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Biomedical subjects

J Levy

Publications and source records attributed to J Levy.

At least 289 records · Page 16Linked to original sources
PubMed1990

Effects of food restriction and insulin treatment on (Ca2+ + Mg2+)-ATPase response to insulin in kidney basolateral membranes of noninsulin-dependent diabetic rats.

Insulin increases (Ca2+ + Mg2+)-ATPase activity in cell membranes of normal rats but fails to do so in membranes of non-insulin-dependent diabetic (NIDD) rats. The loss of regulatory effect of the hormone on the enzyme might contribute to the insulin resistance observed in the NIDD animals. To further test this hypothesis, the effects of insulin treatment and acute food restriction on the ability of insulin to regulate the ATPase activity in kidney basolateral membranes (BLM) of NIDD rats were studied. Although insulin levels in NIDD and control rats were similar, plasma glucose was higher in the NIDD rats (18.3 +/- 1.5 v 19.3 +/- 1.7 microU/mL and 236 +/- 32 v 145 +/- 3 mg/dL, respectively). Insulin treatment (2 U/100 g), which increased plasma insulin in the NIDD rats (47.8 +/- 11.5 microU/mL; P less than .05), did not decrease their glucose (221 +/- 25 mg/dL). Higher insulin dose (4 U/100 g) decreased glucose level in the NIDD rats (73 +/- 3 mg/dL; P less than .001) but increased their plasma insulin 10-fold (202.5 +/- 52.5 microU/mL). Acute food restriction decreased glucose levels in the NIDD rats to levels seen in controls (135 +/- 3 mg/dL), while their insulin decreased by half (8.5 +/- 1.0 microU/mL; P less than .05). Basal (Ca2+ + Mg2+)-ATPase activity in BLM of all diabetic rats was higher than in controls (P less than .05). None of the treatments reversed this defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The previous visual field: effects of lateralization and response accuracy on current performance.

The accuracy of performance in identifying syllables flashed to the RVF (right visual field) or LVF (left visual field) was strongly affected by the lateralization of and response accuracy for the previous stimulus, presented 10-20 sec earlier. For both the LVF and RVF, performance was better on Pre-LVF trials (previous stimulus in LVF) than on Pre-RVF trials (previous stimulus in RVF). The Pre-LVF advantage was the same in subjects with a strong RVF advantage and those with no asymmetry. Their performance was better when a previous stimulus had received adequate attention for correct encoding (Pre-Correct) than when it had not (Pre-Wrong), for both fields on Pre-LVF trials and the LVF, but not RVF, on Pre-RVF trials. Relations are discussed in terms of the capacities and properties of the RH (right hemisphere) and LH (left hemisphere) cerebral arousal systems.

Adult↗
PubMed1990

Adaptation of craniofacial muscles in subjects with craniomandibular disorders.

The purpose of this study was to examine muscle function in subjects with muscle pain. Forty-three subjects with pain in the craniomandibular muscles, clinically determined by manual palpation, were studied for alteration in recruitment of temporalis, masseter, and suprahyoid muscles during a series of phasic movements. Seventeen normal subjects were used as controls. The subjects with muscle pain were divided into three subgroups: (1) those with pain in both mandibular and neck muscles; (2) those with pain in these two muscle groups with joint degeneration; and (3) those subjects with pain only in mandibular muscles. Surface electromyographic (EMG) recordings were taken as each subject performed 16 different responses in which mandibular incisor movement was tracked simultaneously. The results show that the subjects with muscle pain use their anterior temporalis muscles with less frequency (i.e., probability) and with less intensity in several responses than normal subjects. These responses include rapid vertical closing movements, retrusion, ipsilateral laterotrusion, and natural as well as contralateral mastication. The masseter muscle is impaired much less in its function, and the recruitment of the suprahyoid muscles is not affected in the patients with muscle pain. Comparison of the bilateral activity in the anterior temporalis muscles during intercuspal clenching shows that the subjects with muscle pain often demonstrate a more severe asymmetrical recruitment of these muscles than the more symmetrical recruitment seen in normal subjects. Similar observations were made for the masseter muscle. These studies demonstrate that subjects with muscle pain in craniomandibular muscles alter the recruitment of their jaw muscles, thus supporting the concept that the neuromuscular system is altered in patients with craniomandibular disorders.

