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| 1 | Generation of sp3111 transgenic RNAi mice via permanent integration of small hairpin RNAs in repopulating spermatogonial cells in vivo显示文摘spermatid 特定的基因, sp3111,是 four-transmembrane 基因家庭的一个新成员。然而,它的繁殖生物功能留下逃犯。这研究的目的是为进一步在它的繁殖功能上学习 sp3111 基因表示的抑制的效果建立一个 sp3111 击倒的雄的老鼠模型。pSUPER-sp3111-shRNA 的 Recombinant 向量,对老鼠 sp3111 mRNA 的不同区域包含抄录功能的小发卡 RNA 顺序,被构造并且识别。然后,线性化的 recombinant 向量被 electroporation 注入成熟老鼠睾丸和 transfected 到 spermatogonial 房间产生 sp3111 转基因的 RNAi 老鼠。这些 electroporated 男性老鼠与野类型的女性一起被交配在 electroporation 和他们的子孙以后的 30 天被荧光显微镜学和 PCR 两个都检验。在 vivo 的 sp3111 mRNA 的睾丸表达式上的 RNAi 的抑制效率是超过30%并且能稳定地被传给 F3 产生,这被发现,并且与野类型的雄的鼠标相比,吗 sp3111 RNAi 雄的鼠标的后代的吝啬的数字从 11 被减少???????????????????????栠吗?? | Weili Shi Tingyan Shi Zheyu Chen Jufang Lin Xiaofeng Jia Jian Wang Huijuan Shi | 2010 | Acta Biochimica et Biophysica Sinica2010，42，2： | 2 |
| 2 | 白细胞介素-18抑制Lewis肺癌小鼠移植瘤生长与诱导移植瘤细胞凋亡的研究(英文)显示文摘Objective:The aim of our study was to investigate the effects of interleukin-18(IL-18) on implanted Lewis lung cancer in suppressing tumor growth and inducing tumor cells apoptosis.Methods:One week after hypodermic inoculation of Lewis cells, sixteen tumor-bearing syngeneic mice were randomly divided into two groups.The mice in the treatment group were intraperitoneal injected with the IL-18, in the control group were intraperitoneal injected with normal saline.The health conditions of the mice were measured, the morphology of the tumors was studied and the apoptosis of implanted lung cancer cells was detected by TUNEL to evaluated the effects of IL-18.Results:IL-18 had no significant effects on the health conditions of the mice, but it could suppress the implanted tumor growth(inhibition rate was 75%) and induce tumor cells apoptosis.Conclusion:IL-18 can suppress the implanted Lewis lung cancer cells by way of inducing tumor cells apoptosis.It could be used as a new strategy for lung cancer. | Sheng Yang Huishan Lu Xiangqi Chen Tingyan Lin Zhiying Li Mingqiang Kang | 2010 | The Chinese-German Journal of Clinical Oncology2010，9，3： | 1 |
| 3 | Plasmacytoid dendritic cells promote acute kidney injury by producing interferon-α显示文摘Acute kidney injury(AKI)is a common clinical complication associated with high mortality in patients.Immune cells and cytokines have recently been described to play essential roles in AKI pathogenesis.Plasmacytoid dendritic cells(pDCs)are a unique DC subset that specializes in type Ⅰ interferon(IFN)production.Here,we showed that pDCs rapidly infiltrated the kidney in response to AKI and contributed to kidney damage by producing IFN-α.Deletion of pDCs using DTR^(BDCA2) transgenic(Tg)mice suppressed cisplatin-induced AKI,accompanied by marked reductions in proinflammatory cytokine production,immune cell infiltration and apoptosis in the kidney.In contrast,adoptive transfer of pDCs during AKI exacerbated kidney damage.We further identified IFN-α as the key factor that mediated the functions of pDCs during AKI,as IFN-α neutralization significantly attenuated kidney injury.Furthermore,IFN-α produced by pDCs directly induced the apoptosis of renal tubular epithelial cells(TECs)in vitro.In addition,our data demonstrated that apoptotic TECs induced the activation of pDCs,which was inhibited in the presence of an apoptosis inhibitor.Furthermore,similar deleterious effects of pDCs were observed in an ischemia reperfusion(IR)-induced AKI model.Clinically,increased expression of IFN-α in kidney biopsies was observed in kidney transplants with AKI.Taken together,the results of our study reveal that pDCs play a detrimental role in AKI via IFN-α. | Bo Deng Yuli Lin Yusheng Chen Shuai Ma Qian Cai Wenji Wang Bingji Li Tingyan Liu Peihui Zhou Rui He Feng Ding | 2021 | Cellular & Molecular Immunology2021，18，1： | 1 |
| 4 | Quantitative monitoring and mutations of ctDNA before and after non-small cell lung cancer radical surgery显示文摘Objective The aim of this study was to study the quantitative expression of circulating tumour DNA(ctDNA) in patients with non-small cell lung cancer(NSCLC) before and after radical operation and to explore the correlation between gene mutations in non-small cell lung cancer tissues and those in ctDNA.Methods We randomly assigned 5 NSCLC patients from the Department of Thoracic Surgery of Fujian Medical University Union Hospital. All the patients had undergone radical surgery. Venous blood samples were collected from the 5 NSCLC patients at two time points(before the operation and 21–37 days after the operation) for monitoring ctDNA levels. This was done by isolating plasma from venous blood using high velocity centrifugation, extracting DNA from the plasma using the QIAamp Circulating Nucleic Acid kit, and then quantifying the ctDNA levels. The results were analyzed using the Wilcoxon Rank Sum Test. Moreover, the ctDNA levels were compared with those of carcinoembryonic antigen(CEA), which was detected simultaneously with the ctDNA. Then, DNA samples from the tumor tissues and peripheral blood cells and ctDNA were sequenced using the Hiseq2000 sequencing platform(Illumina) and the mutant genes were screened out. Mutations that occurred within the tumor tissues were used as positive control, whereas those found in the pre-operative blood cells were used as a negative control. Based on the mutational analysis of ctDNA genes, a total of 508 cancer-related genes were screened. Results The median values of the pre-and post-operative ctDNA levels in the 5 patients with NSCLC were 0.612(0.518–0.876) and 0.430(0.372–0.612) ng/μL, respectively. There was a significant difference between the two groups(P < 0.05). The pre-operative CEA level was slightly higher than the post-operative level(P > 0.05). In one of the cases, LC tissues showed multiple mutations, consistent with pre-operative ctDNA. Moreover, isogenic mutations of the same type were not detected in post-operative ctDNA or peripheral blood cells. Conclusion Mutations found in the lung cancer(LC) ctDNA gene were consistent with the mutation type of LC tissue. Hence, the quantitative and qualitative analysis of ctDNA is a promising novel molecular biomarker for the evaluation of tumor burden changes in NSCLC. | Xiangqi Chen Tingyan Lin Zhisen Gao Jiangjiang Xu Rui Feng Sheng Yang Shuchen Chen Mingqiang Kang | 2019 | Oncology and Translational Medicine2019，5，3： | 0 |
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