86 results on '"Laudenbach, V."'
Search Results
2. Conséquences neurologiques de la sédation en réanimation
- Author
-
Dahmani, S., Tourrel, F., Blanc, T., Marret, S., Jegou-Colleter, S., and Laudenbach, V.
- Published
- 2012
- Full Text
- View/download PDF
3. Anaesthesia mode for caesarean section and mortality in very preterm infants: An epidemiologic study in the EPIPAGE cohort
- Author
-
Laudenbach, V., Mercier, F.J., Rozé, J.-C., Larroque, B., Ancel, P.-Y., Kaminski, M., Bréart, G., Diemunsch, P., Subtil, D., Lejus, C., Fresson, J., Arnaud, C., Rachet, B., Burguet, A., and Cambonie, G.
- Published
- 2009
- Full Text
- View/download PDF
4. Interactions of PACAP and Ceramides in the Control of Granule Cell Apoptosis During Cerebellar Development
- Author
-
Falluel-Morel, A., Aubert, N., Vaudry, D., Desfeux, A., Allais, A., Burel, D., Basille, M., Vaudry, H., Laudenbach, V., and Gonzalez, B. J.
- Published
- 2008
- Full Text
- View/download PDF
5. PRENATAL ALCOHOL EXPOSURE AFFECTS THE DEVELOPMENT OF THE BRAIN MICROVASCULAR SYSTEM: INVOLVEMENT OF THE VEGF SYSTEM: S040
- Author
-
Jégou, S., El Ghazi, F., de Lendeu, Kwetieu P., Marret, S., Laudenbach, V, Marcorelles, P., Laquerrière, A., and Gonzalez, B. J.
- Published
- 2010
6. Anti-mullerian hormone (AMH)-dependent regulation of the brain serine protease inhibitor, neuroserpin: O10–05
- Author
-
Lebeurrier, N, Launay, S, Maubert, E, Legros, H, Leclerc, A, Jamin, S, Picard, J-Y, Marret, S, and Laudenbach, V
- Published
- 2008
7. Journée d’actualités en néonatologie : JALON 2001, Nancy, 6 octobre 2001 Interactions fentanyl-récepteur ORL-1 en phase périnatale : le « principe de précaution » doit-il être appliqué au prématuré ?
- Author
-
Laudenbach, V. and Gressens, P.
- Published
- 2001
- Full Text
- View/download PDF
8. Mécanismes d'action des anesthésiques généraux
- Author
-
Laudenbach, V.
- Published
- 2006
- Full Text
- View/download PDF
9. Perforations iléales précoces sans signes d'entérocolite ulcéronécrosante : à propos de quatre cas survenus chez des prématurés
- Author
-
Arsac, M., Devaux, A.-M., Blanc, T., Pinquier, D., Bachy, B., Adde, C., Staquet, P., Marret, S., and Laudenbach, V.
- Published
- 2005
- Full Text
- View/download PDF
10. Mécanismes d'action des substances psycho-actives au cours de l'ontogenèse cérébrale
- Author
-
Laudenbach, V and Gressens, P
- Published
- 2004
- Full Text
- View/download PDF
11. Évaluation d’un protocole de sédation analgésie piloté par les infirmier(e)s en réanimation pédiatrique et néonatale
- Author
-
Dame-Sghaier, H., Galène-Gromez, S., Blanc, T., Laudenbach, V., Lepiney, G., Catel, M., Lemarchand, C., and Marret, S.
- Published
- 2012
- Full Text
- View/download PDF
12. Sédation et analgésie en réanimation – Aspects pédiatriques
- Author
-
Nolent, P. and Laudenbach, V.
- Subjects
- *
MIDAZOLAM , *BENZODIAZEPINES , *CLINICAL medicine , *PREVENTIVE medicine - Abstract
Abstract: Sedation and analgesia are a constant challenging issue in paediatric intensive care units, for ethical reasons among others. Basically, goals and available treatments in that context do not differ from those in adults. For instance, while we propose midazolam as the first choice benzodiazepine, there is no evidence for encouraging the use of one morphinomimetic rather than others in children. On the other hand, numerous paediatric specificities do exist: understanding and expression of pain both different and difficult, presence and involvement of the parents, pain assessment methods, pharmacology, pathologies. It is therefore mandatory to know these specificities to ensure a proper use of evaluation tools and therapeutics. The paucity of strong evidence from the literature does not allow producing definitive consensus guidelines. However, some practices can be highlighted such as the use of written protocol on pain/sedation evaluation and therapeutics adapted to children, literature data and local habits, the training of medical/nursing staff and the constitution of local referring team. A particular attention should be paid to propofol: its use longer than several hours should be strongly discouraged in infants and children due to the risk of Propofol Infusion Syndrome. Further clinical studies should be conducted in an attempt to provide answers to routine, daily issues and questions, for example, how to tailor the level of sedation to the needs of the patient, how to stop it, which drug must be preferred or what place for non-pharmacological approaches. [Copyright &y& Elsevier]
- Published
- 2008
- Full Text
- View/download PDF
13. Bax siRNA promotes survival of cultured and allografted granule cell precursors through blockade of caspase-3 cleavage.
- Author
-
Zhokhov, S. S., Desfeux, A., Aubert, N., Falluel-Morel, A., Fournier, A., Laudenbach, V., Vaudry, H., and Gonzalez, B. J.
- Subjects
CENTRAL nervous system ,NEURODEGENERATION ,CELL transplantation ,CEREBELLUM ,NEUROPEPTIDES ,APOPTOSIS - Abstract
Transplantation of neuronal precursor cells (NPCs) into the central nervous system could represent a powerful therapeutical tool against neurodegenerative diseases. Unfortunately, numerous NPCs die shortly after transplantation, predominantly due to caspase-dependent apoptosis. Using a culture of cerebellar neuronal precursors, we have previously demonstrated protective effect of the neuropeptide PACAP, which suppresses ceramide-induced apoptosis by blockade of the mitochondrial apoptotic pathway. The main objective of this study was to determine whether Bax repression can promote survival of NPCs allotransplanted into a host animal. In vivo and ex vivo experiments revealed that C2-ceramide increases Bax expression, while PACAP reverses this effect. In vitro tests using cerebellar NPCs demonstrated that the Bax-specific small interfering RNA (siRNA) could reduce their death and caspase-3 cleavage within the first 24 h. BrdU-labelled NPCs were subjected to transfection procedure with or without siRNA introduction before using for in vivo transplantation. Twenty-four hours after, the allografted NPCs containing siRNA showed significantly reduced level of caspase-3 cleavage, and the volume of their implants was almost twofold higher than in the case of empty-transfected precursors. These data evidence an important role of Bax in life/death decision of grafted NPCs and suggest that RNA interference strategy may be applicable for maintaining NPCs survival within the critical first hours after their transplantation.Cell Death and Differentiation (2008) 15, 1042–1053; doi:10.1038/cdd.2008.29; published online 7 March 2008 [ABSTRACT FROM AUTHOR]
- Published
- 2008
- Full Text
- View/download PDF
14. Ontogenic study of the influence of tissue plasminogen activator (t-PA) in neonatal excitotoxic brain insult and the subsequent microglia/macrophage activation
- Author
-
Hennebert, O., Laudenbach, V., Laquerriere, A., Verney, C., Carmeliet, P., Marret, S., and Leroux, P.
- Subjects
- *
FIBRINOLYTIC agents , *MACROPHAGES , *MICROGLIA , *NEWBORN infants' injuries - Abstract
Abstract: Intracerebral injections of ibotenic acid in neonatal mice produced white and gray matter lesions that mimic some aspects of the acquired cerebral injuries observed in human newborns (i.e. periventricular leukomalacias in preterm newborns and post-ischemic cortical necrosis in at term infants). We have evaluated the effects of tissue plasminogen activator inactivation (t-PA−/−) on the effects of ibotenic acid (0.01–20 μg), and on F4/80 labeling of microglia/macrophages at different stages. Three ontogenic periods have been identified. In mice injected the day of birth, postnatal (P) day 0, ibotenic acid induced neuronal migration disorders together with low local microglial activation in wild-type and t-PA−/− mice. In P2 and P5 mice, ibotenic acid induced diffuse microglial activation in the whole cortex and subcortical areas; e.g. caudate nucleus and septum. In wild-type mice, cystic lesions of the white matter were consistently observed, surrounded by macrophages. In t-PA−/− mice, noncystic lesions filled of macrophages were more frequent than cysts. Macrophages were virtually absent in the gray matter. White and gray matter lesions were reduced in t-PA−/− mice. The plasmin inhibitor aprotinin reduced white and gray matter lesions only in wild-type mice injected with high ibotenic acid doses (2.5–5 μg). During this period, a transient F4/80 immunoreactive cell population was detected in the cingulum. At P10, the salient lesion characteristic was a large gray matter lesion containing macrophage accumulation. Microglial activation was confined to the injection site in the white matter. t-PA−/− mice showed reduced lesion size under high doses (>5 μg) of ibotenic acid. Similarly, aprotinin diminished the lesion in wild-type animals exposed to 10 μg ibotenic acid. These data demonstrate that t-PA and microglia do not actively participate in the migration disorders induced in P0 mice. Conversely, t-PA was implicated in cyst formation in older (P2-P10) mice, and in their subsequent growth. t-PA was also involved in GM lesions, probably through an inflammatory process involving macrophages. [Copyright &y& Elsevier]
