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Biomedical subjects

C Marie

Publications and source records attributed to C Marie.

At least 55 records · Page 3Linked to original sources
PubMed1996

Expression and localization of HrpA1, a protein of Xanthomonas campestris pv. vesicatoria essential for pathogenicity and induction ofthe hypersensitive reaction.

The hrp cluster of the pepper and tomato pathogen Xanthomonas campestris pv. vesicatoria is required for both pathogenicity on susceptible host plants and induction of the hypersensitive reaction on resistant plants. The hrpA locus is located at the left end of the 25-kb hrp region and encodes a single 64-kDa Hrp protein, HrpA1, which belongs to the PulD superfamily of proteins involved in type II and type III protein secretion. In this study, we developed a defined medium without any plant-derived molecules that induces expression of hrpA in vitro. The hrpA transcription start site was mapped in the coding region of the hrpB8 gene, which is the last gene of the hrpB operon. The inducible hrpA promoter shows no homology to known promoter elements or other hrp loci of X. campestris pv. vesicatoria. hrpA expression was shown to be independent of the hrp regulatory gene hrpX. The amino acid sequence of the HrpA1 protein is predicted to contain an N-terminal signal sequence and no further transmembrane domains and to be rich in beta-sheet stretches. Expression of HrpA1 in Escherichia coli cells causes induction of the psp operon like some of its counterparts, suggesting some commonality of function and that HrpA1 forms multimers. The protein product of hrpA1 was identified by using a specific polyclonal antibody. Cell fractionation studies demonstrated that the HrpA1 protein is localized in the outer membrane of X. campestris pv. vesicatoria. HrpA1 is the first component of the Hrp secretion system whose localization has been determined in the original organism.

Amino Acid Sequence↗
PubMed1995

Hemodynamic effects of acute and chronic treatment with aladotril, a mixed inhibitor of neutral endopeptidase and angiotensin I-converting enzyme, in conscious rats with myocardial infarction.

The aim of the present study was to determine, in rats with myocardial infarction, the systemic and cardiac hemodynamic effects of aladotrilat and of its prodrug, aladotril, both of which display inhibitory activity toward both neutral endopeptidase (NEP, EC. 3.4.24.11) and angiotensin I-converting enzyme (ACE). The effects of acute intravenous injection of aladotrilat (30 mg/kg bolus injection plus 30 mg/kg/hr infusion) were measured for 1 hr in conscious infarcted rats and compared with the effects of SQ 28,603, a selective NEP inhibitor (30 mg/kg bolus injection plus 30 mg/kg/hr infusion), and captopril, a selective ACE inhibitor (10 mg/kg bolus injection plus 10 mg/kg/hr infusion). Unlike SQ 28,603, aladotrilat and captopril produced a slight fall in mean arterial blood pressure. The three treatments had no significant effect on heart rate and rate of increase of left ventricular pressure (LV + dP/dt) but caused significant decreases in left ventricular end-diastolic pressure (LVEDP). The effect of aladotrilat on decreasing LVEDP was faster than those of captopril or SQ 28,603. In chronic experiments, groups of rats received orally, twice daily, captopril (10 mg/kg), aladotril (100 mg/kg) or vehicle. Treatments were started 18 to 20 hr after coronary artery ligation and continued for 4 weeks. Hemodynamic parameters and cardiac hypertrophy were measured at the end of therapy. Unlike aladotril, captopril treatment resulted in significant decreases in mean arterial blood pressure and left ventricular systolic pressure (approximately 15 mm Hg) and produced renal vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1994

Neurologic and cytologic outcome following repeated ischemia. Effect of pentobarbital.

We examined clinical recovery from repeated brain ischemic insults that have been reported to affect cytologic outcome. Brain ischemia was induced in the rat by four-vessel occlusion. A 30-min ischemia was given as a single insult or induced in animals made ischemic 24 h earlier by a 10-min insult but exempt both of brain hypoperfusion and neurologic deficit in spite of a partial necrosis of the CA1 sector of hippocampus. Repeated ischemia was associated with a significantly poorer clinical outcome as indicated by an increase in percentage of rats that exhibited postischemic seizure activity combined with the percentage of unconvulsive rats exhibiting neurologic deficits after 72 h of reperfusion (81% vs. 50% after a single 30-min ischemia). Examination of hippocampal damage showed that neurons surviving the first ischemia did not acquire resistance to the second ischemia. Pentobarbital given from start of overt seizures (30 to 60 mg/kg, IP, thrice daily) was able to stop convulsions and to antagonize processes involved in ischemia-induced neuronal death of CA1 hippocampus.

