Self-reported illness and household strategies for coping with health-care payments in Bangladesh

Objective

To investigate self-reported illness and household strategies for coping with payments for health care in a city in Bangladesh.

Methods

A cluster-sampled probability survey of 1593 households in the city of Rajshahi, Bangladesh, was conducted in 2011. Multilevel logistic regression – with adjustment for any clustering within households – was used to examine the risk of self-reported illness in the previous 30 days. A multilevel Poisson regression model, with adjustment for clustering within households and individuals, was used to explore factors potentially associated with the risk of health-care-related “distress” financing (e.g. paying for health care by borrowing, selling, reducing food expenditure, removing children from school or performing additional paid work).

Findings

According to the interviewees, about 45% of the surveyed individuals had suffered at least one episode of illness in the previous 30 days. The most frequently reported illnesses among children younger than 5 years and adults were common tropical infections and noncommunicable diseases, respectively. The risks of self-reported illness in the previous 30 days were relatively high for adults older than 44 years, women and members of households in the poorest quintile. Distress financing, which had been implemented to cover health-care payments associated with 13% of the reported episodes, was significantly associated with heart and liver disease, asthma, typhoid, inpatient care, the use of public outpatient facilities, and poverty at the household level.

Conclusion

Despite the subsidization of public health services in Bangladesh, high prevalences of distress financing – and illness – were detected in the surveyed, urban households.     

The Effect of a Low Fructose and Low Glycemic Index/Load (FRAGILE) Dietary Intervention on Indices of Liver Function,Cardiometabolic Risk Factors,and Body Composition in Children and Adolescents With Nonalcoholic Fatty Liver Disease (NAFLD)

Background: Nonalcoholic fatty liver disease (NAFLD) is a common liver disease in obese children. Diets high in added fructose (high fructose corn syrup; HFCS) and glycemic index (GI)/glycemic load (GL) are associated with increased risk of NAFLD. Lifestyle modification is the main treatment, but no guidelines regarding specific dietary interventions for childhood NAFLD exist. We hypothesized that reductions in dietary fructose (total, free, and HFCS)/GI/GL over 6 months would result in improvements in body composition and markers of liver dysfunction and cardiometabolic risk in childhood NAFLD. Methods: Children and adolescents with NAFLD (n = 12) and healthy controls (n = 14) 7–18 years were studied at baseline and 3 and 6 months post–dietary intervention. Plasma markers of liver dysfunction (ALT, AST, γGT), cardiometabolic risk (TG, total cholesterol, LDL‐HDL cholesterol, Apo‐B100, Apo‐B48, Apo‐CIII, insulin, homeostasis model of assessment of insulin resistance [HOMA‐IR]), inflammation (TNF‐α, IL‐6, IL‐10), anthropometric, and blood pressure (BP) were studied using validated methodologies. Results: Significant reductions in systolic BP (SBP), percentage body fat (BF), and plasma concentrations of ALT (P = .04), Apo‐B100 (P < .001), and HOMA‐IR were observed in children with NAFLD at 3 and 6 months (P < .05). Dietary reductions in total/free fructose/HFCS and GL were related to reductions in SBP (P = .01), ALT (P = .004), HOMA‐IR (P = .03), and percentage BF in children with NAFLD. Reductions in dietary GI were associated with reduced plasma Apo‐B100 (P = .02) in both groups. With the exception of Apo‐B100, no changes in laboratory variables were observed in the control group. Conclusion: Modest reductions in fructose (total/free, HFCS) and GI/GL intake result in improvements of plasma markers of liver dysfunction and cardiometabolic risk in childhood NAFLD.     

Vaccination with a modified vaccinia virus Ankara (MVA)-vectored HIV-1 immunogen induces modest vector-specific T cell responses in human subjects

We investigated whether vaccination of healthy HIV-seronegative and HIV-1-seropositive antiretroviral therapy-treated subjects with recombinant modified vaccinia virus Ankara expressing an HIV-1 immunogen (MVA.HIVA) induced MVA-specific T cell responses. Using IFN-γ Elispot assays, we observed new or increased responses to MVA virus in 52% of HIV-seronegative subjects and 93% HIV-1 seropositive subjects; MVA-specific T cell frequencies were generally low and correlated poorly with T cell responses to the HIV-1 immunogen. In two vaccinees, responses were mapped to CD8+ T cell epitopes present in replication-competent vaccinia virus. These data support further evaluation of MVA as a viral vector for HIV-1 immunogens.     

