Improvements to water purification and sanitation infrastructure may reduce the diarrheal burden in a marginalized and flood prone population in remote Nicaragua

<p>Abstract</p> <p>Background</p> <p>The isolated northern region of Nicaragua has one of the highest rates of diarrheal disease in Central America. Political and environmental hardships faced by inhabitants of this region are contributing factors to this health inequity. The aim of this study was to assess the relationship between water and latrine infrastructure and the prevalence of diarrhea in this region.</p> <p>Methods</p> <p>A population-based, cross-sectional survey of women of reproductive age was conducted in the Sahsa region of northern Nicaragua in July, 2009. Households were selected by two stage cluster sampling methodology. A questionnaire was administered in Spanish and Miskito with assessment of household and socioeconomic conditions, sanitation practices, and health care access. Diarrhea prevalence differences at the household level over a two week reporting period were estimated with a standardized instrument which included assessment of water treatment and latrine use and maintenance.</p> <p>Results</p> <p>There were 189 women enrolled in the current study. The use of water purification methods, such as chlorine and filters, and latrine ownership were not associated with reduced prevalence of household diarrhea in the two week reporting period. Latrine overflow, however, was associated with an increased prevalence of diarrhea during the same two week period [adjusted prevalence difference and 95% CI: 0.19 (0.03, 0.36)].</p> <p>Conclusions</p> <p>Simple, low cost interventions that improve water and latrine infrastructure may reduce the prevalence of diarrheal disease in the isolated regions of Nicaragua and Central America.</p

Avoidable mortality attributable to anthropogenic fine particulate matter (Pm2.5) in Australia

Ambient fine particulate matter 2.5) air pollution increases premature mortalityglobally. Some PM2.5 is natural, but anthropogenic PM2.5 is comparatively avoidable. We determinedthe impact of long-term exposures to the anthropogenic PM component on mortality in Australia.PM2.5-attributable deaths were calculated for all Australian Statistical Area 2 (SA2; n = 2310) regions.All-cause death rates from Australian mortality and population databases were combined withannual anthropogenic PM2.5 exposures for the years 2006–2016. Relative risk estimates were derivedfrom the literature. Population-weighted average PM2.5 concentrations were estimated in eachSA2 using a satellite and land use regression model for Australia. PM2.5-attributable mortality wascalculated using a health-impact assessment methodology with life tables and all-cause death rates.The changes in life expectancy (LE) from birth, years of life lost (YLL), and economic cost of lostlife years were calculated using the 2019 value of a statistical life. Nationally, long-term populationweighted average total and anthropogenic PM2.5 concentrations were 6.5 µg/m3(min 1.2–max 14.2)and 3.2 µg/m3(min 0–max 9.5), respectively. Annually, anthropogenic PM2.5-pollution is associatedwith 2616 (95% confidence intervals 1712, 3455) deaths, corresponding to a 0.2-year (95% CI 0.14, 0.28)reduction in LE for children aged 0–4 years, 38,962 (95%CI 25,391, 51,669) YLL and an average annualeconomic burden of $6.2 billion (95$4.0 billion, $8.1 billion). We conclude that the anthropogenicPM2.5-related costs of mortality in Australia are higher than community standards should allow,and reductions in emissions are recommended to achieve avoidable mortality

The Myeloid Receptor PILRβ Mediates the Balance of Inflammatory Responses through Regulation of IL-27 Production

Paired immunoglobulin-like receptors beta, PILRβ, and alpha, PILRα, are related to the Siglec family of receptors and are expressed primarily on cells of the myeloid lineage. PILRβ is a DAP12 binding partner expressed on both human and mouse myeloid cells. The potential ligand, CD99, is found on many cell types, such as epithelial cells where it plays a role in migration of immune cells to sites of inflammation. Pilrb deficient mice were challenged with the parasite Toxoplasma gondii in two different models of infection induced inflammation; one involving the establishment of chronic encephalitis and a second mimicking inflammatory bowel disease in order to understand the potential role of this receptor in persistent inflammatory responses. It was found that in the absence of activating signals from PILRβ, antigen-presenting cells (APCs) produced increased amounts of IL-27, p28 and promoted IL-10 production in effector T cells. The sustained production of IL-27 led ultimately to enhanced survival after challenge due to dampened immune pathology in the gut. Similar protection was also observed in the CNS during chronic T. gondii infection after i.p. challenge again providing evidence that PILRβ is important for regulating aberrant inflammatory responses

