985 resultados para Project 2003-026-C : 2003-026-C
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Mode of access: Internet.
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Submitted to Illinois Department of Natural Resources.
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Provides statistics and trends of reported sexually transmitted diseases (STDs) in Illinois for 1993-2003 and consists of five sections: Illinois 2003 epidemiologic summary; Illinois statewide statistics tables; and chlamydia, gonorrhea and syphilis cases, rates and county demographics statistics tables. Laboratory data on viral STDs (herpes and hepatits C) testing at STD clinic and outreach sites are also included in the summary section.
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Includes index.
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"GAO/03-658."
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[Conceptual Sketch of Ideal Embassy], untitled. Black and orange ink sketch on graph paper, 8 1/2 x 11 inches [from photographic copy by Lance Burgharrdt]
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Top Row: (20 Staff) Andy Godek, Phil Johnson, Paul Schmidt, Brad Labade, Mark Collins, Mike Gittleson, Steve Morrison, Ron English, Bill Sheridan, Jim Herrmann, Scot Draper, Fred Jackson, Terry Malone, Andy Moeller, Erik Campbell, Scot Loeffler, Jim Boccher, Max Glowacki, Phil Bromley, Jon Falk
8th Row: (18 Staff) Dr. Gerald O'Connor, Dr. James Carpenter, Dr. C. Daniel Hendrickson, Vahan Agbabian, Kevin Tolbert, Kyle Bierlein, Jason Chesney, Dan Geraci, Kolby Wells, Dan Simelis, Matt Kernen, Jim Schneider, Senior Manager Devon Wilson, Taylor Morgan, Kyle Zink, Kevin Undeen, Rick Brandt, Bob Bland.
7th Row: (13 players) Kyle Myers, David Hull, Craig Moore, Ross Ryan, Garrett Rivas, Brandent Englemon, Will Paul, Prescott Burgess, Anton Campbell, Jerome Jackson, Quinton McCoy, Matt Wilde, Jeff Jansen.
6th Row: (19) Alijah Bradley, Mike Carl, Ryan Mundy, Leon Hall, Turner Booth, Jeff Kastl, Paul Sarantos, Clayton Richard, Shawn Crable, Jake Long, Adam Kraus, Patrick Sharrow, Lamarr Woodley, Jim Presley, David Schoonover, Mike Kaselitz, Mark Spencer, B.J. Opong-Owusu, Joseph Leoni.
5th Row: (18) Chris Matsos, Willis Barringer, Darnell Hood, Jason Avant, Steve Breaston, Matt Studenski, Derek Bell, Rondell Biggs, Kevin Murphy, Reuben Riley, Dave Harris, Mike Mandich, Carl Tabb, Brian Thompson, Pierre Rembert, Jacob Stewart, Obinna Oluigbo, Jonathan Borden.
4th Row: (19) Luke Perl, David Underwood, Lawrence Reid, Joey Sarantos, Alex Ofili, Matt Gutierrez, Mark Bihl, Tom Berishaj, Tyler Ecker, Mike Kolodziej, Gabriel Watson, Jeremy Van Alstyne, Larry Harrison, Scott McClintock, Marlin Jackson, Markus Curry, Jeremy Read, Brian Lafer.
3rd Row: (16) Brent Cummings, Charles Young III, Ross Mann, Braylon Edwards, Leo Henige, Tim Massaquoi, Matt Lentz, Zia Combs, Pat Massey, Jim Fisher, Pierre Woods, Earnest Shazor, Adam Stenavich, Andy Stejskal, Ross Kesler, Troy Nienberg.
2nd Row: (15) Phil Brabbs, Roy Manning, Andy Christopfel, Calvin Bell, David Baas, Larry Stevens, Alain Kashama, Demeterius Solomon, Spencer Brinton, Jeff Gaston, Adam Finley, Jermaine Gonzales, Zach Kaufman, Kevin Dudley, Tim Bracken.
Front Row: (13): Jon Shaw, Andy Mignery, Jeremy LeSueur, Courtney Morgan, Tony Pape, John Navarre, Lloyd Carr, Carl Diggs, Norman Heuer, Chris Perry, Grant Bowman, Dave Pearson, Tyrece Butler.
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Mode of access: Internet.
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The Southern Ocean (SO) plays a key role in modulating atmospheric CO2 via physical and biological processes. However, over much of the SO, biological activity is iron-limited. New in situ data from the Antarctic zone south of Africa in a region centered at -20°E - 25°E reveal a previously overlooked region of high primary production, comparable in size to the northwest African upwelling region. Here, sea ice together with enclosed icebergs is channeled by prevailing winds to the eastern boundary of the Weddell Gyre, where a sharp transition to warmer waters causes melting. This cumulative melting provides a steady source of iron, fuelling an intense phytoplankton bloom that is not fully captured by monthly satellite production estimates. These findings imply that future changes in sea-ice cover and dynamics could have a significant effect on carbon sequestration in the SO.
