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  • 1
    Publication Date: 2023-05-12
    Keywords: Area/locality; Conductivity, average; ELEVATION; Heat flow; LATITUDE; LONGITUDE; Method comment; Number; Number of temperature data; Sample, optional label/labor no; Temperature gradient
    Type: Dataset
    Format: text/tab-separated-values, 72 data points
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 20 (1928), S. 552-552 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] High-resolution images covering large areas of the seafloor reveal numerous discontinuities along the mid-ocean ridge. These discontinuities occur at a range of scales (10–1,000 km) and define a fundamental segmentation of seafloor spreading centres. Some are transient; others persist for ...
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1438-2199
    Keywords: Amino acids ; N-(Carboxyalkyl)amino acids ; N6-(Carboxymethyl)lysine ; N5-(carboxymethyl)ornithine ; Lactococcus lactis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This report describes the enzyme-catalyzed synthesis, characterization, and chromatographic separation of N6-(carboxymethyl)-L-lysine and N5-(carboxymethyl)-L-ornithine. The two N ω -(carboxyalkyl)amino acids are formed via a reductive condensation between glyoxylate and theε- orδ-amino groups of lysine and ornithine, respectively. Both reactions are catalyzed by the NADPH-dependent enzyme, N5-(carboxyethyl)ornithine synthase [EC 1.5.1.24], found in some strains of the lactic acid bacteriumLactococcus lactis subsp.lactis.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Marine geophysical researches 4 (1979), S. 37-70 
    ISSN: 1573-0581
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences , Physics
    Notes: Abstract The Tamayo transform fault occurs at the north end of the East Pacific Rise where it enters the Gulf of California. The two deep-tow surveys reported here show that the transform fault zone changes significantly as a function of distance from the spreading center intersections. At site 1, near the intersection, one side of the fault is young and the fault zone is narrow and well-defined. Strike slip occurs in a zone approximately 1-km wide suggesting a correspondingly narrow zone of decoupling between the Pacific and North American plates. On the young side of the strike-slip zone, normal faults occur along shear zones which are 45°–50° oblique to the transform strike. They occur parallel to the short axis of the strain ellipse for transform fault strain here, i.e., perpendicular to the least compressive stress. The transform walls are formed by normal faulting as has been pointed out in previous detailed surveys. Here, however, the age contrast of 2.5 m.y. across the transform valley is apparent in the morphology of the normal fault scarps. While the scarps are steep and well-defined on the young side, the scarps on the older side have gradual 10°–30° slopes and appear to be primarily talus ramps. Apparently, the scarps have been tectonically eroded by continued strike slip activity after the initial stages of normal faulting. Thus, transform valleys should be quite asymmetric in cross-section where there is a significant age contrast and one side is less than approximately 0.5 m.y. old. Also, along older sections of the transform valley walls, normal faulting may not be at all obvious due to degradation of the scarps by tectonic erosion. This phenomenon makes the likelihood of transform faults providing ‘windows’ into the oceanic crust most unlikely except in special cases. The picture of transform deformation is more complex at site 2 in the central portion of the fault where both sides of the fault are greater than 1 m.y. old. Here the transform valley is wider (25–30 km as opposed to 2–5 km). There is no clear simple zone of strike slip tectonics. In fact, the only clear evidence for deformation is the intrusion of magmatic or serpentinite diapirs through the sediments of the transform valley floor. The diapirs have deformed the turbidite layers flooring the valley and in one carefully studied case the turbidite sequence has been uplifted, perched atop the diapir. The pattern of deformation on this outcropping diapir shows radial and concentric fractures which can be modeled by a vertical intrusion circular in plan view. Magnetic studies limit the possible composition to basalt or serpentinite. A 60-km-long median ridge is also likely to be the product of intrusion along the transform fault. The survey at site 2 pointed out the importance of vertical tectonics in the transform valley floor and in particular the importance of diapiric intrusions of either basaltic or serpentinite composition. Based on initial boundary conditions and present tectonic elements in the Tamayo fault zone, a possible history of the mouth of the Gulf of California is outlined. The median ridge was emplaced starting approximately 0.8 m.y. ago by regional extension across the transform fault, the result of ‘leaky’ transform faulting. The diapirs occur along a possible ‘relay’ zone of extension midway along the fault which began approximately 0.15 m.y. ago. The extension in this case is parallel to the trend of the transform fault, is still occurring at present, and may evolve into a true spreading center.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-0581
