Background/Objectives:To investigate the effect of folate status on cervical intraepithelial neoplasia (CIN) progression and its relationship with high-risk human papillomavirus (hrHPV).Subjects/Methods:We evaluated 20 000 sexually active women aged <65 years in Yangqu County by using a questionnaire; the subjects were also screened using the ThinPrep cytologic test (TCT). Patients with abnormal TCT results (other than glandular cell abnormalities) who were willing to provide informed consent were further diagnosed using colposcopy and histopathological examination. We investigated 247 cases of low-grade cervical squamous intraepithelial lesions (LSIL), 125 cases of high-grade cervical squamous intraepithelial lesions (HSIL) and 877 controls. A 24-item food frequency questionnaire was filled out by the investigator to estimate the consumption of dietary folate. Positivity for hrHPV from residual exfoliated cervical cells was tested; serum folate was also measured.Results:The hrHPV infection rate in HSIL patients (77.6%) was higher than that in LSIL (33.2%) and control (32.0%) patients. Dietary folate intakes in controls, LSIL and HSIL were 306.9±176.6, 321.8±168.0 and 314.7±193.8 μg/kcal, respectively. The levels of serum folate in controls, LSIL and HSIL were 18.2±7.9, 15.9±7.1 and 14.3±7.5 nmol/l, respectively. Increased CIN correlated with higher rates of hrHPV infection and lower levels of serum folate.Conclusions:Low levels of serum folate may increase the risk of CIN progression. Furthermore, potential synergy may exist between low serum folate levels and hrHPV infection to promote CIN development.

Cardiomyocyte death is one major factor in the development of heart dysfunction, thus, understanding its mechanism may help with the prevention and treatment of this disease. Previously, we reported that anti-β1-adrenergic receptor autoantibodies (β1-AABs) decreased myocardial autophagy, but the role of these in cardiac function and cardiomyocyte death is unclear. We report that rapamycin, an mTOR inhibitor, restored cardiac function in a passively β1-AAB-immunized rat model with decreased cardiac function and myocardial autophagic flux. Next, after upregulating or inhibiting autophagy with Beclin-1 overexpression/rapamycin or RNA interference (RNAi)-mediated expression of Beclin-1/3-methyladenine, β1-AAB-induced autophagy was an initial protective stress response before apoptosis. Then, decreased autophagy contributed to cardiomyocyte death followed by decreases in cardiac function. In conclusion, proper regulation of autophagy may be important for treating patients with β1-AAB-positive heart dysfunction.

Bacterial vaginosis (BV) is the most-common cause of abnormal vaginal discharge among women of reproductive age, though many are asymptomatic. It is caused by the replacement of normal vaginal Lactobacillus with Gram-negative and anaerobic organisms. BV has assumed increasing public health importance through associations with numerous adverse outcomes in both gravid and non-gravid women. Risk factors for BV include smoking, non-White race, prior BV, current other sexually transmitted diseases (STDs), inserting items in the vagina (e.g., sex, douching), and menses. Symptomatic BV has been associated with pelvic inflammatory disease (PID), miscarriage, premature rupture of membranes, chorioamnionitis, premature labor and delivery, postpartum endometritis, and post-hysterectomy vaginal cuff cellulitis. Anaerobic Gram-negative rods common to BV have also been independently associated with endometritis or PID, even in the absence of clinical BV. BV has also been independently associated with an increased risk of acquiring STDs, including acquiring and transmitting HIV. BV is not an STD, though recent sexual intercourse and multiple sexpartners are risk factors. BV causes a malodorous, white or gray vaginal discharge and is diagnosed through Amsel’s criteria. Treatment with metronidazole or clindamycin is important for symptom relief and to prevent adverse obstetric consequences, particularly among high-risk women who have had a previous preterm delivery or have a pre-pregnancy weight <50 kg.