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Purpose. The aim of this study was to report the influence of hepatitis C virus (HCV) genotype and rejection episodes on the outcome of orthotopic liver transplantation (OLT), hepatitis recurrence, and progression to graft cirrhosis after OLT. Methods. Fifty-three patients who all had undergone OLT for end-stage liver cirrhosis were selected for this study. Hepatitis C genotype was determined. Recurrent hepatitis and rejection were diagnosed based on elevated liver function tests and a liver biopsy. Results. The patients were followed up for a mean of 51.9 +/- 34.3 months. The cumulative survival rate was no different in OLT for hepatitis C and OLT for all other liver diseases. After OLT, serum HCV RNA was detected in 93%. Histological recurrence occurred in 85% of all patients. The 1-, 3-, and 5-year recurrence rates were 48%, 77%, and 85%, respectively. Of the 41 patients with recurrent hepatitis C, 4 (10%) had cirrhosis, 18 (44%) had hepatitis with fibrosis, and 91 (46%) had hepatitis without fibrosis at the end of follow-up. A total of 32% of the patients were infected by HCV genotype 1b and 68% by other HCV genotypes. The recurrence rates were significantly higher in patients infected with genotype 1b than in those with other genotypes (p = 0.04). Twenty of 48 patients (42%) experienced acute rejection. There was a strong association between the number of rejection episodes and the incidence of HCV-related cirrhosis (p < 0.01). Conclusion. Our findings showed the genotype 1b to result in a higher recurrence rate after OLT. On the other hand, rejection episodes were associated with a more rapid progression to graft cirrhosis.
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Background: Increased levels of tumor necrosis factor (TNF)-alpha and oxidative stress have been implicated as factors contributing to hepatic injury in fatty liver diseases. As steatosis is associated with an accelerated progression of fibrosis in chronic hepatitis C (HCV), we hypothesized that the messenger (m)RNA expression of genes involved with the production of reactive oxygen species, inflammation and cellular injury would be increased in liver tissue from subjects with steatosis and chronic HCV. Methods: Real-time polymerase chain reaction was performed to determine relative mRNA expression levels of collagen I, TNF-alpha, cytochrome P450 2E1 (CYP 2E1), transforming growth factor-beta1 and CD14 in liver biopsies from 38 patients with chronic HCV. The mRNA expression levels were compared between subjects with and without steatosis, fibrosis, and inflammation. Results: Multivariate analysis demonstrated that collagen I mRNA expression was increased by 199% in steatosis (P = 0.02), 85% in moderate to severe fibrosis (P = 0.02) and 157% in inflammation (P = 0.03). Livers of patients with steatosis also had an increase in TNF-alpha mRNA expression by 50% (P = 0.03) and CYP 2E1 expression by 37% (P = 0.04) compared with non-steatotic livers. Tumor necrosis factor-alpha protein was localized to Kupffer cells, bile ducts and portal inflammatory cells by immunohistochemistry. Conclusion: Increased expression of TNF-alpha may be involved in the pathogenesis of liver injury and progression of fibrosis in individuals who have steatosis in association with chronic HCV. (C) 2003 Blackwell Publishing Asia Pty Ltd.
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The C2 domain is one of the most frequent and widely distributed calcium-binding motifs. Its structure comprises an eight-stranded beta-sandwich with two structural types as if the result of a circular permutation. Combining sequence, structural and modelling information, we have explored, at different levels of granularity, the functional characteristics of several families of C2 domains. At the coarsest level,the similarity correlates with key structural determinants of the C2 domain fold and, at the finest level, with the domain architecture of the proteins containing them, highlighting the functional diversity between the various subfamilies. The functional diversity appears as different conserved surface patches throughout this common fold. In some cases, these patches are related to substrate-binding sites whereas in others they correspond to interfaces of presumably permanent interaction between other domains within the same polypeptide chain. For those related to substrate-binding sites, the predictions overlap with biochemical data in addition to providing some novel observations. For those acting as protein-protein interfaces' our modelling analysis suggests that slight variations between families are a result of not only complementary adaptations in the interfaces involved but also different domain architecture. In the light of the sequence and structural genomic projects, the work presented here shows that modelling approaches along with careful sub-typing of protein families will be a powerful combination for a broader coverage in proteomics. (C) 2003 Elsevier Ltd. All rights reserved.