Biomedical subjects
Publications and source records attributed to J Marin.
From a large number of different kinds of protective gloves currently on the market, 19 were selected for virus permeability testing using a special model. Most of the gloves tested offered poor mechanical protection against penetration of adenovirus and poliovirus, while vaccinia virus was found to traverse the gloves less freely.
1. The aim of this study is to review the mechanisms implicated in nausea and vomiting and the treatment of these symptoms. 2. Metoclopramide, a benzamide, is the drug most frequently used to alleviate or abolish the majority of nausea and vomiting of different origin. Domperidone, which scarcely penetrates the central nervous system (CNS), is less used. 3. The treatment of vomiting induced by cytotoxic drugs is necessary to use a combination (two or more) of antiemetic drugs (metoclopramide, glucocorticoids, antihistamines, butyrophenones, anticholinergics, cannabinoids). Recently, antagonists of serotonergic (5-HT) receptors of the subtype 5-HT3 appear to possess interesting antiemetic properties and they have a promising future in this field. 4. Antagonists of dopamine receptors (benzamides, phenotiazines, butyrophenones and domperidone) induce adverse reactions in CNS (mainly extrapyramidal disorders), which are scarce with metoclopramide and practically absent with domperidone. These disorders must not suppress antiemetic therapy when it is needed.
5-Hydroxytryptamine (5-HT), noradrenaline (NA) and histamine induced concentration-dependent contractions in segments of human chorionic arteries and veins, whereas clonidine, an alpha 2-adrenoceptor agonist, had no effect. 5-HT and histamine induced strong contractions, while NA elicited weak contractions in some segments. The maximal response was similar for 5-HT and histamine. The order of potency (EC50 values) was: 5-HT greater than or equal to NA greater than or equal to histamine. These agonists induced tachyphylaxis, and single concentrations caused transient contractions. Contractions elicited by 5-HT were antagonized by ketanserin, a 5-HT2-receptor antagonist, which also antagonized the responses to NA and histamine, but at greater concentrations than those needed for 5-HT responses. Contractions elicited by histamine were reduced by diphenydramine. Low concentrations of 5-HT amplified contractions caused by NA and histamine. The results indicate that: (i) 5-HT is the most potent constrictor agent tested in these vessels; (ii) its effects are mediated by 5-HT2-receptors; and (iii) ketanserin at therapeutic plasma concentrations (10(-7) M) seems to block mainly 5-HT2-receptors, and alpha 1-adrenergic- and H1-receptors to a small extent only.
Field electrical stimulation (ES), K+ (50 mM) or ionophore X-537A (0.01 mM) induced tritium release from cat cerebral arteries preincubated with [3H]noradrenaline (NA). Adenosine and AMP (0.5 mM) did not modify tritium release caused by ionophore X-537A, but these agents and ATP (0.5 mM) significantly reduced that elicited by ES and K+; this reduction was antagonized by 1-methyl-3-isobutylxanthine (MIX; 0.05 mM). Inosine (0.5 mM) and the agonist of purinergic A2-receptors, 5'N-ethyl-carboxamide adenosine (NECA; 0.5 mM) had no effect, but the agonist of purinergic A2-receptors L-N6-phenylisopropyl adenosine (L-PIA; 0.1 mM) diminished tritium efflux caused by ES and K+. The adenosine inhibition of ES-induced radioactivity release was not affected by indomethacin (0.05 mM). MIX (0.05 mM) increased tritium release evoked by ES and K+. Agents that increase intracellular cyclic (c)AMP levels, such as dibutyryl cAMP (0.5 mM), the phosphodiesterase inhibitor Ro 20-1724 (0.1 mM), and the activators of adenylate cyclase, forskolin (0.005 mM) and NaF (2 mM) reduced tritium secretion elicited by ES and K+. However, the intracellular increase of cyclic GMP (cGMP) caused by 8-Br-cGMP did not affect this secretion. Dipyridamole (0.05 mM) and the adenosine deaminase inhibitor erythro-9-2-hydroxy-3 nonyl adenosine (EHNA; 0.1 mM) also produced inhibition of tritium secretion elicited by ES and K+. Dipyridamole reduced both the uptake of [3H]NA and [3H]adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
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Aneurysms of the popliteal vein are rare. They often seem to be favored by parietal dysplasia, but this is not a consistent finding. From a clinical viewpoint, the lesion is often asymptomatic. It may be detected fortuitously through the occurrence of a popliteal mass. In more severe cases, pulmonary emboli originating at the aneurysmal site will occur. As a rule, diagnosis is based on results from investigations such as phlebography and, more recently, echography which is bound to have a more important role in this field. Management must take the patient's history and background into account, depending upon which treatment will consist of either mere surveillance of asymptomatic patients, or resection possibly followed by restoration of venous circulation--placement of a caval block being restricted to very particular cases.
