3,219 research outputs found

    Growth and form of the mound in Gale Crater, Mars: Slope wind enhanced erosion and transport

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    Ancient sediments provide archives of climate and habitability on Mars. Gale Crater, the landing site for the Mars Science Laboratory (MSL), hosts a 5-km-high sedimentary mound (Mount Sharp/Aeolis Mons). Hypotheses for mound formation include evaporitic, lacustrine, fluviodeltaic, and aeolian processes, but the origin and original extent of Gale’s mound is unknown. Here we show new measurements of sedimentary strata within the mound that indicate ∼3° outward dips oriented radially away from the mound center, inconsistent with the first three hypotheses. Moreover, although mounds are widely considered to be erosional remnants of a once crater-filling unit, we find that the Gale mound’s current form is close to its maximal extent. Instead we propose that the mound’s structure, stratigraphy, and current shape can be explained by growth in place near the center of the crater mediated by wind-topography feedbacks. Our model shows how sediment can initially accrete near the crater center far from crater-wall katabatic winds, until the increasing relief of the resulting mound generates mound-flank slope winds strong enough to erode the mound. The slope wind enhanced erosion and transport (SWEET) hypothesis indicates mound formation dominantly by aeolian deposition with limited organic carbon preservation potential, and a relatively limited role for lacustrine and fluvial activity. Morphodynamic feedbacks between wind and topography are widely applicable to a range of sedimentary and ice mounds across the Martian surface, and possibly other planets

    Host-parasite dynamics in Chagas disease from systemic to hyper-local scales

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    Trypanosoma cruzi is a remarkably versatile parasite. It can parasitize almost any nucleated cell type and naturally infects hundreds of mammal species across much of the Americas. In humans it is the cause of Chagas disease, a set of mainly chronic conditions predominantly affecting the heart and gastrointestinal tract that can progress to become life threatening. Yet around two thirds of infected people are long-term asymptomatic carriers. Clinical outcomes depend on many factors, but the central determinant is the nature of the host-parasite interactions that play out over the years of chronic infection in diverse tissue environments. In this review, we aim to integrate recent developments in the understanding of the spatial and temporal dynamics of T. cruzi infections with established and emerging concepts in host immune responses in the corresponding phases and tissues

    Prospectus, February 14, 1996

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    https://spark.parkland.edu/prospectus_1996/1004/thumbnail.jp

    Testosterone and resistance training effects on muscle nitric oxide synthase isoforms in COPD men

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    SummaryBackgroundSkeletal muscle dysfunction contributes to exercise limitation in COPD. The role of the nitric oxide synthase (NOS) system in muscle dysfunction is ill defined. Reduced levels of endothelial NOS (eNOS) and elevated levels of inducible NOS (iNOS) in the skeletal muscle of COPD patients have been recently reported. We hypothesized that resistance exercise training (R) and/or testosterone supplementation (T) would alter the transcription and expression of the NOS isoenzymes in COPD skeletal muscle.MethodsVastus lateralis biopsies were obtained before and after a 10-week intervention in 40 men with severe COPD(age 67.7 ± 8.3, FEV1 41.4 ± 12.6% predicted): placebo + no training (P) (n = 11), placebo + resistance training (PR) (n = 8), testosterone + no training (T) (n = 11) and testosterone + resistance training (TR) (n = 10) groups. eNOS, nNOS and iNOS mRNA and protein levels were measured in each sample. mRNA and protein levels were measured using real-time PCR and enzyme-linked immunosorbant assay, respectively.ResultseNOS mRNA increased in the TR group compared to P and T groups (P < 0.001). eNOS protein was increased in TR and T groups after intervention (P < 0.05) but not in the PR group. nNOS protein increased in the PR, T, and TR groups (P < 0.05). iNOS protein decreased only in the TR group (P = 0.01).ConclusionResistance training and testosterone supplementation increased eNOS and nNOS proteins and decreased iNOS protein in the skeletal muscles of men with COPD. These changes in NO system might explain some of the favorable effects of these therapies

    Ulocuplumab (BMS-936564 / MDX1338): a fully human anti-CXCR4 antibody induces cell death in chronic lymphocytic leukemia mediated through a reactive oxygen species-dependent pathway.

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    The CXCR4 receptor (Chemokine C-X-C motif receptor 4) is highly expressed in different hematological malignancies including chronic lymphocytic leukemia (CLL). The CXCR4 ligand (CXCL12) stimulates CXCR4 promoting cell survival and proliferation, and may contribute to the tropism of leukemia cells towards lymphoid tissues. Therefore, strategies targeting CXCR4 may constitute an effective therapeutic approach for CLL. To address that question, we studied the effect of Ulocuplumab (BMS-936564), a fully human IgG4 anti-CXCR4 antibody, using a stroma--CLL cells co-culture model. We found that Ulocuplumab (BMS-936564) inhibited CXCL12 mediated CXCR4 activation-migration of CLL cells at nanomolar concentrations. This effect was comparable to AMD3100 (Plerixafor--Mozobil), a small molecule CXCR4 inhibitor. However, Ulocuplumab (BMS-936564) but not AMD3100 induced apoptosis in CLL at nanomolar concentrations in the presence or absence of stromal cell support. This pro-apoptotic effect was independent of CLL high-risk prognostic markers, was associated with production of reactive oxygen species and did not require caspase activation. Overall, these findings are evidence that Ulocuplumab (BMS-936564) has biological activity in CLL, highlight the relevance of the CXCR4-CXCL12 pathway as a therapeutic target in CLL, and provide biological rationale for ongoing clinical trials in CLL and other hematological malignancies

    The Influence of Structure and Processing on the Behavior of TiO_2 Protective Layers for Stabilization of n-Si/TiO_2/Ni Photoanodes for Water Oxidation

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    Light absorbers with moderate band gaps (1–2 eV) are required for high-efficiency solar fuels devices, but most semiconducting photoanodes undergo photocorrosion or passivation in aqueous solution. Amorphous TiO_2 deposited by atomic-layer deposition (ALD) onto various n-type semiconductors (Si, GaAs, GaP, and CdTe) and coated with thin films or islands of Ni produces efficient, stable photoanodes for water oxidation, with the TiO_2 films protecting the underlying semiconductor from photocorrosion in pH = 14 KOH(aq). The links between the electronic properties of the TiO_2 in these electrodes and the structure and energetic defect states of the material are not yet well-elucidated. We show herein that TiO_2 films with a variety of crystal structures and midgap defect state distributions, deposited using both ALD and sputtering, form rectifying junctions with n-Si and are highly conductive toward photogenerated carriers in n-Si/TiO_2/Ni photoanodes. Moreover, the photovoltage of these electrodes can be modified by annealing the TiO_2 in reducing or oxidizing environments. All of the polycrystalline TiO_2 films with compact grain boundaries investigated herein protected the n-Si photoanodes against photocorrosion in pH = 14 KOH(aq). Hence, in these devices, conduction through the TiO_2 layer is neither specific to a particular amorphous or crystalline structure nor determined wholly by a particular extrinsic dopant impurity. The coupled structural and energetic properties of TiO_2, and potentially other protective oxides, can therefore be controlled to yield optimized photoelectrode performance
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