1997 University of Michigan Football Team

<div><p><b>Back Row</b>: Todd Jager, Kevin Lynch, Paul Schmidt, Mike Gittleson, Rick Clark, Vance Bedford, Brady Hoke, Jim Herrmann, Mike DeBord, Fred Jackson, Bobby Morrison, Stan Parrish, Erik Campbell, Terry Malone, Harold Goodwin, Scott Draper, Jon Falk, Phil Bromley, Mike Elston, Chris Kurpeikis</p><p><b>8th Row</b>: Eddie Davis, Eric Dean, Eddie Magnus, Ethan Perkins, Toni Grant, Brodie Killian, Jake Malacos, Jeremy Miller, Gary Rose, Rudy Smith, Jamie Young, Bob Bland, Rick Brandt, Steve Connelly, Kelly Cox, Peter Clifford, Matt Hamilton, Scott Loeffler</p><p><b>7th Row</b>: Patrick McCall, James Whitley, DeWayne Patmon, Anthony Jordan, Eric Brackins, Ray Jackson, Adam Adkins, Bob Fraumann, Shawn Thompson, Todd Mossa, Bill Seymour, Eric Rosel, Demetrius Smith, Anthony Thomas, William Peterson, Johathan West, P.J. Cwayna</p><p><b>6th Row</b>: David Downs, Chad Henman, Jeff Del Verne, Ryan Parini, Mark Bergin, Eric Wilson, Eric Warner, Jake Frysinger, Kurt Anderson, Maurice Williams, Ben Mast, Jason Brooks, Andy Sechler, Dan Williams, Chris Roth, Matt Johnson</p><p><b>5th Row</b>: LeAundre Brown, Ian Gold, Grady Brooks, Cory Sargent, Kevin Brandt, Steve Hutchinson, Jason Kapsner, Jeff Backus, Paul Tannous, Chad Carpenter, Jerry Johnson, Tommy Hendricks, Dhani Jones, Marcus Knight, Aaron Wright</p><p><b>4th Row</b>: J.R. Ford, Kenneth Jackson, Tate Schanski, Jason Cummings, Rob Renes, Jeff Holtry, Pat Kratus, Lance Ostram, Jason Clyne, Jared Chandler, Kevin Bryant, Jeff Smokevitch, Chad Stock, Brandon Kornblue, Manus Edwards</p><p><b>3rd Row</b>: Clarence Williams, DaydrionTaylor, Charles Woodson, DiAllo Johnson, James Hall, Steve Frazier, Tom Brady, Jeff Potts, Chris Ziemann, Tai Streets, Aaron Shea, Josh Williams, Jason Vinson, Brent Washington, Darren Petterson</p><p><b>2nd Row</b>: Jay Feely, Todd Brooks, Marcus Ray, Kraig Baker, Sam Sword, Nate Miller, Juaquin Feazell, Mark Campbell, JerameTuman, Clint Copenhaver, Noah Parker, Mike Singletary, Scott Parachek, Andre Weathers, Russell Shaw</p><p><b>Front Row</b>: Dr. Gerald O'Connor, Brian Griese, Colby Keefer, Eric Mayes, Rob Swett, Zach Adami, Glen Steele, Head Coach Lloyd Carr, Ben Huff, Chris Howard, Chris Floyd, David Crispin, Jon Jansen, Scott Dreisbach, Terrence Quinn</p></div>

Mowat-wilson Syndrome.

73

Mania as the first manifestation of Wilson`s disease

Background: Although mental changes are frequent in Wilson`s disease, severe psychiatric disorders occur uncommonly and usually accompany the neurological picture. There are few reports in the literature of Wilson`s disease patients with typical bipolar affective disorder (BPAD). Case report: The authors report the case of a patient with Wilson`s disease whose initial manifestation was a manic episode followed by depression. Tremor in the upper limbs appeared one year after the onset of symptoms. The diagnosis of Wilson`s disease was established three years after the first symptoms appeared, based on the neuropsychiatric picture, the detection of Kayser-Fleischer rings and the results of diagnostic tests indicating chronic liver disease and copper excess. ATP7B genotyping and magnetic resonance imaging of the brain with proton spectroscopy study were also performed. The patient became asymptomatic two years after starting treatment with penicillamine and remained non-symptomatic controlled during the eight-year follow-up period, without any specific treatment for the BPAD. Conclusions: To our knowledge, this is a singular report of a case of Wilson`s disease in which a manic episode preceded the onset of neurological symptoms. The association between Wilson`s disease and bipolar disorder is discussed.

