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Biomedical subjects

M Levin

Publications and source records attributed to M Levin.

At least 91 records · Page 5Linked to original sources
PubMed1989

Effect of glucocorticoid deficiency on arterial pressure in conscious spontaneously hypertensive rats.

The effect of selective glucocorticoid or mineralocorticoid deficiency upon arterial pressure was evaluated in unanesthetized adult spontaneously hypertensive rats (SHR). Adrenalectomized SHR were replaced with 6 micrograms/24 h aldosterone (ALDO), 10 microgram/24 h dexamethasone (DEX), or both aldosterone and dexamethasone (ALDO + DEX) by IP osmotic mini-pumps. These were compared to sham-operated SHR (SHAM) and adrenalectomized SHR given no steroid replacement (ADX). Drinking fluid for all groups was 1% NaCl + 2.5% glucose. Six days after adrenalectomy, intra-arterial mean arterial pressure (MAP) fell from 174 +/- 2 to 149 +/- 6 mm Hg in ALDO (n = 8, P less than .01) and from 179 +/- 4 to 125 +/- 4 in ADX (n = 6, P less than .01). In contrast, MAP rose in SHAM from 171 +/- 4 to 179 +/- 5 mm Hg (n = 7, P less than .01), in ALDO + DEX from 161 +/- 3 to 184 +/- 4 mm Hg (n = 7, P less than .01), and in DEX from 162 +/- 2 to 181 +/- 4 mm Hg (n = 7, P less than .01). The results indicate that when diet salt intake is high, glucocorticoid action is necessary for the full expression of hypertension in adult SHR.

Adrenalectomy↗
PubMed1989

Early markers of the renal complications of insulin dependent diabetes mellitus.

We investigated the associations between albuminuria, metabolic control, glomerular filtration, blood pressure, and platelet function in children with insulin dependent diabetes mellitus. The geometric mean (95% tolerance levels) albumin excretion (expressed as the geometric mean albumin to creatinine ratio on two overnight urine collections (UA/UC], in 60 diabetic children was 0.72 (0.80-6.9) mg/mmol, significantly greater than in 45 normal children (geometric mean 0.41 (0.14-1.17]. Mean (SD) glomerular filtration rate, measured by 51Cr edetic acid clearance during constant infusion, was significantly greater in diabetic children (129 (20) ml/min/1.73 m2) compared with normal controls (109 (13]. Mean (SD) renal length for height standard deviation score was +0.25 (1.1); systolic blood pressure standard deviation score was 0.15 (0.65), and diastolic blood pressure was 0.51 (0.82). Spontaneous platelet aggregation, expressed as percentage fall in platelet count in stirred whole blood after 2 minutes was 17.8 (9.2)% in the diabetic compared with 12.3 (7.9)% in normal children. UA/UC correlated with renal length and of the children with UA/UC above the normal range, 70% also had a glomerular filtration rate above the normal range. There was a weak correlation between UA/UC and glycated haemoglobin (HbA1c). All children with spontaneous platelet aggregation above normal had had diabetes for more than seven years. These cross sectional data define some of the early markers and inter-relationships that may be important in the development of nephropathy.

Adolescent↗
PubMed1989

Effects of systemic alkalosis on urinary magnesium excretion in the rat.

