Monitoring and prevalence rates of metabolic syndrome in military veterans with serious mental illness

Background: Cardiovascular disease is the leading cause of mortality among patients with serious mental illness (SMI) and the prevalence of metabolic syndrome-a constellation of cardiovascular risk factors-is significantly higher in these patients than in the general population. Metabolic monitoring among patients using second generation antipsychotics (SGAs)-a risk factor for metabolic syndrome-has been shown to be inadequate despite the release of several guidelines. However, patients with SMI have several factors independent of medication use that predispose them to a higher prevalence of metabolic syndrome. Our study therefore examines monitoring and prevalence of metabolic syndrome in patients with SMI, including those not using SGAs. Methods and Findings: We retrospectively identified all patients treated at a Veterans Affairs Medical Center with diagnoses of schizophrenia, schizoaffective disorder or bipolar disorder during 2005-2006 and obtained demographic and clinical data. Incomplete monitoring of metabolic syndrome was defined as being unable to determine the status of at least one of the syndrome components. Of the 1,401 patients included (bipolar disorder: 822; schizophrenia: 222; and schizoaffective disorder: 357), 21.4% were incompletely monitored. Only 54.8% of patients who were not prescribed SGAs and did not have previous diagnoses of hypertension or hypercholesterolemia were monitored for all metabolic syndrome components compared to 92.4% of patients who had all three of these characteristics. Among patients monitored for metabolic syndrome completely, age-adjusted prevalence of the syndrome was 48.4%, with no significant difference between the three psychiatric groups. Conclusions: Only one half of patients with SMI not using SGAs or previously diagnosed with hypertension and hypercholesterolemia were completely monitored for metabolic syndrome components compared to greater than 90% of those with these characteristics. With the high prevalence of metabolic syndrome seen in this population, there appears to be a need to intensify efforts to reduce this monitoring gap

Parallel assessment of male reproductive function in workers and wild rats exposed to pesticides in banana plantations in Guadeloupe

<p>Abstract</p> <p>Background</p> <p>There is increasing evidence that reproductive abnormalities are increasing in frequency in both human population and among wild fauna. This increase is probably related to exposure to toxic contaminants in the environment. The use of sentinel species to raise alarms relating to human reproductive health has been strongly recommended. However, no simultaneous studies at the same site have been carried out in recent decades to evaluate the utility of wild animals for monitoring human reproductive disorders. We carried out a joint study in Guadeloupe assessing the reproductive function of workers exposed to pesticides in banana plantations and of male wild rats living in these plantations.</p> <p>Methods</p> <p>A cross-sectional study was performed to assess semen quality and reproductive hormones in banana workers and in men working in non-agricultural sectors. These reproductive parameters were also assessed in wild rats captured in the plantations and were compared with those in rats from areas not directly polluted by humans.</p> <p>Results</p> <p>No significant difference in sperm characteristics and/or hormones was found between workers exposed and not exposed to pesticide. By contrast, rats captured in the banana plantations had lower testosterone levels and gonadosomatic indices than control rats.</p> <p>Conclusion</p> <p>Wild rats seem to be more sensitive than humans to the effects of pesticide exposure on reproductive health. We conclude that the concept of sentinel species must be carefully validated as the actual nature of exposure may varies between human and wild species as well as the vulnerable time period of exposure and various ecological factors.</p

Frequency of human immunodeficiency virus (HIV) testing in urban vs. rural areas of the United States: Results from a nationally-representative sample

