格列美脲对高糖环境下大鼠下颌骨成骨细胞增殖、分化及矿化的影响

目的:探讨格列美脲对高糖培养的大鼠下颌骨成骨细胞增殖、分化和矿化功能的影响。方法:分离培养大鼠下颌骨成骨细胞,分别给予5.5 mmol/L(生理糖浓度)、16.5 mmol/L葡萄糖浓度的培养液培养,加入或不加入10μmol/L格列美脲后,用噻唑蓝法(MTT)观察成骨细胞7 d时的增殖情况,生化法测定7 d时的碱性磷酸酶(alkaline phosphatase,ALP)活性,Western免疫印迹检测7 d和14d时Ⅰ型胶原(collagenⅠ,ColⅠ)的表达,实时定量PCR检测21 d时的骨钙素(osteocalcin,OCN)mRNA的表达,采用SPSS13.0软件包对数据进行统计学分析。结果:高糖浓度降低了成骨细胞的增殖、ALP活性和OCN的mRNA表达,提高了14 d时的ColⅠ的表达。格列美脲能够促进2种糖浓度下的成骨细胞增殖、ALP活性、ColⅠ的蛋白表达和OCN的mRNA表达。结论:高糖浓度降低了大鼠下颌骨成骨细胞的增殖、分化和矿化能力,在2种糖浓度下,格列美脲促进大鼠下颌骨成骨细胞的增殖、分化和矿化。     

Down-regulation of MeCP2 in Hirschsprung's disease

Background/Purpose

Hirschsprung's disease (HSCR) is a congenital disorder characterized by the absence of intramural ganglion cells which are highly associated with impaired proliferation and migration of neural crest cells. Whether methyl CpG binding protein 2 (MeCP2) is related with HSCR still remains unknown. This study investigates the involvement of MeCP2 in HSCR.

Methods

Quantitative real time PCR and western blot were used to detect the expression level of MeCP2 both in the aganglionic/diseased segment and the ganglionic/normal segment. In vitro assays we used siRNAs to knock-down the expression of MeCP2 in SH-SY5Y cell lines, and furthermore, MTT and transwell assays were used to detect the proliferation and migration ability, respectively. In addition, bisulfite sequencing (BSP) and miRNA analysis were used to examine why MeCP2 is decreased in HSCR samples.

Results

MeCP2 exhibited a lower expression level in tissues of HSCR patients compared with the controls. The down-regulation may also suppress the proliferative ability of the cells. However, there was no significant difference in the MeCP2 methylation level between cases and controls. Similarly, there was no difference between cases and controls in miRNA-34b (miR-34b) which is predicted to regulate MeCP2 through complementary binding to the 3′-untranslated region of MeCP2.

Conclusion

Our results indicated that an aberrant decreased level of MeCP2 may play an important role in the pathogenesis of HSCR.     

Therapeutic strategies of iatrogenic portal vein injury after cholecystectomy

Background

The incidence of vascular injury after a cholecystectomy is often underestimated. Although injuries to the portal vein are rare, they are devastating. The aim of the present study was to analyze suitable therapeutic strategies regarding portal vein injury in the absence of biliary injury.

Materials and methods

Eleven patients with portal vein injuries after laparoscopic or open cholecystectomy were referred to our hospital between 2004 and 2010. The clinical presentation, diagnosis, and management of patients with severe portal vein injuries were reviewed. All the patients were discharged without outstanding clinical conditions. During retrospective analysis, these patients were divided into early, middle, and late stages.

Results

All the 11 patients had a portal vein and/or right hepatic artery injury, but no biliary injuries were observed. Among these patients, different management strategies were managed according to the stage of the injury. Eight patients received a direct suture at the time of injury by an experienced hepatobiliary surgeon. Two patients received thrombolytic and anticoagulation therapy after cholecystectomy, without additional surgery. One patient received a liver transplant 3 mo after the injury. After long-term follow-up, these patients had no clinical conditions.

Conclusions

Direct repair or suture is important during the early stage of portal vein injury. Conservative thrombolytic and anticoagulation therapy may serve an important role in the treatment of acute massive thrombus in portal vein injury during the middle stage. Liver transplantation is a salvage therapy that should be used during the late stage.     

Polymorphisms in XPC provide prognostic information in acute myeloid leukemia

Acute myeloid leukemia (AML) is the most common type of adult leukemia for which cytosine arabinoside-based chemotherapy is the main treatment. Single nucleotide polymorphisms within the nucleotide excision repair pathway may alter the susceptibility of leukemia cells to chemotherapy. We investigated the roles of six single nucleotide polymorphisms (ERCC5rs76871136, ERCC5rs77569659, ERCC5rs873601, XPCrs2228000, XPCrs2228001, and XPCrs1870134) in the nucleotide excision repair pathway in influencing the outcome of patients with AML treated with cytosine arabinoside-based chemotherapy. One hundred fifty-one patients with AML in a Chinese population were enrolled in this study. Genotypes were determined by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. We found that the distribution of three genotypes of XPCrs1870134 significantly differed in the cytogenetic risk groups (P?=?0.04). A statistically significant correlation between polymorphisms of XPCrs2228001 and gender was found among the gender groups (P?=?0.03). Moreover, patients carrying at least one variant allele (XPCrs2228001AA+CC) were more likely to respond better than those who did not carry a variant. However, no significant association was detected between polymorphisms in ERCC5 and treatment response. These findings suggest that XPC polymorphisms are important markers for the outcome of patients with AML in the Chinese population.     

肺结核患者抗结核药物治疗不良反应

目的探讨肺结核在抗结核药物治疗过程中发生的不良反应。方法对247例行抗结核药物治疗的肺结核患者出现不良反应进行分类分析。结果不良反应主要表现为肝肾功能损害,消化道症状和中枢神经症状等;年龄超过50岁者不良反应发生率明显高于年龄低于50岁者(P<0.05)。结论肺结核患者使用抗结核药治疗应加强督导和随访,定期复查肝肾功能,及时有效处理药物不良反应。