- Published
- 2005
- Full Text
- View/download PDF
15. Open vs thorascopic surgical management of bronchogenic cysts.
- Author
-
Tölg, C, Abelin, K., Laudenbach, V., De Heaulme, O., Dorgere, S., Lipsyc, E. Sèguier, Aigrain, T., De Lagausie, P., Tölg, C, Dorgeret, S, Lipsyc, E Séguier, and Aigrain, Y
- Subjects
CYSTS (Pathology) ,TUMORS ,THORACIC surgery ,PEDIATRIC surgery ,THORACOSCOPY ,ENDOSCOPY ,BRONCHIAL diseases ,COMPARATIVE studies ,RESEARCH methodology ,MEDICAL cooperation ,RESEARCH ,EVALUATION research ,RETROSPECTIVE studies ,THORACOTOMY - Abstract
Background: The aim of this study was to compare the operative outcome in children undergoing open vs thoracoscopic resection of bronchogenic cysts.Methods: The medical records of children who underwent the resection of bronchogenic cysts from 1990 through 2000 were reviewed. Four cyst resections were performed by the open technique and five using a thoracoscopic procedure. The age of the patients, length of hospital stay, duration of drainage, operating time, and outcome were investigated.Results: The mean age of patients undergoing the open procedure was 3 years and 3 months; the mean age for thoracoscopy patients was 7 years and 10 months (p < 0.05). The operating time for the open procedure was 70 +/- 25 min; for the laparoscopic procedure, it was 78 +/- 6 min (p, NS), except in one case with a main bronchial tail that required conversion (320 min). Duration of surgical drainage was 6.5 +/- 3 days for the open procedure and 2.5 +/- 1 days for the thoracoscopic one (p < 0.05). Hospital stay for open patients was 12 days +/- 0 days; it was 6 +/- 1.6 days for thoracoscopic patients (p < 0.01). There were no deaths. The thoracoscopic procedure failed once due to a main bronchial tail and had to be converted to an open procedure. Other early complications included a bronchopulmonary infection after an open cyst excision and an atelectasis after a thoracoscopic cyst excision. Late complications included one reoperation for incomplete excision in each of the two groups.Conclusion: Bronchogenic cyst resection can be performed safely. For complete treatment of these patients, total excision of the wall cyst is needed. In selected patients, the thoracoscopic procedure may decrease the duration of surgical drainage and length of hospital stay without increasing the operating time or MSK for complications. [ABSTRACT FROM AUTHOR]- Published
- 2005
- Full Text
- View/download PDF
16. Anesthesia Mode for Cesarean Section and Mortality in Very Preterm Infants: An Epidemiologic Study in the EPIPAGE Cohort.
- Author
-
Laudenbach, V., Mercier, F.j., Rozé, J.c., Larroque, B., Ancel, P.y., Kaminski, M., Bréart, G., Diemunsch, P., Subtil, D., Lejus, C., Fresson, J., Arnaud, C., Rachet, B., Burguet, A., and Cambonie, G.
- Published
- 2010
- Full Text
- View/download PDF
17. Impact of psychoactive substances on brain development
- Author
-
Laudenbach, V. and Gressens, P.
- Published
- 2004
- Full Text
- View/download PDF
18. NOP7 Hemorragie sous-piale : espace peu connu des hemorragies intracraniennes
- Author
-
Grévent, D., Proust, F., Laudenbach, V., Laquerriere, A., Cellier, C., and Eurin, D.
- Published
- 2004
- Full Text
- View/download PDF
19. Adarpef 2010 : le congrès de la transversalité
- Author
-
Courrèges, P. and Laudenbach, V.
- Published
- 2010
- Full Text
- View/download PDF
20. Congrès annuel de l’Adarpef
- Author
-
Courrèges, P. and Laudenbach, V.
- Published
- 2009
- Full Text
- View/download PDF
21. Effets des agents anesthésiques sur le cerveau en développement
- Author
-
Mons, F., Kwetieu de Lendeu, P., Marret, S., and Laudenbach, V.
- Subjects
- *
DEVELOPMENTAL neurobiology , *ANESTHETICS , *NEUROTOXICOLOGY , *LABORATORY rodents , *CLINICAL trials , *APOPTOSIS , *COGNITIVE development , *NEURAL development - Abstract
Abstract: Objective: To expose the current knowledge about the anaesthetic effects on the developing brain. Data sources: Publications (original articles and reviews) in English and in French language from 1980 were obtained from the Medline database using alone or in combination following keywords: anaesthetics, developing brain, neurodevelopment, neurogenesis, synaptogenesis, neurotoxicity, apoptosis. Data synthesis: Several lines of evidence resulting from animal experiments conducted in rodents and non-human primates have suggested that exposing the developing brain to anaesthetic drugs may elicit an increase a physiological programmed neuronal death (i.e. apoptosis). This neuronal death is not only seen at the cellular level but also results in alterations in some behavioural abilities in the adult animal. However, the vast majority of experiments reported have been conducted in animals not exposed to any surgical or painful stimulation. Moreover, the literature raises contradictory results, some authors not confirming this neurotoxic effect of anaesthetic drugs. Last, available clinical data are scarce and do not allow to claim that exposure to general anaesthesia definitely alters the cognitive development of children. Conclusion: This review raises the question of the innocuity of anaesthetic agents on the developing brain; further clinical trials are required in order to test this effect on human babies. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
22. Neuroprotective effects vary across nonsteroidal antiinflammatory drugs in a mouse model of developing excitotoxic brain injury
- Author
-
Leroux, P., Hennebert, C., Catteau, J., Legros, H., Hennebert, O., Laudenbach, V., and Marret, S.
- Subjects
- *
NEUROPROTECTIVE agents , *PHARMACODYNAMICS , *NONSTEROIDAL anti-inflammatory agents , *BRAIN injuries , *LABORATORY mice , *ANALYSIS of variance , *CYCLOOXYGENASES - Abstract
Abstract: Glutamate excitotoxicity is among the main cellular mechanisms leading to perinatal insults in human newborns. We used intracerebral injection of the glutamatergic glutamate N-methyl-d-aspartate-receptor agonist ibotenate to produce excitotoxic lesions mimicking the acquired white matter lesions seen in human preterm infants. We evaluated whether nonsteroidal antiinflammatory drugs (NSAIDs) protected against glutamate excitotoxicity. Aspirin (0.01–100 μg/d), indomethacin (0.1–10 μg/d), paracetamol (10–100 μg/d), or NS-398 (12.5 μg/d) was given daily before ibotenate (P1 to P5) or after ibotenate (P5 to P9). Lesion size was measured on Cresyl Violet-stained brain sections collected on P10. None of the drugs tested alone or in combination increased lesion size. Pretreatment with low- or high-dose aspirin and post-treatment with paracetamol or NS-398 protected against white matter lesions, whereas cortical lesions were decreased by pretreatment with low- or high-dose aspirin or post-treatment with NS-398. The corticosteroid betamethasone (0.18 μg/d) was neuroprotective when given before or after ibotenate and this effect was reversed by concomitant aspirin therapy (10 μg/d). In conclusion, perinatal NSAID administration may have beneficial effects on brain injury if appropriately timed. [Copyright &y& Elsevier]
- Published
- 2010
- Full Text
- View/download PDF
23. Role of tissue-plasminogen activator (t-PA) in a mouse model of neonatal white matter lesions: Interaction with plasmin inhibitors and anti-inflammatory drugs
- Author
-
Leroux, P., Hennebert, O., Legros, H., Laudenbach, V., Carmeliet, P., and Marret, S.