Animals↗
PubMed1994

Ischemia-induced brain iron delocalization: effect of iron chelators.

Tissue damage in cerebral ischemia may be produced by acidosis-induced delocalization of intracellular iron which acts as a catalyst in oxidative reactions. Acidosis was induced either by homogenization and incubation of rat cortical homogenates in acidified buffers or by submitting hyperglycemic rats to complete ischemia, a procedure that leads to intracellular lactic acidosis. The level of low molecular weight species (LMWS) iron was measured after filtration of tissue homogenates through a 10,000 Mr ultrafiltration membrane. When cortical tissue was homogenized in buffer pH 7, the level of LMWS iron was equal to 0.21 microgram/g. It was significantly enhanced by acidification of the homogenization medium, reaching 0.34 microgram/g at pH 6 and 0.75 microgram/g at pH 5. When the tissue was homogenized in water, the LMWS iron level reached 0.17 microgram/g in normoglycemic rats and 0.38 microgram/g (p < .05) in hyperglycemic rats. Both aerobic incubation of homogenates for 1 h at 37 degrees C and inclusion of EDTA in the homogenization medium led to further increases in the iron level. In order to demonstrate the deleterious role of iron in brain ischemia, the effect of treatment with bipyridyl, an iron-chelating agent, was assessed by measuring regional brain edema by the specific gravity method, 24 h following induction of thrombotic brain infarction. The treatment significantly attenuated the development of brain edema, reducing the water content of the infarcted area by about 2.5%. Taken together, these results support the hypothesis that a significant component of brain ischemic injury involves an iron-dependent mechanism.

2,2'-Dipyridyl↗
PubMed1994

Changes in extracellular and rat brain tissue concentrations of D-beta-hydroxybutyrate after 1,3-butanediol treatment.

1,3-Butanediol (BD) treatment was previously shown to produce a dose-related increase of the plasma levels of D-beta-hydroxybutyrate (BHB) and to protect brain tissue against hypoxia and ischemia. The purpose of this study was to test whether BD-induced hyperketonemia was associated with changes in brain extracellular and tissue concentrations of BHB. Changes in extracellular levels of BHB were continuously monitored in anesthetized rats before and after intraperitoneal injection of BD (25 mmol/kg), using intracerebral microdialysis coupled to online analysis of BHB in the dialysate. Cortical tissue concentrations of BHB were determined in control and BD-treated rats (25 and 50 mmol/kg, i.p.) after freezing of the brain in situ. Butanediol produced a rapid increase in dialysate levels of BHB, with a linear relationship between dialysate and plasma BHB concentrations (r = 0.81, p < 0.001). In contrast, and although brain tissue levels of BHB were markedly increased after BD treatment, they were not related to the plasma concentration of BHB. Our results suggest that BHB produced from BD did not accumulate in brain and that BD protects against hypoxia or ischemia by increasing brain BHB availability.

3-Hydroxybutyric Acid↗
PubMed1994

Hrp Mutants of Pseudomonas solanacearum as Potential Biocontrol Agents of Tomato Bacterial Wilt.

