1,721,102 research outputs found
Post cardiac surgery diaphragmatic spasm successfully treated with gabapentin
We describe the case of an 82 year old woman developing severe respiratory functional impairment after open heart surgery and subsequent surgical pericardial drainage inducing diaphragmatic spasm and successfully treated with gabapentin. (c) 2005 Elsevier Ireland Ltd. All rights reserved.We describe the case of an 82 year old woman developing severe respiratory functional impairment after open heart surgery and subsequent surgical pericardial drainage inducing diaphragmatic spasm and successfully treated with gabapentin. (c) 2005 Elsevier Ireland Ltd. All rights reserved. RI Corti, Angelo/F-7046-201
Combination product (Use of IDO inhibitors in cancer therapy with targeted interferon gamma)
Chromogranin A and the Tumor Microenvironment
Chromogranin A (CgA) is an acidic glycoprotein belonging to a family of regulated secretory proteins stored in the dense core granules of the adrenal medulla and of many other neuroendocrine cells and neurons. This protein is frequently used as a diagnostic and prognostic serum marker for a range of neuroendocrine tumors. Circulating CgA is also increased in patients with other diseases, including subpopulations of patients with non-neuroendocrine tumors, with important prognostic implications. A growing body of evidence suggests that CgA is more than a diagnostic/prognostic marker for cancer patients. Indeed, results of in vitro experiments and in vivo studies in animal models suggest that this protein and its fragments can affect several elements of the tumor microenvironment, including fibroblasts and endothelial cells. In this article, recent findings implicating CgA as a modulator of the tumor microenvironment and suggesting that abnormal secretion of CgA could play important roles in tumor progression and response to therapy in cancer patients are reviewed and discussed
Tumour necrosis factor: Strategies for improving the therapeutic index
Tumour Necrosis Factor (TNF) is a cytokine initially discovered for its capacity to induce haemorragic necrosis of experimental tumours and later found to be endowed with potent proinflammatory activities. It was soon realised that these latter properties were at the origin of unacceptable systemic toxicity in all trials aimed at exploiting the anti-tumour activities of TNF. The present review intends to reconsider the efforts that have been devoted over the past ten years to increase the therapeutic index of TNF so to make it a useful drug for the treatment of malignancies. Overall, attempts to achieve this goal with systemically administered TNF have met little success so far. On the other hand, impressive results have been obtained with locoregional administration of TNF. Although of relatively limited clinical utility, these observations have indicated a realistic possibility for a therapeutic exploitation of TNF in tumour therapy: the delivery of systemically administered TNF to the site of tumour growth. On this basis, different targeting and pre-targeting strategies have been developed to achieve this goal. While still in their infancy, these approaches have yielded encouraging results in experimental tumour models. In the forthcoming years it will be possible to evaluate if they represent a practicable means of delivering high doses of TNF to the tumour while sparing the organism from systemic, toxic effects
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