The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
Aijia Shang - One of the best experts on this subject based on the ideXlab platform.
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proteomic analysis on Infantile Spasm and prenatal stress
Epilepsy Research, 2014Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Aijia ShangAbstract:Summary Infantile Spasms (IS) are an age-dependent epileptic encephalopathy with severe cognitive dysfunction. Prenatal stress (PS) has been reported to increase the risk for IS through clinical and animal studies. We aim to investigate the mechanism of brain damage caused by IS and the effect of PS. Animals were divided into 4 groups: PS-Spasm model, PS-saline control, NS-Spasm model, and saline control. N-methyl-d-aspartate (NMDA) was used to induce Spasm and swimming in cold water was used to induce PS. A proteomics-based approach was used to compare the NS-Spasm model vs. saline control, and PS-Spasm model vs. NS-Spasm model. Gel image analysis was followed by mass spectrometric protein identification and bioinformatics analysis. We observed an increased Spasm frequency ( t =8.65, P t =3.96, P The biological function of differentially expressed proteins indicates the pathogenesis of IS maybe relevant to energy metabolism, brain development, and neural remodeling. PS aggravated seizures in the NMDA-induced Spasm model, YWHAZ, and CFL1 may be involved.
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proteomic analysis of adrenocorticotropic hormone treatment of an Infantile Spasm model induced by n methyl d aspartic acid and prenatal stress
PLOS ONE, 2012Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Wenjing Zhou, Aijia ShangAbstract:Infantile Spasms is an age-specific epileptic syndrome associated with poor developmental outcomes and poor response to nearly all traditional antiepileptic drugs except adrenocorticotropic hormone (ACTH). We investigated the protective mechanism of ACTH against brain damage. An Infantile Spasm rat model induced by N-methyl-d-aspartate (NMDA) in neonate rats was used. Pregnant rats were randomly divided into the stress-exposed and the non-stress exposed groups, and their offspring were randomly divided into ACTH-treated Spasm model, untreated Spasm model, and control groups. A proteomics-based approach was used to detect the proteome differences between ACTH-treated and untreated groups. Gel image analysis was followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometric protein identification and bioinformatics analysis. Prenatal stress exposure resulted in more severe seizures, and ACTH treatment reduced and delayed the onset of seizures. The most significantly up-regulated proteins included isoform 1 of tubulin β-5 chain, cofilin-1 (CFL1), synaptosomal-associated protein 25, malate dehydrogenase, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1, annexin A3 (ANXA3), and rho GDP-dissociation inhibitor 1 (ARHGDIA). In contrast, tubulin α-1A chain was down-regulated. Three of the identified proteins, ARHGDIA, ANXA3, and CFL1, were validated using western blot analysis. ARHGDIA expression was assayed in the brain samples of five Infantile Spasm patients. These proteins are involved in the cytoskeleton, synapses, energy metabolism, vascular regulation, signal transduction, and acetylation. The mechanism underlying the effects of ACTH involves the molecular events affected by these proteins, and protein acetylation is the mechanism of action of the drug treatment.
Jing Wang - One of the best experts on this subject based on the ideXlab platform.
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proteomic analysis on Infantile Spasm and prenatal stress
Epilepsy Research, 2014Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Aijia ShangAbstract:Summary Infantile Spasms (IS) are an age-dependent epileptic encephalopathy with severe cognitive dysfunction. Prenatal stress (PS) has been reported to increase the risk for IS through clinical and animal studies. We aim to investigate the mechanism of brain damage caused by IS and the effect of PS. Animals were divided into 4 groups: PS-Spasm model, PS-saline control, NS-Spasm model, and saline control. N-methyl-d-aspartate (NMDA) was used to induce Spasm and swimming in cold water was used to induce PS. A proteomics-based approach was used to compare the NS-Spasm model vs. saline control, and PS-Spasm model vs. NS-Spasm model. Gel image analysis was followed by mass spectrometric protein identification and bioinformatics analysis. We observed an increased Spasm frequency ( t =8.65, P t =3.96, P The biological function of differentially expressed proteins indicates the pathogenesis of IS maybe relevant to energy metabolism, brain development, and neural remodeling. PS aggravated seizures in the NMDA-induced Spasm model, YWHAZ, and CFL1 may be involved.
