Measuring health program effectiveness in the field: an assessment tool

To assist field workers in program evaluation and to explicitly discuss program strengths and weaknesses, a practical method to estimate the effectiveness of public health interventions within the existing program capacity was developed. The method and materials were tested in seven countries (Afghanistan, Zimbabwe, Tanzania, Uganda, Guatemala, the Philippines, and Ghana). In this method, four core components are assessed using a questionnaire: (1) the efficacy of the intervention; (2) the level of existing human resources (i.e., quality of recruitment, training, and continuing education); (3) the infrastructure (i.e., supplies, salary, transportation, and supervision); and (4) the level of community support (i.e., access and demand). Using the assessment tool provided, program staff can determine if all necessary elements are in place for a successful program that can deliver the specific intervention. Based on the results of the assessment program, weaknesses can be identified, explicitly discussed, and addressed. The usefulness of this tool in humanitarian relief may be twofold: (1) to assess the design and implementation of effective programs; and (2) to highlight the inevitable need for capacity building as the disaster situation evolves.     

A high-fat diet and regulatory T cells influence susceptibility to endotoxin-induced liver injury

In nonalcoholic fatty liver disease, the pathogenesis of progression from simple steatosis to steatohepatitis has not been fully clarified. Many factors, including oxidative stress and hepatic immune regulation, contribute to the inflammation in steatosis. Because regulatory T cells (Tregs) are important components of immune regulation, we have now investigated their role in the pathogenesis of nonalcoholic steatohepatitis. Wild-type C57BL/6 mice were fed a high-fat (HF) diet to induce steatosis, and the hepatic lymphocyte population was analyzed by flow cytometry. HF-induced steatosis was associated with the depletion of hepatic Tregs and led to up-regulation of the inflammatory tumor necrosis factor-alpha signaling pathway. When challenged by exogenous lipopolysaccharide, the HF-fed mice developed liver inflammation. In contrast, the adoptive transfer of Tregs decreased inflammation in HF-fed mice. In comparison with effector T cells, Tregs had a lower expression of Bcl-2 and, therefore, increased susceptibility to oxidative stress-induced apoptosis. The treatment of mice with the antioxidant Mn(III)tetrakis(4-benzoic acid)porphyrin chloride reduced Treg apoptosis, increased the number of hepatic Tregs, and decreased hepatic inflammation in HF-fed mice. CONCLUSION: Our results indicate that increased oxidative stress in a fatty liver causes the apoptosis of Tregs, reduces the number of hepatic Tregs, and leads to a lowered suppression of inflammatory responses. This scenario is likely one of the pathogenetic mechanisms that facilitate the transformation of simple steatosis into steatohepatitis when a fatty liver is exposed to second or third hits.     

Cost-analysis of different management policies for patients with mild hepatitis A virus infection in Kazakhstan

Objective

For patients with mild hepatitis A virus (HAV) infection, this study compared estimates of total costs associated with managing cases under a policy of mandatory hospitalization in the Republic of Kazakhstan and estimates of total costs associated with managing cases in outpatient settings. Costs were estimated both from the perspective of the Ministry of Health and from a broader societal perspective.

Methods

Data were collected by using a standardized structured questionnaire. For cases of mild HAV infection, medical records were obtained from 200 patients managed by hospitalization and from 251 patients managed in an outpatient setting. Personal interviews were also conducted to collect information on productivity losses and out-of-pocket expenses.

Results

Nationally, we estimated about 21,600 cases of mild HAV infection annually. The mean annual treatment costs in hospital for mild HAV infection was estimated at US$3.39 million (2001 US$) (95% confidence interval [CI] = [US$3.26 million – US$3.52 million]). The total annual mild HAV infection cost to the society, including direct medical and nonmedical costs and productivity losses due to 721,440 lost work days, was estimated at US$6.26 million (95% CI [US$6.05 million – US$6.47 million]). In sensitivity analyses, the total annual cost of mild HAV infection ranged from US$4.37 million to US$24.66 million. The survey results showed that a relatively minor change in the current policy of mandatory hospitalization could result in an estimated total annual savings of US$4.62 million (2001 US$) in Kazakhstan.

