[Bone scintigraphy in the pathology of the hindfoot].
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Adolescent↗
Biomedical subjects
P Martin
Publications and source records attributed to P Martin.
[The value of breast lymphoscintigraphy in the definition of axillary staging in cancer of the breast].
Axillary lymphoscintigraphy (ALS) has been investigated in 51 patients with operable breast carcinoma between July 1982 and February 1984. Pre-operative intra-tumoral injection of 2.5 cm Ci of technetium 99 m antimony sulfide colloid has been performed before axillary dissection. We compared the scans produced by ALS with the results of pre-operative clinical examination of the axilla (UICC criterias) and to the histological status of the nodes surgically removed. We focused on the statistical methodology because, for us, most of the studies use inadequate tests. Axillary lymphoscintigraphy did not predict axillary metastase in breast cancer with precision. Its score was under clinical exam. Today, we are not allowed to abandon axillary dissection for pre-operative ALS. That simple and non traumatic examination appeared to be of no value in order to determine the axillary metastatic nodal status in breast cancer.
Axilla↗
[Spontaneous rupture of the esophagus in neurogenic muscular atrophy. A contribution to the etiology of Boerhaave syndrome].
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Aged↗
[A case of myopathy with carnitine deficiency].
Clinical and biological criteria of myopathies associated with carnitine deficiency allow to distinguish a muscular and a systemic form of the condition. In this report, the results of clinical, pathological and electrophysiological data obtained from a patient with carnitine deficiency-linked myopathy are described. The patient was a 23-year-old girl who was previously known to suffer from muscle weakness when suddenly acidosis associated with a severe drop in plasma carnitine appeared. In addition there were hypermetabolic symptoms similar to those described in Luft's syndrome. Biopsy from the quadriceps femoris muscle before treatment revealed that all type I fibers were either hypotrophic or atrophic. They showed lipid overloading manifested by triglyceride droplets adjacent to the mitochondrial membrane. Furthermore, the level of soluble muscle carnitine was 83 p. 100 less than in controls and membrane linked muscle carnitine was also 73.5 p. 100 less than in controls. The patient rapidly recovered after the initiation of daily treatment with 4.40 g carnitine chlorhydrate associated with 50 g Lipogram 20. Nine months later, lipid overloading completely disappeared and the level of plasma carnitine returned to near normal whereas the level of both soluble and linked carnitine remained very low. To provide more information on the origin of the myopathy (myogenic, neurogenic or humoral) we carried out an electrophysiological investigation of cultured skeletal muscle cells from the patient and from biopsies of patients not known to be suffering from myopathy. The electrophysiological data showed that the patient myotubes were less polarized than myotubes from control patients. Furthermore, the amplitude of the action potential was smaller than the amplitude of the action potential measured in control cells. Daily addition of 50 microM carnitine chlorhydrate to the cultured myotubes induced a recovery of the action potential amplitude. Taken together these results indicate that the carnitine deficiency reported here was probably of systemic origin in addition to a myogenic component. Muscle deficiency could be either linked to an alteration in the carnitine pathway or to overconsumption of carnitine by muscle. This latter point is discussed.
Action Potentials↗
Partially reversible osteopenia after surgery for primary hyperparathyroidism.
Bone mineral content of the radius in 30 patients with primary hyperparathyroidism was determined by single-photon absorptiometry before and one year after the removal of a parathyroid adenoma. When compared with normal age- and sex-matched subjects, preoperative bone mineral content was decreased by more than 1 SD in 24 patients 3 cm from the styloid apophysis (distal site) and in 23 patients 8 cm from the styloid apophysis (proximal site). The decrease at the distal site, where there is more trabecular bone, was significantly greater than at the proximal site (74% +/- 13% of the normal mean vs 79% +/- 13%). Bone mineral content values were not different in the female and male populations. One year after surgery, the bone mineral content was significantly increased but was still lower than normal at both sites (81% and 84% of the normal mean, respectively). In some patients, seen up to three years after surgery, the bone mineral content remained lower than normal. We conclude that primary hyperparathyroidism causes an osteopenia that affects both cortical and trabecular bone and that is only partially reversible, even in the long term.
Adenoma↗
Kinetic study of the action of bovine chymosin and pepsin A on bovine kappa-casein.
