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Article ; Online: Pituitary stalk interruption syndrome: diagnostic delay and sensitivity of the auxological criteria of the growth hormone research society.

Gascoin-Lachambre, Géraldine / Brauner, Raja / Duche, Laetitia / Chalumeau, Martin

PloS one

2011 Volume 6, Issue 1, Page(s) e16367

Abstract: Objectives: To study the diagnostic delay for pituitary stalk interruption syndrome (PSIS) with growth hormone deficiency (GHD) and the sensitivity of the auxological criteria of the Growth Hormone Research Society (GHRS) consensus guidelines.: ... ...

Abstract	Objectives: To study the diagnostic delay for pituitary stalk interruption syndrome (PSIS) with growth hormone deficiency (GHD) and the sensitivity of the auxological criteria of the Growth Hormone Research Society (GHRS) consensus guidelines. Methods: A single-center retrospective case-cohort study covering records from January 2000 through December 2007 evaluated the performance of each GHRS auxological criterion for patients with GHD and PSIS. Diagnostic delay was calculated as the difference between the age at which the earliest GHRS criterion could have been observed and the age at diagnosis of PSIS with GHD. A diagnostic delay exceeding one year was defined as late diagnosis. Results: The study included 21 patients, 16 (76%) of whom had isolated GHD and 5 (24%) multiple pituitary hormone deficiencies. The median age at diagnosis was 3.6 years (interquartile range, IQR, 2.6-5.5). The median diagnostic delay was 2.3 years (range 0-12.6; IQR 1.5-3.6), with late diagnosis for 17 patients (81%). Height more than 1.5 SDS below target height was the most effective criterion: 90% of the patients met the criterion before diagnosis at a median age of 1 year, and it was the first criterion to be fulfilled for 84%. Conclusion: In our cohort, the delay for diagnosis of PSIS with GHD was long and could have been reduced by using the GHRS criteria, in particular, height more than 1.5 SDS below the target height. The specificity of such a strategy needs to be tested in healthy populations.
MeSH term(s)	Body Height ; Child, Preschool ; Dwarfism, Pituitary/diagnosis ; Guidelines as Topic ; Humans ; Hypopituitarism ; Pituitary Gland ; Retrospective Studies
Language	English
Publishing date	2011-01-27
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0016367
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Implementation of an antenatal magnesium sulfate protocol for fetal neuroprotection in preterm infants.

Bouet, Pierre-Emmanuel / Brun, Stéphanie / Madar, Hugo / Baisson, Anne-Laure / Courtay, Véronique / Gascoin-Lachambre, Géraldine / Lasocki, Sigismond / Sentilhes, Loïc

Scientific reports

2015 Volume 5, Page(s) 14732

Abstract: The aim of our study was to assess the feasibility of implementing a protocol for the use of magnesium sulfate to prevent cerebral palsy. This retrospective single-center study included all women with fetuses of gestational age <33 weeks of gestation ... ...

Abstract	The aim of our study was to assess the feasibility of implementing a protocol for the use of magnesium sulfate to prevent cerebral palsy. This retrospective single-center study included all women with fetuses of gestational age <33 weeks of gestation whose birth was planned or expected within 24 hours from September 2011 to December 2012. They were to receive magnesium sulfate, administered intravenously as a 4-g bolus followed by a constant infusion of 1 g per hour. If delivery had not occurred after 12 hours and was no longer considered imminent, the infusion was to be discontinued. The study included 119 women, 81 (68.1%) of whom received magnesium sulfate. Among the latter, 71 (87.5%) gave birth within 24 hours. The reasons treatment was not given were: omission by medical team (19/38, 50%), urgent delivery (18/38, 47.4%), and contraindication to treatment (1/38, 2.6%). The mean gestational age at protocol implementation was 29.6 +/- 2.1 weeks. Maternal monitoring, especially at the onset of infusion, appeared suboptimal. No major maternal side effects were observed. Our study shows that implementing a protocol for prevention of cerebral palsy by magnesium sulfate is feasible in a tertiary obstetric center.
MeSH term(s)	Adult ; Cerebral Palsy/physiopathology ; Cerebral Palsy/prevention & control ; Drug Administration Schedule ; Female ; Gestational Age ; Humans ; Infant, Newborn ; Infant, Premature ; Magnesium Sulfate/therapeutic use ; Monitoring, Physiologic ; Neuroprotective Agents/therapeutic use ; Obstetric Labor, Premature/physiopathology ; Pregnancy ; Retrospective Studies ; Tertiary Care Centers
Chemical Substances	Neuroprotective Agents ; Magnesium Sulfate (7487-88-9)
Language	English
Publishing date	2015-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep14732
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Pituitary stalk interruption syndrome