Fine root chemistry and decomposition in model communities of north-temperate tree species show little response to elevated atmospheric CO 2 and varying soil resource availability

Rising atmospheric [CO 2 ] has the potential to alter soil carbon (C) cycling by increasing the content of recalcitrant constituents in plant litter, thereby decreasing rates of decomposition. Because fine root turnover constitutes a large fraction of annual NPP, changes in fine root decomposition are especially important. These responses will likely be affected by soil resource availability and the life history characteristics of the dominant tree species. We evaluated the effects of elevated atmospheric [CO 2 ] and soil resource availability on the production and chemistry, mycorrhizal colonization, and decomposition of fine roots in an early- and late-successional tree species that are economically and ecologically important in north temperate forests. Open-top chambers were used to expose young trembling aspen ( Populus tremuloides ) and sugar maple ( Acer saccharum ) trees to ambient (36 Pa) and elevated (56 Pa) atmospheric CO 2 . Soil resource availability was composed of two treatments that bracketed the range found in the Upper Lake States, USA. After 2.5 years of growth, sugar maple had greater fine root standing crop due to relatively greater allocation to fine roots (30% of total root biomass) relative to aspen (7% total root biomass). Relative to the low soil resources treatment, aspen fine root biomass increased 76% with increased soil resource availability, but only under elevated [CO 2 ]. Sugar maple fine root biomass increased 26% with increased soil resource availability (relative to the low soil resources treatment), and showed little response to elevated [CO 2 ]. Concentrations of N and soluble phenolics, and C/N ratio in roots were similar for the two species, but aspen had slightly higher lignin and lower condensed tannins contents compared to sugar maple. As predicted by source-sink models of carbon allocation, pooled constituents (C/N ratio, soluble phenolics) increased in response to increased relative carbon availability (elevated [CO 2 ]/low soil resource availability), however, biosynthetically distinct compounds (lignin, starch, condensed tannins) did not always respond as predicted. We found that mycorrhizal colonization of fine roots was not strongly affected by atmospheric [CO 2 ] or soil resource availability, as indicated by root ergosterol contents. Overall, absolute changes in root chemical composition in response to increases in C and soil resource availability were small and had no effect on soil fungal biomass or specific rates of fine root decomposition. We conclude that root contributions to soil carbon cycling will mainly be influenced by fine root production and turnover responses to rising atmospheric [CO 2 ], rather than changes in substrate chemistry.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47710/1/442_2005_Article_191.pd

Smoking, Alcohol, Diabetes, Obesity, Socioeconomic Status, and the Risk of Colorectal Cancer in a Population-Based Case–Control Study

Purpose: Although previous research has identified factors that may determine willingness to participate in research, relatively few studies have attempted to quantify the impact non-participation may have on exposure–disease associations. The aims of this study were to (a) investigate the associations between smoking, alcohol, diabetes, obesity, and socioeconomic status and the risk of colorectal cancer in a case–control study (59.7 and 47.2 % response fractions among cases and controls, respectively); and (b) perform sensitivity analyses to examine the possible influence of non-participation. Methods: Logistic regression was used to estimate the exposure–disease associations. We then investigated the associations between various demographic and health factors and the likelihood that an individual would participate in the case–control study and then performed two sensitivity analyses (sampling weights and multiple imputation) to examine whether non-participation bias may have influenced the exposure–disease associations. Results: The exposures alcohol, smoking, and diabetes were associated with an increased risk of colorectal cancer. We found some differences between cases and controls when examining the factors associated with the participation in the study, and in the sensitivity analyses, the exposure–disease associations were slightly attenuated when compared with those from the original analysis. Conclusion: Non-participation may have biased the risk estimates away from the null, but generally not enough to change the conclusions of the study

Effects of multidisciplinary teamwork on lead times and patient flow in the emergency department: A longitudinal interventional cohort study

