INTRODUCTION: Persistent lung inflammation, with an influx of polymorphonuclear leukocytes and monocytes, occurs early in bronchopulmonary dysplasia. We hypothesized that: 1) that interleukin-10, a potent anti-inflammatory cytokine, would cause a markedly different gene expression profile compared to dexamethasone in these cells, and 2) monocyte insensitivity to dexamethasone was related to glucocorticoid receptor expression.
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Specimen part
View SamplesIntroduction: Increasing evidence now supports the association between the fetal inflammatory response syndrome (FIRS) with the pathogenesis of preterm labor, intraventricular hemorrhage and bronchopulmonary dysplasia. These disorders are among the most important causes of mortality and morbidity in the perinatal period. During the fetal inflammatory response syndrome (FIRS) polymorphonuclear leukocytes (PMNs) and monocytes (MONOs) are sequentially recruited into the placenta; the same process occurs in the lung of the newborn during the development of bronchopulmonary dysplasia (BPD). The aim of the study was to reveal cell-specific differences in gene expression and cytokine release in response to endotoxin that would elucidate inflammatory control mechanisms in the newly born.
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Treatment
View SamplesHuman B-1 cells (CD20+CD27+CD43+CD38lo/int) and pre-plasmablast like cells (CD20+CD27hiCD38hi) are new antibody secreting cells identified in circulation. We used microarray to compare and contrast expressed genes between these two cell population
Distinctions among Circulating Antibody-Secreting Cell Populations, Including B-1 Cells, in Human Adult Peripheral Blood.
Specimen part
View SamplesThe goal of this study was to determine the differential expression of specific genes within the papilloma tissues themselves and to characterize the array of host genes that might be important in the pathophysiology of recurrent respiratory papillomatosis.
Immune dysregulation and tumor-associated gene changes in recurrent respiratory papillomatosis: a paired microarray analysis.
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View SamplesBlood pressure regulation is known to be maintained by a neuro-endocrine circuit, but whether immune cells contribute to blood pressure homeostasis has not been determined. We previously showed that CD4+ T lymphocytes that express choline acetyltransferase (ChAT), which catalyzes the synthesis of the vasorelaxant acetylcholine, relay neural signals.
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Specimen part
View SamplesWe used microarrays to detail genome-wide gene expression underlying cardiac myocyte pathologies and identified candidate genes and specific pathways affecting cardiac myopathies
Reduced phosphoinositide 3-kinase (p110alpha) activation increases the susceptibility to atrial fibrillation.
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View SamplesCardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity.
PI3K(p110 alpha) protects against myocardial infarction-induced heart failure: identification of PI3K-regulated miRNA and mRNA.
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View SamplesCell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p.
Cell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p.
Treatment
View SamplesSirtuin deacetylases and forkhead box class O (FOXO) transcription factors are central regulators of cell survival, cell cycle and cellular resistance to stress in response to signals from hormones, growth factors and oxidative stress. FOXO activity is modulated by the sirtuins, which function in a NAD+-dependent manner. Sirtuin activity, on the other hand is subject to inhibition by a natural compound nicotinamide (NAM). This study aims to investigate the effects of NAM on the
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View SamplesSirtuin deacetylases and forkhead box class O (FOXO) transcription factors are central regulators of cell survival, cell cycle and cellular resistance to stress in response to signals from hormones, growth factors and oxidative stress. FOXO activity is modulated by the sirtuins, which function in a NAD+-dependent manner. Sirtuin activity, on the other hand is subject to inhibition by a natural compound nicotinamide (NAM). This study aims to investigate the effects of NAM on the
No associated publication
No sample metadata fields
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