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Objective: A number of health care initiatives seek to improve health outcomes by increasing access to outpatient services while reducing preventable acute events. We evaluated disparities between American Indian and Alaska Native (AI/AN) and non-Hispanic white (white) Medicare enrollees in access to outpatient preventive, primary, and specialty services by comparing their potentially preventable hospitalizations (PPHs)., Research Design: The study population included 121,311 adult AI/AN Medicare enrollees registered to use services funded by the Indian Health Service and 5,915,011 adult white enrollees living in the same counties. Medicare 2010 data and a nationally recognized algorithm were used to identify PPHs., Results: Among AI/AN Medicare enrollees, 58.6% had either diabetes, cardiovascular disease, or both conditions; the AI/AN age-adjusted prevalence of either or both conditions was 1.2 times that of the white enrollees (P<0.001). The age-adjusted PPH rate for all AI/ANs was 74 admissions per 1000 adults, 1.5 times that of white enrollees (P<0.001). Nearly 90% of AI/AN PPHs were among AI/ANs with diabetes, cardiovascular disease, or both conditions; their PPH rate was 114 admissions per 1000 adults, 1.2 times that of white enrollees (P<0.001) with those conditions., Conclusions: Differences in disease burden and access to outpatient services may partly explain the higher PPH rates for AI/AN Medicare enrollees. The health care quality measure used in this study (PPH) was developed for the US general population. It is important to consider AI/AN socioeconomic and other characteristics when interpreting findings for such measures and enhancing programs and policies to improve AI/AN health outcomes.

The idiopathic inflammatory bowel diseases (IBDs), consisting of Crohn's disease and ulcerative colitis, are complex genetic disorders involving chronic inflammation of the intestines. Multiple genetic loci have been implicated through genome-wide searches, but refinement of localization sufficient to undertake positional cloning efforts has been problematic. This difficulty can be obviated through identification of ancestrally shared regions in genetic isolates, such as the Chaldean population, a Roman Catholic group from Iraq. We analyzed four multiply affected American Chaldean families with inflammatory bowel disease not known to be related. We observed evidence for linkage and linkage disequilibrium in precisely the same region of chromosome band 1p36 reported previously in an outbred population. Maximal evidence for linkage was observed near D1S1597 by multipoint analysis (MLOD = 3.01, P = 6.1 x 10(-5)). A shared haplotype (D1S507 to D1S1628) was observed over 27 cM between two families. There was homozygous sharing of a 5 cM portion of that haplotype in one family and over a <1 cM region in the second family. Homozygous sharing of this haplotype near D1S2697 and D1S3669 was observed in one individual in a third multiply affected family, with heterozygous sharing in a fourth family. Linkage in outbred families as well as in this genetic isolate indicates that a pathophysiologically crucial IBD susceptibility gene is located in 1p36. These findings provide a unique opportunity to refine the localization and identify a major susceptibility gene for a complex genetic disorder.

The Childrens Cancer Study Group conducted a case-control study of occupational exposures of parents of 204 children (under 18 yr of age) with acute nonlymphoblastic leukemia. The most consistent finding was an association of acute nonlymphoblastic leukemia risk with pesticide exposure. Controls matched by date of birth and race were obtained through random digit dialing. Odds ratio (OR) for paternal pesticide exposure in jobs held for longer than 1000 days was 2.7 (95% confidence interval, 1.0 to 7.0; trend, P = 0.06), and seven case mothers and no control mothers had prolonged exposure (trend, P = 0.008). Risk estimates for parental pesticide exposure were substantially increased for children under age 6 at diagnosis (OR for prolonged exposure to either parent = 11.4; trend, P = 0.003) and for those with myelomonocytic and monocytic subtypes (OR, 13.6; trend, P = 0.007). Moreover, there were significantly elevated risks for direct exposure of the child to pesticides in the household (OR for exposure most days = 3.5; trend, P = 0.04) and for maternal exposure to household pesticides at the time of pregnancy (eight case mothers versus no controls for exposure most days; trend, P = 0.05). Paternal exposures to solvents (OR, 2.1; P = 0.003) and petroleum products (OR, 2.4; P = 0.002) were reported more commonly for cases than controls. Other occupational exposures reported significantly more often by case parents were paternal exposure to plastics or lead and maternal exposure to paints and pigments, metal dusts, and sawdust. These data provide further evidence for a role of occupational risk factors in the etiology of childhood cancer.

Northern blot analysis was used to assess the level of expression of five protooncogenes and histone H3 in the bone marrow cells of patients with acute nonlymphocytic leukemia (ANLL). The relationship between the level of gene expression and the clinical characteristics of the disease and response to therapy was studied. The levels of expression of c-myc and c-myb are weakly correlated and are unrelated to French-American-British (FAB) type of ANLL. The levels of expression of c-fms, c-fes, and c-fos are highly correlated with each other and are highest in leukemia with a monocytic component (c-fms v FAB = .71, c-fes v FAB = .75). High levels of c-myc expression are associated with a high probability of not responding to remission induction therapy (P = .004). The converse is true for c-fms expression levels. High levels of expression of c-myc or c-myb are associated with short remissions (P = .059 and .065, respectively), perhaps because they are associated with a high capacity for leukemic cell self-renewal and/or an inability of leukemic cells to differentiate in response to chemotherapy.