There have been many attempts to control bacterial wilt with antagonistic bacteria or spontaneous nonpathogenic mutants of Pseudomonas solanacearum that lack the ability to colonize the host, but they have met with limited success. Since a large gene cluster (hrp) is involved in the pathogenicity of P. solanacearum, we developed a biological control strategy using genetically engineered Hrp mutants of P. solanacearum. Three pathogenic strains collected in Guadeloupe (French West Indies) were rendered nonpathogenic by insertion of an omega-Km interposon within the hrp gene cluster of each strain. The resulting Hrp mutants were tested for their ability to control bacterial wilt in challenge inoculation experiments conducted either under growth chamber conditions or under greenhouse conditions in Guadeloupe. Compared with the colonization by a pathogenic strain which spread throughout the tomato plant, colonization by the mutants was restricted to the roots and the lower part of the stems. The mutants did not reach the fruit. Moreover, the presence of the mutants did not affect fruit production. When the plants were challenge inoculated with a pathogenic strain, the presence of Hrp mutants within the plants was correlated with a reduction in disease severity, although pathogenic bacteria colonized the stem tissue at a higher density than the nonpathogenic bacteria. Challenge inoculation experiments conducted under growth chamber conditions led, in some cases, to exclusion of the pathogenic strain from the aerial part of the plant, resulting in high protection rates. Furthermore, there was evidence that one of the pathogenic strains used for the challenge inoculations produced a bacteriocin that inhibited the in vitro growth of the nonpathogenic mutants.

Journal Article↗
PubMed1994

Effects of alatriopril, a mixed inhibitor of atriopeptidase and angiotensin I-converting enzyme, on cardiac hypertrophy and hormonal responses in rats with myocardial infarction. Comparison with captopril.

The aim of the study was to compare, in a rat model of congestive heart failure, the effect of captopril, a selective angiotensin-converting enzyme (ACE; EC 3.4.15.1) inhibitor, to that of alatriopril, a mixed inhibitor of ACE and atriopeptidase (EC 3.4.24.11), an enzyme implicated in the degradation of atrial natriuretic factor (ANF). Myocardial infarction was induced by ligation of the left coronary artery. Groups of rats received orally twice daily captopril (10 mg/kg), alatriopril (100 mg/kg) or vehicle. Treatments were started 18 to 20 h after ligation and continued for 4 weeks. Hypertrophic and hormonal changes reflecting congestive heart failure were assessed in rats with large infarcts by measuring the relative weight of cardiac tissues as well as by assaying ANF in heart and plasma and by measuring renin activity in plasma. Both treatments significantly reduced cardiac hypertrophy, but alatriopril showed a greater efficacy than captopril--the increase in relative heart weight reaching 38% with captopril and only 22% with alatriopril (P < .05). The hypertrophy of right ventricle was reduced by 47% with alatriopril and by 35% with captopril (N.S.), whereas the corresponding reductions for atria were 47% vs. 21% (P < .05). Both treatments prevented the ligation-induced increase of ANF level in the right ventricle. In contrast, plasma ANF level was significantly reduced after captopril but not after alatriopril treatment, a difference that probably reflects the protection of endogenous ANF in circulation resulting from atriopeptidase inhibition. Plasma renin was increased by 36-fold after captopril but only by 1.6-fold after alatriopril, a difference that presumably reflects the inhibition of renal renin secretion by endogenous ANF after alatriopril. These data suggest that enhancement of ANF levels in circulation via atriopeptidase inhibition magnifies the capacity of ACE inhibitors to prevent cardiac hypertrophy, and they show the potential therapeutic value of mixed ACE-atriopeptidase inhibitors in congestive heart failure.

Alanine↗
PubMed1993

Adhesion of CHO cells to fibronectin is mediated by functionally and structurally distinct adhesion plaques.

We have investigated the dynamics between free fibronectin receptors and clusters of them organized into adhesion plaques on CHO cells using the ability of these free integrins to be endocytosed and recycled to the plasma membrane. Indirect inhibition of the endocytic cycle by monensin resulted in the subsequent internalization of free receptors, which we followed by indirect immunostaining and confocal microscopy. Consequently, all the adhesive structures that were in equilibrium with free integrins became progressively disorganized. The cellular morphological changes were analyzed and correlated with the distribution of cell-substratum contacts viewed by confocal images obtained after immunostaining with antibodies raised against the fibronectin receptor, talin, vinculin and actin. After cell adhesion to fibronectin, blockage of the endocytic cycle induced disruption of the adhesion plaques that were mainly localized at the cell periphery, and disappearance of the stress fibers. However, the cells remained firmly attached to the substratum through focal contacts localized in the central part of the cell. These central focal contacts, but not the peripheral adhesion plaques, could form when the vesicular traffic was blocked prior to adhesion and they allowed the cells to attach and flatten onto the substratum. Whereas both adhesive structures contained the same receptors linked to talin and vinculin, the central adhesive structures were attached to a short stretch of actin but never permitted the organization of stress fibers.

