Clinical and Epidemiological Factors Associated with Methicillin Resistance in Community-Onset Invasive Staphylococcus aureus Infections: Prospective Multicenter Cross-Sectional Study in Korea

Successful empirical therapy of Staphylococcus aureus infections requires the ability to predict methicillin resistance. Our aim was to identify predictors of methicillin resistance in community-onset (CO) invasive S. aureus infections. Sixteen hospitals across Korea participated in this study from May to December 2012. We prospectively included cases of S. aureus infection in which S. aureus was isolated from sterile clinical specimens ≤72 hours after hospitalization. Clinical and epidemiological data were gathered and compared in methicillin-resistant S. aureus (MRSA) and methicillin-susceptible S. aureus (MSSA) cases. Community-associated (CA) infections were defined as in previous studies. In total, there were 786 cases of community-onset S. aureus infection, 102 (13.0%) of which were CA-MRSA. In addition to known risk factors, exposure to 3rd generation cephalosporins in the past 6 months [odds ratio (OR), 1.922; 95% confidence interval (CI), 1.176–3.142] and close contact with chronically ill patients in the past month (OR, 2.647; 95% CI, 1.189–5.891) were independent risk factors for MRSA infection. However, no clinical predictors of CA-MRSA were identified. Methicillin resistance, CO infection, and appropriateness of empirical antibiotics were not significantly related to 30-day mortality. MRSA infection should be suspected in patients recently exposed to 3rd generation cephalosporins or chronically-ill patients. There were no reliable predictors of CA-MRSA infection, and mortality was not affected by methicillin resistance.     

Clinic Network Collaboration and Patient Tracing to Maximize Retention in HIV Care

BackgroundUnderstanding retention and loss to follow up in HIV care, in particular the number of people with unknown outcomes, is critical to maximise the benefits of antiretroviral therapy. Individual-level data are not available for these outcomes in Australia, which has an HIV epidemic predominantly focused amongst men who have sex with men.ConclusionsThe network demonstrated low numbers of people with unknown outcomes and high levels of retention in care. Increased levels of retention in care and reductions in unknown outcomes identified after the intervention largely reflected confirmation of clinic transfers while a smaller number were successfully re-engaged in care. Factors associated with disengagement from care were identified. Systems to monitor patient retention, care transfer and minimize disengagement will maximise individual and population-level outcomes for populations with HIV.     

The V471A Polymorphism in Autophagy-Related Gene ATG7 Modifies Age at Onset Specifically in Italian Huntington Disease Patients

The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis.     

Sex Differences in Colorectal Cancer Survival: Population-Based Analysis of 164,996 Colorectal Cancer Patients in Germany

Risk of colorectal cancer (CRC) is considerably higher in men compared to women; however, there is inconclusive evidence of sex differences in CRC prognosis. We aimed to assess and explain sex differences in 5-year relative survival using standard and model-based period analysis among 164,996 patients diagnosed with CRC from 1997 to 2006 and reported to 11 German cancer registries covering a population of 33 million inhabitants. Age-adjusted 5-year relative survival was higher in women (64.5% vs. 61.9%, P<0.0001). A substantial survival advantage of women was confirmed in multivariate analysis after adjusting for CRC stage and subsite in subjects under 65 years of age (relative excess risk, RER 0.86, 95% CI 0.82–0.90), but not in older subjects (RER 1.01, 95% CI 0.98–1.04); this pattern was similar in the 1st and in the 2nd to 5th year after diagnosis. The survival advantage of women varied by CRC stage and age and was most pronounced for localized disease (RERs 0.59–0.88 in various age subgroups) and in patients under 45 years of age (RERs 0.59, 0.72 and 0.76 in patients with localized, regional or advanced disease, respectively). On the contrary, sex differences in survival did not vary by location of CRC. In conclusion, our large population-based study confirmed a survival advantage of female compared to male CRC patients, most notably in young and middle aged patients and patients with localized disease. The effect of sex hormones, either endogenous or through hormonal replacement therapy, might be the most plausible explanation for the observed patterns.     

Current Status of Alligator sinensis

1IntroductionAlligatorsinensisisakindofvaluablebutrareanimalwhichisdistributedonlyinChi-na.Chinesealligatorsliveinreservoirsandpondsinthehillsidesbetweenthemiddleandup-perreachesoftheYangtzeRiver.Historically,thedistributionareaoftheChinesealligatorsreached34.5millionhectaresandthenumberreachedthelevelofbeing"tooeasytogetanddisgust"duringtheWesternHanDynasty(206B.C.-24A.D.).Withtheinterruptionofhumanactivities,thedistributionareaofA.sinensisisdecreasingcontinuouslyandthenumberisreducinggr…     

Fetal Liver Blood Flow Distribution: Role in Human Developmental Strategy to Prioritize Fat Deposition versus Brain Development

Among primates, human neonates have the largest brains but also the highest proportion of body fat. If placental nutrient supply is limited, the fetus faces a dilemma: should resources be allocated to brain growth, or to fat deposition for use as a potential postnatal energy reserve? We hypothesised that resolving this dilemma operates at the level of umbilical blood distribution entering the fetal liver. In 381 uncomplicated pregnancies in third trimester, we measured blood flow perfusing the fetal liver, or bypassing it via the ductus venosus to supply the brain and heart using ultrasound techniques. Across the range of fetal growth and independent of the mother''s adiposity and parity, greater liver blood flow was associated with greater offspring fat mass measured by dual-energy X-ray absorptiometry, both in the infant at birth (r = 0.43, P<0.001) and at age 4 years (r = 0.16, P = 0.02). In contrast, smaller placentas less able to meet fetal demand for essential nutrients were associated with a brain-sparing flow pattern (r = 0.17, p = 0.02). This flow pattern was also associated with a higher degree of shunting through ductus venosus (P = 0.04). We propose that humans evolved a developmental strategy to prioritize nutrient allocation for prenatal fat deposition when the supply of conditionally essential nutrients requiring hepatic inter-conversion is limited, switching resource allocation to favour the brain if the supply of essential nutrients is limited. Facilitated placental transfer mechanisms for glucose and other nutrients evolved in environments less affluent than those now prevalent in developed populations, and we propose that in circumstances of maternal adiposity and nutrient excess these mechanisms now also lead to prenatal fat deposition. Prenatal developmental influences play important roles in the human propensity to deposit fat.