[Tasks of all physicians in the prevention of infectious intestinal diseases. Epidemiology and health education].
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Biomedical subjects
Publications and source records attributed to J Deutsch.
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Cardiac glycosides such as digoxin or ouabain have long been known to influence the strength of contraction of cardiac muscle. Although the mechanism of action of these compounds remains unknown, all the proposed modes of action are based on initial binding to specific membrane receptors which are part of the (Na+ + K+)ATPase complex. These receptors, well characterized and defined, suggest the existence of an endogenous substance capable of binding to them, in analogy with endogenous opiates, discovered long after morphine and its receptors. As glycosides affect (Na+ + K+)ATPase activity, an endogenous substance may be a regulator of this important enzyme. Indeed, the search for endogenous regulators of the (Na+ + K+)ATPase or ouabain-like compounds (OLC) has recently intensified. These compounds, extracted and partially purified from mammalian brain, heart, blood and urine, and from toad skin and plasma, have been shown to inhibit 3H-ouabain binding and (Na+ + K+)ATPase activity. We report here that in addition to these effects, the OLC, highly purified from toad skin and sheep brain, increases the force of contraction of frog and guinea pig atrium.
BACKGROUND: Enlargement of peripheral lymph nodes most commonly caused by a local inflammatory process is frequently seen in childhood. The aim of the present study was to analyze the most common causes of peripheral lymphadenopathy and to develop a simple algorithm for the primary diagnostic evaluation of peripheral lymph node enlargement in this age group. PATIENTS: Between April and September 1999 87 unselected children (median age: 5 1/2 years) with peripheral lymphadenopathy were referred to the Department of Pediatrics, University of Graz, for further investigation. RESULTS: EBV infection was diagnosed in 20 (23.0%) children. 19 (21.8%) patients had acute bacterial lymphadenitis. In 21 (24.1%) patients lymph node enlargement was classified as "post/parainfectious (viral)". Four patients each had toxoplasmosis and cat scratch disease. In 11 (12.6%) patients neither physical nor laboratory examinations revealed pathologic results. Among the remaining 8 children sarcoidosis and Hodgkin disease was diagnosed in one patient each. Small, soft, mobile, nontender, cervical, axillary or inguinal lymph nodes do not require further investigations. In case of enlarged, tender lymph nodes with overlying skin erythema and fever diagnostic evaluation should include complete blood count, erythrocyte sedimentation rate and/or c-reactive protein level, supplemented by appropriate antibody testing (EBV, CMV, Toxoplasma gondii, Bartonella henselae). Firm, enlarged, painless lymph nodes which are matted together and fixed to the skin or underlying tissues necessitate a more detailed diagnostic evaluation in order to exclude malignant or granulomatous diseases. CONCLUSIONS: Our study demonstrated that primary diagnostic evaluation of childhood peripheral lymphadenopathy is mainly based on clinical grounds. In most cases a small number of additionally performed laboratory tests allow to correctly identify the cause of the peripheral lymph node enlargement.
CASE REPORT: A three month old girl, with recurrent hypoglycemia and neonatal cholestasis, is reported. A metabolic disease could be excluded. The liver biopsy revealed giant cell hepatitis and intrahepatic bile duct hypoplasia. ACTH, Cortisol and hGH measured during hypoglycemia were low. Magnetic tomography (MR) of the brain showed an "empty sella". After beginning a replacement therapy with hydrocortisone, growth hormone and thyroxine there was no further episode of hypoglycemia. Transaminases and bilirubin levels normalized. The girl is in good condition, growth and development are normal. DISCUSSION: Hypoglycemia is often the first sign in childrens with neonatal hypopituitarism. The association of liver disease and hypopituitarism has been documented in a few reports. The pathophysiological mechanism leading to the liver dysfunction is not well understood. The prognosis of neonatal hypopituitarism as well as the concomitant liver disease is good under sufficient replacement therapy.
A cross-sectional study was performed to define patients at risk of developing liver disease due to long-term treatment with anticonvulsive drugs. The activities of gamma-glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase and the concentrations of primidone, phenobarbital, phenytoin, and valproic acid in serum were estimated. Epileptic children before therapy were used as controls. The results indicated enzyme induction due to phenobarbital and both enzyme induction and liver cell damage or plasma membrane leakage due to phenytoin. Gamma-glutamyltransferase may be an early indicator of liver disease due to valproic acid.
Material extracted and partially purified from plasma of the Sabra hypertension prone rats was found to be capable of 1) inhibiting the binding of 3H-ouabain to rat brain synaptosomes, 2) inhibiting the activity of rat brain microsomal Na, K activated adenosine triphosphatase, and 3) increasing the contractile force of rat heart muscle. The results demonstrate the presence of a ouabainlike compound in the plasma of these rats. The plasma concentration of this compound in Sabra hypertension prone rats was 698 +/- 199 nmol/ml in ouabain equivalents (SEM; n = 11) versus 2543 +/- 1140 nmol/ml (n = 9) in the Sabra normotensive strain. The presence of ouabainlike compound in the plasma is consistent with the hypothesis that this compound functions as a hormone that regulates Na, K activated adenosine triphosphatase activity and the physiological processes in which this enzyme is involved.
