52 resultados para Bracken


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Polycomb-like proteins 1-3 (PCL1-3) are substoichiometric components of the Polycomb-repressive complex 2 (PRC2) that are essential for association of the complex with chromatin. However, it remains unclear why three proteins with such apparent functional redundancy exist in mammals. Here we characterize their divergent roles in both positively and negatively regulating cellular proliferation. We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predominantly expressed in quiescent cells. Ectopic expression of any PCL protein recruits PRC2 to repress the INK4A gene; however, only PCL2 and PCL3 confer an INK4A-dependent proliferative advantage. Remarkably, PCL1 has evolved a PRC2- and chromatin-independent function to negatively regulate proliferation. We show that PCL1 binds to and stabilizes p53 to induce cellular quiescence. Moreover, depletion of PCL1 phenocopies the defects in maintaining cellular quiescence associated with p53 loss. This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution. This study illustrates the functional bifurcation of PCL proteins, which act in both a chromatin-dependent and a chromatin-independent manner to regulate the INK4A and p53 pathways.

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Evidence is presented of widespread changes in structure and species composition between the 1980s and 2003–2004 from surveys of 249 British broadleaved woodlands. Structural components examined include canopy cover, vertical vegetation profiles, field-layer cover and deadwood abundance. Woods were located in 13 geographical localities and the patterns of change were examined for each locality as well as across all woods. Changes were not uniform throughout the localities; overall, there were significant decreases in canopy cover and increases in sub-canopy (2–10 m) cover. Changes in 0.5–2 m vegetation cover showed strong geographic patterns, increasing in western localities, but declining or showing no change in eastern localities. There were significant increases in canopy ash Fraxinus excelsior and decreases in oak Quercus robur/petraea. Shrub layer ash and honeysuckle Lonicera periclymenum increased while birch Betula spp. hawthorn Crataegus monogyna and hazel Corylus avellana declined. Within the field layer, both bracken Pteridium aquilinum and herbs increased. Overall, deadwood generally increased. Changes were consistent with reductions in active woodland management and changes in grazing and browsing pressure. These findings have important implications for sustainable active management of British broadleaved woodlands to meet silvicultural and biodiversity objectives.

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Giant planets helped to shape the conditions we see in the Solar System today and they account for more than 99% of the mass of the Sun’s planetary system. They can be subdivided into the Ice Giants (Uranus and Neptune) and the Gas Giants (Jupiter and Saturn), which differ from each other in a number of fundamental ways. Uranus, in particular is the most challenging to our understanding of planetary formation and evolution, with its large obliquity, low self-luminosity, highly asymmetrical internal field, and puzzling internal structure. Uranus also has a rich planetary system consisting of a system of inner natural satellites and complex ring system, five major natural icy satellites, a system of irregular moons with varied dynamical histories, and a highly asymmetrical magnetosphere. Voyager 2 is the only spacecraft to have explored Uranus, with a flyby in 1986, and no mission is currently planned to this enigmatic system. However, a mission to the uranian system would open a new window on the origin and evolution of the Solar System and would provide crucial information on a wide variety of physicochemical processes in our Solar System. These have clear implications for understanding exoplanetary systems. In this paper we describe the science case for an orbital mission to Uranus with an atmospheric entry probe to sample the composition and atmospheric physics in Uranus’ atmosphere. The characteristics of such an orbiter and a strawman scientific payload are described and we discuss the technical challenges for such a mission. This paper is based on a white paper submitted to the European Space Agency’s call for science themes for its large-class mission programme in 2013.

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Basic concept knowledge of children who were deaf/hard of hearing was tested using the Bracken Basic Concept Scale: 3rd Edition. These children were given both the receptive and expressive portions of the test. Results indicate delays in overall basic concept knowledge in children who are deaf compared to their normal-hearing peers.

