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E André

Publications and source records attributed to E André.

At least 19 recordsLinked to original sources
PubMed2006

Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung.

High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach. Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 microg x m(-3)) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation. Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6-1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells. In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.

Air Pollutants↗
PubMed2005

[Netherton syndrome: a type of infantile erythroderma with failure to thrive, immune deficiency, rickets. Report of 3 cases].

We report the cases of 2 boys and 1 girl suffering from Netherton syndrome. Both boys presented with a non-bullous congenital erythroderma and were diagnosed early as Netherton syndrome with hair biopsies. Both had severe failure to thrive, signs of atopy, several episodes of bacterial infection, and rickets (with a high blood level of vitamin D in the first boy, and vitamin D deficiency in the second). In the third case, the pilar abnormality appeared at the age of 3 years. The girl had ichtyosis linearis circumflexa, failure to thrive and severe constipation. Netherton syndrome is a rare disorder characterized by severe ichtyosis, signs of atopy, immune deficiency and failure to thrive. The disease is severe and comprises many complications in early infancy. It is due to a genetic disorder of recessive autosomal transmission, and the gene, SPINK5, is located in the chromosome 5. Prenatal diagnosis is possible. Two of our patients had rickets, which has never been described in such patients population.

Carrier Proteins↗
PubMed2002

Haemodynamic effects of an angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist during hypovolaemia in the anaesthetized pig.

BACKGROUND: Renin-angiotensin system antagonists, either angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor (AT(1)) antagonists, may interfere with regulation of arterial pressure during anaesthesia. This study aimed to compare the haemodynamic profile of anaesthetized pigs, which were subjected to haemorrhage in the presence of the ACE inhibitor enalaprilat or the AT(1) antagonist valsartan. METHODS: Thirty-six pigs were assigned randomly to placebo, enalaprilat or valsartan groups. After a 30-min period of stabilization following anaesthesia and injection of the study drug, the animals were bled in two equal steps of 20% of their estimated blood volume (20% BV and 40% BV). RESULTS: After bleeding of 20% BV, the mean arterial pressure (MAP) decreased significantly but similarly in each group (20-25%) but the placebo and the enalaprilat groups had a significant decrease in cardiac index (CI, 22% and 16%, respectively) without significant change in systemic vascular resistance (SVR). Conversely, in the valsartan group, SVR decreased significantly (23%, P<0.02 vs other groups) without significant change in CI (-4%). After bleeding of 40% BV, the CI decreased significantly compared with 20% BV in the three groups (19% in the placebo and enalaprilat groups, 14% in the valsartan group) but the MAP decreased significantly in the enalaprilat group only (23%). The SVR increased significantly in the placebo group (P<0.01 vs each of the other groups), but there were no differences in the change in SVR between the other groups. CONCLUSION: Blockade of the renin-angiotensin system by either enalaprilat or valsartan leads to a similar decrease in arterial pressure during anaesthesia and haemorrhage but the haemodynamic profiles are quite different.

Angiotensin Receptor Antagonists↗
PubMed2001

[An experience with transthoracic echocardiography after heart surgery].

OBJECTIVE: In order to determine if routine use of transthoracic echocardiography (TTE) shortly after heart surgery could have a role in postoperative management, we carried out TTE in postoperative patients operated on for CABG or valvular repair. PATIENTS AND METHODS: For a 3 months period, we prospectively enrolled 51 patients for TTE. We performed a TTE using a Hewlett Packard Sonos 1500 and a 2.5 MHz probe. Feasibility, left ventricular kinesis, valve function, intracardiac thrombi, and pericardial effusion were noted for each patient. Patients have been divided into 2 groups: patients with or, without haemodynamic disturbance (HD, mean arterial blood pressure < or = 80 mmHg). RESULTS: Nine TTE were impossible for bad acoustic images. Feasibility was about 82% (42 TTE/51 patients). Two ETT views were easily obtained: the apical 4-chambers (75%) and the subcostal (30%) views. TTE examination induced treatment change in 12 patients for hypovolaemia (ten patients), left ventricular dysfunction (one patient), and systolic anterior motion of mitral valve (one patient). In patients without HD (41 patients) only hypovolaemia was found (three patients) and TTE returned to normal with fluid challenge. In patients with HD (ten patients), one patient returned to the operating room for valvular replacement, one patient was treated with dobutamine for left ventricular dysfunction, seven patients with hypovolaemia recovered with fluid challenge. CONCLUSION: TTE can guide postoperative management of patients operated on for heart surgery especially in patients with haemodynamic disturbance. Because of its safety and easiness, TTE may be the first-line examination in these patients before any invasive evaluation.

