2,738 research outputs found

    Innovations and revolutions in reducing retinal ganglion cell loss in glaucoma

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    Introduction: Glaucoma remains the leading cause of irreversible blindness. Although the loss of retinal ganglion cells (RGCs) is an established hallmark of glaucoma, reduction of intraocular pressure (IOP) is a widely used evidence-based management approach, even in normotensive patients. However, despite optimal pressure control, some patients progress to lose vision. / Areas covered: This review provides a summary of the latest methods aimed at reducing RGC loss with the objective of preserving vision, categorized by the mechanism of action. We discuss both the newest ways in which IOP can be reduced, alongside ‘pressure-independent’ pharmacological therapies and developments in bioengineering. The conducted PubMed search included the terms: ‘glaucoma pathophysiology,’ ‘IOP-lowering agents,’ ‘retinal ganglion cell apoptosis,’ ‘neuroprotection,’ ‘stem cells,’ ‘imaging.’ / Expert opinion: With many agents failing to successfully translate into clinical use, further understanding of the underlying disease process is required, along with novel biomarkers that will enable timely and reliable quantification of treatment effect

    Transplantation Pneumonia

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    A clinically distinct pneumonitis occurred in six renal transplant recipients receiving azathioprine and prednisone immunosuppressive therapy. The patients ranged in age from 3 to 20 years. The onset was 42 to 102 days postoperatively, coinciding with decrease in prednisone dosage below approximately 1 mg per kilogram of body weight per day. Mild nonproductive cough, fever, and cynanosis were present. Chest x-rays demonstrated extensive hazy to nodular infiltrates usually involving both hila and lower lung fields. Cold agglutinins were present in five patients. Pulmonary function studies demonstrated an alveolar capillary block. The duration of illness was 12 to 34 days and was not influenced by antibiotic therapy. Autopsy of the single case in which death occurred revealed Pneumocystis carinii pneumonia and disseminated cytomegalic inclusion-body disease. © 1964, American Medical Association. All rights reserved

    History of clinical transplantation

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    The emergence of transplantation has seen the development of increasingly potent immunosuppressive agents, progressively better methods of tissue and organ preservation, refinements in histocompatibility matching, and numerous innovations is surgical techniques. Such efforts in combination ultimately made it possible to successfully engraft all of the organs and bone marrow cells in humans. At a more fundamental level, however, the transplantation enterprise hinged on two seminal turning points. The first was the recognition by Billingham, Brent, and Medawar in 1953 that it was possible to induce chimerism-associated neonatal tolerance deliberately. This discovery escalated over the next 15 years to the first successful bone marrow transplantations in humans in 1968. The second turning point was the demonstration during the early 1960s that canine and human organ allografts could self-induce tolerance with the aid of immunosuppression. By the end of 1962, however, it had been incorrectly concluded that turning points one and two involved different immune mechanisms. The error was not corrected until well into the 1990s. In this historical account, the vast literature that sprang up during the intervening 30 years has been summarized. Although admirably documenting empiric progress in clinical transplantation, its failure to explain organ allograft acceptance predestined organ recipients to lifetime immunosuppression and precluded fundamental changes in the treatment policies. After it was discovered in 1992 that long-surviving organ transplant recipient had persistent microchimerism, it was possible to see the mechanistic commonality of organ and bone marrow transplantation. A clarifying central principle of immunology could then be synthesized with which to guide efforts to induce tolerance systematically to human tissues and perhaps ultimately to xenografts

    Evidence of triggered star formation in G327.3-0.6. Dust-continuum mapping of an infrared dark cloud with P-ArT\'eMiS

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    Aims. Expanding HII regions and propagating shocks are common in the environment of young high-mass star-forming complexes. They can compress a pre-existing molecular cloud and trigger the formation of dense cores. We investigate whether these phenomena can explain the formation of high-mass protostars within an infrared dark cloud located at the position of G327.3-0.6 in the Galactic plane, in between two large infrared bubbles and two HII regions. Methods: The region of G327.3-0.6 was imaged at 450 ? m with the CEA P-ArT\'eMiS bolometer array on the Atacama Pathfinder EXperiment telescope in Chile. APEX/LABOCA and APEX-2A, and Spitzer/IRAC and MIPS archives data were used in this study. Results: Ten massive cores were detected in the P-ArT\'eMiS image, embedded within the infrared dark cloud seen in absorption at both 8 and 24 ?m. Their luminosities and masses indicate that they form high-mass stars. The kinematical study of the region suggests that the infrared bubbles expand toward the infrared dark cloud. Conclusions: Under the influence of expanding bubbles, star formation occurs in the infrared dark areas at the border of HII regions and infrared bubbles.Comment: 4 page

    Gluteal compartment syndrome: a case report

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    This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

    Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection

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    Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome-associated coronavirus (SARS-CoV). Not only can these cells support the growth of SARS-CoV infection, but they are also capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelial signaling to SARS-CoV is crucial for paving the way to better understand SARS pathogenesis. Based on microarray-based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derived from Calu-3 cells. Specifically, we found a temporal and spatial activation of nuclear factor (NF)κB, activator protein (AP)-1, and interferon regulatory factor (IRF)-3/7 in infected 2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.), resulting in the activation of many antiviral genes, including interferon (IFN)-β, -λs, inflammatory mediators, and many IFN-stimulated genes (ISGs). We also showed, for the first time, that IFN-β and IFN-λs were capable of exerting previously unrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detected in infected 2B4 bronchial epithelial cells until 48 hrs p.i. Collectively, our results highlight the mechanics of the sequential events of antiviral signaling pathway/s triggered by SARS-CoV in bronchial epithelial cells and identify novel cellular targets for future studies, aiming at advancing strategies against SARS

    Accessing ratios of quantized resistances in graphene p–n junction devices using multiple terminals

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    The utilization of multiple current terminals on millimeter-scale graphene p–n junction devices has enabled the measurement of many atypical, fractional multiples of the quantized Hall resistance at the ν = 2 plateau (RH ≈ 12 906 Ω). These fractions take the form abRH and can be determined both analytically and by simulations. These experiments validate the use of either the LTspice circuit simulator or the analytical framework recently presented in similar work. Furthermore, the production of several devices with large-scale junctions substantiates the approach of using simple ultraviolet lithography to obtain junctions of sufficient sharpness.The utilization of multiple current terminals on millimeter-scale graphene p–n junction devices has enabled the measurement of many atypical, fractional multiples of the quantized Hall resistance at the ν = 2 plateau (RH ≈ 12 906 Ω). These fractions take the form abRH and can be determined both analytically and by simulations. These experiments validate the use of either the LTspice circuit simulator or the analytical framework recently presented in similar work. Furthermore, the production of several devices with large-scale junctions substantiates the approach of using simple ultraviolet lithography to obtain junctions of sufficient sharpness
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