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Biomedical subjects

A Drash

Publications and source records attributed to A Drash.

At least 19 recordsLinked to original sources
PubMed1989

Substrate and hormone responses to exercise following a marathon run.

The aim of this study was to examine selected substrate and hormone responses to 30-min treadmill runs performed several days before and after a competitive marathon (42.2 km) to determine the time course for return of altered responses to pre-race levels. Six experienced male runners (30.8 +/- 9.1 years) ran at their predicted race pace (77.1% +/- 4.1% of VO2max) 8-7 days prior (S-1) to the Boston Marathon and 2-3 (S-2), 6-7 (S-3), and 13-14 days (S-4) post-marathon. All 30-min runs were performed in the morning at a constant time for each subject following a 12-h fast. Blood samples were drawn immediately before and immediately after (within 1 min) the 30-min runs. Post-exercise glucose responses were higher (P less than 0.05) during S-2 and S-3 compared with S-1 values. S-2 post-exercise lactate concentrations were also higher than the corresponding S-1 value. Pre-exercise free fatty acid (FFA) levels during S-4, and the post-exercise FFA values during S-2, S-3, and S-4, were lower (P less than 0.05) than the corresponding S-1 concentrations. Pre- and post-exercise alanine levels during S-2 were higher (P less than 0.05) than the S-1 values. Both pre- and post-exercise insulin levels during S-2, S-3, and S-4 were greater (P less than 0.05) than corresponding S-1 concentrations. Glucagon concentrations were unchanged across all sessions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Initial pathogenic events in IDDM.

A workshop sponsored by the National Institute of Child Health and Human Development was held in June 1988 to discuss the initial events in the pathogenesis of insulin-dependent diabetes and to make recommendations for future studies. Better definition of immunological markers to reliably predict the disease will enable the detection and study of the earliest pathogenic events involved. The precise autoimmune mechanisms and the role of the environment, both in the initiation of the disease process and precipitation of clinically overt disease, need to be accurately determined to define strategies that might eventually lead to its prevention.

Animals↗
PubMed1986

HLA-DR 3 is associated with a more slowly progressive form of type 1 (insulin-dependent) diabetes.

The presence of HLA-DR 3 was analysed in 745 patients with Type 1 (insulin-dependent) diabetes with age at diagnosis between 1-19 years. HLA-DR 3 and/or 4 was found in 678/745 (91%) of the patients. Presence of DR2 with neither DR 3 nor 4 was demonstrated in 15 patients. Patients with HLA-DR 3 without DR 4 presented with Type 1 diabetes more evenly over the year; they also presented without incidence peaks at 7 years or 10-11 years, as seen especially in DR 3/4 patients. The DR 3 patients more often had mild disease with less ketonuria at diagnosis, less often ketoacidotic symptoms and more often a subsequent partial remission. The apparently more severe disease among diabetic girls may, at least to some extent, be explained by their higher prevalence of HLA-DR 4. The differences found were similar in North America and Europe. The results suggest that Type 1 diabetes is a genetically heterogeneous disease and that HLA-typing may be a useful marker of this heterogeneity.

Adolescent↗
PubMed1986

Why do children with diabetes die?

While the treatment of children with Type I diabetes mellitus has dramatically improved since the introduction of insulin in 1922, significant acute mortality still remains. To better ascertain the causes of death in younger children and adolescents with diabetes mellitus, a retrospective review was undertaken of diabetes associated mortality in the patient population followed at the Children's Hospital of Pittsburgh between the years 1950 and 1985. Fifty-five deaths were identified of which 20 occurred during the initial presentation of diabetes and 35 occurred between 2 months and 11 years following the diagnosis of diabetes mellitus. Diabetic ketoacidosis (DKA) was associated with 64% of the total mortality with 85% of the early onset and 54% of the late onset deaths being ketoacidosis related. Of these ketoacidosis associated deaths, cerebral edema was documented in 31%, or 20% of the total group mortality. Non ketoacidosis deaths in both early and late onset groups were caused by heterogeneous events. There were no deaths associated with the traditional late vascular complications of diabetes mellitus. Since diabetic ketoacidosis is a potentially preventable acute complication of diabetes mellitus and represented a predominant cause of mortality in these children, early recognition and prompt treatment might substantially reduce childhood mortality in patients with Type I diabetes mellitus.

Adolescent↗
PubMed1985

Cognitive deficits in adolescents who developed diabetes early in life.

