Correction to: Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder / Andrew W. ZIMMERMAN in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 44 p. Titre : Correction to: Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder Type de document : texte imprimé Auteurs : Andrew W. ZIMMERMAN, Auteur ; Kanwaljit SINGH, Auteur ; Susan L. CONNORS, Auteur ; Hua LIU, Auteur ; Anita A PANJWANI, Auteur ; Li-Ching LEE, Auteur ; Eileen DIGGINS, Auteur ; Ann FOLEY, Auteur ; Stepan MELNYK, Auteur ; Indrapal N. SINGH, Auteur ; S. Jill JAMES, Auteur ; Richard E. FRYE, Auteur ; Jed W. FAHEY, Auteur Article en page(s) : 44 p. Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1186/s13229-021-00451-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 [article] Correction to: Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder [texte imprimé] / Andrew W. ZIMMERMAN, Auteur ; Kanwaljit SINGH, Auteur ; Susan L. CONNORS, Auteur ; Hua LIU, Auteur ; Anita A PANJWANI, Auteur ; Li-Ching LEE, Auteur ; Eileen DIGGINS, Auteur ; Ann FOLEY, Auteur ; Stepan MELNYK, Auteur ; Indrapal N. SINGH, Auteur ; S. Jill JAMES, Auteur ; Richard E. FRYE, Auteur ; Jed W. FAHEY, Auteur . - 44 p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 44 p. Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1186/s13229-021-00451-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459

Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress / Patrick M. HECHT in Autism Research, 9-11 (November 2016)  

Public ISBD [article]  inAutism Research > 9-11 (November 2016) . - p.1151-1160 Titre : Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress Type de document : texte imprimé Auteurs : Patrick M. HECHT, Auteur ; Melissa HUDSON, Auteur ; Susan L. CONNORS, Auteur ; Michael R. TILLEY, Auteur ; Xudong LIU, Auteur ; David Q. BEVERSDORF, Auteur Article en page(s) : p.1151-1160 Langues : Anglais (eng) Mots-clés : autism spectrum disorders  serotonin  stress  prenatal stress  development  environmental influences Index. décimale : PER Périodiques Résumé : Stress exposure during gestation is implicated in several neuropsychiatric conditions, including autism spectrum disorder (ASD). Previous research showed that prenatal stress increases risk for ASD with peak exposure during the end of the second and the beginning of the third trimester. However, exposures to prenatal stress do not always result in ASD, suggesting that other factors may interact with environmental stressors to increase ASD risk. The present study examined a maternal genetic variation in the promoter region of the serotonin transporter gene (5-HTTLPR) affecting stress tolerance and its interaction with the effect of environmental stressors on risk for ASD. Two independent cohorts of mothers of ASD children recruited by the University of Missouri and Queen's University were surveyed regarding the prenatal environment and genotyping on 5-HTTLPR was performed to explore this relationship. In both samples, mothers of children with ASD carrying the stress susceptible short allele variant of 5-HTTLPR experienced a greater number of stressors and greater stress severity when compared to mothers carrying the long allele variant. The temporal peak of stressors during gestation in these mothers was consistent with previous findings. Additionally, increased exposure to prenatal stress was not reported in the pregnancies of typically developing siblings from the same mothers, regardless of maternal genotype, suggesting against the possibility that the short allele might increase the recall of stress during pregnancy. The present study provides further evidence of a specific maternal polymorphism that may affect the risk for ASD with exposure to prenatal stress. En ligne : http://dx.doi.org/10.1002/aur.1629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=297 [article] Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress [texte imprimé] / Patrick M. HECHT, Auteur ; Melissa HUDSON, Auteur ; Susan L. CONNORS, Auteur ; Michael R. TILLEY, Auteur ; Xudong LIU, Auteur ; David Q. BEVERSDORF, Auteur . - p.1151-1160. Langues : Anglais (eng) in Autism Research > 9-11 (November 2016) . - p.1151-1160 Mots-clés : autism spectrum disorders  serotonin  stress  prenatal stress  development  environmental influences Index. décimale : PER Périodiques Résumé : Stress exposure during gestation is implicated in several neuropsychiatric conditions, including autism spectrum disorder (ASD). Previous research showed that prenatal stress increases risk for ASD with peak exposure during the end of the second and the beginning of the third trimester. However, exposures to prenatal stress do not always result in ASD, suggesting that other factors may interact with environmental stressors to increase ASD risk. The present study examined a maternal genetic variation in the promoter region of the serotonin transporter gene (5-HTTLPR) affecting stress tolerance and its interaction with the effect of environmental stressors on risk for ASD. Two independent cohorts of mothers of ASD children recruited by the University of Missouri and Queen's University were surveyed regarding the