Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort / Xueqi QU in Autism Research, 15-4 (April 2022)  

Public ISBD [article]  inAutism Research > 15-4 (April 2022) . - p.740-750 Titre : Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort Type de document : Texte imprimé et/ou numérique Auteurs : Xueqi QU, Auteur ; Li-Ching LEE, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Yuelong JI, Auteur ; Luther G. KALB, Auteur ; Heather E. VOLK, Auteur ; Xiaobin WANG, Auteur Article en page(s) : p.740-750 Langues : Anglais (eng) Mots-clés : Asthma/complications/epidemiology  Attention Deficit Disorder with Hyperactivity/complications/epidemiology  Autism Spectrum Disorder/complications/epidemiology  Birth Cohort  Child  Dermatitis, Atopic/complications/epidemiology  Female  Humans  Infant, Newborn  Risk Factors  atopic diseases  children  neurodevelopmental disability  the United States  relevant to this article to disclose. Index. décimale : PER Périodiques Résumé : Reports on the association between the prevalence of atopic diseases and neurodevelopmental disabilities (NDs) have been inconsistent in the literature. We investigated whether autism spectrum disorder (ASD), attention deficit-hyperactivity disorders (ADHD), and other NDs are more prevalent in children with asthma, atopic dermatitis (AD) and allergic rhinitis (AR) compared to those without specific atopic conditions. A total of 2580 children enrolled at birth were followed prospectively, of which 119 have ASD, 423 have ADHD, 765 have other NDs, and 1273 have no NDs. Atopic diseases and NDs were defined based on physician diagnoses in electronic medical records. Logistic regressions adjusting for maternal and child characteristics estimated the associations between NDs (i.e., ASD, ADHD, and other NDs) and asthma, AD and AR, respectively. Children with asthma, AD or AR had a greater likelihood of having ADHD or other NDs compared with children without specific atopic conditions. The association between ASD and asthma diminished after adjusting for maternal and child factors. Either mothers or children having atopic conditions and both mothers and children with atopic conditions were associated with a higher prevalence of ADHD in children, compared with neither mothers nor children having atopic conditions. Children diagnosed with multiple atopic diseases were more likely to have NDs compared with those without or with only one type of atopic disease. In conclusion, in this U.S. urban birth cohort, children with atopic diseases had a higher co-morbidity of NDs. The findings have implications for etiologic research that searches for common early life antecedents of NDs and atopic conditions. Findings from this study also should raise awareness among health care providers and parents about the possible co-occurrence of both NDs and atopic conditions, which calls for coordinated efforts to screen, prevent and manage NDs and atopic conditions. En ligne : https://dx.doi.org/10.1002/aur.2680 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Association between atopic diseases and neurodevelopmental disabilities in a longitudinal birth cohort [Texte imprimé et/ou numérique] / Xueqi QU, Auteur ; Li-Ching LEE, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Yuelong JI, Auteur ; Luther G. KALB, Auteur ; Heather E. VOLK, Auteur ; Xiaobin WANG, Auteur . - p.740-750. Langues : Anglais (eng) in Autism Research > 15-4 (April 2022) . - p.740-750 Mots-clés : Asthma/complications/epidemiology  Attention Deficit Disorder with Hyperactivity/complications/epidemiology  Autism Spectrum Disorder/complications/epidemiology  Birth Cohort  Child  Dermatitis, Atopic/complications/epidemiology  Female  Humans  Infant, Newborn  Risk Factors  atopic diseases  children  neurodevelopmental disability  the United States  relevant to this article to disclose. Index. décimale : PER Périodiques Résumé : Reports on the association between the prevalence of atopic diseases and neurodevelopmental disabilities (NDs) have been inconsistent in the literature. We investigated whether autism spectrum disorder (ASD), attention deficit-hyperactivity disorders (ADHD), and other NDs are more prevalent in children with asthma, atopic dermatitis (AD) and