Animals↗
PubMed1992

Alpha-methyl-para-tyrosine pretreatment protects from striatal neuronal death induced by four-vessel occlusion in the rat.

Rats were treated with alpha-methyl-para-tyrosine (AMT, 250 mg/kg, i.p), an hydroxylase inhibitor, in order to decrease brain levels of catecholamines. Six hours later, when cerebral dopamine (DA) and norepinephrine were reduced by about 80%, a transient forebrain ischemia of 30 min duration was induced by four-vessel occlusion technique. Evaluation of brain damage 72 hours after ischemia showed that AMT treatment significantly decreased neuronal necrosis in the striatum but had no cytoprotective effect in the CA1 sector of the hippocampus and in the neocortex. AMT treatment reduced mortality within the ischemic period but did not affect either the mortality within the recirculation period or the postischemic neurologic deficit. These results suggest that the striatal cytoprotective effect of AMT is linked to cerebral DA depletion and that excessive release of DA during ischemia or dopaminergic hyperactivity during recirculation play a detrimental role in the development of ischemic cell damage in the striatum.

Animals↗
PubMed1992

Rhizobium leguminosarum has two glucosamine synthases, GlmS and NodM, required for nodulation and development of nitrogen-fixing nodules.

The Rhizobium leguminosarum nodM gene product shows strong homology to the Escherichia coli glmS gene product that catalyses the formation of glucosamine 6-P from fructose 6-P and glutamine. DNA hybridization with nodM indicated that, in addition to nodM on the symbiotic plasmid, another homologous gene was present elsewhere in the R. leguminosarum genome. A glucosamine-requiring mutant was isolated and its auxotrophy could be corrected by two different genetic loci. It could grow without glucosamine when the nodM gene on the symbiotic plasmid was induced or if the cloned nodM gene was expressed from a vector promoter. Alternatively, it could be complemented by a second fragment of R. leguminosarum DNA that carries a region homologous to E. coli glmS. Biochemical assays of glucosamine 6-P formation confirmed that the two R. leguminosarum genes nodM and glmS have interchangeable functions. No nodulation of peas or vetch was observed with a double nodM glmS mutant, and this block occurred at a very early stage since no root-hair deformation or infection threads were seen. Nodulation and root-hair deformation did occur with either the nodM or the glmS mutant, showing that the gene products of either of these genes can be involved in the formation of the lipo-oligosaccharide nodulation signal. However, the glmS mutant formed nodules that had greatly reduced nitrogen fixation. Constitutive expression of nodM restored nitrogen fixation to the glmS mutant. Therefore the reduced nitrogen fixation probably occurs because glmS is absent and nodM is not normally expressed in nodules and, in the absence of glucosamine precursors, normal bacteroid maturation is blocked.

Cloning, Molecular↗
PubMed1992

Effects of tilting in the anaesthetized and mechanically ventilated rat: a model of orthostatic hypotension.

The main of the present study was to determine the experimental conditions for an animal model of orthostatic hypotension based on tilting in rats. Blood pressure, heart rate and plasma catecholamine levels were measured before and after tilting in conscious and anaesthetized rats either breathing spontaneously or mechanically ventilated. In conscious rats, tilting did not alter arterial blood pressure, but increased heart rate and plasma catecholamine levels. In anaesthetized rats, tilting induced a drop in arterial blood pressure without any modification in plasma catecholamine concentrations. Mechanical ventilation significantly increased the postural hypotension and the percentage of rats showing a decrease in heart rate. Tyramine infusion increased plasma noradrenaline levels, and reduced or counteracted the postural hypotension and bradycardia. The results show that anaesthetized mechanically ventilated rats might constitute an appropriate model of orthostatic hypotension.

Anesthesia↗
PubMed1991

Semi-intact CHO and endothelial cells: a tool to probe the control of integrin activity?