- Subjects
- *
FIBRINOLYTIC agents , *BLOOD plasma , *ADRENOCORTICAL hormones , *TUMOR necrosis factors - Abstract
Abstract: Ibotenic acid injected intracerebrally over a broad dose range to 5-day-old mice induces cystic white matter (WM) lesions that mimic periventricular leukomalacia (PVL) of preterm infants. With both low (0.1 μg) and high (5 μg) ibotenic acid doses, tissue-plasminogen activator (t-PA) is involved in cyst formation. Subsequent cyst growth depends on high doses. We evaluated the effects of human recombinant tissue-plasminogen activator (hrt-PA), plasmin inhibitors (tranexamic acid, alpha2-antiplasmin, and aprotinin), and anti-inflammatory drugs (betamethasone, NS-398) in wild-type and t-PA−/− mice given high-dose or low-dose ibotenic acid. Intracerebral hrt-PA induced WM cystic lesions in t-PA−/− mice and had an additive effect when co-injected with high-dose ibotenic acid. Plasmin inhibitors reduced lesion growth in wild-type mice given high-dose, but not low-dose, ibotenic acid but had no effect in t-PA−/− mice. Similarly the anti-inflammatory drugs betamethasone and NS-398 (a cyclooxygenase 2 and NFκB inhibitor) were neuroprotective in wild-type animals exposed to high-dose, but not low-dose, ibotenic acid. Thus, the t-PA-dependent effect of low-dose ibotenic acid on cyst formation appeared independent from plasmin activity or inflammation. Conversely, a t-PA-dependent inflammatory process occurred with high-dose ibotenic acid. Potential strategies for PVL in preterm neonates may include fibrinolytic monitoring for prevention and anti-inflammatory agents for treatment. [Copyright &y& Elsevier]
- Published
- 2007
- Full Text
- View/download PDF
24. R012 Analyse de la surexpression du récepteur nicotinique de l'acétylcholine (nrach) dans le muscle dénervé
- Author
-
Laudenbach, V., Bessereau, J.L., M.A.ntz, J., Desmonts, J.M., and C.H.angeux, J.P.
- Published
- 1998
- Full Text
- View/download PDF
25. Devenir neuromoteur à 2 ans des grands prématurés avec leucomalacie périventriculaire : étude rétrospective sur 11 ans à l’hôpital universitaire de Rouen
- Author
-
Gobalakichenane, P., Labarre, A., Mons, F., Galène-Gromez, S., Laudenbach, V., and Marret, S.
- Published
- 2009
- Full Text
- View/download PDF
26. Est-il possible de protéger le cerveau de l’enfant né prématuré et de diminuer le taux de séquelles neuro-développementales ?
- Author
-
Marret, S., Foix-l’Hélias, L., Ancel, P.-Y., Kaminski, M., Larroque, B., Marcou-Labarre, A., and Laudenbach, V.
- Subjects
- *
NEWBORN infants' injuries , *PREMATURE infant diseases , *BRAIN damage , *ANIMAL models in research , *CLINICAL trials , *DRUG delivery systems - Abstract
Summary: With improving neonatal survival for very premature babies, the challenge for neonatalogists is to ameliorate outcome of surviving babies. Several pharmacological molecules have been shown to have protective effects in different types of in vitro or in vivo animal models of acquired cerebral brain damages. However translational research and conduction of therapeutic trials in human remain difficult due to failure to recognize start of deleterious cascade leading to cerebral damage and additional toxic effect of potential protective molecules. This review concentrates on best evidence emerging in recent years on prevention on brain damage by early drug administration. It has been shown in two randomised trials that prenatal low-dose of magnesium sulphate does not increase paediatric mortality in very-preterm infants and has non significant neuroprotective effects on occurrence of motor dysfunction (with a 0.62 odds ratio in the French trial Premag and 0.71 relative risk in the Australian trial ACTOMgSO4), justifying that magnesium sulphate should be discussed as a stand-alone treatment or as part of a combination treatment, at least in the context of clinical trials. Antenatal corticosteroid therapy increases the survival of very-preterm infants, including the most immature. Moreover in an observational recent study of the Epipage cohort, it has been observed a significant decrease in white matter injury in the 28-32 weeks’ gestation group but no effect on long term outcome and behaviour. Conversely in the most immature of the 24-27 weeks’ gestation group, no effect has been detected either in white matter injury incidence or in long term outcome rates. Caffeine has a protective effect since a decrease in cerebral palsy has been noted in the caffeine group in a randomised trial studying caffeine versus placebo. For what concern other widely used potential protective molecules during the perinatal period, there is no evidence of cerebral protection with indometacine, nitric oxide, eythropoietin, phenobarbital, and etamsylate. Due to their specific properties, a careful evaluation of aspirin, anaesthetic drugs and tocolytics should be done in the next months. [Copyright &y& Elsevier]
- Published
- 2008
- Full Text
- View/download PDF
27. Conditions requiring hospitalisations, more than general anaesthesia itself, are associated with diagnosis of learning disorders in children.
- Author
-
Laudenbach V, Charollais A, Radi S, Stumpf MH, Vincent A, Kaltwasser I, Tomczyk T, Benichou J, Leroux P, and Marret S
- Subjects
- Child, Hospitalization, Humans, Prospective Studies, Retrospective Studies, Anesthesia, General adverse effects, Learning Disabilities diagnosis, Learning Disabilities epidemiology
- Abstract
Background: Anaesthesia is neurotoxic in developing primates. Retrospective clinical studies show a correlation between exposure to anaesthesia during infancy and the occurrence of learning disorders (LD). Prospective studies failed to detect any influence of a single exposure to anaesthesia on neurodevelopment. We hypothesised that some specific populations of children were electively sensitive to anaesthesia-related neurotoxicity., Methods: Using a case-control design, we analysed the medical histories of children with LD, compared to those of their normally reading siblings. Interviews were conducted and medical records were reviewed. The numbers of hospitalisations and anaesthesia exposures before the age of five years were determined., Results: Four hundred fourteen dyslexic children were screened over a one-year period. Two hundred and seventy patients were excluded due to confounding variables (single child, all siblings showing LD or any condition placing the neurological prognosis at risk (N = 107/414 for the latter)) or inability to accurately collect evaluation criteria. In the 144 case-control pairs studied, the mean number of hospitalisations was significantly different (N = 1.097 ± 0 .135/case versus 0.667 ± 0.097/control, p = 0.0052), as was the proportion of hospitalised patients (54.2% versus 38.9%, p = 0.0031). The mean number of anaesthesia exposures per individual was not statistically different (N = 0.958 ± 0.183/case versus 0.569 ± 0.107/control, p = 0.0732), but the proportion of children anaesthetised at least once was (43.8% (cases) versus 33.3% (controls), p = 0.0301)., Discussion: One or more hospitalisation(s) may reflect a health status and/or have an iatrogenic effect disrupting the normal setting up of learning abilities. Anaesthesia may play a role, but a correlation between LD and anaesthesia is of a lower magnitude than between LD and hospitalisation., (Copyright © 2020 Société française d'anesthésie et de réanimation (Sfar). Published by Elsevier Masson SAS. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF
28. Neurotoxicity of anaesthetics on developing brain: a relevant question or just a "bias"?
- Author
-
Dahmani S and Laudenbach V
- Subjects
- Anesthesia, General, Brain, Child, Humans, Anesthesia, Conduction, Anesthetics, Neurotoxicity Syndromes
- Published
- 2019
- Full Text
- View/download PDF
29. Determining the editorial policy of Anaesthesia Critical Care and Pain Medicine (ACCPM).
- Author
-
Lefrant JY, Lorne E, Asehnoune K, Ausset S, Beaulieu P, Biais M, Brichant JF, Charbit B, Constantin JM, Cuvillon P, Dadure C, Dahmani S, David JS, Fuchs-Buder T, Geeraerts T, Godier A, Hanouz JL, Joannes-Boyau O, Kipnis E, Laudenbach V, Le Guen M, Legrand M, Lescot T, Marret E, Mongardon N, Ouattara A, Pierre S, Roberts J, Schneider A, Tourtier JP, Tran L, Pirracchio R, and Capdevila X
- Subjects
- Anesthesia, Anesthesiology, Critical Care, Editorial Policies, Pain Management, Periodicals as Topic
- Published
- 2018
- Full Text
- View/download PDF
30. T H 17 Cell Frequency in Peripheral Blood Is Elevated in Overweight Children without Chronic Inflammatory Diseases.
- Author
-
Schindler TI, Wagner JJ, Goedicke-Fritz S, Rogosch T, Coccejus V, Laudenbach V, Nikolaizik W, Härtel C, Maier RF, Kerzel S, and Zemlin M
- Abstract
Background: The prevalence of obesity has dramatically increased in children in the last few decades and is associated with chronic inflammatory diseases. Fat tissue produces IL-6 and TNF-α, which are stimuli for T
H 17 cell differentiation. These cells are characterized by expression of the transcription factor receptor-related orphan receptor C (RORC) and by IL-17A production. In murine models, obesity has been linked with elevated TH 17 cell frequencies. The aim of this study was to explore whether being overweight was associated with an elevated frequency of circulating TH 17 cells or elevated messenger RNA (mRNA)-levels of IL-17A and RORC in children without chronic inflammatory diseases., Methods: We studied peripheral blood samples from 15 overweight and 50 non-overweight children without a history of autoimmune diseases, asthma, atopic dermatitis or allergic rhinoconjunctivitis. TH 17 cells were quantified in Ionomycin stimulated peripheral blood mononuclear cells by flow cytometry using intracellular IL-17A staining. RORC- and IL-17A expressions were measured by real-time PCR., Results: We found significantly elevated TH cell frequencies in overweight children compared then on-overweight controls with 34.7 ± 1.5% of CD3+ CD4+ cells versus 25.4 ± 2.4% (mean ± SEM, p = 0.0023), respectively. Moreover, TH cell frequencies correlated positively with body mass index ( r = 0.42, p = 0.0005, respectively). The relative mRNA expression of RORC ( p = 0.013) and IL-17A ( p = 0.014) were upregulated in overweight compared to non-overweight children., Conclusion: Childhood obesity is an independent factor that is associated with an elevated frequency of circulating TH 17 cells and higher expression of RORC- and IL-17A-mRNA after in vitro stimulation with Ionomycin. This might be due to the inflammatory activity of the fat tissue. Studies on TH 17 immunity should not only be adjusted for acute and chronic inflammatory diseases but also for overweight.- Published
