28 research outputs found
Vesicle adhesion in the electrostatic strong-coupling regime studied by time-resolved small-angle X-ray scattering
We have used time-resolved small-angle X-ray scattering (SAXS) to study the adhesion of lipid vesicles in the electrostatic strong-coupling regime induced by divalent ions. The bilayer structure and the interbilayer distance dw between adhered vesicles was studied for different DOPC:DOPS mixtures varying the surface charge density of the membrane, as well as for different divalent ions, such as Ca2+, Sr2+, and Zn2+. The results are in good agreement with the strong coupling theory predicting the adhesion state and the corresponding like-charge attraction based on ion-correlations. Using SAXS combined with the stopped-flow rapid mixing technique, we find that in highly charged bilayers the adhesion state is only of transient nature, and that the adhering vesicles subsequently transform to a phase of multilamellar vesicles, again with an inter-bilayer distance according to the theory of strong binding. Aside from the stopped-flow SAXS instrumentations used primarily for these results, we also evaluate microfluidic sample environments for vesicle SAXS in view of future extension of this work
Global Transcriptome Analysis of RNA Abundance Regulation by ADAR in Lung Adenocarcinoma
Despite tremendous advances in targeted therapies against lung adenocarcinoma, the majority of patients do not benefit from personalized treatments. A deeper understanding of potential therapeutic targets is crucial to increase the survival of patients. One promising target, ADAR, is amplified in 13% of lung adenocarcinomas and in-vitro studies have demonstrated the potential of its therapeutic inhibition to inhibit tumor growth. ADAR edits millions of adenosines to inosines within the transcriptome, and while previous studies of ADAR in cancer have solely focused on protein-coding edits, >99% of edits occur in non-protein coding regions. Here, we develop a pipeline to discover the regulatory potential of RNA editing sites across the entire transcriptome and apply it to lung adenocarcinoma tumors from The Cancer Genome Atlas. This method predicts that 1413 genes contain regulatory edits, predominantly in non-coding regions. Genes with the largest numbers of regulatory edits are enriched in both apoptotic and innate immune pathways, providing a link between these known functions of ADAR and its role in cancer. We further show that despite a positive association between ADAR RNA expression and apoptotic and immune pathways, ADAR copy number is negatively associated with apoptosis and several immune cell types' signatures
1979 Farm Business Analysis Report Dairy Summary by Herd Size
Exact date of working paper unknown
PTR Explorer: An approach to identify and explore Post Transcriptional Regulatory mechanisms using proteogenomics
Toxicol Sci
Triclosan is an antimicrobial chemical incorporated into many personal, medical and household products. Approximately, 75% of the U.S. population has detectable levels of triclosan in their urine, and although it is not typically considered a contact sensitizer, recent studies have begun to link triclosan exposure with augmented allergic disease. We examined the effects of dermal triclosan exposure on the skin and lymph nodes of mice and in a human skin model to identify mechanisms for augmenting allergic responses. Triclosan (0%-3%) was applied topically at 24-h intervals to the ear pinnae of OVA-sensitized BALB/c mice. Skin and draining lymph nodes were evaluated for cellular responses and cytokine expression over time. The effects of triclosan (0%-0.75%) on cytokine expression in a human skin tissue model were also examined. Exposure to triclosan increased the expression of TSLP, IL-1\u3b2, and TNF-\u3b1 in the skin with concomitant decreases in IL-25, IL-33, and IL-1\u3b1. Similar changes in TSLP, IL1B, and IL33 expression occurred in human skin. Topical application of triclosan also increased draining lymph node cellularity consisting of activated CD86(+)GL-7(+) B cells, CD80(+)CD86(+) dendritic cells, GATA-3(+)OX-40(+)IL-4(+)IL-13(+) Th2 cells and IL-17\u2009A(+) CD4 T cells. In\ua0vivo antibody blockade of TSLP reduced skin irritation, IL-1\u3b2 expression, lymph node cellularity, and Th2 responses augmented by triclosan. Repeated dermal exposure to triclosan induces TSLP expression in skin tissue as a potential mechanism for augmenting allergic responses.CC999999/Intramural CDC HHSUnited States/CAN 927ZLCU/PHS HHSUnited States
