1.The study of apolipoprotein E gene polymorphism in the elderly
Zhimian ZHANG ; Haiqing GAO ; Yongle SUN
Chinese Journal of Geriatrics 2003;0(07):-
0.05). Conclusions E 3/3 and the prevalence of ? 3 allele were significantly higher in Shandong elderly population.
2.Laparoscopic colorectomy for colorectal cancer.
Min TAN ; Baoxian GUO ; Zhimian WU ; Guotai CHEN ; Zhaoxu ZHENG ; Zhenxian ZHAO
Chinese Journal of Surgery 2002;40(10):769-772
OBJECTIVETo evaluate the result of laparoscopic colorectomy in treatment of colorectal cancer.
METHODSLaparoscopic colorectal surgery was performed in 78 patients with colorectal cancer. Operative procedures, complications and postoperative recovery were studied.
RESULTNone of the 78 patients died of laparoscopic colorectal surgery or complications. Eleven patients died from tumor metastasis and 2 from other causes. Twenty-one, 17, 8 patients for 1, 3, 5 years survived respectively. In nine patients who had received operation less than 1 year, no tumor recurrence or metastasis was found except in 1 patient 11 months after operation.
CONCLUSIONLaparoscopic colorectal cancer resection is essential to colectomy for colon and rectum cancer when indicated.
Adult ; Aged ; Aged, 80 and over ; Colectomy ; methods ; Colorectal Neoplasms ; mortality ; pathology ; surgery ; Female ; Humans ; Laparoscopy ; Male ; Middle Aged ; Neoplasm Staging ; Rectum ; surgery
3.Research progress of ferroptosis in aortic dissection
Yaoyao WU ; Na LI ; Minghui SUN ; Bingxiang WANG ; Zhimian ZHANG
Chinese Journal of Geriatrics 2023;42(2):229-233
Aortic dissection, especially Stanford type A aortic dissection, is an acutely progressive and highly fatal cardiovascular disease.Early prevention and timely treatment can greatly reduce mortality and reduce the burden on families and society.However, due to the etiological mechanism is still unclear, the clinical treatment is still mainly surgery, and the early prevention and drug application are very limited.And some recent studies have found that ferroptosis may play an important role in the occurrence and development of aortic dissection, revealing the relationship between them may provide ideas for the prevention, treatment and scientific research of the disease.
4.Calenduloside E inhibits hepatocellular carcinoma cell proliferation and migration by down-regulating GPX4 and SLC7A11 expression through the autophagy pathway
Qianyi CHEN ; Shuhan SHANG ; Huan LU ; Sisi LI ; Zhimian SUN ; Xirui FAN ; Zhilin QI
Journal of Southern Medical University 2024;44(7):1327-1335
Objective To investigate the molecular mechanism through which calenduloside E inhibits hepatocellular carcinoma(HCC)cell proliferation and migration.Methods HCC cell lines HepG2 and Huh7 treated with calenduloside E were examined for changes in cell viability using CCK-8 assay and expressions of GPX4,SLC7A11,LC3,P62 and phosphorylation of Akt/mTOR using Western blotting.The effects LY294002 and Rapamycin(the inhibitor and activator of autophagy,respectively)on proliferation and migration of calenduloside E-treated HCC cells were evaluated using EdU and Transwell assays.The TCGA database was used to explore the expression levels of GPX4 and SLC7A11 in HCC and normal liver tissues and their correlation with the patients'survival outcomes.GPX4 and SLC7A11 expressions were also detected in HCC cells and normal hepatocytes using RT-qPCR and Western blotting.Results Calenduloside E obviously inhibited the viability of HCC cells.GPX4 and SLC7A11 were highly expressed in HCC tissues and cell lines,and their expression levels were negatively correlated with the patients'survival.In HCC cell lines,calenduloside E significantly inhibited the expressions of GPX4 and SLC7A11 proteins,activated the Akt-mTOR pathway,and enhanced the expression of LC3 II.The inhibitory effect of calenduloside E on GPX4 and SLC7A11 expressions was significantly enhanced by rapamycin but attenuated by LY294002.Inhibiting the autophagy pathway obviously diminished the inhibitory effect of calenduloside E on proliferation and migration of HCC cells,while activating this pathway produced the opposite effect.Conclusion Calenduside E inhibits the proliferation and migration of HCC cells by down-regulating GPX4 and SLC7A11 expression via the autophagy pathway.