A study was carried out to determine the Michaelian parameters relative to the action of chymosin and pepsin A on bond Phe105-Met106 of bovine kappa0-casein (carbohydrate-free fraction in micellar state). The reaction was performed in citrate buffer, pH 6.2, at 30 degrees C. The reaction mixture was analysed by reverse phase HPLC. Dosages of peptide 106-169 (caseino macropeptide) at different reaction times from recordings of its absorbance at 220 nm gave the initial rates of reaction at each substrate concentration. From these values the following parameters were determined: kcat = 68.5 s-1, Km = 0.048 mM, kcat/Km = 1,413 mM-1 s-1 for chymosin, and kcat = 45 s-1, Km = 0.018 mM, kcat/Km = 2,439 mM-1 s-1 for pepsin A. For chymosin they are similar to those obtained previously in dimethyl glutarate buffer, pH 6.6, at 30 degrees C, using fragment 98-111 of kappa-casein as substrate. It can thus be concluded that neither the micellar state nor the presence of the whole peptide chain of kappa-casein (our conditions) significantly affect the action of chymosin on fragment 98-111, which seems to contain all information that makes bond 105-106 highly sensitive to chymosin. For pepsin A, only the information contained in fragment 103-108 appears to be required.
Amino Acids↗
Comparison of clenbuterol enantiomers using four psychopharmacological tests sensitive to beta-agonists.
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.
5-Hydroxytryptophan↗
Does a single priming injection of clenbuterol alter behavioral response to beta-adrenoceptor agonists and antagonists in mice through a time-dependent process?
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.
Adrenergic beta-Agonists↗
Effects of triiodothyronine on the 5-hydroxytryptophan-induced head twitch and its potentiation by antidepressants in mice.
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.
5-Hydroxytryptophan↗
Oncogene expression in human tumors.
The expression of 9 oncogenes in primary tumors and in human tumors passaged in nude mice was tested: a total of 28 tumor types was analyzed. Oncogenes src, fps, and mos were not expressed in any of the tumors tested but oncogene myc was transcribed in most of the tumors and myc was over-expressed in 3 tumors passaged in nude mice (Ewing sarcoma, large intestine carcinoma and kidney carcinoma) and in primary fibrous histiocytoma. Enhanced transcription of ras and fos genes was observed nonspecifically in different tumors. Oncogene sis was activated specifically in metastases of different tumors in lymph nodes.
Animals↗
Phenotype of recovering lymphoid cell populations after marrow transplantation.
Four patients who received bone marrow transplants were studied sequentially during the posttransplant period to define the pattern of recovering lymphoid cell types. Three patients received T cell-depleted, HLA-matched marrow, and one received untreated marrow from an identical twin. Blood lymphoid cells were labeled with 25 different pairs of monoclonal antibodies. In each sample, one antibody was conjugated to fluorescein and one to phycoerythrin, thus allowing simultaneous assessment of the expression of the two markers using the fluorescence activated cell sorter. A total of 14 antibodies were used, routinely including HLE, Leu-M3, Leu-4, Leu-1, Leu-5, Leu-9, Leu-6, Leu-2, Leu-3, HLA-DR, Leu-7, Leu-11, Leu-15, and Leu-12. Other antibodies were used to further define some populations. This study has allowed us to define six distinct cell types that have appeared in all four patients by day 90 posttransplantation, and which account for 90-100% of all circulating lymphoid cells. These cell types are (a) T helper cells expressing Leu-1, Leu-4, Leu-9, Leu-5, Leu-3, and variable amounts of HLA-DR; (b) T suppressor cells expressing Leu-1, Leu-4, Leu-9, Leu-5, Leu-2, and variable amounts of HLA-DR; (c) B cells expressing Leu-12, B1, HLA-DR, IgD, and IgM, but none of the T cell antigens; (d) an unusual B cell phenotype (Leu-1 B) expressing all of the B cell markers, and also having low amounts of Leu-1, but none of the other T cell antigens; (e) natural killer (NK) cells expressing Leu-11, Leu-15, Leu-5 but none of the other T cell or B cell markers; (f) NK cells expressing Leu-11, Leu-15, Leu-5, and low levels of Leu-2. Both NK types also express Leu-7 on some, but not all cells. The relative frequencies of these cell types varied among the patients and with time, but the striking findings were the presence of relatively few mature T cells, large numbers of NK cells, and the preponderance of the unusual Leu-1 B cell over conventional B cells in all three patients who developed B cells. Sorting experiments confirmed the NK activity of the major NK cell phenotypes, and DNA analysis confirmed that all of the cells studied were of donor origin. In addition, analysis of Ig genes in one patient showed that the Leu-1 B cells were not clonally rearranged.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
Marker chromosomes in direct preparations of human large bowel tumors.
