Proliferative retinopathy in a woman with growth hormone deficiency and diabetes mellitus.
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Adult↗
Biomedical subjects
P Chatelain
Publications and source records attributed to P Chatelain.
Assay of growth hormone levels in human plasma using commercial kits: analysis of some factors influencing the results.
The reliability of growth hormone (GH) assays, performed in 39 different laboratories, using five different immunoassay kits was evaluated. It was found that the variability in GH levels measured by different commercial assay kits may be due to human factors, as well as differences between the kits. The influence of the variation in amount of circulating GH, during provocative testing and spontaneous secretory episodes, on the results of GH assay was also evaluated. It was found that large molecular weight forms of GH may be underestimated by some assay kits.
Child↗
Growth hormone response to a bolus injection of 1-44 growth-hormone-releasing hormone in very short children with intrauterine onset of growth failure.
The release of growth hormone (GH) during the 120 min following a bolus venous injection of 1-44 GH-releasing hormone (GHRH) 2 micrograms/kg was studied in 52 prepubertal children aged 8.4 +/- 2.1 years, having a nonfamilial growth deficiency of prenatal onset (-3.26 +/- 1.13 SDS at birth, -3.22 +/- 0.88 SDS at the time of study) and a normal response to conventional GH stimulation tests. GH release reached a peak level of 96.1 +/- 60.2 microU/ml, being significantly higher than that found in 68 non-GH-deficient very short children whose growth failure had a postnatal onset, and not significantly correlated with the response to conventional tests. 26 of the 52 intrauterine growth retardation (IUGR) patients were re-tested with GHRH in similar conditions after 6-12 months of daily subcutaneous injections of GH and 2 days without. They reached at the second test a peak plasma GH level of 91.7 +/- 56.1 microU/ml, not different from their response to the first test. These data could be taken into consideration for long-term studies of the clinical effects of GH in IUGR children with persisting severe growth deficiency.
Child↗
Coronary angioplasty in silent and painful myocardial ischemia.
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Adult↗
Amiodarone pretreatment effects on ischemic isovolumic rat hearts: a P-31 nuclear magnetic resonance study of intracellular pH and high-energy phosphates contents evolutions.
Effects of amiodarone injected intravenously (i.v.) at two doses (10 and 20 mg/kg) on perfused isovolumic rat hearts were assessed by P-31 nuclear magnetic resonance (NMR). P-31 NMR is used to measure intracellular myocardial pH, phosphocreatine (PCr), and ATP contents time evolutions. Myocardial mechanical function is estimated by heart rate (HR), left ventricular developed pressure (LVP), and coronary flow (CF). In experimental procedure A (2-h retrograde perfusion), drug injection induced a dose-dependent bradycardia (10-20%) and a slight decrease in LVP but did not affect CF, pH, PCr, or ATP contents. Experimental procedure B consisted of 30-min stabilization, 18-min ischemia, and 72-min reperfusion. During ischemia, amiodarone did not preserve ATP and PCr pools and did not alleviate acidosis. ATP decreased to 30% of its control values, whereas the PCr peak was hardly detectable after 12 min of ischemia. After 24 min of reflow, HR, PCr, and pH of treated hearts recovered. LVP recovered after 36 min, whereas for control hearts, HR, PCr, and pH recovered after 42 min and LVP did not reach its control values at the end of reperfusion time. Faster pH recovery is explained by a preservation of Na+/K+ ATPase due to the influence of amiodarone on membrane lipid dynamics.
Adenosine Triphosphate↗
SR 33557, a novel calcium entry blocker. I. In vitro isolated tissue studies.
