Central America & Caribbean Region, 1858 (Raster Image)

This layer is a georeferenced raster image of the historic paper map entitled: A new map of tropical-America, north of the Equator : comprising the West-Indies, Central-America, Mexico, New Cranada [sic] and Venezuela by H. Kiepert. It was published by Dietrich Reimer in 1858. Scale [ca. 1:3,600,000].The image inside the map neatline is georeferenced to the surface of the earth and fit to the World Miller Cylindrical projected coordinate system. All map collar and inset information is also available as part of the raster image, including any inset maps, profiles, statistical tables, directories, text, illustrations, index maps, legends, or other information associated with the principal map. This map shows features such as drainage, roads, cities and other human settlements, territorial boundaries and colonial claims, shoreline features, and more. Relief shown by hachures and spot heights. Includes also text and inset map: Central part of the Mexican Republic on an enlarged scale, based upon the surveys published by A. v. Humboldt, v. Gerolt, Heller, Smith and the Sociedad Mejicana de Geografía y Estadística. Scale 1:1,000,000.This layer is part of a selection of digitally scanned and georeferenced historic maps from the Harvard Map Collection. These maps typically portray both natural and manmade features. The selection represents a range of originators, ground condition dates, scales, and map purposes.

The Aleut language, the elements of Aleut grammar with a dictionary in two parts containing basic vocabularies of Aleut and English,

"Aleut-English dictionary, compiled by Richard Henry Geoghegan. A vocabulary of the Aleutian or Unangan language as spoken on the eastern Aleutian Islands and on the Alaska Peninsula, being a translation of the Russian, 'Slovarʹ aleutsko-lisʹevskago yazyka' or 'Dictionary of the Aleut-Fox language', by Ivan Veniaminov, 1834, with additions and annotations by the compiler": p. 89-124.

Fulham palace, formerly called Fulham house, and Fulham manor : a short account of the old manor house of Fulham, written at the wish of the bishop on the occasion of His Lordship's visit to America and Canada, 1907 /

"The bishop of London and the mission field": p. 43-91.

Essays by the late Mark Pattison, sometime rector of Lincoln college;

Vol. 1. Gregory of Tours.--Early intercourse of England and Germany.--Antecedents of the Reformation.--The Stephenses.--Muretus.--Joseph Scaliger.--Life of Joseph Scaliger (Fragment).--Peter Daniel Huet.--A chapter of university history.--F.A. Wolf.--Oxford Studies.--Vol. 2. Calvin at Geneva.--Tendencies of religious thought in England, 1688-1750.--Life of Bishop Warburton.--The Calas tragedy.--Present state of theology in Germany (1857).--Learning in the Church of England.--Philanthropic societies in the reign of Queen Anne.--Life of Montaigne.--Pope and his editors.--Buckle's History of civilization in England.

Hymnes de Synésius ... : précédés d'une étude sur sa vie et ses écrits ; accompagnés d'un Hymne au Christ par Saint Clement Alexandrin ... ; et suivis des hymnes sacrés de Manzoni /

Mode of access: Internet.

Chronicles of the crusades;

Mode of access: Internet.

Materials for the history of Thomas Becket : archbishop of Canterbury (canonized by Pope Alexander III., A. D. 1173) /

Vol. 7 edited by James Craigie Robertson ... and J. Brigstocke Sheppard.

Discourses on some of the doctrinal articles of the church of England; also lectures on the history of Saint Peter.

First American from the last London edition.

The life of Saint Patrick, Apostle of Ireland, to which is added Saint Fiech's Irish Hymn; also a copious appendix of the various ecclesiastical institutions, &c. in Ireland,

Includes a hymn on the life, virtues and miracles of St. Patrick, composed by St. Fiech.

Food for Thought: Emergence of Food-Based Historical Museum Walking Tours

Thesis (Master's)--University of Washington, 2016-06

Characterization of heparin-binding site of tissue transglutaminase:its importance in cell surface targeting, matrix deposition, and cell signaling

Tissue transglutaminase (TG2) is a multifunctional Ca2+ activated protein crosslinking enzyme secreted into the extracellular matrix (ECM), where it is involved in wound healing and scarring, tissue fibrosis, celiac disease and metastatic cancer. Extracellular TG2 can also facilitate cell adhesion important in wound healing through a non-transamidating mechanism via its association with fibronectin (FN), heparan sulphates (HS) and integrins. Regulating the mechanism how TG2 is translocated into the ECM therefore provides a strategy for modulating these physiological and pathological functions of the enzyme. Here, through molecular modelling and mutagenesis we have identified the HS binding site of TG2 202KFLKNAGRDCSRRSSPVYVGR222. We demonstrate the requirement of this binding site for translocation of TG2 into the ECM through a mechanism involving cell surface shedding of HS. By synthesizing a peptide NPKFLKNAGRDCSRRSS corresponding to the HS binding site within TG2, we also demonstrate how this mimicking peptide can in isolation compensate the RGD-induced loss of cell adhesion on FN via binding to syndecan-4, leading to activation of PKCa, pFAK-397 and ERK1/2 and the subsequent formation of focal adhesions and actin cytoskeleton organization. A novel regulatory mechanism for TG2 translocation into the extracellular compartment that depends upon TG2 conformation and the binding of HS is proposed.

