Effects of prophylaxis on latex sensitization in children with spina bifida.
Explore the source record for details and available documents.
Child↗
Biomedical subjects
A Hoppe
Publications and source records attributed to A Hoppe.
The influence of shunted hydrocephalus on the prevalence of allergy to latex in patients with spina bifida.
Explore the source record for details and available documents.
Case-Control Studies↗
Rapid purification of malate synthase from cotyledons of Brassica napus L.
A rapid and efficient method for the purification of malate synthase, an enzyme uniquely confined to glyoxysomes, from cotyledons of Brassica napus L. has been developed. The two step purification procedure is based on the consequent utilization of the tendency of malate synthase to form high molecular weight aggregates. Malate synthase was purified 75-fold to apparent homogeneity with a specific activity of 180 nkat/mg protein. The estimated molecular weight of malate synthase subunits was 63 kDa. Polyclonal antibodies raised against malate synthase in rabbits detect on Western blots only one single polypeptide with an identical molecular weight.
Brassica↗
Potent photoaffinity labelled and iodinated antagonists of bradykinin.
Continuing the studies on photoaffinity labelled analogues of the peptide hormone bradykinin (BK), several labelled antagonists were synthesized and characterized regarding their biological activities on rat uterus (RUT) and guinea pig ileum (GPI). The photoreactive amino acid p-benzoyl-phenylalanine (Bpa) was incorporated in potent, iodinated BK analogues at positions -2, -1, 0 and 7. The newly synthesized BK antagonists were derived from HOE 140 ([DArg0, Hyp3, Thi5, D-Tic7, Oic8]-BK) or [D-Phe7]-BK. Because the application of Bpa requires an additional group for the introduction of 125I, iodinated tyrosine was inserted at different positions as a model for radioiodination. Suitable positions for incorporation of tyrosine residues are -1, 0, 3 and 7, whereas the compound with 3-I-Tyr at position 4 had only a low biological activity. The antagonists obtained by modification of HOE 140 generally retained a high antagonistic potency. In this group [D-Bpa-2, 3-I-D-Tyr-1, D-Arg0, Hyp3, Thi5, D-Tic7, Oic8]-BK (pA2 values 8.06 on RUT and 8.15 on GPI) and [Bpa-1, D-Arg0, 3-I-Tyr3, Thi5, D-Tic7, Oic8]-BK (pA2 values 7.55 on RUT and 8.07 on GPI) belong to the most active compounds. The incorporation of D-Bpa at position 7 also resulted in potent analogues. The antagonists [3-I-Tyr-1, D-Arg0, D-Bpa7]-BK (pA2 on RUT 7.69) and [3-I-Tyr-1, D-Arg0, D-Bpa7, Oic8]-BK (pA2 on GPI 7.53) are an alternative to the N-terminal modified HOE 140 analogues. Compounds with D-Bpa7 act as pure competitive antagonists, whereas the HOE 140 derivatives show a mixed antagonism. The comparison of the results between photoaffinity labelled agonists and antagonists suggests that modifications in the series of BK antagonists were better tolerated.
Affinity Labels↗
[Can parathormone be used to treat osteoporosis?].
Explore the source record for details and available documents.
Animals↗
Urinary excretion of metals during treatment with D-penicillamine and 2-mercaptopropionylglycine in normal and cystinuric dogs.
Urinary excretion of metals during treatment with 2-mercaptopropionylglycine (2-MPG) was studied in 11 normal and 20 cystinuric male dogs. The results were compared with those obtained during D-penicillamine treatment. Twenty-four-h urine and morning samples of urine were taken for determination of 13 metals before and during treatment. After single intravenous and oral D-penicillamine treatment of the normal dogs, significant increases were found in the 24-h urinary excretion of Ca, Cu and Zn. Oral intake of D-penicillamine increased the excretion of Co, Cr, Fe and Mg as well. No effect on renal metal excretion was observed after single intravenous and up to 2 months of daily oral treatment with 2-MPG. In 14 cystinuric dogs no effect was found after single intravenous and oral administrations of 2-MPG. However, after oral treatment of six cystinuric dogs with 2-MPG for 2-4 months, significantly increased excretions of Ca and Mg were found. Fourteen of the cystinuric dogs were also investigated after 2-6 years of continuous 2-MPG treatment, and after this period no significant elevation in the urinary excretion of metals was found. The present study shows that in contrast to D-penicillamine, 2-MPG does not increase the urinary excretion of metals to any appreciable extent. Observed increases in the excretion of Ca and Mg seemed to be a temporary effect only.