- 2017
- Full Text
- View/download PDF
31. The antiapoptotic effect of remifentanil on the immature mouse brain: an ex vivo study.
- Author
-
Tourrel F, de Lendeu PK, Abily-Donval L, Chollat C, Marret S, Dufrasne F, Compagnon P, Ramdani Y, Dureuil B, Laudenbach V, Gonzalez BJ, and Jégou S
- Subjects
- Analgesics, Opioid pharmacokinetics, Animals, Animals, Newborn, Blotting, Western, Caspase 3 metabolism, Cell Death drug effects, Cell Nucleus drug effects, Cell Nucleus ultrastructure, Drug Synergism, Glycine pharmacology, Half-Life, Immunohistochemistry, In Vitro Techniques, L-Lactate Dehydrogenase metabolism, Mice, Microscopy, Electron, Mitochondria drug effects, Mitochondria ultrastructure, Piperidines pharmacokinetics, Receptors, N-Methyl-D-Aspartate drug effects, Remifentanil, bcl-2-Associated X Protein metabolism, Analgesics, Opioid pharmacology, Apoptosis drug effects, Brain cytology, Brain drug effects, Piperidines pharmacology
- Abstract
Background: The use of remifentanil in a context of potential prematurity led us to explore ex vivo the opioid effects on the immature mouse brain. Remifentanil enhances medullary glutamatergic N-methyl-D-aspartate (NMDA) receptor activity. Furthermore, in neonatal mouse cortex, NMDA was previously shown to exert either excitotoxic or antiapoptotic effects depending on the cortical layers. With the use of a model of acute cultured brain slices, we evaluated the potential necrotic and apoptotic effects of remifentanil, alone or associated with its glycine vehicle (commercial preparation of remifentanil, C.P. remifentanil), on the immature brain., Methods: Cerebral slices from postnatal day 2 mice were treated up to 5 hours with the different compounds, incubated alone or in the presence of NMDA. The necrotic effect was studied by measuring lactate dehydrogenase activity and 7-Aminoactinomycin D labeling. Apoptotic death was evaluated by measurement of caspase-3 activity and cleaved caspase-3 protein levels, using Western blot and immunohistochemistry. Extrinsic and intrinsic apoptotic pathways were investigated by measuring caspase-8, caspase-9 activities, Bax protein levels, and mitochondrial integrity., Results: C.P. remifentanil was ineffective on necrotic death, whereas it significantly reduced caspase-3 activity and cortical cleaved caspase-3 levels. C.P. remifentanil inhibited cortical Bax protein expression, caspase-9 activity, and preserved mitochondrial integrity, whereas it had no effect on caspase-8 activity. Its action targeted the neocortex superficial layers, and it was reversed by the opioid receptors antagonist naloxone and the NMDA antagonist MK801. Remifentanil and glycine acted synergistically to inhibit apoptotic death. In addition, C.P. remifentanil enhanced the antiapoptotic effect of NMDA, whereas it did not improve NMDA excitotoxicity in brain slices., Conclusion: The present data indicate that at a supraclinical concentration C.P. remifentanil had no pronecrotic effect but exerted ex vivo antiapoptotic action on the immature mouse brain, involving the opioid and NMDA receptors, and the mitochondrial-dependent apoptotic pathway. Assessment of the impact of the antiapoptotic effect of remifentanil in in vivo neonatal mouse models of brain injury will also be essential to measure its consequences on the developing brain.
- Published
- 2014
- Full Text
- View/download PDF
32. High t-PA release by neonate brain microvascular endothelial cells under glutamate exposure affects neuronal fate.
- Author
-
Henry VJ, Lecointre M, Laudenbach V, Ali C, Macrez R, Jullienne A, Berezowski V, Carmeliet P, Vivien D, Marret S, Gonzalez BJ, and Leroux P
- Subjects
- Animals, Animals, Newborn, Brain pathology, Immunohistochemistry, Mice, Mice, Inbred C57BL, Neurons pathology, Organ Culture Techniques, Apoptosis physiology, Brain metabolism, Endothelial Cells metabolism, Glutamic Acid metabolism, Neurons metabolism, Tissue Plasminogen Activator metabolism
- Abstract
Glutamate excitotoxicity is a consolidated hypothesis in neonatal brain injuries and tissue plasminogen activator (t-PA) participates in the processes through proteolytic and receptor mediated effects. In brain microvascular endothelial cell (nBMEC) cultures from neonates, t-PA content and release upon glutamate are higher than in adult (aBMECs) cultures. Owing to the variety of t-PA substrates and receptor targets, the study was aimed at determining the putative roles of endothelial t-PA in the neonatal brain parenchyma under glutamate challenge. Basal t-PA release was 4.4 fold higher in nBMECs vs aBMECs and glutamate was 20 fold more potent to allow Evans blue vascular permeability in neonate microvessels indicating that, under noxious glutamate (50 μM) exposure, high amounts of endothelial t-PA stores may be mobilized and may access the nervous parenchyma. Culture media from nBMECS or aBMECs challenged by excitotoxic glutamate were applied to neuron cultures at DIV 11. While media from adult cells did not evoke more LDH release in neuronal cultures that under glutamate alone, media from nBMECs enhanced 2.2 fold LDH release. This effect was not observed with media from t-PA(-/-) nBMECs and was inhibited by hr-PAI-1. In Cortical slices from 10 day-old mice, hrt-PA associated with glutamate evoked neuronal necrosis in deeper (more mature) layers, an effect reversed by NMDA receptor GluN1 amino-terminal domain antibody capable of inhibiting t-PA potentiation of the receptor. In superficial layers (less mature), hrt-PA alone inhibited apoptosis, an effect reversed by the EGF receptor antagonist AG1478. Applied to immature neurons in culture (DIV5), media from nBMEC rescued 85.1% of neurons from cell death induced by serum deprivation. In cortical slices, the anti-apoptotic effect of t-PA fitted with age dependent localization of less mature neurons. These data suggest that in the immature brain, propensity of vessels to release high amounts of t-PA may not only impact vascular integrity but may also influence neuronal fate, via regulation of apoptosis in immature cells and, as in adult by potentiating glutamate toxicity in mature neurons. The data point out putative implication of microvessels in glutamate neurotoxicity in the development, and justify research towards vessel oriented neuroprotection strategies in neonates., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
33. Prenatal alcohol exposure affects vasculature development in the neonatal brain.
- Author
-
Jégou S, El Ghazi F, de Lendeu PK, Marret S, Laudenbach V, Uguen A, Marcorelles P, Roy V, Laquerrière A, and Gonzalez BJ
- Subjects
- Age Factors, Animals, Animals, Newborn, CD13 Antigens metabolism, Calcium metabolism, Cell Death drug effects, Cerebral Cortex drug effects, Cerebral Cortex embryology, Cerebral Cortex growth & development, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Interactions, Endothelial Cells metabolism, Endothelial Cells pathology, Female, Fetal Alcohol Spectrum Disorders metabolism, Fetus, Gene Expression Regulation, Developmental drug effects, Glucose Transporter Type 1 genetics, Glucose Transporter Type 1 metabolism, Glutamic Acid pharmacology, Humans, In Vitro Techniques, Locomotion drug effects, Male, Maze Learning drug effects, Mice, Microscopy, Video, Microvessels metabolism, Muscle Strength physiology, Neovascularization, Pathologic pathology, Platelet Endothelial Cell Adhesion Molecule-1 genetics, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Pregnancy, Prenatal Exposure Delayed Effects physiopathology, Receptors, N-Methyl-D-Aspartate genetics, Receptors, N-Methyl-D-Aspartate metabolism, Receptors, Vascular Endothelial Growth Factor genetics, Receptors, Vascular Endothelial Growth Factor metabolism, Time Factors, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Central Nervous System Depressants adverse effects, Cerebral Cortex pathology, Ethanol adverse effects, Fetal Alcohol Spectrum Disorders pathology, Microvessels growth & development, Microvessels pathology, Prenatal Exposure Delayed Effects pathology
- Abstract
Objective: In humans, antenatal alcohol exposure elicits various developmental disorders, in particular in the brain. Numerous studies focus on the deleterious effects of alcohol on neural cells. Although recent studies suggest that alcohol can affect angiogenesis in adults, the impact of prenatal alcohol exposure on brain microvasculature remains poorly understood., Methods: We used a mouse model to investigate effects of prenatal alcohol exposure on the cortical microvascular network in vivo and ex vivo and the action of alcohol, glutamate, and vascular endothelial growth factor A (VEGF) on activity, plasticity, and survival of microvessels. We used quantitative reverse transcriptase polymerase chain reaction, Western blot, immunohistochemistry, calcimetry, and videomicroscopy. We characterized the effect of prenatal alcohol exposure on the cortical microvascular network in human controls and fetal alcohol syndrome (FAS)/partial FAS (pFAS) patients at different developmental stages., Results: In mice, prenatal alcohol exposure induced a reduction of cortical vascular density, loss of the radial orientation of microvessels, and altered expression of VEGF receptors. Time-lapse experiments performed on brain slices revealed that ethanol inhibited glutamate-induced calcium mobilization in endothelial cells, affected plasticity, and promoted death of microvessels. These effects were prevented by VEGF. In humans, we evidenced a stage-dependent alteration of the vascular network in the cortices of fetuses with pFAS/FAS. Whereas no modification was observed from gestational week 20 (WG20) to WG22, the radial organization of cortical microvessels was clearly altered in pFAS/FAS patients from WG30 to WG38., Interpretation: Prenatal alcohol exposure affects cortical angiogenesis both in mice and in pFAS/FAS patients, suggesting that vascular defects contribute to alcohol-induced brain abnormalities., (Copyright © 2012 American Neurological Association.)
