Piscataquis County, Maine, 1858 (Image 2 of 2) (Raster Image)

This layer is a georeferenced raster image of the historic paper map entitled: Map of Piscataquis County Maine, from surveys under the direction of H. F. Walling; field notes under the direction of L. H. Eaton Esq. civil engineer. It was published by Lee & Marsh in 1858. Scale [ca 1:63,360]. This layer is image 2 of 2 total images, representing the northwest portion of the four sheet source map. The image inside the map neatline is georeferenced to the surface of the earth and fit to the Universal Transverse Mercator projection (UTM Zone 19N, meters, NAD1983). 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 roads, railroads, drainage, public buildings, schools, churches, cemeteries, industry locations (e.g. mills, factories, mines, etc.), private buildings with names of property owners, town boundaries, and more. Relief shown by hachures. It includes many cadastral insets of individual county towns and villages. It also includes illustrations, business directories, and tables of statistics and distances.This layer is part of a selection of digitally scanned and georeferenced historic maps of New England from the Harvard Map Collection. These maps typically portray both natural and manmade features. The selection represents a range of regions, originators, ground condition dates, scales, and map purposes.

Chicago, Illinois, and vicinity, 1910 (Raster Image)

This layer is a georeferenced raster image of the historic paper map entitled: Blanchard's map of Chicago and suburbs. It was published by Rufus Blanchard in 1910. Scale [ca. 1:49,600]. The image inside the map neatline is georeferenced to the surface of the earth and fit to the Illinois East State Plane Coordinate System NAD83 (in Feet) (Fipszone 1201). 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 roads, elevated roads, railroads, railroad stations, street car lines, drainage, selected industry locations, parks and boulevards, city limits and ward boundaries, and more. Includes insets: Lake shore north of Chicago -- Cook, Dupage, and Will counties, also parts of Kane County, Ill., and Lake County, Ind.. This layer is part of a selection of digitally scanned and georeferenced historic maps from The Harvard Map Collection as part of the Imaging the Urban Environment project. Maps selected for this project represent major urban areas and cities of the world, at various time periods. These maps typically portray both natural and manmade features at a large scale. The selection represents a range of regions, originators, ground condition dates, scales, and purposes.

Cross-country insurance mechanisms in currency unions. Bruegel Working Paper 2014/04, 27 March 2014

Countries in a monetary union can adjust to shocks either through internal or external mechanisms. We quantitatively assess for the European Union a number of relevant mechanisms suggested by Mundell’s optimal currency area theory, and compare them to the United States. For this purpose, we update a number of empirical analyses in the economic literature that identify (1) the size of asymmetries across countries and (2) the magnitude of insurance mechanisms relative to similar mechanisms and compare results for the European Monetary Union (EMU) with those obtained for the US. To study the level of synchronization between EMU countries we follow Alesina et al. (2002) and Barro and Tenreyro (2007). To measure the effect of an employment shock on employment levels, unemployment rates and participation rates we perform an analysis based on Blanchard and Katz (1992) and Decressin and Fatas (1995). We measure consumption smoothing through capital markets, fiscal transfers and savings, using the approach by Asdrubali et al. (1996) and Afonso and Furceri (2007). To analyze risk sharing through a common safety net for banks we perform a rudimentary simulation analysis. |

A new eosinophilic esophagitis (EoE)-like disease without tissue eosinophilia found in EoE Families

BACKGROUND Eosinophilic esophagitis (EoE) is a rapidly emerging, chronic inflammatory, genetically impacted disease of the esophagus, defined clinically by symptoms of esophageal dysfunction and, pathologically, by an eosinophil-predominant tissue infiltration. However, in four EoE-families, we have identified patients presenting with EoE-typical and corticosteroid-responsive symptoms, but without tissue eosinophilia. It was the aim of this study to clinically and immunologically characterize these patients with EoE-like disease. METHODS Five patients suffering from an EoE-like disease were evaluated with endoscopic, histologic, functional and quantitative immunohistologic examinations, and mRNA expression determination. RESULTS The frequency of first generation offspring of EoE-like disease patients affected by EoE or EoE-like disease was 40%. Immunofluorescence analysis confirmed an almost complete absence of eosinophils in the esophageal tissues of patients with EoE-like disease, but revealed a considerable T cell infiltration, comparable to EoE. In contrast to EoE, eotaxin-3 mRNA and protein were markedly reduced in EoE-like disease (P < 0.05). The mRNA expression levels of three selected EoE genes (eotaxin-3, MUC4 and CDH26) allowed to discriminate between EoE-like disease, EoE and normal epithelium. CONCLUSIONS Patients suffering from "EoE without eosinophilia" do not fulfill formally the diagnostic criteria for EoE. However, their clinical manifestation, immunohistology and gene-expression pattern, plus the fact that they bequeath EoE to their offspring, suggest a uniform underlying pathogenesis. Conventional EoE, with its prominent eosinophilia, therefore appears to be only one phenotype of a broader "inflammatory dysphagia syndrome" spectrum. In this light, the role of the eosinophils, the definition of EoE, and its diagnostic criteria must likely be reconsidered. This article is protected by copyright. All rights reserved.