    Keywords: plate tectonics ; seafloor spreading ; rift propagation ; rift failure ; lithospheric transfer ; magmatic differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences , Physics
    Notes: Abstract ALVIN investigations have defined the fine-scale structural and volcanic patterns produced by active rift and spreading center propagation and failure near 95.5° W on the Galapagos spreading center. Behind the initial lithospheric rifting, which is propagating nearly due west at about 50 km m.y.−1, a triangular block of preexisting lithosphere is being stretched and fractured, with some recent volcanism along curving fissures. A well-organized seafloor spreading center, an extensively faulted and fissured volcanic ridge, develops ~ 10 km (~ 200,000 years) behind the tectonic rift tip. Regional variations in the chemical compositions of the youngest lavas collected during this program contrast with those encompassing the entire 3 m.y. of propagation history for this region. A maximum in degree of magmatic differentiation occurs about 9 km behind the propagating rift tip, in a region of diffuse rifting. The propagating spreading center shows a gentle gradient in magmatic differentiation culminating at the SW-curving spreading center tip. Except for the doomed rift, which is in a constructional phase, tectonic activity also dominates over volcanic activity along the failing spreading system. In contrast to the propagating rift, failing rift lavas show a highly restricted range of compositions consistent with derivation from a declining upwelling zone accompanying rift failure. The lithosphere transferred from the Cocos to the Nazca plate by this propagator is extensively faulted and characterized by ubiquitous talus in one of the most tectonically disrupted areas of seafloor known. The pseudofault scarps, where the preexisting lithosphere was rifted apart, appear to include both normal and propagator lavas and are thus more lithologically complex than previously thought. Biological communities, probably vestimentiferan tubeworms, occur near the top of the outer pseudofault scarp, although no hydrothermal venting was observed.
    Type of Medium: Electronic Resource
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  • 7
    Publication Date: 2014-03-14
    Description: Fossil fuel combustion has increased atmospheric CO 2 by ≈ 115 µmol mol -1 since 1750, and decreased its carbon isotope composition (δ 13 C) by 1.7-2 ‰ (the 13 C Suess effect). Because carbon is stored in the terrestrial biosphere for decades and longer, the δ 13 C of CO 2 released by terrestrial ecosystems is expected to differ from the δ 13 C of CO 2 assimilated by land plants during photosynthesis. This isotopic difference between land-atmosphere respiration (δ R ) and photosynthetic assimilation (δ A ) fluxes gives rise to the 13 C land disequilibrium (D). Contemporary understanding suggests that over annual and longer time scales, D is determined primarily by the Suess effect, and thus D is generally positive (δ R  〉 δ A ). A seven-year record of biosphere-atmosphere carbon exchange was used to evaluate the seasonality of δ A and δ R , and the 13 C land disequilibrium, in a subalpine conifer forest. A novel isotopic mixing model was employed to determine the δ 13 C of net land-atmosphere exchange during day and night, and combined with tower-based flux observations to assess δ A and δ R . The disequilibrium varied seasonally, and when flux-weighted was opposite in sign than expected from the Suess effect (D = -0.75 ± 0.21 ‰ or -0.88 ± 0.10 ‰ depending on method). Seasonality in D appeared to be driven by photosynthetic discrimination (Δ canopy ) responding to environmental factors. Possible explanations for negative D include: 1) changes in Δ canopy over decades as CO 2 and temperature have risen, and/or 2) post-photosynthetic fractionation processes leading to sequestration of isotopically-enriched carbon in long-lived pools like wood and soil.