- Published
- 2012
- Full Text
- View/download PDF
34. NO-dependent protective effect of VEGF against excitotoxicity on layer VI of the developing cerebral cortex.
- Author
-
El Ghazi F, Desfeux A, Brasse-Lagnel C, Roux C, Lesueur C, Mazur D, Remy-Jouet I, Richard V, Jégou S, Laudenbach V, Marret S, Bekri S, Prevot V, and Gonzalez BJ
- Subjects
- Analysis of Variance, Animals, Animals, Newborn, Calcium metabolism, Caspase 3 metabolism, Cerebral Cortex cytology, Cerebral Cortex drug effects, Citrulline metabolism, Dose-Response Relationship, Drug, Electron Spin Resonance Spectroscopy methods, Enzyme Inhibitors pharmacology, Enzyme-Linked Immunosorbent Assay methods, Excitatory Amino Acid Agents pharmacology, Gene Expression Regulation, Developmental drug effects, Glutamate Decarboxylase genetics, Glutamic Acid toxicity, Green Fluorescent Proteins genetics, In Vitro Techniques, L-Lactate Dehydrogenase metabolism, Mice, Mice, Transgenic, NADPH Dehydrogenase metabolism, Neurons drug effects, Nitric Oxide Synthase metabolism, RNA, Small Interfering genetics, RNA, Small Interfering metabolism, S-Nitroso-N-Acetylpenicillamine pharmacology, Time Factors, Apoptosis drug effects, Cerebral Cortex growth & development, Neurons metabolism, Neuroprotective Agents pharmacology, Nitric Oxide metabolism, Vascular Endothelial Growth Factor A pharmacology
- Abstract
In industrialized countries, cerebral palsy affects 2.5‰ of preterm and term infants. At a neurochemical level, the massive release of glutamate constitutes a major process leading to excitotoxicity and neonatal brain lesions. Previous studies, conducted in the laboratory, revealed that, in (δ/δ)VEGF(A) transgenic mice, glutamate-induced brain lesions are exacerbated suggesting that VEGF(A) could play a protective action against excitotoxicity. Using a model of cultured cortical brain slices, the aim of the study was to characterize the central effects of VEGF against glutamate-induced excitotoxicity in neonates. Exposure of brain slices to glutamate induced a strong increase of necrotic cell death in the deep cortical layer VI and a decrease of apoptotic death in superficial layers II-IV. When administered alone, a 6-h treatment with VEGF(A) had no effect on both apoptotic and necrotic deaths. In contrast, VEGF(A) abolished the glutamate-induced necrosis observed in layer VI. While MEK and PI3-K inhibitors had no effect on the protective action of VEGF(A), L-NAME, a pan inhibitor of NOS, abrogated the effect of VEGF(A) and exacerbated the excitotoxic action of glutamate. Calcimetry experiments performed on brain slices revealed that VEGF(A) reduced the massive calcium influx induced by glutamate in layer VI and this effect was blocked by L-NAME. Neuroprotective effect of VEGF(A) was also blocked by LNIO and NPLA, two inhibitors of constitutive NOS, while AGH, an iNOS inhibitor, had no effect. Nitrite measurements, electron paramagnetic resonance spectroscopy and immunohistochemistry indicated that glutamate was a potent inducer of NO production via activation of nNOS in the cortical layer VI. In vivo administration of nNOS siRNA promoted excitotoxicity and mimicked the effects of L-NAME, LNIO and NPLA. A short-term glutamate treatment increased nNOS Ser1412 phosphorylation, while a long-term exposure inhibited nNOS/NR2B protein-protein interactions. Altogether, these findings indicate that, in deep cortical layers of mice neonates, glutamate stimulates nNOS activity. Contrasting with mature brain, NO production induced by high concentrations of glutamate is neuroprotective and is required for the anti-necrotic effect of VEGF(A)., (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Published
- 2012
- Full Text
- View/download PDF
35. [Neurological consequences after long-term sedation in the ICU].
- Author
-
Dahmani S, Tourrel F, Blanc T, Marret S, Jegou-Colleter S, and Laudenbach V
- Subjects
- Aging physiology, Anesthetics, General antagonists & inhibitors, Anesthetics, General pharmacology, Anesthetics, General toxicity, Animals, Cesarean Section, Critical Care, Excitatory Amino Acid Agonists pharmacology, Female, Fetal Alcohol Spectrum Disorders physiopathology, Humans, Hypnotics and Sedatives pharmacology, Hypnotics and Sedatives toxicity, Infant, Newborn, Infant, Premature, Intensive Care Units, N-Methylaspartate pharmacology, Nervous System Diseases pathology, Neurotoxicity Syndromes etiology, Neurotoxicity Syndromes therapy, Pregnancy, Primates physiology, Synaptic Transmission drug effects, Teratogens, gamma-Aminobutyric Acid pharmacology, Conscious Sedation adverse effects, Nervous System Diseases etiology
- Abstract
Experiments performed in mammals, including non-human primates, have demonstrated an increase in neuronal death rates normally seen in normal brain development. Such an increase is encountered in diseases but also after exposure of the brain to various class of anaesthetics. In living animals, it can (but not always) result in persistent cognitive impairment. Most of the experiments have been conducted in animals which were never exposed to any pain, which questions their relevancy. On the clinical side, all data comes from retrospective studies. Given the multiple bias, they cannot definitely state that a protocol, if toxic, is more or less when compared to another. Until now, prospective follow-up of children exposed to anaesthetics in utero or during the first months of life do not suggest a major deleterious effect. Yet, a minor one, if existing, would be hard to detect among polluting variables (e.g. pathology requiring anaesthesia, long hospitalization after birth, preterm birth, environmental stress...). For sure, when surgery is mandatory during pregnancy, it is generally for maternal indication and should not be a motif strong enough for foetal extraction, especially in terms where the baby has few chances to survive. Second, it is known for years than anaesthesia before 1 year of age is much riskier than after 1 year, whatever the theorical neurotoxicity is. Third, this enforces the need to develop tools enhancing the precision of anaesthesia as much as possible. Meanwhile, when an infant has undergone numerous general anaesthesias, we strongly recommend a long-time neurological follow-up., (Copyright © 2011. Published by Elsevier SAS.)
- Published
- 2012
- Full Text
- View/download PDF
36. Effects of antenatal uteroplacental hypoperfusion on neonatal microvascularisation and excitotoxin sensitivity in mice.
