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Background Childhood obesity has been rising rapidly in the USA. The rate is higher among those at a lower socioeconomic status and racial/ethnic minority groups. In Alabama, nearly half of the children from rural African American families are overweight or obese. Studies suggest that children's eating behaviours and weight could be influenced by surrounding food environments. The purpose of this paper is to assess the community food environment and examine the associations with childhood obesity in Alabama's Black Belt region. Methods This research uses both qualitative and quantitative methods. Weight status of 613 African American students in four elementary schools in a rural county of Alabama was assessed. We examined community food environments around children's home through GIS (Geographic Information System) and statistical methods. The interrelations between children's weight and community food environments are explored with multi-level models. Results Approximately 42.1% of surveyed children were overweight or obese, much higher than the national average, 30.6%. In Model 1, convenience stores (3.44; P < 0.01), full service restaurants (8.99; P < 0.01) and supermarkets (−37.69; P < 0.01) were significantly associated with the percentile of body mass index. Fast food stores (−0.93; P = 0.88) were not related to children's weight. In Model 2, the additions of sociodemographic factors and school effects cause significant changes of the relationships between children's weight and four types of food outlets. The percentage of African American population (90.23, P < 0.01) and school (6.68, P < 0.01) were positively associated with children's weight; while median household income (−39.6; P < 0.01) was negatively related to it. Conclusion Children's weight is influenced by community food environments, sociodemographic factors and school context. Findings suggest that policymakers and planners need to improve community food environments of low-income minority communities. Parents and schools should pay more attention to reduce the negative impacts of food environments on children.

Effects of weather variables on suicide are well-documented, but there is still little consistency among the results of most studies. Nevertheless, most studies show a peak in suicides during the spring season, and this is often attributed to increased temperatures. The purpose of this study is to test the relationship between monthly temperature and monthly suicide, independent of months or seasons, for five counties located across the United States. Harmonic analysis shows that four of the five counties display some seasonal components in the suicide data. However, simple linear regression shows no correlation between suicide and temperature, and discriminant analysis shows that monthly departure from mean annual suicide rates is not a useful tool for identifying months with temperatures that are colder or warmer than the annual average. Therefore, it appears that the seasonality of suicides is due to factors other than temperature.

In organ culture of fetal human and fetal murine pancreas under “conventional” conditions (10% CO2 in air), the islet cells of both species survive, proliferate and function but the acinar tissue rapidly degenerates. Fetal mouse islet cells also survive in 90% CO2 but nonendocrine cells, including fibroblasts and macrophages, degenerate. Fetal mouse islets grown in 90% O2 show diminished immunogenicity when transplanted into recipients differing across the entire MHC, but a reduced allograft response by the host is frequently still present in the absence of immunosuppresslon. Fetal human islets, grown in 10% C02 in air, produce insulin in vitro for prolonged periods, and as xenografts, differentiate under the kidney capsule of athymlc mice, suggesting that under appropriate conditions both in vitro and in vivo, the fetal human islets can survive. However, fetal human pancreatic cells of all types are highly susceptible to high oxygen concentrations and are rapidly killed. Because of the susceptibility of fetal human pancreas to oxygen, conditions for the culture of fetal human islets for allotransplantation may need to be modified from those tolerated by fetal mouse islets. Fetal human islets may be a useful source of transplant material in human insulin-dependent diabetes, but it is likely that tissue matching and immunosuppression may be required in addition to modification of islet immunogenicity by prior organ culture.

Organ-cultured fetal mouse pancreas was transplanted into syngeneic diabetic mice and the insulin content of the graft measured. Insulin content of each 17-day-old uncultured fetal mouse pancreas was 90 ± 10 ng, rising to 457 ± 123 ng after 16 days in organ culture (P < 0.001); however, after 35 days in vitro, it decreased to 108 ± 59 ng. Diabetes was induced in mice with streptozotocin (STZ), and 3 wk later each animal was grafted under the kidney capsule with one syngeneic fetal pancreas cultured for 16 days. Total insulin content of fetal pancreata increased from 457 ± 123 ng on the day of transplantation to peak at 12,125 ± 3679 ng by 9 wk after grafting (P < 0.001), at which time insulin content of grafts was comparable to that extracted from normal adult mouse pancreas (8917 ± 436 ng). Random blood glucose in mice following STZ was 15.7 ± 0.9 mmol/L and declined to normal levels (5.6 ± 0.5 mmol/L) 6 wk after transplantation. Insulin content of the pancreas after STZ injection decreased from 8917 ± 436 ng to 906 ± 410 ng at 15 wk (P < 0.001) in diabetic mice that were not islet grafted. However, pancreatic insulin content of grafted mice was significantly greater than in ungrafted mice 15 wk after STZ (3168 ± 532 ng versus 906 ± 410 ng, P 0.01), which suggests that islet transplantation protects residual pancreatic function. It is concluded that fetal islets have a large capacity to produce and accumulate insulin in vitro and in vivo, and each grafted fetal pancreas may attain an insulin content equivalent to that of a normal adult pancreas. The potential of fetal islets to accumulate large insulin reserves may make possible the use of tissue from one donor to treat multiple recipients.

The control of diabetes and the prevention of renal complications were studied in mice that received different treatment regimes for six months. Transplantation of syngeneic cultured fetal pancreas completely reversed streptozotocin-induced diabetes (mean FBG 5.1 +/- 0.4 mmole/liter six months after transplantation, versus 5.8 +/- 0.2 mmole/liter in normal mice). The mean fasting blood glucose (FBG) level of insulin-treated mice was lower than the mean FBG level of untreated diabetic mice (9.0 +/- 1.2 mmole/liter versus 11.5 +/- 1.3 mmole/liter, P less than 0.05) but exceeded the FBG level of transplanted mice (P less than 0.001) or normal controls (P less than 0.001). There were no significant differences between the mean level of glycosylated hemoglobin (HbA1c) of normal (4.8 +/- 0.3%), transplanted (4.5 +/- 0.3%), or insulin-treated mice (5.3 +/- 0.4%), but the HbA1c level in the untreated diabetic group was increased (7.0 +/- 0.5%; P less than 0.001). Six months after transplantation, the thickness of the glomerular capillary basement membrane (GCBM) was not different in the transplanted group and normal controls (156.4 +/- 5.7 nm versus 157.3 +/- 12.6 nm); the GCBM was thicker in the insulin-treated mice than in the transplanted mice (179.8 +/- 4.2 nm versus 156.4 +/- 5.7 nm; P less than 0.02), but thinner than in untreated diabetic mice (179.8 +/- 4.2 nm versus 202.2 +/- 4.4 nm; P less than 0.001). It is concluded that islet transplantation, in contrast to good control as judged by normalization of HbA1c levels achieved with parenteral insulin, prevents GCBM thickening in experimental diabetes.