Search

Background: Pectus carinatum may be a major issue for adolescent patients, as chest-wall malformations can have a negative impact on body image and induce self-esteem disorders. Bracing has become the first line treatment for adolescent patients whose anterior chest wall is still flexible. The main obstacle is the tolerability of the bracing device along with the patient's compliance to the device. The aim of this study was to examine the quality of life of adolescent patients treated with bracing to correct pectus carinatum in our institution. From November 2021 to July 2023, 28 patients with pectus carinatum were treated with bracing therapy in our chest wall deformities unit. We used a bivalve brace, manufactured with computer-aided design. All patients were asked to answer a multiple-choice questionnaire designed to assess how bracing therapy impacts their daily life, treatment compliance, and overall satisfaction. Patients who wore the brace for at least 3 months, and at least 5 days per week and 10 h per day, are defined as compliant with the bracing protocol. Results: The mean age of the patients was 14 ± 1.36 years. Patients wore the brace for an average of 10.1 ± 6.9 months in the compliance group (n = 18), and 2.2 ± 2.5 months in the non-compliance group (n = 10). Our results show that compliant patients are fairly satisfied of the comfort of the brace, with a limited impact of the device on their daily activities and social life. However, non-compliant patients report the following dissatisfactions regarding the brace: higher pain scores, difficulty in breathing, and issues sleeping with the brace. The compliant patients noted a significant improvement in the appearance of their chest, and were satisfied with the appearance of their chest. The non-compliant patients did not notice any changes. Conclusions: Compliant patients treated with a bi-valve brace for pectus carinatum seem to have a good quality of life with a limited impact on their daily life and social activities. The bi-valve brace also seems to be an effective therapy in compliant patients. [ABSTRACT FROM AUTHOR]

Erythropoiesis-stimulating agents (ESAs) remain the first-line treatment of anemia in lower risk myelodysplastic syndromes (MDS) without 5q deletion. A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias. We conducted a prospective multicenter study of EPO-β and ATRA in anemic MDS patients with marrow blasts <10% and either previous ESA failure or relapse, endogenous EPO >500 U/l or other cytopenia(s) (absolute neutrophilic count <1.0 G/l or platelets <50 G/l). A total of 59 patients were evaluable after 12 weeks of treatment. The erythroid response rates according to IWG 2000 and 2006 criteria, respectively, were as follows: overall: 49 and 36%; patients with previous ESA failure (n=28): 43 and 32%; patients with endogenous EPO >500 U/l (n=18): 11 and 19%; patients transfused >2 red blood cells units/month (n=28) 43 and 39%. Only one neutrophil, but no platelet response, and no major side effect were observed. EPO-β–ATRA combination appears a possible therapeutic option in anemia of MDS having failed an ESA alone, but not in patients with high endogenous EPO level, and does not improve neutropenia and thrombocytopenia.Leukemia (2009) 23, 673–678; doi:10.1038/leu.2008.362; published online 8 January 2009 [ABSTRACT FROM AUTHOR]

Corrosion-Electrochemical behavior of a commercial API5CT grade L80 type 13Cr tubing enriched with microalloying elements is studied in 6, 7.5, 9, 12 and 15% HCl solutions by electrochemical methods. The objective is to contribute to the comprehension of corrosion phenomena caused by HCl of similar concentrations, generally used in acidizing job. The corrosion morphology is examined by scanning electron microscopy (SEM) coupled with EDAX. The soluble corrosion products are analyzed by atomic absorption spectroscopy and colorimetric methods. General, as well as localized, corrosion is present. The severest general corrosion with a maximum rate of 26 mm/year is obtained at 15% HCl. The localized corrosion which morphologically differs as function of HCl concentrations is revealed by SEM investigation. In all the above HCl solutions, the commercial 13% Cr martensitic stainless steel tubing shows no passive state. Above 6% HCl, the microalloying elements promote forming a discontinuous film of the corrosion products. The corrosion rate slightly decreases in 15% HCl compared to the published data on a conventional 13% Cr martensitic stainless steel tubing. This is due to both the chemical composition (silicon, manganese and vanadium) and microstructural properties. Copper seems to additionally accelerate the corrosion of the alloy. [ABSTRACT FROM AUTHOR]