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Pteridium aquilinum (bracken fern) is one of the most common plants. Epidemiological studies have revealed a higher risk of certain types of cancers (i.e., esophageal, gastric) in people who consume bracken fern directly ( as crosiers or rhizomes) or indirectly through the consumption of milk from livestock that fed on the plant. In animals, evidence exists regarding the associations between chronic bracken fern intoxication, papilloma virus infection, and the development of carcinomas. While it is possible that some carcinogens in bracken fern could be responsible for these cancers in both humans and animals, it is equally plausible that the observed increases in cancers could be related to induction of an overall immunosuppression by the plant/its various constituents. Under the latter scenario, normal tumor surveillance responses against nascent (non-bracken-induced) cancers or responses against viral infections ( specifically those linked to induction of cancers) might be adversely impacted by continuous dietary exposure to this plant. Therefore, the overall objective of this study was to evaluate the immunomodulatory effects of bracken fern following daily ingestion of its extract by a murine host over a period of 14 ( or up to 30) days. In C57BL/6 mice administered ( by gavage) the extract, histological analyses revealed a significant reduction in splenic white pulp area. Among a variety of immune response parameters/functions assessed in these hosts and isolated cells, both delayed-type hypersensitivity (DTH) analysis and evaluation of IFN gamma. production by NK cells during T(H)1 priming were also reduced. Lastly, the innate response in these hosts-assessed by analysis of NK cell cytotoxic functionality-was also diminished. The results here clearly showed the immunosuppressive effects of P. aquilinum and that many of the functions that were modulated could contribute to the increased risk of cancer formation in exposed hosts.

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Numa área situada no município de Lavras, MG, o desmatamento realizado há cerca de dez anos propiciou a formação de uma comunidade infestante dominada por Pteridium aquilium (L.) Khun., te ndo como codominantes Imperara brasiliensis Trin. e Andropogon bicornis L.. Como fatores que mantém esta comu nidade devem ser considerados: a) as queimadas intermiten te s; b) a acidez do solo; c) a alta percentagem de saturação de aluminio ; d) a ação fitotóxica do próprio P. aquilinum; e) a falta de palatabilidade das espécies dominantes.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Chronic kidney diseasemineral bone disorder (CKD-MBD) is defined by abnormalities in mineral and hormone metabolism, bone histomorphometric changes, and/or the presence of soft-tissue calcification. Emerging evidence suggests that features of CKD-MBD may occur early in disease progression and are associated with changes in osteocyte function. To identify early changes in bone, we utilized the jck mouse, a genetic model of polycystic kidney disease that exhibits progressive renal disease. At 6 weeks of age, jck mice have normal renal function and no evidence of bone disease but exhibit continual decline in renal function and death by 20 weeks of age, when approximately 40% to 60% of them have vascular calcification. Temporal changes in serum parameters were identified in jck relative to wild-type mice from 6 through 18 weeks of age and were subsequently shown to largely mirror serum changes commonly associated with clinical CKD-MBD. Bone histomorphometry revealed progressive changes associated with increased osteoclast activity and elevated bone formation relative to wild-type mice. To capture the early molecular and cellular events in the progression of CKD-MBD we examined cell-specific pathways associated with bone remodeling at the protein and/or gene expression level. Importantly, a steady increase in the number of cells expressing phosphor-Ser33/37-beta-catenin was observed both in mouse and human bones. Overall repression of Wnt/beta-catenin signaling within osteocytes occurred in conjunction with increased expression of Wnt antagonists (SOST and sFRP4) and genes associated with osteoclast activity, including receptor activator of NF-?B ligand (RANKL). The resulting increase in the RANKL/osteoprotegerin (OPG) ratio correlated with increased osteoclast activity. In late-stage disease, an apparent repression of genes associated with osteoblast function was observed. These data confirm that jck mice develop progressive biochemical changes in CKD-MBD and suggest that repression of the Wnt/beta-catenin pathway is involved in the pathogenesis of renal osteodystrophy. (C) 2012 American Society for Bone and Mineral Research.