Adult↗
PubMed1990

Abnormal Ca2(+)-ATPase activity in erythrocytes of non-insulin-dependent diabetic rats.

Non-insulin-dependent diabetic (NIDD) rats have an increased Ca2(+)-ATPase activity in their kidney basolateral membranes. We find that a similar increased activity occurs in erythrocytes of the NIDD animals. This alteration in membrane ATPase activity appears to be specific for the Ca2(+)-ATPase as (Na(+) + K+) and Mg2(+)-ATPase and Na, K and Mg concentrations in the erythrocyte were not affected by the diabetic condition in these animals. Thus, abnormalities in membrane Ca2(+)-ATPase activity in the NIDD rats are not restricted to one tissue and appear to be a generalized pathology in the NIDD animals.

Animals↗
PubMed1990

Essential fatty acid deficiency mimicking porphyria cutanea tarda in a patient with chronic cholestasis.

Essential fatty acid deficiency was documented in a 3-year-old boy with chronic cholestasis secondary to paucity of intrahepatic bile ducts (Alagille's syndrome). Dietary management had consisted almost exclusively of a proprietary formula with over 80% of the fat as medium-chain triglycerides. The bullous lesions involved mostly sun-exposed areas and were diagnosed initially as being compatible with acquired porphyria cutanea tarda. Improvement followed correction of the fatty acid abnormalities with a polyunsaturated fat supplement administered orally. We postulate that the association of fatty acid deficiency and abnormal vitamin E status contributed to skin damage, possibly involving photosensitizing compounds poorly cleared by the markedly cholestatic liver.

Child, Preschool↗
PubMed1990

Nonocclusive mesenteric ischemia associated with propranolol overdose: implications regarding splanchnic circulation.

We describe a case of massive propranolol overdose in a healthy 19-year-old woman associated with isolated mesenteric ischemia following shock. We postulate that endogenous catecholamine release from shock combined with massive beta-adrenergic blockade led to severe splanchnic vasoconstriction from unopposed alpha-adrenergic activity. This case supports current thinking regarding the effect of vasoactive mediators on the gastrointestinal tract in humans and might be relevant to the mechanism of action of propranolol in the prophylaxis of variceal bleeding.

Adrenergic beta-Antagonists↗
PubMed1990

Characterization and description of "Campylobacter upsaliensis" isolated from human feces.

During a 3-year period, "Campylobacter upsaliensis" was isolated from 99 patients. Phenotypic characterization and numerical analysis of protein electrophoregrams showed evidence that "C. upsaliensis" is a distinct Campylobacter species with unique characteristics. The MBCs of 13 antibiotics were determined. In general, these organisms were highly susceptible to drugs that were present in the selective isolation media, making none of the available selective media suitable for the isolation of "C. upsaliensis." Ten strains were found to be resistant to erythromycin (MBCs, greater than or equal to 12.50 mg/liter). Plasmid DNA was detectable in 89 of the 99 strains; 16 plasmid profiles could be identified. Plasmid pattern 16, containing four plasmids of 52, 32, 5.5, and 2.6 megadaltons, represented 60.7% of the plasmid-containing strains. None of the "C. upsaliensis" strains could be agglutinated with antisera against heat-labile antigens from C. jejuni, C. coli, or C. laridis. "C. upsaliensis" was found to be susceptible to serum killing and was readily phagocytized by human polymorphonuclear cells.

Bacterial Proteins↗
PubMed1990

Insulin antagonistic effects of insulin receptor antibodies on plasma membrane (Ca2+ + Mg2+) ATPase activity: a possible etiology of type B insulin resistance.