Handling-induced convulsions in the quaking mouse can be blocked by: phenobarbital, pentobarbital or phenytoin; postsynaptic alpha-adrenoceptor agonists (noradrenaline, phenylephrine, CRL 40028); presynaptic alpha-adrenoceptor blockers (yohimbine, mianserine); catecholamine liberating agent (amphetamine); noradrenaline reuptake inhibitors (cocaine, imipramine, desipramine). Moreover, the protective effect of yohimbine was antagonized by clonidine, prazosin or alpha-methylparatyrosine, and the protective effect of CRL 40028 was antagonized by prazosin but not by alpha-methyltyrosine. Drugs acting by other mechanisms (pilocarpine, atropine, trihexyphenidyl, (−)-5-HTP, methysergide, pimozide, clonidine, alpha-methyl DOPA, prazosin, isoprenaline, salbutamol) did not protect against convulsions. A slight protection was obtained with high doses of apomorphine and also with (±)-propranolol. This effect is probably not related, to blockade of betaadrenoceptors because the same effect was obtained with (+)propranolol. In young quaking mice, where susceptibility to convulsions is low, both postsynaptic alpha-adrenoceptor blockers and presynaptic alpha-adrenoceptor antagonist lowered the convulsive threshold. Thus, this seems to constitute an interesting model for the in vivo study of substances which affect the central alpha-adrenoceptors either pre- or postsynaptically. [ABSTRACT FROM AUTHOR]

Eleven benzodiazepines were evaluated in the staircase test in mice. The behavioural parameters measured were the number of steps climbed and the number of rears during a 3-min test. Climbing and to a lesser extent rears were enhanced at low doses, whereas both parameters, particularly rearing, were reduced at higher doses. The differential effects of the drugs on the two parameters were used to determine indices of anxiolytic efficacy for each drug where increases in climbing were taken to indicate the onset of anxiolytic activity and decreases in rearing the onset of sedative activity. The compounds could be ranked according to these indices in a manner which appears to reflect their therapeutic profile in man. [ABSTRACT FROM AUTHOR]

A novel test procedure for antidepressants was designed in which a mouse is suspended by the tail from a lever, the movements of the animal being recorded. The total duration of the test (6 min) can be divided into periods of agitation and immobility. Several psychotropic drugs were studied: amphetamine, amttriptyline, atropine, desipramine, mianserin, nomifensine and viloxazine. Antidepressant drugs decrease the duration of immobility, as do psychostimulants and atropine. If coupled with measurement of locomotor activity in different conditions, the test can separate the locomotor stimulant doses from antidepressant doses. Diazepam increases the duration of immobility. The main advantages of this procedure are (1) the use of a simple, objective test situation, (2) the concordance of the results with the validated 'behavioral despair' test from Porsolt and, (3) the sensitivity to a wide range of drug doses. [ABSTRACT FROM AUTHOR]

Male Wistar rats were trained to press a lever with food reinforcement according to a continuously reinforced schedule (CRF). Afterwards, rats were subjected to three experimental sessions (30 min each) during which responding was rewarded according to a progressive ratio schedule (following an initial 2-min CRF period, the number of presses necessary for the pellet delivery was doubled every second minute). Responding during the first half of each session, i.e., pressing for food, was maintained at a significant level, whereas it was almost suppressed during the second part of the session. As compared to controls (200±20 presses/30 min) animals given amfonelic acid (0.5, 1 mg/kg IP), methylphenidate (4, 8 mg/kg IP), caffeine (16 mg/kg IP), cocaine (4 mg/kg IP), oxolinic acid (32 mg/kg IP), nomifensine (4 mg/kg IP), DR 250 (2, 4 mg/kg IP) and d-amphetamine (0.25, 0.5, 1 mg/kg IP) showed an increased rate of responding ranging from 400 to 950 presses/30 min. In contrast, apomorphine, MK 486+ l-dopa, trihexyphenidyl, imipramine, salbutamol and diazepam did not increase responding. These results suggested that this test is highly sensitive for psychomotor stimulants and perhaps for their ability to enhance the reinforcing value of the reward or stimuli associated with the reward. Such activity seemed related to a catecholaminergic substrate since the increase of responding induced by amphetamine was blocked by pimozide, d,l-propranolol and prazosin. [ABSTRACT FROM AUTHOR]

