Del origen, fundacion, privilegios y excelencias de la Universidad de Osuna [...] : Apuntes para la historia de tan insigne y extinguida escuela

Copia digital. realizada por la Biblioteca de Andalucí

First lunar outpost

Design and research efforts at the University of Puerto Rico have focused on the evaluation and refinement of the Habitability Criteria for a prolonged human presence in space during the last four years. Living quarters for a Mars mission and a third generation lunar base concept were proposed. This academic year, 1991-92, work on further refinement of the habitability criteria and design of partial gravity furniture was carried on. During the first semester, design alternatives for furniture necessary in a habitat design optimized for lunar and Martian environments were developed. Designs are based on recent research data from lunar and Mars gravity simulations, and current NASA standards. Artifacts will be submitted to NASA architects to be tested in KC-135 flights. Test findings will be submitted for incorporation in future updates to NASA habitat design standards. Second semester work was aimed at integrating these findings into the First Lunar Outpost (FLO), a mission scenario currently being considered by NASA. The mission consists of a manned return to the moon by crews of four astronauts for periods of 45 days. The major hardware components of the mission are as follows: (1) a Crew Module for the delivery of the crew and their supplies, and (2) the Habitat Module, which will arrive on the Moon unmanned. Our design efforts concentrated on this Habitat Module and on application of habitability criteria. Different geometries for the pressure vessel and their impact on the interior architecture were studied. Upon the selection of a geometry, a more detailed analysis of the interior design was performed, taking into consideration the reduced gravity, and the protection against radiation, micrometeorites, and the extreme temperature variation. A proposal for a FLO was submitted by the students, consisting essentially of a 24-feet (7.3 m.) by 35-feet (10.67 m) high vertical cylinder with work areas, crew quarters, galley, wardroom, leisure facilities, health maintenance, waste management, EVA operations facilities, and safe havens

A Facile Nanoparticle Immunoassay for Cancer Biomarker Discovery

<p>Abstract</p> <p>Background</p> <p>Gold nanoparticles (AuNPs) scatter light intensely at or near their surface plasmon wavelength region. Using AuNPs coupled with dynamic light scattering (DLS) detection, we developed a facile nanoparticle immunoassay for serum protein biomarker detection and analysis. A serum sample was first mixed with a citrate-protected AuNP solution. Proteins from the serum were adsorbed to the AuNPs to form a protein corona on the nanoparticle surface. An antibody solution was then added to the assay solution to analyze the target proteins of interest that are present in the protein corona. The protein corona formation and the subsequent binding of antibody to the target proteins in the protein corona were detected by DLS.</p> <p>Results</p> <p>Using this simple assay, we discovered multiple molecular aberrations associated with prostate cancer from both mice and human blood serum samples. From the mice serum study, we observed difference in the size of the protein corona and mouse IgG level between different mice groups (i.e., mice with aggressive or less aggressive prostate cancer, and normal healthy controls). Furthermore, it was found from both the mice model and the human serum sample study that the level of vascular endothelial growth factor (VEGF, a protein that is associated with tumor angiogenesis) adsorbed to the AuNPs is decreased in cancer samples compared to non-cancerous or less malignant cancer samples.</p> <p>Conclusion</p> <p>The molecular aberrations observed from this study may become new biomarkers for prostate cancer detection. The nanoparticle immunoassay reported here can be used as a convenient and general tool to screen and analyze serum proteins and to discover new biomarkers associated with cancer and other human diseases.</p

Experimental Zika Virus Infection in the Pregnant Common Marmoset Induces Spontaneous Fetal Loss and Neurodevelopmental Abnormalities.

During its most recent outbreak across the Americas, Zika virus (ZIKV) was surprisingly shown to cause fetal loss and congenital malformations in acutely and chronically infected pregnant women. However, understanding the underlying pathogenesis of ZIKV congenital disease has been hampered by a lack of relevant in vivo experimental models. Here we present a candidate New World monkey model of ZIKV infection in pregnant marmosets that faithfully recapitulates human disease. ZIKV inoculation at the human-equivalent of early gestation caused an asymptomatic seroconversion, induction of type I/II interferon-associated genes and proinflammatory cytokines, and persistent viremia and viruria. Spontaneous pregnancy loss was observed 16-18 days post-infection, with extensive active placental viral replication and fetal neurocellular disorganization similar to that seen in humans. These findings underscore the key role of the placenta as a conduit for fetal infection, and demonstrate the utility of marmosets as a highly relevant model for studying congenital ZIKV disease and pregnancy loss

A Universal Phase Diagram for PMN-xPT and PZN-xPT

The phase diagram of the Pb(Mg1/3Nb2/3)O3 and PbTiO3 solid solution (PMN-xPT) indicates a rhombohedral ground state for x < 0.32. X-ray powder measurements by Dkhil et al. show a rhombohedrally split (222) Bragg peak for PMN-10%PT at 80 K. Remarkably, neutron data taken on a single crystal of the same compound with comparable q-resolution reveal a single resolution-limited (111) peak down to 50 K, and thus no rhombohedral distortion. Our results suggest that the structure of the outer layer of these relaxors differs from that of the bulk, which is nearly cubic, as observed in PZN by Xu et al.Comment: Replaced Fig. 3 with better versio

Hit-and-run transcriptional control by bZIP1 mediates rapid nutrient signaling in Arabidopsis

