979 resultados para 150-905


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Continental rise Site 905 yielded upper Miocene and Pliocene uniform hemipelagic mud (a contourite) from approximately 215 to 540 meters below seafloor. The nannofossil biostratigraphy of this interval was reexamined using closely spaced samples from core interiors. Additionally, total nannofossil abundances and dominant species and species group abundances were determined to evaluate the potential of this section for extracting sequence stratigraphic information. The data indicate that the putative hiatuses at the end of the late Pliocene (Zones NN17 and NN18) and in the early Pliocene (Zones NN13 and NN14) probably are condensed intervals, but the base of the late Miocene is almost certainly marked by an unconformity. Judging from carbonate content and sedimentation rate both, nannofossil abundance may be governed by carbonate dissolution or by siliciclastic dilution. Consequently, condensed sections cannot be identified by the abundance of pelagic component in the sediment alone, as is possible in equivalent age Gulf of Mexico sediments. Where nannofossil preservation is adequate in consecutive samples, as in the early Pliocene and latest late Miocene, total nannofossil abundance fluctuates regularly and with a periodicity of less than 105 yr, which suggests that dilution of the pelagic component occurred with a frequency probably related to astronomical forcing.

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Mendel's paper 'Versuche über Pflanzen-Hybriden' is the best known in a series of studies published in the late 18th and 19th centuries that built our understanding of the mechanism of inheritance. Mendel investigated the segregation of seven gene characters of pea (Pisum sativum), of which four have been identified. Here, we review what is known about the molecular nature of these genes, which encode enzymes (R and Le), a biochemical regulator (I) and a transcription factor (A). The mutations are: a transposon insertion (r), an amino acid insertion (i), a splice variant (a) and a missense mutation (le-1). The nature of the three remaining uncharacterized characters (green versus yellow pods, inflated versus constricted pods, and axial versus terminal flowers) is discussed.

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Digital Image

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postwar version of F 38352

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In an attempt to unravel the role of conserved histidine residues in the structure-function of sheep liver cytosolic serine hydroxymethyltransferase (SHMT), three site-specific mutants (H134N, H147N, and H150N) were constructed and expressed, H134N and H147N SHMTs had K-m values for L-serine, L-allo-threonine and beta-phenylserine similar to that of wild type enzyme, although the k(cat) values were markedly decreased, H134N SHMT was obtained in a dimeric form with only 6% of bound pyridoxal 5'-phosphate (PLP) compared with the wild type enzyme, Increasing concentrations of PLP (up to 500 mu M) enhanced the enzyme activity without changing its oligomeric structure, indicating that His-134 may be involved in dimer-dimer interactions, H147N SHMT was obtained in a tetrameric form but with very little PLP (3%) bound to it, suggesting that this residue was probably involved in cofactor binding, Unlike the wild type enzyme, the cofactor could be easily removed by dialysis from H147N SHMT, and the apoenzyme thus formed was present predominantly in the dimeric form, indicating that PLP binding is at the dimer-dimer interface, H150N SHMT was obtained in a tetrameric form with bound PLP, However, the mutant had very little enzyme activity (<2%). The k(cat)/K-m values for L-serine, L-allo-threonine and beta-phenylserine were 80-, 56-, and SS-fold less compared with wild type enzyme, Unlike the wild type enzyme, it failed to form the characteristic quinonoid intermediate and was unable to carry out the exchange of 2-S proton from glycine in the presence of H-4-folate. However, it could form an external aldimine with serine and glycine, The wild type and the mutant enzyme had similar K-d values for serine and glycine, These results suggest that His-150 may be the base that abstracts the alpha-proton of the substrate, leading to formation of the quinonoid intermediate in the reaction catalyzed by SHMT.

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A steel ball was slid on a steel flat lubricated by molybdenum disulfide (MoS2) particles suspended in hexadecane oil at 150 degrees C. The friction data is compared with that obtained when the ball was slid on the flat sprayed apriori with nominally dry MoS2 particles. The friction in the dry experiment was found to increase with temperature while the friction in wet condition was found to decrease with increasing temperature. Micro-Raman and Fourier transform IR spectroscopy are used to explore the roles of environmental moisture and chemical degradation of oil on the formation of antifriction film on the steel substrate.

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Hedgehog (HH) signaling is a significant regulator of cell fate decisions during embryogenesis, development, and perpetuation of various disease conditions. Testing whether pathogen-specific HH signaling promotes unique innate recognition of intracellular bacteria, we demonstrate that among diverse Gram-positive or Gram-negative microbes, Mycobacterium bovis BCG, a vaccine strain, elicits a robust activation of Sonic HH (SHH) signaling in macrophages. Interestingly, sustained tumor necrosis factor alpha (TNF-alpha) secretion by macrophages was essential for robust SHH activation, as TNF-alpha(-/-) macrophages exhibited compromised ability to activate SHH signaling. Neutralization of TNF-alpha or blockade of TNF-alpha receptor signaling significantly reduced the infection-induced SHH signaling activation both in vitro and in vivo. Intriguingly, activated SHH signaling downregulated M. bovis BCG-mediated Toll-like receptor 2 (TLR2) signaling events to regulate a battery of genes associated with divergent functions of M1/M2 macrophages. Genome-wide expression profiling as well as conventional gain-of-function or loss-of-function analysis showed that SHH signaling-responsive microRNA 31 (miR-31) and miR-150 target MyD88, an adaptor protein of TLR2 signaling, thus leading to suppression of TLR2 responses. SHH signaling signatures could be detected in vivo in tuberculosis patients and M. bovis BCG-challenged mice. Collectively, these investigations identify SHH signaling to be what we believe is one of the significant regulators of host-pathogen interactions.