Employment Status and Health: Understanding the Health of the Economically Inactive Population in Scotland

ABSTRACT: BACKGROUND: Although the association between health and unemployment has been well examined, less attention has been paid to the health of the economically inactive (EI) population. Scotland has one of the worst health records compared to any Western European country and the EI population account for 23% of the working age population. The aim of this study is to investigate and compare the health outcomes and behaviours of the employed, unemployed and the EI populations (further subdivided into the permanently sick, looking after home and family [LAHF] and others) in Scotland. METHODS: Using data from the 2003 Scottish Health Survey, the differences in health and health behaviours among the employed, unemployed and the subgroups of the EI population were examined. RESULTS: Both low educational attainment and residence in a deprived community were more likely in the permanently sick group. The LAHF and the unemployed showed worse self-reported health and limiting longstanding illness compared to the employed but no significant differences were observed between these groups. The permanently sick group had significantly poorer health outcomes than all the other economic groups. Similar to the unemployed and LAHF they are more likely to smoke than the employed but less likely (along with LAHF and 'others') to exhibit heavy alcohol consumption. Interestingly, the LAHF showed better mental health than the rest of the EI group, but a similar mental health status to the unemployed. On the physical health element of lung function, the LAHF were no worse than the employed. CONCLUSION: While on-going health promotion and vocational rehabilitation efforts need to be directed towards all, our data suggests that the EI group is at higher risk and policies and strategies directed at this group may need particular attention.     

Mortality in dioxin-exposed mice infected with influenza: mitochondrial toxicity (reye's-like syndrome) versus enhanced inflammation as the mode of action.

Increased mortality following influenza A infection was reported in B6C3F1 mice exposed to a low (0.01 micro g/kg) dose of dioxin. However, mortality was not associated with increased viral load and antibody titers to the virus were not decreased at doses of TCDD < or = 10 micro g/kg, suggesting that viral overgrowth, secondary to immunosuppression, was not the proximate cause of death. We tested the hypothesis that mitochondrial toxicity and dysfunction, similar to Reye's syndrome (RS) in humans, is responsible for increased mortality in dioxin-exposed, infected B6C3F1 female mice, based on similarities in the biochemical and immunological events that occur in RS and in TCDD-exposed animals. Endpoints were also included to test the hypothesis that increased pulmonary inflammation following dioxin exposure, in the absence of mitochondrial toxicity, was associated with increased mortality. Dose-related effects of TCDD alone, infection with influenza A alone, and combined TCDD exposure/influenza infection were evaluated. Mice were given a single ip injection of 0, 0.001, 0.01, 0.1, or 1.0 micro g TCDD/kg, 7 days before infection by intranasal instillation of an estimated LD(10-20) of influenza A Hong Kong/8/68 (H3N2) and were terminated 1, 7, and 10 days after infection. Serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for various measurements, including clinical chemistries, cell counts, cytokine analysis, and viral titers. Exposure to < or = 1.0 micro g TCDD/kg did not increase mortality; virus titers were similar at all doses of TCDD and there was no dioxin-related effect on serum NH(3) or glucose concentrations, two prominent indicators of the altered mitochondrial oxidative metabolism typically observed in RS. A study was therefore conducted over a wider range of TCDD doses. A single injection of 0, 0.025, 0.5, or 10 micro g TCDD/kg preceded infection by 7 days; subgroups of noninfected control and highest dose group (10 micro g TCDD/kg) mice were also evaluated for biochemical and immunological endpoints on the equivalent of infection day 4 to provide baseline data. Five days after infection the same endpoints described above were evaluated. The 10 micro g TCDD/kg dose increased mortality, but once again did not increase virus titer; as in previous experiments, serum biochemistry endpoints did not support mitochondrial dysfunction. These results suggest that RS is an unlikely explanation for increased influenza mortality in TCDD-exposed mice. Rather, constituents in BALF implicate increased pulmonary inflammation as the mode of TCDD action.     

Diesel Exhaust Enhanced Susceptibility to Influenza Infection is Associated with Decreased Surfactant Protein Expression

We have previously shown that exposure of respiratory epithelial cells to diesel exhaust (DE) enhances susceptibility to influenza infection and increases the production of interleukin (IL)-6 and interferon (IFN)-β. The purpose of this study was to confirm and expand upon these in vitro results by assessing the effects of DE exposure on the progression of influenza infection and on development of associated pulmonary immune and inflammatory responses in vivo. BALB/c mice were exposed to air or to DE containing particulate matter at concentrations of 0.5 or 2 mg/m³ for 4 h/day for 5 days and subsequently instilled with influenza A/Bangkok/1/79 virus. Exposure to 0.5 mg/m³ (but not the higher 2-mg/m³ dose) of DE increased susceptibility to influenza infection as demonstrated by a significant increase in hemagglutinin (HA) mRNA levels, a marker of influenza copies, and greater immunohistochemical staining for influenza virus protein in the lung. The enhanced susceptibility to infection observed in mice exposed to 0.5 mg/m³ of DE was associated with a significant increase in the expression of IL-6, while antiviral lung IFN levels were unaffected. Analysis of the expression and production of surfactant proteins A and D, which are components of the interferon-independent antiviral defenses, showed that these factors were decreased following exposure to 0.5 mg/m³ of DE but not to the higher 2-mg/m³ concentration. Taken together, the results demonstrate that exposure to DE enhances the susceptibility to respiratory viral infections by reducing the expression and production of antimicrobial surfactant proteins.     

