997 resultados para Walker, John, 1732-1807.
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We present an integrated palaeoecological and archaeobotanical study of pre-Columbian raised-field agriculture in the Llanos de Moxos, a vast seasonally inundated forest–savanna mosaic in the Bolivian Amazon. Phytoliths from excavated raised-field soil units, together with pollen and charcoal in sediment cores from two oxbow lakes, were analysed to provide a history of land use and agriculture at the El Cerro raised-field site. The construction of raised fields involved the removal of savanna trees, and gallery forest was cleared from the area by AD 310. Despite the low fertility of Llanos de Moxos soils, we determined that pre-Columbian raised-field agriculture sufficiently improved soil conditions for maize cultivation. Fire was used as a common management practice until AD 1300, at which point, the land-use strategy shifted towards less frequent burning of savannas and raised fields. Alongside a reduction in the use of fire, sweet potato cultivation and the exploitation of Inga fruits formed part of a mixed resource strategy from AD 1300 to 1450. The pre-Columbian impact on the landscape began to lessen around AD 1450, as shown by an increase in savanna trees and gallery forest. Although agriculture at the site began to decline prior to European arrival, the abandonment of raised fields was protracted, with evidence of sweet potato cultivation occurring as late as AD 1800.
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praemittitur Christoph. Matthaei Pfaffii
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Existing descriptions of bi-directional ammonia (NH3) land–atmosphere exchange incorporate temperature and moisture controls, and are beginning to be used in regional chemical transport models. However, such models have typically applied simpler emission factors to upscale the main NH3 emission terms. While this approach has successfully simulated the main spatial patterns on local to global scales, it fails to address the environment- and climate-dependence of emissions. To handle these issues, we outline the basis for a new modelling paradigm where both NH3 emissions and deposition are calculated online according to diurnal, seasonal and spatial differences in meteorology. We show how measurements reveal a strong, but complex pattern of climatic dependence, which is increasingly being characterized using ground-based NH3 monitoring and satellite observations, while advances in process-based modelling are illustrated for agricultural and natural sources, including a global application for seabird colonies. A future architecture for NH3 emission–deposition modelling is proposed that integrates the spatio-temporal interactions, and provides the necessary foundation to assess the consequences of climate change. Based on available measurements, a first empirical estimate suggests that 5°C warming would increase emissions by 42 per cent (28–67%). Together with increased anthropogenic activity, global NH3 emissions may increase from 65 (45–85) Tg N in 2008 to reach 132 (89–179) Tg by 2100.
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The synthesis of DNA in mitochondria requires the uptake of deoxynucleotides into the matrix of the organelle. We have characterized a human cDNA encoding a member of the family of mitochondrial carriers. The protein has been overexpressed in bacteria and reconstituted into phospholipid vesicles where it catalyzed the transport of all four deoxy (d) NDPs, and, less efficiently, the corresponding dNTPs, in exchange for dNDPs, ADP, or ATP. It did not transport dNMPs, NMPs, deoxynucleosides, nucleosides, purines, or pyrimidines. The physiological role of this deoxynucleotide carrier is probably to supply deoxynucleotides to the mitochondrial matrix for conversion to triphosphates and incorporation into mitochondrial DNA. The protein is expressed in all human tissues that were examined except for placenta, in accord with such a central role. The deoxynucleotide carrier also transports dideoxynucleotides efficiently. It is likely to be medically important by providing the means of uptake into mitochondria of nucleoside analogs, leading to the mitochondrial impairment that underlies the toxic side effects of such drugs in the treatment of viral illnesses, including AIDS, and in cancer therapy.
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Neuropathological and brain imaging studies suggest that schizophrenia may result from neurodevelopmental defects. Cytoarchitectural studies indicate cellular abnormalities suggestive of a disruption in neuronal connectivity in schizophrenia, particularly in the dorsolateral prefrontal cortex. Yet, the molecular mechanisms underlying these findings remain unclear. To identify molecular substrates associated with schizophrenia, DNA microarray analysis was used to assay gene expression levels in postmortem dorsolateral prefrontal cortex of schizophrenic and control patients. Genes determined to have altered expression levels in schizophrenics relative to controls are involved in a number of biological processes, including synaptic plasticity, neuronal development, neurotransmission, and signal transduction. Most notable was the differential expression of myelination-related genes suggesting a disruption in oligodendrocyte function in schizophrenia.
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Brassinosteroid-insensitive 1 (BRI1) of Arabidopsis thaliana encodes a cell surface receptor for brassinosteroids. Mutations in BRI1 severely affect plant growth and development. Activation tagging of a weak bri1 allele (bri1-5) resulted in the identification of a new locus, brs1-1D. BRS1 is predicted to encode a secreted carboxypeptidase. Whereas a brs1 loss-of-function allele has no obvious mutant phenotype, overexpression of BRS1 can suppress bri1 extracellular domain mutants. Genetic analyses showed that brassinosteroids and a functional BRI1 protein kinase domain are required for suppression. In addition, overexpressed BRS1 missense mutants, predicted to abolish BRS1 protease activity, failed to suppress bri1-5. Finally, the effects of BRS1 are selective: overexpression in either wild-type or two other receptor kinase mutants resulted in no phenotypic alterations. These results strongly suggest that BRS1 processes a protein involved in an early event in the BRI1 signaling.
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The CLAVATA1 (CLV1) gene encodes a putative receptor kinase required for the proper balance between cell proliferation and differentiation in Arabidopsis shoot and flower meristems. Impaired CLV1 signaling results in masses of undifferentiated cells at the shoot and floral meristems. Although many putative receptor kinases have been identified in plants, the mechanism of signal transduction mediated by plant receptor-like kinases is largely unknown. One potential effector of receptor kinase signaling is kinase-associated protein phosphatase (KAPP), a protein that binds to multiple plant receptor-like kinases in a phosphorylation-dependent manner. To examine a possible role for KAPP in CLV1-dependent plant development, the interaction of CLV1 and KAPP was investigated in vitro and in vivo. KAPP binds directly to autophosphorylated CLV1 in vitro and co-immunoprecipitates with CLV1 in plant extracts derived from meristematic tissue. Reduction of KAPP transcript accumulation in an intermediate clv1 mutant suppresses the mutant phenotype, and the degree of suppression is inversely correlated with KAPP mRNA levels. These data suggest that KAPP functions as a negative regulator of CLV1 signaling in plant development. This may represent a general model for the interaction of KAPP with receptor kinases.
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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
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Supersedes NACA technical note 4231.
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Mode of access: Internet.