52 resultados para Melita.
Resumo:
Back Row: Asst. coaches Bob Thornbladh, Tom Reed, Jerry Hanlon, Tirrel Burton, Tim Davis, Bill McCartney, Jack Harbaugh, Paul Schudel, Dennis Brown, Don Nehlen, Barry Pierson, Jerry Zuver, Eqp. Mgr. Jon Falk, Trainer Lindsy McLean
8th Row: Marcus Bond, Chuck Christian, Greg Wunderli, Kurt Becker, Tony Osbun, Dan Kwiatkowski, Tom Wandersleben, Fred Motley, Andy Cannavino, Mike Kligis, Jim Breaugh, Oliver Johnson
7th Row: Kirk Yearian, B.J. Dickey, Alan Mitchell, Rodney Feaster, Stanley Edwards, Mike Trgovac, Dave Nicolau, Jeff Jackson, Neal Ginley, Kelley Keough, John Prepolec, Ben Needham, Stuart Harris, Rick Jones
6th Row: Derek Williams, Tony Woodford, Jay Allen, James Humphries, David Payne, Tom Keller, Ron Pratl, Rich Novak, David Angood, Craig Page, Dan Murray, Thomas Moss, Larry Jones, Brian Virgil
5th Row: Roger Gaudette, Virgil Williams, Gerald Diggs, Gene Bell, Dave Kadela, Gary Quinn, Ralph Clayton, Chuck Hetts, Mel Owens, Gary Weber, John Wangler, Keith Gilmore, Irvin Johnson, Tony Leoni, Jim Kozlowski
4th Row: Sr. Mgr. Don DiPaolo, Nick Labun, Mike Harden, Michael Davis, Lawrence Reid, Mike Jolly, John Powers, Chris Godfrey, Jeff Bednarek, George Lilja, Mike Leoni, Doug Marsh, Ron Simpkins, Roosevelt Smith, Gregg Willner, Tim Malinak
3rd Row: Ed Kasparek, Mark Braman, Bob Patek, Stacy Johnson, Dale Keitz, John Arbeznik, Curtis Greer, Jon Giesler, Chip Pederson, Mark DeSantis, Mark Torzy, Rock Lindsay, William Jackson, Bob Hollway, Tom Melita</p>
2nd Row: Max Richardson, Curt Stephenson, Derek Howard, Steve Graves, John Anderson, Bill Dufek, Mark Donahue, Co-captain Walt Downing, Garry Szara, Mike Kenn, Rick White, Dominic Tedesco, Jim Pickens, Kevin King, Co-captain Dwight Hicks, Head Coach Bo Schembechler
Front Row: Raymond Johnson, Roger Bettis, Mike Smith, Russell Davis, Tom Seabron, Gene Johnson, Steve Nauta, Rex Mackall, Greg Bartnick, Dave Harding, Mark Schmerge, Jerry Meter, Rick Leach, Harlan Huckleby, Woody Brown
Resumo:
Back Row: Coaches Bob Patek, Jerry Zuver, Mike Gittleson, Milan Vooletich, Dennis Brown, Jack Harbaugh, Bill McCartney, Jerry Hanlon, Don Nehlen, Tirrel Burton, Paul Schudel, Bob Thornbladh, Barry Pierson, Mike Smith, Curt Stephenson, Trainer Lindsy McLean, Eqp. Mgr. Jon Falk.