The regulatory effect of insulin on plasma membrane (Ca2+ + Mg2+)ATPase activity in target tissues for insulin was proposed to be of importance in mediating the hormone's cellular action. Consequently, polyclonal insulin receptor antibodies from patients with type B insulin resistance (B7 and B10) were used as probes to further explore a possible role for this ATPase in insulin action. The antibodies B7 and B10 obtained during the active phase of the disease manifested insulinomimetic actions in rat renal cortical basolateral membranes by displacing [125I]insulin bound to the membranes and stimulating the tyrosine kinase activity of solubilized insulin receptors in a dose-dependent manner. In contrast, these antibodies had insulin antagonistic effects on the membrane (Ca2+ + Mg2+)ATPase activity. While insulin stimulated, both antibodies inhibited the ATPase basal activity in a dose-dependent manner. Furthermore, the stimulatory effect of insulin on the ATPase was completely abolished by the antibodies. Immunoglobulin fractions obtained from patient B10 in the clinically inactive phase of the disease and from pooled normal human sera did not affect basal or insulin-stimulated ATPase activity. The effects of insulin receptor antibodies on basal and insulin-stimulated (Ca2+ + Mg2+)ATPase activities were specific. The receptor antibody did not affect PTH-stimulated (Ca2+ + Mg2+) ATPase activity, nor did it affect other kidney basolateral membrane ATPase basal activities. The data reveal that insulin receptor antibodies have a direct regulatory effect on the plasma membrane (Ca2+ + Mg2+) ATPase. We suggest that the insulin antagonistic effects of the insulin receptor antibodies on the ATPase might explain in part the impaired insulin action in type B insulin resistance.

Animals↗
PubMed1990

Correlation of urinary albumin and beta-2-microglobulin and growth hormone excretion in patients with diabetes mellitus and short stature.

We examined the correlation between urinary GH, urinary albumin, and beta-2-microglobulin excretion to determine how the excretion of GH relates to markers of renal glomerular and tubular function. Urinary albumin and GH excretion was determined in timed daytime and nighttime urine collections obtained from both subjects with diabetes mellitus and subjects with short stature. For subjects with diabetes, urinary GH excretion rate correlated highly with urinary albumin concentration and excretion rate in both the range of 0 to 1.6 g/L (r = 0.75), P less than 0.001) and in the microalbuminuria range, 0 to 0.4 g/L (r = 0.53, P less than 0.001). Changes in GH and albumin excretion occurred in parallel in 71% of the subjects with diabetes and elevated albumin excretion. The mean GH excretion rate was higher in the group with elevated albumin excretion rate (AER) during both day and night compared to the group with microalbuminuria during the day and normal AER at night. For subjects with short stature, the mean albumin excretion rate was 0.7 +/- 1.3 micrograms/min (range 0.05-8.3 micrograms/min) using a sensitive enzyme-linked immunosorbent assay to measure albumin concentration. The correlation of GH and albumin excretion rates for the subjects with short stature was not statistically significant (r = 0.14, P less than 0.5). About half of the subjects with diabetes and elevated AER (greater than 10 micrograms/min) had a GH excretion rate within the range observed in subjects with short stature. The GH and albumin excretion rate were not correlated in this group. There was a positive correlation of both albumin and GH excretion rate with age in the subjects with diabetes. Urinary GH and beta-2-microglobulin excretion rates were determined in a larger group of subjects with diabetes and a separate group with short stature. Urinary GH and beta-2-microglobulin excretion were correlated both in subjects with diabetes (r = 0.46, P less than 0.001) and with short stature (r = 0.64, P less than 0.001). The association was present in urine collected either during the day or night. The mean GH excretion rate of the group with diabetes was greater than the group with short stature. In conclusion, there was an association of urinary GH and albumin excretion rate in subjects with abnormal glomerular function as indicated by elevated albumin excretion rate. An association of urinary GH and beta-2-microglobulin excretion was observed in subjects with normal tubular function.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

High-fat feeding induces tissue-specific alteration in proportion of activated insulin receptors in rats.

High dietary fat intake causes glucose intolerance and insulin resistance in man and in laboratory rats. We studied possible mechanisms of this insulin resistance in rat kidney, muscle and liver. In high-fat fed rats the body weight, plasma insulin concentration, plasma glucose levels, and serum triglyceride concentration were significantly higher than in the control rats. 125I-insulin binding to kidney basolateral membrane insulin receptors from high-fat fed rats was lower than in control rats. Basal as well as insulin-stimulated tyrosine kinase activity per insulin receptor was higher in the high-fat fed group, accompanied by increased autophosphorylation of the beta-subunit of the receptor and higher proportion of tyrosine-phosphorylated insulin receptors. In contrast, both in the skeletal muscle and the liver the insulin-stimulated tyrosine kinase activity per insulin receptor was significantly lower in high-fat fed animals, accompanied by diminished autophosphorylation of the beta-subunit of the receptor and lower proportion of tyrosine-phosphorylated receptors. Our results indicate tissue-specific alterations in transmembrane signaling induced by high-fat feeding in target tissues for insulin which in turn might contribute to the observed insulin resistance.