Conclusion

Adoption of an outpatient management policy for cases of mild HAV infection would generate substantial cost savings to the Ministry of Health and society.     

Occupational exposure to crystalline silica dust in the United States, 1988-2003

The purposes of this study were a) to summarize measurements of airborne (respirable) crystalline silica dust exposure levels among U.S. workers, b) to provide an update of the 1990 Stewart and Rice report on airborne silica exposure levels in high-risk industries and occupations with data for the time period 1988-2003, c) to estimate the number of workers potentially exposed to silica in industries that the Occupational Safety and Health Administration (OSHA) inspected for high exposure levels, and d) to conduct time trend analyses on airborne silica dust exposure levels for time-weighted average (TWA) measurements. Compliance inspection data that were taken from the OSHA Integrated Management Information System (IMIS) for 1988-2003 (n = 7,209) were used to measure the airborne crystalline silica dust exposure levels among U.S. workers. A second-order autoregressive model was applied to assess the change in the mean silica exposure measurements over time. The overall geometric mean of silica exposure levels for 8-hr personal TWA samples collected during programmed inspections was 0.077 mg/m3, well above the applicable American Conference of Governmental Industrial Hygienists threshold limit value of 0.05 mg/m3. Surgical appliances supplies industry [Standard Industrial Classification (SIC) 3842] had the lowest geometric mean silica exposure level of 0.017 mg/m3, compared with the highest level, 0.166 mg/m3, for the metal valves and pipe fitting industry (SIC 3494), for an 8-hr TWA measurement. Although a downward trend in the airborne silica exposure levels was observed during 1988-2003, the results showed that 3.6% of the sampled workers were exposed above the OSHA-calculated permissible exposure limit.     

Urinary cadmium levels in the U S working population, 1988-1994

Few studies have estimated the prevalence and mean urinary cadmium levels in U.S. workers and the factors associated with high cadmium exposure. In this study, urinary cadmium measurements were obtained on 11228 U.S. workers aged 18 to 64 years who participated in the Third National Health and Nutrition Examination Survey (NHANES III, 1988-1994). Urinary cadmium levels ranged from 0.01 to 15.57 microg/L, with a geometric mean of 0.30 microg/L (0.28 microg/g creatinine) for all U.S. workers. The prevalence of urinary cadmium levels >or=5 microg/L was 0.42% (551000) for U.S. workers aged 18 to 64 years. Among U.S. workers in the metal industry (two-digit Standard Industrial Classification or SIC codes 33 and 34), the geometric mean urinary cadmium level was 0.48 microg/L (0.39 microg/g creatinine), and 0.45% of these workers had urinary cadmium levels >or=10 microg/L. The prevalence of urinary cadmium levels >or=15 microg/L was 0.0028% (3907). The agriculture industry (two-digit SIC codes 01, 02, and 07-09) was associated with low urinary cadmium levels, compared with repair services industries (two-digit SIC codes 75 and 76). Results from ordinary least squares regression analyses indicated that smokers had significantly higher urinary cadmium levels than nonsmokers (p 相似文献   

Cost of lost work and bed days for us workers in private industry--national health interview survey, 2003

Data from the 2003 National Health Interview Survey (n = 12,943) of US workers aged 18 to 64 years were used to estimate the annual cost of lost work (ACLW) and lost productivity (ACLP) due to bed days. The average lost workdays (LWDs) was estimated to be 8.39 for US workers compared with 5.62 bed days (BDs). The prevalence of high LWDs (>or=30 days) was 2.9% for US workers compared with 1.3% for BDs (>or=30 days). Regression analyses showed that female workers had higher adjusted mean LWDs and BDs than did male workers. Workers in the mining industry had the highest mean of 26.71 LWDs compared with 5.58 LWDs for workers in the wholesale industry. The total ACLW and ACLP was estimated to be $62.8 billion ($US 2003; 95% CI = $57.53-$67.52 billion).     

