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Biomedical subjects

I Gottesman

Publications and source records attributed to I Gottesman.

9 recordsLinked to original sources
PubMed1997

Workshop on schizophrenia.

On November 29-30, 1995, the National Academy of Sciences and the Institute of Medicine brought together experts in schizophrenia and specialists in other areas of the biological sciences in a workshop aimed at promoting the application of the latest biological information to this clinical problem. The workshop paid particular attention to evidence of pathology in the brains of people with schizophrenia, and to the possibility that this reflects an abnormality in brain development that eventually leads to the appearance of symptoms. The participants were impressed with the complexity of the problem, and felt that multiple approaches would be required to understand this disease. They recommended that a major focus should be on the search for predisposing genes, but that there should be parallel research in many other areas.

Brain↗
PubMed1996

A broader phenotype of autism: the clinical spectrum in twins.

The diagnostic boundaries of the behavioural phenotype for autism were examined in 28 MZ pairs and 20 DZ same-sex twin pairs, where one or both twins had autism. In the non-autistic cotwin (i.e. in twin pairs discordant for autism) it was common to find language impairments in childhood and social deficits persisting into adulthood. Concordance for this broader phenotype was much greater in MZ pairs than DZ pairs, indicating a strong genetic component. Behavioural and cognitive manifestations of autism were compared both within and between MZ twin pairs. The variation was as great within MZ twin pairs as between pairs, suggesting that it does not index genetic heterogeneity (although aetiological heterogeneity probably exists). Current diagnostic practices need re-evaluation.

Activities of Daily Living↗
PubMed1995

Autism as a strongly genetic disorder: evidence from a British twin study.

Two previous epidemiological studies of autistic twins suggested that autism was predominantly genetically determined, although the findings with regard to a broader phenotype of cognitive, and possibly social, abnormalities were contradictory. Obstetric and perinatal hazards were also invoked as environmentally determined aetiological factors. The first British twin sample has been re-examined and a second total population sample of autistic twins recruited. In the combined sample 60% of monozygotic (MZ) pairs were concordant for autism versus no dizygotic (DZ) pairs; 92% of MZ pairs were concordant for a broader spectrum of related cognitive or social abnormalities versus 10% of DZ pairs. The findings indicate that autism is under a high degree of genetic control and suggest the involvement of multiple genetic loci. Obstetric hazards usually appear to be consequences of genetically influenced abnormal development, rather than independent aetiological factors. Few new cases had possible medical aetiologies, refuting claims that recognized disorders are common aetiological influences.

Abnormalities, Multiple↗
PubMed1994

Comparison of Neuropsychological Test Performance in PTSD, Generalized Anxiety Disorder, and Control Vietnam Veterans

Although impairment in cognitive functioning is theoretically linked to the presence of post-traumatic stress disorder (PTSD), the actual impact of this disorder on neuropsychological performance remains largely unknown. While a modest amount of empirical attention has been directed toward examining the neuropsychological correlates of PTSD, several methodological problems, most notably small sample sizes and the resulting lack of power, have greatly restricted generalizability of findings. The present study examined the neuropsychological performance pattern of Vietnam veterans with PTSD (n = 241) as compared to those with generalized anxiety disorder (n = 241) and no history of psychiatric diagnosis (n = 241). A one-way MANOVA revealed no significant differences among the groups on any of the dependent measures of cognitive functioning, including the Wechsler Adult Intelligence Scale-Revised Block Design subtest, the California Verbal Learning Test, the Rey-Osterrieth Complex Figure Drawing Test, and the Paced Auditory Serial Addition Test. The results are reconciled as they relate to previous research examining the theoretical constructs of PTSD, clinical applications, and directions for future research.

Journal Article↗
PubMed1988

The parathyroid adenoma: an imaging/surgical perspective.

The clinical picture of hyperparathyroidism has changed since the implementation of routine serum calcium testing, resulting in more asymptomatic patients undergoing early surgical exploration. Although operative complications (e.g., recurrent laryngeal nerve paralysis, hypocalcemia, etc.) are not prevalent, the risk can be minimized by minimizing tissue dissection. For this reason, we feel that preoperative tumor localization is of great importance. We report our imaging results of parathyroid adenomas, utilizing ultrasonography, technetium-thallium subtraction scanning, digital subtraction angiography and magnetic resonance imaging. We also present an imaging protocol which, we have found, maximizes preoperative identification of these tumors.

