24 research outputs found
Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes
Type 1 diabetes (T1D) is a common autoimmune disorder that arises from the action of multiple genetic and environmental risk factors. We report the findings of a genome-wide association study of T1D, combined in a meta-analysis with two previously published studies. The total sample set included 7,514 cases and 9,045 reference samples. Forty-one distinct genomic locations provided evidence for association with T1D in the meta-analysis (P 10 6). After excluding previously reported associations, we further tested 27 regions in an independent set of 4,267 cases, 4,463 controls and 2,319 affected sib-pair (ASP) families. Of these, 18 regions were replicated (P 0.01; overall P 5 × 10 8) and 4 additional regions provided nominal evidence of replication (P 0.05). The many new candidate genes suggested by these results include IL10, IL19, IL20, GLIS3, CD69 and IL27
Grass Mud Horse - a Maquette for Ai Weiwei
cast iron and cast aluminum sculpture
A one finger salute in support of Ai Weiwei. The aluminum finger is cast in an empty Chinese handcuff . You are only trapped if you resist in the way expected.https://digitalcommons.buffalostate.edu/noreaster_art/1001/thumbnail.jp
Nonketotic Hyperosmolal Diabetic Coma in a Child: Management With Low-Dose Insulin Infusion and Intracranial Pressure Monitoring
Nonketotic hyperosmolal diabetic coma, which is rare in children, is associated with a high mortality in both children and adults. We report a case of nonketotic hyperosmolal diabetic coma in a 3½-year-old child, who was successfully managed with low-dose insulin infusion and invasive intracranial pressure monitoring and recovered without sequelae. Despite severely elevated serum glucose (2,660 mg/dL) and osmolality (435 mosm/kg) levels, there was no elevation of intracranial pressure during her treatment. This case illustrates that insulin should be used cautiously and at low dose in this disease, and that intracranial pressure monitoring is of use in the management of such patients. The pathogenesis and clinical features of nonketotic hyperosmolal diabetic coma are briefly reviewed.</jats:p
Factitious Hypoglycemia
Insulin abuse resulting in hypoglycemia was originally reported in 1947.1,2 However, not until the 1970s was the serum C-peptide level recognized to be a reliable marker of pancreatic β-cell activity.3 Human C-peptide radioimmunoassay has been advocated recently as a useful test in diagnosing insulin-induced factitious hypoglycemia.4,5 This report describes a case of child abuse presenting as hypoglycemic coma secondary to insulin injection. The diagnosis was made by the presence of the pathognomonic triad: hypoglycemia, hyperinsulinemia, and low serum levels of C-peptide.
CASE REPORT
A 2-year-old black boy was brought to the emergency room in an unresponsive state. He was said to be unarousable after his regular afternoon nap.</jats:p
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Racial differences in metabolic control of children and adolescents with type I diabetes mellitus
This study evaluated racial differences in the metabolic control of children and adolescents with insulin-dependent (type I) diabetes mellitus and examined the interactive effects of race with age and sex.
Data on several demographic and clinical variables were obtained for 102 black and 108 white children, including the percentage of total HbA1, age, age at diagnosis, duration of diabetes, pubertal status, insulin dose (U.kg-1.day-1), body mass index, number of clinic visits kept and missed, number of hospitalizations for diabetic ketoacidosis (DKA) for the year, and socioeconomic status (SES).
Black children had higher insulin dosages (P less than 0.05) and lower SESs (P less than 0.001) than white children. HbA1 was higher in black than white children (P less than 0.01) after statistically adjusting for the effects of insulin dose, diabetes duration, and SES. With HbA1-based criteria, more black than white children were in poor and fewer in good metabolic control (P less than 0.001). Older children (greater than or equal to 13 yr) had higher HbA1 levels than younger (less than 13 yr) children (P less than 0.002), but there were no differences in HbA1 between males and females nor were there interactive effects of race, sex, and age-group. Black children were hospitalized for DKA more frequently than white children (P less than 0.04). More black than white children missed clinic visits (P less than 0.01), but they did not differ in number of visits kept.
Black youths with type I diabetes mellitus are in poorer metabolic control than white youths
