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Biomedical subjects

S Craft

Publications and source records attributed to S Craft.

48 records · Page 3Linked to original sources
PubMed1993

Mechanism of awareness of hypoglycemia. Perception of neurogenic (predominantly cholinergic) rather than neuroglycopenic symptoms.

We sought 1) to determine which symptoms of hypoglycemia are reproducible, 2) to pharmacologically distinguish neurogenic (autonomic) from neuroglycopenic symptoms, and 3) to test the hypothesis that awareness of hypoglycemia is the result of perception of neurogenic rather than neuroglycopenic symptoms. Awareness of hypoglycemia and 19 symptoms were quantitated in 10 normal, young adults, each studied on four occasions in random sequence, during 1) clamped euglycemia (approximately 5 mM), 2) clamped hypoglycemia (approximately 2.5 mM), 3) clamped hypoglycemia with combined alpha- and beta-adrenergic blockade (phentolamine and propranolol), and 4) clamped hypoglycemia with pan-autonomic blockade (phentolamine, propranolol and atropine). Significant (ANOVA, P < 0.001) treatment effects on the awareness of hypoglycemia ("blood sugar low") were noted. No change occurred in the score for this during euglycemia, but the mean +/- SE increase was 2.1 +/- 0.4 during hypoglycemia. This increase was not reduced significantly by adrenergic blockade (1.6 +/- 0.5), but was reduced significantly and substantially (approximately 70%) by pan-autonomic blockade (0.6 +/- 0.3). Significant neurogenic symptoms included shaky/tremulous (P < 0.001), heart pounding (P < 0.001), and nervous/anxious (P = 0.002), all adrenergic; and sweaty (P < 0.001), hungry (P < 0.001), and tingling (P = 0.009), all cholinergic. Significant neuroglycopenic symptoms, those produced by hypoglycemia but not reduced by pan-autonomic blockade, included warm (P < 0.001), weak (P = 0.011), difficulty thinking/confused (P = 0.004), and tired/drowsy (P = 0.003). We conclude that muscarinic cholinergic mechanisms mediate an important and previously uncharacterized component of the neurogenic symptoms of hypoglycemia and awareness of hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1992

Lateralized deficits in visual attention in males with developmental dopamine depletion.

Children with early treated phenylketonuria (ETPKU), a disorder associated with developmental dopamine depletion, were tested with a visual orienting paradigm to determine the existence of lateralized deficits in specific attentional operations. Male ETPKU subjects showed a right visual field impairment in disengaging attention, indicating left hemisphere dysfunction, and overall slowed reaction times. Female ETPKU and normal subjects did not differ. The results suggest that for males, dopamine depletion disrupts left hemisphere function. This finding has important implications for disorders with suspected developmental dopamine abnormalities, and may also illustrate how sex differences in functional lateralization develop in the normal brain.

Attention↗
PubMed1992

Glucose and memory in mild senile dementia of the Alzheimer type.

Glucose utilization appears to play a role in memory, and patients with Senile Dementia of the Alzheimer Type (SDAT) show particular abnormalities of the glucose system. The present study examined the effects of glucose administration on memory in subjects with mild SDAT and age-matched controls. SDAT subjects demonstrated greater overall increases in blood glucose levels following glucose administration. Normal subjects whose blood glucose levels returned to near baseline following glucose administration showed facilitated memory performance, whereas SDAT subjects whose blood glucose levels remained elevated showed significant improvement following glucose administration. The results suggest that impaired glucose regulation contributes to memory impairment in SDAT.

Aged↗
PubMed1991

Higher glycemic thresholds for symptoms during beta-adrenergic blockade in IDDM.

We tested the hypotheses that nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations and that neither neuroglycopenic symptoms nor cognitive impairments during hypoglycemia are altered by beta-adrenergic blockade. To do so, we applied the euglycemic and stepped hypoglycemic clamp techniques to patients with moderately controlled insulin-dependent diabetes mellitus (IDDM) in the absence (n = 8) and presence (n = 9) of the nonselective beta-adrenergic antagonist propranolol. Compared with the corresponding euglycemic clamps, total symptom scores first increased at the 4.4-mM plasma glucose step (a higher level than that of 2.8 mM in nondiabetic subjects studied previously) in the absence of propranolol. Beta-adrenergic blockade did not produce absolute hypoglycemia unawareness. Indeed, at the frankly hypoglycemic step of 2.8 mM, total symptom scores tended to be higher in the presence than in the absence of propranolol. This was largely the result of greater (P less than 0.01) perception of diaphoresis. However, symptom scores did not increase until the 3.3-mM plasma glucose step during beta-adrenergic blockade. The perception of hunger, and perhaps that of tremulousness, was reduced by propranolol at the higher glucose steps. Neuroglycopenic symptoms were not reduced by propranolol. The cognitive function of memory, but not that of attention, was impaired, also starting at the 4.4-mM glucose step. This was not impaired further by propranolol. Thus, we formed the following conclusions. 1) Nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations in patients with IDDM. 2) Beta-adrenergic blockade does not reduce neuroglycopenic symptoms, and it does not further impair cognitive function during hypoglycemia in IDDM patients.

