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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.

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.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.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; P0.01), full service restaurants (8.99; P0.01) and supermarkets (-37.69; P0.01) 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, P0.01) and school (6.68, P0.01) were positively associated with children's weight; while median household income (-39.6; P0.01) was negatively related to it.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.

Suppressor of Cytokine Signaling-1 (SOCS-1) is an essential physiological inhibitor of IFN-γ signaling. Mice lacking this gene die in the early postnatal period from a disease characterized by hyperresponsiveness to endogenous IFN-γ. The SOCS box is a C-terminal domain shared with over 30 other proteins that links SOCS proteins to an E3 ubiquitin ligase activity and the proteasome, but whether it contributes to inhibition of cytokine signaling is currently disputed. We have deleted only the SOCS box of the SOCS-1 gene in mice and show that such mice have an increased responsiveness to IFN-γ and slowly develop a fatal inflammatory disease. These results demonstrate that deletion of the SOCS box leads to a partial loss of function of SOCS-1.

Evidence is presented that the mAb 25E11, directed against the platelet integrin alpha IIb beta 3 (glycoprotein IIbIIIa;CD41b/CD61) also binds the distinct myeloid cell integrin alpha M beta 2 (Mac-1;CDIIb/CD18). The Ab is shown to identify only the alpha IIb beta 3 integrin complex and not the individual subunits in crossed Ab immunoelectrophoresis of platelet lysate. From cultured human macrophages, sequential immunoprecipitation of labeled glycoproteins indicated that 25E11 also bound the Mac-1 (CD11b/CD18) complex. This was confirmed using COS-7 and WOP cells doubly transfected with alpha M (CD11b) and beta 2 (CD18) or with alpha L (CD11a) and beta 2 when it was found that the Ab bound only the alpha M beta 2 transfectants. Studies with these cells and the RC2A myeloid cell line stimulated with tetradecanoyl phorbol acetate or FMLP indicated that the 25E11 epitope on Mac-1 did not depend on cell activation for its expression. The rationale for this cross-reactivity is not known, but since the 25E11 Ab inhibits the function of both platelets and myeloid cells, it is likely that this shared epitope is important to integrin function. Given the expression of this epitope on IIbIIIa and Mac-1, the dominant integrins of platelets and granulocyte/macrophage cells, but not on other integrins, a role of this epitope in the early events of inflammation is suggested.

Advances in screening technologies allowing the identification of growth factor receptors solely by virtue of DNA or protein sequence comparison call for novel methods to isolate corresponding ligand growth factors. The EPH-like receptor tyrosine kinase (RTK) HEK (human EPH-like kinase) was identified previously as a membrane antigen on the LK63 human pre-B-cell line and overexpression in leukemic specimens and cell lines suggested a role in oncogenesis. We developed a biosensor-based approach using the immobilized HEK receptor exodomain to detect and monitor purification of the HEK ligand. A protein purification protocol, which included HEK affinity chromatography, achieved a 1.8 X 10(6)-fold purification of an approximately 23-kDa protein from human placental conditioned medium. Analysis of specific sHEK (soluble extracellular domain of HEK) ligand interactions in the first and final purification steps suggested a ligand concentration of 40 pM in the source material and a Kd of 2-3 nM. Since the purified ligand was N-terminally blocked, we generated tryptic peptides and N-terminal amino acid sequence analysis of 7 tryptic fragments of the S-pyridylethylated protein unequivocally matched the sequence for AL-1, a recently reported ligand for the related EPH-like RTK REK7 (Winslow, J.W., Moran, P., Valverde, J., Shih, A., Yuan, J.Q., Wong, S.C., Tsai, S.P., Goddard, A., Henzel, W.J., Hefti, F., Beck, K.D., & Caras, I.W. (1995) Neuron 14, 973-981). Our findings demonstrate the application of biosensor technology in ligand purification and show that AL-1, as has been found for other ligands of the EPH-like RTK family, binds more than one receptor.

Evidence is presented that the mAb 25E11, directed against the platelet integrin alpha IIb beta 3 (glycoprotein IIbIIIa;CD41b/CD61) also binds the distinct myeloid cell integrin alpha M beta 2 (Mac-1;CDIIb/CD18). The Ab is shown to identify only the alpha IIb beta 3 integrin complex and not the individual subunits in crossed Ab immunoelectrophoresis of platelet lysate. From cultured human macrophages, sequential immunoprecipitation of labeled glycoproteins indicated that 25E11 also bound the Mac-1 (CD11b/CD18) complex. This was confirmed using COS-7 and WOP cells doubly transfected with alpha M (CD11b) and beta 2 (CD18) or with alpha L (CD11a) and beta 2 when it was found that the Ab bound only the alpha M beta 2 transfectants. Studies with these cells and the RC2A myeloid cell line stimulated with tetradecanoyl phorbol acetate or FMLP indicated that the 25E11 epitope on Mac-1 did not depend on cell activation for its expression. The rationale for this cross-reactivity is not known, but since the 25E11 Ab inhibits the function of both platelets and myeloid cells, it is likely that this shared epitope is important to integrin function. Given the expression of this epitope on IIbIIIa and Mac-1, the dominant integrins of platelets and granulocyte/macrophage cells, but not on other integrins, a role of this epitope in the early events of inflammation is suggested.

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.

Fetal mouse pancreatic isotransplantation was performed in CBA mice, previously made diabetic with streptozotocin. Either 17- or 12-day-old fetal tissue was used, either uncultured or after 14 days in organ culture. Grafts were placed under the renal capsule, and their effect on fasting blood glucose levels was assessed over a 10-week postgraft period. The grafts and the host pancreas were then examined by light microscopy. Uncultured 12- and 17-day fetal pancreases produced poorly developed grafts with small islets, numerous ducts, and copious adipose tissue. By contrast, if organ cultured for 14 days before transplantation, both 12- and 17-day tissue resulted in large grafts composed predominantly of well-stained islet cells, few ducts, and little connective and adipose tissue. The most functionally effective grafts were derived from cultured 17-day pancreas, and a single graft per recipient always ameliorated diabetes. By contrast, grafts from single or multiple uncultured 12-day pancreases did not function, but, after culture, grafts derived from three (but not from one) 12-day pancreas lowered blood glucose levels to almost normal levels. It is concluded that grafts of fetal mouse pancreas can function in experimental diabetes provided they are first cultured and are of adequate gestational age.