Géraldine Gascoin-Lachambre / Raja Brauner / Laetitia Duche / Martin Chalumeau

PLoS ONE, Vol 6, Iss 1, p e

diagnostic delay and sensitivity of the auxological criteria of the growth hormone research society.

2011 Volume 16367

Abstract: OBJECTIVES: To study the diagnostic delay for pituitary stalk interruption syndrome (PSIS) with growth hormone deficiency (GHD) and the sensitivity of the auxological criteria of the Growth Hormone Research Society (GHRS) consensus guidelines. METHODS: A ...

Abstract	OBJECTIVES: To study the diagnostic delay for pituitary stalk interruption syndrome (PSIS) with growth hormone deficiency (GHD) and the sensitivity of the auxological criteria of the Growth Hormone Research Society (GHRS) consensus guidelines. METHODS: A single-center retrospective case-cohort study covering records from January 2000 through December 2007 evaluated the performance of each GHRS auxological criterion for patients with GHD and PSIS. Diagnostic delay was calculated as the difference between the age at which the earliest GHRS criterion could have been observed and the age at diagnosis of PSIS with GHD. A diagnostic delay exceeding one year was defined as late diagnosis. RESULTS: The study included 21 patients, 16 (76%) of whom had isolated GHD and 5 (24%) multiple pituitary hormone deficiencies. The median age at diagnosis was 3.6 years (interquartile range, IQR, 2.6-5.5). The median diagnostic delay was 2.3 years (range 0-12.6; IQR 1.5-3.6), with late diagnosis for 17 patients (81%). Height more than 1.5 SDS below target height was the most effective criterion: 90% of the patients met the criterion before diagnosis at a median age of 1 year, and it was the first criterion to be fulfilled for 84%. CONCLUSION: In our cohort, the delay for diagnosis of PSIS with GHD was long and could have been reduced by using the GHRS criteria, in particular, height more than 1.5 SDS below the target height. The specificity of such a strategy needs to be tested in healthy populations.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genetic and epigenetic mechanisms collaborate to control SERPINA3 expression and its association with placental diseases.

Chelbi, Sonia T / Wilson, Melissa L / Veillard, Anne-Clémence / Ingles, Sue A / Zhang, Jim / Mondon, Françoise / Gascoin-Lachambre, Géraldine / Doridot, Ludivine / Mignot, Thérèse-Marie / Rebourcet, Régis / Carbonne, Bruno / Concordet, Jean-Paul / Barbaux, Sandrine / Vaiman, Daniel

Human molecular genetics

2012 Volume 21, Issue 9, Page(s) 1968–1978

Abstract: SERPINA3 (Serpin peptidase inhibitor clade A member 3), also known as a1-antichymotrypsin, is a serine protease inhibitor involved in a wide range of biological processes. Recently, it has been shown to be up-regulated in human placental diseases in ... ...

