Women with PCO have a unique but poorly characterized disorder of insulin action. Obese (n = 16) and nonobese (n = 14) PCO women and age- and weight-matched normal, nondiabetic ovulatory women (obese, n = 15; nonobese, n = 17) had insulin action determined in vivo with sequential multiple insulin dose euglycemic clamps and in isolated abdominal adipocytes to clarify the mechanisms of insulin resistance. PCO resulted in significant increases in the ED50 insulin for glucose utilization in vivo (P < 0.001) and in adipocytes (P < 0.01), without significant changes in adipocyte insulin-binding sites. PCO also resulted in significant decreases in maximal insulin-stimulated rates of glucose utilization in vivo (P < 0.01) and in adipocytes (P < 0.01). Obesity resulted in smaller decreases in insulin sensitivity than PCO (ED50 insulin, P < 0.001 in vivo and P < 0.05 in adipocytes), but greater decreases in insulin responsiveness (Vmax P < 0.001 in vivo and in adipocytes). The ED50 insulin for suppression of HGP was increased only in obese PCO women (P < 0.001), and the interactions between PCO and obesity on this parameter were statistically significant. No significant correlations between androgen or estrogen levels and adipocyte insulin binding or action were found. Because insulin binding was not changed, we conclude that the major lesion causing insulin resistance in PCO is a striking decrease in insulin sensitivity secondary to a defect in the insulin receptor and/or postreceptor signal transduction. PCO also is associated with modest but significant decreases in glucose transport. These defects in insulin action appear to represent intrinsic abnormalities that are independent of obesity, metabolic derangements, body fat topography, and sex hormone levels. Conversely, changes in hepatic insulin sensitivity appear to be acquired with obesity.

Sub-Saharan Africa (SSA) is facing a double burden of disease with a rising prevalence of non-communicable diseases (NCDs) while the burden of communicable diseases (CDs) remains high. Despite these challenges, there remains a significant need to understand how or under what conditions health interventions implemented in sub-Saharan Africa are sustained. The purpose of this study was to conduct a systematic review of empirical literature to explore how health interventions implemented in SSA are sustained. We searched MEDLINE, Biological Abstracts, CINAHL, Embase, PsycInfo, SCIELO, Web of Science, and Google Scholar for available research investigating the sustainability of health interventions implemented in sub-Saharan Africa. We also used narrative synthesis to examine factors whether positive or negative that may influence the sustainability of health interventions in the region. The search identified 1819 citations, and following removal of duplicates and our inclusion/exclusion criteria, only 41 papers were eligible for inclusion in the review. Twenty-six countries were represented in this review, with Kenya and Nigeria having the most representation of available studies examining sustainability. Study dates ranged from 1996 to 2015. Of note, majority of these studies (30 %) were published in 2014. The most common framework utilized was the sustainability framework, which was discussed in four of the studies. Nineteen out of 41 studies (46 %) reported sustainability outcomes focused on communicable diseases, with HIV and AIDS represented in majority of the studies, followed by malaria. Only 21 out of 41 studies had clear definitions of sustainability. Community ownership and mobilization were recognized by many of the reviewed studies as crucial facilitators for intervention sustainability, both early on and after intervention implementation, while social and ecological conditions as well as societal upheavals were barriers that influenced the sustainment of interventions in sub-Saharan Africa. The sustainability of health interventions implemented in sub-Saharan Africa is inevitable given the double burden of diseases, health care worker shortage, weak health systems, and limited resources. We propose a conceptual framework that draws attention to sustainability as a core component of the overall life cycle of interventions implemented in the region.

The trend of e-cigarette use among teens is ever increasing. Here we show the dysbiotic oral microbial ecology in e-cigarette users influencing the local host immune environment compared with non-smoker controls and cigarette smokers. Using 16S rRNA high-throughput sequencing, we evaluated 119 human participants, 40 in each of the three cohorts, and found significantly altered beta-diversity in e-cigarette users (p = 0.006) when compared with never smokers or tobacco cigarette smokers. The abundance of Porphyromonas and Veillonella (p = 0.008) was higher among vapers. Interleukin (IL)-6 and IL-1β were highly elevated in e-cigarette users when compared with non-users. Epithelial cell-exposed e-cigarette aerosols were more susceptible for infection. In vitro infection model of premalignant Leuk-1 and malignant cell lines exposed to e-cigarette aerosol and challenged by Porphyromonas gingivalis and Fusobacterium nucleatum resulted in elevated inflammatory response. Our findings for the first time demonstrate that e-cigarette users are more prone to infection.

Introduction: Electronic cigarette (EC) use is growing dramatically with use highest among young adults and current smokers. One of the most common reasons for using ECs is interest in quitting or reducing cigarettes per day (CPD); however there are few randomized controlled trials (RCT) on the effect of ECs on smoking abstinence and reduction. Methods: We conducted a two-arm; double-blind RCT. Subjects were randomized to receive 3-weeks of either disposable 4.5% nicotine EC (intervention) or placebo EC. The primary outcome was self-reported reduction of at least 50% in the number of CPDs smoked at week 3 (end of treatment) compared to baseline. Study subjects (n = 99) were young adult (21–35), current smokers (smoked ≥ 10 CPDs) living in NYC. Results: Compared with baseline, a significant reduction in CPDs was observed at both study time periods (1 and 3 weeks) for intervention (P < .001) and placebo (P < .001) groups. Between-group analyses showed significantly fewer CPDs in the intervention group compared to the placebo group at week 3 (P = .03), but not at any other follow-up periods. The logistic regression analysis showed that using a greater number of ECs, treatment condition and higher baseline readiness to quit were significantly associated with achieving at least 50% reduction in CPDs at the end of treatment. Conclusion: A diverse young adult sample of current everyday smokers, who were not ready to quit, was able to reduce smoking with the help of ECs. Further study is needed to establish the role of both placebo and nicotine containing ECs in increasing both reduction and subsequent cessation. Implications: Despite the critical need for well-designed clinical trials on the effect of ECs on cessation and cigarette reduction, the majority of studies have been observational or noncomparative intervention designs. Only three RCTs studying ECs as a cessation or reduction intervention have been published, and none were conducted in the United States. The current study adds knowledge to current literature on the feasibility of using ECs to aid smoking reduction among young smokers in US urban populations.

The New York City Clinical Data Research Network (NYC-CDRN), funded by the Patient-Centered Outcomes Research Institute (PCORI), brings together 22 or