Pelvic inflammatory disease in the People's Republic of China: aetiology and management.

OBJECTIVES: To study the causes of pelvic inflammatory disease (PID) in Shenyang, Northeastern China, and to assess the efficacy of the syndromic management flowchart for PID recommended by World Health Organization (WHO). METHODS: 200 outpatients with PID attending Gynaecologic Clinic of No. 1 and No. 2 hospital of China Medical University in Shenyang, and 155 control women without symptoms underwent pelvic examination, and were tested for Chlamydia trachomatis (CT), Neisseria gonorrhoeae (NG), Mycoplasma hominis (MH), bacterial vaginosis (BV), Candida albicans (CA) and Trichomonas vaginalis (TV). RESULTS: In PID patients, the prevalence of MH was 26%, of BV 26%, of CT 16%, of CA 11%, of TV 4% and of NG 2.5%. In the control population, prevalences were 5.2%, 8.4%, 0%, 5.2%, 0.7%, 0% respectively. MH, BV and CT were significantly more common in PID patients than in controls (P<0.01). One hundred and thirty-seven of the 200 patients with PID (68.5%) returned for follow-up. Symptoms had resolved completely in 64 (47%), and had improved in 68 (50%). There was no improvement in five (4%). CONCLUSIONS: The management protocol for female lower abdominal pain recommended by WHO is effective in this setting

Uterine Insulin Sensitivity Defects Induced Embryo Implantation Loss Associated with Mitochondrial Dysfunction-Triggered Oxidative Stress

Scope. Implantation loss is a considerable cause of early pregnancy loss in humans and mammalian animals. It is not addressed how proliferative uterine defects implicate in implantation loss. Methods and Results. Herein, a comprehensive proteomic analysis was conducted on proliferative endometria from sows with low and normal reproductive performance (LRP and NRP, respectively). Enrichment analysis of differentially expressed proteins revealed alterations in endometrial remodeling, substance metabolism (mainly lipid, nitrogen, and retinol metabolism), immunological modulation, and insulin signaling in LRP sows. Importantly, aberrant lipid metabolite accumulation and dysregulation of insulin signaling were coincidently confirmed in endometria of LPR sows, proving an impaired insulin sensitivity. Furthermore, established high-fat diet- (HFD-) induced insulin-resistant mouse models revealed that uterine insulin resistance beginning before pregnancy deteriorated uterine receptivity and decreased implantation sites and fetal numbers. Mitochondrial biogenesis and fusion were decreased, and reactive oxygen species was overproduced in uteri from the HFD group during the implantation period. Ishikawa and JAR cells directly demonstrated that oxidative stress compromised implantation in vitro. Conclusions. This study demonstrated that uterine insulin sensitivity impairment beginning before pregnancy resulted in implantation and fetal loss associated with oxidative stress induced by mitochondrial dysfunction