Adult↗
PubMed2000

Contribution of nitric oxide, prostanoids and Ca(2+)-activated K+ channels to the relaxant response of bradykinin in the guinea pig bronchus in vitro.

In the guinea pig bronchus with epithelium, pre-contracted with histamine, bradykinin (BK), lysyl-BK, prostaglandin E2 (PGE2), cromakalim and S-nitroso-N-acetylpenicillamine each caused graded relaxation with mean EC50s of 34 nM, 11 nM, 0.1 nM, 0.3 microM and 3.4 microM, respectively. The addition of NO synthase inhibitors N(W)-nitro-L-arginine (L-NOARG), N(G)-monomethyl-L-arginine or 7-nitroindazole reduced BK-induced relaxation by 41+/-6%, 59+/-4% and 51+/-2%, respectively. The inhibition of BK response caused by L-NOARG was completely reversed by L-, but not by D-arginine. Methylene blue and 6-(phenylamino)-5,8-quinolinedione (LY 83583) inhibited the BK response by 88+/-5% and 64+/-4%, while 1H-[1,2,4]oxadiazolo[4,3-a]quinolaxin- -one (ODQ) had no effect. However, ODQ almost abolished SNAP-induced relaxation. Indomethacin and the cyclo-oxygenase 2 (COX-2) inhibitor 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanon e (DFU) caused graded inhibtion of BK responses with mean IC50s of 60 nM and 0.6 nM, respectively. Addition of tetraethylammonium (TEA), charybdotoxin (ChTx), or iberotoxin (IbTx) inhibited BK-induced relaxation by 76+/-4%, 30+/-4% and 99+/-1%, respectively, but the relaxations of PGE2 and cromakalim were unaffected. In contrast, 4-aminopyridine, apamin or glibenclamide did not affect BK-induced relaxation. These results indicate that BK-induced epithelium-dependent relaxation in the guinea pig bronchus is partially mediated by release of NO or by NO-related substances, involving an activation of both cyclo-oxygenase 1 (COX-1) and COX-2 enzymes, through a cyclic guanosine monophosphate (cGMP)-independent mechanism. Furthermore, BK-induced relaxation involves an activation of high-conductance Ca(2+)-activated K+ channels highly sensitive to IbTx, and to a lesser extent to ChTx and TEA.

Animals↗
PubMed1999

Mechanisms underlying the relaxation caused by the sesquiterpene polygodial in vessels from rabbit and guinea-pig.

