ABSTRACT
OBJECTIVE: To investigate the relationship of Ureaplasma urealyticum(UU)and Chlamydia trachomatis(CT)infections with reproductive tract microenvironment changes and clinical infertility.METHODS: From July 2018 to May2019,85 cases of tubal infertility were collected as the infertility group from the Outpatient Department of Reproductive Medicine Center,the Seventh Affiliated Hospital of Sun Yat-sen University.The ultrasonography and hysterosalpingography(HSG)showed normal size and shape of uterine cavity,and complete or incomplete obstruction of one or both fallopian tubes;infertility caused by other factors was excluded. The control group consisted of 45 normal women during the same period who had no previous pregnancy history and HSG showed no obvious abnormal fallopian tube. Vaginal and cervical secretions were collected to detect vaginal cleanliness and UU and CT infection.RESULTS: The vaginal cleanliness（Ⅲ-Ⅳ）of infertility group(18.82%)was more than that of control group(4.4%)(P<0.05).CT(18.82%),U(38.82%),CT+UU(15.29%)and total infection rates(72.94%)in infertility group were higher than those in control group(4.44%,8.89%,2.22% and 15.56%). The difference was statistically significant(P<0.01). Multivariate logistic regression analysis showed that tubal infertility was closely related to CT,UU and CT+UU infection(CT:P=0.046,OR=3.291;UU:P=0.025,OR=2.789;CT+UU:P=0.017,OR=7.528).CONCLUSION: CT and UU infections are strongly associated with tubal infertility. It is necessary to screen all women at childbearing age,especially infertile women,in order to clarify the relationship between these pathogens and impaired fertility and adverse pregnancy outcomes.
ABSTRACT
Fanconi anaemia (FA) is an autosomal recessive inherited disorder caused by defects in hematopoietic stem cells. The clinical manifestations of FA are diverse and complicated. FA cells display high hypersensitivity to agents which produce interstrand DNA cross-links such as mitomycin C (MMC) or diepoxybutane (DEB). At least eight complementation groups with defects in eight genes (FANCA, FANCB, FANCC, FANCD(1), FANCD(2), FANCE, FANCF and FANCG) have been identified by gene analysis. Six genes (corresponding to subtypes A, C, D(2), E, F and G) have been coloned, and the encoded FA proteins interact in a common cellular pathway - "FA Pathway", through which modulate DNA repair. The progress of research on FA molecular mechanism provides gene therapy of FA with theory basis. FA cells transduced with the use of retrovirus carring the normal FA gene cDNA manifestate phenotypic correction of hypersensitivity to DNA cross-linking agents, such as MMC. In this review the clinical manifestations and gene composition of FA, and the functions of encoded FA proteins were summarized. The hematopoietic stem cell transplantation and gene therapy for FA patients were discussed.