Administration, Oral↗
Simultaneous multi-element determination of selected elements in dog urine by direct current plasma-atomic emission spectrometry.
Urine samples from dogs were analyzed for 15 important elements (Ca, Cd, Co, Cr, Cu, Fe, K, Mg, Mn, Na, Ni, P, Pb, V, and Zn) by using wet-ashing and simultaneous DCP atomic emission spectrometry. As K, Na and P influence the spectral emission of elements to be determined, matrix-matching was applied to ensure accurate metal determinations. The method was checked by analyzing standard reference materials of urine. The values found were generally in agreement (accuracy within 100 +/- 10%) with the certified values. Short- and long-term stabilities of the instrument for the elements determined ranged from 0.4 to 2.2% and from 1.2 to 6.9%, respectively. Simultaneous multi-element determination gives increased information on trace- and minor elements in urine. In the present study DCP atomic emission spectrometry is successfully applied for this purpose.
Animals↗
Visual field defects in vascular lesions of the lateral geniculate body.
Corresponding retinal nerve fibres begin their path in the eyes and end in a single visual cortical cell. Because of this arrangement, lesions in the anterior visual pathway produce incongruent visual field defects and in the posterior pathway congruent field defects. The lateral geniculate body is on the anterior third of the visual pathway. A lesion of this nucleus produces moderately to completely congruent visual field defects. Five patients with ischaemic lesions of the lateral geniculate body are reported. Two patients had a wedge-shaped homonymous hemianopia, two other cases had congruent superior homonymous quadratic defects and the fifth a quadruple sector defect. The lateral geniculate body has a dual blood supply from the anterior choroidal artery (branch from internal carotid artery) and from the lateral choroidal artery (branch from the posterior cerebral artery). A schematic diagram has been devised which shows that a knowledge of the visual field disrupted can identify the arterial system involved.
Aged↗
Quantitation of the Na(+)-Pi cotransporter in renal cortical brush border membranes. [14C]phosphonoformic acid as a useful probe to determine the density and its change in response to parathyroid hormone.
To determine the density of Na(+)-Pi symporters in brush border membranes (BBM) from rat renal cortex, [14C] phosphonoformic acid [( 14C] PFA), a competitive inhibitor of Na(+)-Pi cotransport, was employed as a probe. The [14C]PFA binding was measured in BBM vesicles (BBMV) under equilibrated conditions (extra-vesicular Na+, K+, and H+ = intravesicular Na+, K+, and H+) to avoid modulatory effects of these solutes. BBMV were preincubated in media without or with addition of molar excess of Pi (greater than 20 times) to determine the Pi-protectable PFA-binding sites, and then [14C] PFA binding was determined. Only the [14C]PFA binding in the presence of Na+ displaceable by an excess of Pi was saturated and was independent of intravesicular volume of BBMV. This value denoted as "Pi-protectable Na(+)-[14C]PFA binding," was analyzed by Scatchard plot showing BmaxPFA = 375 +/- 129 pmol of PFA/mg protein, KDPFA = 158 +/- 18 microM; the Hill coefficient was congruent to 1. For Na(+)-dependent binding of [3H]phlorizin, in the same BBMV, Bmax = 310 +/- 37 pmol/mg protein and KD V 2.2 +/- 0.5 microM. BBMV prepared from cortex of thyroparathyroidectomized rats infused with phosphaturic doses of parathyroid hormone (PTH) were compared with vehicle-infused controls. Administration of PTH resulted in decrease of BmaxPFA (-38%) and of Na(+)-gradient-dependent uptake of 32Pi (-35%), but KDPFA was not changed. Neither BmaxPhl and KDPhl for Na(+)-phlorizin binding, nor the Na(+)-gradient-dependent uptake of [3H]D-glucose differed between PTH-treated and control rats. We conclude: (a) measurement of Pi-protectable Na(+)-[14C]PFA binding determines numbers and affinity of Na(+)-Pi symporters in renal BBMV; (b) the affinity of PFA for Na(+)-Pi symporter is similar to apparent affinity for Pi (KmPi), as determined from measurements of Na(+)-gradient-dependent 32Pi uptake by BBMV; (c) both Na(+)-Pi symporter and [Na+]D-glucose symporters are present within renal BBM in a similar range of density; (d) PTH decreases the number of Na(+)-Pi cotransporters in BBMV commensurate with the parallel decrease of Na(+)-gradient-dependent Pi transport, whereas the affinity of Na(+)-Pi symporters for Pi is not changed. These observations support the hypothesis that PTH decreases capacity for Na(+)-dependent Pi reabsorption by internalization of Na(+)-Pi symporters in BBM of renal proximal tubules.
