Bird metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559752 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13151400_1.fastq.gz | Fastqsanger.gz | |||
| SRR13151400_2.fastq.gz | Fastqsanger.gz | |||
| SRR13151401_1.fastq.gz | Fastqsanger.gz | |||
| SRR13151401_2.fastq.gz | Fastqsanger.gz | |||
| SRR13151402_1.fastq.gz | Fastqsanger.gz |
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Project description:Male song sparrows (Melospiza melodia) are territorial year-round; however, neuroendocrine responses to simulated territorial intrusion (STI) differ between breeding (spring) and non-breeding seasons (autumn). In spring, exposure to STI leads to increases in luteinizing hormone and testosterone, but not in autumn. These observations suggest that there are fundamental differences in the mechanisms driving neuroendocrine responses to STI between seasons. Microarrays, spotted with EST cDNA clones of zebra finch, were used to explore gene expression profiles in the hypothalamus after territorial aggression in two different seasons. Free-living territorial male song sparrows were exposed to either conspecific or heterospecific (control) males in an STI in spring and autumn. Behavioral data were recorded, whole hypothalami were collected, and microarray hybridizations were performed. Quantitative PCR was performed for validation. Our results show 262 cDNAs were differentially expressed between spring and autumn in the control birds. There were 173 cDNAs significantly affected by STI in autumn; however, only 67 were significantly affected by STI in spring. There were 88 cDNAs that showed significant interactions in both season and STI. Results suggest that STI drives differential genomic responses in the hypothalamus in the spring vs. autumn. The number of cDNAs differentially expressed in relation to season was greater than in relation to social interactions, suggesting major underlying seasonal effects in the hypothalamus which may determine the differential response upon social interaction. Functional pathway analyses implicated genes that regulate thyroid hormone action and neuroplasticity as targets of this neuroendocrine regulation. For condition experiment, SC (spring control), AC (autumn control), SE (spring STI), AE (autumn STI) Biological replicates: 7 in SC, 8 in AC, SE, AE. One Melospiza melodia subject and one universal SoNG reference (pooled Taeniopygia guttata brain) per array.
2010-05-18 | E-GEOD-18970 | biostudies-arrayexpress
Project description:Male song sparrows (Melospiza melodia) are territorial year-round; however, neuroendocrine responses to simulated territorial intrusion (STI) differ between breeding (spring) and non-breeding seasons (autumn). In spring, exposure to STI leads to increases in luteinizing hormone and testosterone, but not in autumn. These observations suggest that there are fundamental differences in the mechanisms driving neuroendocrine responses to STI between seasons. Microarrays, spotted with EST cDNA clones of zebra finch, were used to explore gene expression profiles in the hypothalamus after territorial aggression in two different seasons. Free-living territorial male song sparrows were exposed to either conspecific or heterospecific (control) males in an STI in spring and autumn. Behavioral data were recorded, whole hypothalami were collected, and microarray hybridizations were performed. Quantitative PCR was performed for validation. Our results show 262 cDNAs were differentially expressed between spring and autumn in the control birds. There were 173 cDNAs significantly affected by STI in autumn; however, only 67 were significantly affected by STI in spring. There were 88 cDNAs that showed significant interactions in both season and STI. Results suggest that STI drives differential genomic responses in the hypothalamus in the spring vs. autumn. The number of cDNAs differentially expressed in relation to season was greater than in relation to social interactions, suggesting major underlying seasonal effects in the hypothalamus which may determine the differential response upon social interaction. Functional pathway analyses implicated genes that regulate thyroid hormone action and neuroplasticity as targets of this neuroendocrine regulation.
2009-12-16 | GSE18970 | GEO
Project description:Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the M-bM-^@M-^\TNFR1 signalingM-bM-^@M-^] as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered. In this study, we analyzed the expression profiles of 6 biological replicates of blood monocytes from ACHF patients pre- and post-treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). All RNAs from pre-treatment monocytes were hybridized against RNAs from post-treatment RNAs. We performed a total of 11 technical replicates.
2013-10-31 | E-GEOD-51888 | biostudies-arrayexpress
Project description:Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the “TNFR1 signaling” as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered.
2013-10-31 | GSE51888 | GEO
Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of STAT3 on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of STAT3 in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for STAT3. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE35514 | GEO
Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of NF-kappaB RelA (p65) on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with functional deletion of NF-kappaB RelA (p65) in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE35513 | GEO
Project description:Photoperiod and hormonal cues drive dramatic seasonal changes in structure and function of the avian song control system. Little is known, however, about the patterns of gene expression associated with seasonal changes. Here we address this issue by exposing Gambel’s white-crowned sparrows to season-appropriate cues and extracting RNA from the telencephalic song control nuclei HVC and RA across multiple time points that capture different stages of growth and regression. We chose HVC and RA because while both nuclei change in volume across seasons, the cellular mechanisms underlying these changes differ. We thus hypothesized that different genes would be expressed between HVC and RA. We tested this by using the extracted RNA to perform a cDNA microarray hybridization developed by the SoNG initiative. We then validated these results using qRT-PCR. Supporting our hypothesis, only 59 of the 363 genes of interest were found to vary by more than |1.5| fold in expression in both nuclei, while 132 gene expression changes were HVC specific and 172 genes were RA specific. We then assigned many of these genes to functional categories relevant to the different mechanisms underlying seasonal change in HVC and RA, including neurogenesis, apoptosis, cell growth, dendrite arborization and axonal growth, angiogenesis, endocrinology, growth factors, and electrophysiology. This revealed categorical differences in the kinds of genes regulated in HVC and RA. These results show that different molecular programs underlie seasonal changes in HVC and RA, and that gene expression is time specific across different reproductive conditions. Our results provide insights into the complex molecular pathways that underlie adult neural plasticity.
2012-10-01 | GSE28347 | GEO
Project description:A common response to physiological duress is the hepatic acute phase response, a process during which the expression of many genes is altered in the liver. Amongst these transcripts are those encoding acute phase proteins, defined as circulating proteins with significantly changed concentrations during an acute phase response. The goal of this study was to determine the influence of two transcription factors, STAT3 and NF-kappaB p65 (RelA), on hepatic gene changes including but not limited to acute phase proteins during bacterial pneumonia. Using the Cre-LoxP system, mice were generated with combined functional deletions of both STAT3 and RelA in hepatocytes. In mutant mice, Cre-recombinase was expressed under transcriptional control of an albumin promoter in the presence of homozygous floxed alleles for both STAT3 and RelA. Wild-type control mice lacked the Cre-recombinase transgene. Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE32105 | GEO
Project description:The immune response plays a pivotal role in initiating cardiac repair and remodeling in both the acute and chronic phase after ST-Elevated myocardial infarction (STEMI). To dissect the longitudinal character of the immune response in STEMI patients over time, we performed single-cell RNA-sequencing (scRNA-seq) on a total of 95,995 peripheral blood mononuclear cells (PBMCs) collected from 38 STEMI patients at hospital admission, 24 hours (acute phase) and 6-8 weeks (chronic phase) after STEMI. Additionally, comparison to healthy controls was performed using previously generated scRNA-seq data on 33,878 PBMCs from 38 age- and sex-matched healthy controls from the Dutch population cohort Lifelines DEEP.
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