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E Petit

Publications and source records attributed to E Petit.

At least 37 records · Page 2Linked to original sources
PubMed2001

Children of chernobyl cleanup workers do not show elevated rates of mutations in minisatellite alleles.

The disaster at the Chernobyl Nuclear Power Plant in April 1986 was accompanied by the release of large amounts of radioisotopes, resulting in the contamination of extensive regions of the Ukraine, Byelorus and the Russian Federation. Cleanup workers (liquidators) and people living on land contaminated with radioactive materials were most exposed. To assess the genetic effects of exposure to ionizing radiation after the Chernobyl accident, we have measured the frequency of inherited mutant alleles at seven hypermutable minisatellite loci in 183 children born to Chernobyl cleanup workers (liquidators) and 163 children born to control families living in nonirradiated areas of the Ukraine. There was no significant difference in the frequency of inherited mutant alleles between the exposed and control groups. The exposed group was then divided into two subgroups according to the time at which the children were conceived with respect to the fathers' work at the power plant. Eighty-eight children were conceived either while their fathers were working at the facility or up to 2 months later (Subgroup 1). The other 95 children were conceived at least 4 months after their fathers had stopped working at the Chernobyl site (Subgroup 2). The frequencies of mutant alleles were higher for the majority of loci (i.e. 1.44 times higher for CEB1) in Subgroup 1 than in Subgroup 2. This result, if confirmed, would reconcile the apparently conflicting results obtained in the chronically exposed Byelorus population and the Hiroshima-Nagasaki A-bomb survivors.

Alleles↗
PubMed2000

A possible role of the Na(+)/K(+)-ATPase for O(2) production from H(2)O(2).

We are attempting to supply a new insight on interaction between Na(+)/K(+)-ATPase and H(2)O(2). We demonstrate that in vitro the Na(+)/K(+)-ATPase, a non heme-protein, is able to disproportionate H(2)O(2) catalatically into dioxygen and water, as well as C(40) catalase. By polarography, we quantify O(2) production and by Raman spectroscopy H(2)O(2) consumption. A comparative analysis of kinetics parameters relative to O(2) production shows that for Na(+)/K(+)-ATPase the affinity of the catalytic site able to transform H(2)O(2) into O(2) is twice weaker than that for C(40) catalase. It also shows that the molar activity for O(2) production is 300-fold weaker for ATPase than for catalase. Inhibitors, pH and GSH studies highlight the differences between the heme- and nonheme-proteins. Indeed, for C(40), NaN(3) is strongly inhibiting, but much less for ATPase. The pH range for the catalatic activity of ATPase is wide (6.5 to 8.5), while it is not for C(40) catalase (optimum at pH 8). The Na(+)/K(+)-ATPase catalatic activity is reduced in presence of glutathione, while it is not the case with C(40) catalase.

Animals↗
PubMed2000

[Meningeal metastases of ovarian cancer. Contribution of imaging].

BACKGROUND: Secondary meningeal localizations are uncommon and may disclose reactivation of a malignant disease. Most meningeal metastases occur in breast cancer, exceptionally in primary ovarian cancer. CASE REPORT: We report 2 cases of secondary meningeal localizations of ovarian cancer. The diagnosis was clinical, supported by cerebrospinal fluid analysis and computed tomography and magnetic resonance imaging. DISCUSSION: Establishing the diagnosis of carcinomatous meningitis may be difficult. Clinical signs and biological data are not always conclusive. If spinal tap is contraindicated or negative, imaging, particularly magnetic resonance imaging is highly contributive in establishing the diagnosis of secondary localization. A precise evaluation of the invaded tissues is quite helpful in guiding therapeutic management based on chemotherapy, tumor resection or radiotherapy.

Adult↗
PubMed2000

Glial responses, clusterin, and complement in permanent focal cerebral ischemia in the mouse.

There is considerable evidence that complement activation occurs within the CNS in inflammatory and degenerative disorders, but little is known about its involvement in the pathophysiology of cerebral ischemia. Our study sought to characterize the glial response and the expression of complement factors after permanent focal cerebral ischemia in the mouse, using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemistry. mRNA expression of glial fibrillary acidic protein (GFAP) increased at day 1 and peaked 3 days after middle cerebral artery (MCA) occlusion in the perifocal area. Immunohistochemical staining for GFAP indicated that astroglia were activated the day after MCA occlusion. Microglial activation, as assessed by lectin-binding experiments, increased by 1 day after MCA occlusion in the perifocal area and peaked at 3 days postocclusion. RT-PCR experiments demonstrated an increased expression of clusterin, C1qB, and C4 mRNA in the ischemic cortex, with a peak level at 3 days after MCA occlusion. Clusterin, C1qB, and C4 mRNA were located in the perifocal area, as assessed by in situ hybridization. Reactive astrocytes within the cortex medial to the ischemic lesion were found to be strongly immunoreactive for clusterin. In addition, we observed C1q-positive macrophage-like cells within the infarcted core at 3 days postocclusion. At 7 days after the onset of ischemia, increased C4 immunostaining was restricted to perifocal neurons. We conclude that local expression of complement components may contribute to the inflammation observed in this model, thereby representing an important process in secondary injury mechanisms after focal cerebral ischemia.

