Biomedical subjects
Publications and source records attributed to P Simon.
The interstitial nephritis associated with sicca syndrome is usually symptomless or responsible for mild renal impairment. The authors report five cases in which renal failure was severe, requiring haemodialysis in two patients. The physiopathological mechanisms and the treatment of interstitial nephritis in sicca syndrome are discussed. Corticosteroids improved renal function in three of these five patients.
We will present data from the comparison between four tests in mice of 10 1,4-benzodiazepines and one 1,5-benzodiazepine (clobazam). The tests used were: the "4 plates test" of anxiolytic activity; the electroshock test to determine the anticonvulsive effects; actimetry to predict the sedative effect on motricity; and traction test to predict the myorelaxant effect. The latter two tests have been suggested to be predictive of side-effects that damage psychomotor efficiency in human patients. A comparison of ED50s determined from the predictive tests of the therapeutic effect and those of the side-effects led to the calculation of ratios considered to be predictive of the safety margin. A classification according to this margin shows the advantages of the 1,5-benzodiazepine compared with the 1,4-benzodiazepines. Despite the caution needed in the extrapolation of the results from animals to humans, this work stresses the interesting place that the 1,5-benzodiazepine seem to hold as anticonvulsant in clinical practice.
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In order to compare the level of agreement between four evaluation criteria, data from an 18-month clinical trial with 181 schizophrenic patients were reanalyzed. In that study, assessments of the subjects were carried out with two psychiatric rating scales, Brief Psychiatric Rating Scale and Nurses' Observation Scale for Inpatient Evaluation (BPRS and NOSIE), and two clinical evaluations (psychiatrist and nurse). Results show that there was total agreement on the four outcome measures for only half of the subjects. After further analyses, we observed that the best agreement was between the two clinical assessments. The NOSIE had poor agreement with the other criteria and appeared less sensitive to moderate levels of improvement in the patients' clinical status. These results are discussed with respect to reliability and validity issues.
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In the brown hare, fertile mating takes place from the beginning of December to September. Pituitary and ovarian response to a monthly i.v. injection of 5 micrograms LHRH was studied from September 1983 to October 1984 in 2 groups of 6 hares. The basal concentrations of LH remained undetectable until the end of January, rose from 0.23 +/- 0.14 ng/ml from February to a maximum of 1.44 +/- 0.57 ng/ml in July. LHRH injection was always followed by a release of LH. Between September and December, the LH value peaked 15 min after injection and returned to basal concentrations 2 h later. From January, this pattern altered and a second peak of LH appeared 2 h after injection. Peak levels 15 min after LHRH were around 10 ng/ml between September and December, increased from 47.0 +/- 8.0 ng/ml in January to 106 +/- 33 ng/ml in July and decreased in August (69.4 +/- 10.6 ng/ml). The values of the second peak rose from 11.0 +/- 2.2 ng/ml in January to 90.6 +/- 12.4 ng/ml between March and July and decreased in August (24.5 +/- 5.1 ng/ml). The LH surge induced by LHRH was always followed by a transient rise in progesterone. During the breeding season, this progesterone secretion increased considerably. Ovulation was possible between January and August and the number of ovulating females was maximum between March and July. The amount and duration of progesterone secretion during the resulting pseudopregnancies increased during the breeding season.
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A preventive technique of radiation injuries to small intestines with intrapelvic mammary prosthesis is described. It has been used for twelve cases in which 9 concerned rectal adenocarcinomas (local recurrences 7 and fixated tumors 2). After this short experience, we can recommend this reliable technique without important local complication and describe the irradiation technique. The indications of this method are precised because it is finally an unfrequent therapeutic.
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Between January 1976 and December 1985, renal biopsy was indicated in 663 adults (greater than 15 yrs) patients who were born and lived in a rural area of 400,000 inhabitants. Annual incidence (AI) was 16.5/100,000. Primary GN was diagnosed in 418 pts (63%) corresponding to a prevalence (P) for 10 yrs of 1/1000. The results have been compared for two periods: A (1976-1980) and B (1981-1985) for which the number of patients with primary GN was similar (205 vs 213, AI: 10.3 vs 10.6/100,000). Sex-ratio M/F (2.1 vs 1.8) and mean age (+/- SD) at the time of renal biopsy (45 +/- 17) were not different. P (%) among primary GN, P (nb/1000) among global population, AI (nb/100,000) and sex-ratio (A vs B) were evaluated for each histological type: lipoid nephrosis (MC and HSF): 9.8%, 0.1/1000, 1.2 vs 0.8/100,000 (ns), 1 vs 1.5 (ns). Membranous nephropathy 12.4%, 0.13/1000, 1.1 vs 1.5/100,000 (ns), 1.75 vs 0.8 (less than 0.02). IgAGN (Berger): 27%, 0.28/1000, 2.6 vs 3/100,000 (ns), 3 vs 3.3 (ns). IgAGN (Schönlein-Henoch): 5%, 0.05/1000, 0.45 vs 0.6/100,000 (ns), 3 vs 5 (ns). MPGN: 5.9%, 0.06/1000, 1 vs 0.25/100,000 (less than 0.01), 2.3 vs 1.5 (ns). Post streptococcal AGN: 2.8%, 0.03/1000, 0.55 vs 0.05/100,000 (less than 0.01). Non post-streptococcal AGN: 6.7%, 0.07/1000, 0.65 vs 0.75/100,000 (ns), 1.2 vs 0.6. Idiopathic crescentic GN: 4.7%, 0.05/1000, 0.25 vs 0.75/100,000 (less than 0.01) 1.5 vs 1.5. S and F proliferative GN: 1.9%, 0.02/1000, 0.15 vs 0.25/100,000 (ns), 2 vs 0.2.(ABSTRACT TRUNCATED AT 250 WORDS)
Iron as ferrous ammonium sulfate was injected into the cerebral spinal fluid of rats. After three consecutive days of injection of 4 mumol of iron, the total iron content of brain cortex synaptosomes from the iron-treated animals was 2-fold higher than that from control animals receiving the saline vehicle only. Spin label studies of the synaptosomal membranes demonstrated that the lipid region of the membranes became more rigid and, in addition, the mobility of labeled SH groups of membrane proteins decreased after the iron treatment. The cholesterol content was significantly higher in iron-treated animals as compared to controls. Centrophenoxine pretreatment (100 mg/kg body weight daily for 6 weeks) diminished the iron effects. Synaptosomal membrane alterations observed after iron treatment were similar to changes observed previously during aging. This lends support to the notion that free-radical induced damage occurs in brain membranes with increasing age.