Animals↗
PubMed1990

Effect of insulin on glucose utilization in epitrochlearis muscle of rats with streptozocin-induced NIDDM.

Because skeletal muscle plays a major role in glucose disposal, it may be the primary site of insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM). Rates of glycogen synthesis (GS), glucose utilization via glycolysis, glycolytic utilization (GU), and glucose transport (GT) were studied in epitrochlearis muscles (EMs) obtained from 10-wk-old nonfasted Sprague-Dawley rats in which NIDDM was neonatally induced with streptozocin. Plasma glucose in NIDDM rats was elevated (P less than 0.001), whereas plasma insulin was similar in NIDDM and control rats. No differences in muscle weight, protein, glycogen, ATP, phosphocreatine, lactate, lactate-pyruvate ratios, or glucose-6-phosphate were noted in EMs of control and NIDDM rats. EMs were incubated in medium containing 5.6 or 11.2 mM glucose with tracer D-[5-3H]glucose and insulin from 0 to 7.18 x 10(-7) M for 1 or 2 h, and GS, GT, and GU were evaluated. Similar rates of basal (non-insulin-mediated) and insulin-stimulated GS, GU, and GT were observed in EMs of NIDDM and control rats incubated in 5.6 mM glucose for 2 h. Insulin dose-response curves revealed similar sensitivities and responsiveness. Increasing glucose concentration (from 5.6 to 11.2 mM) induced significant increases in basal rates of GS, GU, and GT in EMs of control but not NIDDM rats. Insulin dose-response curves for GS and GT revealed decreased sensitivity and no change in responsiveness in EMs of control and NIDDM rats, even though GU of EMs of NIDDM rats was significantly lower at basal and all other insulin concentrations. These data revealed that both insulin resistance and glucose resistance contribute to the impaired glucose metabolism in EMs of the NIDDM rat.

Adenosine Triphosphate↗
PubMed1990

Intraocular pressures during high-flux hemodialysis.

The intraocular pressures of 16 patients with end stage renal failure treated with high-flux dialysis were measured before and during a high-flux dialysis treatment. The patients were selected so as not to have glaucoma or history of glaucoma. Intraocular pressures did not change significantly in any patients during or following a high-flux hemodialysis treatment. These data suggest that high-flux hemodialysis does not result in increases in intraocular pressure nor does it precipitate acute glaucoma in well-dialyzed patients undergoing intermittent in-center hemodialysis.

Adult↗
PubMed1990

Antibiotic resistance in Europe and the current use of antibiotics in severe pediatric infections.

The prevalence of antibiotic resistance among bacteria responsible for severe infections in childhood is increasing. In H. influenzae, clinically relevant resistance to ampicillin and chloramphenicol is caused by plasmid mediated enzymatic drug inactivation whereas penicillin resistant pneumococci emerge as the result of alterations in their penicillin binding proteins. In N. meningitidis both mechanisms have recently been implicated in penicillin resistance. Although antibiotic resistant H. influenzae, S. pneumoniae and, to much less extent, N. meningitidis have a widespread distribution, marked geographical variations exist in their prevalence. In areas where these drug resistant bacteria are reported, cefotaxime or ceftriaxone should be used for the empiric treatment of suspected severe bacterial infections in childhood.

Anti-Bacterial Agents↗
PubMed1990

Abnormal insulin receptor tyrosine kinase activity in kidney basolateral membranes from non-insulin-dependent diabetic rats.

