentrations were measured, and the quantitative insulin sensitivity check index (QUICKI) and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) were calculated. Eight weeks postoperation, the hepatic IRS-2 and GLUT-2 protein and mRNA levels were measured using western blotting and reverse transcription polymerase chain reaction, respectively. RESULTS: The fasting blood glucose in the DO group decreased from a preoperative level of 20.21 ± 2.14 mmol/L to 8.50 ± 2.19 mmol/L (P < 0.05) 8 wk post-DJE. A change in the QUICKI revealed a dramatic increase, and HOMA-IR showed a significant decrease in the DO group (P < 0.05). Additionally, the IRS-2 and GLUT-2 protein and mRNA levels at 8 wk postoperation were significantly increased in the DO group compared with the DC group. CONCLUSIONS: DJE led to upregulated hepatic IRS-2 and GLUT-2 expression in the hepatic insulin signaling pathway and improved insulin sensitivity in type 2 diabetic rats.

Enforced expression of miR-101 enhances cisplatin sensitivity in human bladder cancer cells by modulating the cyclooxygenase-2 pathway.

Alterations in microRNA (miRNA) expression have been shown to be involved in the tumor response to chemotherapy. However, the possible role of miR­101 in cisplatin sensitivity in human bladder cancer cells remains unclear. In this study, quantitative polymerase chain reaction and western blotting were utilized to determine the expression profiles of miR­101 and cyclooxygenase­2 (COX­2) in human bladder cancer cells. The effect of miR­101 and small interfering RNA (siRNA) against COX­2 on cell viability was evaluated using MTT assays, and apoptosis levels were determined using fluorescence­activated cell sorting analysis of Annexin V/propidium iodide­stained cells. Luciferase reporter plasmids were constructed to confirm direct targeting. This study found that the expression of miR­101 was downregulated in the cisplatin­resistant cell line T24/CDDP as compared with that in the parental line, T24. Furthermore, overexpression of miR­101 significantly increased the anti­proliferative effects and apoptosis induced by cisplatin, whereas knockdown of miR­101 significantly decreased the anti­proliferative effects and apoptosis induced by cisplatin. In addition, downregulation of miR­101 induced cell survival and cisplatin resistance through the upregulation of COX­2 expression. Luciferase gene reporter assays confirmed that COX­2 was a direct target gene of miR­101. Inhibition of COX­2 using COX­2 siRNA abrogated the cisplatin resistance induced by miR­101 downregulation. These results suggest that miR­101 may provide a novel mechanism for understanding cisplatin resistance in bladder cancer by modulating the COX­2 pathway.