Abstract	SERPINA3 (Serpin peptidase inhibitor clade A member 3), also known as a1-antichymotrypsin, is a serine protease inhibitor involved in a wide range of biological processes. Recently, it has been shown to be up-regulated in human placental diseases in association with a hypomethylation of the 5' region of the gene. In the present study, we show that the promoter of SERPINA3 is transcriptionally activated by three transcription factors (TFs) (SP1, MZF1 and ZBTB7B), the level of induction being dependent on the rs1884082 single nucleotide polymorphism (SNP) located inside the promoter, the T allele being consistently induced to a higher level than the G, with or without added TFs. When the promoter was methylated, the response to ZBTB7B was allele specific (the G allele was strongly induced, while the T allele was strongly down-regulated). We propose an adaptive model to explain the interest of such a regulation for placental function and homeostasis. Overexpression of SERPINA3 in JEG-3 cells, a trophoblast cell model, decreased cell adhesion to the extracellular matrix and to neighboring cells, but protects them from apoptosis, suggesting a way by which this factor could be deleterious at high doses. In addition, we show in different human populations that the T allele appears to predispose to Intra Uterine Growth Restriction (IUGR), while a G allele at a second SNP located in the second exon (rs4634) increases the risk of preeclampsia. Our results provide mechanistic views inside the involvement of SERPINA3 in placental diseases, through its regulation by a combination of epigenetic, genetic and TF-mediated regulations.
MeSH term(s)	Alleles ; Apoptosis ; Base Sequence ; Case-Control Studies ; Cell Adhesion ; Cell Line ; DNA Methylation ; DNA-Binding Proteins/metabolism ; Epigenesis, Genetic ; Female ; Fetal Growth Retardation/genetics ; Fetal Growth Retardation/metabolism ; Gene Expression Regulation ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Hypoxia/genetics ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Kruppel-Like Transcription Factors/metabolism ; Models, Biological ; Placenta Diseases/genetics ; Placenta Diseases/metabolism ; Polymorphism, Single Nucleotide ; Pre-Eclampsia/genetics ; Pre-Eclampsia/metabolism ; Pregnancy ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Serpins/genetics ; Sp1 Transcription Factor/metabolism ; Transcription Factors/metabolism ; Transcriptional Activation ; Trophoblasts/cytology ; Trophoblasts/metabolism ; Zinc Fingers
Chemical Substances	DNA-Binding Proteins ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Kruppel-Like Transcription Factors ; MZF1 protein, human ; RNA, Messenger ; SERPINA3 protein, human ; Serpins ; Sp1 Transcription Factor ; Transcription Factors ; ZBTB7B protein, human
Language	English
Publishing date	2012-05-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/dds006
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The intensity of IUGR-induced transcriptome deregulations is inversely correlated with the onset of organ function in a rat model.

Vaiman, Daniel / Gascoin-Lachambre, Géraldine / Boubred, Farid / Mondon, Françoise / Feuerstein, Jean-Marc / Ligi, Isabelle / Grandvuillemin, Isabelle / Barbaux, Sandrine / Ghigo, Eric / Achard, Vincent / Simeoni, Umberto / Buffat, Christophe

PloS one

2011 Volume 6, Issue 6, Page(s) e21222

Abstract: A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult ...

Abstract	A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult metabolic anomalies, such as diabetes and cardiovascular disease. Development and function of many organs are affected by environmental conditions such as those inducing fetal and early postnatal growth restriction. This phenomenon, termed "fetal programming" has been studied unconnectedly in some organs, but very few studies (if any) have investigated at the same time several organs, on a more comparative basis. However, it is quite probable that IUGR affects differentially most organ systems, with possible persistent changes in gene expression. In this study we address transcriptional alterations induced by IUGR in a multi-organ perspective, by systematic analysis of 20-days rat fetuses. We show that (1) expressional alterations are apparently stronger in organs functioning late in foetal or postnatal life than in organs that are functioning early (2) hierarchical classification of the deregulations put together kidney and placenta in one cluster, liver, lungs and heart in another; (3) the epigenetic machinery is set up especially in the placenta, while its alterations are rather mild in other organs; (4) the genes appear deregulated in chromosome clusters; (5) the altered expression cascades varies from organ to organ, with noticeably a very significant modification of the complement and coagulation cascades in the kidney; (6) we found a significant increase in TF binding site for HNF4 proteins specifically for liver genes that are down-regulated in IUGR, suggesting that this decrease is achieved through the action of HNF transcription factors, that are themselves transcriptionnally induced in the liver by IUGR (x 1.84 fold). Altogether, our study suggests that a combination of tissue-specific mechanisms contributes to bring about tissue-driven modifications of gene cascades. The question of these cascades being activated to adapt the organ to harsh environmental condition, or as an endpoint consequence is still raised.
MeSH term(s)	Animals ; Chromosomes, Mammalian/genetics ; Cluster Analysis ; Disease Models, Animal ; Down-Regulation/genetics ; Epigenesis, Genetic ; Female ; Fetal Growth Retardation/genetics ; Fetal Growth Retardation/physiopathology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genomic Imprinting/genetics ; Organ Specificity/genetics ; Pregnancy ; Promoter Regions, Genetic/genetics ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/genetics ; Stress, Physiological/genetics
Language	English
Publishing date	2011-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0021222
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Combination of promoter hypomethylation and PDX1 overexpression leads to TBX15 decrease in vascular IUGR placentas.