Animals↗
Pharmacokinetics and bioavailability of 2-mercaptopropionylglycine administered intravenously and orally in dogs.
The pharmacokinetic disposition of 2-mercaptopropionylglycine (2-MPG) given as a single intravenous injection and/or as a single oral dose was studied in 9 normal and 13 cystinuric dogs. After intravenous injection of approximately 10 or 20 mg/kg body weight the pharmacokinetics were best described by a three-exponential function. The first phase involved a distribution process apparently including establishment of drug-plasma protein and drug-tissue binding. The second phase involved rapid renal elimination and 60% of the drug was excreted within 3 h of administration. There was also a slow terminal third phase with a long half-life after both intravenous (t1/2 = 23 h) and oral (t1/2 = 22 h) administration. No dose dependency was observed. A deep pool of reversibly tissue-bound 2-MPG was indicated by a Vss of 3.3 +/- 0.9 l/kg body weight and the long terminal elimination phase. Total clearance was estimated as 4.1 +/- 0.9 ml/min/kg body weight. 2-MPG was eliminated mainly by renal excretion, but there was a difference in recovery of dose between normal and cystinuric dogs. During the first 24 h after intravenous and oral administration, 69% and 54%, respectively, of the drug was recovered in the urine of normal dogs. The corresponding figures in cystinuric dogs were 44% and 29%, respectively. The absolute bioavailability (FAUC) was 88 +/- 20% in normal dogs.
Administration, Oral↗
Renal denervation enhances the phosphaturic effect of parathyroid hormone.
Hyperventilation/hypocapnia increases renal phosphate reabsorption and decreases the phosphaturic effect of parathyroid hormone (PTH). Recent studies suggest that the blunted phosphaturic effect of PTH in hyperventilated/hypocapnic rats may be mediated by the stimulation of renal beta-adrenoreceptors. In the present study, no differences in plasma catecholamine levels were detected in hyperventilated/hypocapnic rats as compared to hyperventilated/normocapnic rats. Therefore, studies were performed to determine the role of the renal nerves in the blunted phosphaturic effect of PTH in hyperventilated/hypocapnic rats. In clearance experiments in acutely thyroparathyroidectomized male Sprague-Dawley rats, PTH infusion increased the fractional excretion of phosphate (FEPi) in the denervated left kidney of hyperventilated/hypocapnic rats (n = 8), from 2.4 +/- 1.1 to 18.6 +/- 2.7%, as compared to 1.0 +/- 0.3 to 9.1 +/- 2.1% in the contralateral innervated kidney. Denervation of the left kidney in hyperventilated/normocapnic rats (n = 8) also significantly increased the phosphaturic response to PTH by 2.5 +/- 1.5 to 26.9 +/- 3.0% as compared to 0.9 +/- 0.5 to 18.6 +/- 2.6% in the contralateral innervated kidney. The phosphaturic responses to PTH were similar when comparing the denervated kidney in hyperventilated/hypocapnic rats with the innervated kidney of hyperventilated/normocapnic rats. Thus, renal denervation enhanced the phosphaturic effect of PTH in both hyperventilated/hypocapnic and hyperventilated/normocapnic rats. These results suggest that renal nerves play a role in the modulation of the phosphaturic effect of PTH.
Animals↗
Site of restoration of the effect of PTH by propranolol in respiratory alkalosis.
