73 research outputs found

    Geographic Variation in Wood Specific Gravity: Effects of Latitude, Temperature, and Precipitation

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    Wood basic specific gravity (SG) was compared at sites located along a gradient from 52°N latitude to the equator. Mean SG increased by 0.0049 per °C mean annual temperature (MAT), and decreased by 0.00017 per cm of mean annual precipitation (MAP). Considered alone, MAT was a better predictor of mean SG across the temperate zone (3-22°C MAT, latitude north of 29°N; r2 = 0.80) than it was across the entire MAT range (r2 = 0.62) or across warm tropical sites alone (MAT > 23°C; r2 = 0.33, p = 0.67). In contrast, MAP considered alone was a better predictor of mean SG in the warm tropical sites (r2 = 0.62) than across all sites (r2 = 0.04, p = 0.39).Variability in SG among the sites was compared using two measures of dispersion: range and standard deviation. As MAT increased across the temperate zone, maximum SG increased and minimum SG remained constant, resulting in an increase in SG range; SG standard deviation, however, remained constant. Both SG range and SG standard deviation increased dramatically in the warm tropical zone relative to the temperate zone, demonstrating that variability in SG in the warm tropics is much greater than would be predicted from greater species richness alone

    Extreme Radial Changes in Wood Specific Gravity in Some Tropical Pioneers

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    Twelve Hampea appendiculata, six Heliocarpus appendiculatus, and twelve Ochroma pyramidale trees from tropical wet forest in Costa Rica were sampled across their radii. Wood from all three species increased linearly in specific gravity from pith to bark. The magnitude of the increase was about 0.1 units of specific gravity per 10 cm of radius, although there were differences between the species and between trees within each species. All three species colonize clearings and disturbed sites, and these extreme changes in specific gravity may be associated with the pioneer habit in the wet forest

    Radiocarbon and geologic evidence reveal Ilopango volcano as source of the colossal ‘mystery’ eruption of 539/40 CE

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    Highlights ‱ Major eruption of Ilopango volcano, El Salvador occurred in the first half of the 6th century. ‱ Ilopango eruption is consistent with ‘mystery’ eruption of 540 CE that caused global cooling. ‱ Magnitude 7 event ranks as one of the 10 largest on Earth in past 7000 years. ‱ Impacts on the Maya of Central America were severe, including estimated 100,000 + fatalities. Abstract Ilopango volcano (El Salvador) erupted violently during the Maya Classic Period (250–900 CE) in a densely-populated and intensively-cultivated region of the southern Maya realm, causing regional abandonment of an area covering more than 20,000 km2. However, neither the regional nor global impacts of the Tierra Blanca Joven (TBJ) eruption in Mesoamerica have been well appraised due to limitations in available volcanological, chronological, and archaeological observations. Here we present new evidence of the age, magnitude and sulfur release of the TBJ eruption, establishing it as one of the two hitherto unidentified volcanic triggers of a period of stratospheric aerosol loading that profoundly impacted Northern Hemisphere climate and society between circa 536 and 550 CE. Our chronology is derived from 100 new radiocarbon measurements performed on three subfossil tree trunks enveloped in proximal TBJ pyroclastic deposits. We also reassess the eruption magnitude using terrestrial (El Salvador, Guatemala, Honduras) and near-shore marine TBJ tephra deposit thickness measurements. Together, our new constraints on the age, eruption size (43.6 km3 Dense Rock Equivalent of magma, magnitude = 7.0) and sulfur yield (∌9–90 Tg), along with Ilopango's latitude (13.7° N), squarely frame the TBJ as the major climate-forcing eruption of 539 or 540 CE identified in bipolar ice cores and sourced to the tropics. In addition to deepening appreciation of the TBJ eruption's impacts in Mesoamerica, linking it to the major Northern Hemisphere climatic downturn of the mid-6th century CE offers another piece in the puzzle of understanding Eurasian history of the period

    Stem cells in liver regeneration and therapy

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    The liver has adapted to the inflow of ingested toxins by the evolutionary development of unique regenerative properties and responds to injury or tissue loss by the rapid division of mature cells. Proliferation of the parenchymal cells, i.e. hepatocytes and epithelial cells of the bile duct, is regulated by numerous cytokine/growth-factor-mediated pathways and is synchronised with extracellular matrix degradation and restoration of the vasculature. Resident hepatic stem/progenitor cells have also been identified in small numbers in normal liver and implicated in liver tissue repair. Their putative role in the physiology, pathophysiology and therapy of the liver, however, is not yet precisely known. Hepatic stem/progenitor cells also known as “oval cells” in rodents have been implicated in liver tissue repair, at a time when the capacity for hepatocyte and bile duct replication is exhausted or experimentally inhibited (facultative stem/progenitor cell pool). Although much more has to be learned about the role of stem/progenitor cells in the physiology and pathophysiology of the liver, experimental analysis of the therapeutic value of these cells has been initiated. Transplantation of hepatic stem/progenitor cells or in vivo pharmacological activation of the pool of hepatic stem cells may provide novel modalities for the therapy of liver diseases. In addition, extrahepatic stem cells (e.g. bone marrow cells) are being investigated for their contribution to liver regeneration. Hepatic progenitor cells derived from embryonic stem cells are included in this review, which also discusses future perspectives of stem cell-based therapies for liver diseases

    Hepatic progenitor cells of biliary origin with liver repopulation capacity

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    Hepatocytes and cholangiocytes self-renew following liver injury. Following severe injury hepatocytes are increasingly senescent, but whether hepatic progenitor cells (HPCs) then contribute to liver regeneration is unclear. Here, we describe a mouse model where the E3 ubiquitin ligase Mdm2 is inducibly deleted in more than 98% of hepatocytes, causing apoptosis, necrosis and senescence with nearly all hepatocytes expressing p21. This results in florid HPC activation, which is necessary for survival, followed by complete, functional liver reconstitution. HPCs isolated from genetically normal mice, using cell surface markers, were highly expandable and phenotypically stable in vitro. These HPCs were transplanted into adult mouse livers where hepatocyte Mdm2 was repeatedly deleted, creating a non-competitive repopulation assay. Transplanted HPCs contributed significantly to restoration of liver parenchyma, regenerating hepatocytes and biliary epithelia, highlighting their in vivo lineage potency. HPCs are therefore a potential future alternative to hepatocyte or liver transplantation for liver disease
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