112 research outputs found

    Secondary Forest Age and Tropical Forest Biomass Estimation Using TM

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    The age of secondary forests in the Amazon will become more critical with respect to the estimation of biomass and carbon budgets as tropical forest conversion continues. Multitemporal Thematic Mapper data were used to develop land cover histories for a 33,000 Square kM area near Ariquemes, Rondonia over a 7 year period from 1989-1995. The age of the secondary forest, a surrogate for the amount of biomass (or carbon) stored above-ground, was found to be unimportant in terms of biomass budget error rates in a forested TM scene which had undergone a 20% conversion to nonforest/agricultural cover types. In such a situation, the 80% of the scene still covered by primary forest accounted for over 98% of the scene biomass. The difference between secondary forest biomass estimates developed with and without age information were inconsequential relative to the estimate of biomass for the entire scene. However, in futuristic scenarios where all of the primary forest has been converted to agriculture and secondary forest (55% and 42% respectively), the ability to age secondary forest becomes critical. Depending on biomass accumulation rate assumptions, scene biomass budget errors on the order of -10% to +30% are likely if the age of the secondary forests are not taken into account. Single-date TM imagery cannot be used to accurately age secondary forests into single-year classes. A neural network utilizing TM band 2 and three TM spectral-texture measures (bands 3 and 5) predicted secondary forest age over a range of 0-7 years with an RMSE of 1.59 years and an R(Squared) (sub actual vs predicted) = 0.37. A proposal is made, based on a literature review, to use satellite imagery to identify general secondary forest age groups which, within group, exhibit relatively constant biomass accumulation rates

    Effects of a large-scale, natural sediment deposition event on plant cover in a Massachusetts salt marsh

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    In mid-winter 2018, an unprecedented sediment deposition event occurred throughout portions of the Great Marsh in Massachusetts. Evaluation of this event in distinct marsh areas spanning three towns (Essex, Ipswich, and Newbury) revealed deposition covering 29.2 hectares with an average thickness of 30.1±2.1 mm measured shortly after deposition. While sediment deposition helps marshes survive sea level rise by building elevation, effects of such a large-scale deposition on New England marshes are unknown. This natural event provided an opportunity to study effects of large-scale sediment addition on plant cover and soil chemistry, with implications for marsh resilience. Sediment thickness did not differ significantly between winter and summer, indicating sediment is not eroding or compacting. The deposited sediment at each site had similar characteristics to that of the adjacent mudflat (e.g., texture, bivalve shells), suggesting that deposited materials resulted from ice rafting from adjacent flats, a natural phenomenon noted by other authors. Vegetative cover was significantly lower in plots with rafted sediment (75.6±2.3%) than sediment-free controls (93.1±1.6%) after one growing season. When sorted by sediment thickness categories, the low thickness level (1–19 mm) had significantly greater percent cover than medium (20–39 mm) and high (40–90 mm) categories. Given that sediment accretion in the Great Marsh was found to average 2.7 mm per year, the sediment thickness documented herein represents ~11 years of sediment accretion with only a 25% reduction in plant cover, suggesting this natural sediment event will likely increase long-term marsh resilience to sea level rise

    A longer vernal window: The role of winter coldness and snowpack in driving spring thresholds and lags

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    Climate change is altering the timing and duration of the vernal window, a period that marks the end of winter and the start of the growing season when rapid transitions in ecosystem energy, water, nutrient, and carbon dynamics take place. Research on this period typically captures only a portion of the ecosystem in transition and focuses largely on the dates by which the system wakes up. Previous work has not addressed lags between transitions that represent delays in energy, water, nutrient, and carbon flows. The objectives of this study were to establish the sequence of physical and biogeochemical transitions and lags during the vernal window period and to understand how climate change may alter them. We synthesized observations from a statewide sensor network in New Hampshire, USA, that concurrently monitored climate, snow, soils, and streams over a three-year period and supplemented these observations with climate reanalysis data, snow data assimilation model output, and satellite spectral data. We found that some of the transitions that occurred within the vernal window were sequential, with air temperatures warming prior to snow melt, which preceded forest canopy closure. Other transitions were simultaneous with one another and had zero-length lags, such as snowpack disappearance, rapid soil warming, and peak stream discharge. We modeled lags as a function of both winter coldness and snow depth, both of which are expected to decline with climate change. Warmer winters with less snow resulted in longer lags and a more protracted vernal window. This lengthening of individual lags and of the entire vernal window carries important consequences for the thermodynamics and biogeochemistry of ecosystems, both during the winter-to-spring transition and throughout the rest of the year