Metabolic alkalosis has previously been shown to have an antimagnesiuric influence. To further clarify this phenomenon, short-term clearance studies were performed on intact anesthetized rats subjected to 0.9% saline infusion, 0.15 M NaHCO3 infusion or acute respiratory alkalosis. The experimental protocols resulted in a similar degree of natriuresis in each of the three groups. The increase in plasma pH value was similar both in animals treated with NaHCO3 and animals with respiratory alkalosis. Filtered loads of Mg did not differ in the three experimental groups. However, only acute metabolic alkalosis was associated with a reduction in the absolute rate of Mg excretion (saline: 0.49 +/- 0.05 mu Eq/min; 0.15 M NaHCO3: 0.29 +/- 0.04 mu Eq/min; acute respiratory alkalosis: 0.48 +/- 0.03 mu Eq/min) and fractional Mg excretion (saline: 40.3 +/- 5.3%; 0.15 NaHCO3: 18.7 +/- 1.4%; acute respiratory alkalosis: 37.2 +/- 6.9%). A similar decrease in urinary Mg excretion in animals treated with bicarbonate infusion was observed following removal of the parathyroid gland. Moreover, for any given rate of urinary Na excretion, Mg excretion was lower in bicarbonate-treated animals than in rats infused with saline solution. Intact animals treated with increasing doses of NaHCO3 revealed a statistically significant inverse correlation between the Mg to Na clearance ratio and urinary and plasma bicarbonate concentration. In contrast, such a correlation was not observed during respiratory alkalosis. The findings suggest that bicarbonate ion directly stimulates tubular magnesium reabsorption independent of the presence or absence of parathyroid hormone.

Alkalosis↗
PubMed1989

Clinical, radiographic, SEM evaluation and assessment of microleakage of Class II composite restorations.

The influence of incremental or bulk filling techniques, and reapplication of unfilled resin (impregnation) to the margins with an enamel bonding agent, on marginal adaptation was evaluated in Class II composite restorations by clinical, radiographic, scanning electron microscope (SEM) and dye penetration techniques. Cavities were prepared in 80 extracted permanent posterior teeth. All cavity walls were treated with polyacrylic acid for 10 seconds. The enamel was etched for 1 minute, rinsed, dried, and lined with Scotchbond. Forty cavities were filled by increments of P30 and 40 cavities in bulk. The margins of the restorations of 20 teeth in each group were re-etched for 30 seconds and Concise Enamel Bond reapplied. The clinical scores were excellent for all restorations. Radiographic examination showed twice as many bubbles in the incrementally filled restoration than in the group filled in bulk. In 53 teeth, a radiolucent area between the dentin and the restorative material was found. After sectioning, this area was found to correspond to a hard material. The SEM revealed excellent margins in the groups of teeth that were impregnated with an unfilled resin, whereas 13 teeth without impregnation showed defective margins. The dye penetration, as a test for marginal leakage, was minimal at the occlusal surface of all teeth. At the cervical surface, 10.5% of the impregnated teeth showed severe dye penetration compared to 18% of the nonimpregnated teeth. No correlation was found between dye penetration at the cervical surface and the thickness of the residual enamel in this area.(ABSTRACT TRUNCATED AT 250 WORDS)

Composite Resins↗
PubMed1989

Hemolytic uremic syndrome.

HUS has now emerged as a common clinical and pathologic syndrome that may result from a variety of disease processes. On the basis of clinical and epidemiologic criteria, several distinct subgroups of the disorder have been distinguished, the most common of which are the result of infectious processes, whereas the rarer forms may be genetically determined or acquired defects in vascular homeostasis. A related group of bacterial toxins, verotoxins, and Shiga toxin, produced by a variety of species of enteric pathogens, have been implicated in the pathogenesis of typical childhood HUS. In the few years since verotoxin-producing organisms were first incriminated as the possible etiologic agents of HUS, there has been a remarkable growth in knowledge of the biology of verotoxin and its role, not only in HUS but in hemorrhagic colitis and childhood diarrhea. The availability of purified toxin and new tools for detection of verotoxin and verotoxin-producing organisms, such as monoclonal antibodies and probes for DNA hybridization, should enable definitive studies of the epidemiology and pathogenesis of verotoxin-associated HUS to be undertaken. The growing understanding of HUS should eventually lead to improved treatment and ultimately to prevention of this serious childhood disorder.

Child↗
PubMed1988

Intravascular platelet activation in the hemolytic uremic syndrome.