Inhibition of transglutaminase activity reduces extracellular matrix accumulation induced by high glucose levels in proximal tubular epithelial cells

Diabetic nephropathy affects 30-40% of diabetics leading to end-stage kidney failure through progressive scarring and fibrosis. Previous evidence suggests that tissue transglutaminase (tTg) and its protein cross-link product epsilon(gamma-glutamyl)lysine contribute to the expanding renal tubulointerstitial and glomerular basement membranes in this disease. Using an in vitro cell culture model of renal proximal tubular epithelial cells we determined the link between elevated glucose levels with changes in expression and activity of tTg and then, by using a highly specific site directed inhibitor of tTg (1,3-dimethyl-2[(oxopropyl)thio]imidazolium), determined the contribution of tTg to glucose-induced matrix accumulation. Exposure of cells to 36 mm glucose over 96 h caused an mRNA-dependent increase in tTg activity with a 25% increase in extracellular matrix (ECM)-associated tTg and a 150% increase in ECM epsilon(gamma-glutamyl)lysine cross-linking. This was paralleled by an elevation in total deposited ECM resulting from higher levels of deposited collagen and fibronectin. These were associated with raised mRNA for collagens III, IV, and fibronectin. The specific site-directed inhibitor of tTg normalized both tTg activity and ECM-associated epsilon(gamma-glutamyl)lysine. Levels of ECM per cell returned to near control levels with non-transcriptional reductions in deposited collagen and fibronectin. No changes in transforming growth factor beta1 (expression or biological activity) occurred that could account for our observations, whereas incubation of tTg with collagen III indicated that cross-linking could directly increase the rate of collagen fibril/gel formation. We conclude that Tg inhibition reduces glucose-induced deposition of ECM proteins independently of changes in ECM and transforming growth factor beta1 synthesis thus opening up its possible application in the treatment other fibrotic and scarring diseases where tTg has been implicated.

Mechanisms of ion channel activation in primary cultured and clonal cell lines

The effects of hypotonic shock upon membrane C1 permeability of ROS 17/2.8 osteoblast-like cells was investigated using the patch-clamp technique. Hypotonic shock produced cell swelling that was accompanied by large amplitude, outwardly rectifying, currents that were active across the entire physiological range of membrane potentials (-80 to +100 mV). At strong depolarisations (> +50 mV) the currents exhibited time-dependent inactivation that followed a monoexponential time course. The currents were anion selective and exhibited a selectivity sequence of SCN- > I > Br- > Cl- > F- > gluconate. Current activation was unaffected by inhibitors of protein kinase (A (H-89) and tyrosine kinase (tyrphostin A25), and could not be mimicked by elevation of intracellular Ca2+ or activation of protein kinase C. Similarly, disruption of actin filaments by dihydrocytochalsin B, or generation of membrane tension by dipyridamole failed to elicit significant increases in cell chloride permeability. The mechanism of current activation is as yet undetermined. The currents were effectively inhibited by the chloride channel inhibitors NPPB and DIDS but resistant to DPC. A Cl- conductance with similar characteristics was found to be present in mouse primary cultured calvarial osteoblasts. The volume-sensitive Cl- current in ROS 17/2.8 cells was inhibited by arachidonic acid in two distinct phases. A rapid block that developed within 10 s, preceding a slower developing inhibitory phase that occurred approximately 90 s after onset of arachidonate superfusion. Arachidonic acid also induced kinetic modifications of the current which were evident as an acceleration of the time-dependent· inactivation exhibited at depolarised potentials. Inhibitors of cyclo-oxygenases, lipoxygenases and cytochrome P-4S0 were ineffectual against arachidonic acid's effects sugtgesting that arachidonic acid may elicit it's effects directly. Measurements of cell volume under hypotonic conditions showed that ROS 17/2,8 cells could effectively regulate their volume, However, effective inhibitors of the volume-sensitive CI" current drastically impaired this response suggesting that physiologically this current may have a vital role in cell volume regulation, In L6 skeletal myocytes, vasopressin was found to rapidiy hyperpolarise cells. This appears to occur as the result of activation of Ca2+ -sensitive K+ channels in a process dependent upon the presence of extracellular Ca2+.