4,015 research outputs found

    Zircon LA-ICPMS geochronology of the Cornubian Batholith, SW England

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    AcceptedArticleAvailable U-Pb age data for the Cornubian Batholith of SW England is based almost entirely on monazite and xenotime, and very little zircon U-Pb age data has been published. As a result, no zircon inheritance data is available for the batholith, by which the nature of the unexposed basement of the Rhenohercynian Zone in SW England might be constrained. Zircon LA-ICPMS data for the Cornubian Batholith provides Concordia ages (Bodmin Moor granite: 316 ± 4 Ma, Carnmenellis granite: 313 ± 3 Ma, Dartmoor granite: ~ 310 Ma, St. Austell granite: 305 ± 5 Ma, and Land's End granite: 300 ± 5 Ma) that are consistently 20–30 Ma older than previously published emplacement ages for the batholith and unrealistic in terms of geologic relative age relationships with respect to the country rock. This discrepancy is likely as a consequence of minor pre-granitic Pb inheritance. Several of the batholith's granite plutons contain a component of late-Devonian inheritance that may record rift-related, lower crustal melting or arc-related magmatism associated with subduction of the Rheic Ocean. In addition, the older granites likely contain Mesoproterozoic inheritance, although the highly discordant nature of the Mesoproterozoic ages precludes their use in assigning an affinity to the Rhenohercynian basement in SW England.This project was supported by the Department of Geological Sciences at Ohio University and by NSERC (Canada) through Discovery grants to JBM. Thanks are also extended to the faculty and staff in the School of Earth and Environmental Sciences at the University of Portsmouth, the British Geological Survey, and the Department of Earth Systems Science at Morehead State University for the use of their facilities

    Mantle evolution in the Variscides of SW England: geochemical and isotopic constraints from mafic rocks

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    This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record.The geology of SW England has long been interpreted to reflect Variscan collisional processes associated with the closure of the Rhenohercynian Ocean and the formation of Pangea. The Cornish peninsula is composed largely of Early Devonian to Late Carboniferous volcanosedimentary successions that were deposited in pre- and syncollisional basins and were subsequently metamorphosed and deformed during the Variscan orogeny. Voluminous Early Permian granitic magmatism (Cornubian Batholith) is broadly coeval with the emplacement of ca. 280-295 Ma lamprophyric dykes and flows. Although these lamprophyres are well mapped and documented, the processes responsible for their genesis and their relationship with regional Variscan tectonic events are less understood. Pre- to syn-collisional basalts have intra-continental alkalic affinities, and have REE profiles consistent with derivation from the spinel-garnet lherzolite boundary. εNd values for the basalts range from +0.37 to +5.2 and TDM ages from 595 Ma to 705 Ma. The lamprophyres are extremely enriched in light rare earth elements, large iron lithophile, and depleted in heavy rare earth elements suggesting a deep, garnet lherzolite source that was previously metasomatised. They display εNd values ranging from -1.4 to +1.4, initial Sr values of ca. 0.706, and TDM ages from 671 Ma to 1031 Ma, suggesting that metasomatism occurred in the Neoproterozoic. Lamprophyres and coeval granite batholiths of similar chemistry to those in Cornwall occur in other regions of the Variscan orogen, including Iberia and Bohemia. By using new geochemical and isotopic data to constrain the evolution of the mantle beneath SW England and the processes associated with the formation of these post-collisional rocks, we may be able to gain a more complete understanding of mantle processes during the waning stages of supercontinent formation

    Fgf2 Regulates Proliferation of Neural Crest Cells, with Subsequent Neuronal Differentiation Regulated by Lif or Related Factors