9th Row: Kevin Smith, Doug Agnew, * , Mike Butts, Steve Zarnata, Brad Fischer, Kevin Gilligan, * , Karl Tech, Jerome Jelinek, Bill Welch, * , Vince Shaw, Mgr. Nick Uriah
8th Row: Marion Body, Dave Brewster, Rich Strenger, Sanford Washington, Steve Reilly, Tom Neal, Norm Betts, Mike Petsch, Mike Lemirande, Gary Snell, Jeff Reeves, Tony Jackson, Jeff Felten, Tony Kelsie
7th Row: Mike Webster, Butch Woolfolk, Cedric Coles, Bubba Paris, Chuck Rowland, Ed Muransky, Mark Warth, Tom Garrity, Robert Thompson, Jim Paciorek, Gary Lee, Zeke Wallace, Brian Carpenter, John Sandberg
6th Row: Tom Moss, Tim Carrier, Jay Allen, Jim Breaugh, Larry Jones, David Angood, Tom Wandersleben, Fred Motley, Dave Payne, Rod Vaughn, Gasper Calindrino, Kevin Long, Bryan Virgil, *
5th Row: Brad Bates, Irvin Johnson, Kelly Keough, Tom Keller, Rick Novak, Ben Needham, Oliver Johnson, Jeff Jackson, Dan Kwiatkowski, John Prepolec, Greg Wunderli, Kurt Becker, Tony Osbun, Mike Kligis, Chuck Christian
4th Row: Craig Page, B.J. Dickey, Rodney Peaster, Dan Murray, Andy Cannavino, Dave Nicolau, Stanley Edwards, Michael Davis, Mike Trgovac, Stuart Harris, Roger Gaudette, Jim Kozlowski, Alan Mitchell, Rick Jones, Head Coach Bo Schembechler
3rd Row: Gerald Diggs, Tony Leoni, Roosevelt Smith, Gary Weber, Lawrence Reid, Mel Owens, George Lilja, John Powers, Chris Godfrey, John Wangler, Gene Bell, Michael Harden, Mike Leoni, Gary Quinn, Jim Humphries
2nd Row: Gregg Willner, William Jackson, Mike Jolly, Ralph Clayton, Chip Pederson, Rock Lindsay, John Arbeznik, Ron Simpkins, Doug Marsh, Dale Keitz, Tom Melita, Mark Torzy, Tim Malinak, Ed Kasparek, Chuck Netts
Front Row: Mark Braman, Mark DeSantis, Mark Schmerge, Curtis Greer, Greg Bartnick, Harlan Huckleby, Co-Captain Russell Davis, Bill Dufek, Rick Leach, Co-Captain Jerry Meter, Gene Johnson, Jon Giesler, Tom Seabron, Steve Nauta, Bob Hollway
* = left the team
Resumo:
Metastatic melanoma is poorly responsive to treatment, and immunotherapeutic approaches are potentially beneficial. Predictors of clinical response are needed to identify suitable patients. We sought factors associated with melanoma-specific clinical response following intradermal vaccination with autologous melanoma peptide and particulate hepatitis B antigen (HBsAg)-exposed immature monocyte-derived dendritic cells (MDDC). Nineteen patients with metastatic melanoma received a maximum of 8, 2-weekly vaccinations of DC, exposed to HBsAg in addition to autologous melanoma peptides. A further 3 patients received an otherwise identical vaccine that did not include HBsAg. Patients were assessed 1-2 monthly for safety, disease volume, and cellular responses to HBsAg and melanoma peptide. There was no significant toxicity. Of 19 patients receiving HBsAg-exposed DC, 9 primed or boosted a cellular response to HBsAg, and 10 showed no HBsAg response. HBsAg-specific responses were associated with in vitro T cell responses to melanoma peptides and to phytohemagglutinin (PHA). Zero out of 10 non-HBsAg-responding and 4/9 HBsAg-responding patients achieved objective melanoma-specific clinical responses or disease stabilization- 1 complete and 2 partial responses and I case of stable disease (P=0.018). Development of melanoma-specific cellular immunity and T cell responsiveness to mitogen were greater in the group of patients responding to HBsAg. Therefore stimulation of an immune response to nominal particulate antigen was necessary when presented by melanoma peptide-exposed immature DC, to achieve clinical responses in metastatic melanoma. Since general immune competence may be a determinant of treatment response, it should be assessed in future trials on DC immunotherapy.
Resumo:
Current methods of understanding microbiome composition and structure rely on accurately estimating the number of distinct species and their relative abundance. Most of these methods require an efficient PCR whose forward and reverse primers bind well to the same, large number of identifiable species, and produce amplicons that are unique. It is therefore not surprising that currently used universal primers designed many years ago are not as efficient and fail to bind to recently cataloged species. We propose an automated general method of designing PCR primer pairs that abide by primer design rules and uses current sequence database as input. Since the method is automated, primers can be designed for targeted microbial species or updated as species are added or deleted from the database. In silico experiments and laboratory experiments confirm the efficacy of the newly designed primers for metagenomics applications.