allergic rhinitis (AR) compared to those without specific atopic conditions. A total of 2580 children enrolled at birth were followed prospectively, of which 119 have ASD, 423 have ADHD, 765 have other NDs, and 1273 have no NDs. Atopic diseases and NDs were defined based on physician diagnoses in electronic medical records. Logistic regressions adjusting for maternal and child characteristics estimated the associations between NDs (i.e., ASD, ADHD, and other NDs) and asthma, AD and AR, respectively. Children with asthma, AD or AR had a greater likelihood of having ADHD or other NDs compared with children without specific atopic conditions. The association between ASD and asthma diminished after adjusting for maternal and child factors. Either mothers or children having atopic conditions and both mothers and children with atopic conditions were associated with a higher prevalence of ADHD in children, compared with neither mothers nor children having atopic conditions. Children diagnosed with multiple atopic diseases were more likely to have NDs compared with those without or with only one type of atopic disease. In conclusion, in this U.S. urban birth cohort, children with atopic diseases had a higher co-morbidity of NDs. The findings have implications for etiologic research that searches for common early life antecedents of NDs and atopic conditions. Findings from this study also should raise awareness among health care providers and parents about the possible co-occurrence of both NDs and atopic conditions, which calls for coordinated efforts to screen, prevent and manage NDs and atopic conditions. En ligne : https://dx.doi.org/10.1002/aur.2680 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication / Ozlem BOZDAGI in Molecular Autism, (December 2010)  

Public ISBD [article]  inMolecular Autism > (December 2010) . - 47 p. Titre : Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication Type de document : Texte imprimé et/ou numérique Auteurs : Ozlem BOZDAGI, Auteur ; Takeshi SAKURAI, Auteur ; Danae PAPAPETROU, Auteur ; Xiaobin WANG, Auteur ; Dara L. DICKSTEIN, Auteur ; Nagahide TAKAHASHI, Auteur ; Yuji KAJIWARA, Auteur ; Mu YANG, Auteur ; Adam M. KATZ, Auteur ; Maria Luisa SCATTONI, Auteur ; Mark J. HARRIS, Auteur ; Roheeni SAXENA, Auteur ; Jill L. SILVERMAN, Auteur ; Jacqueline N. CRAWLEY, Auteur ; Qiang ZHOU, Auteur ; Patrick R. HOF, Auteur ; Joseph D. BUXBAUM, Auteur Année de publication : 2010 Article en page(s) : 47 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : SHANK3 is a protein in the core of the postsynaptic density (PSD) and has a critical role in recruiting many key functional elements to the PSD and to the synapse, including components of alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid (AMPA), metabotropic glutamate (mGlu) and N-methyl-D-aspartic acid (NMDA) glutamate receptors, as well as cytoskeletal elements. Loss of a functional copy of the SHANK3 gene leads to the neurobehavioral manifestations of 22q13 deletion syndrome and/or to autism spectrum disorders. The goal of this study was to examine the effects of haploinsufficiency of full-length Shank3 in mice, focusing on synaptic development, transmission and plasticity, as well as on social behaviors, as a model for understanding SHANK3 haploinsufficiency in humans. Methods We used mice with a targeted disruption of Shank3 in which exons coding for the ankyrin repeat domain were deleted and expression of full-length Shank3 was disrupted. We studied synaptic transmission and plasticity by multiple methods, including patch-clamp whole cell recording, two-photon time-lapse imaging and extracellular recordings of field excitatory postsynaptic potentials. We also studied the density of GluR1-immunoreactive puncta in the CA1 stratum radiatum and carried out assessments of social behaviors. Results In Shank3 heterozygous mice, there was reduced amplitude of miniature excitatory postsynaptic currents from hippocampal CA1 pyramidal neurons and the input-output (I/O) relationship at Schaffer collateral-CA1 synapses in acute hippocampal slices was significantly depressed; both of these findings indicate a reduction in basal neurotransmission. Studies with specific inhibitors demonstrated that