The dynamic nature of gene regulatory networks allows cells to rapidly respond to environmental change. However, the underlying temporal connections are missed, even in kinetic studies, as transcription factor (TF) binding within at least one time point is required to identify primary targets. The TF-regulated but unbound genes are dismissed as secondary targets. Instead, we report that these genes comprise transient TF-target interactions most relevant to rapid signal transduction. We temporally perturbed a master TF (Basic Leucine Zipper 1, bZIP1) and the nitrogen (N) signal it transduces and integrated TF regulation and binding data from the same cell samples. Our enabling approach could identify primary TF targets based solely on gene regulation, in the absence of TF binding. We uncovered three classes of primary TF targets: (i) poised (TF-bound but not TF-regulated), (ii) stable (TF-bound and TF-regulated), and (iii) transient (TF-regulated but not TF-bound), the largest class. Unexpectedly, the transient bZIP1 targets are uniquely relevant to rapid N signaling in planta, enriched in dynamic N-responsive genes, and regulated by TF and N signal interactions. These transient targets include early N responders nitrate transporter 2.1 and NIN-like protein 3, bound by bZIP1 at 1-5 min, but not at later time points following TF perturbation. Moreover, promoters of these transient targets are uniquely enriched with cis-regulatory motifs coinherited with bZIP1 binding sites, suggesting a recruitment role for bZIP1. This transient mode of TF action supports a classic, but forgotten, "hit-and-run" transcription model, which enables a "catalyst TF" to activate a large set of targets within minutes of signal perturbation

Engineering HIV-1-resistant T-cells from short-hairpin RNA-expressing hematopoietic stem/progenitor cells in humanized BLT mice

Down-regulation of the HIV-1 coreceptor CCR5 holds significant potential for long-term protection against HIV-1 in patients. Using the humanized bone marrow/liver/thymus (hu-BLT) mouse model which allows investigation of human hematopoietic stem/progenitor cell (HSPC) transplant and immune system reconstitution as well as HIV-1 infection, we previously demonstrated stable inhibition of CCR5 expression in systemic lymphoid tissues via transplantation of HSPCs genetically modified by lentiviral vector transduction to express short hairpin RNA (shRNA). However, CCR5 down-regulation will not be effective against existing CXCR4-tropic HIV-1 and emergence of resistant viral strains. As such, combination approaches targeting additional steps in the virus lifecycle are required. We screened a panel of previously published shRNAs targeting highly conserved regions and identified a potent shRNA targeting the R-region of the HIV-1 long terminal repeat (LTR). Here, we report that human CD4+ T-cells derived from transplanted HSPC engineered to co-express shRNAs targeting CCR5 and HIV-1 LTR are resistant to CCR5- and CXCR4- tropic HIV-1-mediated depletion in vivo. Transduction with the combination vector suppressed CXCR4- and CCR5- tropic viral replication in cell lines and peripheral blood mononuclear cells in vitro. No obvious cytotoxicity or interferon response was observed. Transplantation of combination vector-transduced HSPC into hu-BLT mice resulted in efficient engraftment and subsequent stable gene marking and CCR5 down-regulation in human CD4+ T-cells within peripheral blood and systemic lymphoid tissues, including gut-associated lymphoid tissue, a major site of robust viral replication, for over twelve weeks. CXCR4- and CCR5- tropic HIV-1 infection was effectively inhibited in hu-BLT mouse spleen-derived human CD4+ T-cells ex vivo. Furthermore, levels of gene-marked CD4+ T-cells in peripheral blood increased despite systemic infection with either CXCR4- or CCR5- tropic HIV-1 in vivo. These results demonstrate that transplantation of HSPCs engineered with our combination shRNA vector may be a potential therapy against HIV disease.This work was supported by grants from the California Institute for Regenerative Medicine (CIRM grant DR1-01431 to ISYC), the National Institutes of Health (1RO1HL086409 and 3RO1HL086409-03S1 to DSA and 5T32AI060567), and the University of California Los Angeles AIDS Institute/Center for AIDS Research (5P30AI028697). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

La Histoplasmosis Aviar – Aún un Problema de Salud Pública

La histoplasmosis es una micosis sistémica que afecta al sistema retículo endotelial, producida por el hongo dimórfico termal y nutricional Histoplasma capsulatum (var. capsulatum) [1-3]. Su distribución geográfica es en zonas tropicales, subtropicales y templadas. Su fase saprofitica filamentosa tiene un hábitat natural en suelos ricos de nitrógeno, en cuevas, minas y edificios deshabitados, enriquecidos con excrementos de murciélagos, gallinas, palomas y otras aves; que contraen al inhalar los bioaerosoles o polvo con los microconidios (forma infectante del hongo) comienza afectar a las vías respiratorias de animales como: perros, gatos, ganado bovino, ovejas, roedores, caballos o animales salvajes, también se puede producir por la contaminación de heridas y por la inoculación accidental por medio de pinchazos con algún elemento contaminado y pueden ocurrir infecciones locales en laboratorios por el contacto con mucosas o fluidos biológicos [1-3]

La Histoplasmosis Aviar – Aún un Problema de Salud Pública

La histoplasmosis es una micosis sistémica que afecta al sistema retículo endotelial, producida por el hongo dimórfico termal y nutricional Histoplasma capsulatum (var. capsulatum) [1-3]. Su distribución geográfica es en zonas tropicales, subtropicales y templadas. Su fase saprofitica filamentosa tiene un hábitat natural en suelos ricos de nitrógeno, en cuevas, minas y edificios deshabitados, enriquecidos con excrementos de murciélagos, gallinas, palomas y otras aves; que contraen al inhalar los bioaerosoles o polvo con los microconidios (forma infectante del hongo) comienza afectar a las vías respiratorias de animales como: perros, gatos, ganado bovino, ovejas, roedores, caballos o animales salvajes, también se puede producir por la contaminación de heridas y por la inoculación accidental por medio de pinchazos con algún elemento contaminado y pueden ocurrir infecciones locales en laboratorios por el contacto con mucosas o fluidos biológicos [1-3]