Respiratory alkalosis decreases the phosphaturic response to parathyroid hormone (PTH). beta-adrenoreceptor blockade by propranolol infusion restores the phosphaturic effect of PTH in respiratory alkalotic rats; however, the nephron site of these changes in phosphate reabsorption by propranolol is not known. The present study was performed to localize the nephron segment(s) involved in the restoration of the phosphaturic effect of PTH by propranolol infusion in respiratory alkalotic rats. PTH infusion increased the fractional delivery of phosphate (FDPi) to the late proximal tubule to similar levels in the propranolol and vehicle-infused respiratory alkalotic rats (FDPi 46.6 +/- 4.4% and 48.6 +/- 4.2%, respectively). In contrast, PTH only increased FDPi to the early distal tubules (to 17.1 +/- 0.9%) in the absence of propranolol compared to FDPi 41.9 +/- 2.5% in the presence of propranolol in respiratory alkalotic animals. We conclude that the restoration of the phosphaturic effect of PTH in respiratory alkalotic rats by propranolol infusion is due primarily to decreased reabsorption of phosphate by the straight segment of the proximal tubule.
Alkalosis, Respiratory↗
Irreversible inhibition of renal Na(+)-Pi cotransporter by alpha-bromophosphonoacetic acid.
We investigated the suitability of alpha-bromophosphonoacetic acid (alpha-BrPAA) to act as a possible irreversible inhibitor of Na(+)-dependent transport of Pi across renal brush-border membrane (BBM). When added directly into the Pi uptake medium, alpha-BrPAA causes specific, competitive [apparent inhibition constant (Ki) = 0.33 mM; no change in maximum velocity (Vmax)], and reversible (by washing) inhibition of Na+ gradient [Na+o greater than Na+i]-dependent uptake of Pi by BBM vesicles (BBMV). Next, BBMV were preincubated with 5 mM alpha-BrPAA in alkaline (pH 9) medium for 30 min, then twice washed by 1:100 dilution and recentrifugation, and tested for transport and other properties. This preincubation of BBMV with alpha-BrPAA in alkaline medium resulted in a different type of inhibition [lower Vmax; no change in Michaelis constant (Km)] of the Na+ gradient-dependent uptake of 32Pi, whereas the uptakes of D-[3H]glucose and other solutes were not altered. This inhibition of Pi transport was not reversed by dilution and washing of BBMV. The BBMV Na(+)-dependent binding of [14C]phosphonoformic acid, but not of [3H]phlorizin, was decreased; activities of BBM marker enzymes were not changed. Results suggest that alpha-BrPAA binds onto the same locus on luminal surface of BBM on which Pi and Na+ bind and inhibits Na(+)-Pi cotransporter similar to phosphonoformic acid. Furthermore, after a 30-min incubation in alkaline medium, alpha-BrPAA apparently forms a more stable association with BBM in the vicinity of the Na(+)-Pi cotransporter. We thus suggest that alpha-BrPAA acts under these conditions as an apparently irreversible inhibitor of Na(+)-Pi cotransporter in BBM.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Propranolol restores phosphaturic effect of PTH in short-term phosphate deprivation.
Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone (PTH). The present study evaluated the role of the beta-adrenergic system in this resistance phenomenon. In clearance experiments performed on acutely thyroparathyroidectomized male Sprague-Dawley rats, the phosphaturic response to PTH was determined in the presence and absence of propranolol in rats fed a low-phosphate diet (LPD) for 0.5, 1, 2, 3, or 4 days. Fractional excretion of phosphate (FEPi) in control rats fed a normal-phosphate diet (NPD) increased from 4.37 +/- 1.6 to 38.5 +/- 3.4% in response to PTH infusion. Propranolol did not change FEPi in NPD animals in the absence or in the presence of PTH (2.0 +/- 1.1 vs. 36.7 +/- 1.6%). LPD resulted in a gradual decrease in the phosphaturic response to PTH infusion as compared with NPD animals. PTH increased FEPi to 24.2 +/- 6.0% after one-half day of LPD, but when the infusion was supplemented with propranolol, PTH increased FEPi to 38.0 +/- 4.7%, similar to that in NPD animals. In the group fed LPD for one day, PTH increased FEPi to 16.9 +/- 4.3%, whereas in the presence of propranolol FEPi was restored to a similar level as in the NPD group (36.0 +/- 5.9%). Two days of LPD markedly decreased FEPi in response to PTH to 7.9 +/- 3.8% as compared with NPD rats, and propranolol infusion did not change this value significantly. Three and 4 days of LPD induced complete resistance to the phosphaturic effect of PTH in the presence as well as in the absence of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of propranolol on phosphate reabsorption by superficial nephron segments in response to parathyroid hormone in phosphate-deprived rats.
Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone. The decreased phosphaturic response to parathyroid hormone in rats fed a low phosphate diet for 1 day can be restored by propranolol infusion. Free-flow micropuncture studies were performed to localize the nephron site of restoration of the phosphaturic effect of parathyroid hormone by propranolol in rats deprived of phosphate for one day. In animals fed low phosphate diet and in the presence of parathyroid hormone, propranolol infusion did not change phosphate delivery to the late proximal tubule; however, fractional delivery of phosphate to the early distal tubule was significantly increased from 18.3 +/- 2.9 to 32.2 +/- 4.1%. In rats fed a normal phosphate diet, propranolol infusion did not change phosphate delivery along the nephron. We conclude that the restoration of the phosphaturic effect of parathyroid hormone by propranolol infusion in rats deprived of phosphate for 1 day is primarily due to decreased reabsorption of phosphate by superficial loop segments, most likely the pars recta segment of the proximal tubule.
Absorption↗
[Methods of treatment of preschool children used in the orthodontics department, Institute of Stomatology, Medical Academy in Warsaw].
The reported analysis was based on 288 clinical cards of patients aged 2 to 6 years, admitted for treatment in the years 1980-1985. The greatest group was that of children aged 3 years (28%), followed by those aged 6 years (25%). Abnormalities from the group of distocclusion prevailed (28%), followed by teeth abnormalities (26%), and cross-bite (16%). In 165 cases functional apparatus was used initially, in 66 cases Schwarz or Adams plates, in 31 cases dental prostheses, and in 22 cases chin sling. Four cases were observed after removal of malocclusion cause. Besides treatment with removable devices myotherapy and spatula exercises were used.
Child↗
Different mechanisms of adaptive increase in Na+-Pi cotransport across renal brush-border membrane.
We explored the biochemical mechanism by which thyroid hormone (T3) and low-phosphate diet (LPD) cause an adaptive increase in Na+-Pi cotransport across renal brush-border membrane (BBM). The rate of Na+-Pi cotransport was determined by 32Pi uptake by BBM vesicles (BBMV), and the number of Na+-Pi symporters was assessed by binding of [14C]phosphonoformic acid (PFA) on BBMV. In BBMV of both T3-treated rats and LPD-fed rats, the Na+ gradient-dependent 32Pi uptake increased (Vmax increased; Km Pi was not changed). The Na+-dependent [14C]PFA binding on BBMV increased (higher Vmax, no change in Km PFA) in response to T3, but it remained unchanged in rats fed LPD. Both the increase of Na+-Pi cotransport and of Na+-dependent [14C]PFA binding in response to T3 were blocked by actinomycin D or cycloheximide. Addition of benzyl alcohol to BBMV in vitro increased Na+-Pi cotransport, but [14C]PFA binding did not change; the [3H]phlorizin binding and cotransports of other solutes decreased or did not change. The exposure of BBMV to cholesterol decreased Na+-Pi cotransport without changing [14C]PFA binding. We suggest that the adaptive increase of Na+-Pi cotransport elicited by T3 is due to an increase in number of Na+-Pi cotransporters in BBM. In contrast, in response to LPD the number of Na+-Pi cotransporters is unchanged, and the increased Na+-Pi cotransport is due to faster translocation of Na+ with Pi due to enhanced fluidity of BBM.
Adaptation, Physiological↗
alpha-Cl-alpha-Br-phosphonoacetic acid is a potent and selective inhibitor of Na+/Pi cotransport across renal cortical brush border membrane.
We found that alpha-Cl-alpha-Br-phosphonoacetate (ClBrPAA) is a competitive, solute-specific inhibitor of Na+/Pi cotransport across renal cortical brush border membrane. Inhibition by ClBrPAA (Ki = 62 microM) is more than three times more effective than inhibition by phosphonoformate (PFA), the most potent Na+/Pi cotransport inhibitor known to date, and 26 times more effective than the parent compound, phosphonoacetate (PAA). These observations indicate that substitution of bromine and chlorine atoms at the alpha-carbon of PAA greatly enhances its efficacy as a competitive inhibitor of Na+/Pi cotransport. As ClBrPAA is much less inhibitory than PAA and PFA towards viral DNA polymerases and did not inhibit human alpha-DNA polymerase (ref. 10), the results also demonstrate that Na+/Pi cotransport inhibition can be dissociated from inhibition of DNA polymerases by phosphonocarboxylate compounds.
Animals↗