Ontology highlight
ABSTRACT:
PROVIDER: PRJEB46005 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6150260.fastq.gz | Fastqsanger.gz | |||
| ERR6150261.fastq.gz | Fastqsanger.gz | |||
| ERR6150262.fastq.gz | Fastqsanger.gz | |||
| ERR6150263.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.
2013-12-31 | GSE23319 | GEO
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage.
2013-12-31 | GSE23317 | GEO
Project description:In this data set, we compared the expression data of song nuclei HVC, visual cortex entopallium, and the molecular layer of the cerebellum dissected from females and males of 3 songbird species (S. canaria, U. cyanocephalus, P. bicolor) to identify sex-specific stimulated gene expression. Testosterone-treated male and female canaries were also included in order to study whether testosterone effect on transcriptomes is sex-specific. Finally, testosterone-treated female canaries were compared with a rare group of spontaneously singing female canaries to study whether testosterone stimulation would be different from natural stimulation.
2019-03-31 | GSE83674 | GEO
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage. Microarray analysis was performed on the cortex of neonatal brains using Illumina mouse Ref8 V2 genechips. The right common carotid artery was exposed through a ventral midline neck incision and permanently occluded by electrocoagulation, The wound was sutured and mouse pups were returned to their mother for 1.5M-bM-^@M-^S2 h. Sham control and pre-conditioned mice (n = 4) underwent the identical procedure, without carotid artery occlusion. Pups were then placed in an 8% O2/92% N2 humidified chamber at 37M-BM-0C for 1 h with tissue extraction taking place 3h, 8h and 24h thereafter (n=4 respectively). Sham controls were included in this study too (n=4 respectively).
2013-12-31 | E-GEOD-23317 | biostudies-arrayexpress
Project description:Hypoxia-ischemia (HI) brain damage is one of the most common causes of neonatal brain injuries, amidst other conditions such as intrauterine infection and perinatal cerebral hemorrhage (Bracci et al., 2006). HI, occurring during the perinatal period, severely affects brain integrity resulting in detrimental long-term neurological morbidity in terms of motor, intellectual, educational and neuropsychological performance deficits (e.g. cerebral palsy, mental retardation, learning disability and epilepsy), and even neonatal mortality (Cowan et al., 2003; Ferriero, 2004; van Handel et al., 2007; Shalak and Perlman, 2004). Current therapeutic interventions fail to provide substantial reversal of HI brain injuries and improvement in overall cognitive function. Recent clinical studies demonstrated that post-HI hypothermia provide moderate neuroprotection but fail to show any significant reduction in neonatal morbidity and mortality (Shankaran et al., 2005). We would like to investigate the transcriptional effects of HI on neonatal brain, and if hypoxic pre-conditioning is beneficial to the reduction of brain damage. Microarray analysis was performed on the striatum of neonatal brains using Illumina mouse Ref8 V2 genechips. The right common carotid artery was exposed through a ventral midline neck incision and permanently occluded by electrocoagulation, The wound was sutured and mouse pups were returned to their mother for 1.5M-bM-^@M-^S2 h. Sham control and pre-conditioned mice (n = 4) underwent the identical procedure, without carotid artery occlusion. Pups were then placed in an 8% O2/92% N2 humidified chamber at 37M-BM-0C for 1 h with tissue extraction taking place 3h, 8h and 24h thereafter (n=4 respectively). Sham controls were included in this study too (n=4 respectively).
2013-12-31 | E-GEOD-23319 | biostudies-arrayexpress
Project description:Background: Colorectal cancer (CRC) remains the second leading cause of cancer mortality in the U.S., with significant racial and ethnic disparities in incidence, survival, and mortality rates. The rising incidence of early-onset CRC and the frequent presentation at advanced stages of CRC among the Hispanics makes this an important ethnic group to study. A deeper understanding of the complex interplay between molecular, genetic, and environmental factors is critical for developing targeted therapies to reduce the prevalence in specific racial and ethnic groups, such as Hispanics. This study explores the role of stress-survival pathway (SSP) genes in early-onset and late-stage CRC, primarily focusing on disparities between Hispanics and Non-Hispanic Whites (NHWs). Additionally, this study investigates the role of MCM10, in contributing to CRC disparities among the Hispanic populations with an emphasis of early-onset and late-stage CRC Hispanics. Methods: One of our previous studies had identified some SSP protein coding genes associated with CRC. The expressions of these genes were validated in CRC cell lines, cDNA arrays, tissue microarrays, and tissue samples using qRT-PCR, and immunohistochemistry. The transcript-level expressions of differentially expressed SSP genes were further evaluated in Hispanic and NHWs tumor tissues, including early onset and late-stage cohorts. Additionally, we performed cellular physiological and functional assays to explore the role of MCM10 in tumor progression, before and after siRNA mediated knockdown. High-throughput transcriptomic and proteomic analyses were performed to reveal the underlying molecular mechanism. Results: We observed differential expressions of twelve SSP genes in CRC cell lines, at the transcript level; that of ten genes in early and late stages using cDNA arrays, and nine genes at the protein levels using tissue microarrays and immunohistochemistry. Hispanic CRC samples showed differential expression of all nine SSP genes compared to NHWs, in early-onset, and late-stage CRC, with all genes being upregulated other than CDK4 and PRDX4 in late-stage CRC and CDK4 in early-onset CRC. Our functional study demonstrated that MCM10 knockdown in CRC cell lines significantly reduced cell proliferation, growth, invasion and migration by inducing cell cycle arrest, apoptosis and reactive oxygen species pathways. The integrative RNA-sequencing and proteomics study reported that the novel gene PPFI1A could be associated with MCM10 mediated cancer progression. The role of MCM10 and PPFI1A in cancer progression has been validated using a Hispanic CRC patient derived organoid. Conclusion: This study highlights the role of SSP genes, particularly MCM10, in colorectal cancer progression and its potential as a biomarker and therapeutic target to address Hispanic CRC disparities.
2025-08-06 | GSE304110 | GEO