- Author
-
Catteau J, Gernet JI, Marret S, Legros H, Gressens P, Leroux P, and Laudenbach V
- Subjects
- Animals, Animals, Newborn, Excitatory Amino Acid Agonists pharmacology, Excitatory Amino Acid Agonists toxicity, Female, Fetal Growth Retardation, Humans, Ibotenic Acid pharmacology, Ibotenic Acid toxicity, Mice, Platelet Endothelial Cell Adhesion Molecule-1 genetics, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Pregnancy, Receptors, N-Methyl-D-Aspartate genetics, Receptors, N-Methyl-D-Aspartate metabolism, Receptors, Vascular Endothelial Growth Factor genetics, Receptors, Vascular Endothelial Growth Factor metabolism, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Brain drug effects, Brain metabolism, Brain pathology, Ischemia physiopathology, Microcirculation, Neurotoxins pharmacology, Placenta blood supply, Regional Blood Flow physiology, Uterus blood supply
- Abstract
Vascular intrauterine growth restriction (IUGR) occurs in about 5% of pregnancies and may reduce the incidence of periventricular leukomalacia in preterm newborns. We evaluated neonatal excitotoxicity in a murine model of vascular IUGR involving unilateral uterine ligation on embryonic day (E)13.5. Birth weight was significantly decreased in the ligation group compared with the sham group (p < 0.001). VEGFs, VEGF receptors (VEGFRs), and NMDA receptor subunit mRNAs in brain extracts were assayed using quantitative RT-PCR. Ligation was associated with increased mRNAs for the vascular marker PECAM-1 on postnatal day (PD)2 and VEGFR-3 on PD2 and PD10, contrasting with decreased VEGFA and VEGFC on PD10. Microvessel density was increased on PD7. Ligated and sham pups received intracerebral ibotenate (NMDA agonist) on PD2 or PD10. Cortical and white matter (WM) lesions after 5 d were reduced in ligated versus sham pups injected on PD2 (p < 0.001 and p < 0.01, respectively); this effect persisted on PD42 (p < 0.01 and p < 0.05, respectively). With ibotenate on PD10, lesions were exacerbated after 5 d in the ligated group in the cortex (p < 0.05) and WM (p < 0.05) and on PD42 in the cortex (p < 0.05). In conclusion, vascular IUGR offered only transient protection against neonatal excitotoxic lesions, possibly via angiogenesis.
- Published
- 2011
- Full Text
- View/download PDF
37. Influence of gestational age on fibrinolysis from birth to postnatal day 10.
- Author
-
Sentilhes L, Leroux P, Radi S, Ricbourg-Schneider A, Laudenbach V, Marpeau L, Bénichou J, Vasse M, and Marret S
- Subjects
- Biomarkers, Carboxypeptidase B2 blood, Humans, Infant, Newborn, Plasminogen Activator Inhibitor 1 blood, Plasminogen Activator Inhibitor 2 blood, Tissue Plasminogen Activator blood, Fibrinolysis physiology, Gestational Age, Infant, Premature
- Abstract
Objective: To compare components of the fibrinolytic cascade in newborns of gestational age ranging from extreme prematurity to full term, at birth and for the next 10 days, and in their mothers at delivery., Study Design: We studied 10 extremely preterm neonates, 10 very preterm neonates, 10 moderately preterm neonates, 10 full-term neonates, and their mothers (n = 40). We measured the antigen levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitors 1 (PAI-1) and 2 (PAI-2), and thrombin-activatable fibrinolysis inhibitor, as well as PAI-1 activity, in neonates at birth and on postnatal days 3 and 10 and in mothers at delivery., Results: On day 10, both PAI-1 antigen and activity were higher in extremely preterm neonates than in full-term neonates (P = .004 and <.0006, respectively), and the t-PA/PAI-1 activity ratio was lower in the extremely preterm and very preterm neonates compared with the full-term neonates (P = .002 and .017, respectively). No significant differences in the fibrinolytic system components were seen among the 4 groups of mothers., Conclusions: The development of fibrinolysis suppression in extremely preterm infants within 10 days after birth may contribute to the increased risk of periventricular hemorrhagic infarction in these infants., (Copyright © 2011 Mosby, Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
38. [The Adarpef 2010 Congress: transversality was the keyword].
- Author
-
Courrèges P and Laudenbach V
- Subjects
- Cardiopulmonary Resuscitation, Critical Care standards, France, Humans, Workforce, Intensive Care Units trends, Nursing Staff statistics & numerical data
- Published
- 2010
- Full Text
- View/download PDF
39. Dual effect of glutamate on GABAergic interneuron survival during cerebral cortex development in mice neonates.
- Author
-
Desfeux A, El Ghazi F, Jégou S, Legros H, Marret S, Laudenbach V, and Gonzalez BJ
- Subjects
- 6-Cyano-7-nitroquinoxaline-2,3-dione pharmacology, Analysis of Variance, Animals, Animals, Newborn, Apoptosis drug effects, Calcium metabolism, Caspase 3 metabolism, Dizocilpine Maleate pharmacology, Dose-Response Relationship, Drug, Excitatory Amino Acid Agonists pharmacology, Excitatory Amino Acid Antagonists pharmacology, Gene Expression Regulation, Developmental drug effects, Glutamate Decarboxylase genetics, Green Fluorescent Proteins genetics, In Vitro Techniques, L-Lactate Dehydrogenase metabolism, Membrane Potential, Mitochondrial drug effects, Mice, Mice, Transgenic, N-Methylaspartate pharmacology, Necrosis chemically induced, RNA, Small Interfering pharmacology, bcl-2-Associated X Protein genetics, bcl-2-Associated X Protein metabolism, Cerebral Cortex cytology, Cerebral Cortex growth & development, Glutamic Acid pharmacology, Interneurons physiology, gamma-Aminobutyric Acid metabolism
- Abstract
In term and preterm neonates, massive glutamate release can lead to excitotoxic white-matter and cortical lesions. Because of its high permeability toward calcium, the N-methyl-D-aspartic acid (NMDA) receptor is thought to play an important role in excitotoxic lesions and NMDA antagonists therefore hold promise for neuroprotection. We found that, in neonatal mouse cortex, a given NMDA concentration exerted either excitotoxic or antiapoptotic effects depending on the cortical layers. In layer VI, NMDA led to excitotoxicity, sustained calcium mobilization, and necrosis of Gad67GFP neurons. In the immature layers II-IV, NMDA decreased apoptosis and induced transient calcium mobilization. The NMDA antagonist MK801 acted as a potent caspase-3 activator in immature layers II-IV and affected gamma aminobutyric acid (GABA)ergic interneurons. The apoptotic effect of MK801-induced BAX expression, mitochondrial potential collapse and caspase-9 activation. In vivo Bax small interfering ribonucleic acid and a caspase-9 inhibitor abrogated MK801-induced apoptosis and pyknotic nucleus formation. Ketamine, an anesthetic with NMDA antagonist properties, mimicked the apoptotic effects of MK801. These data indicate a dual effect of glutamate on survival of immature and mature GABAergic neurons and suggest that ketamine may induce apoptosis of immature GABAergic neurons.
- Published
- 2010
- Full Text
- View/download PDF
40. Vascular endothelial growth factor and its high-affinity receptor (VEGFR-2) are highly expressed in the human forebrain and cerebellum during development.
- Author
-
Sentilhes L, Michel C, Lecourtois M, Catteau J, Bourgeois P, Laudenbach V, Marret S, and Laquerrière A
- Subjects
- Cerebellum cytology, Child Development, Embryonic Development, Humans, Immunohistochemistry, Infant, Newborn, Microscopy, Confocal, Neurons metabolism, Prosencephalon cytology, Tissue Distribution, Aging metabolism, Cerebellum embryology, Cerebellum metabolism, Embryo, Mammalian metabolism, Prosencephalon embryology, Prosencephalon metabolism, Vascular Endothelial Growth Factor A metabolism, Vascular Endothelial Growth Factor Receptor-2 metabolism
- Abstract
Vascular endothelial growth factor (VEGF) is an angiogenic and neurotrophic factor in both adult and neonatal animals, but its expression and role have been incompletely studied in the developing human brain. We analyzed the distribution of VEGF and its high-affinity receptor VEGFR-2 in the human forebrain and cerebellum at developmental stages from 14 weeks' gestation (WG) to the13th postnatal month. Tissue samples free of detectable neuropathologic abnormalities were assessed by immunohistochemistry and confocal microscopy using anti-human VEGF and VEGFR-2 antibodies. The VEGFR-2 was first expressed in the whole cerebral mantle and in migrating cells in the intermediate zone, whereas VEGFwas found in superficial layers of the cortical plate, in radial glia, and in the cerebellar external germinal cell layer. From 23 WG, temporospatial VEGFR-2 expression was superimposable on that ofVEGF in the cortical plate, intermediate zone, basal ganglia, limbicstructures, and external germinal cell layer. The VEGF/VEGFR-2-positive astrocytes were observed during their generation and migration from 23 WG to the first postnatal month. The VEGF-positive mature oligodendrocytes were observed in myelinating structures in the forebrain from birth and in the cerebellum from 24WG. These data suggest that VEGF and VEGFR-2 are likely involved in several aspects of human brain development.
- Published
- 2010
- Full Text
- View/download PDF
41. [The annual congress of Adarpef].
- Author
-
Courrèges P and Laudenbach V
- Subjects
- Europe, France, Anesthesiology
- Published
- 2009
- Full Text
- View/download PDF
42. [Neuromotor outcome at 2 years of age in children born between 27 and 32 GW with periventricular leukomalacia. Retrospective 11-year study at the Rouen University Hospital].
