Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128705 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A Novel Model of Common TLR4- and Injury induced transcriptional themes in Human Leukocytes (supported by NIH grant GM34695)
2015-09-15 | E-GEOD-22278 | ExpressionAtlas
Project description:A comparison of gene expression between control versus IPF human lung MPC using human Affy 1.0st chips. This work was funded by grants to S.M. Majka from the NIH R01HL091105 and NIH R01HL11659701. Additional funding was also provided by PPG-5P01HL108800-04 (PI:J. Loyd). Experiments were performed using the University of Colorado Cancer Center Microarray core (NCI P30 CA 46934-14). The project was supported in part by the National Center for Research Resources, Grant UL1 RR024975-01, and is now at the National Center for Advancing Translational Sciences, Grant 2 UL1 TR000445-06.
2017-03-23 | GSE94060 | GEO
Project description:This study examines the mechanisms underlying fumarate- and glyoxylate-mediated changes in tobraymcyin sensitivity in PAO1 cells Grant ID: NIH Grant K99 GM 118907 Grant title: Effects of Host Metabolic Variation on Antibiotic Susceptibility Funding Source: NIH NIGMS Name: Jason Yang
2016-12-20 | GSE90620 | GEO
Project description:In order to better understand the effects of social stress on the prefrontal cortex, we investigated gene expression in mice subjected to acute and repeated social encounters of different duration using microarrays. The observed up-regulation of genes associated with vascular system and brain injury suggests that stressful social encounters may affect brain function through the stress-induced dysfunction of the vascular system. The study was supported by Grant N N311 604938, 2011/03/N/NZ29/05222 and partially by IP2011 030371. Statistical analysis of microarray data was supported with Grant N N519 657940.
2015-01-07 | GSE64734 | GEO
Project description:Colorectal cancer (CRC) remains the third most common cancer in the US, with 15% of cases displaying Microsatellite Instability (MSI) secondary to Lynch Syndrome (LS) or somatic hypermethylation of the MLH1 promoter. A cohort of rhesus macaques from our institution developed spontaneous mismatch repair deficient (MMRd) CRC with a notable fraction harboring a pathogenic germline mutation in MLH1. DNA methylation and transcriptome analysis was used to evaluate the rhesus macaque as a model organism to study carcinogenesis, develop immunotherapies and vaccines, and implement chemoprevention approaches pertinent to sporadic MSI-H and LS CRC in humans. NIH grant(s): Grant ID: 5 P30 CA016672-44 Grant title: Cancer Center Support Grant Affiliation: The University of Texas MD Anderson Cancer Center Grantor: NCI
2022-03-31 | GSE178381 | GEO
Project description:Colorectal cancer (CRC) remains the third most common cancer in the US, with 15% of cases displaying Microsatellite Instability (MSI) secondary to Lynch Syndrome (LS) or somatic hypermethylation of the MLH1 promoter. A cohort of rhesus macaques from our institution developed spontaneous mismatch repair deficient (MMRd) CRC with a notable fraction harboring a pathogenic germline mutation in MLH1. DNA methylation and transcriptome analysis was performed to evaluate the rhesus macaque as a model organism to study carcinogenesis, develop immunotherapies and vaccines, and implement chemoprevention approaches pertinent to sporadic MSI-H and LS CRC in humans. NIH grant(s): Grant ID: 5 P30 CA016672-44 Grant title: Cancer Center Support Grant Affiliation: The University of Texas MD Anderson Cancer Center Grantor: NCI
2022-03-31 | GSE178377 | GEO
Project description:Comparison of Enteral versus Parenteral Feeding in Healthy Human Subjects (Supported by NIH grant GM34695)
| PRJNA125941 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below. NIH grant(s): Grant ID: 5 P30 CA016672-44 Grant title: Cancer Center Support Grant Affiliation: The University of Texas MD Anderson Cancer Center Grantor: NCI
2022-03-31 | GSE178383 | GEO
Project description:Toll like receptor 4 (TLR4), an innate immunity gene, is involved in responses to several pulmonary agonists including endotoxin (LPS; Poltorak et al.,1998), ozone (O3 ,Kleeberger et. al., 2001), Pseudomonas aeruginosa (Faure et al, 2004), and hyperoxia (Zhang et al, 2005). TLR4 appears to partially mediate the response to LPS- and O3-induced lung injury, however, TLR4 is protective for prevention of injury in Pseudomonas aeruginosa infection and against acute lung injury (hyperoxia). The mechanism behind this protection is unclear. We previously demonstrated that TLR4 was also protective against BHT-induced chronic inflammation and tumor promotion (Bauer et al, 2005). C.C3H-Tlr4Lps-d (BALBLps-d) mice, congenic for a 10 cM region of C3H/HeJ chromosome 4 that contains Tlr4 (Vogel et al, 1994), have a missence mutation that renders TLR4 dysfunctional. The Tlr4 mutation likely abrogates signaling by disrupting a direct point of contact with other signaling molecules (Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol 2004;4(7):499-511.). Bronchoalveolar lavage fluid (BALF) alveolar macrophages, lymphocytes, and total protein content were significantly elevated in BALBLps-d mice compared to BALB/c (BALB; Tlr4 sufficient) mice following chronic BHT (Bauer et al., 2005). BALBLps-d mice also had a significant increase in tumor multiplicity (60%) over that of BALB mice in response to an MCA/BHT tumor promotion protocol. While this was the first model to demonstrate a protective role for TLR4 in chronic lung inflammation and tumorigenesis, the downstream mechanism regulating this protective response remains unknown. Using Affymetrix microarray analysis followed by GeneSpring and Ingenuity pathway analyses, we herein identified known and novel downstream pathways and their interactions that may be involved in the protective mechanism elicited by TLR4. We therefore hypothesize that these pathways and interactions amongst the genes identified during the tumor promotion/chronic inflammation stage are in part influencing the differential strain response observed during tumorigenesis. Keywords: time course, tumor study Protocol 1 - 3 biological replicates after chronic dosing in each mouse strain Protocol 2 - multiple replicates after MCA/BHT tumor progression model used
2009-12-12 | E-GEOD-8504 | biostudies-arrayexpress
Project description:Radiation-induced lung injury is a common late side-effect of thoracic radiotherapy. The inflammatory microenvironment plays a key role in this process. Endothelial cells are the goalkeeper of inflammation. Endothelial dysfunction following leukocytes infiltrated is a prominent feature in the pathogenesis of radiation-induced lung injury. Tyrosine phosphatase Shp2 is a key regulator of endothelial functions and inflammation. Here, we established a clinical-mimicking mouse model of radiation-induced lung injury and found that Shp2 activity was elevated in endothelium after injury. Mice with endothelium-specific Shp2 deletion showed relieved collagen deposition along with disrupted radiation-induced Jag1 expression in the endothelium. Furthermore, endothelium-derived Jag1 activated the alternative activation of macrophages in vitro and in vivo by paracrine Notch signaling. Consistently, Notch pathway was significant activated by chest irradiation in the peripheral blood leukocytes of cancer patients. Collectively, this is the first demonstration of radiation-induced lung injury regulation by endothelial Shp2. Shp2 participates in the radiation-induced endothelial dysfunction and subsequently inflammatory microenvironment producing.
2021-12-18 | GSE191056 | GEO