Animals↗
PubMed2000

Expression of receptors for complement anaphylatoxins C3a and C5a following permanent focal cerebral ischemia in the mouse.

In the present study, we have examined the expression of anaphylatoxin C3a and C5a receptors (C3aR and C5aR) at the mRNA and protein levels in ischemic brain tissues following permanent middle cerebral artery (MCA) occlusion in the mouse. C3aR and C5aR mRNAs were both detected by semiquantitative reverse transcription and polymerase chain reaction (RT-PCR) and the cellular distribution of each receptor was analyzed by immunohistochemistry. Significant increases in the expression of C3aR and C5aR mRNAs in the ischemic cortex were observed; the expression of both reached a peak at 2 days after MCA occlusion (4.3- and 3.4-fold increases, respectively, compared with nonoperated control cortical samples; P < 0.00625 with Bonferroni's correction, n = 3). C3aR and C5aR stainings were found constitutively on neurons and astrocytes. In ischemic tissues, we observed that C3aR and C5aR were expressed de novo on endothelial cells of blood vessels, at 6 h and 2 days after MCA occlusion, respectively. C3aR and C5aR immunostaining was increased in macrophage-like cells and reactive astrocytes 7 days postocclusion. C3a and C5a may play an important role in promoting inflammatory and/or repair processes in the ischemic brain by regulating glial cell activation and chemotaxis.

Animals↗
PubMed2000

Hypoxia-induced vascular endothelial growth factor expression precedes neovascularization after cerebral ischemia.

We investigated the hypothesis that hypoxia induces angiogenesis and thereby may counteract the detrimental neurological effects associated with stroke. Forty-eight to seventy-two hours after permanent middle cerebral artery occlusion we found a strong increase in the number of newly formed vessels at the border of the infarction. Using the hypoxia marker nitroimidazole EF5, we detected hypoxic cells in the ischemic border of the neocortex. Expression of vascular endothelial growth factor (VEGF), which is the main regulator of angiogenesis and is inducible by hypoxia, was strongly up-regulated in the ischemic border, at times between 6 and 24 hours after occlusion. In addition, both VEGF receptors (VEGFRs) were up-regulated at the border after 48 hours and later in the ischemic core. Finally, the two transcription factors, hypoxia-inducible factor-1 (HIF-1) and HIF-2, known to be involved in the regulation of VEGF and VEGFR gene expression, were increased in the ischemic border after 72 hours, suggesting a regulatory function for these factors. These results strongly suggest that the VEGF/VEGFR system, induced by hypoxia, leads to the growth of new vessels after cerebral ischemia. Exogenous support of this natural protective mechanism might lead to enhanced survival after stroke.

Animals↗
PubMed2000

A population genetic analysis of migration: the case of the noctule bat (Nyctalus noctula).

Although rarely assessed, the population genetics of hibernating colonies can help to understand some aspects of population structure, even when samples from nursery or mating colonies are not available, or in studies of migration when both types of samples are available and can be compared. Here we illustrate both points in a survey of mitochondrial DNA (mtDNA) control region sequences used to study the population genetics of hibernating colonies of a migrating species, the noctule bat (Nyctalus noctula). Lacking samples from Scandinavian nursery colonies, we use a North European hibernacula to suggest that Scandinavian populations are isolated from Central and East European colonies. Then, we compare genetic diversities of nursery and hibernating colonies. We find a significantly higher haplotype diversity in hibernacula, confirming that they consist of individuals from different nursery colonies. Finally, we show that pairwise comparisons of the haplotype frequencies of nursery and hibernating colonies contain some information on the migration direction of the noctule bat.

Animals↗
PubMed2000

Neurons and astrocytes express EPO mRNA: oxygen-sensing mechanisms that involve the redox-state of the brain.