prenatal environment and genotyping on 5-HTTLPR was performed to explore this relationship. In both samples, mothers of children with ASD carrying the stress susceptible short allele variant of 5-HTTLPR experienced a greater number of stressors and greater stress severity when compared to mothers carrying the long allele variant. The temporal peak of stressors during gestation in these mothers was consistent with previous findings. Additionally, increased exposure to prenatal stress was not reported in the pregnancies of typically developing siblings from the same mothers, regardless of maternal genotype, suggesting against the possibility that the short allele might increase the recall of stress during pregnancy. The present study provides further evidence of a specific maternal polymorphism that may affect the risk for ASD with exposure to prenatal stress. En ligne : http://dx.doi.org/10.1002/aur.1629 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=297

Prenatal β2-Adrenergic Receptor Signaling and Autism : Dysmaturation and Retained Fetal Function / Susan L. CONNORS

Public ISBD contenu dans Autism / Andrew W. ZIMMERMAN Titre : Prenatal β2-Adrenergic Receptor Signaling and Autism : Dysmaturation and Retained Fetal Function Type de document : texte imprimé Auteurs : Susan L. CONNORS, Auteur Année de publication : 2008 Importance : p.147-182 Langues : Anglais (eng) Mots-clés : Récepteur adrénergique  prenatalité  Foetal  Polymorphie  Adénylate cyclase  cAMP Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=704 contenu dans Autism / Andrew W. ZIMMERMAN Prenatal β2-Adrenergic Receptor Signaling and Autism : Dysmaturation and Retained Fetal Function [texte imprimé] / Susan L. CONNORS, Auteur . - 2008 . - p.147-182. Langues : Anglais (eng) Mots-clés : Récepteur adrénergique  prenatalité  Foetal  Polymorphie  Adénylate cyclase  cAMP Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=704

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Prenatal exposure to beta2-adrenergic receptor agonists and risk of autism spectrum disorders / Lisa A. CROEN in Journal of Neurodevelopmental Disorders, 3-4 (December 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-4 (December 2011) . - p.307-15 Titre : Prenatal exposure to beta2-adrenergic receptor agonists and risk of autism spectrum disorders Type de document : texte imprimé Auteurs : Lisa A. CROEN, Auteur ; Susan L. CONNORS, Auteur ; Marilyn MATEVIA, Auteur ; Yinge QIAN, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Andrew W. ZIMMERMAN, Auteur Article en page(s) : p.307-15 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This study aims to investigate the association between prenatal exposure to terbutaline and other beta2 adrenergic receptor (B2AR) agonists and autism spectrum disorders (ASDs). The methodology used is a case-control study among children born from 1995 to 1999 at Kaiser Permanente Northern California hospitals. Cases (n = 291) were children with an ASD diagnosis; controls (n = 284) were children without ASDs, randomly sampled and frequency-matched to cases on sex, birth year, and delivery hospital. Exposure to B2AR agonists during 30 days prior to conception and each trimester of pregnancy was ascertained from prenatal medical records and health plan databases. The frequency of exposure to any B2AR agonist during pregnancy was similar for mothers of children with ASD and mothers of controls (18.9% vs. 14.8%, P = 0.19). Exposure to B2AR agonists other than terbutaline was not associated with an increased risk for ASDs. However, terbutaline exposure for >2 days during the third trimester was associated with more than a fourfold increased risk for ASDs independent of indication although the limited sample size resulted in an imprecise and nonsignificant effect estimate (OR(adj) = 4.4; 95% confidence interval, 0.8-24.6). This analysis does not offer evidence linking B2AR exposure in pregnancy with autism risk. However, exposure to terbutaline during the third trimester for >2 days may be associated with an increased risk of autism. Should this result be confirmed in larger samples, it would point to late pregnancy as an etiologic window of interest in autism risk factor research. En ligne : http://dx.doi.org/10.1007/s11689-011-9093-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Prenatal exposure to beta2-adrenergic receptor agonists and risk of autism spectrum disorders [texte imprimé] / Lisa A. CROEN, Auteur ; Susan L. CONNORS, Auteur ; Marilyn MATEVIA, Auteur ; Yinge QIAN, Auteur ; Craig J. NEWSCHAFFER, Auteur ; Andrew W. ZIMMERMAN, Auteur . - p.307-15. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-4 (December 2011) . - p.307-15 Index. décimale : PER Périodiques Résumé : This study aims to investigate the association between prenatal exposure to terbutaline and other beta2 adrenergic receptor (B2AR) agonists and autism spectrum disorders (ASDs). The methodology used is a case-control study among children born from 1995 to 1999 at Kaiser Permanente Northern California hospitals. Cases (n = 291) were children with an ASD diagnosis; controls (n = 284) were children without ASDs, randomly sampled and frequency-matched to cases on sex, birth year, and delivery hospital. Exposure to B2AR agonists during 30 days prior to conception and each trimester of pregnancy was ascertained from prenatal medical records and health plan databases. The frequency of exposure to any B2AR agonist during pregnancy was similar for mothers of children with ASD and mothers of controls (18.9% vs. 14.8%, P = 0.19). Exposure to B2AR agonists other than terbutaline was not associated with an increased risk for ASDs. However, terbutaline exposure for >2 days during the third trimester was associated with more than a fourfold increased risk for ASDs independent of indication although the limited sample size resulted in an imprecise and nonsignificant effect estimate (OR(adj) = 4.4; 95% confidence interval, 0.8-24.6). This analysis does not offer evidence linking B2AR exposure in pregnancy with autism risk. However, exposure to terbutaline during the third trimester for >2 days may be associated with an increased risk of autism. Should this result be confirmed in larger samples, it would point to late pregnancy as an etiologic window of interest in autism risk factor research. En ligne : http://dx.doi.org/10.1007/s11689-011-9093-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder / Andrew W. ZIMMERMAN in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 38 p. Titre : Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder Type de document : texte imprimé Auteurs : Andrew W. ZIMMERMAN, Auteur ; Kanwaljit SINGH, Auteur ; Susan L. CONNORS, Auteur ; Hua LIU, Auteur ; Anita A PANJWANI, Auteur ; Li-Ching LEE, Auteur ; Eileen DIGGINS, Auteur ; Ann FOLEY, Auteur ; Stepan MELNYK, Auteur ; Indrapal N. SINGH, Auteur ; S. Jill JAMES, Auteur ; Richard E. FRYE, Auteur ; Jed W. FAHEY, Auteur Article en page(s) : 38 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder (ASD)  Biomarkers  Clinical trial  Placebo effects  Sulforaphane  defendants in matters related to pediatric neurology and Autism Spectrum Disorder.  JWF retired from the full-time faculty at Johns Hopkins in mid-2020, and now serves  as a scientific advisor to Brassica Protection Products LLC (Baltimore, MD, USA),  which produces a glucoraphanin-rich broccoli seed extract that it supplies to the  supplement industry. AWZ is named on a patent on the use of sulforaphane for the  treatment of autism that has been assigned to Johns Hopkins University. Index. décimale : PER Périodiques Résumé : BACKGROUND: Sulforaphane (SF), an isothiocyanate in broccoli, has potential benefits relevant to autism spectrum disorder (ASD) through its effects on several metabolic and immunologic pathways. Previous clinical trials of oral SF demonstrated positive clinical effects on behavior in young men and changes in urinary metabolomics in children with ASD. METHODS: We conducted a 15-week randomized parallel double-blind placebo-controlled clinical trial with 15-week open-label treatment and 6-week no-treatment extensions in 57 children, ages 3-12 years, with ASD over 36 weeks. Twenty-eight were assigned SF and 29 received placebo (PL). Clinical effects, safety and tolerability of SF were measured as were biomarkers to elucidate mechanisms of action of SF in ASD. RESULTS: Data from 22 children taking SF and 23 on PL were analyzed. Treatment effects on the primary outcome measure, the Ohio Autism Clinical Impressions Scale (OACIS), in the general level of autism were not significant between SF and PL groups at 7 and 15 weeks. The effect sizes on the OACIS were non-statistically significant but positive, suggesting a possible trend toward greater improvement in those on treatment with SF (Cohen's d 0.21; 95% CI - 0.46, 0.88 and 0.10; 95% CI - 0.52, 0.72, respectively). Both groups improved in all subscales when on SF during the open-label phase. Caregiver ratings on secondary outcome measures improved significantly on the Aberrant Behavior Checklist (ABC) at 15 weeks (Cohen's d - 0.96; 95% CI - 1.73, - 0.15), but not on the Social Responsiveness Scale-2 (SRS-2). Ratings on the ABC and SRS-2 improved with a non-randomized analysis of the length of exposure to SF, compared to the pre-treatment baseline (p < 0.001). There were significant changes with SF compared to PL in biomarkers of glutathione redox status, mitochondrial respiration, inflammatory markers and heat shock proteins. Clinical laboratory studies confirmed product safety. SF was very well tolerated and side effects of treatment, none serious, included rare insomnia, irritability and intolerance of the taste and smell. LIMITATIONS: The sample size was limited to 45 children with ASD and we did not impute missing data. We were unable to document significant changes in clinical assessments during clinical visits in those taking SF compared to PL. The clinical results were confounded by placebo effects during the open-label phase. CONCLUSIONS: SF led to small yet non-statistically significant changes in the total and all subscale scores of the primary outcome measure, while for secondary outcome measures, caregivers' assessments of children taking SF showed statistically significant