the decrease in basal transmission reflected reduced AMPA receptor-mediated transmission. This was further supported by the observation of reduced numbers of GluR1-immunoreactive puncta in the stratum radiatum. Long-term potentiation (LTP), induced either with theta-burst pairing (TBP) or high-frequency stimulation, was impaired in Shank3 heterozygous mice, with no significant change in long-term depression (LTD). In concordance with the LTP results, persistent expansion of spines was observed in control mice after TBP-induced LTP; however, only transient spine expansion was observed in Shank3 heterozygous mice. Male Shank3 heterozygotes displayed less social sniffing and emitted fewer ultrasonic vocalizations during interactions with estrus female mice, as compared to wild-type littermate controls. Conclusions We documented specific deficits in synaptic function and plasticity, along with reduced reciprocal social interactions in Shank3 heterozygous mice. Our results are consistent with altered synaptic development and function in Shank3 haploinsufficiency, highlighting the importance of Shank3 in synaptic function and supporting a link between deficits in synapse function and neurodevelopmental disorders. The reduced glutamatergic transmission that we observed in the Shank3 heterozygous mice represents an interesting therapeutic target in Shank3-haploinsufficiency syndromes. En ligne : http://dx.doi.org/10.1186/2040-2392-1-15 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=114 [article] Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication [Texte imprimé et/ou numérique] / Ozlem BOZDAGI, Auteur ; Takeshi SAKURAI, Auteur ; Danae PAPAPETROU, Auteur ; Xiaobin WANG, Auteur ; Dara L. DICKSTEIN, Auteur ; Nagahide TAKAHASHI, Auteur ; Yuji KAJIWARA, Auteur ; Mu YANG, Auteur ; Adam M. KATZ, Auteur ; Maria Luisa SCATTONI, Auteur ; Mark J. HARRIS, Auteur ; Roheeni SAXENA, Auteur ; Jill L. SILVERMAN, Auteur ; Jacqueline N. CRAWLEY, Auteur ; Qiang ZHOU, Auteur ; Patrick R. HOF, Auteur ; Joseph D. BUXBAUM, Auteur . - 2010 . - 47 p. Langues : Anglais (eng) in Molecular Autism > (December 2010) . - 47 p. Index. décimale : PER Périodiques Résumé : SHANK3 is a protein in the core of the postsynaptic density (PSD) and has a critical role in recruiting many key functional elements to the PSD and to the synapse, including components of alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid (AMPA), metabotropic glutamate (mGlu) and N-methyl-D-aspartic acid (NMDA) glutamate receptors, as well as cytoskeletal elements. Loss of a functional copy of the SHANK3 gene leads to the neurobehavioral manifestations of 22q13 deletion syndrome and/or to autism spectrum disorders. The goal of this study was to examine the effects of haploinsufficiency of full-length Shank3 in mice, focusing on synaptic development, transmission and plasticity, as well as on social behaviors, as a model for understanding SHANK3 haploinsufficiency in humans. Methods We used mice with a targeted disruption of Shank3 in which exons coding for the ankyrin repeat domain were deleted and expression of full-length Shank3 was disrupted. We studied synaptic transmission and plasticity by multiple methods, including patch-clamp whole cell recording, two-photon time-lapse imaging and extracellular recordings of field excitatory postsynaptic potentials. We also studied the density of GluR1-immunoreactive puncta in the CA1 stratum radiatum and carried out assessments of social behaviors. Results In Shank3 heterozygous mice, there was reduced amplitude of miniature excitatory postsynaptic currents from hippocampal CA1 pyramidal neurons and the input-output (I/O) relationship at Schaffer collateral-CA1 synapses in acute hippocampal slices was significantly depressed; both of these findings indicate a reduction in basal neurotransmission. Studies with specific inhibitors demonstrated that the decrease in basal transmission reflected reduced AMPA receptor-mediated transmission. This was further supported by the observation of reduced numbers of GluR1-immunoreactive puncta in the stratum radiatum. Long-term potentiation (LTP), induced either with theta-burst pairing (TBP) or high-frequency stimulation, was impaired in Shank3 