<p>Abstract</p> <p>Background</p> <p>Studies in the United States show that rural persons with HIV are more likely than their urban counterparts to be diagnosed at a late stage of infection, suggesting missed opportunities for HIV testing in rural areas. To inform discussion of HIV testing policies in rural areas, we generated nationally representative, population-based estimates of HIV testing frequencies in urban vs. rural areas of the United States.</p> <p>Methods</p> <p>Secondary analysis of 2005 and 2009 Behavioral Risk Factor Surveillance System (BRFSS) data. Dependent variables were self-reported lifetime and past-year HIV testing. Urban vs. rural residence was determined using the metropolitan area framework and Urban Influence Codes and was categorized as 1) metropolitan, center city (the most urban); 2) metropolitan, other; 3) non-metropolitan, adjacent to metropolitan; 4) non-metropolitan, micropolitan; and 4) remote, non-metropolitan (the most rural).</p> <p>Results</p> <p>The 2005 sample included 257,895 respondents. Lifetime HIV testing frequencies ranged from 43.6% among persons residing in the most urban areas to 32.2% among persons in the most rural areas (P < 0.001). Past-year testing frequencies ranged from 13.5% to 7.3% in these groups (P < 0.001). After adjusting for demographics (age, sex, race/ethnicity, and region of residence) and self-reported HIV risk factors, persons in the most remote rural areas were substantially less likely than persons in the most urban areas to report HIV testing in the past year (odds ratio 0.65, 95% CI 0.57-0.75). Testing rates in urban and rural areas did not change substantively following the 2006 Centers for Disease Control and Prevention recommendation for routine, population-based HIV testing in healthcare settings. In metropolitan (urban) areas, 11.5% (95% CI 11.2-11.8) reported past-year HIV testing in 2005 vs. 11.4% (95% CI 11.1%-11.7%) in 2009 (P = 0.93). In non-metropolitan areas, 8.7% (95% CI 8.2%-9.2%) were tested in 2005 vs. 7.7% (95% CI 7.2%-8.2%) in 2009 (P = 0.03).</p> <p>Conclusions</p> <p>Rural persons are less likely than urban to report prior HIV testing, which may contribute to later HIV diagnosis in rural areas. There is need to consider strategies to increase HIV testing in rural areas.</p

Mechanical compression attenuates normal human bronchial epithelial wound healing

Background: Airway narrowing associated with chronic asthma results in the transmission of injurious compressive forces to the bronchial epithelium and promotes the release of pro-inflammatory mediators and the denudation of the bronchial epithelium. While the individual effects of compression or denudation are well characterized, there is no data to elucidate how these cells respond to the application of mechanical compression in the presence of a compromised epithelial layer. Methods: Accordingly, differentiated normal human bronchial epithelial cells were exposed to one of four conditions: 1) unperturbed control cells, 2) single scrape wound only, 3) static compression (6 hours of 30 cmH(2)O), and 4) 6 hours of static compression after a scrape wound. Following treatment, wound closure rate was recorded, media was assayed for mediator content and the cytoskeletal network was fluorescently labeled. Results: We found that mechanical compression and scrape injury increase TGF-beta 2 and endothelin-1 secretion, while EGF content in the media is attenuated with both injury modes. The application of compression after a pre-existing scrape wound augmented these observations, and also decreased PGE(2) media content. Compression stimulated depolymerization of the actin cytoskeleton and significantly attenuated wound healing. Closure rate was partially restored with the addition of exogenous PGE(2), but not EGF. Conclusion: Our results suggest that mechanical compression reduces the capacity of the bronchial epithelium to close wounds, and is, in part, mediated by PGE(2) and a compromised cytoskeleton

The Effects of Overexpression of Histamine Releasing Factor (HRF) in a Transgenic Mouse Model

Asthma is a disease that affects all ages, races and ethnic groups. Its incidence is increasing both in Westernized countries and underdeveloped countries. It involves inflammation, genetics and environment and therefore, proteins that exacerbate the asthmatic, allergic phenotype are important. Our laboratory purified and cloned a histamine releasing factor (HRF) that was a complete stimulus for histamine and IL-4 secretion from a subpopulation of allergic donors' basophils. Throughout the course of studying HRF, it was uncovered that HRF enhances or primes histamine release and IL-13 production from all anti-IgE antibody stimulated basophils. In order to further delineate the biology of HRF, we generated a mouse model.We constructed an inducible transgenic mouse model with HRF targeted to lung epithelial cells, via the Clara cells. In antigen naïve mice, overproduction of HRF yielded increases in BAL macrophages and statistical increases in mRNA levels for MCP-1 in the HRF transgenic mice compared to littermate controls. In addition to demonstrating intracellular HRF in the lung epithelial cells, we have also been able to document HRF's presence extracellularly in the BAL fluid of these transgenic mice. Furthermore, in the OVA challenged model, we show that HRF exacerbates the allergic, asthmatic responses. We found statistically significant increases in serum and BAL IgE, IL-4 protein and eosinophils in transgenic mice compared to controls.This mouse model demonstrates that HRF expression enhances allergic, asthmatic inflammation and can now be used as a tool to further dissect the biology of HRF

The p.V37I Exclusive Genotype Of GJB2: A Genetic Risk-Indicator of Postnatal Permanent Childhood Hearing Impairment