Adenoma↗
PubMed1986

Efficacy, pharmacokinetics and tolerability of a somatostatin analogue (L-363,586) in insulin-dependent diabetes mellitus.

To assess the pharmacologic properties and possible use in the treatment of diabetes mellitus of a recently developed analogue somatostatin (L-363,586), the analogue (2, 5, 10 or 40 micrograms/hr), somatostatin (200 micrograms/hr), or placebo were infused intravenously for 5 hours in 6 insulin-dependent diabetic subjects who were given a standard meal containing xylose. The metabolic clearance rate of the analogue (approximately 300 ml/min) was 1/6 that previously reported for somatostatin (approximately 2000 ml/min) and its half-life was approximately 20 times as great as that reported for somatostatin (45 vs 2 min). At a dose of 10 micrograms/hr, the analogue produced suppression of plasma glucagon, growth hormone, glucose, xylose and triglyceride responses to meal ingestion which were comparable to those observed when somatostatin was infused at a rate of 200 micrograms/hr. We conclude that L-363,586 is a long-acting and potent analogue of somatostatin, which has the potential for use as an adjunct to insulin in the treatment of diabetes mellitus.

Adult↗
PubMed1983

Estimation and kinetic analysis of insulin-independent glucose uptake in human subjects.

Using the glucose clamp technique, glucose uptake was determined isotopically in normal human volunteers at plasma glucose concentrations of congruent to 60, 95, and 160 mg/dl during insulin infusions that increased plasma insulin to congruent to 20, 80, and 160 microU/ml. Because glucose uptake was found to be a linear function of plasma insulin at each plasma glucose concentration (r greater than 0.92, P less than 0.01), glucose uptake at 0 plasma insulin was estimated by linear regression analysis. The values thus derived (1.30, 1.62, and 2.59 mg . kg-1 . min-1 for plasma glucose concentrations of 60, 95, and 160 mg/dl, respectively) produced a linear Eadie-Hofstee plot, suggesting that insulin-independent glucose uptake followed Michaelis-Menten kinetics. The Km for glucose uptake at 0 plasma insulin (congruent to 10 mM) was similar to those observed for glucose uptake at the other plasma insulin concentrations studied (congruent to 9-12 mM), but its Vmax was less (5.2 vs. 6.4, 18.5, and 26.8 mg . kg-1 . min-1 for congruent to 20, 80, and 160 U/ml, respectively). These results indicate that in postabsorptive human subjects 75-85% of glucose uptake is noninsulin-mediated and provide additional support for the concept that insulin may increase glucose uptake merely by providing additional transport sites. The method described herein provides an assessment of insulin-independent glucose uptake in vivo that may prove useful in distinguishing between intrinsic defects of the glucose transport system and those due to defects in insulin action.

Adult↗
PubMed1982

Insulin increases the maximum velocity for glucose uptake without altering the Michaelis constant in man. Evidence that insulin increases glucose uptake merely by providing additional transport sites.

The present studies were undertaken to assess the mechanism by which insulin increases glucose uptake in man. Because glucose uptake in most mammalian tissues occurs predominantly by a facilitated transport system that follows Michaelis-Menten kinetics, glucose uptake was measured isotopically in normal volunteers over the physiologic range of plasma glucose and insulin concentrations and was subjected to Lineweaver-Burk and Eadie-Hofstee analysis. With both methods, increases in plasma insulin from 18 microunits/ml to 80 and 150 microunits/ml were found to increase the maximum velocity (Vmax) for glucose uptake nearly three- and fivefold, respectively, (P less than 0.025 and P less than 0.001) without significantly altering the Michaelis constant (Km). Because an increase in the affinity or molecular activity of transport sites or provision of additional transport sites that differed from those present basally should have altered the Km, whereas a mere increase in the number of transport sites would have only increased the Vmax, our results indicate that in man, insulin may increase glucose uptake merely by providing additional transport sites.

Adult↗