The sesquiterpene polygodial produces graded relaxation in rings of rabbit pulmonary artery or thoracic aorta and guinea-pig pulmonary artery with endothelium. In rings with rubbed endothelium its vasorelaxant action was largely reduced. The N(omega)-nitro-L-arginine (L-NOARG), N(G)-nitro-L-arginine methyl ester (L-NAME), 6-anilino-5,8-quinolinedione (LY 83583) and 1H-[1,2, 4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), inhibited the endothelium-dependent vasorelaxant action of polygodial. In contrast, N(omega)-nitro-D-arginine (D-NOARG), indomethacin, N(2)-[(4R)-4-hydroxy-1-(1methyl-1H-indol-3yl)carbonyl-L-prol yl]-N-met hyl-N-phenylmethyl-3-(2-naphthyl)-L-alaninamide (FK 888), (S)-N-methyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3, 4-dichlorophenyl)butyl]benzamide (SR 48968), (8R,9S, 11S)-(-)-9-hydroxy-9-n-hexyloxy-carbonyl-8-methyl-2,3,9, 20-tetrahydro-8,11-epoxy-1H,8H,11H-2,7b,11a-triaqzadibenzo[a, g]cycloocta[c,d,e]-trinden-1-one (KT 5720), calcitocin gene-related peptide receptor antagonist (CGRP-(8-37), apamin, charybdotoxin and 4-aminopyridine had no effect on polygodial action. However, glibenclamide inhibited partially, but significantly, its relaxant responses. These results demonstrate that the vasorelaxation of polygodial is partly dependent on the release of nitric oxide (NO )or an NO-derived substance from the vascular endothelium through an activation of a guanylyl cyclase-dependent mechanism. Finally, results demonstrate that the polygodial vasorelaxant action is not related with the opening of potassium (K(+)) channels, release of prostacyclin, substance P, or with the activation of adenylyl cyclase-dependent mechanisms.

Acetylcholine↗
PubMed1999

The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event.

During apoptosis induced by various stimuli, cytochrome c is released from mitochondria into the cytosol where it participates in caspase activation. This process has been proposed to be an irreversible consequence of mitochondrial permeability transition pore opening, which leads to mitochondrial swelling and rupture of the outer mitochondrial membrane. Here we present data demonstrating that NGF-deprived sympathetic neurons protected from apoptosis by caspase inhibitors possess mitochondria which, though depleted of cytochrome c and reduced in size, remained structurally intact as viewed by electron microscopy. After re-exposure of neurons to NGF, mitochondria recovered their normal size and their cytochrome c content, by a process requiring de novo protein synthesis. Altogether, these data suggest that depletion of cytochrome c from mitochondria is a controlled process compatible with function recovery. The ability of sympathetic neurons to recover fully from trophic factor deprivation provided irreversible caspase inhibitors have been present during the insult period, has therapeutical implications for a number of acute neuropathologies.

Amino Acid Chloromethyl Ketones↗
PubMed1999

[Heparin-induced thrombopenia].

Heparin-induced thrombocytopenia remains a topical subject for at least two reasons. The first reason is the increasing prescription of low molecular weight heparins (LMWH) rather than unfractionated heparins, with limited laboratory surveillance, raising the question concerning the need for twice-weekly platelet counts, according to the recommendations of the Vidal drug directory. The second reason is the recent release onto the market of two products, danaparoid (Orgaran) and lepirudin (Refludin) for this precise indication of heparin-induced thrombocytopenia. These products greatly facilitate the management of this complication. Many basic research teams are trying to optimize the detection of heparin-dependent antibodies and to more clearly elucidate the mechanism of this particular thrombocytopenia, which carries a risk of very severe thrombotic complications when the diagnosis is delayed.

Antibodies↗
PubMed1998

A novel isoform of the orphan nuclear receptor RORbeta is specifically expressed in pineal gland and retina.

RORbeta is a member of the nuclear hormone receptor superfamily whose ligand is unknown. Expression of RORbeta is confined to the central nervous system and its pattern suggests that this orphan nuclear receptor is implicated in the processing of sensory information and in circadian timing. In rats, RORbeta mRNA levels oscillate robustly in pineal gland and retina, displaying a 24h rhythm. Here we report the cloning of the cDNA of a novel isoform of RORbeta from rat pineal tissue. Expression of this isoform, called RORbeta2, is confined to pineal gland and retina and strongly increases at night. RORbeta2 shares common DNA- and putative ligand-binding domains with the canonical RORbeta (referred to as RORbeta1), but is characterized by a different amino-terminal domain. This structural difference renders RORbeta2 much more selectively binding to DNA than RORbeta1. Moreover, in contrast to RORbeta1, the novel isoform efficiently activates transcription also in non-neuronal cell lines. Thus, the two RORbeta isoforms are likely to regulate different sets of genes in different physiological contexts. 1998 Elsevier Science B.V.