The Severity of Dependence Scale (SDS) in an adolescent population of cannabis users: reliability, validity and diagnostic cut-off

The Severity of Dependence Scale (SDS) is a five-item scale that has been reported to be a reliable and valid screening instrument for dependence and a measure of dependence severity in adults across several substance classes. To date no data have been reported on its performance in a population of adolescent cannabis users. The current study assessed the psychometric properties of the SDS in a community sample of 14-18-year-old adolescent cannabis users (n=100). Internal consistency (alpha=0.83) and test-retest coefficients (ICC=0.88) were high and a principal components analysis of the scale found all items to load on a single factor. Total SDS score correlated significantly with frequency of cannabis use and number of DSM-IV dependence criteria met, indicating good concurrent validity. Receiver Operating Characteristic curve analysis was used to determine the most appropriate SDS cut-off score for use as an indicator of cannabis dependence, with optimal discrimination at an SDS score of 4. These findings indicate that the SDS is a reliable and valid measure of severity of cannabis dependence among adolescents, has high diagnostic utility, and that an SDS score of 4 may be indicative of cannabis dependence.     

Source apportionment of particulate matter in the U.S. and associations with lung inflammatory markers

Size-fractionated particulate matter (PM) samples were collected from six U.S. cities and chemically analyzed as part of the Multiple Air Pollutant Study. Particles were administered to cultured lung cells and the production of three different proinflammatory markers was measured to explore the association between the health effect markers and PM. Ultrafine, fine, and coarse PM samples were collected between December 2003 and May 2004 over a 4-wk period in each city. Filters were pooled for each city and the PM samples were extracted then analyzed for trace metals, ions, and elemental carbon. Particle extracts were applied to cultured human primary airway epithelial cells, and the secreted levels of interleukin-8 (IL-8), heme oxygenase-1, and cyclooxygenase-2 were measured 1 and 24 h following exposure. Fine PM sources were quantified by the chemical mass balance (CMB) model. The relationship between toxicological measures, PM sources, and individual species were evaluated using linear regression. Ultrafine and fine PM mass were associated with increases in IL-8 (r(2) = .80 for ultrafine and r(2) = .52 for fine). Sources of fine PM and their relative contributions varied across the sampling sites and a strong linear association was observed between IL-8 and secondary sulfate from coal combustion (r(2) = .79). Ultrafine vanadium, lead, copper, and sulfate were also associated with increases in IL-8. Increases in inflammatory markers were not observed for coarse PM mass and source markers. These findings suggest that certain PM size fractions and sources are associated with markers of lung injury or inflammation.     

Effects of atrial natriuretic peptide on systemic haemodynamics and cardiac function in normal man

Atrial natriuretic peptides (ANP) reduce blood pressure. Animal experiments suggest that this depressor action results from a reduction in cardiac output rather than peripheral vascular resistance but it is unresolved whether this is wholly due to their effect of reducing left ventricular filling or whether they have a negatively inotropic effect. We have therefore investigated the effects of ANP in normal man using Doppler measurements of ascending aortic blood flow. Six normal volunteers underwent infusions of placebo and incremental doses of ANP in the range 0.25 to 12 micrograms.min-1. Each infusion was given for 15 min and measurements made both in the supine and erect positions (passive tilt). In both positions ANP had dose dependent effects of increasing heart rate (HR) and maximal acceleration whilst lowering an index of systemic vascular resistance (ISVR). In the erect position ANP also lowered systolic blood pressure. In the 30 min after completion of the infusions there were significant decreases in peak velocity and cardiac output with increases in ISVR in both positions, but HR fell and diastolic pressure increased only when supine. During the course of the experiment mean haematocrit (SEM) increased from 43.9 (1.2) to 46.7 (1.0), indicating a mean reduction in plasma volume of 10.5%. This occurred despite a negative fluid balance of only 31(7) ml over the 2 h. These data suggest that ANP is not negatively inotropic and that, at pharmacological doses, it is an arteriolar dilator of rapid offset and reduces cardiac filling pressures by a mechanism of slower offset.