Chelbi, Sonia T / Doridot, Ludivine / Mondon, Françoise / Dussour, Chloé / Rebourcet, Régis / Busato, Florence / Gascoin-Lachambre, Géraldine / Barbaux, Sandrine / Rigourd, Virginie / Mignot, Thérèse-Marie / Tost, Jörg / Vaiman, Daniel

Epigenetics

2011 Volume 6, Issue 2, Page(s) 247–255

Abstract: Preeclampsia (PE) and vascular intra-uterine growth restriction (vIUGR) are two pathological obstetrical conditions originating from placental dysfunction. Recently, methylation changes at the placental level have been shown to be indicative of these ... ...

Abstract	Preeclampsia (PE) and vascular intra-uterine growth restriction (vIUGR) are two pathological obstetrical conditions originating from placental dysfunction. Recently, methylation changes at the placental level have been shown to be indicative of these diseases. The alteration of such epigenetic marks is therefore a novel pathway that might be critical for these pathologies. Here, we identified a region located in the distal promoter of the T-box-containing transcription factor TBX15 that is differentially methylated in pathological placentas. The level of methylation correlated significantly with the weight and stature of the newborn. The promoter was found to be hypomethylated in vIUGR coinciding with the down-regulation of its expression. PDX1, a transcription factor important for the regulation of insulin metabolism regulation was able to repress the TBX15 promoter in a methylation-dependent manner, which might, at least partially, explain the specific mRNA decrease of TBX15 observed in vIUGR placentas. Overall, the data presented herein suggest that TBX15 might be involved in the pathophysiology of placental diseases.
MeSH term(s)	Adult ; Base Sequence ; Cell Line ; DNA Methylation/genetics ; Epigenomics ; Female ; Fetal Growth Retardation/genetics ; Gene Expression/genetics ; Homeodomain Proteins/genetics ; Humans ; Infant, Newborn ; Molecular Sequence Data ; Placenta/metabolism ; Placenta Diseases/genetics ; Pre-Eclampsia/genetics ; Pregnancy ; Promoter Regions, Genetic/genetics ; T-Box Domain Proteins/genetics ; Trans-Activators/genetics
Chemical Substances	Homeodomain Proteins ; T-Box Domain Proteins ; TBX15 protein, human ; Trans-Activators ; pancreatic and duodenal homeobox 1 protein
Language	English
Publishing date	2011-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.4161/epi.6.2.13791
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A genome-wide approach reveals novel imprinted genes expressed in the human placenta.

Barbaux, Sandrine / Gascoin-Lachambre, Géraldine / Buffat, Christophe / Monnier, Paul / Mondon, Françoise / Tonanny, Marie-Béatrice / Pinard, Amélie / Auer, Jana / Bessières, Bettina / Barlier, Anne / Jacques, Sébastien / Simeoni, Umberto / Dandolo, Luisa / Letourneur, Franck / Jammes, Helene / Vaiman, Daniel

Epigenetics

2012 Volume 7, Issue 9, Page(s) 1079–1090

Abstract: Genomic imprinting characterizes genes with a monoallelic expression, which is dependent on the parental origin of each allele. Approximately 150 imprinted genes are known to date, in humans and mice but, though computational searches have tried to ... ...