The effect of phorbol 12-myristate, 13-acetate (PMA), an activator of protein kinase C, on noradrenaline (NA) release from cat cerebral arteries preincubated with [3H]NA was investigated in order to examine the role of that enzyme in this secretion. PMA (3 microM) potentiated tritium release elicited by electrical stimulation (2 Hz, 0.3 ms) without modification of spontaneous secretion, whereas 4 alpha-phorbol 12,13 didecanoate (3 microM), an inactive compound, had no effect. Tritium release evoked by tyramine was not modified by PMA. The electrically evoked tritium secretion was reduced by clonidine (1 microM) or B-HT 920 (0.1 microM), alpha 2-adrenoceptor agonists, and unaffected by yohimbine (1 microM), an alpha 2-adrenoceptor antagonist. The presence of clonidine, B-HT 920 or yohimbine reduced the action of PMA. The facilitatory effect of PMA was not increased by the Ca2+ ionophore A23187 (5 microM). These results suggest that: (1) protein kinase C of perivascular adrenergic nerve endings participates in the exocytotic release of NA; (2) the effects of PMA could be partially due to an interference with prejunctional autoinhibitory alpha 2-adrenoceptors, and (3) the increase of intracellular Ca2+ produced by A23187 appears to be inadequate for potentiating the action of PMA.
A case of pulmonary infection caused by Trichosporon beigelii is reported in an asthmatic patient undergoing steroid treatment who developed fever and lung infiltrates. Arthroconidia and blastoconidia were isolated from repeated sputum, bronchial aspirate and telescopic catheter samples. The infection coincided with neutropenia resulting from pyrazolone treatment. The response to amphotericin B treatment was favourable.
1. Nifedipine (5 x 10(-9) M) reduced and the Ca agonists CGP 28392 (10(-6) M) and Bay K 8644 (10(-7) M) increased the contractions elicited by K+ in segments of rat aorta, whereas those caused by noradrenaline (NA) were unaffected. 2. CGP 28392 and Bay K 8644 evoked concentration-dependent contractions in segments moderately depolarized with 15 mM K+; these responses were reduced by nifedipine. 3. 45Ca uptake induced by 50 mM K+ or NA (10(-7) M) was reduced by nifedipine (10(-6) M). Bay K 8644 (10(-6) M) only increased the 45Ca uptake induced by K+, which was inhibited by nifedipine (10(-6) M). 4. These results indicate that in this vascular preparation: (a) Ca agonists only activate voltage-dependent Ca channels (VDCs), the potency of Bay K 8644 being higher than of CGP 28392, and (b) VDCs and receptor-operated Ca channels have different pharmacological properties.
During a 5-year period 203 previously untreated patients with acute myeloblastic leukemia entered an intensive induction chemotherapy regimen with daunorubicin, cytosine arabinoside, 6-thioguanine, vincristine and prednisone (DATOP). The complete remission rate was 64%. Patients in complete remission were randomly assigned to 3 courses of early consolidation with DATOP at lower dosage followed by maintenance chemotherapy, or to the same maintenance regimen in the absence of any consolidation courses. No significant differences were found between these options concerning disease-free survival (median 7.0 vs. 9.8 months; p greater than 0.10) or survival (median 15.8 vs. 19.4 months; p greater than 0.10). This study, in addition to the few previously reported randomized trials, suggests that early low-dose consolidation adds no benefit to maintenance chemotherapy in acute myeloblastic leukemia once complete remission has been achieved.
In 1932, Horton, Magath and Brown reported two cases of a "new form of arteritis affecting the temporal vessels ... which probably represents a new clinical syndrome". In reality, several publications, devoted to the same pathology already preceded this article. The most ancient is that of an ophthalmologist from Baghdad, Ali Ibn Isa (940 to 1010). In his memories, translated and published in english in 1936, the author states that "he undertook excision and cauterisation of arteries to treat patients who were suffering from heat and inflammation of their temporal muscles and which sometimes ended in loss of vision ...". In 1890, J. Hutchinson, an English surgeon, reported a case "... of inflammed and swollen temporal arteries ...". This article was only brought to light in 1946. In 1930, M. Schmidt, published a probable case of temporal arteritis, subsequently reported in 1947. In 1934 and 1936, Horton published new cases of temporal arteritis and defined the clinical characteristics of the disease and its histology. In 1938, Jennings made a particular contribution in reporting the first case of blindness. From this time on, cases of temporal arteritis became increasingly common in the literature. The first French case was described by J. Paviot et al. in 1934, but remained largely unrecognized until 1942. In 1936, J. Chavany was the first to describe the pillow sign, but more particularly in 1948, he prescribed the first treatment with steroids, with spectacular results. It was only in 1950 that R.M. Shick et al. published the effects of steroid therapy in temporal arteritis.(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in left ventricular (LV) meridional and circumferential end-systolic wall stress during isometric and isotonic exercises were determined noninvasively in 12 healthy subjects using echocardiography and cuff blood pressure measurements. Isometric exercise was performed at 20 and 40% of maximal voluntary contraction using a handgrip dynamometer, and isotonic exercise was done on a cycle ergometer at 150 kpm/min increments every 3 minutes to a maximum of 600 kpm/min. Although the increase in systolic blood pressure was similar in both forms of exercise, LV systolic stress in the circumferential and meridional planes increased markedly during isometric exercise but decreased slightly during higher intensity isotonic exercise. Isometric exercise also produced a significant decrease in fractional shortening, whereas isotonic exercise significantly increased fractional shortening. Wall stress and fractional shortening were linearly and inversely related, but isometric and isotonic exercise produced divergent and significantly different linear regressions. In normal subjects isometric exercise produces a significant increase in LV afterload that leads to a decrease in LV global function. In contrast, isotonic exercise causes an increase in LV global function, most likely from an unchanged or slight decrease in afterload associated with increased LV contractility from greater catecholamine release.
