1.Vitamin E Succinate inhibits growth and induces apoptosis of prostate cancer cell line PC-3
Lihang YU ; Bo YANG ; Linhui WANG ; Yinghao SUN
Academic Journal of Second Military Medical University 2001;0(09):-
Objective:To study the inhibitory and apoptosisinducing effect of vitamin E succinate(VES) on androgen-independent prostate cancer cell line PC-3 in vitro.Methods: VES was dissolved with ethanol to obtain VES solution.PC-3 cells of logarithmic growth phase were treated with various concentrations of VES solution(25,50,75,100,and 125mg/L);cells in control group were treated with 1.25% ethanol.MTT method was used to measure the viability and inhibitory rate of cells in each group 24h,48h and 72h after VES treatment;flow cytometry was employed to determine the apoptosis rate of the PC-3 cells.Results: The viability of cells in the experimental groups was significantly lower than that in the control group(P
2.Is semen polymorphonuclear leucocytes count a good predictor of male genital tract infection?
Lihang CHEN ; Su Ling YU ; Hemashree RAJESH
Singapore medical journal 2013;54(6):328-331
INTRODUCTIONThis study aims to evaluate whether an increased polymorphonuclear leucocyte (PMN) count in semen is a good predictor of male genital tract infection, which is detected by semen culture.
METHODSA retrospective cross-sectional study examining the semen of 388 men was conducted at the in vitro fertilisation centre of a tertiary hospital. We compared the culture results of 109 men with increased semen PMN count against those of 279 men with normal semen PMN count.
RESULTSThere was no significant difference in the percentage of positive cultures between men with increased PMN count in their semen and those without PMN count elevation (original sensitivity 20.8%, specificity 70.3%; p = 0.1289). The overall percentage of positive semen cultures among all 388 patients was 18.6%.
CONCLUSIONBased on the positive cultures of significant organisms in the semen of our cohort, an increased semen PMN count is not a good predictor of genital tract infection in men.
Adult ; Bacterial Infections ; diagnosis ; microbiology ; Cross-Sectional Studies ; Humans ; Leukocyte Count ; Male ; Middle Aged ; Neutrophils ; cytology ; microbiology ; Reproductive Tract Infections ; diagnosis ; microbiology ; Retrospective Studies ; Semen ; cytology ; microbiology ; Sensitivity and Specificity ; Young Adult
3.Missense mutation analysis of the COL7A1 gene in a pedigree with dominant dystrophic epidermolysis bullosa
Linhong YU ; Huaiyu WANG ; Changhua ZHU ; Linxin DONG ; Baofeng WU ; Lihang LIN ; Xuemin XIAO
Chinese Journal of Dermatology 2024;57(5):455-458
Objective:To detect gene mutations in a pedigree with dominant dystrophic epidermolysis bullosa (DDEB) .Methods:A 20-year-old male proband presented with repeated blisters, ulceration, pigmentation, scars on the limbs, and deformation of the nails/toenails after birth. There were 5 patients in the 3-generation family, and they all presented with typical skin lesions. Peripheral blood samples were obtained from 14 members of the pedigree (including the 5 patients) and 100 unrelated healthy controls. Whole-exome sequencing was performed in the proband to identify relevant mutation sites, which were then confirmed in the family by Sanger sequencing.Results:Genetic testing indicated that the proband and the other 4 patients all carried a missense mutation (c.7885G>A) in exon 107 of the COL7A1 gene, resulting in the substitution of glycine by arginine at amino acid position 2629 (p.G2629R). The mutation was identified neither in the 9 healthy relatives nor in the 100 unrelated healthy controls. The mutation co-segregated with DDEB in the family, and was not included in databases such as Pubmed, HGMD or ClinVar, suggesting it was a novel missense mutation. The amino acid encoded by this mutation may alter the structure of type Ⅶ collagen, thereby affecting its function.Conclusion:A novel missense mutation was identified in exon 107 of the COL7A1 gene in the family with DDEB, expanding the spectrum of mutations in the COL7A1 gene.