A survey of 257 marker chromosomes in 48 primary human large bowel adenocarcinomas showed that 44% were markers with recognized patterns. Chromosomes #1, #3, #5, #8, #9, #13, and #17 were involved most frequently. Markers related to chromosomes #7 and X were not seen in any recognizable form. The unidentified chromosomes were classified as markers with abnormal banding regions. In correlating tumor location and stage of invasion with markers, there were fewer markers in tumors from the right side. However, there was little difference in the number of markers seen in the left-sided tumors, irrespective of histopathologic stage, suggesting that function and microenvironmental conditions between various parts of the colon may be related to these differences. The most striking observation is that 21% of all tumors analyzed were without any obvious markers.
Adenocarcinoma↗
Chromosomal banding patterns in human large bowel adenomas.
Chromosome studies were performed on direct preparations of 38 benign human large bowel adenomas by fluorescent banding techniques. Five adenomas had a normal diploid karyotype line. Six adenomas had numerical abnormalities, and seven polypoid lesions exhibited structural and numerical changes. In 20 adenomas without analyzable metaphases, it was presumed that the cells were dividing at a lower rate. Mosaics were observed in 25% of cases. The most common finding was trisomy of 7, 8, or 13.
Adenoma↗
Effects of phencyclidine on active avoidance and escape in rats.
Rats trained to avoid electrical shock in a shuttle box were given phencyclidine (0.0, 1.0, 5.0, or 10.0 mg/kg) prior to testing for 5 consecutive days. There was a dose-dependent increase in both avoidance and escape failures although animals continued to cross the barrier during intertrial intervals, indicating that they were capable of making the appropriate response. Little evidence of tolerance was found during the 5-day testing period.
Animals↗
The specific protective effect of diazepam and valproate against isoniazid-induced seizures is not correlated with increased GABA levels.
Amino acid concentrations were measured in the cortex, cerebellum and hippocampus of the mouse brain before and during seizures induced by isoniazid (250 mg/kg i.p.), an inhibitor of L-glutamate-1-decarboxylase (EC 4.1.1.15: GAD). Valproate sodium and diazepam dose-dependently delay the onset of convulsive fits caused by isoniazid. However, neither diazepam nor valproate prevented the decrease in GABA concentrations produced by isoniazid alone. Also, these antiepileptic drugs did not modify the rate of GABA depletion elicited by isoniazid. These results, observed in four different brain structures, strengthen those first obtained with beta-vinyllactic acid, another inhibitor of GAD.
Amino Acids↗
Triiodothyronine-induced reversal of learned helplessness in rats.
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Animals↗
Dissociation of head twitches and tremors during the study of interactions with 5-hydroxytryptophan in mice.
Intraperitoneal injection of 5-hydroxytryptophan and 5-methoxy-N,N-dimethyltryptamine is shown to provoke characteristic behaviors in mice that can be quantified. The two principal phenomena described here are head twitches and tremors. Tremors became more frequent when doses of the two substances studied were increased. Head twitches appeared at lower doses, but beyond a certain dose, they decreased and even disappeared. The effects on these movements of agents that modify serotonin function were then studied. The results pose problems of interpretation that are discussed.
Animals↗
Effect of brief bursts of carotid sinus stimuli on heart rate and atrioventricular conduction.
The effect of a single brief stimulus burst applied simultaneously to both carotid sinus nerves on atrioventricular conduction (PR) was examined in paced and unpaced preparations of anesthetized open-chest dogs. The relative timing of the stimulus burst was varied to encompass the complete cardiac cycle. Carotid sinus/vagal effect curves were constructed to identify the time course of the response. In paced preparations the maximum increase in PR was 20.3 +/- 2.7 msec and this occurred 458.0 +/- 22.8 msec after the stimulus. There was a latency of 246.0 +/- 12.4 msec after the electrical stimulus before the PR began to increase. In unpaced heart preparations the effect of single carotid sinus nerve stimuli on heart period (PP) and PR was also determined. PP was maximally lengthened by 251.4 +/- 49.4 msec at 644.2 +/- 50.9 msec after the stimulus. There was a latency of 251.4 +/- 10.5 msec before the first noticeable change in PP occurred. The PR response was biphasic. The maximum lengthening of the PR interval was 16.2 +/- 4.2 msec. This response occurred at 361 +/- 22.0 msec after the electrical stimulus. The PR decreased to a minimum value of 13.6 +/- 2.2 msec below control values at 767.1 +/- 44.0 msec after the stimulus. The overall effect of carotid sinus activity on atrioventricular conduction depends not only on the direct nodal effect of acetylcholine but also on the indirect heart rate changes. We conclude that brief bursts of carotid sinus nerve stimulation produce cardiac electrophysiological effects qualitatively similar to the effects of direct vagal stimulation, differing only in having a lower amplitude, a longer latency and a somewhat wider time dispersion.
Animals↗