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The minerals sillimanite, kyanite, andalusite, dumortierite, and topaz comprise a group of minerals whose high alumina content and physical properties are particularly desirable in the manufacture of refractory products. Sillimanite is the least plentiful of the minerals of this group, and for this reason it is not used extensively at the present time. However, it would be very desirable to the refractory industry if a suitable domestic source of supply could be established.

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Background. Increasing rates of maternal employment highlight the need for non-maternal child care for infants at an earlier age. Several studies have shown that employment induced maternal depression or psychological distress is associated with the child's socio-emotional and cognitive development. However, separation anxiety, a common phenomenon observed among employed mothers during early years, has seldom been studied. Therefore, the purpose of this study was to evaluate the role of maternal separation anxiety in the child's cognitive development.^ Methods. Data were obtained from Phase I (birth to 36 months) of the National Institute of Child Health and Human Development, Study of Early Child Care and Youth Development (NICHD SECCYD). Bivariate and multivariate analyses were performed to determine the association between separation anxiety groups and child outcomes. Multivariate analysis was also used to examine the mediating and/or moderating effect of sensitivity and moderating effect of difficult temperament.^ Results. Separation anxiety showed a negative association with the Bracken, attachment security, maternal sensitivity and psychological state. Children whose mothers never reported high levels of separation anxiety showed higher levels of school readiness and attachment security compared to those whose mothers experienced high levels of separation anxiety at least once. There was a significant interaction between separation anxiety and maternal sensitivity for the Bracken and attachment security indicating the moderating effect of sensitivity. Maternal sensitivity was also found to partially mediate the association between high levels of separation anxiety and school readiness or attachment security. However, the interaction between difficult temperament and separation anxiety was not significant for any of the child outcomes. ^ Conclusions. High levels of separation anxiety have a negative impact on school readiness, attachment security, maternal sensitivity and psychological state. In addition, mothers who experience high levels of separation anxiety but are sensitive during the mother-child interaction have children with high school readiness and attachment security compared to those who are less sensitive.^ Keywords. Maternal separation anxiety, School readiness. ^

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To address growing concern over the effects of fisheries non-target catch on elasmobranchs worldwide, the accurate reporting of elasmobranch catch is essential. This requires data on a combination of measures, including reported landings, retained and discarded non-target catch, and post-discard survival. Identification of the factors influencing discard vs. retention is needed to improve catch estimates and to determine wasteful fishing practices. To do this we compared retention rates of elasmobranch non-target catch in a broad subset of fisheries throughout the world by taxon, fishing country, and gear. A regression tree and random forest analysis indicated that taxon was the most important determinant of retention in this dataset, but all three factors together explained 59% of the variance. Estimates of total elasmobranch removals were calculated by dividing the FAO global elasmobranch landings by average retention rates and suggest that total elasmobranch removals may exceed FAO reported landings by as much as 400%. This analysis is the first effort to directly characterize global drivers of discards for elasmobranch non-target catch. Our results highlight the importance of accurate quantification of retention and discard rates to improve assessments of the potential impacts of fisheries on these species.

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Back Row: Fred Mushinski, Jerry Hanlon, Lloyd Carr, Fritz Seyferth, Jerry Meter, Ron Vanderlinden, Milan Wooletich, Mike Gittleson, Les Miles, Paul Schudel, Bob Thornbladh, Bill McCartney, Tim Davis, Tirrel Burton

8th Row: Dennis Hammond, Jon Falk, Brad Maxon, Mike Melnyk, Fritz Burgess, Roger Joseph, John Lanman, Rolie Zagnoli, John Ferens, Larry Cerasi, Jeff Nate, Cedric Smith, Russ Miller

7th Row: Evan Cooper, Vincent Bean, Tom Dixon, Glen Dwyer, Nate Rodgers, Jeff Shaw, Mike Wilson, Larry Sweeney, Ron Prusa, Doug James, Bob Dana, Mike Boren, Carlton Rose, Tim Anderson