Neonatal rats that receive injections of streptozotocin develop insulin resistance and non-insulin-dependent diabetes mellitus (NIDDM). Insulin resistance precedes development of overt diabetes, and some insulin bioeffects are known to be impaired at the postreceptor level in several target tissues of this rat model. We studied a possible contribution of altered insulin receptor function to the impaired insulin action in these animals. Activity of the insulin-sensitive tyrosine kinase of receptors from kidney cortical basolateral membranes (BLMs) obtained from these nonobese, normoinsulinemic, insulin-resistant rats was examined at the age of 5 weeks (before overt hyperglycemia developed) and at 10 weeks (after NIDDM was fully manifested). In experimental animals, at both 5 and 10 weeks, binding of insulin labeled with iodine 125 to crude kidney BLM was higher than in their control littermates. However, no such difference was found with insulin binding to purified insulin receptors from BLM. The insulin receptor, tyrosine kinase activity (TKA), to an exogenous substrate was higher in diabetic tissue both at basal condition and after insulin stimulation at both 5 and 10 weeks of age. Autophosphorylation of the beta-subunit of the insulin receptor and the proportion of tyrosine-phosphorylated ("active") insulin receptors from BLM was also higher in diabetic rats. There was an age-related increase in the receptor TKA between 5 and 10 weeks in both diabetic and control animals. A 24-hour fast normalized insulin binding and nearly abolished the difference in TKA of the BLM receptors from 5-week-old insulin-resistant rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Adenovirus-related hemophagocytic syndrome after bone marrow transplantation.

Four weeks following autologous bone marrow transplantation for Wilms' tumor, a patient developed fever, hepatomegaly, coagulation disorders and pancytopenia. Bone marrow studies showed progressively increased hemophagocytosis of normal hematopoietic progenitors by histiocytes resulting in aplasia. Adenovirus type 11 was consistently isolated from urine and stool cultures, and one of the marrow aspirates. At autopsy, adenovirus was isolated from the lungs, liver, heart, intestine and spleen. These findings are consistent with the previously described virus-associated hemophagocytic syndrome, which have not been associated with bone marrow transplantation. This case suggests that this diagnosis should be considered in any bone marrow transplant patient who has evidence of secondary graft failure.

Adenovirus Infections, Human↗
PubMed1989

Role of cellular calcium metabolism in abnormal glucose metabolism and diabetic hypertension.

The prevalence of hypertension in patients with non-insulin-dependent diabetes mellitus (NIDDM) is considerably higher than in the non-diabetic population. Insulin resistance may contribute to this increased prevalence. Abnormal cellular calcium (Ca2+) homeostasis may link insulin resistance and high blood pressure in patients with NIDDM. Observations of abnormal cellular Ca2+ homeostasis in animal models of NIDDM and obesity as well as in diabetic patients are consistent with this hypothesis. Abnormalities in cellular Ca2+ homeostasis are also found in hypertensive animals and humans. Alterations in cell membrane phospholipid content and distribution may be the primary cause of abnormal plasma membrane Ca2+ fluxes in patients with NIDDM and hypertension.

Animals↗
PubMed1989

Beta cell desensitization to glucose induced by hyperglycemia is augmented by increased calcium.

Chronic hyperglycemia has been shown to induce a decrease in beta cell sensitivity to a subsequent glucose challenge. Calcium is a necessary cofactor in the insulin secretory process and glucose elevates cytoplasmic levels. This study was designed to study whether chronic exposure to different extracellular calcium and glucose concentrations would affect the islets' subsequent response to regulatory stimuli. Islets were isolated and cultured in TC 199 plus 10% beta calf serum, glucose (5.5 or 27.5 mM) and calcium (0.5, 2.5 or 4.0 mM) for 48 h. Following culture, the islets were harvested and incubated a second time in the presence of glucose and/or arginine, theophylline, and trifluoperazine (TFP). Some islets were used for insulin content, protein synthesis studies and/or CO2 production from labelled glucose. Islets cultured in a normal glucose environment with low or normal calcium concentration maintained the capacity to respond to a subsequent glucose or arginine challenge. However, islets cultured in a high glucose or high calcium medium failed to respond to a second glucose or arginine stimulus. Theophylline stimulated insulin secretion from both glucose-sensitive and non-sensitive islets, while trifluoperazine inhibited glucose-stimulated insulin secretion in previously sensitive islets and increased insulin secretion in previously non-sensitive islets. The different culture conditions did not alter insulin content, protein synthesis or glucose conversion to labelled CO2. We conclude that chronic exposure to high glucose decreases beta cell responsiveness to glucose and amino acids. Increased extracellular calcium augmented this response. However, the beta cell remained sensitive to theophylline-induced insulin secretion, while TFP paradoxically increased insulin secretion in the glucose-insensitive beta cells. Protein synthesis and glucose oxidation were not affected by culture conditions. Thus we suggest that the glucose-induced desensitization of the beta cells may be due to alterations in the calcium-dependent release mechanism.

Animals↗