The effects of the enantiomers of clenbuterol were compared in four psychopharmacological tests in which beta-adrenergic agonists are known to be active. In mice (+/-)-clenbuterol 0.06 mg/kg decreased motor activity and antagonized the hypothermia induced by 16 mg/kg of apomorphine; at 0.5 mg/kg it increased head-twitches and tremors induced by 1-5-hydroxytryptophan (4 mg/kg) and decreased the number of bites of a food pellet by mice which had been maintained on a water only diet for 24-27 h ('Tantale' test). The present results show that the (-) form is responsible for this activity and that the (+) form has no effect per se and does not antagonize the (-) enantiomer.
The present study investigated the extent to which a single priming injection of clenbuterol, a beta-adrenoceptor agonist, could alter the behavioral response (locomotor activity recorded for 30 min with photocell counters) of mice to the subsequent administration of beta-adrenoceptor agonists or antagonists. In mice pretreated with clenbuterol (0.25 mg/kg), the dose-response curve of clenbuterol (0.06 to 2 mg/kg) for reducing locomotor activity was shifted to the right with minimal alteration of the maximal response. The magnitude of the shift was dependent on both the priming dose of clenbuterol and the time interval between the priming and the test injections (maximum between 15 to 24 h, disappearance for intervals exceeding 72 h). The coadministration of propranolol (0.5; 2; 8 mg/kg) dose dependently antagonized the effects of the priming injection of clenbuterol. A previous injection of clenbuterol was also found to reduce the ability of another beta-adrenoceptor stimulant, salbutamol (8 mg/kg), but not apomorphine, to reduce locomotor activity. Finally, previous beta-adrenoceptor stimulation resulted in an enhanced ability of two beta-adrenoceptor antagonists, propranolol (0.125 to 8 mg/kg) and penbutolol (0.5 to 32 mg/kg), to reduce locomotor activity in mice. All these data add to the evidence concerning the remarkable plasticity of central beta-adrenoceptors and indicate that initial stimulation of a class of beta-adrenoceptors may trigger a relatively important, time-dependent alteration in the behavioral reactivity to beta-adrenoceptor agonists and antagonists.
The effects of enantiomers of nomifensine were compared in five psychopharmacological tests in which (+/-)-nomifensine is active. In mice, (+)-nomifensine increased motor activity at 16 mg/kg, 8 mg/kg reduced the hypothermia and ptosis induced by reserpine and antagonized the hypothermia induced by 16 mg/kg of apomorphine. (+)-Nomifensine 4 mg/kg potentiated yohimbine toxicity. (-)-Nomifensine 4,8, or 16 mg/kg was inactive in all these tests. In rats, (+)-nomifensine 8 mg/kg induced stereotyped movements whereas (-)-nomifensine 64 mg/kg did not produce stereotypies.
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Daily injection of triiodothyronine (T3) for 3 consecutive days dose dependently enhanced 1-5-HTP (4 mg/kg)-induced head twitches in mice. This effect was blocked by 1-penbutolol. Pretreatment with a sub-effective dose of T3 (0.06 mg/kg) markedly enhanced the ability of clenbuterol but not indalpine to potentiate the response to 1-5-HTP. Likewise, the effects of T3 were more pronounced on the desipramine- or maprotiline-induced potentiation of head-twitches than on the action of citalopram or clomipramine. These data suggest that the increased responsiveness to 1-5-HTP caused by T3 involves an indirect (noradrenalin-mediated) rather than a direct effect on serotonergic processes.
Previous experiments have shown that a number of xenobiotics such as halogenated ethylenes cause an experimental acetonemia. In addition, under exposure of rats to vinylidene fluoride (one of the agents producing this effect), the urinary excretion rates of acetoacetate and 3-hydroxybutyrate are enhanced. The enhanced formation of ketone bodies is theoretically explained by a covalent interaction of reactive metabolites of the applied xenobiotic with hepatic cytosolic coenzyme A. This theory is further corroborated by the following experiments: Microsomal incubations of [14C]vinyl chloride and [3H]coenzyme A lead to one metabolite containing 2 moles vinyl chloride/mole coenzyme A and two other with equimolar ratios of both components. Exposure of rats to vinyl chloride leads to a progressive depletion of hepatic cytosolic CoASH, but not of CoASH in mitochondria. In the cytosol acetyl-CoA is also diminished after vinyl chloride exposure. These changes may cause secondary effects in lipid metabolism which are regarded as responsible for the enhancement of ketone bodies.