The antagonism of hypothermia induced by two doses of apomorphine (1 or 16 mg/kg) is proposed as an improved screening test for both neuroleptics and antidepressants. Low dose apomorphine-induced hypothermia (1 mg/kg) differentiates sulpiride-like neuroleptics (which better antagonize this effect of apomorphine than other effects such as stereotyped behavior) from haloperidol-like drugs. The latter equally antagonize the two effects of apomorphine. The effects of sulpiride are also distinct from those of chlorpromazine-like drugs which strongly antagonize stereotyped behavior, but not hypothermia induced by apomorphine. Hypothermia induced by a high dose of apomorphine (16 mg/kg) is not antagonized by neuroleptics, but is strongly antagonized by antidepressants (imipramine-like drugs, amineptine, amoxapine, nomifensine, viloxazine) and potential antidepressants (beta-adrenergic stimulants). The use of these two tests rapidly screens both antidepressants and neuroleptics and classifies neuroleptics according to their profile of action on the dopaminergic system. [ABSTRACT FROM AUTHOR]

The stimulant effects of oxolinic acid were investigated in rats and mice. This drug, given orally, consistantly induced, in doses ranging from 16 to 256 mg·kg, locomotor stimulation and stereotyped behavior. These effects were antagonized by pimozide (1 mg·kg), α-methyltyrosine (64 mg·kg) or reserpine (4 mg·kg, 24 h before testing) pretreatment, suggesting a facilitatory role of oxolinic acid on catecholaminergic processes. Diazepam (4-16 mg·kg) reduced the stimulant effects induced by oxolinic acid but not those induced by amphetamine; oxolinic acid (8 mg·kg) markedly reduced the antipunishment effect elicited in rats by diazepam (2 mg·kg). Since benzodiazepines have been reported to enhance GABA functioning, these data suggest that oxolinic acid may impair GABA transmission. However, neither muscimol (0.5-1 mg·kg) or γ-acetylenic-GABA (16-64 mg·kg) selectively reduced the stimulant effects elicited by oxolinic acid. Therefore, the possible facilitation exerted by this drug on catecholaminergic systems may not derive from the release of an inhibitory GABAergic control. [ABSTRACT FROM AUTHOR]

Common effects of four beta-adrenergic blocking drugs have been investigated in mice using classical and new psychopharmacological tests. Propranolol, alprenolol, practolol and penbutolol reduced the increase in locomotor activity produced by reserpine after MAO inhibition; they produce hypothermia when associated with amphetamine and they increase oxotremorine-induced hypothermia. Regarding these three tests the studied substances ranged themselves in the same order of potency: penbutolol > propranolol > alprenolol > practolol. Propranolol and penbutolol decreased the toxicity provoked in crowded mice by amphetamine or by the association pargyline-reserpine; alprenolol and practolol did not. Propranolol, penbutolol and alprenolol antagonized the amphetamine-induced increase in motor activity; practolol did not. When used at doses for which d-l propranolol was active, the dextrogyre isomer of propranolol was without effect whatever the test studied. It is suggested that for the selection of a beta-blocking drug, regarding central effects in man, the tests described would deserve consideration. [ABSTRACT FROM AUTHOR]

Behavioral and pharmacological tests were performed on rats (males Wistar A.F.) maintained either during 6 weeks at 20 or 5 in a cage (40×40×17 cm) or during 6 weeks at 20 and during 8 days at 5 in cage. When compared to 5/cage-reared rats, overcrowded rats (20/cage) exhibit a lessened locomotor activity in the open field, staircase test, and Y maze; rearings, intrasession habituation, and spontaneous alternation were not altered. It seems difficult to relate this lessened locomotor activity to an enhanced emotionality level. Although overcrowded rats showed heavier adrenals, their susceptibility to restraint-induced gastric ulcers, their 'neophobic' responses to new food, and their sensitivity to the stimulating effect of oxazepam in the Y maze were not modified. Sensitivity to amphetamine-induced stereotyped behavior and to pentobarbital-induced hypnosis was found to be increased in overcrowded rats. Apomorphine-induced stereotypy and barbital sleeping time were not modified. All these data (except the fact that barbital onset of hypnosis was delayed in overcrowded rats) may suggest an altered hepatic metabolism in rats reared at 20 in a cage. In overcrowded rats an enhanced amphetamine-induced stereotyped behavior was associated with a lessened locomotor activity. Moreover, after 8 days at 5 in a cage, this increased sensitivity to amphetamine (and to pentobarbital) completely disappeared, whereas locomotor activity was not fully restored. This suggests that amphetamine sensitivity is not related to the predrug activity level of the animals. [ABSTRACT FROM AUTHOR]