Microglial Cells Prevent Hemorrhage in Neonatal Focal Arterial Stroke

Perinatal stroke leads to significant morbidity and long-term neurological and cognitive deficits. The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. To understand whether microglial cells limit injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/ALK5 signaling, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO). Microglial depletion by intracerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage and triggered hemorrhages in injured regions 24 h after tMCAO. Lack of microglia did not alter expression or intracellular redistribution of several tight junction proteins, did not affect degradation of collagen IV induced by the tMCAO, but altered cell types producing TGFβ1 and the phosphorylation and intracellular distribution of SMAD2/3. Selective inhibition of TGFbr2/ALK5 signaling in microglia via intracerebral liposome-encapsulated SB-431542 delivery triggered hemorrhages after tMCAO, demonstrating that TGFβ1/TGFbr2/ALK5 signaling in microglia protects from hemorrhages. Consistent with observations in neonatal rats, depletion of microglia before tMCAO in P9 Cx3cr1(GFP/+)/Ccr2(RFP/+) mice exacerbated injury and induced hemorrhages at 24 h. The effects were independent of infiltration of Ccr2(RFP/+) monocytes into injured regions. Cumulatively, in two species, we show that microglial cells protect neonatal brain from hemorrhage after acute ischemic stroke. SIGNIFICANCE STATEMENT The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. We assessed whether microglial cells preserve neurovascular integrity after neonatal stroke. In neonatal rats, microglial depletion or pharmacological inhibition of TGFbr2/ALK5 signaling in microglia triggered hemorrhages in injured regions. The effect was not associated with additional changes in expression or intracellular redistribution of several tight junction proteins or collagen IV degradation induced by stroke. Consistent with observations in neonatal rats, microglial depletion in neonatal mice exacerbated stroke injury and induced hemorrhages. The effects were independent of infiltration of monocytes into injured regions. Thus, microglia protect neonatal brain from ischemia-induced hemorrhages, and this effect is consistent across two species.

The youth of Shakspeare /

"Slips from Shakespeare's tree" (newspaper clipping) mounted on inside front cover.

En la colonia, 1800-1815; poema.

Mode of access: Internet.

1987 University of Michigan Football Team

1988 University of Michigan Football Team

University of Michigan Men's Basketball Team, 2000

Back Row: Assistant Tom Sorboro, Assistant Kurtis Townsend, Darius Taylor, Rotolu Adebiyi, Brandon Smith, Josh Asselin, Peter Vignier, Chris Young, Leland Anderson, LaVell Blanchard, Herb Gibson, Assistant Scott Trost, Assistant Lorenzo Neely.

Front Row: Trainer Steve Stricker, Mike Gotfredson, Gavin Groninger, Kevin Gaines, head coach Brian Ellerbe, Jamal Crawford, Leon Jones, Ramal Hunter, equip. mngr. Bob Bland.

University of Michigan Men's Basketball Team, 2001

Back Row: assoc. head coach Scott Trost, asst. coach Kurtis Townsend, asst. coach Terence Greene, LaVell Blanchard, Bernard Robinson Jr., Chris Young, Josh Moore, Josh Asselin, Rotolu Adebiyi, director of basketball operations Tom Sorboro, trainer Steve Stricker, equip. mngr. Bob Bland.

Front Row: Avery Queen, Mike Gotfredson, Leon Jones, head coach Brian Ellerbe, Gavin Groninger, Herb Gibson, Maurice Searight

University of Michigan Men's Basketball Team, 2002

Back Row (standing): Coach Tommy Amaker, director of basketball operations Kirsten Green, strength coach Jim Plocki, asst. coach Charles E. Ramsey, Dommanic Ingerson, Bernard Robinson Jr., Chuck Bailey, Josh Moore, Ron Garber, Colin Dill, LaVell Blanchard, Herb Gibson, asst. coach Billy Schmidt, equip. mngr. Bob Bland, asst. coach Chuck Swenson.

Front Row: admin. asst. Steve Grialou, mngr. Alan Hibino, Avery Queen, Marcus Bennett, captain Rotolu Adebiyi, captain Chris Young, captain Leon Jones, Gavin Groninger, Mike Gotfredson, mngr. Lucien St. Gerard, trainer Eric Broekhuizen.

University of Michigan Men's Basketball Team, 2003

Back Row:: academic advisor Angie Heath, head coach Tommy Amaker, director of basketball operations Kirsten Green, asst. coach Billy Schmidt, asst. coach Charles E. Ramsey, Lester Abram, Chuck Bailey, J.C. Mathis, Graham Brown, Chris Hunter, Amadou Ba, Colin Dill, Bernard Robinson Jr., admin. asst. Andy Moore, strength coach Jim Plocki, asst. coach Chuck Swenson, equip. mngr. Bob Bland.

Front Row: trainer Eric Broekhuizen, sr. mngr. Michael Oh, Sherrod Harrell, Dommanic Ingerson, Gavin Groninger, LaVell Blanchard, Rotolu Adebiyi, Daniel Horton, Avery Queen, sr. mngr. Jesse Grasty, sr. mngr. Lucien St. Gerard.

University of Michigan Men's Basketball Team, 2003

Back Row: Lester Abram, Chuck Bailey, J.C. Mathis, Graham Brown, Chris Hunter, Amadou Ba, Colin Dill, Bernard Robinson Jr.

Front Row: Sherrod Harrell, Dommanic Ingerson, Gavin Groninger, LaVell Blanchard, Rotolu Adebiyi, Daniel Horton, Avery Queen.