    QT Interval Prolongation and Torsade De Pointes in Patients with COVID-19 treated with Hydroxychloroquine/Azithromycin

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    Background: There is no known effective therapy for patients with COVID-19. Initial reports suggesting the potential benefit of Hydroxychloroquine/Azithromycin (HY/AZ) have resulted in massive adoption of this combination worldwide. However, while the true efficacy of this regimen is unknown, initial reports have raised concerns regarding the potential risk of QT prolongation and induction of torsade de pointes (TdP). Objective: to assess the change in QTc interval and arrhythmic events in patients with COVID-19 treated with HY/AZ METHODS: This is a retrospective study of 251 patients from two centers, diagnosed with COVID-19 and treated with HY/AZ. We reviewed ECG tracings from baseline and until 3 days after completion of therapy to determine the progression of QTc and incidence of arrhythmia and mortality. Results: QTc prolonged in parallel with increasing drug exposure and incompletely shortened after its completion. Extreme new QTc prolongation to > 500 ms, a known marker of high risk for TdP had developed in 23% of patients. One patient developed polymorphic ventricular tachycardia (VT) suspected as TdP, requiring emergent cardioversion. Seven patients required premature termination of therapy. The baseline QTc of patients exhibiting extreme QTc prolongation was normal. Conclusion: The combination of HY/AZ significantly prolongs the QTc in patients with COVID-19. This prolongation may be responsible for life threating arrhythmia in the form of TdP. This risk mandates careful consideration of HY/AZ therapy in lights of its unproven efficacy. Strict QTc monitoring should be performed if the regimen is given

    T-lymphocyte subsets in liver tissues of patients with primary biliary cirrhosis (PBC), patients with primary sclerosing cholangitis (PSC), and normal controls

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    T lymphocytes infiltrating hepatic tissues were typed and enumerated in liver biopsies of patients with primary biliary cirrhosis (PBC), patients with primary sclerosing cholangitis (PSC), and normal controls using monoclonal antibodies and the avidin-biotin-immunoperoxidase technique. The peripheral blood mononuclear cells were studied also by flow cytometry. In PBC, T lymphocytes were decreased (P<0.001) in the blood [absolute number was 426±200 (SE) vs 1351±416 in 15 controls], as was the helper/suppressor (T4/T8) ratio (1.0±0.1 vs normal 2.3±0.3). T lymphocytes were the most numerous mononuclear cells infiltrating portal areas of PBC livers: 749±93/5 high-power fields (HPF) in PBC vs 98±15/5 HPF (P<0.01) in controls. The T4/T8 ratios varied from 0.9 to 2.3 (mean, 1.8±0.1) in the portal triads (normal mean, 1.6±0.1), with the T4+ cells accounting for more than 75% of infiltrating T cells. In contrast, the mean T4/T8 ratio in portal triads of PSC was reduced (1.0±0.3) due to a significant increase (P<0.001) in the number of T8+ cells. The T cells around and in the walls of bile ducts in PBC were mostly T8+, and the T4/T8 ratio was 0.8±0.2. No T8+ cells were seen in this location in PSC and normal livers. Few mononuclear cells were present in hepatic lobules. Subtyping of T lymphocytes in liver tissues of patients with PBC and PSC may be helpful in the differential pathologic diagnosis. In patients with advanced PBC, a decrease in T4+ cells in the blood appeared to be accompanied by their accumulation in the portal triads. In contrast, T8+ cells accumulated preferentially around bile ducts. © 1984 Plenum Publishing Corporation

    Meta-Analysis for Genome-Wide Association Study Identifies Multiple Variants at the BIN1 Locus Associated with Late-Onset Alzheimer's Disease