Postnatal permanent childhood hearing impairment (PCHI) is frequent (0.25%–0.99%) and difficult to detect in the early stage, which may impede the speech, language and cognitive development of affected children. Genetic tests of common variants associated with postnatal PCHI in newborns may provide an efficient way to identify those at risk. In this study, we detected a strong association of the p.V37I exclusive genotype of GJB2 with postnatal PCHI in Chinese Hans (P = 1.4×10−10; OR 62.92, 95% CI 21.27–186.12). This common genotype in Eastern Asians was present in a substantial percentage (20%) of postnatal PCHI subjects, and its prevalence was significantly increased in normal-hearing newborns who failed at least one newborn hearing screen. Our results indicated that the p.V37I exclusive genotype of GJB2 may cause subclinical hearing impairment at birth and increases risk for postnatal PCHI. Genetic testing of GJB2 in East Asian newborns will facilitate prompt detection and intervention of postnatal PCHI

Could albumin level explain the higher mortality in hemodialysis patients with pulmonary hypertension?

BACKGROUND: The pathogenesis of pulmonary hypertension (PH) in hemodialysis is still unclear. The aim of this study was to identify the risk factors associated with the presence of PH in chronic hemodialysis patients and to verify whether these factors might explain the highest mortality among them. METHODS: We conducted a retrospective study of hemodialysis patients who started treatment from August 2001 to October 2007 and were followed up until April 2011 in a Brazilian referral medical school. According to the results of echocardiography examination, patients were allocated in two groups: those with PH and those without PH. Clinical parameters, site and type of vascular access, bioimpedance, and laboratorial findings were compared between the groups and a logistic regression model was elaborated. Actuarial survival curves were constructed and hazard risk to death was evaluated by Cox regression analysis. RESULTS: PH > 35 mmHg was found in 23 (30.6%) of the 75 patients studied. The groups differed in extracellular water, ventricular thickness, left atrium diameter, and ventricular filling. In a univariate analysis, extracellular water was associated with PH (relative risk = 1.194; 95% CI of 1.006 – 1.416; p = 0.042); nevertheless, in a multiple model, only left atrium enlargement was independently associated with PH (relative risk =1.172; 95% CI of 1.010 – 1.359; p = 0.036). PH (hazard risk = 3.008; 95% CI of 1.285 – 7.043; p = 0.011) and age (hazard risk of 1.034 per year of age; 95% CI of 1.000 – 7.068; p = 0.047) were significantly associated with mortality in a multiple Cox regression analysis. However, when albumin was taken in account the only statistically significant association was between albumin level and mortality (hazard risk = 0.342 per g/dL; 95% CI of 0.119 – 0.984; p = 0.047) while the presence of PH lost its statistical significance (p = 0.184). Mortality was higher in patients with PH (47.8% vs 25%) who also had a statistically worse survival after the sixth year of follow up. CONCLUSIONS: PH in hemodialysis patients is associated with parameters of volume overload that sheds light on its pathophysiology. Mortality is higher in hemodialysis patients with PH and the low albumin level can explain this association

Understory Bird Communities in Amazonian Rainforest Fragments: Species Turnover through 25 Years Post-Isolation in Recovering Landscapes

Inferences about species loss following habitat conversion are typically drawn from short-term surveys, which cannot reconstruct long-term temporal dynamics of extinction and colonization. A long-term view can be critical, however, to determine the stability of communities within fragments. Likewise, landscape dynamics must be considered, as second growth structure and overall forest cover contribute to processes in fragments. Here we examine bird communities in 11 Amazonian rainforest fragments of 1–100 ha, beginning before the fragments were isolated in the 1980s, and continuing through 2007. Using a method that accounts for imperfect detection, we estimated extinction and colonization based on standardized mist-net surveys within discreet time intervals (1–2 preisolation samples and 4–5 post-isolation samples). Between preisolation and 2007, all fragments lost species in an area-dependent fashion, with loss of as few as <10% of preisolation species from 100-ha fragments, but up to 70% in 1-ha fragments. Analysis of individual time intervals revealed that the 2007 result was not due to gradual species loss beginning at isolation; both extinction and colonization occurred in every time interval. In the last two samples, 2000 and 2007, extinction and colonization were approximately balanced. Further, 97 of 101 species netted before isolation were detected in at least one fragment in 2007. Although a small subset of species is extremely vulnerable to fragmentation, and predictably goes extinct in fragments, developing second growth in the matrix around fragments encourages recolonization in our landscapes. Species richness in these fragments now reflects local turnover, not long-term attrition of species. We expect that similar processes could be operating in other fragmented systems that show unexpectedly low extinction