Indenture, signed by John Rutledge, 1786.

Indenture for Ephraim Mitchell for 295 pounds, signed by John Rutledge in Charleston, South Carolina, August 29, 1786. Rutledge was an American statesman and judge from South Carolina.https://digitalcommons.wofford.edu/littlejohnmss/1092/thumbnail.jp

A systems biology analysis of brain microvascular endothelial cell lipotoxicity.

BackgroundNeurovascular inflammation is associated with a number of neurological diseases including vascular dementia and Alzheimer's disease, which are increasingly important causes of morbidity and mortality around the world. Lipotoxicity is a metabolic disorder that results from accumulation of lipids, particularly fatty acids, in non-adipose tissue leading to cellular dysfunction, lipid droplet formation, and cell death.ResultsOur studies indicate for the first time that the neurovascular circulation also can manifest lipotoxicity, which could have major effects on cognitive function. The penetration of integrative systems biology approaches is limited in this area of research, which reduces our capacity to gain an objective insight into the signal transduction and regulation dynamics at a systems level. To address this question, we treated human microvascular endothelial cells with triglyceride-rich lipoprotein (TGRL) lipolysis products and then we used genome-wide transcriptional profiling to obtain transcript abundances over four conditions. We then identified regulatory genes and their targets that have been differentially expressed through analysis of the datasets with various statistical methods. We created a functional gene network by exploiting co-expression observations through a guilt-by-association assumption. Concomitantly, we used various network inference algorithms to identify putative regulatory interactions and we integrated all predictions to construct a consensus gene regulatory network that is TGRL lipolysis product specific.ConclusionSystem biology analysis has led to the validation of putative lipid-related targets and the discovery of several genes that may be implicated in lipotoxic-related brain microvascular endothelial cell responses. Here, we report that activating transcription factors 3 (ATF3) is a principal regulator of TGRL lipolysis products-induced gene expression in human brain microvascular endothelial cell

I Kiss\u27d You In A Dream : Song And Chorus

https://digitalcommons.library.umaine.edu/mmb-vp/1663/thumbnail.jp

De Old Churchyard In De Lane

Old man reading to young girl under treehttps://scholarsjunction.msstate.edu/cht-sheet-music/13648/thumbnail.jp

The Politics of Annexation: Oligarchic Power in a Southern City

This Open Access Edition of The Politics of Annexation presents a newly formatted version of the original 1982 edition. The text itself has been edited only for non-substantive style changes and corrections. The Preface, the new Introduction (“Fifty Years Later”), and the index were prepared especially for this edition. The original edition was published by Schenkman Publishing Company, Cambridge, Massachusetts, and is available online through the UR Scholarship Repository at https://scholarship.richmond.edu/bookshelf/307/ The Politics of Annexation examines the process of American cities using annexation of suburban areas as a tool to increase their tax base and generate new revenue. The authors find that the annexation by Richmond, Virginia of part of Chesterfield County in 1970 was in fact racially motivated, and a way to dilute the black vote. They examine the details behind the annexation as well as its aftermath in subsequent litigation, leading to the Supreme Court. They also study annexation cases in Houston and San Antonio, drawing parallels with Richmond regarding their racially-based annexation efforts. The Politics of Annexation is one of the first scholarly attempts to explain the uniqueness of civil rights activism in Richmond --Julian Maxwell Hayter, from his Preface.https://scholarscompass.vcu.edu/politics_annexation/1000/thumbnail.jp

Downscaling Storm Surge Models for Engineering Applications

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Postprandial apoE isoform and conformational changes associated with VLDL lipolysis products modulate monocyte inflammation.

ObjectivePostprandial hyperlipemia, characterized by increased circulating very low-density lipoproteins (VLDL) and circulating lipopolysaccharide (LPS), has been proposed as a mechanism of vascular injury. Our goal was to examine the interactions between postprandial lipoproteins, LPS, and apoE3 and apoE4 on monocyte activation.Methods and resultsWe showed that apoE3 complexed to phospholipid vesicles attenuates LPS-induced THP-1 monocyte cytokine expression, while apoE4 increases expression. ELISA revealed that apoE3 binds to LPS with higher affinity than apoE4. Electron paramagnetic resonance (EPR) spectroscopy of site-directed spin labels placed on specific amino acids of apoE3 showed that LPS interferes with conformational changes normally associated with lipid binding. Specifically, compared to apoE4, apoE bearing the E3-like R112→Ser mutation displays increased self association when exposed to LPS, consistent with a stronger apoE3-LPS interaction. Additionally, lipolysis of fasting VLDL from normal human donors attenuated LPS-induced TNFα secretion from monocytes to a greater extent than postprandial VLDL, an effect partially reversed by blocking apoE. This effect was reproduced using fasting VLDL lipolysis products from e3/e3 donors, but not from e4/e4 subjects, suggesting that apoE3 on fasting VLDL prevents LPS-induced inflammation more readily than apoE4.ConclusionPostprandial apoE isoform and conformational changes associated with VLDL dramatically modulate vascular inflammation