8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, heart obtained at 12 weeks (thus animals were diabetic for 4 weeks). Left vent of heart.
Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart.
No sample metadata fields
View SamplesEffect of type 1 diabetes (induced by streptozotocin 60 mg/kg) on lung gene expression. Wistar rats, male. At age 8 weeks control rats got IP buffer, diabetic rats got streptozotocin. At age 12 weeks animals were anesthetized and lungs removed. RNA was extracted with Trizol, and gene expression array analysis was performed using Affymetrix RAE 230A microarrays according to the directions from the manufacturer. Arrays were scanned using a Hewlett Packard Gene Array scanner, and analyzed with Affymetrix MAS 5.0 software. Expression levels reported are the output from the MAS software.
Alterations in lung gene expression in streptozotocin-induced diabetic rats.
Age, Specimen part
View SamplesNormal young adult Sprague Dawley rats (male)
Differential expression of lipid and carbohydrate metabolism genes in upper airway versus diaphragm muscle.
No sample metadata fields
View SamplesComparison of gene expression of heart (left vent) and diaphragm of normal Sprague Dawley rats, young adult
Contrast between cardiac left ventricle and diaphragm muscle in expression of genes involved in carbohydrate and lipid metabolism.
No sample metadata fields
View SamplesVaccinia virus infection of mouse lungs produces a focal infection within the lung remaining at the large bronchi throughout the course of infection. Animals die of respiratory failure with little edema and few infiltrating immune cells. It is well established that poxviruses control the host immune system by encoding multiple host defense pathway antagonists.
Roles of vaccinia virus genes E3L and K3L and host genes PKR and RNase L during intratracheal infection of C57BL/6 mice.
Specimen part
View SamplesIn this study, we evaluated global Mtb-induced gene expression in airway immune cells obtained by bronchoalveolar lavage of individuals with latent tuberculosis infection (LTBI) and in Mtb-naïve control subjects
<i>Mycobacterium tuberculosis</i>-Induced Bronchoalveolar Lavage Gene Expression Signature in Latent Tuberculosis Infection Is Dominated by Pleiotropic Effects of CD4<sup>+</sup> T Cell-Dependent IFN-γ Production despite the Presence of Polyfunctional T Cells within the Airways.
Specimen part, Disease
View SamplesEfforts to unravel the mechanisms underlying taste sensation (gustation) have largely focused on rodents. The first comprehensive database of gene expression in primate (Macaca fascicularis) taste buds is presented. This database provides a foundation for further studies in diverse aspects of taste biology. A taste bud gene expression database was generated using laser capture microdissection (LCM) of tissue freeze medium OTC embedded macaque tongue tissue blocks. We collected fungiform (FG) taste buds at the front of the tongue, circumvallate (CV) taste buds at the back of the tongue, as well as non-gustatory lingual epithelium (LE). Gene expression was also analyzed in the top and bottom portions of CV taste buds collected using LCM. Samples were collected from 10 animals - 7 female, 3 male.
Genome-wide analysis of gene expression in primate taste buds reveals links to diverse processes.
Sex, Age, Specimen part
View SamplesBACKGROUND: Young age at portoenterostomy has been linked to improved outcome in biliary atresia, but pre-existing biological factors may influence the rate of disease progression. In this study, we aimed to determine whether molecular profiling of the liver identifies stages of disease at diagnosis. METHODS: We examined liver biopsies from 47 infants with biliary atresia enrolled in a prospective observational study. Biopsies were scored for inflammation and fibrosis, used for gene expression profiles, and tested for association with indicators of disease severity, response to surgery, and survival at 2 years. RESULTS: Fourteen of 47 livers displayed prominent features of inflammation (N=9) or fibrosis (N=5), with the remainder showing similar levels of both simultaneously. Differential profiling of gene expression of the 14 livers displayed a unique molecular signature containing 150 gene probes. Applying prediction analysis models, the probes classified 29 of the remaining 33 livers into inflammation or fibrosis. Molecular classification into the two groups was validated by the findings of increased hepatic population of lymphocyte subsets or tissue accumulation of matrix substrates. The groups had no association with traditional markers of liver injury or function, response to surgery, or complications of cirrhosis. However, infants with an inflammation signature were younger, while those with a fibrosis signature had decreased transplant-free survival. CONCLUSION: Molecular profiling at diagnosis of biliary atresia uncovers a signature of inflammation or fibrosis in most livers. This signature may relate to staging of disease at diagnosis and has implications to clinical outcomes.
Staging of biliary atresia at diagnosis by molecular profiling of the liver.
Specimen part
View SamplesPurpose: The goal of this study is to investigate the role of CBS enzyme in colorectal carcinogenesis Methods: RNA-Seq transcriptome analysis of CBS-overexpression in NCM356 cels compared to control vector cells Overall design: RNA-seq transcriptome profiling of NCM356-CBS overexpressing cells vs. vector cells
Upregulation of Cystathionine-β-Synthase in Colonic Epithelia Reprograms Metabolism and Promotes Carcinogenesis.
Subject
View SamplesCell lines bearing MLL translocations (MV4-11 and MOLM-13) were treated with a potent, selective inhibitor of the DOT1L histone methyl transferase. Treatment of MLL-rearranged cell lines with the DOT1L inhibitor selectively inhibits H3K79 methylation and blocks expression of leukemogenic genes. Here we provide expression profiling data of cells treated with DOT1L inhibitor or vehicle control.
Selective killing of mixed lineage leukemia cells by a potent small-molecule DOT1L inhibitor.
Cell line, Time
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