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    Two of the key early events in the development of the peripheral nervous system are the proliferation of neural crest precursor cells and their subsequent differentiation into different neural cell types, We present evidence that members of the fibroblast growth factor family, (FGF1 or FGF2) act directly on the neural crest cells in vitro to stimulate proliferation in the presence of serum, These findings correlate with in situ hybridisation analysis, which shows FGF2 mRNA is expressed in cells both in the neural tube and within newly formed sensory ganglia (dorsal root ganglia, DRG) at embryonic day 10 in the mouse, when neural crest precursors are proliferating within the DRG, This data infers an autocrine/paracrine loop for FGF regulation of proliferation, Evidence supporting this notion is provided by the finding that part of the endogenous proliferative activity in the NC cultures is related to FGF, It was also found, in early neural crest cultures, that exogenous FGF completely inhibited neuronal differentiation, probably as a direct consequence of its mitogenic activity, In order to stimulate neuronal differentiation significantly, it was necessary to remove the FGF and replace it with leukemia inhibitory factor (LIF) or related factors, Under these conditions, 50% of the cells differentiated into neurons, which developed a sensory neuron morphology and were immunoreactive for the sensory markers CGRP and substance P. These data support a model of neural crest development, whereby multipotential neural crest precursor cells are stimulated to divide by FGF and subsequent development into sensory neurons is regulated by LIF or other cytokines with a similar signalling mechanism

    The results of compression forces applied to the isolated human calvaria

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    Data for the force necessary to fracture the isolated calvaria (skull cap) are not available in the extant literature. Twenty dry adult calvaria were tested to failure quasistatically at the vertex using a 15-kN load cell. The forces necessary to fracture or cause diastasis of calvarial sutures were then documented and gross examination of the specimens made. Failure forces had a mean measurement of 2772 N. Initial fractures did not cross suture lines. Prior to complete destruction of the calvaria there were 7 specimens in which all sutures of the calvaria became diastatic, 6 specimens in which the calvaria became diastatic along only the coronal sutures, 2 specimens in which the calvaria became diastatic along only the sagittal suture and 5 specimens in which there were diagonal linear parietal bone fractures. Our hopes are that these data may contribute to the structural design of more safer protective devices for use in our society, assist in predicting injury and aid in the construction of treatment paradigms

    Comparison of cellular responses to TGF-β1 and BMP-2 between healthy and torn tendons

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    Background: Tendons heal by fibrotic repair, increasing the likelihood of reinjury. Animal tendon injury and overuse models have identified transforming growth factor beta (TGF-β) and bone morphogenetic proteins (BMPs) as growth factors actively involved in the development of fibrosis, by mediating extracellular matrix synthesis and cell differentiation. Purpose: To understand how TGF-β and BMPs contribute to fibrotic processes using tendon-derived cells isolated from healthy and diseased human tendons. Study Design: Controlled laboratory study. Methods: Tendon-derived cells were isolated from patients with a chronic rotator cuff tendon tear (large to massive, diseased) and healthy hamstring tendons of patients undergoing anterior cruciate ligament repair. Isolated cells were incubated with TGF-β1 (10 ng/mL) or BMP-2 (100 ng/mL) for 3 days. Gene expression was measured by real-time quantitative polymerase chain reaction. Cell signaling pathway activation was determined by Western blotting. Results: TGF-β1 treatment induced ACAN mRNA expression in both cell types but less in the diseased compared with healthy cells (P < .05). BMP-2 treatment induced BGN mRNA expression in healthy but not diseased cells (P < .01). In the diseased cells, TGF-β1 treatment induced increased ACTA2 mRNA expression (P < .01) and increased small mothers against decapentaplegic (SMAD) signaling (P < .05) compared with those of healthy cells. Moreover, BMP-2 treatment induced ACTA2 mRNA expression in the diseased cells only (P < .05). Conclusion: Diseased tendon–derived cells show reduced expression of the proteoglycans aggrecan and biglycan in response to TGF-β1 and BMP-2 treatments. These same treatments induced enhanced fibrotic differentiation and canonical SMAD cell signaling in diseased compared with healthy cells. Clinical Relevance: Findings from this study suggest that diseased tendon–derived cells respond differently than healthy cells in the presence of TGF-β1 and BMP-2. The altered responses of diseased cells may influence fibrotic repair processes during tendon healing
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