The main goal of the research was to find some new biomarkers for the monitoring of the Minimal Residual Disease in Acute Lymphoblastic Leukemia patients.
No associated publication
Sex, Age
View SamplesHelicobacter pylori is a well-recognized bacterium associated with the development of several histopathological lesions in the stomach. The chronic infection produces an inflammatory lesion known as gastritis. This lesion can later progress to more serious lesions such as intestinal metaplasia. Some attempts in the transcriptome of these conditions have been made; these however, have yielded limited information. Given the potential of high-throughput technologies for understanding biological processes altered and in the description of biomarkers of disease, we performed a genome-wide gene expression analysis in gastric biopsies. The aim of this study was to describe the altered molecular mechanism and potential biomarkers of follicular gastritis, chronic gastritis and intestinal metaplasia, through the identification of characteristic gene expression profiles in each histopathological lesion. The exploratory set comprised twenty-one biopsies from patients with follicular gastritis (n=7), chronic gastritis (n=7), and intestinal metaplasia (n=7), which were analyzed by whole-genome gene expression microarrays. The enrichment analyses and functional annotation of genes using computational tools were performed. The bioinformatics data of the same 21 biopsies were validated by real time PCR analysis while 79 FFPE samples were analyzed by immunohistochemistry.
No associated publication
Sex, Age
View SamplesGlioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3-THP) similarly promotes cell proliferation in the U87 human GBM cell line.
Allopregnanolone Alters the Gene Expression Profile of Human Glioblastoma Cells.
Specimen part, Cell line, Treatment
View SamplesWe analyzed the changes in the spinal cord transcriptome after a spinal cord contusion injury and MSC or OEC transplantation. The cells were injected immediately or 7 days after the injury. The mRNA of the spinal cord injured segment was extracted and analyzed by microarray at 2 and 7 days after cell grafting.
Gene expression changes in the injured spinal cord following transplantation of mesenchymal stem cells or olfactory ensheathing cells.
Treatment
View SamplesThe GeneChip Porcine Genome Array was used to identify the transcriptional response upon Salmonella typhimurium infection in three porcine intestinal sections (jejumun, ileum and colon) along a time course of 1,2 and 6 days post infection.
No associated publication
Specimen part, Treatment
View SamplescAMP receptor protein (CRP, also known as the catabolite activator protein [CAP]) is arguably the best-studied of the global transcription factors of E coli. CRP alone is responsible for regulating at least 283 operons. Upon binding cAMP, the CRP dimer binds DNA and directly interacts with RNA polymerase (RNAP). At Class II promoters, CRP binds near position -41,5 relative to the transcription start site and contacts the amino-terminal domain of the RNAP subunit (RNAP-NTD). This interaction requires AR2, a patch of primarily positively charged residues (H19, H21, E96, and K101) that interact with negatively charged residues on RNAP-NTD. Acetylome analyses consistently detect lysine 100 (K100) of CRP as acetylated. Since K100 is adjacent to the positively charged AR2, we hypothesized that the K100 positive charge may also play a role in CRP function. We further hypothesized that acetylation of K100 would neutralize this positive charge, leading to a potential regulatory mechanism
Influence of Glucose Availability and CRP Acetylation on the Genome-Wide Transcriptional Response of <i>Escherichia coli</i>: Assessment by an Optimized Factorial Microarray Analysis.
No sample metadata fields
View SamplesThe genomic causes of inbreeding depression are poorly known. Several studies have found widespread transcriptomic alterations in inbred organisms, but it remains unclear which of these alterations are causes of the depression and which are mere responses to the ensuing physiological stress.
No associated publication
Specimen part
View SamplesA detailed knowledge of the mechanisms underlying brain aging is fundamental to understand its functional decline and the baseline upon which brain pathologies superimpose. Endogenous protective mechanisms must contribute to the adaptability and plasticity still present in the healthy aged brain. Apolipoprotein D (ApoD) is one of the few genes with a consistent and evolutionarily conserved up-regulation in the aged brain. ApoD protecting roles upon stress or injury are well known, but a study of the effects of ApoD expression in the normal aging process is still missing. Using an ApoD-knockout mouse we analyze the effects of ApoD on factors contributing to the functional maintenance of the aged brain. We focused our cellular and molecular analyses in cortex and hippocampus at an age representing the onset of senescence where mortality risks are below 25%, avoiding bias towards long-lived animals. Lack of ApoD causes a prematurely aged brain without altering lifespan. Age-dependent hyperkinesia and memory deficits are accompanied by differential molecular effects in cortex and hippocampus. Transcriptome analyses reveal distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus, with different cell-type contributions to age-regulated gene expression. Markers of glial reactivity, proteostasis, and oxidative and inflammatory damage reveal early signs of aging and enhanced brain deterioration in the ApoD-knockout brain. The lack of ApoD results in an age-enhanced significant reduction in neuronal calcium-dependent functionality markers and signs of early reduction of neuronal numbers in the cortex, thus impinging upon parameters clearly differentiating neurodegenerative conditions from healthy brain aging. Our data support the hypothesis that the physiological increased brain expression of ApoD represents a homeostatic anti-aging mechanism.
Aging without Apolipoprotein D: Molecular and cellular modifications in the hippocampus and cortex.
Sex, Age, Specimen part
View SamplesMonocytes play a critical role during infection with Mycobacterium tuberculosis (Mtb). They are recruited to the lung where they participate in the contention of infection. Alternatively, inflammatory monocytes may help in prolonging inflammation or serve as niches for Mtb infection. Also, monocyte response to infection may vary depending on the particularities of the clinical isolate of Mtb from which they are infected. In this pilot study, using microarrays we have examined the global mRNA profiles of circulating human monocytes from healthy individuals and patients with active tuberculosis (TB).
Infection of Monocytes From Tuberculosis Patients With Two Virulent Clinical Isolates of <i>Mycobacterium tuberculosis</i> Induces Alterations in Myeloid Effector Functions.
Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
NF-κB activation impairs somatic cell reprogramming in ageing.
Specimen part, Disease, Disease stage, Treatment
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