Erythropoietin (Epo), the major hormone controlling the hypoxia-induced increase in the number of erythrocytes, has also a functional role in the brain. However, few data exist as to the cellular source of brain-derived Epo as well as to the molecular mechanisms that control Epo expression in the central nervous system. Using patch-clamp and RT-PCR methods, we provide direct evidence that, besides astrocytes, neurons are a source of Epo in the brain. Both the astrocytic and neuronal expression of Epo mRNA are induced not only by hypoxia, but also by desferrioxamine (DFX) and cobalt chloride (CoCl(2)), two agents known to mimic the hypoxic induction of Epo in hepatoma cells. This induction is blocked by cycloheximide suggesting that de novo protein synthesis is required. Furthermore, the addition of H(2)O(2) decreases the hypoxia-induced Epo mRNA levels. These data indicate that, following hypoxia, a common oxygen sensing and signaling pathway leads to increased Epo gene expression in both nervous and hepatoma cells; this pathway would be dependent on the redox-state of the brain. Furthermore, we show that the in vivo administration of CoCl(2) and DFX to mice induces an increased Epo mRNA level in the neocortex. As Epo protects the brain against ischemia, our in vivo experiments suggest that the use of molecules such as CoCl(2) or DFX, that provoke an increased Epo gene expression in the brain, could be useful in the development of potential therapeutic strategies for the treatment of hypoxic or ischemic brain injury.

Animals↗
PubMed1999

Male dispersal in the noctule bat (Nyctalus noctula): where are the limits?

Studying the dispersal behaviour of small, volant, and nocturnal animals such as microchiropterans with direct methods (banding--recapture, telemetry) is a very difficult task. The development of easily scorable and highly variable genetic markers nowadays allows us to study some aspects of dispersal indirectly, using population genetics. Here, we applied these indirect methods to characterize male dispersal behaviour in a European bat species. The eight microsatellite loci analysed were highly variable in all the nursing colonies assessed (h = 0.63-0.93). Contrary to what we found in the mtDNA, an AMOVA and F-statistics showed that the overall European population structure of the noctule bat was very weak, indicating a high male dispersal rate. Nevertheless, the population was not totally panmictic (theta = 0.006, p < 0.001), and neither isolation by distance, nor influence of migration could account for this result. Rather, an analysis of pairwise theta-values showed that the population structure might be explained partly by a geographical barrier to gene flow (the Alps), and partly by the fact that there is some limit to the distance the males can disperse.

Animals↗
PubMed1999

A potential role for erythropoietin in focal permanent cerebral ischemia in mice.

The present study describes, for the first time, a temporal and spatial cellular expression of erythropoietin (Epo) and Epo receptor (Epo-R) with the evolution of a cerebral infarct after focal permanent ischemia in mice. In addition to a basal expression of Epo in neurons and astrocytes, a postischemic Epo expression has been localized specifically to endothelial cells (1 day), microglia/macrophage-like cells (3 days), and reactive astrocytes (7 days after occlusion). Under these conditions, the Epo-R expression always precedes that of Epo for each cell type. These results support the hypothesis that there is a continuous formation of Epo, with its corresponding receptor, during the active evolution of a focal cerebral infarct and that the Epo/Epo-R system might be implicated in the processes of neuroprotection and restructuring (such as angiogenesis and gliosis) after ischemia. To support this hypothesis, a significant reduction in infarct volume (47%; P < 0.0002) was found in mice treated with recombinant Epo 24 hours before induction of cerebral ischemia. Based on the above, we propose that the Epo/Epo-R system is an endogenous mechanism that protects the brain against damages consequent to a reduction in blood flow, a mechanism that can be amplified by the intracerebroventricular application of exogenous recombinant Epo.

Animals↗
PubMed1999

Finding new human minisatellite sequences in the vicinity of long CA-rich sequences.

Microsatellites and minisatellites are two classes of tandem repeat sequences differing in their size, mutation processes, and chromosomal distribution. The boundary between the two classes is not defined. We have developed a convenient, hybridization-based human library screening procedure able to detect long CA-rich sequences. Analysis of cosmid clones derived from a chromosome 1 library show that cross-hybridizing sequences tested are imperfect CA-rich sequences, some of them showing a minisatellite organization. All but one of the 13 positive chromosome 1 clones studied are localized in chromosomal bands to which minisatellites have previously been assigned, such as the 1pter cluster. To test the applicability of the procedure to minisatellite detection on a larger scale, we then used a large-insert whole-genome PAC library. Altogether, 22 new minisatellites have been identified in positive PAC and cosmid clones and 20 of them are telomeric. Among the 42 positive PAC clones localized within the human genome by FISH and/or linkage analysis, 25 (60%) are assigned to a terminal band of the karyotype, 4 (9%) are juxtacentromeric, and 13 (31%) are interstitial. The localization of at least two of the interstitial PAC clones corresponds to previously characterized minisatellite-containing regions and/or ancestrally telomeric bands, in agreement with this minisatellite-like distribution. The data obtained are in close agreement with the parallel investigation of human genome sequence data and suggest that long human (CA)s are imperfect CA repeats belonging to the minisatellite class of sequences. This approach provides a new tool to efficiently target genomic clones originating from subtelomeric domains, from which minisatellite sequences can readily be obtained. [The sequence data described in this paper have been submitted to the EMBL data library under accession nos. AJ000377-AJ000383.]