heterozygous mice, with no significant change in long-term depression (LTD). In concordance with the LTP results, persistent expansion of spines was observed in control mice after TBP-induced LTP; however, only transient spine expansion was observed in Shank3 heterozygous mice. Male Shank3 heterozygotes displayed less social sniffing and emitted fewer ultrasonic vocalizations during interactions with estrus female mice, as compared to wild-type littermate controls. Conclusions We documented specific deficits in synaptic function and plasticity, along with reduced reciprocal social interactions in Shank3 heterozygous mice. Our results are consistent with altered synaptic development and function in Shank3 haploinsufficiency, highlighting the importance of Shank3 in synaptic function and supporting a link between deficits in synapse function and neurodevelopmental disorders. The reduced glutamatergic transmission that we observed in the Shank3 heterozygous mice represents an interesting therapeutic target in Shank3-haploinsufficiency syndromes. En ligne : http://dx.doi.org/10.1186/2040-2392-1-15 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=114

Interaction between Maternal Immune Activation and Antibiotic Use during Pregnancy and Child Risk of Autism Spectrum Disorder / Calliope HOLINGUE in Autism Research, 13-12 (December 2020)  

Public ISBD [article]  inAutism Research > 13-12 (December 2020) . - p.2230-2241 Titre : Interaction between Maternal Immune Activation and Antibiotic Use during Pregnancy and Child Risk of Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Calliope HOLINGUE, Auteur ; Martha BRUCATO, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Heather E. VOLK, Auteur ; Noel T. MUELLER, Auteur ; Xiaobin WANG, Auteur ; M. Daniele FALLIN, Auteur Article en page(s) : p.2230-2241 Langues : Anglais (eng) Mots-clés : anti-bacterial agents  autism spectrum disorder  environmental exposure  epidemiology  maternal exposure  minority health  risk factors Index. décimale : PER Périodiques Résumé : Prenatal exposure to maternal immune activation (MIA) has been implicated as a risk factor for the development of autism spectrum disorder (ASD), though the conditions under which this elevated risk occurs are unclear. Animal literature demonstrates that antibiotic use, which affects the composition of the maternal gut microbiota, modifies the effect of MIA on neurodevelopmental outcomes in the offspring. The aim of this study was to assess whether antibiotic use during pregnancy modifies the association between MIA and subsequent risk of ASD, in a prospective birth cohort with 116 ASD cases and 860 typically developing (TD) child controls. There was no evidence of interaction between fever or genitourinary infection and antibiotic use on the odds of ASD in unadjusted or adjusted analyzes. However, we found evidence of an interaction between flu, specifically in second trimester, and antibiotic use at any point during pregnancy on the odds of ASD in the child. Among women who received an antibiotic during pregnancy, flu in trimester two was not associated with ASD (adjusted odds ratio [aOR] = 0.99 [0.43-2.28]). Among women who were not exposed to an antibiotic at any point during pregnancy, flu in second trimester was significantly associated with increased odds of ASD (aOR = 4.05 [1.14-14.38], P = .03), after adjustment for child sex, child birth year, maternal age, gestational age, C-section delivery, and low birthweight. These findings should be treated as hypothesis-generating and suggest that antibiotic use may modify the influence that MIA has on autism risk in the child. LAY SUMMARY: We looked at whether the association between activation of the immune system during pregnancy and risk of the child developing autism spectrum disorder (ASD) differed among women who did or did not take an antibiotic at any point during pregnancy. We examined 116 children with ASD and 860 without ASD and found that flu in second trimester was associated with increased ASD, but only among women who did not take an antibiotic during pregnancy. No other immune activation exposures seemed to interact with antibiotic use. En ligne : http://dx.doi.org/10.1002/aur.2411 