6th Row: Don Bracken, Greg Armstrong, Kerry Smith, Steve Smith, Dave Hall, Vince DeFelice, Stefan Humphries, Milt Carthens, Rod Lyles, Jerry DiOrio, Dave Meredith, Harry Gosier, Tom Hassel, Greg Powell

5th Row: Ali Haji-Sheikh, Nate Davis, Ricky Davis, John Lott, Duke Haynes, Jim Herrmann, Dan Yarano, Todd Triplett, Joe Mosketti, Scott Roberts, Marshall Parks, Kevin Smith, Bill Jacoby, Frank Raiford

4th Row: Anthony Carter, Larry Ricks, Rich Hewlett, Jerry Burgei, Keith Bostic, Jerald Ingram, Winfred Carraway, Craig Dunaway, Tom Neal, Vincent Shaw, Jeff Cohen, Don Ryan, Brad Fischer, Paul Girgash, Kenny Gear

3rd Row: Mike Czarnota, Fred Brockington, Robert Thompson, Jeff Felten, Tom Garrity, Bubba Paris, Ed Muransky, Rich Strenger, Mike Lemirande, Mark Warth*, Zeke Wallace, Cedric Coles, Sanford Washington, Tony Kelsie

2nd Row: Oliver Johnson, Brian Carpenter, Tony Jackson, Butch Woolfolk, Jim Breaugh, Fred Motley, Chuck Christian, Kelly Keough, Tom Wandersleben, Brad Bates, Norm Betts, Jeff Reeves, Marion Body, Karl Tech

Front Row: Alan Mitchell, Tony Osbun, Kurt Becker, Mike Trgovac, John Wangler, George Lilja, Mel Owens, John Powers, Gerald Diggs, Andy Cannavino, Dave Nicolau, Stan Edwards, Rod Feaster, Stu Harris, Coach Bo Schembechler

* = left the team

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Back Row: Fritz Seyferth, Bob Chmiel, Alex Agase, Jerry Meter, Elliot Uzelac, Paul Schudel, Jerry Hanlon, Gary Moeller, Tirrell Burton, Milan Vooletich, Lloyd Carr, Bob Thornbladh, Dennis Doornbos, Mike Gittleson

9th Row: Chuck Ritter, Jon Falk, Ken Gear, Bob Kimball, Ed Hood, Camp Fellin, Marc Shevrin, Joe Mosketti, Charlie Fromm, Russ Miller

8th Row: Pat Moons, Derek Woodmore, Greg Randall, Triando Markray, Andy Moeller, Mike Krauss, Dan Decker, Jerry Quaerna, Rick Frazer, Dieter Heren, Ben Logue, Keith Cowan, Robert Harris

7th Row: Tony Gant, Steve Johnson, Thomas Wilcher, Eddie Garrett, Paul Schmerge, Mike Reinhold, Marty Shimko, John Mihic, Mark Hammerstein, Jim Harbaugh, Dan Rice, Bob Perryman, Gilvanni Johnson, Ivan Hicks

6th Row: Joe English, Todd Schlopy, Mike Melnyk, John Ferens, Mike Sessa, John Ghindia, Sim Nelson, Gil Zimmerman, Eric Kempthorn, Bruce Brown, Dave Simon, Sylvester Ogletree, John Paciorek, Bob Bergeron

5th Row: Tom Knoebel, Mike Odioso, Phil Lewandowski, Bob Popowski, Clay Miller, Jeff Akers, Kevin Brooks, Art Balourdos, Mike Hammerstein, Brian Mercer, Bob Tabachino, Joe Gray, Jim Scarcelli, Riley McPhee

4th Row: Greg Powell, Brad Cochran, Al Sincinch, Mike Mallory, Eric Kattus, Vince DeFelice, Tim Anderson, Dave Meredith, Larry Sweeney, Mike Wilson, Nate Rodgers, Robert Dana, Rick Rogers, Fritz Burgess