    Print ISSN: 0886-6236
    Electronic ISSN: 1944-9224
    Topics: Biology , Chemistry and Pharmacology , Geography , Geosciences , Physics
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  • 8
    Publication Date: 2016-05-17
    Description: The number of patients surviving with congenital heart disease (CHD) has soared over the last 3 decades. Adults constitute the fastest-growing segment of the CHD population, now outnumbering children. Research to date on the heart-brain intersection in this population has been focused largely on neurodevelopmental outcomes in childhood and adolescence. Mutations in genes that are highly expressed in heart and brain may cause cerebral dysgenesis. Together with altered cerebral perfusion in utero, these factors are associated with abnormalities of brain structure and brain immaturity in a significant portion of neonates with critical CHD even before they undergo cardiac surgery. In infancy and childhood, the brain may be affected by risk factors related to heart disease itself or to its interventional treatments. As children with CHD become adults, they increasingly develop heart failure, atrial fibrillation, hypertension, diabetes mellitus, and coronary disease. These acquired cardiovascular comorbidities can be expected to have effects similar to those in the general population on cerebral blood flow, brain volumes, and dementia. In both children and adults, cardiovascular disease may have adverse effects on achievement, executive function, memory, language, social interactions, and quality of life. Against the backdrop of shifting demographics, risk factors for brain injury in the CHD population are cumulative and synergistic. As neurodevelopmental sequelae in children with CHD evolve to cognitive decline or dementia during adulthood, a growing population of CHD can be expected to require support services. We highlight evidence gaps and future research directions.
    Keywords: Cardiovascular Disease, Congenital Heart Disease, Vascular Disease
    Electronic ISSN: 1524-4539
    Topics: Medicine
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  • 9
    Publication Date: 2012-12-08
    Description: The microtubule-associated protein targeting protein for Xenopus kinesin-like protein 2 (TPX2) plays a key role in spindle assembly and is required for mitosis in human cells. In interphase, TPX2 is actively imported into the nucleus to prevent its premature activity in microtubule organization. To date, no function has been assigned to nuclear TPX2. We now report that TPX2 plays a role in the cellular response to DNA double strand breaks induced by ionizing radiation. Loss of TPX2 leads to inordinately strong and transient accumulation of ionizing radiation-dependent Ser-139-phosphorylated Histone 2AX (γ-H2AX) at G0 and G1 phases of the cell cycle. This is accompanied by the formation of increased numbers of high intensity γ-H2AX ionizing radiation-induced foci. Conversely, cells overexpressing TPX2 have reduced levels of γ-H2AX after ionizing radiation. Consistent with a role for TPX2 in the DNA damage response, we found that the protein accumulates at DNA double strand breaks and associates with the mediator of DNA damage checkpoint 1 (MDC1) and the ataxia telangiectasia mutated (ATM) kinase, both key regulators of γ-H2AX amplification. Pharmacologic inhibition or depletion of ATM or MDC1, but not of DNA-dependent protein kinase (DNA-PK), antagonizes the γ-H2AX phenotype caused by TPX2 depletion. Importantly, the regulation of γ-H2AX signals by TPX2 is not associated with apoptosis or the mitotic functions of TPX2. In sum, our study identifies a novel and the first nuclear function for TPX2 in the cellular responses to DNA damage.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
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  • 10
    Publication Date: 2014-05-21
    Description: DNA-dependent protein kinase (DNA-PK) orchestrates DNA repair by regulating access to breaks through autophosphorylations within two clusters of sites (ABCDE and PQR). Blocking ABCDE phosphorylation (by alanine mutation) imparts a dominant negative effect, rendering cells hypersensitive to agents that cause DNA double-strand breaks. Here, a mutational approach is used to address the mechanistic basis of this dominant negative effect. Blocking ABCDE phosphorylation hypersensitizes cells to most types of DNA damage (base damage, cross-links, breaks, and damage induced by replication stress), suggesting that DNA-PK binds DNA ends that result from many DNA lesions and that blocking ABCDE phosphorylation sequesters these DNA ends from other repair pathways. This dominant negative effect requires DNA-PK's catalytic activity, as well as phosphorylation of multiple (non-ABCDE) DNA-PK catalytic subunit (DNA-PKcs) sites. PSIPRED analysis indicates that the ABCDE sites are located in the only contiguous extended region of this huge protein that is predicted to be disordered, suggesting a regulatory role(s) and perhaps explaining the large impact ABCDE phosphorylation has on the enzyme's function. Moreover, additional sites in this disordered region contribute to the ABCDE cluster. These data, coupled with recent structural data, suggest a model whereby early phosphorylations promote initiation of nonhomologous end joining (NHEJ), whereas ABCDE phosphorylations, potentially located in a "hinge" region between the two domains, lead to regulated conformational changes that initially promote NHEJ and eventually disengage NHEJ.
    Print ISSN: 0270-7306
    Electronic ISSN: 1098-5549
    Topics: Biology , Medicine
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