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proteomic analysis of adrenocorticotropic hormone treatment of an Infantile Spasm model induced by n methyl d aspartic acid and prenatal stress
PLOS ONE, 2012Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Wenjing Zhou, Aijia ShangAbstract:Infantile Spasms is an age-specific epileptic syndrome associated with poor developmental outcomes and poor response to nearly all traditional antiepileptic drugs except adrenocorticotropic hormone (ACTH). We investigated the protective mechanism of ACTH against brain damage. An Infantile Spasm rat model induced by N-methyl-d-aspartate (NMDA) in neonate rats was used. Pregnant rats were randomly divided into the stress-exposed and the non-stress exposed groups, and their offspring were randomly divided into ACTH-treated Spasm model, untreated Spasm model, and control groups. A proteomics-based approach was used to detect the proteome differences between ACTH-treated and untreated groups. Gel image analysis was followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometric protein identification and bioinformatics analysis. Prenatal stress exposure resulted in more severe seizures, and ACTH treatment reduced and delayed the onset of seizures. The most significantly up-regulated proteins included isoform 1 of tubulin β-5 chain, cofilin-1 (CFL1), synaptosomal-associated protein 25, malate dehydrogenase, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1, annexin A3 (ANXA3), and rho GDP-dissociation inhibitor 1 (ARHGDIA). In contrast, tubulin α-1A chain was down-regulated. Three of the identified proteins, ARHGDIA, ANXA3, and CFL1, were validated using western blot analysis. ARHGDIA expression was assayed in the brain samples of five Infantile Spasm patients. These proteins are involved in the cytoskeleton, synapses, energy metabolism, vascular regulation, signal transduction, and acetylation. The mechanism underlying the effects of ACTH involves the molecular events affected by these proteins, and protein acetylation is the mechanism of action of the drug treatment.
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rapamycin in tuberous sclerosis patient with Infantile Spasm a case report and literature review
Chinese Journal of Neuromedicine, 2012Co-Authors: L I Xiaoyan, Jing WangAbstract:Objective To analyze the clinical features of tuberous sclerosis (TS) patient with Infantile Spasm and investigate its treatment efficacy with rapamycin. Methods The clinical manifestations of a tuberous sclerosis patient with Infantile Spasm before and after the treatment with rapamycin were retrospectively analyzed; and the related literature was reviewed. Results Dermatological abnormalities were evidcnt in the child and mainly shown as hypomelanotic macules.His neurological abnormalities included Infantile Spasm and backward psychomotor development.Head MRI and CT had abnormal changes.Treatment with rapamycin 3 months later disclosed improvement in many ways: the convulsion seizure of the patient decreased apparently, and MRI showed decreased subependymal tuber size; meanwhile,the intellectual development of the patient improved obviously,and there was no adverse reaction. Conclusion Rapamycin,enjoying good effect,would be a new and safety method to treat TS patients with Infantile Spasm. Key words: Rapamycin; Tuberous sclerosis; Infantile Spasm
Guang Yang - One of the best experts on this subject based on the ideXlab platform.
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proteomic analysis on Infantile Spasm and prenatal stress
Epilepsy Research, 2014Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Aijia ShangAbstract:Summary Infantile Spasms (IS) are an age-dependent epileptic encephalopathy with severe cognitive dysfunction. Prenatal stress (PS) has been reported to increase the risk for IS through clinical and animal studies. We aim to investigate the mechanism of brain damage caused by IS and the effect of PS. Animals were divided into 4 groups: PS-Spasm model, PS-saline control, NS-Spasm model, and saline control. N-methyl-d-aspartate (NMDA) was used to induce Spasm and swimming in cold water was used to induce PS. A proteomics-based approach was used to compare the NS-Spasm model vs. saline control, and PS-Spasm model vs. NS-Spasm model. Gel image analysis was followed by mass spectrometric protein identification and bioinformatics analysis. We observed an increased Spasm frequency ( t =8.65, P t =3.96, P The biological function of differentially expressed proteins indicates the pathogenesis of IS maybe relevant to energy metabolism, brain development, and neural remodeling. PS aggravated seizures in the NMDA-induced Spasm model, YWHAZ, and CFL1 may be involved.