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=434 [article] Interaction between Maternal Immune Activation and Antibiotic Use during Pregnancy and Child Risk of Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Calliope HOLINGUE, Auteur ; Martha BRUCATO, Auteur ; Christine LADD-ACOSTA, Auteur ; Xiumei HONG, Auteur ; Heather E. VOLK, Auteur ; Noel T. MUELLER, Auteur ; Xiaobin WANG, Auteur ; M. Daniele FALLIN, Auteur . - p.2230-2241. Langues : Anglais (eng) in Autism Research > 13-12 (December 2020) . - p.2230-2241 Mots-clés : anti-bacterial agents  autism spectrum disorder  environmental exposure  epidemiology  maternal exposure  minority health  risk factors Index. décimale : PER Périodiques Résumé : Prenatal exposure to maternal immune activation (MIA) has been implicated as a risk factor for the development of autism spectrum disorder (ASD), though the conditions under which this elevated risk occurs are unclear. Animal literature demonstrates that antibiotic use, which affects the composition of the maternal gut microbiota, modifies the effect of MIA on neurodevelopmental outcomes in the offspring. The aim of this study was to assess whether antibiotic use during pregnancy modifies the association between MIA and subsequent risk of ASD, in a prospective birth cohort with 116 ASD cases and 860 typically developing (TD) child controls. There was no evidence of interaction between fever or genitourinary infection and antibiotic use on the odds of ASD in unadjusted or adjusted analyzes. However, we found evidence of an interaction between flu, specifically in second trimester, and antibiotic use at any point during pregnancy on the odds of ASD in the child. Among women who received an antibiotic during pregnancy, flu in trimester two was not associated with ASD (adjusted odds ratio [aOR] = 0.99 [0.43-2.28]). Among women who were not exposed to an antibiotic at any point during pregnancy, flu in second trimester was significantly associated with increased odds of ASD (aOR = 4.05 [1.14-14.38], P = .03), after adjustment for child sex, child birth year, maternal age, gestational age, C-section delivery, and low birthweight. These findings should be treated as hypothesis-generating and suggest that antibiotic use may modify the influence that MIA has on autism risk in the child. LAY SUMMARY: We looked at whether the association between activation of the immune system during pregnancy and risk of the child developing autism spectrum disorder (ASD) differed among women who did or did not take an antibiotic at any point during pregnancy. We examined 116 children with ASD and 860 without ASD and found that flu in second trimester was associated with increased ASD, but only among women who did not take an antibiotic during pregnancy. No other immune activation exposures seemed to interact with antibiotic use. En ligne : http://dx.doi.org/10.1002/aur.2411 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=434

Maternal Dyslipidemia, Plasma Branched-Chain Amino Acids, and the Risk of Child Autism Spectrum Disorder: Evidence of Sex Difference / Anita A PANJWANI in Journal of Autism and Developmental Disorders, 50-2 (February 2020)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 50-2 (February 2020) . - p.540-550 Titre : Maternal Dyslipidemia, Plasma Branched-Chain Amino Acids, and the Risk of Child Autism Spectrum Disorder: Evidence of Sex Difference Type de document : Texte imprimé et/ou numérique Auteurs : Anita A PANJWANI, Auteur ; Yuelong JI, Auteur ; Jed W FAHEY, Auteur ; Amanda PALMER, Auteur ; Guoying WANG, Auteur ; Xiumei HONG, Auteur ; Barry S. ZUCKERMAN, Auteur ; Xiaobin WANG, Auteur Article en page(s) : p.540-550 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Branched-chain amino acids  Maternal cholesterols  Metabolomics  Pre- and perinatal risk factors  Sex differences Index. décimale : PER Périodiques Résumé : In contrast to the well-observed associations between obesity, diabetes, and autism spectrum disorder (ASD), the roles of maternal dyslipidemia and sex disparity in ASD have not been well-studied. We examined the joint associations of maternal plasma cholesterols, branched-chain amino acids (BCAAs) and child sex on child ASD risk. We analyzed data from 756 mother-infant