The effects of SR 33557 on isolated cardiovascular preparations were compared to those of nifedipine, verapamil and diltiazem. In rat aortic strips, SR 33557, like nifedipine, verapamil and diltiazem, caused a significant and simultaneous inhibition of potassium-induced 45Ca++ influx and contractile responses (nifedipine greater than SR 33557 greater than verapamil greater than diltiazem). SR 33557 also antagonized Ca(++)-induced contractions in K(+)-depolarized aorta preparations (pA2:9.08 +/- 0.03) and is the first calcium channel antagonist, structurally not related to 1,4-dihydropyridines, to inhibit competitively contractions induced by BAY K8644. In spike-generating vascular smooth muscle (rat portal vein), contractures evoked by noradrenaline (4 microM) or KCl (100 mM) were reduced by all four antagonists, the pharmacological potency being nifedipine greater than SR 33557 greater than verapamil greater than diltiazem. Unlike SR 33557, nifedipine, verapamil and diltiazem showed a parallel enhancement of frequency of spontaneous contractions in rat portal vein in spite of a concentration-related reduction in amplitude. By using rabbit atrial preparations, spontaneous right atrial rate and electrically stimulated (120/min) basal contractions of left atria were used as indices of chronotropy and inotropy. The potency series for negative chronotropic effects was nifedipine greater than SR 33557 greater than verapamil greater than diltiazem. For negative inotropic effects the potency order was verapamil greater than nifedipine greater than SR 33557 greater than diltiazem, respectively. Thus, SR 33557 should depress heart rate to a greater extent than ventricular contractility. These results suggest that SR 33557 is a potent calcium entry blocker that (unlike verapamil and diltiazem) is particularly selective for vascular smooth muscle and devoid of any potent negative inotropic actions.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
[Hypotensive effect of a new calcium antagonist, SR 33557 in conscious rats].
SR 33557 (SR) is a new calcium channel blocker belonging to the chemical class of indolizinsulfones (IC50 = 0.6 nM, 3H-nitrendipine). Its hypotensive effects were studied in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and compared to those of Nitrendipine (Nit) (IC50 = 0.8 nM, 3H-nitrendipine). SR was given intravenously (IV) at 0.3, 1 and 3 mg/kg (n = 4 to 6) and orally (PO) at 3, 10, 30 and 60 mg/kg (n = 4 to 7). Nitrendipine was studied at 0.3 mg/kg (IV) and 10 mg/kg (PO). Blood pressure (BP) and heart rate (HR) were measured for 120 min, and for 24 h at 30 mg/kg. The IV injection of SR induced an immediate and dose-dependent decrease in BP. The maximal diastolic hypotension was situated between 11 p. 100 at 0.3 mg/kg and 45 p. 100 at 3 mg/kg (basal values: 133 +/- 6 and 131 +/- 5 mmHg). These effects lasted between 30 min and over 2 hours. The oral administration of SR induced a dose-dependent fall in BP at 3 mg/kg and upwards. The maximal diastolic hypotension appeared within 60 and 120 min and were situated between 8 p. 100 at 3 mg/kg and 28 p. 100 at 60 mg/kg (basal values: 130 +/- 7 and 133 +/- 2 mmHg). At 30 mg/kg, the hypotension lasted for 8 hours. SR was roughly 10 times less hypotensive in WKY than in SHR. HR did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
SR 33557, a novel calcium entry blocker. II. Interactions with 1,4-dihydropyridine, phenylalkylamine and benzothiazepine binding sites in rat heart sarcolemmal membranes.
We have assessed the binding characteristics of a structurally novel calcium entry blocker, SR 33557, to purified rat heart sarcolemma. SR 33557 prevented completely the binding of (+)-[3H]PN200-110, (-)-[3H]D888 and cis-(+)-[3H]diltiazem to their specific binding sites in an apparently competitive manner (nH congruent to 1.0) and with a high affinity (Ki = 0.5-2.0 nM). Equilibrium and kinetic studies suggest that SR 33557 does not act as a simple competitive antagonist at the 1,4-dihydropyridine, the phenylalkylamine or the benzothiazepine-selective sites associated with the L-type calcium channel: 1) inhibition of (-)-[3H]D888 and cis-(+)-[3H]diltiazem binding by SR 33557 resulted in a decrease in maximum binding, 2) cis-(+)-diltiazem and (+)-PN200-110 allosterically increased the inhibition of (+)-[3H]PN200-110 binding and of (-)-[3H]D888 and cis-(+)-[3H]diltiazem binding by SR 33557, respectively and 3) dissociation kinetics of the three radioligands were accelerated by SR 33557. Calcium (in millimolar concentrations) decreased the apparent affinity of SR 33557 for its high-affinity binding sites. This observation was similar to that seen with the phenylalkylamines and cis-(+)-diltiazem, but contrasted from that seen with the 1,4-dihydropyridines. These results indicate that SR 33557 interacts with a high affinity to a novel binding site associated with the L-type calcium channel and has a strong negative allosteric interaction with the well-characterized binding sites for 1,4-dihydropyridines, phenylalkylamines and benzothiazepines.
Animals↗
[Virilizing ovarian tumor in an adolescent].