Resumo:
BACKGROUND: Multiyear epidemics of Salmonella enterica serovar Typhi have been reported from countries across eastern and southern Africa in recent years. In Blantyre, Malawi, a dramatic increase in typhoid fever cases has recently occurred, and may be linked to the emergence of the H58 haplotype. Strains belonging to the H58 haplotype often exhibit multidrug resistance and may have a fitness advantage relative to other Salmonella Typhi strains.
METHODS: To explore hypotheses for the increased number of typhoid fever cases in Blantyre, we fit a mathematical model to culture-confirmed cases of Salmonella enterica infections at Queen Elizabeth Central Hospital, Blantyre. We explored 4 hypotheses: (1) an increase in the basic reproductive number (R0) in response to increasing population density; (2) a decrease in the incidence of cross-immunizing infection with Salmonella Enteritidis; (3) an increase in the duration of infectiousness due to failure to respond to first-line antibiotics; and (4) an increase in the transmission rate following the emergence of the H58 haplotype.
RESULTS: Increasing population density or decreasing cross-immunity could not fully explain the observed pattern of typhoid emergence in Blantyre, whereas models allowing for an increase in the duration of infectiousness and/or the transmission rate of typhoid following the emergence of the H58 haplotype provided a good fit to the data.
CONCLUSIONS: Our results suggest that an increase in the transmissibility of typhoid due to the emergence of drug resistance associated with the H58 haplotype may help to explain recent outbreaks of typhoid in Malawi and similar settings in Africa.
Resumo:
INTRODUCTION: Between 1998 and 2010, S. Typhi was an uncommon cause of bloodstream infection (BSI) in Blantyre, Malawi and it was usually susceptible to first-line antimicrobial therapy. In 2011 an increase in a multidrug resistant (MDR) strain was detected through routine bacteriological surveillance conducted at Queen Elizabeth Central Hospital (QECH).
METHODS: Longitudinal trends in culture-confirmed Typhoid admissions at QECH were described between 1998-2014. A retrospective review of patient cases notes was conducted, focusing on clinical presentation, prevalence of HIV and case-fatality. Isolates of S. Typhi were sequenced and the phylogeny of Typhoid in Blantyre was reconstructed and placed in a global context.
RESULTS: Between 1998-2010, there were a mean of 14 microbiological diagnoses of Typhoid/year at QECH, of which 6.8% were MDR. This increased to 67 in 2011 and 782 in 2014 at which time 97% were MDR. The disease predominantly affected children and young adults (median age 11 [IQR 6-21] in 2014). The prevalence of HIV in adult patients was 16.7% [8/48], similar to that of the general population (17.8%). Overall, the case fatality rate was 2.5% (3/94). Complications included anaemia, myocarditis, pneumonia and intestinal perforation. 112 isolates were sequenced and the phylogeny demonstrated the introduction and clonal expansion of the H58 lineage of S. Typhi.
CONCLUSIONS: Since 2011, there has been a rapid increase in the incidence of multidrug resistant, H58-lineage Typhoid in Blantyre. This is one of a number of reports of the re-emergence of Typhoid in Southern and Eastern Africa. There is an urgent need to understand the reservoirs and transmission of disease and how to arrest this regional increase.
Resumo:
The purpose of this study was to examine the reliability and validity of the School Anxiety Inventory (SAI) using a sample of 646 Slovenian adolescents (48% boys), ranging in age from 12 to 19 years. Single confirmatory factor analyses replicated the correlated four-factor structure of scores on the SAI for anxiety-provoking school situations (Anxiety about School Failure and Punishment, Anxiety about Aggression, Anxiety about Social Evaluation, and Anxiety about Academic Evaluation), and the three-factor structure of the anxiety response systems (Physiological Anxiety, Cognitive Anxiety, and Behavioral Anxiety). Equality of factor structures was compared using multigroup confirmatory factor analyses. Measurement invariance for the four- and three-factor models was obtained across gender and school-level samples. The scores of the instrument showed high internal reliability and adequate test–retest reliability. The concurrent validity of the SAI scores was also examined through its relationship with the Social Anxiety Scale for Adolescents (SASA) scores and the Questionnaire about Interpersonal Difficulties for Adolescents (QIDA) scores. Correlations of the SAI scores with scores on the SASA and the QIDA were of low to moderate effect sizes.
