Gastric cancer is a common malignant tumor with a high mortality rate. Abnormal APOBEC3B (apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3B) expression increases tumor susceptibility. However, the exact molecular mechanism of APOBEC3B expression in the development of gastric cancer is still unknown. We investigated the effect of APOBEC3B on the malignant biological behavior of gastric cancer cells and discussed the role of APOBEC3B in the development and progression of gastric cancer. APOBEC3B protein levels were measured in 161 gastric cancer samples using western blotting and immunohistochemistry. Both in vitro and in vivo assays were performed, and molecules were analyzed using bioinformatics analysis and western blotting. APOBEC3B was overexpressed in gastric cancer. Moreover, APOBEC3B significantly enhanced cell proliferation in vitro and tumorigenicity in vivo. Regarding the underlying mechanism, APOBEC3B promoted the proliferation of gastric cancer cells by upregulating P53, MCM2 (minichromosome maintenance protein 2), and cyclin D1. Our results suggest that APOBEC3B is involved in cancer progression, providing a new theoretical basis for the prevention and treatment of gastric cancer.

Accurate and timely genetic material replication is essential for preserving genomic integrity. The replication process begins with chromatin licensing and DNA replication factor 1 (CDT1). It has been demonstrated that dysregulated CDT1 expression causes genomic instability, damages DNA, and may even cause cancer. Although this protein is overexpressed in several malignancies, its significance in gastric cancer is still unknown. This work aims to investigate the biological function and molecular mechanism of CDT1 in gastric cancer. Bioinformatics studies were carried out using TCGA database, Kaplan-Meier and GEPIA online data analysis software. The expression of CDT1 in stomach cancer tissues was determined by immunohistochemistry, and its relationship to clinicopathological features was examined. Using siRNA and cell function experiments, the impact of CDT1 expression on the capacity of gastric cancer cell lines to proliferate, migrate, and invade was investigated. In gastric cancer tissues, CDT1 is overexpressed and is linked to a dismal prognosis. Through the up-regulation of M-cyc, MCM5 (microchromosome maintenance protein 5), CyclinD1, N-cadherin, and the down-regulation of E-cadherin, CDT1 facilitated the proliferation and invasion of gastric cancer cells. The study's findings shed insight on the possible molecular processes behind CDT1's function in promoting the start and progression of gastric cancer and demonstrate the potential predictive and diagnostic use of CDT1 expression in gastric cancer.

Aims DX5(+)NKT cells' distribution and population change in BALB/c and FVB mice infected byC sinensisand their function in liver damage were investigated. Methods and results Mice were infected byClonorchis sinensismetacercariae, and lymphocytes were isolated from the livers, spleens and peripheral blood. NK, DX5(+)NKT, INF-gamma(+)DX5(+)NKT cells and liver fibrosis were analysed. The DX5(+)NKT cells displayed the largest amount in normal BALB/c mice liver followed by peripheral blood and spleen. Although the hepatic DX5(+)NKT cells of BALB/c mice were more than that of FVB mice, they did not show significant percentage change afterC sinensisinfection. The hepatic DX5(+)NKT cells of FVB mice increased remarkably after infection accompanied with heavier liver injury and fibrosis than the BALB/c mice. And hydroxyproline content was also positively correlated with DX5(+)NKT cells only in FVB mice. However, the increase of IFN-gamma producing DX5(+)NKT cells was lower in FVB mice than in BALB/c mice which showed sharp increase with mild liver damage after infection. The frequencies of anti-fibrotic NK cells were similar in both of the two mouse strains. Conclusions C sinensiscould induce different DX5(+)NKT cells responses in different mouse strains which may play roles in liver injury and fibrosis in FVB mice.

目的 探讨华支睾吸虫感染对FVB和BALB/c小鼠肝纤维化及DX5+ NKT细胞的影响. 方法 解剖麦穗鱼,分离获取华支睾吸虫囊蚴,分别灌胃感染FVB和BALB/c小鼠.无菌分离小鼠肝脏、脾脏并采集外周血,HE和Masson染色法检测两种小鼠肝脏病理变化和纤维化程度,流式细胞术检测外周血淋巴细胞中DX5+ NKT细胞的比例.结果 华支睾吸虫囊蚴感染4周后,FVB小鼠肝脏和脾脏均明显增大,肝纤维化程度较BALB/c小鼠严重.感染组BALB/c小鼠肝脏中DX5+ NKT细胞比例为(5.40±0.40)％,外周血为(3.44±0.60)％,脾脏(2.27±0.20)％,与对照组相比差异均无统计学意义(P＞0.05),且在感染1、4、7周后均无明显变化.对照组FVB小鼠的DX5+ NKT细胞在肝脏、脾脏和外周血中的水平相似,为1.5％左右.其中肝脏和外周血DX5+ NKT细胞比例均显著低于对照组BALB/c小鼠(P＜0.05或P＜0.01),脾脏DX5+ NKT细胞在两种小鼠间差异无统计学意义(P＞0.05).感染4周后,FVB小鼠肝脏DX5+ NKT细胞比例为(3.54±0.15)％,对照组为(1.53±0.19)％,差异有统计学意义(P＜0.01). 结论 BALB/c和FVB小鼠感染华支睾吸虫后DX5+ NKT细胞表现出不同的变化和分布,提示其可能在FVB小鼠肝纤维化中发挥作用.

