[Hypokalemia with severe rhythm disorders induced by Vichy water].
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Biomedical subjects
Publications and source records attributed to P Benoit.
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Various lines of evidence from in vivo and in vitro experiments suggest that muscle-derived factors may enhance the survival and axonal outgrowth of spinal neurons. Our previous results using cultures of embryonic spinal neurons showed that denervation of skeletal muscle increased levels of a neurite-promoting activity in soluble muscle extracts. Here, two other experimental models in which muscle activity was also lowered were investigated. The mutant mouse 'paralysé' exhibits a spontaneous regression of motor nerve endings, with concomitant paralysis. In 'paralysé' mutant muscle extracts, specific neurite-promoting activity was up to 10-fold higher than in extracts prepared from control littermates. Tenotomy is known to retard the regression of polyneuronal motor innervation in skeletal muscle from neonatal rats. Three days after operation, levels of neurite-promoting activity were increased 2-fold with respect to total protein. These results suggest that skeletal muscle activity might regulate the synthesis of molecules affecting nerve growth.
Two commonly used methods for screening hybridoma supernatants against cell-surface antigens were performed simultaneously on the supernatant culture fluids of different hybridizations, and compared with the detection of Ig secretion. Supernatants reacting with glutaraldehyde-fixed cells (ELISA (Enzyme-linked immunosorbent assay) on fixed cells) are mostly non-specific for the immunogen; in addition, with this method, only half of the antibodies detected by immunofluorescence are identified. These results can be explained by the frequent occurrence of hybridomas secreting antibodies displaying 'natural antibody' properties, which are strongly reactive with intracellular antigens, and apparently made accessible by the fixation procedure. Since artefacts impair the interpretation of results with ELISA on fixed cells, and complement-mediated cytotoxicity usually as a low yield, membrane immunofluorescence remains the best method for screening hybridoma antibodies.
A 35 year-old caucasian man suffered from paroxysmal nocturnal haemoglobinuria (PNH) or Marchiafava-Micheli's disease diagnosed in 1976 and complicated by several thrombotic episodes. He developed a benign intracranial hypertension. A digitalized intravenous angiography showed occlusion of both lateral sinuses. Partial improvement followed lombo-peritoneal shunting and steroid therapy. Cerebral venous thrombosis is a well-known complication of PNH but only a few cases have been radiologically and/or pathologically proven. It usually involves the superior longitudinal sinus and/or cortical veins resulting in hemorrhagic infarction of poor outcome. Benign intracranial hypertension due to a venous occlusion is rare. In 3 published cases, as in our own, the neurologic outcome was good. Steroid therapy seems useful. The risks of anticoagulant therapy are discussed.
The aim of this paper is to study the clinical and haemodynamic tolerance of intravenous diltiazem in a bolus dose of 10 mg followed by an infusion of 360 mg over 24 hours in 12 patients in the acute phase of myocardial infarction. We did not observe any significant modification in the heart rate or in the pulmonary artery diastolic pressure. The mean blood pressure decreased from 111.5 +/- 11.8 mmHg to 92.8 +/- 12.7 mmHg (p less than 0.001) after a 24 infusion. The cardiac index increased from 2.34 +/- 0.62 1 X min1 X m-2 to 3.05 +/- 0.95 1 X min-1 X m-2 (p less than 0.05) and the systemic vascular resistance decreased from 2 150 +/- 640 dyn. s.cm-5 to 1 403 +/- 308 dyn.s.cm-5 (p +/- 0.005). Three patients presented a rise in the pulmonary artery diastolic pressure of more than 30 mmHg and in one of these patients, the diltiazem had to be stopped. These three patients all had a high initial pulmonary capillary pressure (greater than 18 mmHg). The drug was well tolerated clinically. On electrocardiography, four patients presented conduction disorders, all of which regressed when the diltiazem was stopped (a 3rd degree atrioventricular block with narrow QRS complexes, a Luciani-Wenckebach type of 2nd degree atrioventricular block and two cases of 1st degree atrioventricular block. Overall, intravenous diltiazem was well tolerated in terms of clinical and haemodynamic parameters in these patients in the acute phase of a myocardial infarction, provided the left ventricular filling pressure was not excessively elevated.(ABSTRACT TRUNCATED AT 250 WORDS)