The following behavioral modifications were observed after a single i.p. administration of T.R.H. (thyreo-tropin-releasing hormone) in mice or rats at doses higher than 4mg · kg: I. an increased reactivity to stimuli, II. periods of excitation alternating with periods of aggressivity, III. unusual movements ('tail-rattling' and 'wet-dog'), IV. the reserpine- or oxotremorine-induced hypothermia was antagonized in mice by T.R.H. in doses of 1 mg · kg and higher, but only a few other symptoms were influenced. The prochlorperazine-induced catalepsy in rats was antagonized by T.R.H.; under the experimental conditions, sudden hyperkinetic episodes were observed. The toxicity of pargyline- l-Dopa association was slightly increased, amphetamine- or apomorphine-induced stereotyped behavior was unchanged. This spectrum of activity is different from other known psychotropic drugs. [ABSTRACT FROM AUTHOR]

The role of atrial distension and/or adrenergic mechanisms in the regulation of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP, norepinephrine (NE), epinephrine (E) and left atrial diameter at rest, during and after graded bicycle exercise has been studies in 8 healthy male subjects after single doses of placebo, tertatolol 5 mg (a non-selective β-adrenoceptor blocker), prazosin 1 mg (an α-adrenoceptor antagonist) and their combination. Systolic and diastolic left atrial diameters were measured before, during and just after exercise by bidimensional echocardiography. Exercise caused an increase in plasma ANP, which was greater after tertatolol alone, and tertatolol plus prazosin, than after placebo or prazosin alone; the mean area under the plasma ANP concentration curve was increased by 35% after tertatolol alone, by 45% after tertatolol and prazosin compared to placebo, and by 82% and 94%, respectively when compared to prazosin alone. The rise in plasma ANP was more marked during the post-exercise period: 80% after tertatolol alone, 67% after tertatolol and prazosin compared to placebo, and 133% and 115%, respectively, compared to prazosin alone. The rise in plasma ANP was accompanied by an increase in both the systolic and diastolic atrial diameter, which was also significantly greater after tertatolol alone and the combination than placebo, or after prazosin alone. β-Adrenoceptor blockade alone did not affect the plasma catecholamine concentrations, but the exercise-induced increase in plasma norepinephrine was significantly potentiated by prazosin and by prazosin plus tertatolol, and that of plasma epinephrine by the drug combination. We conclude that potentiation of the exercise-induced increase in plasma ANP by β-blockers may be due to atrial stretching consequent on the decreased myocardial contractility and relaxation, and not to alpha-1 adrenoceptor stimulation. Any increase in plasma catecholamines did not play an important role in ANP secretion. [ABSTRACT FROM AUTHOR]

The influence of three beta-adrenergic blocking agents was studied on the stereotyped behavior induced in rats by a range of doses of d-amphetamine or apomorphine. The stereotyped behavior was assessed either clinically (quotation from 0 to 3 at various times for each rat) or using the confinement motor activity test. From 8 mg/kg (i.p.) onwards, propranolol and prinodolol clearly potentiated the amphetamine-induced stereotyped behavior without any modification of the apomorphine-induced stereotyped behavior. Practolol, known for its poor passage through the blood-brain barrier had only a slight effect. [ABSTRACT FROM AUTHOR]

In mice, pilocarpine - or oxotremorine - induced decrease in locomotor activity and increase of the reaction time to pain were antagonized by atropine and not by methylatropinium. Identical doses of atropine and methylatropinium suppressed the antagonism of the cholinergics towards reserpine-induced palpebral ptosis. Cholinergics-induced hypothermia was not clearly antagonized by atropine or methylatropinium. [ABSTRACT FROM AUTHOR]