- Author
-
Gobalakichenane P, Labarre A, Mons F, Galène-Gromez S, Laudenbach V, and Marret S
- Subjects
- Brain Damage, Chronic epidemiology, Cerebral Palsy epidemiology, Child, Preschool, Cross-Sectional Studies, Disability Evaluation, Echoencephalography, Female, Follow-Up Studies, France, Humans, Incidence, Infant, Infant, Newborn, Infant, Premature, Diseases epidemiology, Leukomalacia, Periventricular epidemiology, Pregnancy, Pregnancy Trimester, Third, Prognosis, Retrospective Studies, Risk Assessment, Brain Damage, Chronic diagnosis, Cerebral Palsy diagnosis, Infant, Low Birth Weight, Infant, Premature, Diseases diagnosis, Leukomalacia, Periventricular diagnosis
- Published
- 2009
- Full Text
- View/download PDF
43. Newborn- and adult-derived brain microvascular endothelial cells show age-related differences in phenotype and glutamate-evoked protease release.
- Author
-
Legros H, Launay S, Roussel BD, Marcou-Labarre A, Calbo S, Catteau J, Leroux P, Boyer O, Ali C, Marret S, Vivien D, and Laudenbach V
- Subjects
- Animals, Animals, Newborn, Biomarkers, Brain cytology, Brain drug effects, Cell Shape, Cells, Cultured, Endothelial Cells cytology, Endothelial Cells metabolism, Excitatory Amino Acid Transporter 2 metabolism, Gene Expression Regulation drug effects, Gene Expression Regulation genetics, Matrix Metalloproteinase 2 metabolism, Matrix Metalloproteinase 9 metabolism, Mice, Microvessels cytology, Microvessels drug effects, Microvessels metabolism, Monocarboxylic Acid Transporters metabolism, Phenotype, Protein Subunits genetics, Protein Subunits metabolism, Receptors, N-Methyl-D-Aspartate metabolism, Symporters metabolism, Tissue Culture Techniques, Aging physiology, Brain blood supply, Brain enzymology, Endothelial Cells drug effects, Endothelial Cells enzymology, Glutamic Acid pharmacology, Microvessels enzymology
- Abstract
Few data are available on the involvement of brain microvascular endothelial cells (BMECs) in excitotoxic neonatal brain lesions. Therefore, we developed an original approach for investigating mouse-derived BMECs in vitro. We hypothesized that newborn and adult BMEC cultures would show age-related differences in phenotype and sensitivity to glutamate. Expression of the monocarboxylate transporter, MCT1, was higher in neonatal than in adult BMECs, whereas expression of the glucose transporter, GLUT1, was higher in adult than in neonatal BMECs that overexpressed the N-methyl-D-aspartate receptor NR1 subunit (NMDAR1) compared with adult BMECs. The ability of neonatal and adult BMECs to be activated by glutamate was confirmed through intracellular calcium ([Ca2+]i) recording. The glutamate-induced [Ca2+]i increase was blocked by the selective NMDAR antagonist, MK-801. Significant glutamate-evoked concentration-dependent release of tissue-type plasminogen activator (t-PA) and matrix metalloproteinases (MMPs) activities was found in supernatants of neonatal, but not in adult BMECs. The glutamate-mediated release of t-PA, MMP-2, and MMP-9 proteolytic activities in neonatal BMECs was blocked by MK-801. Conceivably, this protease release from neonatal BMECs may participate in neonatal brain lesions.
- Published
- 2009
- Full Text
- View/download PDF
44. Anti-Mullerian-hormone-dependent regulation of the brain serine-protease inhibitor neuroserpin.
- Author
-
Lebeurrier N, Launay S, Macrez R, Maubert E, Legros H, Leclerc A, Jamin SP, Picard JY, Marret S, Laudenbach V, Berger P, Sonderegger P, Ali C, di Clemente N, and Vivien D
- Subjects
- Animals, Anti-Mullerian Hormone genetics, Astrocytes cytology, Astrocytes metabolism, Bone Morphogenetic Protein Receptors, Type I genetics, Bone Morphogenetic Protein Receptors, Type I metabolism, Brain cytology, Cell Survival physiology, Male, Mice, Mice, Knockout, Neurons cytology, Neuropeptides genetics, Receptors, Peptide genetics, Receptors, Transforming Growth Factor beta genetics, Serpins genetics, Smad5 Protein genetics, Smad5 Protein metabolism, Neuroserpin, Anti-Mullerian Hormone metabolism, Brain metabolism, Neurons metabolism, Neuropeptides metabolism, Receptors, Peptide metabolism, Receptors, Transforming Growth Factor beta metabolism, Serpins metabolism, Signal Transduction physiology
- Abstract
The balance between tissue-type plasminogen activator (tPA) and one of its inhibitors, neuroserpin, has crucial roles in the central nervous system, including the control of neuronal migration, neuronal plasticity and neuronal death. In the present study, we demonstrate that the activation of the transforming growth factor-beta (TGFbeta)-related BMPR-IB (also known as BMPR1B and Alk6)- and Smad5-dependent signalling pathways controls neuroserpin transcription. Accordingly, we demonstrate for the first time that anti-Mullerian hormone (AMH), a member of the TGFbeta family, promotes the expression of neuroserpin in cultured neurons but not in astrocytes. The relevance of these findings is confirmed by the presence of both AMH and AMH type-II receptor (AMHR-II) in brain tissues, and is supported by the observation of reduced levels of neuroserpin in the brain of AMHR-II-deficient mice. Interestingly, as previously demonstrated for neuroserpin, AMH protects neurons against N-methyl-D-aspartate (NMDA)-mediated excitotoxicity both in vitro and in vivo. This study demonstrates the existence of an AMH-dependent signalling pathway in the brain leading to an overexpression of the serine-protease inhibitor, neuroserpin, and neuronal survival.
- Published
- 2008
- Full Text
- View/download PDF
45. PACAP prevents toxicity induced by cisplatin in rat and primate neurons but not in proliferating ovary cells: involvement of the mitochondrial apoptotic pathway.
- Author
-
Aubert N, Vaudry D, Falluel-Morel A, Desfeux A, Fisch C, Ancian P, de Jouffrey S, Le Bigot JF, Couvineau A, Laburthe M, Fournier A, Laudenbach V, Vaudry H, and Gonzalez BJ
- Subjects
- Animals, Apoptosis drug effects, CHO Cells, Callithrix, Cell Proliferation drug effects, Cells, Cultured, Cisplatin therapeutic use, Cisplatin toxicity, Cricetinae, Cricetulus, Female, Macaca fascicularis, Male, Neurons cytology, Neurons drug effects, Organ Culture Techniques, Ovary drug effects, Rats, Rats, Wistar, Signal Transduction drug effects, Signal Transduction physiology, Apoptosis physiology, Apoptosis Regulatory Proteins physiology, Cisplatin antagonists & inhibitors, Mitochondrial Proteins physiology, Neurons physiology, Ovary cytology, Ovary physiology, Pituitary Adenylate Cyclase-Activating Polypeptide physiology
- Abstract
Cisplatin is a chemotherapeutic agent whose use is limited by side effects including neuropathies. In proliferating cells, toxic action of cisplatin is based on DNA interactions, while, in quiescent cells, it can induce apoptosis by interacting with proteins. In the present study, we compared cytotoxic mechanisms activated by cisplatin in primate and rodent neurons and in ovary cells in order to determine whether the anti-apoptotic peptide PACAP could selectively reduce neurotoxicity. In quiescent neurons, JNK and sphingomyelinase inhibitors blocked cisplatin-induced cell death. Toxicity was associated with DNA laddering, caspase-3 and -9 activations and Bax induction. These effects were prevented by PACAP. In proliferating cells, cisplatin activated caspase-8 but had no effect on caspase-9. PACAP exerted no protective effect. These data indicate that cisplatin activates distinct apoptotic pathways in quiescent neurons and proliferating cells and that PACAP may reduce neurotoxicity of cisplatin without affecting its chemotherapeutic efficacy.
- Published
- 2008
- Full Text
- View/download PDF
46. [Is it possible to protect the preterm infant brain and to decrease later neurodevelopmental disabilities?].
