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Irvin L. Paradis

Bio: Irvin L. Paradis is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Transplantation & Lung. The author has an hindex of 34, co-authored 58 publications receiving 3673 citations.


Papers
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TL;DR: Recipients with obliterative bronchiolitis detected in the preclinical stage were significantly more likely to be in remission than recipients who had clinical disease at the time of diagnosis and results indicate that acute rejection is the most significant risk factor for development of obliteration and that obliteration responds to treatment with augmented immunosuppression when it is detected early by surveillance transbronchial biopsy.

412 citations

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TL;DR: This trial demonstrates the advantage of tacrolimus in reducing the risk of obliterative bronchiolitis, the most important cause of long-term morbidity and mortality after lung transplantation.

201 citations

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TL;DR: Although mortality and morbidity have been high, the experiences gained through this series will likely result in an improved outlook for future recipients and provide insight into the immunobiology of the transplanted lung.

174 citations

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TL;DR: The hazard for death, infection, and rejection after pulmonary transplantation appears biphasic, and prevention of cytomegalovirus disease should improve survival by decreasing the prevalence of infection and rejection.

165 citations

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TL;DR: Despite the formidable barrier that infection of the lung allograft poses, the procedure of pulmonary transplantation clearly holds sufficient promise that all efforts possible should be made to hurdle this barrier and ensure a place formonary transplantation in the armamentarium of treatment for irreversible pulmonary disease.

158 citations


Cited by
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Journal ArticleDOI
TL;DR: As compared with conventional therapy, the continuous intravenous infusion of epoprostenol produced symptomatic and hemodynamic improvement, as well as improved survival in patients with severe primary pulmonary hypertension.
Abstract: Background Primary pulmonary hypertension is a progressive disease for which no treatment has been shown in a prospective, randomized trial to improve survival. Methods We conducted a 12-week prospective, randomized, multicenter open trial comparing the effects of the continuous intravenous infusion of epoprostenol (formerly called prostacyclin) plus conventional therapy with those of conventional therapy alone in 81 patients with severe primary pulmonary hypertension (New York Heart Association functional class III or IV). Results Exercise capacity was improved in the 41 patients treated with epoprostenol (median distance walked in six minutes, 362 m at 12 weeks vs. 315 m at base line), but it decreased in the 40 patients treated with conventional therapy alone (204 m at 12 weeks vs. 270 m at base line; P<0.002 for the comparison of the treatment groups). Indexes of the quality of life were improved only in the epoprostenol group (P<0.01). Hemodynamics improved at 12 weeks in the epoprostenol-treated pat...

2,495 citations

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TL;DR: The molecular and biochemical characterization of HOs is reviewed, with a discussion on the mechanisms of signal transduction and gene regulation that mediate the induction of HO-1 by environmental stress, to lay a foundation for potential future clinical applications of these systems.
Abstract: The heme oxygenases, which consist of constitutive and inducible isozymes (HO-1, HO-2), catalyze the rate-limiting step in the metabolic conversion of heme to the bile pigments (i.e., biliverdin and bilirubin) and thus constitute a major intracellular source of iron and carbon monoxide (CO). In recent years, endogenously produced CO has been shown to possess intriguing signaling properties affecting numerous critical cellular functions including but not limited to inflammation, cellular proliferation, and apoptotic cell death. The era of gaseous molecules in biomedical research and human diseases initiated with the discovery that the endothelial cell-derived relaxing factor was identical to the gaseous molecule nitric oxide (NO). The discovery that endogenously produced gaseous molecules such as NO and now CO can impart potent physiological and biological effector functions truly represented a paradigm shift and unraveled new avenues of intense investigations. This review covers the molecular and biochemical characterization of HOs, with a discussion on the mechanisms of signal transduction and gene regulation that mediate the induction of HO-1 by environmental stress. Furthermore, the current understanding of the functional significance of HO shall be discussed from the perspective of each of the metabolic by-products, with a special emphasis on CO. Finally, this presentation aspires to lay a foundation for potential future clinical applications of these systems.

2,111 citations

DOI
05 Nov 2009
TL;DR: 结节病易误诊,据王洪武等~([1])收集国内18篇关于此第一印象中拟诊 结核5例,为此应引起临床对本 病诊
Abstract: 结节病易误诊,据王洪武等~([1])收集国内18篇关于此病误诊的文献,误诊率高达63.2%,当然有误诊就会有误治,如孙永昌等~([2])报道26例结节病在影像学检查诊断的第一印象中拟诊结核5例,其中就有2例完成规范的抗结核治疗,为此应引起临床对本病诊治的重视。

1,821 citations

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TL;DR: The hypothesis that idiopathic pulmonary fibrosis is a fibrotic rather than an inflammatory disease is examined, and the therapeutic implications of these findings are discussed.
Abstract: Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.

1,696 citations