http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Upregulation of MicroRNA 181c Expression in Gastric Cancer Tissues and Plasma
Cui, Mei-Hua,Hou, Xiao-Lin,Lei, Xiao-Yan,Mu, Fang-Hong,Yang, Gui-Bin,Yue, Lin,Fu, Yi,Yi, Guo-Xing Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.5
Objective: To test the microRNA-181c (miR-181c) expression in tissues and plasma of gastric cancer (GC) cases, analyze any correlations, and explore the possibility of miR-181c as a potential molecular marker for GC diagnosis. Materials and Methods: Relative miR-181c expression levels in cancers and plasma from 30 GC patients was tested using reverse transcription-real-time fluorescent quantitation PCR and compared to that in samples from 30 gastric ulcer and 30 chronic gastritis patients. Results: The miR-181c expression level in the GC tissues was significantly higher than that in the gastric ulcer and chronic gastritis tissues (P = 0.000), as was the miR-181c expression level in the GC plasma (P = 0.000). We determined that miR-181c expression in GC plasma was positively correlated to its expression in the GC tissues (P = 0.000). Conclusions: The expression of miR-181c is upregulated in GC tissues and plasma, and the miR-181c expression level in GC plasma is positively correlated to that in the corresponding cancer tissues. Plasma miR-181c is possibly a new serological marker for GC diagnosis.
Jun Wang,Li Jiang,Sheng Ding,Si-Yi He,Shun-Bi Liu,Zhong-Jie Lu,Yuan-Zhang Liu,Li-Wen Hou,Bin-Su Wang,Jin-Bao Zhang 연세대학교의과대학 2023 Yonsei medical journal Vol.64 No.4
Purpose: We aimed to analyze the optimal timing of enteral nutrition (EN) in the treatment of sepsis and its effect on sepsis-asso ciated acute kidney injury (SA-AKI.)Materials and Methods: The MIMIC-III database was employed to identify patients with sepsis who had received EN. With AKI as the primary outcome variable, receiver operating characteristic (ROC) curves were utilized to calculate the optimal cut-off time of early EN (EEN). Propensity score matching (PSM) was employed to control confounding effects. Logistic regressions and propen sity score-based inverse probability of treatment weighting were utilized to assess the robustness of our findings. Comparisons within the EEN group were performed. Results: 2364 patients were included in our study. With 53 hours after intensive care units (ICU) admission as the cut-off time of EEN according to the ROC curve, 1212 patients were assigned to the EEN group and the other 1152 to the delayed EN group. The risk of SA-AKI was reduced in the EEN group (odds ratio 0.319, 95% confidence interval 0.245–0.413, p<0.001). The EEN patients re ceived fewer volumes (mL) of intravenous fluid (IVF) during their ICU stay (3750 mL vs. 5513.23 mL, p<0.001). The mediating ef fect of IVF was significant (p<0.001 for the average causal mediation effect). No significant differences were found within the EEN group (0–48 hours vs. 48–53 hours), except that patients initiating EN within 48 hours spent fewer days in ICU and hospital. Conclusion: EEN is associated with decreased risk of SA-AKI, and this beneficial effect may be proportionally mediated by IVF volume.
Li Cui,Weiquan Bu,Jie Song,Liang Feng,Tingting Xu,Dan Liu,Wenbo Ding,Jianhua Wang,Changyang Li,Binge Ma,Yi Luo,Ziyu Jiang,Chengcheng Wang,Juan Chen,Jian Hou,Hong-mei Yan,Lei Yang,Xiao-bin Jia 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.3
Alantolactone is a sesquiterpene lactone isolatedfrom Inula helenium L. Although alantolactone possessesanti-inflammation and apoptosis-induction activities, theunderlying mechanism of anti-cancer effect on humanbreast cancer cells remains largely unknown. In this study,we explored the possibility of alantolactone as an apoptosis-inducing cytotoxic agent using MDA-MB-231 cells asin vitro model. Alantolactone significantly induced itsapoptosis, demonstrated by cell cycle analysis, annexinV-APC/7-AAD double staining and dUTP nick end labeling. Additionally, alantolactone triggered the mitochondrial-mediated caspase cascade apoptotic pathway, whichwas confirmed by increased Bax/Bcl-2 ratio, loss of MMP,release of cytc from mitochondria to cytoplasm, activationof caspase 9/3, and subsequent cleavage of PARP. Z-VADFMKpartially prevented apoptosis induced by alantolactone. Alantolactone provoked the production of ROS, whileNAC (a scavenger of ROS) reversed alantolactone-mediateddepolarization of MMP and apoptosis. Alantolactonemodulated the activities of MAPKs. As expected, cotreatmentwith SB203580, SP600125 or U0126 could reducedthe apoptotic rate. Furthermore, alantolactone decreasedthe protein expressions of p-NF-kB p65 and p-STAT3,increased p-c-Jun level in a dose-dependent manner. Thesefindings suggested that alantolactone possessed anticanceractivity via ROS-mediated mitochondrial dysfunctioninvolving MAPK pathway, and had an effect on the transcriptionfactors of NF-kB, AP-1 and STAT3.