1. Smooth muscle contraction is related to the intracellular free Ca2+ concentration. 2. Potential dependent Ca2+ channels (PDCs) are generally more sensitive to Ca2+-antagonists (CAts) than receptor-operated Ca2+ channels (ROCs). However, there exists a wide variation in the sensitivity of ROCs and CAts, which largely depends on the vessel studied. 3. Cerebral and coronary arteries seem to be very sensitive to CAts. 4. New dihydropyridines possess selectivity for the cerebrovascular bed. 5. The vasospasm subsequent to subarachnoid hemorrhage appears to be sensitive to CAts. 6. CAts prevent or reduce the neurologic alterations elicited by cerebral ischemia, and some of them induce beneficial effects in the prophylaxis of migraine.
Pentobarbital (PB) induced concentration-dependent vasodilation in cylindrical segments of cat cerebral and femoral arteries precontracted with 75 mM K+ or 10(-5) M serotonin (5-HT). PB (10(-4) or 10(-3) M, 10 min preincubations) caused concentration-dependent inhibition of the contraction produced by both agents. The exposure of the vessels to a Ca2+-free medium annulled the response elicited by K+ in both kinds of arteries. In this medium, the contraction induced by 5-HT in cerebral arteries was abolished, whereas in femoral ones it was significantly reduced. This residual response was abolished by PB. The intracellular 45Ca2+ uptake (La3+ method) elicited by K+ in both kinds of arteries and by 5-HT in cerebral ones was reduced in a concentration-dependent manner by PB (10(-4)-10(-3) M). The spontaneous 45Ca2+ efflux from these arteries and that induced by La3+ (10 mM) were unaffected by PB (10(-3) M). These results indicate that the vasodepressor effects induced by PB are essentially due to an interference of the barbiturate with the Ca2+ entry into the vascular smooth muscle cell in both kinds of arteries and with the intracellular Ca2+ movements in femoral ones. It does not seem to exist a clear selectivity of PB for brain or peripheral arteries for antagonizing the responses caused by K+ or 5-HT.
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Morphine (up to 3 X 10(-4) M) elicited concentration-dependent contractions in cat middle cerebral arteries, higher concentrations induced vasodilation. These responses were annulled in the presence of 1-methyl-3-isobutylxanthine, but unaffected by diphenhydramine, cimetidine, phentolamine or naloxone. Ca2+ suppression blocked the morphine-evoked contractions and Ca2+ addition antagonized its vasodilatory effects. Nifedipine induced a marked relaxation in arteries previously contracted with morphine. Preincubation with nifedipine induced a decrease in the contraction elicited by morphine while it increased the vasodilatory phase. Morphine did not produce a significant effect in femoral arteries. In cerebral arteries previously submitted to an active tone, the opioid-induced vasodilation was unchanged by naloxone, cimetidine, diphenhydramine or ouabain, whereas Ca2+ addition antagonized this effect. These results indicate: that the opioid effects are mediated neither by opiate receptors nor by noradrenaline or histamine release; and that an antagonism exists between Ca2+ and the vasodilation caused by morphine.
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Morphine reduced the [3H]noradrenaline uptake in cat cerebral and femoral arteries and induced a dose-dependent tritium release from these vessels prelabelled with this amine, which was diminished in Ca2+-free medium. The opioid decreased the radioactivity release induced by electrical field stimulation as well as its potentiation by tetraethylammonium. These effects were unaffected by naloxone. These results indicate: the reduction by morphine of tritium release from both kinds of vessels is through a mechanism unrelated to opiate receptors, and the noradrenaline release elicited by morphine could be due in part to inhibition of its reuptake.