A comprehensive battery of neuropsychological tests was administered to 125 adolescents with a history of insulin-dependent diabetes, and to 83 demographically similar nondiabetic control subjects. To test the hypothesis that developing this disease early in life greatly increases the risk of manifesting significant cognitive impairments, diabetic subjects were assigned to an "early-onset" (diagnosis before age 5 years) or a "later-onset" subgroup. Results showed that subjects with early onset of diabetes performed more poorly than either subjects with later onset of diabetes or nondiabetic control subjects on virtually all tests, including measures of intelligence, school achievement, visuospatial ability, memory, motor speed, and eye-hand coordination. Moreover, multiple regression analyses demonstrated that the age at onset and the duration of diabetes seem to affect neuropsychological functioning in very different ways. The duration of the disease best predicted performance on those tests requiring highly overlearned, primarily verbal, skills whereas the age at onset best predicted scores on tests requiring the ability to process relatively unfamiliar, typically nonverbal, information in novel ways. Although the etiology of these deficits remains unclear, there is a possibility that they are secondary to mild brain damage that develops as a consequence of multiple episodes of serious hypoglycemia early in life.

Adolescent↗
PubMed1979

Circulating glucagon antibodies in children who have insulin-dependent diabetes mellitus. Clinical significance and characterization.

A substance present in the sera of diabetic children that interferes with the radioimmunoassay for glucagon was found in six of 66 children who were participating in an inpatient study of diabetic control. Detailed studies documented unequivocally that this glucagon-binding substance is a specific antibody to glucagon and is located in the immunoglobulins. In a survey of diabetic children in the outpatient diabetes clinic and in a diabetes summer camp, antibodies to glucagon were found in about 12% of those evaluated. However, no children who had had diabetes for less than three years were found to have antibodies, and there appeared to be an increase with increasing duration of disease of up to greater than 20% at eight years' duration. The presence of glucagon antibodies may be of pathologic significance in that the patients have a greater tendency to develop hypoglycemia than do diabetic children without glucagon antibodies.

Adolescent↗
PubMed1979

Age, sex, and season of onset of juvenile diabetes in different geographic areas.

Age, sex, and estimated time of onset of insulin-dependent diabetes were determined for children in Pittsburgh (N = 673), Gainesville (N = 976), Galveston (n = 741), and Melbourne (N = 851). The US cities had a decrease in new cases during the summer and peak incidence in January through April. In Melbourne, monthly trends were reversed: there were more cases during May through August. In US cities, but not in Melbourne, children less than 6 years old showed a greater variation by season than children 6 years old and older. Observations of the same fall and winter onset (in different calendar months) of insulin-dependent diabetes in Australia and the United States, and exaggeration of seasonal differences in young US children, suggest that onset of insulin-dependent diabetes is associated with seasonally varying viral diseases. Mumps and rubella infections do not seem to be responsible for much of the seasonal variation. Seasonal peaks of mumps and rubella are later than those observed for insulin-dependent diabetes, and immunization with live mumps and rubella viruses has not been associated with changes in incidence of insulin-dependent diabetes. An increase in disease incidence in boys over girls below age 6 years and in girls over boys at ages 6 through 11 years was consistently observed but not explained.

Adolescent↗
PubMed1979

Cardio-respiratory and perceptual recovery from a marathon run.

Seven male runners (21--42 years) were examined before and after the 1976 Boston Marathon to provide data concerning the cardio-respiratory and perceptual recovery from the performance. Treadmill runs, 30 min in duration, were administered 1 week prior to the marathon and 2--3, 6--7 and 13--15 days following. Treadmill speed was held constant and based on each runner's planned race pace. Maximal performance data were collected 1 week before and 2 weeks after the race. Data were analyzed using a 2-way ANOVA (4 thirty min run data collection periods and 3 exercise time points--5, 15 and 30 min) and "t" tests. Treatment effects were not observed for either HR or VE, however, perceived exertion (RPE) was significantly elevated 2--3 and 6--7 days post-marathon and VO2 was significantly lower at 13--15 days. HR and RPE showed significant time effects indicating a non-steady state response. None of the maximal test variables were significantly displaced. All variables were returned to pre-marathon levels by 13--15 days except VO2 which was lower. Aerobic capacity was not a limiting factor in the recovery from a marathon run. Muscle soreness and stiffness seem to be related to the increased perceptual ratings following a marathon run.

Adult↗
PubMed1978

Immunopathology of juvenile-onset diabetes mellitus. I. IgA deficiency and juvenile diabetes.

There is an increased prevalence (P less than 0.001) of IgA deficiency in children with juvenile-onset insulin-dependent diabetes mellitus (9/366) but not in adults with insulin-dependent diabetes (0/421). The juvenile diabetics with IgA deficiency have other immune-associated diseases, such as thyroiditis and chronic active hepatitis, and have a history of infections. Four of the nine IgA-deficient diabetics we studied have autoantibodies to endocrine organs. Seven of eight have the HLA-B8, a proportion significantly (P less than 0.05) greater than control populations. Based on the clinical findings of IgA deficiency and multiple autoantibodies in patients with ataxia-telangiectasia and chronic mucocutaneous candidiasis, diseases associated with thymus deficiency, we suspect that thymus deficiency and autoimmunity may play a role in the pathogenesis of some types of juvenile-onset diabetes mellitus. In addition, an excess morbidity of the IgA-deficient juvenile diabetic population may explain the lack of IgA deficiency in older insulin-dependent diabetic individuals.

Adolescent↗