BACKGROUND Long waiting times for emergency care are claimed to be caused by overcrowded emergency departments and non-effective working routines. Teamwork has been suggested as a promising solution to these issues. The aim of the present study was to investigate the effects of teamwork in a Swedish emergency department on lead times and patient flow. METHODS The study was set in an emergency department of a university hospital where teamwork, a multi-professional team responsible for the whole care process for a group of patients, was introduced. The study has a longitudinal non-randomized intervention study design. Data were collected for five two-week periods during a period of 1.5 years. The first part of the data collection used an ABAB design whereby standard procedure (A) was altered weekly with teamwork (B). Then, three follow-ups were conducted. At last follow-up, teamwork was permanently implemented. The outcome measures were: number of patients handled within teamwork time, time to physician, total visit time and number of patients handled within the 4-hour target. RESULTS A total of 1,838 patient visits were studied. The effect on lead times was only evident at the last follow-up. Findings showed that the number of patients handled within teamwork time was almost equal between the different study periods. At the last follow-up, the median time to physician was significantly decreased by 11 minutes (p = 0.0005) compared to the control phase and the total visit time was significantly shorter at last follow-up compared to control phase (p = <0.0001; 39 minutes shorter on average). Finally, the 4-hour target was met in 71% in the last follow-up compared to 59% in the control phase (p = 0.0005). CONCLUSIONS Teamwork seems to contribute to the quality improvement of emergency care in terms of small but significant decreases in lead times. However, although efficient work processes such as teamwork are necessary to ensure safe patient care, it is likely not sufficient for bringing about larger decreases in lead times or for meeting the 4-hour target in the emergency department.Åsa Muntlin Athlin, Ulrica von Thiele Schwarz and Nasim Farrohkni

Reactive oxygen species in phagocytic leukocytes

Phagocytic leukocytes consume oxygen and generate reactive oxygen species in response to appropriate stimuli. The phagocyte NADPH oxidase, a multiprotein complex, existing in the dissociated state in resting cells becomes assembled into the functional oxidase complex upon stimulation and then generates superoxide anions. Biochemical aspects of the NADPH oxidase are briefly discussed in this review; however, the major focus relates to the contributions of various modes of microscopy to our understanding of the NADPH oxidase and the cell biology of phagocytic leukocytes

Full-Exon Resequencing Reveals Toll-Like Receptor Variants Contribute to Human Susceptibility to Tuberculosis Disease

Tuberculosis (TB) is the leading cause of death worldwide due to an infectious agent. Data have accumulated over decades suggesting that variability in human susceptibility to TB disease has a genetic component. Toll-like receptors (TLRs) play a critical role in initiating the innate immune response to many pathogens in mouse models, but little is known about their role in human infections. Human TLRs have been reported to recognize mycobacterial antigens and initiate an immune response. We tested the hypothesis that amino acid-altering polymorphisms in five TLRs were associated with susceptibility to TB disease using a population-based case-control study with 1,312 adult TB patients and controls. Full-coding region sequencing of the five TLR genes in all 1,312 subjects yielded a data set in excess of 16 Mb. Rare nonsynonymous polymorphisms in TLR6-TLR1-TLR10 were significantly overrepresented among African-American TB cases compared with ethnically-matched control subjects. Common nonsynonymous polymorphisms in TLR6-TLR1-TLR10 also were significantly associated with TB disease in certain ethnic groups. Among African Americans, homozygotes for the common-variant haplotype TLR1-248S, TLR1-602I, and TLR6-249S had a significantly increased TB disease risk. A transmission/disequilibrium test on an independent sample found that the TLR1-248S variant was preferentially transmitted to diseased children, thereby confirming disease association. These results are consistent with recent reports implicating TLR1 variants, including TLR1-602, in significantly altered innate immune responses. Also consistent with disease association, rare TLR6 variants were defective in their ability to mediate NF-κB signal transduction in transfected human cells. Taken together, the data suggest that variant TLRs contribute to human susceptibility to TB disease. Extensive full-exon resequencing was critical for revealing new information about the role of TLRs in human-pathogen interactions and the genetic basis of innate immune function