985 resultados para 7136-150
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This study investigates the landscape evolution and soil development in the loess area near Regensburg between approximately 6000-2000 yr BP (radiocarbon years), Eastern Bavaria. The focus is on the question how man and climate influenced landscape evolution and what their relative significance was. The theoretical background concerning the factors that controlled prehistoric soil erosion in Middle Europe is summarized with respect to rainfall intensity and distribution, pedogenesis, Pleistocene relief, and prehistoric farming. Colluvial deposits , flood loams, and soils were studied at ten different and representative sites that served as archives of their respective palaeoenvironments. Geomorphological, sedimentological, and pedological methods were applied. According to the findings presented here, there was a high asynchronity of landscape evolution in the investigation area, which was due to prehistoric land-use patterns. Prehistoric land use and settlement caused highly difIerenciated phases of morphodynamic activity and stability in time and space. These are documented at the single catenas ofeach site. In general, Pleistocene relief was substantially lowered. At the same time smaller landforms such as dells and minor asymmetric valleys filled up and strongly transformed. However, there were short phases at many sites, forming short lived linear erosion features ('Runsen'), resulting from exceptional rainfalls. These forms are results of single events without showing regional trends. Generally, the onset of the sedimentation of colluvial deposits took place much earlier (usually 3500 yr BP (radiocarbon) and younger) than the formation of flood loams. Thus, the deposition of flood loams in the Kleine Laaber river valley started mainly as a consequence of iron age farming only at around 2500 yr BP (radiocarbon). A cascade system explains the different ages of colluvial deposits and flood loams: as a result of prehistoric land use, dells and other minor Pleistocene landforms were filled with colluvial sediments. After the filling of these primary sediment traps , eroded material was transported into flood plains, thus forming flood loams. But at the moment we cannot quantify the extent ofprehistoric soil erosion in the investigation area. The three factors that controlled the prehistoric Iandscapc evolution in the Ioess area near Regensburg are as follows: 1. The transformation from a natural to a prehistoric cultural landscape was the most important factor: A landscape with stable relief was changed into a highly morphodynamic one with soil erosion as the dominant process of this change. 2. The sediment traps of the pre-anthropogenic relief determined where the material originated from soil erosion was deposited: either sedimentation took place on the slopes or the filled sediment traps of the slopes rendered flood loam formation possible. Climatic influence of any importance can only be documented as the result of land use in connection with singular and/or statistic events of heavy rainfalls. Without human impact, no significant change in the Holocene landscape would have been possible.
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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.
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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.
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Specific and coordinated regulation of innate immune receptor-driven signaling networks often determines the net outcome of the immune responses. Here, we investigated the cross-regulation of toll-like receptor (TLR)2 and nucleotide-binding oligomerization domain (NOD)2 pathways mediated by Ac2PIM, a tetra-acylated form of mycobacterial cell wall component and muramyl dipeptide (MDP), a peptidoglycan derivative respectively. While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-alpha, VEGF-A, and IL-12 levels was observed. Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively. Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression. Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKC delta-MAPK pathway to suppress beta-catenin-mediated expression of COX-2, SOCS-3, and MMP-9. Our investigation has thus underscored the negative regulatory role of Ac2PIM-TLR2 signaling on NOD2 pathway which could broaden our understanding on vaccine potential or adjuvant utilities of Ac2PIM and/or MDP.
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Consultoria Legislativa - Área III - Tributação, Direito Tributário.