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association of serotonin transporter polymorphisms with responsiveness to adrenocorticotropic hormone in Infantile Spasm
World Journal of Pediatrics, 2013Co-Authors: Guang Yang, Yingxue Ding, Bing HeAbstract:Background: Serotonin or 5-hydroxytryptamine (5-HT) is an important neurotransmitter in the central nervous system. The serotonin transporter (5HTT) is a key regulator of the level of serotonergic neurotransmission. In the present study, the contribution of 5-HTT polymorphisms to the risk of Infantile Spasm (IS) and the responsiveness to adrenocortico tropic hormone (ACTH) were investigated. Methods: Two functional polymorphisms, the 44-bp insertion-deletion polymorphism in the promoter region (5-HTTLPR) and the variable number tandem repeat in the second intron (5-HTTVNTR), were genotyped in a Chinese case-control study involving 112 patients with IS and 120 controls. Results: Genotyping yielded valid data in 111 patients and 118 controls for 5-HTTLPR and 110 patients and 118 controls for 5-HTTVNTR. The polymorphisms were not found to have an allelic or genotypic association with IS. However, responsiveness to ACTH was higher in patients who were homozygous for L (91%) than in those with S/L (56%) or S/S (60%) (P=0.017). Haplotype analysis did not improve the observed association. Conclusions: The results suggest that the 5-HTTLPR genotype may infl uence the responsiveness to ACTH. This interpretation deserves further study. World J Pediatr 2013;9(3):251-255
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proteomic analysis of adrenocorticotropic hormone treatment of an Infantile Spasm model induced by n methyl d aspartic acid and prenatal stress
PLOS ONE, 2012Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Wenjing Zhou, Aijia ShangAbstract:Infantile Spasms is an age-specific epileptic syndrome associated with poor developmental outcomes and poor response to nearly all traditional antiepileptic drugs except adrenocorticotropic hormone (ACTH). We investigated the protective mechanism of ACTH against brain damage. An Infantile Spasm rat model induced by N-methyl-d-aspartate (NMDA) in neonate rats was used. Pregnant rats were randomly divided into the stress-exposed and the non-stress exposed groups, and their offspring were randomly divided into ACTH-treated Spasm model, untreated Spasm model, and control groups. A proteomics-based approach was used to detect the proteome differences between ACTH-treated and untreated groups. Gel image analysis was followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometric protein identification and bioinformatics analysis. Prenatal stress exposure resulted in more severe seizures, and ACTH treatment reduced and delayed the onset of seizures. The most significantly up-regulated proteins included isoform 1 of tubulin β-5 chain, cofilin-1 (CFL1), synaptosomal-associated protein 25, malate dehydrogenase, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1, annexin A3 (ANXA3), and rho GDP-dissociation inhibitor 1 (ARHGDIA). In contrast, tubulin α-1A chain was down-regulated. Three of the identified proteins, ARHGDIA, ANXA3, and CFL1, were validated using western blot analysis. ARHGDIA expression was assayed in the brain samples of five Infantile Spasm patients. These proteins are involved in the cytoskeleton, synapses, energy metabolism, vascular regulation, signal transduction, and acetylation. The mechanism underlying the effects of ACTH involves the molecular events affected by these proteins, and protein acetylation is the mechanism of action of the drug treatment.
Ying Zhang - One of the best experts on this subject based on the ideXlab platform.
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proteomic analysis on Infantile Spasm and prenatal stress
Epilepsy Research, 2014Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Aijia ShangAbstract:Summary Infantile Spasms (IS) are an age-dependent epileptic encephalopathy with severe cognitive dysfunction. Prenatal stress (PS) has been reported to increase the risk for IS through clinical and animal studies. We aim to investigate the mechanism of brain damage caused by IS and the effect of PS. Animals were divided into 4 groups: PS-Spasm model, PS-saline control, NS-Spasm model, and saline control. N-methyl-d-aspartate (NMDA) was used to induce Spasm and swimming in cold water was used to induce PS. A proteomics-based approach was used to compare the NS-Spasm model vs. saline control, and PS-Spasm model vs. NS-Spasm model. Gel image analysis was followed by mass spectrometric protein identification and bioinformatics analysis. We observed an increased Spasm frequency ( t =8.65, P t =3.96, P The biological function of differentially expressed proteins indicates the pathogenesis of IS maybe relevant to energy metabolism, brain development, and neural remodeling. PS aggravated seizures in the NMDA-induced Spasm model, YWHAZ, and CFL1 may be involved.