An in vitro assay has been developed using semi-intact cells, made with the bacterial toxin streptolysin O, in order to measure integrin activity in relation to the cytosol environment. In this assay, the cytosolic content can easily be modified while the receptor binding activity is measured by monitoring the interaction of specific radiolabeled substrates with the cell surface. Using two different cell types, i.e., wild-type Chinese hamster ovary cells and human endothelial cells in culture, it has been shown that the binding activities of the fibronectin and fibrinogen receptors become cytosol-dependent on perforated cells. Furthermore, this control depends on micromolar concentrations of intracellular calcium, suggesting that calcium or calcium binding protein(s) may play a key role in controlling integrin activity.

Animals↗
PubMed1991

Blood glucose level and morphological brain damage following cerebral ischemia.

It is well known that various systemic parameters can modulate the deleterious effects of cerebral ischemia. We have reviewed the experimental data concerning the relationship between blood glucose concentration and brain ischemic morphological damage. Whereas the influence of hyperglycemia has been extensively investigated, the effect of a decrease in blood glucose concentration is not well documented. In models of transient ischemia, the cytologic damage is increased if the insult is induced in glucose-infused fed or fasted animals and decreased if it is induced in fasted animals. A more recent finding is the modulation of the extent of the cellular ischemic injury by manipulation of postischemic blood glucose concentration. In models of focal ischemia, conflicting results (a deleterious, a protective, or no effect) have been reported on the influence of elevated blood glucose concentration. Differences between the models of focal ischemia with respect to the possibility of collateral blood flow to enter the infarcted region may be an important factor for the explanation of the discrepant results. Because glycemia differences may explain some of the divergences on the susceptibility of the brain to ischemia, it becomes obvious (a) that the monitoring of glycemia before, during, and following the ischemic period is a prerequisite for the validation and the comparison of histological results, and (b) that every situation known to interfere with glycemia, such as food intake, anesthesia, or stress, have to be strictly controlled.

Animals↗
PubMed1991

Inhibitory effect of 17 beta-estradiol on thymocyte proliferation and metabolic activity in young rats.

Proliferation of 21-day-old rat thymus lymphocytes has been assessed after 7 daily injections of 17 beta-estradiol (E2). Two methods were used: 1) image cytometry of cell nuclei using the SAMBA 200 image processor, and 2) cell culture making it possible to design cell proliferation assay, mitochondrial activity evaluation and measurement of IL2 activity. Using image cytometry, we found a significant decrease in the proliferation index at the dose of 100 micrograms of E2 per day. When 200 micrograms and 400 micrograms per day were given, this decrease reached 70% of inhibition. 3H-thymidine incorporation was significantly reduced in cell culture even after 5 micrograms of E2 per day. On the other hand, with either 5 micrograms or 50 micrograms of E2, a significant increase of IL2 was found in the supernatant.

Animals↗
PubMed1990

Fasting prior to transient cerebral ischemia reduces delayed neuronal necrosis.

A transient brain ischemia of 30-min duration was induced by the four-vessel occlusion technique in normally fed and in 48-hr-fasted rats. Evaluation of brain damage 72 hr after ischemia showed that fasting reduced neuronal necrosis in the striatum, the neocortex, and the lateral part of the CA1 sector of hippocampus. Signs of status spongiosis in the pars reticulata of the substantia nigra were seen in 75% of fed rats and in only 19% of fasted rats. The protective effect was associated with reduction in mortality and in postischemic seizure incidence. The metabolic changes induced by fasting were evaluated before and during ischemia. After 30 min of four-vessel occlusion, fasted rats showed a marked decrease in brain lactate level (14.7 vs 22.5 mumol/g in fed rats; P less than 0.001). The decrease in brain lactate concentration might explain the beneficial effect of fasting by minimizing the neuropathological consequences of lactic acidosis. Several factors may account for lower lactate production during ischemia in fasted rats: hypoglycemia, reduction in preischemic stores of glucose and glycogen, or increased utilization of ketone bodies aiming at reducing the glycolytic rate.

3-Hydroxybutyric Acid↗