We studied intravascular platelet activation in patients with typical (epidemic) and atypical (sporadic) HUS and found defective aggregation, decreased platelet and increased plasma serotonin in both groups. The findings were present not only on admission during the thrombocytopenic stage of the disease, but persisted for several weeks after recovery of the platelet count. Reduced endothelial PGI2 production was significantly more common in plasma from atypical than typical cases. Plasma from both typical and atypical HUS patients induced aggregation of normal platelets, but this phenomenon was unrelated to both the presence of thrombocytopenia or the stage of the disease. Serum platelet aggregating activity was higher in the atypical HUS patients, and was not associated with immune complexes detectable by polyethylene glycol precipitation. The data indicate that intravascular platelet activation is a feature of both forms of HUS, and may be initiated by different mechanisms in the two subgroups. While abnormal PGI2 synthesis appears to be important in the atypical cases, neither defective PGI2 production nor platelet aggregation by plasma factors adequately accounts for platelet activation in the majority of typical cases.

Adolescent↗
PubMed1988

Acute mercury poisoning and mercurial pneumonitis from gold ore purification.

We describe four men who had symptoms of acute mercury poisoning following exposure to mercury vapor. They were attempting home gold ore purification using a gold-mercury amalgam and sulfuric acid. Three of the four patients required treatment with penicillamine. The clinical and laboratory data are presented along with pulmonary function test results. Long-term follow-up of one patient indicates residual morbidity, with continued reduction in pulmonary diffusing capacity. This suggests permanent impairment of pulmonary function despite prompt chelation therapy.

Acute Disease↗
PubMed1987

Inhibitory and facilitatory effects from the peroneal nerve onto the soleus H-reflex in normal and spinal man.

The effects of conditioning stimulation of a mixed nerve in the leg, the common peroneal nerve (CPN), on the ipsilateral soleus H-reflex were compared with the effects of stimulating its cutaneous branch, the superficial peroneal nerve (SPN), in two groups of subjects--normals and patients with spinal spasticity subsequent to a clinically complete transection of the spinal cord. Condition-test delays of 20 msec to 2 sec, measured from the end of the 20 msec train (3 pulses at 100 Hz), were investigated. In normal subjects, CPN stimulation at 1.4 X MT profoundly depressed the soleus H-reflex. There was an initial depression (peak 40-90 msec) followed by a slow recovery which was incomplete at condition-test delays of 2 sec. One-half of the subjects showed a late facilitation, or disinhibition, peaking at 170-190 msec. The inhibitory effects were attributed to activation of low threshold, groups I and II, muscle afferents because stimulation of the SPN, at 1.5 X threshold for a compound action potential recorded from the CPN, had only facilitatory effects on the soleus H-reflex. Facilitation occurred at condition-test delays of 30-190 msec. The cutaneous stimulation was presumed to activate the largest, A beta, cutaneous afferents as it elicited a weak paraesthesia on the dorsum of the foot. The results suggested that cutaneous afferents may have contributed to the late facilitation seen with CPN conditioning stimulation. In spinal cord-lesioned subjects, CPN stimulation depressed the soleus H-reflex but the decrease was less and the recovery was faster and more complete than in normals. The magnitude of the initial depression at 20-100 msec varied with the severity of the spasticity, subjects with mild spasticity showing less of a depression. Weak cutaneous conditioning stimulation either had no effect or produced a slight depression of the soleus H-reflex, providing clear evidence that transmission in the pathways mediating the facilitatory effects of cutaneous afferents onto extensor motoneuronal pools is depressed in spinal spasticity. This may shift the balance of activity toward the flexor motoneurones, thus favouring the development of, for example, flexor spasms and flexor hypertonia. Since inhibitory effects from cutaneous stimulation are associated with activation of higher threshold afferents in normal man, the present results may reflect a decrease in the threshold for flexor withdrawal reflexes commonly associated with spasticity of spinal origin.

Adolescent↗
PubMed1987

Peroxidatic catecholestrogen production by human breast cancer tissue in vitro.