This clinical case describes a 13 year-old pubertal girl suffering from secondary virilization, amenorrhea, and abdominal mass. Plasma testosterone and androstenedione levels were markedly elevated. Upon surgery, an ovarian tumor containing 5 l of liquid was removed. The histologic examination revealed a macrocystic granulosa cell type tumor of non-juvenile type. After removal of the tumor, which included ipsilateral ovariectomy, the contralateral ovary developed polycystic changes. The role of the tumoral hyperandrogeny in inducing this contralateral polycystic ovary is discussed.
Adolescent↗
[Turner's syndrome: a new era].
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Female↗
[Eosinophilic myocarditis and pulmonary hypertension in a drug-addict. Anatomo-clinical study and brief review of the literature].
We report the clinical and pathological findings in a young female patient who was a chronic drug addict for over eight years. In 1984, she presented with tricuspid endocarditis and three years later, was found to have irreversible pulmonary hypertension. Post-mortem examination revealed not only persistent tricuspid endocarditis and evidence of repeated pulmonary thromboembolism explaining her pulmonary hypertension but also a diffuse eosinophilic myocarditis, with myocardial fibre degeneration. The combined pulmonary and myocardial lesions have rarely been documented in the same drug addict. The relationship of these various pathological findings are discussed in the light of the existing literature.
Adult↗
Differential effects of amiodarone and propranolol on lipid dynamics and enzymatic activities in cardiac sarcolemmal membranes.
The amphiphilic cationic cardioactive drugs (pindolol, propranolol and amiodarone) were tested for their effects on lipid dynamics (measured by fluorescence depolarization) and on enzymatic activities up to 1 mM in purified cardiac sarcolemmal vesicles from adult rat. The vesicles were enriched 12- to 37-fold (with respect to tissue homogenate) in Na+/K+ ATPase, K+-stimulated p-nitrophenylphosphatase, 5'nucleotidase and adenylate cyclase, all of which are believed to be components of sarcolemma. Phospholipids and cholesterol content were enriched 5- and 13-fold respectively. There was very little contamination of the sarcolemmal vesicles by sarcoplasmic reticulum (as judged by Ca2+ ATPase and glucose-6-phosphatase activities) or mitochondria (as judged by cytochrome-c-oxidase activity). Pindolol had no effect on lipid dynamics and enzyme activities except for the isoproterenol-stimulated adenylate cyclase. The latter was also totally inhibited at 1 microM by propranolol which inhibited Mg2+ ATPase and increased fluidity above 20 microM. Amiodarone affected all the enzyme activities (except Na+/K+ ATPase): isoproterenol-stimulated adenylate (IC50 = 30 microM), Mg2+ ATPase (IC50 = 20 microM) and K+-stimulated-p-nitrophenylphosphatase were inhibited; 5'nucleotidase was activated above 2 microM. By contrast with propranolol, amiodarone decreased lipid mobility. The effect was linear with the concentration of the drug above 1 microM.
4-Nitrophenylphosphatase↗
[Leukocyte removal in a closed system of human red-cell concentrates: a technic coupled with the automated extraction of the buffy coat using a sterile connector from a filtration kit].
A technique, integrally run in a closed system, for leucocyte depletion of human red cell concentrates is described. It associates two complementary processes: buffy-coat removal and filtration. The first step is carried out with an automated system for blood component preparation (Compomat, NPBI); its efficiency is improved by a custom made blood collection set with ACD anticoagulant solution in the primary bag. The second step is simplified by a filtration kit requiring only one sterile connection for operation (SCD 312, Dupont de Nemours) and allowing a standardised rinsing of the filter. Quality control of 33 units so prepared shows principally: --an intensive leuko-depletion (4 logs) enabling leukocyte contamination to be kept below 10(6) per unit; --a moderate red cells loss (15 ml for the first step and 20 ml for the second one). This technique provides a permanently available and very pure blood component. Moreover it offers new potential for standardisation and mastery of quality control.
Blood Cell Count↗
[Viability of human red blood cells preserved for 35 days after leukocyte depletion (in vitro study)].
