Severe cerebral ischemia caused by events such as ischemic stroke or cardiac arrest is a relatively common and life-threating condition. Those who survive frequently suffer from significant cerebral dysfunction, often with poor outcome. To date the treatment options are limited. Concomitant hyperglycemia is frequently perceived both in focal and global transient ischemia, augmenting the ischemic brain injury as revealed by experimental and clinical studies.
Hyperglycemia Alters Expression of Cerebral Metabolic Genes after Cardiac Arrest.
Specimen part, TreatmentView Samples
Microarray based mRNA profiling was used to identify the mechanism of action for the small molecule b-AP15.
Inhibition of proteasome deubiquitinating activity as a new cancer therapy.
Cell line, TreatmentView Samples
In this study the gene expression in cells infected with lytic and non-lytic variants of coxsackievirus B2 Ohio (CVB2O) were analyzed using next generation sequencing. This approach was selected with the purpose of elucidating the effects of lytic and non-lytic viruses on host cell transcription. Total RNA was extracted from infected cells, next generation sequencing was performed, and the reads were subsequently mapped against the human and CVB2O genomes. The amount of intracellular virions was measured, showing a relative amount of virus RNA 13 times higher in the cells infected with the lytic variant, vVP1Q164K, compared to cells infected by the non-lytic CVB2Owt. Furthermore, differential gene expression in the cells infected with the two viruses was identified and a number of genes singled out as possible keys to the answer of how the viruses interact with the host cells, resulting in lytic or non-lytic infections. Overall design: 4 samples, two samples of one strain, one sample of a different strain, and one control sample
The Transcriptome of Rhabdomyosarcoma Cells Infected with Cytolytic and Non-Cytolytic Variants of Coxsackievirus B2 Ohio-1.
No sample metadata fieldsView Samples
Vitamin A is the only known compound that produces spontaneous fractures in rats. In an effort to resolve the molecular mechanism behind this effect, we fed young rats high doses of vitamin A and performed a global transcriptional analysis of diaphyseal bone after one week, i.e. just before the first fractures appeared. Microarray gene expression analysis revealed that 68 transcripts were differentially expressed in hypervitaminotic cortical bone and 118 transcripts were found when the bone marrow was also included. 98% of the differentially expressed genes in the bone marrow sample were up-regulated. In contrast, hypervitaminotic cortical bone without marrow showed reduced expression of 37% of differentially expressed genes. Gene Ontology (GO) analysis revealed that only samples containing bone marrow were associated to a GO term, which principally represented extracellular matrix (ECM). This is consistent with the histological findings of increased endosteal bone formation. Four of the genes in this ECM cluster and four other genes, including Cyp26b1 which is known to be up-regulated by vitamin A, were selected and verified by real-time PCR. In addition, immunohistochemical staining of bone sections confirmed that the bone-specific molecule, osteoadherin (Omd) was up-regulated. Further analysis of the major gene expression changes revealed distinct differences between cortical bone and bone marrow, e.g. there appeared to be augmented Wnt signaling in the bone marrow but reduced Wnt signaling in cortical bone. Moreover, induced expression of hypoxia-associated genes was only found in samples containing bone marrow. Together, these results corroborate our previous observations of compartment-specific effects of vitamin A, with reduced periosteal but increased endosteal bone formation, and suggest important roles for Wnt signaling and hypoxia in the processes leading to spontaneous fractures.
Microarray profiling of diaphyseal bone of rats suffering from hypervitaminosis A.
Sex, Age, Specimen part, DiseaseView Samples
We performed microarray analysis to investigate the gene expression profile changes induced by Hmg20b knock down in I/11 cells.
The DNA binding factor Hmg20b is a repressor of erythroid differentiation.
Specimen partView Samples
Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.
The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.
Cell lineView Samples
Bulk RNA Sequencing of Healthy Bone Marrow Mononuclear Cells Overall design: Using standard operating procedures, mononuclear cells from bone marrow aspirates were isolated using Ficoll density gradient separation and cryopreserved in 90% FBS/ 10% DMSO for storage in liquid nitrogen. RNA was harvested from thawed cell vials of BMMCs using AllPrep kits (QIAGEN). Libraries were prepared using TruSeq Stranded Total RNA Sample Preparation Kit (Illumina) with 1ug of RNA input. Sequencing was performed by paired-end 75 nt on Illumina HiSeq 3000.
Human bone marrow assessment by single-cell RNA sequencing, mass cytometry, and flow cytometry.
Age, Specimen part, SubjectView Samples
Malaria infection renders humans more attractive to Anopheles gambiae sensu lato mosquitoes than uninfected people. The mechanisms remain unknown. Here, we show that an isoprenoid precursor produced by Plasmodium falciparum, (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMBPP), affects A. gambiae s.l. blood meal seeking and feeding behaviors, as well as susceptibility to infection. HMBPP acts indirectly by triggering human red blood cells to increase the release of CO2, aldehydes, and monoterpenes, which together enhance vector attraction, and stimulate vector feeding. When offered in a blood meal, HMBPP modulates neural, antimalarial, and oogenic gene transcription without affecting mosquito survival or fecundity, while in a P. falciparum infected blood meal, sporogony is increased. Overall design: Differential expression was quantified from whole body of mosquitoes in biological triplicates at 1, 3, 6 and 24 hours post treatment with either RBCs or hmbRBCs.
A key malaria metabolite modulates vector blood seeking, feeding, and susceptibility to infection.
Subject, TimeView Samples
The specific contribution of the two TNF-receptors Tnfr1 and Tnfr2 to TNF-induced inflammation in the glomerulus is unknown. In mice, TNF exposure induces glomerular expression of inflammatory mediators like adhesion molecules and chemokines in vivo, and glomerular accumulation of leukocytes.
Distinct contributions of TNF receptor 1 and 2 to TNF-induced glomerular inflammation in mice.
Specimen part, TreatmentView Samples
593 FFPE colorectal cancer samples were used to generate three prediction models: Recurrence prediction, 5FU efficacy prediction, and FOLFOX efficacy prediction
Building personalized treatment plans for early-stage colorectal cancer patients.
Specimen partView Samples