Animals↗
PubMed1998

Disruption of retinoid-related orphan receptor beta changes circadian behavior, causes retinal degeneration and leads to vacillans phenotype in mice.

The orphan nuclear receptor RORbeta is expressed in areas of the central nervous system which are involved in the processing of sensory information, including spinal cord, thalamus and sensory cerebellar cortices. Additionally, RORbeta localizes to the three principal anatomical components of the mammalian timing system, the suprachiasmatic nuclei, the retina and the pineal gland. RORbeta mRNA levels oscillate in retina and pineal gland with a circadian rhythm that persists in constant darkness. RORbeta-/- mice display a duck-like gait, transient male incapability to sexually reproduce, and a severely disorganized retina that suffers from postnatal degeneration. Consequently, adult RORbeta-/- mice are blind, yet their circadian activity rhythm is still entrained by light-dark cycles. Interestingly, under conditions of constant darkness, RORbeta-/- mice display an extended period of free-running rhythmicity. The overall behavioral phenotype of RORbeta-/- mice, together with the chromosomal localization of the RORbeta gene, suggests a close relationship to the spontaneous mouse mutation vacillans described >40 years ago.

Animals↗
PubMed1998

staggerer phenotype in retinoid-related orphan receptor alpha-deficient mice.

Retinoid-related orphan receptor alpha (RORalpha) is a member of the nuclear receptor superfamily. To study its physiological role we generated null-mutant mice by targeted insertion of a lacZ reporter gene encoding the enzyme beta-galactosidase. In heterozygous RORalpha+/- mice we found beta-galactosidase activity, indicative of RORalpha protein expression, confined to the central nervous system, skin and testis. In the central nervous system, the RORalpha gene is expressed in cerebellar Purkinje cells, the thalamus, the suprachiasmatic nuclei, and retinal ganglion cells. In skin, RORalpha is strongly expressed in the hair follicle, the epidermis, and the sebaceous gland. Finally, the peritubular cells of the testis and the epithelial cells of the epididymis also strongly express RORalpha. Recently, it was reported that the ataxic mouse mutant staggerer (sg/sg) is caused by a deletion in the RORalpha gene. The analysis of the cerebellar and the behavioral phenotype of homozygous RORalpha-/- mice proves identity to sg/sg mice. Although the absence of RORalpha causes dramatic developmental effects in the cerebellum, it has no apparent morphological effect on thalamus, hypothalamus, and retina. Similarly, testis and skin of RORalpha-/- mice display a normal phenotype. However, the pelage hair of both sg/sg and RORalpha-/- is significantly less dense and when shaved shows reluctance to regrow.

Animals↗
PubMed1998

Venous thrombosis in older people: prevalence of the factor V gene mutation Q506.

OBJECTIVES: Old age is usually considered to be a risk factor for venous thromboembolism, in conjunction with other factors such as heart failure, major surgery, cancer, long-term immobilization, and antiphospholipid antibodies. Genetic risk factors, especially inherited deficiencies in coagulation inhibitors, also play a role in the pathogenesis of thrombosis, but these are usually diagnosed in thrombophilic patients before the age of 50. The factor V Q506 mutation, responsible for activated protein C resistance, was recently linked to thromboembolic disease. We therefore investigated the prevalence of biological risk factors in older hospital patients with venous thromboembolism. DESIGN: A 2-year study period. SETTING: Ivry sur Seine (Paris), France. PARTICIPANTS: Seventy-nine geriatric patients (60 women and 19 men, mean age 83+/-6.8 years, range 70-102 years) who had had at least one proven episode of venous thromboembolism were enrolled over a 2-year period. MEASUREMENTS: Lupus anticoagulant and antithrombin (AT), protein C (PC), and protein S (PS) levels were determined in plasma. The factor V Q506 mutation was detected on genomic DNA. RESULTS: Lupus anticoagulant was detected in two women, one of whom also had a high level of anticardiolipin IgG, leading to the diagnosis of an antiphospholipid syndrome. No hereditary deficiency in AT, PC, or PS was found, but one patient had an acquired AT deficiency. Interestingly, nine of the 79 patients (11.4%, six women and three men) were heterozygous for the factor V Q506 mutation, although none were homozygous. The only major risk factor for thrombosis identified in these patients was prolonged immobilization in four cases. Four of the nine patients who were heterozygous for the factor V Q506 mutation had recurrent thromboembolism, and two of these patients had been immobilized for long periods. CONCLUSIONS: This study confirms that hereditary deficiencies in coagulation inhibitors, and the lupus anticoagulant, are rarely involved in the pathogenesis of venous thromboembolism in older subjects. In contrast, the factor V Q506 mutation was frequently associated with thrombosis (11.4% of our patients) and should, therefore, be considered an important risk factor in the older people.