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proteomic analysis of adrenocorticotropic hormone treatment of an Infantile Spasm model induced by n methyl d aspartic acid and prenatal stress
PLOS ONE, 2012Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Wenjing Zhou, Aijia ShangAbstract:Infantile Spasms is an age-specific epileptic syndrome associated with poor developmental outcomes and poor response to nearly all traditional antiepileptic drugs except adrenocorticotropic hormone (ACTH). We investigated the protective mechanism of ACTH against brain damage. An Infantile Spasm rat model induced by N-methyl-d-aspartate (NMDA) in neonate rats was used. Pregnant rats were randomly divided into the stress-exposed and the non-stress exposed groups, and their offspring were randomly divided into ACTH-treated Spasm model, untreated Spasm model, and control groups. A proteomics-based approach was used to detect the proteome differences between ACTH-treated and untreated groups. Gel image analysis was followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometric protein identification and bioinformatics analysis. Prenatal stress exposure resulted in more severe seizures, and ACTH treatment reduced and delayed the onset of seizures. The most significantly up-regulated proteins included isoform 1 of tubulin β-5 chain, cofilin-1 (CFL1), synaptosomal-associated protein 25, malate dehydrogenase, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1, annexin A3 (ANXA3), and rho GDP-dissociation inhibitor 1 (ARHGDIA). In contrast, tubulin α-1A chain was down-regulated. Three of the identified proteins, ARHGDIA, ANXA3, and CFL1, were validated using western blot analysis. ARHGDIA expression was assayed in the brain samples of five Infantile Spasm patients. These proteins are involved in the cytoskeleton, synapses, energy metabolism, vascular regulation, signal transduction, and acetylation. The mechanism underlying the effects of ACTH involves the molecular events affected by these proteins, and protein acetylation is the mechanism of action of the drug treatment.
Juan Wang - One of the best experts on this subject based on the ideXlab platform.
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proteomic analysis on Infantile Spasm and prenatal stress
Epilepsy Research, 2014Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Aijia ShangAbstract:Summary Infantile Spasms (IS) are an age-dependent epileptic encephalopathy with severe cognitive dysfunction. Prenatal stress (PS) has been reported to increase the risk for IS through clinical and animal studies. We aim to investigate the mechanism of brain damage caused by IS and the effect of PS. Animals were divided into 4 groups: PS-Spasm model, PS-saline control, NS-Spasm model, and saline control. N-methyl-d-aspartate (NMDA) was used to induce Spasm and swimming in cold water was used to induce PS. A proteomics-based approach was used to compare the NS-Spasm model vs. saline control, and PS-Spasm model vs. NS-Spasm model. Gel image analysis was followed by mass spectrometric protein identification and bioinformatics analysis. We observed an increased Spasm frequency ( t =8.65, P t =3.96, P The biological function of differentially expressed proteins indicates the pathogenesis of IS maybe relevant to energy metabolism, brain development, and neural remodeling. PS aggravated seizures in the NMDA-induced Spasm model, YWHAZ, and CFL1 may be involved.
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proteomic analysis of adrenocorticotropic hormone treatment of an Infantile Spasm model induced by n methyl d aspartic acid and prenatal stress
PLOS ONE, 2012Co-Authors: Jing Wang, Juan Wang, Ying Zhang, Guang Yang, Wenjing Zhou, Aijia ShangAbstract:Infantile Spasms is an age-specific epileptic syndrome associated with poor developmental outcomes and poor response to nearly all traditional antiepileptic drugs except adrenocorticotropic hormone (ACTH). We investigated the protective mechanism of ACTH against brain damage. An Infantile Spasm rat model induced by N-methyl-d-aspartate (NMDA) in neonate rats was used. Pregnant rats were randomly divided into the stress-exposed and the non-stress exposed groups, and their offspring were randomly divided into ACTH-treated Spasm model, untreated Spasm model, and control groups. A proteomics-based approach was used to detect the proteome differences between ACTH-treated and untreated groups. Gel image analysis was followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometric protein identification and bioinformatics analysis. Prenatal stress exposure resulted in more severe seizures, and ACTH treatment reduced and delayed the onset of seizures. The most significantly up-regulated proteins included isoform 1 of tubulin β-5 chain, cofilin-1 (CFL1), synaptosomal-associated protein 25, malate dehydrogenase, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1, annexin A3 (ANXA3), and rho GDP-dissociation inhibitor 1 (ARHGDIA). In contrast, tubulin α-1A chain was down-regulated. Three of the identified proteins, ARHGDIA, ANXA3, and CFL1, were validated using western blot analysis. ARHGDIA expression was assayed in the brain samples of five Infantile Spasm patients. These proteins are involved in the cytoskeleton, synapses, energy metabolism, vascular regulation, signal transduction, and acetylation. The mechanism underlying the effects of ACTH involves the molecular events affected by these proteins, and protein acetylation is the mechanism of action of the drug treatment.