3,788 research outputs found

    The MHC-encoded TAP1/LMP2 bidirectional promoter is down-regulated in highly oncogenic adenovirus type 12 transformed cells

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    AbstractCells transformed by human adenovirus 12 (Ad12) exhibit extremely low surface levels of MHC class I molecules and contain reduced levels of class I heavy chain mRNAs. We report that levels of MHC-encoded TAP1 and LMP2 mRNAs are also down-regulated in Ad12-transformed rat cells, and that transcription of rat TAP1 and LMP2 transcripts is directed from a 564 bp intergenic region which is significantly less active in Ad12-transformed cells compared to those transformed with Ad5. Our results suggest that, in common with MHC class I gene expression, TAP1 and LMP2 gene expression is reduced mainly at the level of transcription in Ad12-transformed cells

    Senior Theses: Department of Physical Sciences

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    1993 Fall Semester Senior Theses for the class Physical Science 471: Petrologic Classification of Igneous and Metamorphic Rocks by Frank Baldridge X -Ray Analysis of Cave Sediments From Pigeon Water Cave of Northeastern Pine Mountain by Billy B. Stapleton The Correlation of Stream-deposited Breccias In Bat Cave, Carter Caves, Kentucky by James Bond Jointing and Faulting in Selected Areas of Eastern Kentucky by Mark A. Blai

    The zinc finger transcription factor PLAGL2 enhances stem cell fate and activates expression of ASCL2 in intestinal epithelial cells

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    An Integrated Analysis of Maternal-Infant Sleep, Breastfeeding, and Sudden Infant Death Syndrome Research Supporting a Balanced Discourse

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    Breastfeeding and the place of sleep for the mother and the infant have been controversial internationally due to reported concerns regarding infant deaths despite the known benefits of exclusive and prolonged breastfeeding, which are increased by breastfeeding at night. The aims of this integrated analysis were to (a) review breastfeeding and maternal and infant sleep research literature via historical, epidemiological, anthropological, and methodological lenses; (b) use this information to determine where we are currently in safeguarding both infant lives and breastfeeding; and (c) postulate the direction that research might take from this point forward to improve our knowledge and inform our policy and practice. Despite well-meaning but unsuccessful campaigns in some countries to dissuade parents from sleeping with their babies, many breastfeeding mothers and caregivers do sleep with their infants whether intentionally or unintentionally. Taking cultural contexts and socio-ecological circumstances into consideration, data supports policies to counsel parents and caregivers on safe sleep practices, including bed-sharing in non-hazardous circumstances, particularly in the absence of parental smoking, recent parental alcohol consumption, or sleeping next to an adult on a sofa. Further research with appropriate methodology is needed to drill down on actual rates of infant deaths, paying close attention to the definitions of deaths, the circumstances of the deaths, and confounding factors, in order to ensure we have the best information with which to derive public health policy. Introduction and use of the concept of “breastsleeping” is a plausible way to remove the negative connotations of “co-sleeping” and redirect ongoing data-driven discussions and education of best practices of breastfeeding and sleep

    Secondhand smoke inhibits both Cl- and K+ conductances in normal human bronchial epithelial cells

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    Secondhand smoke (SHS) exposure is an independent risk factor for asthma, rhinosinusitis, and more severe respiratory tract infections in children and adults. Impaired mucociliary clearance with subsequent mucus retention contributes to the pathophysiology of each of these diseases, suggesting that altered epithelial salt and water transport may play an etiological role. To test the hypothesis that SHS would alter epithelial ion transport, we designed a system for in vitro exposure of mature, well-differentiated human bronchial epithelial cells to SHS. We show that SHS exposure inhibits cAMP-stimulated, bumetanide-sensitive anion secretion by 25 to 40% in a time-dependent fashion in these cells. Increasing the amount of carbon monoxide to 100 ppm from 5 ppm did not increase the amount of inhibition, and filtering SHS reduced inhibition significantly. It was determined that SHS inhibited cAMP-dependent apical membrane chloride conductance by 25% and Ba2+-sensitive basolateral membrane potassium conductance by 50%. These data confirm previous findings that cigarette smoke inhibits chloride secretion in a novel model of smoke exposure designed to mimic SHS exposure. They also extend previous findings to demonstrate an effect on basolateral K+ conductance. Therefore, pharmacological agents that increase either apical membrane chloride conductance or basolateral membrane potassium conductance might be of therapeutic benefit in patients with diseases related to SHS exposure
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