Abstract	Genomic imprinting characterizes genes with a monoallelic expression, which is dependent on the parental origin of each allele. Approximately 150 imprinted genes are known to date, in humans and mice but, though computational searches have tried to extract intrinsic characteristics of these genes to identify new ones, the existing list is probably far from being comprehensive. We used a high-throughput strategy by diverting the classical use of genotyping microarrays to compare the genotypes of mRNA/cDNA vs. genomic DNA to identify new genes presenting monoallelic expression, starting from human placental material. After filtering of data, we obtained a list of 1,082 putative candidate monoallelic SNPs located in more than one hundred candidate genes. Among these, we found known imprinted genes, such as IPW, GRB10, INPP5F and ZNF597, which contribute to validate the approach. We also explored some likely candidates of our list and identified seven new imprinted genes, including ZFAT, ZFAT-AS1, GLIS3, NTM, MAGI2, ZC3H12Cand LIN28B, four of which encode zinc finger transcription factors. They are, however, not imprinted in the mouse placenta, except for Magi2. We analyzed in more details the ZFAT gene, which is paternally expressed in the placenta (as ZFAT-AS1, a non-coding antisense RNA) but biallelic in other tissues. The ZFAT protein is expressed in endothelial cells, as well as in syncytiotrophoblasts. The expression of this gene is, moreover, downregulated in placentas from complicated pregnancies. With this work we increase by about 10% the number of known imprinted genes in humans.
MeSH term(s)	Animals ; Cattle ; Female ; Gene Expression Profiling ; Genetic Loci ; Genome, Human/genetics ; Genomic Imprinting/genetics ; Humans ; Mice ; Mice, Inbred C57BL ; Oligonucleotide Array Sequence Analysis ; Placenta/metabolism ; Polymorphism, Single Nucleotide ; Pregnancy ; RNA, Messenger/biosynthesis ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	RNA, Messenger ; Transcription Factors ; ZFAT protein, human
Language	English
Publishing date	2012-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.4161/epi.21495
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The intensity of IUGR-induced transcriptome deregulations is inversely correlated with the onset of organ function in a rat model.

Daniel Vaiman / Géraldine Gascoin-Lachambre / Farid Boubred / Françoise Mondon / Jean-Marc Feuerstein / Isabelle Ligi / Isabelle Grandvuillemin / Sandrine Barbaux / Eric Ghigo / Vincent Achard / Umberto Simeoni / Christophe Buffat

PLoS ONE, Vol 6, Iss 6, p e

2011 Volume 21222

Abstract	A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult metabolic anomalies, such as diabetes and cardiovascular disease. Development and function of many organs are affected by environmental conditions such as those inducing fetal and early postnatal growth restriction. This phenomenon, termed "fetal programming" has been studied unconnectedly in some organs, but very few studies (if any) have investigated at the same time several organs, on a more comparative basis. However, it is quite probable that IUGR affects differentially most organ systems, with possible persistent changes in gene expression. In this study we address transcriptional alterations induced by IUGR in a multi-organ perspective, by systematic analysis of 20-days rat fetuses. We show that (1) expressional alterations are apparently stronger in organs functioning late in foetal or postnatal life than in organs that are functioning early (2) hierarchical classification of the deregulations put together kidney and placenta in one cluster, liver, lungs and heart in another; (3) the epigenetic machinery is set up especially in the placenta, while its alterations are rather mild in other organs; (4) the genes appear deregulated in chromosome clusters; (5) the altered expression cascades varies from organ to organ, with noticeably a very significant modification of the complement and coagulation cascades in the kidney; (6) we found a significant increase in TF binding site for HNF4 proteins specifically for liver genes that are down-regulated in IUGR, suggesting that this decrease is achieved through the action of HNF transcription factors, that are themselves transcriptionnally induced in the liver by IUGR (x 1.84 fold). Altogether, our study suggests that a combination of tissue-specific mechanisms contributes to bring about tissue-driven modifications ...
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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