Activation-induced cytidine deaminase (AID) produces immune-diversity by inducing somatic hypermutations and class-switch recombinations in human immunoglobulin genes. This role of AID in causing genomic mutations, also can potentially cause somatic mutations in various host genes of non-lymphoid tissues, and contribute to tumorigenesis. The goal of the present study was to investigate whether AID expression was involved in the development or progression of colorectal cancer, and the nuclear expression of p53 protein in cancer cells. We examined the pattern of expression of AID and p53 proteins in 71 colorectal adenomas and 122 sporadic colorectal cancers by immunohistochemistry. AID and p53 expression was detected in 57 (46.7%) and 78 (63.9%) out of 122 colorectal cancers, respectively. Statistically, the expression of the AID protein was not associated with the 5-year survival or clinical and pathological parameters, including tumor stage, location, size, and lymph node metastasis (P > 0.05). However, the expression of the AID protein was associated with tumor differentiation (P = 0.004). In addition, a significant association was observed between AID and the nuclear expression of p53 in colorectal cancers (P = 0.0357). Only 3 (4.2%) of the 71 colorectal adenomas showed immunopostivity for AID, resulting in a significant difference between total colorectal cancers and adenomas (P < 0.001). The p53 expression was detected in 7 (9.9%) out of 71 colorectal adenomas. Statistically, AID protein was not associated with the degree of dysplasia and the nuclear expression of p53 in colorectal adenomas (P > 0.05). These results suggest that aberrant expression of the AID protein might play a role in the development of colorectal cancers.

病理学是集医学基础、临床及科研于一体的多学科融合课程.随着现代科学知识的不断更新,夯实基础理论,紧跟医学研究前沿,是当代医学硕士研究生的重要任务.通过构建《病理学新进展》课程体系,将病理学基础理论知识与临床实践能力、科学研究新进展等进行融合,并在教学实践中不断优化更新,以提高研究生病理学知识在临床实践中的应用能力,拓宽知识视野,开发科研思维.

Aims: To investigate whether the BTG3 gene is involved in colorectal carcinogenesis. Methods and results: we have examined the genetic alterations, including somatic mutations and promoter hypermethylation of the BTG3 gene in 78 sporadic colorectal carcinomas. Results revealed that no mutation was detected in the coding region of the BTG3 gene and promoter hypermethylation was detected in 5 colorectal carcinoma samples. The expression of BTG3 proteins was also examined via immunohistochemistry in 78 colorectal carcinomas. There was loss or reduced expression of BTG3 in the 43 (55.1%) of the 78 colorectal carcinomas. Statistically, altered expression of BTG3 was not associated with clinicopathological parameters, including tumor differentiation, location, and lymph node metastasis (P>0.05). Conclusion: Our results suggest that genetic, epigenetic, and protein expression pattern alterations of the BTG3 gene might play a minor role in the development or progression of colorectal carcinomas.

组织芯片可以将数十个甚至上百个不同个体的临床组织标本按预先设计的顺序排列在同一张固相载体如玻璃片或硅片上进行分析研究，是一种高通量、多样本的分析工具。组织芯片具有高信息量、体积小、准确、快速、高效率、低消耗等优点，可根据实验的不同要求进行组合和设计，在医学院校的形态学教学中，该技术也能给形态学教学带来一些帮助和好处。

科研诚信是研究人员具备的基本科研素质。近年来，高等院校及科研院所中科研不端行为时常发生，而研究生是高校科研工作的主要力量，因此，加强研究生的科研诚信教育具有重要的现实意义。本文通过地方医学院校研究生科研诚信问题出现的原因、表现形式及解决策略等方面探讨当下加强医学研究生科研诚信教育的必要性、紧迫性。

目的探讨如何改进或加强对考研实习医师的管理,提高实习效果。方法通过对本科实习医师发放问卷的形式,对合格答卷进行初步统计分析。结果选择考研重要、实习考研不能兼顾者共占29.16%,有41.66%的被调查者认为一个月考研假期少,选择考前应管理松和适当照顾、不值夜班、少管病人及考研书少看、不看者均超过半数,而选择考研和实习可兼顾、考研假期时间、病历文书书写等指标适中,选择管理严的实习单位者均超过50%。结论临床实习过程中大部分的意见或想法有利于在管理中采取"严格管理、硬性指标、弹性安排、适当照顾"的办法,取得一定效果,但更有效的方法尚需进一步探讨和实践。