Bacteriophage P1↗
PubMed1998

Selective neuronal vulnerability and specific glial reactions in hippocampal and neocortical organotypic cultures submitted to ischemia.

Neurons from cerebral neocortex and hippocampus exhibit a striking difference in vulnerability to transient global ischemia. In order to study the contribution of neuronal connections and neuron-glia interactions to this variation in neuronal vulnerability, we used hippocampal and neocortical cultures submitted to various periods of histotoxic ischemia. Organotypic cultures were exposed at 37 degrees C for 0, 7, 30 and 60 min to a glucose-free NaCN-containing medium. Histological analysis using thionin staining and MAP2 immunostaining showed differences in the temporal profile of neuronal damage in hippocampal and neocortical structures, i.e., in decreasing order, CA1 (7 min) > CA3 and neocortical layers II, III, V, VI (30 min) > DG and neocortical layer IV (60 min). In parallel to the neurodegeneration study, the time course and the regional pattern of microglial and astroglial changes were also examined using GS-B4 isolectin and GFAP as immunohistochemical markers, respectively. The GS-B4 isolectin staining revealed an early (at 7 min for the hippocampus) and a specific microglial activation located in areas undergoing neuronal damage. For both organotypic cultures, astrogliosis occurred later (after 30 min of stress) with no specific regional distribution. Both hippocampal and neocortical cultures submitted to histotoxic ischemia allowed the replication of many of the cellular events observed in response to global ischemia in vivo. These findings support the hypothesis that neuron-neuron connections as well as interactions between neurons and glial cells are essential to reproduce in vitro the selective neuronal vulnerability described in vivo.

Adaptation, Physiological↗
PubMed1997

Changes in ouabain affinity of Na+, K+-ATPase during focal cerebral ischaemia in the mouse.

We investigated the effect of focal cerebral ischaemia on the activity and the affinity of the ouabain sites of Na+,K+-ATPase in the mouse. The Na+,K+-ATPase activity was decreased by 38% as early as 30 min following ischaemia. In the sham group, the dose-response curves for ouabain disclosed three inhibitory states which contribute, respectively, 24.9 +/- 6.7%, 39.1 +/- 7.5% and 36.0% of the total activity (low affinity, LA; high affinity, HA and very high affinity, VHA, respectively). Their computed IC50 values are, respectively: 1.3 X 10(-3) M, 4.5 X 10(-6) M and 2.9 X 10(-9) M. Surprisingly, in ischaemic cortices, only two sites for ouabain were detected. The first site exhibits a LA (IC50 = 2.0 X 10[-4] M) but its relative contribution to the total activity (46.1 +/- 5.2%) is twice that noted for the LA site in non-ischaemic tissues. The second site presents an affinity intermediate between those of HA and VHA sites of the sham group (IC50 = 1.7 X 10[-7] M) and contributes 53.9% to the total activity. Loss in the specific activity of the second site explains that of the total activity. The most likely explanation in the presence of only two ouabain sites of Na+,K+-ATPase following ischaemia may be a change in ouabain affinity of alpha2 and/or alpha3 isoforms, as the presence of all three alpha isoforms has been observed by Western blotting. These results suggest that ischaemia induces intrinsic modifications in Na+,K+-ATPase which result from perturbations in membrane integrity and/or association of the alpha isoforms of this enzyme.

Animals↗
PubMed1997

Identification of glucuronan lyase from a mutant strain of Rhizobium meliloti.

The Rhizobium meliloti M5N1CS (NCIMB 40472) mutant strain wich induces nodule formation on alfalfa roots, produces a (1 --> 4)-beta-D-glucuronan partially acetylated. During fermentation under specific conditions, the molecular weight of the polymer decrease, the presence of polysaccharide degrading enzyme was suspected. A glucuronan lyase was identified, this new bacterial lyase produces d.p. 4 oligoglucuronans, substituents (acetates) present on the substrate reduced the enzyme activity.

Acetylation↗
PubMed1997

[Osteoarticular amyloidosis and dysglobulinemia: apropos of 2 cases].

We report two cases of bone and joint amyloidosis involvement related to plasma cell dyscrasia. The radiographic appearances mimic numerous benign or malignant diseases. MR imaging shows a diffuse low signal in T1 and an heterogeneous low or mild low signal in T2 weighted spin-echo sequence.

Aged↗