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  • ISSN: 2333-6625
    Current Issue
    Volume 5, Issue 2
    BS Sharma*, Hari Mohan Meena, Vinita Garg, and Prity Sharma
    Acute respiratory distress syndrome is a syndrome of acute onset characterized by hypoxemia and infiltrates on chest radiographs that affects both adults and children of all ages. It is an important cause of respiratory failure in pediatric intensive care units and is associated with significant morbidity and mortality. The management of pediatric acute respiratory distress syndrome (PARDS) is still difficult because there is no definite guideline available for treatment of this entity. At present, the cornerstone of treatment of PARDS is sound intensive care management and early optimal anticipatory ventilatory support. This article reviews recent updates in definition & management of PARDS.
    Michael L. Scharf*
    Physicians have been warned about ordering too many tests, performing too many procedures and layering of medications on top of medications [1]. Whether it be for financial or patient safety considerations, we have been asked to adhere to the philosophy of "less is more" whenever possible. And in 1996, upon the commercial availability in the U.S. of IV Epoprostenol (FLOLAN) for the treatment of what had then been termed Primary Pulmonary Hypertension (PPH), monotherapy with Epoprostenol became the standard of care. Until Epoprostenol, for those diagnosed with this here to fore considered rare disease, their physicians viewed the diagnosis as a death sentence, if left treated only by the conventional medicines available at that time. Epoprostenol showed efficacy in terms of improved hemodynamics and survival [2].
    Research Article
    Barbas-Filho JV, Parra ER, Waisberg DR and Capelozzi VL*
    In our previous study we showed that in normal areas of usual interstitial pneumonia (UIP), type II alveolar epithelial cells telomerase positive (AEC2T+) expression was significantly inferior when compared to normal lung tissue (NLT). Nevertheless, the density of AEC2 was the same in both UIP and NLT. An inversely significant correlation was observed between AEC2 density and AEC2 apoptosis in this area. These results led us to suggest that the pathogenesis of UIP after numerous mitoses is that AEC2 T- exhausts its telomeres and enters into apoptosis, in patients with small subpopulation of AEC2 T+. If this is correct, AEC2 T+ prevails in the remodeled areas of UIP. Thus, we hypothesized that in remodeled areas, AEC2T+ is predominant.
    Material and Methods: We studied 24 open lung biopsies (12 male and 12 female) from our previous study with IPF/UIP disease [4]. Immunohistochemistry (IHC) analysis was performed to identify AEC2 by surfactant A protein and anti-telomerase antibodies. AEC2 density and telomerase expression in the remodeled areas of UIP were assessed at different time points in ten fields using the point-count technique. Forced vital capacity (FVC) was measured by Collins's computer spirometer in 15 patients
    Results: The mean of AEC2 and with Telomerase did not present significant difference. There was a significant positive correlation between AEC2T+ density and FVC- %.
    Conclusion: Our interpretation on the pathogenesis of IPF/UIP was confirmed by the predominance of AEC2T+. A positive correlation was found between AEC2T+ and FCV%.
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