24 leukocyte poor red cells concentrates (L.P.R.C.) were prepared by sterile connection of a leucocyte filter between the primary bag and the SAGM bag of a blood unit after centrifugation. Their quality was followed up to 42 days by means of a panel of tests including, ATP and 2,3-DPG levels, hemolysis, plasma potassium, lactate and glucose, and counts of the microaggregates. 24 standard units acted as a control group. Results showed better preservation of LPRC and especially less hemolysis, higher ATP levels and at least equal oxyphoric capacity (explored by 2,3-DPG). Microaggregate formation was dramatically reduced and bacteriologic checks (48 at day 25 and 48 at day 42) were all negative. Leucocyte depletion appears as a new way to improve functionality of erythrocytes during storage in the SAGM medium. 35 days shelf life will allow this blood product to be more available and its preparation more standardised.
2,3-Diphosphoglycerate↗
In vitro effect of insulin and insulin-like growth factor-I on cell multiplication and adrenocorticotropin responsiveness of fetal adrenal cells.
The present study examined the effects of both insulin and insulin-like growth factor-I (IGF-I) on cell division and specific functions of cultured adrenocortical cells from 100- to 122-day-old ovine fetuses. When culture was performed in a serum-free medium containing transferrin and ascorbic acid, the number of cells increased only slightly (1.2-fold) over a 4-day period. Addition of insulin or IGF-I in the culture medium enhanced the number of cells counted on Day 5. The effect of both peptides was dose-dependent, but 10 ng/ml IGF-I was as potent as 10 micrograms/ml insulin. The acute cyclic adenosine 3',5'-monophosphate (cAMP) and steroidogenic responses to adrenocorticotropin (ACTH1-24) decreased in fetal cells cultured in the absence of insulin or ACTH. Insulin at micromolar concentrations not only prevented this decrease but enhanced the acute ACTH1-24-induced cAMP output on Day 5 over that observed on Day 2. Treatment of fetal cells for 4 days with increasing concentrations of insulin or IGF-I enhanced the acute cAMP and steroidogenic responses (3- to 4-fold) to ACTH1-24 over that of control cells. The ED50 of IGF-I was about 3 ng/ml (congruent to 0.4 nM) whereas that of insulin was about 10 ng/ml (1.7 nM). However, a second plateau was apparent at concentrations of insulin above 1 microgram/ml. The acute cholera toxin stimulation of cAMP production of cells cultured in the absence of insulin or ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Glands↗
Functional hypersomatotropism in small for gestational age (SGA) newborn infants.
Basal plasma GH levels and the GH responses to an injection of 1 microgram/kg 1-44(NH2) GHRH were determined on day 3 postnatally in 5 small gestational age (SGA) twin newborns and their appropriate gestational age (AGA) co-twins, and in 10 SGA singleton newborns and 6 AGA singleton newborns. The mean basal plasma GH level was higher in the SGA than in the AGA infants but the difference was significant only for singleton newborns (p less than 0.01). The mean peak plasma GH level was markedly increased in SGA compared to AGA infants (p less than 0.05 for twins, p less than 0.01 for singletons). Twelve SGA infants re-tested at 1 month had lower basal and peak plasma GH levels (p less than 0.001 and p less than 0.01). In 21 SGA and 17 AGA infants, serum IGF-I, measured by RIA between 12 and 96 hours after birth, was significantly higher in SGA than in AGA (p less than 0.001). These results suggest that, whatever the mechanism, functional hypersomatotropism is present at day 3 in SGA infants. This hypersomatotropism may participate in the early catch-up growth process.
Gestational Age↗
[Biosynthetic growth hormone: current therapeutic status and perspectives].
This paper covers the practical aspect of GH therapy in both GH deficiency and Turner syndrome. Dose regimen, route and frequency of administration and follow-up are detailed. Prospectives of therapeutic use of growth hormone are discussed.
Age Determination by Skeleton↗
[Hypothalamic dysfunction. 2 cases: the contribution of nuclear magnetic resonance, therapeutic trial of naltrexone].
Two cases of idiopathic hypothalamic dysfunction (one boy and one girl) are reported. Symptoms of hypothalamic dysfunction were noted by the age of 2 years: initial polyphagia and obesity with subsequent anorexia and emaciation were observed in one patient. Thermoregulation and thirst disorders, recurrent accesses of hypernatremia, acrocyanosis and profuse sweating were present. Impaired growth and delayed puberty in one case, and in the other hypogonadism, absence of growth hormone and gonadotrophins release in response to provocative stimuli were observed as well as abnormal thyroid stimulating hormone response to thyrotropin releasing hormone with hyperprolactinemia. Magnetic resonance imaging showed structural lesion in the lateral part of the lentiform nucleus in one case. Treatment with naltrexone, an opiate antagonist, had little if any effect.
Body Height↗