3rd Row: Evan Cooper, Greg Armstrong, Don Bracken, Carlton Rose, Tom Hassell, Kerry Smith, Dave Hall, Jerry Diorio, Ron Prusa, Milt Carthens, Doug James, Rodney Lyles, Mickey Hanlon, Lou Kovacs

2nd Row: Vince Bean, Stefan Humphries, Nate Davis, Ricky Davis, John Lott, Scott Roberts, Todd Triplett, Dan Yarano, Rich Hewlett, Jeff Cohen, Jim Herrman, Steve Smith, Mike Boren, Tom Dixon

Front Row: Marion Body, Jerald Ingram, Mike Lemirande, Winfred Carraway, Craig Dunaway, Keith Bostic, Rich Strenger, Robert Thompson, Anthony Carter, Lawrence Ricks, Paul Girgash, Tom Garrity, Jerry Burgei, Ali Haji-Sheikh, Bo Schembechler

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Back Row: Bill Giarmo, Alex Agase, Jerry Hanlon, Bob Thornbladh, Elliott Uzelac, Gary Moeller, Lloyd Carr, Jerry Meter, Milan Vooletich, Tirrel Burton, Bob Chmiel, Jim Herrmann, Dave Magazu

9th Row: Doug Ham (Mgr.), Mike Gittleson, Lou Kovacs, Joe English, Joe Mosketti, James Rott, Garrett Smith, Phil Logas, John Whitledge, Andy Samosiuk, Dave Garlow, Russ Miller, Fritz Seyferth, Jon Falk

8th Row: Tim Schulte, Mike O'Connor, Billy Harris, Carlitos Bostic, Gene Cecchini, Steve Thibert, Jack Walker, John Balourdos, Pete Wentworth, Todd Schulte, Brandon Johns, Monte Robbins, John Zingales

7th Row: Billy Dawson, Doug Mallory, Gerald White, Garland Rivers, Dave Folkertsma, Andrew Borowski, Glenn Mogle, John Elliott, Andree McIntyre, Dwayne Freeman, Phil Webb, Chris Zurbrugg, Ken Higgins, Russell Rein

6th Row: Gene Lawson, Camp Fellin, Marc Shevrin, Dieter Heren, John Mihic, Jerry Quaerna, Rick Frazer, Marty Shimko, Triando Markray, Dan Decker, Keith Cowan, Pat Moons, Ed Hood, Al Bishop

5th Row: Steve Johnson, Tony Gant, Greg Randall, Ben Logue, Gilvanni Johnson, Paul Schmerge, Mark Hammerstein, Mike Reinhold, Jim Harbaugh, Bob Perryman, Andy Moeller, Mike Krauss, Ivan Hicks

4th Row: Mike Melnyk, Todd Schlopy, John Paciorek, Dave Simon, John Ghindia, Phil Lewandowski, Jim Scarcelli, Brad Cochran, Tom Knoebel, Mike Sessa, Eddie Garrett, Dan Rice, John Ferens, Bob Bergeron, Tom Wilcher

3rd Row: Joe Gray, Mike Mallory, Clay Miller, Eric Kattus, Art Balourdos, Al Sincich, Kevin Brooks, Mike Hammerstein, Sim Nelson, Jeff Akers, Rick Rogers, Bob Popowski, Bob Tabachino, Brian Mercer

2nd Row: Fritz Burgess, Tim Anderson, Mike Wilson, Nate Rogers, Dave Meredith, Vince DeFelice, Greg Armstrong, Milt Carthens, Rodney Lyles, Larry Sweeney, Dan Yarano, Gerald Ingram, Don Bracken, Kerry Smith

Front Row: Jeff Cohen, Jerry Diorio, Dave Hall, Carlton Rose, Steve Smith, Tom Dixon, Stefan Humphries, Mike Boren, Doug James, Evan Cooper, Tom Hassel, John Lott, Vince Bean, Rich Hewlett, Coach Bo Schembechler