Neurological manifestations and ATP7B mutations in Wilson`s disease

Wilson`s disease (WD) is a rare inborn metabolic error characterized by deficient biliary copper excretion secondary to ATP7B gene mutations. Neurological presentations are variable in respect to both pattern and age of onset; commonly a movement disorder presents in the second or third decade. The aim of this study was to ascertain genotype correlations with distinct neurological manifestations in 41 WD patients in a Brazilian center for WD. A total of 23 distinct mutations were detected, and the frameshift 3402de1C had the highest allelic frequency (31.7%). An association between 3402de1C and dysphagia was detected (p = 0.01) but the limited number of patients is insufficient to allow one to draw conclusions. Both clinical studies analyzing larger cohorts and basic research on ATP7B protein function could potentially shed more light on our understanding of WD. (c) 2007 Elsevier Ltd. All rights reserved.

Wilson`s disease: two treatment modalities. Correlations to pretreatment and posttreatment brain MRI

Brain magnetic resonance imaging (MRI) studies on Wilson`s disease (WD) show lack of correlations between neurological and neuroimaging features. Long-term follow-up reports with sequential brain MRI in patients with neurological WD comparing different modalities of treatment are scarce. Eighteen patients with neurological WD underwent pretreatment and posttreatment brain MRI scans to evaluate the range of abnormalities and the evolution along these different periods. All patients underwent at least two MRI scans at different intervals, up to 11 years after the beginning of treatment. MRI findings were correlated with clinical picture, clinical severity, duration of neurological symptoms, and treatment with two different drugs. Patients were divided into two groups according to treatment: d-penicillamine (D-P), zinc (Zn), and Zn after the onset of severe intolerance to D-P. MRI scans before treatment showed, in all patients, hypersignal intensity lesions on T2- and proton-density-weighted images bilaterally and symmetrically at basal nuclei, thalamus, brain stem, cerebellum, brain cortex, and brain white matter. The most common neurological symptoms were: dysarthria, parkinsonism, dystonia, tremor, psychiatric disturbances, dysphagia, risus sardonicus, ataxia, chorea, and athetosis. From the neurological point of view, there was no difference on the evolution between the group treated exclusively with D-P and the one treated with Zn. Analysis of MRI scans with longer intervals after the beginning of treatment depicted a trend for neuroimaging worsening, without neurological correspondence, among patients treated with Zn. Neuroimaging pattern of evolution was more favorable for the group that received exclusively D-P.

Effect of the toxic milk mutation (tx) on the function and intracellular localization of Wnd, the murine homologue of the Wilson copperATPase

Wilson disease is an autosomal recessive copper transport disorder resulting from defective biliary excretion of copper and subsequent hepatic copper accumulation and liver failure if not treated. The disease is caused by mutations in the ATP7B (WND) gene, which is expressed predominantly in the liver and encodes a copper-transporting P-type ATPase that is structurally and functionally similar to the Menkes protein (MNK), which is defective in the X-linked copper transport disorder Menkes disease. The toxic milk (tx) mouse has a clinical phenotype similar to Wilson disease patients and, recently, the tx mutation within the murine WND homologue (Wnd) of this mouse was identified, establishing it as an animal model for Wilson disease. In this study, cDNA constructs encoding the wild-type (Wnd-wt) and mutant (Wnd-tx) Wilson proteins (Wnd) were generated and expressed in Chinese hamster ovary (CHO) cells. The fx mutation disrupted the copper-induced relocalization of Wnd in CHO cells and abrogated Wnd-mediated copper resistance of transfected CHO cells. In addition, co-localization experiments demonstrated that while Wnd and MNK are located in the trans-Golgi network in basal copper conditions, with elevated copper, these proteins are sorted to different destinations within the same cell, Ultrastructural studies showed that with elevated copper levels, Wnd accumulated in large multivesicular structures resembling late endosomes that may represent a novel compartment for copper transport. The data presented provide further support for a relationship between copper transport activity and the copper-induced relocalization response of mammalian copper ATPases, and an explanation at a molecular level for the observed phenotype of fx mice.

For Your Freedom and Ours: The Polish Question in Wilson's Peace Initiatives, 1916 - 1917

The first eighteen months of the Great War witnessed an unprecedented awakening of interest in the Polish Question, when worldwide attention was drawn to the prolonged devastation of the Polish territories. Thereafter, a steady increase in media comment and criticism, highlighting Poland's plight, fostered public indignation at the continual stalling of humanitarian relief efforts for Polish refugees. Such burgeoning popular sentiment focused wider political attention upon a growing movement for recognition of Polish claims to independence. This particularly proved to be the case for Woodrow Wilson and his administration's budding interest in Poland. Subsequently, nowhere did the Polish Question assume a greater role in diplomatic efforts to mediate for peace than in America, and at no time more than during the year preceding the President's hesitant decision to intervene in hostilities.

Transcrição e tradução do audiobook "Eric"

Orientação: Professora Maria Helena Anacleto-Matias