pairs (86 ASD) from the Boston Birth Cohort. Maternal plasma cholesterols and BCAAs were measured in samples collected 24-72 h postpartum. We found that in this urban, low-income prospective birth cohort, low maternal high-density lipoprotein cholesterol (HDL-C), above-median maternal plasma BCAA concentrations, and male sex additively or synergistically increased risk of ASD. Additional studies are necessary to confirm our findings. En ligne : http://dx.doi.org/10.1007/s10803-019-04264-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=416 [article] Maternal Dyslipidemia, Plasma Branched-Chain Amino Acids, and the Risk of Child Autism Spectrum Disorder: Evidence of Sex Difference [Texte imprimé et/ou numérique] / Anita A PANJWANI, Auteur ; Yuelong JI, Auteur ; Jed W FAHEY, Auteur ; Amanda PALMER, Auteur ; Guoying WANG, Auteur ; Xiumei HONG, Auteur ; Barry S. ZUCKERMAN, Auteur ; Xiaobin WANG, Auteur . - p.540-550. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 50-2 (February 2020) . - p.540-550 Mots-clés : Autism spectrum disorder  Branched-chain amino acids  Maternal cholesterols  Metabolomics  Pre- and perinatal risk factors  Sex differences Index. décimale : PER Périodiques Résumé : In contrast to the well-observed associations between obesity, diabetes, and autism spectrum disorder (ASD), the roles of maternal dyslipidemia and sex disparity in ASD have not been well-studied. We examined the joint associations of maternal plasma cholesterols, branched-chain amino acids (BCAAs) and child sex on child ASD risk. We analyzed data from 756 mother-infant pairs (86 ASD) from the Boston Birth Cohort. Maternal plasma cholesterols and BCAAs were measured in samples collected 24-72 h postpartum. We found that in this urban, low-income prospective birth cohort, low maternal high-density lipoprotein cholesterol (HDL-C), above-median maternal plasma BCAA concentrations, and male sex additively or synergistically increased risk of ASD. Additional studies are necessary to confirm our findings. En ligne : http://dx.doi.org/10.1007/s10803-019-04264-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=416

Prenatal exposure to fever is associated with autism spectrum disorder in the boston birth cohort / Martha BRUCATO in Autism Research, 10-11 (November 2017)  

Public ISBD [article]  inAutism Research > 10-11 (November 2017) . - p.1878-1890 Titre : Prenatal exposure to fever is associated with autism spectrum disorder in the boston birth cohort Type de document : Texte imprimé et/ou numérique Auteurs : Martha BRUCATO, Auteur ; Christine LADD-ACOSTA, Auteur ; Mengying LI, Auteur ; Deanna CARUSO, Auteur ; Xiumei HONG, Auteur ; Jamie KACZANIUK, Auteur ; Elizabeth A. STUART, Auteur ; M. Daniele FALLIN, Auteur ; Xiaobin WANG, Auteur Article en page(s) : p.1878-1890 Langues : Anglais (eng) Mots-clés : autism spectrum disorder (ASD)  environmental exposure  maternal exposure  fever  epidemiology  risk factors  minority health Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is phenotypically and etiologically heterogeneous, with evidence for genetic and environmental contributions to disease risk. Research has focused on the prenatal period as a time where environmental exposures are likely to influence risk for ASD. Epidemiological studies have shown significant associations between prenatal exposure to maternal immune activation (MIA), caused by infections and fever, and ASD. However, due to differences in study design and exposure measurements no consistent patterns have emerged revealing specific times or type of MIA exposure that are most important to ASD risk. No prior studies have examined prenatal MIA exposure and ASD risk in an under-represented minority population of African ancestry. To overcome these limitations, we estimated the association between prenatal exposure to fever and maternal infections and ASD in a prospective birth cohort of an understudied minority population in a city in the United States. No association was found between prenatal exposure to genitourinary infections or flu and the risk of ASD in a nested sample of 116 ASD cases and 988 typically developing controls in crude or adjusted analyses. Prenatal exposure to fever was associated with increased ASD risk (aOR 2.02 [1.04–3.92]) after adjustment for educational attainment, marital status, race, child sex, maternal age, birth year, gestational age, and maternal smoking. This effect may be specific to fever during the third trimester (aOR 2.70 [1.00–7.29]). Our findings provide a focus for future research efforts and ASD prevention strategies across diverse populations. Autism Res 2017, 10: 1878–1890. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We looked at whether activation of the immune system during pregnancy increases the chance a child will develop ASD. We examined 116 children with ASD and 988 children without ASD that came from a predominantly low income, urban, minority population. We found that having the flu or genitourinary tract infections during pregnancy is not related to the child being diagnosed with ASD. However, we did find children were at increased risk for ASD when their mothers had a fever during pregnancy. En ligne : http://dx.doi.org/10.1002/aur.1841 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322 [article] Prenatal exposure to fever is associated with autism spectrum disorder in the boston birth cohort [Texte imprimé et/ou numérique] / Martha BRUCATO, Auteur ; Christine LADD-ACOSTA, Auteur ; Mengying LI, Auteur ; Deanna CARUSO, Auteur ; Xiumei HONG, Auteur ; Jamie KACZANIUK, Auteur ; Elizabeth A. STUART, Auteur ; M. Daniele FALLIN, Auteur ; Xiaobin WANG, Auteur . - p.1878-1890. Langues : Anglais (eng) in Autism Research > 10-11 (November 2017) . - p.1878-1890 Mots-clés : autism spectrum disorder (ASD)  environmental exposure  maternal exposure  fever  epidemiology  risk factors  minority health Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is phenotypically and etiologically heterogeneous, with evidence for genetic and environmental contributions to disease risk. Research has focused on the prenatal period as a time where environmental exposures are likely to influence risk for ASD. Epidemiological studies have shown significant associations between prenatal exposure to maternal immune activation (MIA), caused by infections and fever, and ASD. However, due to differences in study design and exposure measurements no consistent patterns have emerged revealing specific times or type of MIA exposure that are most important to ASD risk. No prior studies have examined prenatal MIA exposure and ASD risk in an under-represented minority population of African ancestry. To overcome these limitations, we estimated the association between prenatal exposure to fever and maternal infections and ASD in a prospective birth cohort of an understudied minority population in a city in the United States. No association was found between prenatal exposure to genitourinary infections or flu and the risk of ASD in a nested sample of 116 ASD cases and 988 typically developing controls in crude or adjusted analyses. Prenatal exposure to fever was associated with increased ASD risk (aOR 2.02 [1.04–3.92]) after adjustment for educational attainment, marital status, race, child sex, maternal age, birth year, gestational age, and maternal smoking. This effect may be specific to fever during the third trimester (aOR 2.70 [1.00–7.29]). Our findings provide a focus for future research efforts and ASD prevention strategies across diverse populations. Autism Res 2017, 10: 1878–1890. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary We looked at whether activation of the immune system during pregnancy increases the chance a child will develop ASD. We examined 116 children with ASD and 988 children without ASD that came from a predominantly low income, urban, minority population. We found that having the flu or genitourinary tract infections during pregnancy is not related to the child being diagnosed with ASD. However, we did find children were at increased risk for ASD when their mothers had a fever during pregnancy. En ligne : http://dx.doi.org/10.1002/aur.1841 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322

The impact of COVID-19 on psychiatric clinical encounters among low-income racially-diverse children / Serena A. RUSK in Journal of Child Psychology and Psychiatry, 65-5 (May 2024)  

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