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    Recent GWAS studies focused on uncovering novel genetic loci related to AD have revealed associations with variants near CLU, CR1, PICALM and BIN1. In this study, we conducted a genome-wide association study in an independent set of 1034 cases and 1186 controls using the Illumina genotyping platforms. By coupling our data with available GWAS datasets from the ADNI and GenADA, we replicated the original associations in both PICALM (rs3851179) and CR1 (rs3818361). The PICALM variant seems to be non-significant after we adjusted for APOE e4 status. We further tested our top markers in 751 independent cases and 751 matched controls. Besides the markers close to the APOE locus, a marker (rs12989701) upstream of BIN1 locus was replicated and the combined analysis reached genome-wide significance level (p = 5E-08). We combined our data with the published Harold et al. study and meta-analysis with all available 6521 cases and 10360 controls at the BIN1 locus revealed two significant variants (rs12989701, p = 1.32E-10 and rs744373, p = 3.16E-10) in limited linkage disequilibrium (r2 = 0.05) with each other. The independent contribution of both SNPs was supported by haplotype conditional analysis. We also conducted multivariate analysis in canonical pathways and identified a consistent signal in the downstream pathways targeted by Gleevec (P = 0.004 in Pfizer; P = 0.028 in ADNI and P = 0.04 in GenADA). We further tested variants in CLU, PICALM, BIN1 and CR1 for association with disease progression in 597 AD patients where longitudinal cognitive measures are sufficient. Both the PICALM and CLU variants showed nominal significant association with cognitive decline as measured by change in Clinical Dementia Rating-sum of boxes (CDR-SB) score from the baseline but did not pass multiple-test correction. Future experiments will help us better understand potential roles of these genetic loci in AD pathology

    Differential endothelial cell gene expression by African Americans versus Caucasian Americans: a possible contribution to health disparity in vascular disease and cancer

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    <p>Abstract</p> <p>Background</p> <p>Health disparities and the high prevalence of cardiovascular disease continue to be perplexing worldwide health challenges. This study addresses the possibility that genetic differences affecting the biology of the vascular endothelium could be a factor contributing to the increased burden of cardiovascular disease and cancer among African Americans (AA) compared to Caucasian Americans (CA).</p> <p>Methods</p> <p>From self-identified, healthy, 20 to 29-year-old AA (n = 21) and CA (n = 17), we established cultures of blood outgrowth endothelial cells (BOEC) and applied microarray profiling. BOEC have never been exposed to <it>in vivo </it>influences, and their gene expression reflects culture conditions (meticulously controlled) and donor genetics. Significance Analysis of Microarray identified differential expression of single genes. Gene Set Enrichment Analysis examined expression of pre-determined gene sets that survey nine biological systems relevant to endothelial biology.</p> <p>Results</p> <p>At the highly stringent threshold of False Discovery Rate (FDR) = 0, 31 single genes were differentially expressed in AA. <it>PSPH </it>exhibited the greatest fold-change (AA > CA), but this was entirely accounted for by a homolog (<it>PSPHL</it>) hidden within the <it>PSPH </it>probe set. Among other significantly different genes were: for AA > CA, <it>SOS1, AMFR, FGFR3; and for AA < CA, ARVCF, BIN3, EIF4B. </it>Many more (221 transcripts for 204 genes) were differentially expressed at the less stringent threshold of FDR <.05. Using the biological systems approach, we identified shear response biology as being significantly different for AA versus CA, showing an apparent tonic increase of expression (AA > CA) for 46/157 genes within that system.</p> <p>Conclusions</p> <p>Many of the genes implicated here have substantial roles in endothelial biology. Shear stress response, a critical regulator of endothelial function and vascular homeostasis, may be different between AA and CA. These results potentially have direct implications for the role of endothelial cells in vascular disease (hypertension, stroke) and cancer (via angiogenesis). Also, they are consistent with our over-arching hypothesis that genetic influences stemming from ancestral continent-of-origin could impact upon endothelial cell biology and thereby contribute to disparity of vascular-related disease burden among AA. The method used here could be productively employed to bridge the gap between information from structural genomics (for example, disease association) and cell function and pathophysiology.</p
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