Sexually transmitted infections among male highway coach drivers in Myanmar.

A cross sectional descriptive study was conducted from February 2008 to December 2009 at the largest Highway Terminal, Yangon, Myanmar to determine the prevalence of curable STIs (syphilis, gonorrhea, chlamydial infections, and trichomoniasis), to find out the associated factors for STIs, and to determine the antibiotic susceptibility pattern of gonococcal infection among highway drivers. Urine and blood specimens were collected from 601 male highway coach drivers after an interview about their behavior. Standard laboratory tests were carried out to detect STIs. Multivariate analysis was used to ascertain potential risk factors for STIs. The prevalence rates of syphilis, gonorrhea, chlamydial infections, and trichomoniasis were 4.8, 4.3, 5.7, and 9.8%, respectively. One hundred and two (17.0%) were infected with at least one of the tested four STIs, and 34 (5.7%) had STI co-infections (2STIs). Those who had multiple sexual contacts were likely to be infected with at least one STI, and those who had a history of inconsistent condom use within past two weeks and multiple sexual contacts were more likely to have STI co-infections (p < 0.05). Antimicrobial susceptibility of 21 Neisseria gonorrhoeae isolates showed that 85.7% were susceptible to azithromycin, 80.9% to spectinomycin, 66.7% to cefixime, 61.9% to ceftriaxone, and 38.1% to ciprofloxacin. The high prevalence of STIs in this study and the decreased susceptibility of Neisseria gonorrhoeae to cephalosporin and fluoroquinolone highlighted the role of periodic screening in early diagnosis and effective treatment of STIs among high-risk populations.

Autophagy participants in the dedifferentiation of mouse 3T3-L1 adipocytes triggered by hypofunction of insulin signaling.

Our previous data indicate that both insulin and IGF-1 signallings dysfunction promotes the dedifferentiation of primary human and mouse white adipocytes. Based on the fact that insulin activates mTOR and inhibits autophagy, and autophagy deficiency can inhibit the differentiation of white adipocytes, we speculate that autophagy may be related to the dedifferentiation of white adipocytes. We investigated the underlying mechanism of autophagy during dedifferentiation of mouse 3T3-L1 adipocytes. After incomplete inhibition of insulin and IGF-1 signallings, 3T3-L1 adipocytes manifest dedifferentiation accompanied with an increase of autophagy level. If induction only of autophagy in the adipocytes, then the cells also occur somewhat dedifferentiation, and with a slight decrease of insulin signal, while its degree was weaker than insulin signal inhibited cells. Notably, after inhibition of the insulin and IGF-1 signallings and simultaneously inducing autophagy, the dedifferentiation of 3T3-L1 adipocytes was the most obvious compared with other groups, and the insulin and IGF-1 signallings decreases was greater than the cells with inhibition only of insulin signalling. If inhibition of both insulin signal and autophagy simultaneously, the dedifferentiation of the adipocytes reveals similar tendencies to the cells that insulin signal was inhibited. No significant dedifferentiation occurs of 3T3-L1 cells if only inhibition of autophagy. Taken all together, in this study, we proved that autophagy is positively related to the dedifferentiation of 3T3-L1 adipocytes and is regulated through the insulin-PI3K-AKT-mTOCR1-autophagy pathway. Autophagy may also has a certain degree of negative feedback affect on the insulin signalling of 3T3-L1 cells. Our work may help to better understand the biological properties of mature adipocytes and may help formulate anti-obesity strategies by regulating insulin and insulin signaling level.