Adult↗
PubMed1989

Contributions of clinical neuropsychology to the study of schizophrenia.

Clinical neuropsychological findings are examined with respect to competing hypotheses about localized neuropathology in schizophrenia. Two general models of structural and functional impairment are described. The first addresses deficits in cortical/subcortical processes concerned with arousal, attention, and higher cortical functions. The second addresses impairments in the balance of lateralized functions consistent with left hemisphere overactivation. Empirical data provide support for both models, and suggest that the explanatory power of these models may vary when they are applied to different subtypes of schizophrenia.

Cerebral Cortex↗
PubMed1986

Identification of the crossover site during FLP-mediated recombination in the Saccharomyces cerevisiae plasmid 2 microns circle.

The FLP protein of the Saccharomyces cerevisiae plasmid 2 microns circle catalyzes site-specific recombination between two repeated segments present on the plasmid. In this paper we present results of experiments we performed to define more precisely the features of the FLP recognition target site, which we propose to designate FRT, and to determine the actual recombination crossover point in vivo. We found that essential sequences for the recombination event are limited to an 8-base-pair core sequence and two 13-base-pair repeated units immediately flanking it. This is the region identified as the FLP binding site in vitro and at which FLP protein promotes specific single-strand cleavages (B. J. Andrews, G. A. Proteau, L. G. Beatty, and P. D. Sadowski, Cell 40:795-803, 1985; J. F. Senecoff, R. C. Bruckner, and M. M. Cox, Proc. Natl. Acad. Sci. USA 82:7270-7274, 1985). Mutations within the core domain can be suppressed by the presence of the identical mutation in the chromatid with which it recombines. However, mutations outside the core are not similarly suppressed. We found that strand exchange during FLP recombination occurs most of the time within the core region, proceeding through a heteroduplex intermediate. Finally, we found that most FLP-mediated events are reciprocal exchanges and that FLP-catalyzed gene conversions occur at low frequency. The low level of gene conversion associated with FLP recombination suggests that it proceeds by a breakage-joining reaction and that the two events are concerted.

Base Sequence↗
PubMed1977

Motor conduction of the anterior interosseous nerve.

Motor conduction examinations of the left anterior interosseous nerve were performed on 25 healthy women. The purposes of this study were to determine the optimal position for placement of the active recording electrode, and to report normal motor conduction values for the anterior interosseous nerve. The anterior interosseous nerve (branch of the median nerve) was stimulated proximal to the elbow and the evoked responses were recorded from three sites over the flexor pollicis longus. The optimal site for placement of the active recording electrode was over the lateral distal one-third of the anterior surface of the forearm at a point representing the distal 38% of the length of the forearm. A latency of 4.0 msec and an amplitude of 2.5 mv may serve as the limits of normal values for motor conduction of the anterior interosseous nerve and for action potentials of the flexor pollicis longus muscle, respectively.

Action Potentials↗
PubMedDate not supplied

Memory improvement following induced hyperinsulinemia in Alzheimer's disease.

Dementia of the Alzheimer type (DAT) is accompanied by disruption in glucose regulation and utilization that may contribute to its characteristic memory impairment. Increasing glucose availability by raising plasma glucose improves memory in patients with DAT. Such memory improvement is associated with a secondary elevation in plasma insulin levels, raising the question of whether improvement is due to changes in insulin levels, independent of hyperglycemia. Distributions of insulin receptors in the hippocampus and insulin-mediated increases in glucose utilization in entorhinal cortex provide potential mechanisms for such improvement. We show that raising plasma insulin through intravenous infusion while keeping plasma glucose at a fasting baseline level produces striking memory enhancement for patients with DAT. Previous findings of hyperglycemic memory enhancement were also replicated. Patients with DAT also showed abnormal plasma levels of glucoregulatory hormones and metabolites at baseline and during metabolic manipulations. Our findings suggest that neuroendocrine factors play an important role in the pathophysiology of DAT.

Aged↗
PubMedDate not supplied

Enduring psychiatric and neuropsychologic sequelae in the post-encephalitis patient.

Initial presentations of encephalitis are sometimes misdiagnosed as psychoses due to the predominance of psychiatric symptoms and frequently negative neurological work-ups. It is likely that many of these errors are never discovered. The patient described herein is an exception. Her symptoms, diagnosis, and treatment have now been followed for nearly two years and suggest not only that the initial diagnosis was in error but also that both psychiatric and organic symptoms can endure as sequelae of encephalitis. Questions regarding optimal treatment and reasons for clinical improvement are addressed.

Adult↗