INTRODUCTION: Current lead screening guidelines recommend monitoring lead levels in children under 3 years of age. There are, however, a number of children between the ages of 3 and 6 years who have elevated blood lead levels. Whether these lead elevations are new or chronic has not been examined. OBJECTIVE: To determine the proportion of children with lead levels greater than or equal to 10 microg/dL after their third birthday when all prior testing had been normal. METHODS: Retrospective study based on 39000 venous lead tests obtained between 1993 and 1998. From this group, 2046 children were located who had blood lead levels of less than 10 microg/dL before 36 months and who had a follow-up lead level after 36 months. All lead assays were done by the City of New York laboratories, which had an intrasample variability of 13%. RESULTS: Sixty-six (3.2%) of the 2046 children showed an elevation in blood lead for the first time after their third birthday. The abnormal values ranged from 10 to 25 microg/dL. The majority (72%) of the screen-positive children, however, had lead levels of 10 to 12 microg/dL, and 63.3% of screen-positive children with repeat tests had lead levels that reverted to below 10 microg/dL. CONCLUSIONS: The data indicate that some new cases of lead level elevations did occur after 3 years of age in this 'high-risk' community; however, the current study provides evidence that universal screening for lead poisoning beyond 3 years of age is not warranted in this community as it is not likely to pick up clinically important exposure.
Fluorescence techniques have been used to assess the viscosity of surfactant-containing fluids in vivo and have been successfully employed clinically as indices of lung maturity. However, fluorescence measurements have not been previously used as indicators of fetal lung maturation in an in vitro system. Lung explants derived from 19-, 20-, and 21-day fetal rats were cultured in F-12 medium for 24-72 h. Tissue homogenates and culture medium were eluted on Sephacryl S-300 columns, a diphenylhexatriene (DPH) probe was added to each fraction, and fluorescence anisotropy and intensity were measured after excitation at 357 nm and emission at 435 nm. Elution fractions containing the major fluorescence peak were demonstrated to correspond to the phosphatidylcholine-containing fraction and were shown to contain lamellar bodies. Fluorescence anisotropy of tissue homogenates obtained from 19-day lung explants decreased after 72 h in culture, suggesting lower microviscosity of the surfactant-containing fractions. Assessment of culture media collected at 24-h intervals revealed significant decreases in anisotropy by 48 h for the 19-day explants, and by 24 h for the 20- and 21-day explants. Anisotropy of the final (48-72 h) culture media aliquots was significantly lower for 21-day explants (0.144 +/- 0.004, SE), than for 20-day (0.172 +/- 0.013) or 19-day explants (0.197 +/- 0.008), p < .005. Anisotropy of culture medium tended to be lower than anisotropy of corresponding tissue homogenates, suggesting that viscosity of recently secreted surfactant may be different from viscosity of surfactant within lamellar bodies in type II cells. Relative fluorescence intensity of tissue homogenates also increased with time in culture. These results indicate that fluorescence anisotropy can be used to assess the viscosity of surfactant in vitro and serve as another index of fetal lung maturation in in vitro systems. Estimation of the microviscosity of the surfactant phospholipid bilayer using anisotropy measurements may provide additional insight into such roles of surfactant function as adsorption and spreading.
The biosynthesis of digitalis-like compounds (DLC) was determined in bovine and rat adrenal homogenates by following changes in the concentration of DLC using three independent sensitive bioassays: inhibition of [3H]-ouabain binding to red blood cells and competitive ouabain and bufalin ELISA. The amounts of DLC in bovine and rat adrenal homogenates, as measured by the two first bioassays, increased with time when the mixtures were incubated under tissue culture conditions. These results suggest that Na+, K+-ATPase inhibitors which interact with ouabain antibodies, but not those which interact with bufalin antibodies, are synthesized in bovine and rat adrenals.
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Fluorescence anisotropy was assessed in tracheal and oropharyngeal aspirates to evaluate its use in the diagnosis of respiratory distress syndrome. Samples from 31 neonates at birth were purified by using Sephacryl S-300 column chromatography. After the addition of the molecular probe, 1,6-diphenyl 1,3,5 hexatriene fluorescence was measured and anisotropy calculated. Ten neonates with normal respiratory function had a mean anisotropy (+/- SD) of 0.226 +/- 0.023. Fourteen infants with a diagnosis of respiratory distress syndrome had a mean anisotropy of 0.260 +/- 0.014 (p < 0.001). Seven neonates with respiratory problems other than respiratory distress syndrome had a mean anisotropy of 0.211 +/- 0.027 (p < 0.001 vs respiratory distress syndrome). A diagnosis of respiratory distress syndrome was associated with higher tracheal fluid anisotropy, indicating a qualitative difference in the characteristics of the pulmonary surfactant. We conclude that this 30-minute test could help identify neonates who benefit from surfactant replacement therapy.