Protection from autoimmune diabetes and T-cell lymphoproliferation induced by FasL mutation are differentially regulated and can be uncoupled pharmacologically

Spontaneous mutation of Fas (lpr) or FasL (gld) completely protects nonobese diabetic mice from autoimmune diabetes but also causes massive double-negative T-cell lymphoproliferation. In this study, we used bone marrow chimeras and adoptive transfer analysis to investigate further the role of FasL in the pathogenesis of autoimmune diabetes and to determine whether gld-induced tolerance and double-negative T-cell lymphoproliferation can be uncoupled from each other. We show that FasL expressed on hematopoietic and nonhematopoietic compartments plays nonredundant roles in the pathogenesis of autoimmune diabetes. Mutation of FasL in either compartment interferes with the autoimmune process and prevents onset of diabetes, but FasL expressed in the hematopoietic compartment is the dominant regulator of T-cell homeostasis. Furthermore, pathogenesis of diabetes is dependent on normal FasL expression in both compartments, whereas only minimal FasL function is required to maintain T-cell homeostasis. Consequently, partial disruption of FasL protects from autoimmune diabetes without causing T-cell lymphoproliferation. This is demonstrated genetically in nonobese diabetic-gld/+ mice and pharmacologically by using FasL-neutralizing antibody. These results have important implications for understanding the role of the Fas pathway in pathogenesis of autoimmune diseases and for designing novel FasL-modulating therapies.     

Syndecan‐1 identifies and controls the frequency of IL‐17‐producing naïve natural killer T (NKT17) cells in mice

Invariant natural killer T (iNKT) cells recognize glycolipids as antigens and diversify into NKT1 (IFN‐γ), NKT2 (IL‐4), and NKT17 (IL‐17) functional subsets while developing in the thymus. Mechanisms that govern the balance between these functional subsets are poorly understood due, partly, to the lack of distinguishing surface markers. Here we identify the heparan sulfate proteoglycan syndecan‐1 (sdc1) as a specific marker of naïve thymic NKT17 cells in mice and show that sdc1 deficiency significantly increases thymic NKT17 cells at the expense of NKT1 cells, leading to impaired iNKT cell‐derived IFN‐γ, both in vitro and in vivo. Using surface expression of sdc1 to identify NKT17 cells, we confirm differential tissue localization and interstrain variability of NKT17 cells, and reveal that NKT17 cells express high levels of TCR‐β, preferentially use Vβ8, and are more highly sensitive to ɑ‐GalCer than to CD3/CD28 stimulation. These findings provide a novel, noninvasive, simple method for identification, and viable sorting of naïve NKT17 cells from unmanipulated mice, and suggest that sdc1 expression negatively regulates homeostasis in iNKT cells. In addition, these findings lay the groundwork for investigating the mechanisms by which sdc1 regulates NKT17 cells.     

Blood lead levels in U.S. workers, 1988-1994

Limited research has been conducted to measure the association between elevated blood lead levels and sociodemographic factors among U.S. workers in various industries and occupations using population-based survey data. Data from the Third National Health and Nutrition Examination Survey ( n = 10,127) were used to determine the blood lead levels in the U.S. workers. The prevalence of elevated blood lead levels > or = 50 microg/dL was 0.001% (1560) among U.S. workers compared with 0.2% (19,953) workers with elevated lead levels > or = 40 microg/dL. Regression analyses indicated that workers in the repair service industry were correlated with higher blood lead levels than those workers in the construction industry. Although low blood lead levels were found for the entire working population, the results showed that there were still high blood lead levels in certain occupations and industries during 1988 to 1994.