improvements compared to those taking PL on the ABC but not the SRS-2. Clinical effects of SF were less notable in children compared to our previous trial of a SF-rich preparation in young men with ASD. Several of the effects of SF on biomarkers correlated to clinical improvements. SF was very well tolerated and safe and effective based on our secondary clinical measures. TRIAL REGISTRATION: This study was prospectively registered at clinicaltrials.gov (NCT02561481) on September 28, 2015. Funding was provided by the U.S. Department of Defense. En ligne : http://dx.doi.org/10.1186/s13229-021-00447-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 [article] Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder [texte imprimé] / Andrew W. ZIMMERMAN, Auteur ; Kanwaljit SINGH, Auteur ; Susan L. CONNORS, Auteur ; Hua LIU, Auteur ; Anita A PANJWANI, Auteur ; Li-Ching LEE, Auteur ; Eileen DIGGINS, Auteur ; Ann FOLEY, Auteur ; Stepan MELNYK, Auteur ; Indrapal N. SINGH, Auteur ; S. Jill JAMES, Auteur ; Richard E. FRYE, Auteur ; Jed W. FAHEY, Auteur . - 38 p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 38 p. Mots-clés : Autism spectrum disorder (ASD)  Biomarkers  Clinical trial  Placebo effects  Sulforaphane  defendants in matters related to pediatric neurology and Autism Spectrum Disorder.  JWF retired from the full-time faculty at Johns Hopkins in mid-2020, and now serves  as a scientific advisor to Brassica Protection Products LLC (Baltimore, MD, USA),  which produces a glucoraphanin-rich broccoli seed extract that it supplies to the  supplement industry. AWZ is named on a patent on the use of sulforaphane for the  treatment of autism that has been assigned to Johns Hopkins University. Index. décimale : PER Périodiques Résumé : BACKGROUND: Sulforaphane (SF), an isothiocyanate in broccoli, has potential benefits relevant to autism spectrum disorder (ASD) through its effects on several metabolic and immunologic pathways. Previous clinical trials of oral SF demonstrated positive clinical effects on behavior in young men and changes in urinary metabolomics in children with ASD. METHODS: We conducted a 15-week randomized parallel double-blind placebo-controlled clinical trial with 15-week open-label treatment and 6-week no-treatment extensions in 57 children, ages 3-12 years, with ASD over 36 weeks. Twenty-eight were assigned SF and 29 received placebo (PL). Clinical effects, safety and tolerability of SF were measured as were biomarkers to elucidate mechanisms of action of SF in ASD. RESULTS: Data from 22 children taking SF and 23 on PL were analyzed. Treatment effects on the primary outcome measure, the Ohio Autism Clinical Impressions Scale (OACIS), in the general level of autism were not significant between SF and PL groups at 7 and 15 weeks. The effect sizes on the OACIS were non-statistically significant but positive, suggesting a possible trend toward greater improvement in those on treatment with SF (Cohen's d 0.21; 95% CI - 0.46, 0.88 and 0.10; 95% CI - 0.52, 0.72, respectively). Both groups improved in all subscales when on SF during the open-label phase. Caregiver ratings on secondary outcome measures improved significantly on the Aberrant Behavior Checklist (ABC) at 15 weeks (Cohen's d - 0.96; 95% CI - 1.73, - 0.15), but not on the Social Responsiveness Scale-2 (SRS-2). Ratings on the ABC and SRS-2 improved with a non-randomized analysis of the length of exposure to SF, compared to the pre-treatment baseline (p < 0.001). There were significant changes with SF compared to PL in biomarkers of glutathione redox status, mitochondrial respiration, inflammatory markers and heat shock proteins. Clinical laboratory studies confirmed product safety. SF was very well tolerated and side effects of treatment, none serious, included rare insomnia, irritability and intolerance of the taste and smell. LIMITATIONS: The sample size was limited to 45 children with ASD and we did not impute missing data. We were unable to document significant changes in clinical assessments during clinical visits in those taking SF compared to PL. The clinical results were confounded by placebo effects during the open-label phase. CONCLUSIONS: SF led to small yet non-statistically significant changes in the total and all subscale scores of the primary outcome measure, while for secondary outcome measures, caregivers' assessments of children taking SF showed statistically significant improvements compared to those taking PL on the ABC but not the SRS-2. Clinical effects of SF were less notable in children compared to our previous trial of a SF-rich preparation in young men with ASD. Several of the effects of SF on biomarkers correlated to clinical improvements. SF was very well tolerated and safe and effective based on our secondary clinical measures. TRIAL REGISTRATION: This study was prospectively registered at clinicaltrials.gov (NCT02561481) on September 28, 2015. Funding was provided by the U.S. Department of Defense. En ligne : http://dx.doi.org/10.1186/s13229-021-00447-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459

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