Activated Protein C Resistance↗
PubMed1998

[Murine typhus in Portugal].

Murine typhus or endemic typhus is a wide spread infectious disease, with a low prevalence in developed countries, but surely underdiagnosed. Its relative benignity, the similarity to other infectious diseases and the discretion of its epidemiologic chain, as well as the usual unexpectedness of its existence, makes its diagnosis more difficult. The clinical presentation and evolution of this case illustrate the necessity of being aware of this nosological entity.

Humans↗
PubMed1997

The expression pattern of the orphan nuclear receptor RORbeta in the developing and adult rat nervous system suggests a role in the processing of sensory information and in circadian rhythm.

RORbeta is an orphan nuclear receptor related to retinoid and thyroid hormone receptors and is exclusively expressed in the central nervous system (CNS). Here we present an in situ hybridization analysis of the distribution of RORbeta mRNA in the developing and adult rat CNS. The receptor localizes to areas involved in the processing of sensory information. In the cerebral cortex, RORbeta mRNA was exclusively detected in non-pyramidal neurons of layer IV and, less so, layer V. The highest expression was found in primary sensory cortices. In the thalamus highest RORbeta expression was found in the sensory relay nuclei projecting to the respective cortical areas. In contrast, sensory projection neurons in the periphery, for example retinal ganglion cells and neurons of the sensory ganglia showed only little RORbeta expression. RORbeta is also expressed in areas involved in the generation and maintenance of circadian rhythms - the suprachiasmatic nucleus, the pineal gland and the retina. In the latter two tissues, RORbeta mRNA abundance oscillates with circadian rhythmicity peaking during the hours of darkness. RORbeta mRNA could not be detected in striatum, hippocampus, cerebellum, the motor nuclei of the cranial nerves or the ventral part of the spinal cord. During development, RORbeta is expressed in many areas as early as embryonic day (E) 15, anticipating the distribution pattern in the adult. Our data suggest that RORbeta regulates genes whose products play essential roles in the context of sensory input integration as well as in the context of circadian timing system.

Animals↗
PubMed1996

The metastasis suppressor candidate nucleotide diphosphate kinase NM23 specifically interacts with members of the ROR/RZR nuclear orphan receptor subfamily.

We have cloned proteins that interact with the nuclear orphan receptor RZR beta using the yeast two-hybrid system. We identified, amongst a number of other genes, the nucleoside diphosphate kinase (NDPK)-2 also known as Nm23-2, c-myc regulatory factor PuF and differentiation inhibitory factor, RZR beta specifically interacts with Nm23-2 but not with the closely related tumor metastasis suppressor candidate gene product Nm23-1. In contrast ROR alpha interacts with both Nm23 proteins. These findings were corroborated by in vitro interaction assays based on GST-pulldown experiments. With-n-myc we propose a candidate gene regulated by ROR alpha/RZR beta and Nm23, based on the finding that the respective DNA binding sites in the first intron are conserved in several mammalian species.

Animals↗