The ability of breast cancer tissues from postmenopausal women to form catechol estrogens was examined by using a product isolation assay. Initial assays were carried out in the presence of either: (a) NADPH, the co-factor for monooxygenase mediated catecholestrogen (CE) formation or; (b) light-activated Tween 80 (LAT-80), a putative organic hydroperoxide co-factor for peroxidatic activity. Under monooxygenase conditions, CE formation by homogenates of 10 tumors did not exceed that obtained with heat denatured tissue. In contrast, 17 of 20 tumors incubated with LAT-80 synthesized significant amounts of CE (8.5 +/- 1.17 2-hydroxyestradiol [2-OH-E2] and 12.8 +/- 2.4 nmol/g protein/10 min 4-hydroxyestradiol [4-OH-E2]). Substitution of cumene hydroperoxide, an organic hydroperoxide, for LAT-80 enhanced estrogen 2/4 hydroxylase (E-2/4-H) activity over 200-fold, making it possible to characterize systematically the peroxidatic activity. The properties of peroxidatic E-2/4-H activity were similar to those of soluble peroxidases isolated from brain, including an acidic pH optimum, localization in the soluble fraction, an apparent Km in the range of 80 microM and an apparent Vmax in the range of 4000 nmol/g/protein/10 min for both 2- and 4-OH-E2. Under optimal assay conditions, peroxidatic E-2/4-H activity was identified in 10 of 13 tumors (2480 +/- 580 nmol/g protein/10 min for 2-OH-E2 and 2790 +/- 600 for 4-OH-E2). The level of activity detected suggests a biological relevance for CE formation by breast cancer tissue.

Animals↗
PubMed1987

Decreased sensitivity to heparin in vitro in steroid-responsive nephrotic syndrome.

The in vitro heparin sensitivity of 18 nephrotic children was compared with that of 10 normal children and 13 children with other renal diseases. The influence of age on the heparin sensitivity of 52 normal subjects (aged 12 to 85 years) was also studied. The heparin sensitivity was calculated from the dose-response curve obtained when increasing amounts of heparin were added to plasma and the kaolin partial thromboplastin time (KPTT) was measured. There was a significantly-reduced heparin sensitivity in nephrotic children compared to the control children and a progressive decline in heparin sensitivity with age. In the nephrotic syndrome heparin-sensitivity correlated with albumin and triglyceride concentrations but not with antithrombin III, platelet factor 4, cholesterol, fibrinogen, heparin cofactor II or histidine-rich glycoprotein. Addition of exogenous albumin did not restore the heparin sensitivity of nephrotic plasma. Four patients with Type II hyperlipidemia had a normal sensitivity to heparin. The decreased sensitivity to heparin thus does not appear to be a consequence of the nephrotic state, and may be a reflection of an underlying disturbance of charged macromolecules in steroid-responsive nephrotic syndrome.

Adolescent↗
PubMed1987

Inhibition of lipoprotein lipase by plasma from children with the steroid responsive nephrotic syndrome.

The study was designed to investigate the hyperlipidaemia associated with the steroid responsive nephrotic syndrome in children and in particular to examine the mechanism for the delayed clearance of the circulating triglyceride-rich lipoproteins. The possibility that plasma from patients with steroid responsive nephrotic syndrome may contain an inhibitor of lipoprotein lipase activity was studied by examining the effect of the addition of plasma from patients, on normal postheparin lipoprotein lipase activity. Plasma from children with steroid responsive nephrotic syndrome significantly inhibited lipoprotein lipase activity (p less than 0.001), whereas that from patients with familial hypercholesterolaemia and normal children had no significant effect. The inhibition of lipoprotein lipase activity by plasma from patients with steroid responsive nephrotic syndrome correlated significantly with their increased plasma cholesterol and reduced plasma albumin concentrations (p less than 0.001 and less than 0.02, respectively), but there was no significant correlation with plasma triglyceride concentrations. Thus, the degree of inhibition probably reflected the severity of the condition at the time of study. Neither the cholesterol, albumin nor triglyceride concentrations appeared to directly influence the lipoprotein lipase activity of postheparin plasma.

Adolescent↗