- Author
-
Marret S, Foix-L'hélias L, Ancel PY, Kaminski M, Larroque B, Marcou-Labarre A, and Laudenbach V
- Subjects
- Animals, Humans, Infant, Infant, Newborn, Brain Damage, Chronic prevention & control, Developmental Disabilities prevention & control, Infant, Premature, Neuroprotective Agents therapeutic use
- Abstract
With improving neonatal survival for very premature babies, the challenge for neonatalogists is to ameliorate outcome of surviving babies. Several pharmacological molecules have been shown to have protective effects in different types of in vitro or in vivo animal models of acquired cerebral brain damages. However translational research and conduction of therapeutic trials in human remain difficult due to failure to recognize start of deleterious cascade leading to cerebral damage and additional toxic effect of potential protective molecules. This review concentrates on best evidence emerging in recent years on prevention on brain damage by early drug administration. It has been shown in two randomised trials that prenatal low-dose of magnesium sulphate does not increase paediatric mortality in very-preterm infants and has non significant neuroprotective effects on occurrence of motor dysfunction (with a 0.62 odds ratio in the French trial Premag and 0.71 relative risk in the Australian trial ACTOMgSO4), justifying that magnesium sulphate should be discussed as a stand-alone treatment or as part of a combination treatment, at least in the context of clinical trials. Antenatal corticosteroid therapy increases the survival of very-preterm infants, including the most immature. Moreover in an observational recent study of the Epipage cohort, it has been observed a significant decrease in white matter injury in the 28-32 weeks' gestation group but no effect on long term outcome and behaviour. Conversely in the most immature of the 24-27 weeks' gestation group, no effect has been detected either in white matter injury incidence or in long term outcome rates. Caffeine has a protective effect since a decrease in cerebral palsy has been noted in the caffeine group in a randomised trial studying caffeine versus placebo. For what concern other widely used potential protective molecules during the perinatal period, there is no evidence of cerebral protection with indometacine, nitric oxide, eythropoietin, phenobarbital, and etamsylate. Due to their specific properties, a careful evaluation of aspirin, anaesthetic drugs and tocolytics should be done in the next months.
- Published
- 2008
- Full Text
- View/download PDF
47. Detection of Neisseria meningitidis DNA from skin lesion biopsy using real-time PCR: usefulness in the aetiological diagnosis of purpura fulminans.
- Author
-
Staquet P, Lemee L, Verdier E, Bonmarchand G, Laudenbach V, Michel C, Lemeland JF, Marret S, and Blanc T
- Subjects
- Adult, Biopsy, Blood microbiology, Child, Humans, Intensive Care Units, Intensive Care Units, Pediatric, Neisseria meningitidis genetics, Retrospective Studies, Skin chemistry, DNA, Bacterial isolation & purification, IgA Vasculitis microbiology, Neisseria meningitidis isolation & purification, Polymerase Chain Reaction methods, Skin microbiology
- Abstract
Objective: The present study evaluated the usefulness of a real-time polymerase chain reaction (rtPCR) assay for the detection of Neisseria meningitidis (Nm) and genogrouping on skin lesion biopsies in patients with purpura fulminans (PF)., Design: Retrospective single-centre study., Setting: Adult and paediatric intensive care units at the University Hospital of Rouen., Patients: All patients admitted between January 2000 and January 2006, with a final diagnosis of PF and for which a skin biopsy and blood cultures were performed, were included., Interventions: Skin biopsy and blood cultures were used for culture and rtPCR., Measurements and Main Results: Thirty-four patients fulfilled the criteria (27 children and 7 adults). Nm rtPCR performed on skin biopsy was positive in 100% (34/34) of cases, compared with only 14.7% (5/34) for skin culture (p=0.0001). rtPCR genogrouping on skin biopsy was positive in 58.8% (20/34) of the cases compared with 14.7% (5/34) for skin culture (p=0.0013). For patients (n=17) in whom rtPCR was performed both on blood and skin biopsy, skin biopsy gave a significantly higher rate of Nm detection [100% (17/17) vs. 58.8% (10/17); p=0.023] and genogroup characterisation [76.5% (13/17) vs. 35.3% (6/17); p=0.045] than blood. We encountered no specimen with culture-positive and rtPCR-negative results (negative predictive value of rtPCR 100%)., Conclusion: In suspected PF cases, skin biopsy is more reliable to identify Nm and its genogroup than blood or, probably, CSF, especially when PCR methods are used. This could help the implementation of public health interventions, especially concerning a vaccination policy.
- Published
- 2007
- Full Text
- View/download PDF
48. Neonatal hypoxic preconditioning involves vascular endothelial growth factor.
- Author
-
Laudenbach V, Fontaine RH, Medja F, Carmeliet P, Hicklin DJ, Gallego J, Leroux P, Marret S, and Gressens P
- Subjects
- Aging physiology, Alanine analogs & derivatives, Alanine pharmacology, Animals, Antibodies, Blocking pharmacology, Brain growth & development, Brain pathology, Excitatory Amino Acid Agonists, Hypoxia, Brain pathology, Ibotenic Acid, Injections, Intraperitoneal, Mice, Mice, Transgenic, Mutation physiology, Promoter Regions, Genetic genetics, Pyrimidinones pharmacology, Recombinant Proteins administration & dosage, Recombinant Proteins pharmacology, Uracil pharmacology, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A pharmacology, Vascular Endothelial Growth Factor Receptor-1 antagonists & inhibitors, Vascular Endothelial Growth Factor Receptor-2 antagonists & inhibitors, Weight Loss drug effects, Animals, Newborn physiology, Hypoxia, Brain physiopathology, Vascular Endothelial Growth Factor A physiology
- Abstract
We studied hypoxic preconditioning (HxP) in the murine developing brain, focusing on the role for vascular endothelial growth factor (VEGF). Newborn mice were used as follows: (1) HxP (or normoxia) then intracerebral (i.c.) NMDA or AMPA-kainate agonist; (2) HxP then intraperitoneal (i.p.) anti-VEGFR2/Flk1 or anti-VEGFR1/Flt1 monoclonal blocking antibody (mAb) then i.c. NMDA/AMPA-kainate agonist; (3) i.p. VEGF then i.c. NMDA/AMPA-kainate agonist; and (4) in mutants lacking the hypoxia-responsive element (HRE) of the VEGF-A gene (VEGF( partial differential/ partial differential)) and their wild-type littermates (VEGF(+/+)), HxP followed by i.c. NMDA agonist. HxP reduced the size of NMDA-related cortical and AMPA-kainate-related cortical and white matter excitotoxic lesions. Anti-VEGFR2/Flk1 mAb prevented HxP-induced neuroprotection. VEGF produced dose-dependent reduction in cortical lesions. HxP did not prevent, but instead exacerbated, brain lesions in VEGF( partial differential/ partial differential) mutants. Thus, exogenous as well as endogenous VEGF reduces excitotoxic brain lesions in the developing mouse. The VEGF/VEGFR2/Flk1 pathway is involved in the neuroprotective response to HxP.
- Published
- 2007
- Full Text
- View/download PDF
49. [Early spontaneous ileal perforations in preterm infants: report of 4 cases].
- Author
-
Arsac M, Devaux AM, Blanc T, Pinquier D, Bachy B, Adde C, Staquet P, Marret S, and Laudenbach V
- Subjects
- Diagnosis, Differential, Humans, Ileal Diseases diagnosis, Infant, Newborn, Intestinal Perforation diagnosis, Prognosis, Risk Factors, Ileal Diseases pathology, Infant, Premature, Intestinal Perforation pathology
- Abstract
An ileal perforation occurred shortly after birth in 4 very premature newborns. Diagnosis was made on an abdominal distension with a pneumoperitoneum on X-ray. There were no biological, radiological nor histological signs of necrotizing enterocolitis. There were no digestive short- or long-term complications. According to the few authors who described this syndrome, there are some risk factors, but they were not clearly involved in our cases. Ileal perforation in the absence of signs of necrotizing enterocolitis is rarely reported but should be well known because of its good prognosis.
- Published
- 2005
- Full Text
- View/download PDF
50. Effect of acamprosate on neonatal excitotoxic cortical lesions in in utero alcohol-exposed hamsters.
- Author
-
Adde-Michel C, Hennebert O, Laudenbach V, Marret S, and Leroux P
- Subjects
- Acamprosate, Animals, Animals, Newborn, Central Nervous System Depressants adverse effects, Cerebral Cortex injuries, Cerebral Cortex pathology, Cricetinae, Dose-Response Relationship, Drug, Drug Interactions, Female, Ibotenic Acid toxicity, Male, Pregnancy, Alcohol Deterrents pharmacology, Cerebral Cortex drug effects, Ethanol adverse effects, Prenatal Exposure Delayed Effects, Taurine analogs & derivatives, Taurine pharmacology
- Abstract
Alcohol exposition during pregnancy has irreversible effects on the fetus brain. In hamsters, intrapallial injection of the glutamate receptor agonist ibotenic acid (100ng) on the day of birth (P0) induced neuronal migration disorders. In utero alcohol (7%) exposure from day 5 of gestation to P5, enhanced lesions size measured in pups' brain at P5. The administration for the same period of the taurine derivative acamprosate together with alcohol or in water to pregnant females reduced the rate of occurrence of nodular heterotopia, sub-pial ectopia and microgyria in non-alcohol-exposed pups. In addition acamprosate diminished lesion size in alcohol-exposed and non-exposed pups. A significant dose-related effect of acamprosate was observed. In addition, acamprosate rescued 27% of the pups injected with 10 microg ibotenic acid, a lethal dose in alcohol-exposed animals.
- Published
- 2005
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.