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1.
Zhonghua Yi Xue Za Zhi ; 99(25): 1963-1967, 2019 Jul 02.
Article in Chinese | MEDLINE | ID: mdl-31269601

ABSTRACT

Objective: To investigate the cinical value of FAM19A4promoter methylation in cervicalexfoliated cells for triage of cervical cancer. Methods: A total of 162 high-risk HPV-infected patients who were pathologically confirmed as different cervical lesions from August 2017 to December 2017 were collected in Guangdong Women and Children Hospital. Taqman probe-based quantitative PCR (qPCR) was used to detect the methylation of FAM19A4 promoterin different grades of cervical lesions, and the value of FAM19A4 methylation in predicting cervical HSIL and the above lesions was calculated by diagnostic test. Results: (1)The positive rates of FAM19A4 methylation in cervical exfoliated cells increased with the severity of cervical lesions, which were 7.69% (4/52) , 34.62% (9/26) , 55.56% (20/36) , 95.83% (46/48) in normal cervix/cervicitis, cervical LSIL, HSIL, and cervical cancer, respectively(P<0.05).(2)There was no significant difference in the detection rates of FAM19A4 methylation between different age groups, pathological types, clinical stage, tumor size and lymph node metastasis status (P>0.05). (3) The specificity and positive predictive value of FAM19A4 methylation in detecting cervical HSIL alone and ≥HSIL lesions were the optimal, with the AUC of 0.69 and 0.84, respectively. When combined with HPV16/18 genotyping, the sensitivity was significantly improved. Conclusions: The detection of FAM19A4 promoter methylation in cervical exfoliated cells has a high clinical value of discriminating ≥HSIL lesions; and the cotest of methylated FAM19A4 and HPV16/18 genotyping can identify ≥HSIL lesions more sensitively.


Subject(s)
Cytokines/genetics , Papillomavirus Infections , Uterine Cervical Dysplasia , Uterine Cervical Neoplasms , DNA Methylation , Female , Human papillomavirus 16 , Human papillomavirus 18 , Humans , Promoter Regions, Genetic
2.
Life Sci ; 100(1): 61-6, 2014 Mar 28.
Article in English | MEDLINE | ID: mdl-24530740

ABSTRACT

AIMS: This experiment investigated the effects of sub-chronic aluminum chloride (AlCl3) exposure on rat ovaries. MAIN METHODS: Eighty female Wistar (5weeks old) rats, weighed 110-120g, were randomly divided into four treatment groups: control group (CG), low-dose group (LG, 64mg/kg BW AlCl3), mid-dose group (MG, 128mg/kg BW AlCl3) and high-dose group (HG, 256mg/kg BW AlCl3). The AlCl3 was administered in drinking water for 120days. The ovarian ultrastructure was observed. The activities of acid phosphatase (ACP), alkaline phosphatase (ALP), succinate dehydrogenase (SDH), Na(+)-K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase, the contents of Fe, Cu and Zn, and the protein expression of follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) in the ovary were determined. KEY FINDINGS: The results showed that the structure of the ovary was disrupted, the activities of ALP, ACP, SDH, Na(+)-K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase, the contents of Zn, Fe and the protein expression of FSHR and LHR were lowered, and the content of Cu was increased in AlCl3-treated rats than those in control. SIGNIFICANCE: The results indicate that sub-chronic AlCl3 exposure caused the damage of the ovarian structure, the disturbed metabolism of Fe, Zn and Cu and the decreased activities of Na(+)-K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase in the ovary, which could result in suppressed energy supply in the ovary. A combination of suppression of energy supply and reduction of expression of FSHR and LHR could inhibit ovulation and corpus luteum development, leading to infertility in female rats.


Subject(s)
Aluminum Compounds/toxicity , Chlorides/toxicity , Ovary/drug effects , Acid Phosphatase/metabolism , Alkaline Phosphatase/metabolism , Aluminum Chloride , Animals , Copper/metabolism , Female , Infertility, Female/chemically induced , Iron/metabolism , Ovary/metabolism , Ovary/pathology , Rats , Rats, Wistar , Receptors, FSH/metabolism , Receptors, LH/metabolism , Zinc/metabolism
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