Photodynamic therapy is a promising antitumor treatment modality approved for the management of both early and advanced tumors. The mechanisms of its antitumor action include generation of singlet oxygen and reactive oxygen species that directly damage tumor cells and tumor vasculature. A number of mechanisms seem to be involved in the protective responses to PDT that include activation of transcription factors, heat shock proteins, antioxidant enzymes and antiapoptotic pathways. Elucidation of these mechanisms might result in the design of more effective combination strategies to improve the antitumor efficacy of PDT. Using DNA microarray analysis to identify stress-related genes induced by Photofrin-mediated PDT in colon adenocarcinoma C-26 cells, we observed a marked induction of heme oxygenase-1 (HO-1). Induction of HO-1 with hemin or stable transfection of C-26 with a plasmid vector encoding HO-1 increased resistance of tumor cells to PDT-mediated cytotoxicity. On the other hand, zinc (II) protoporphyrin IX, an HO-1 inhibitor, markedly augmented PDT-mediated cytotoxicity towards C-26 and human ovarian carcinoma MDAH2774 cells. Neither bilirubin, biliverdin nor carbon monoxide, direct products of HO-1 catalysed heme degradation, was responsible for cytoprotection. Importantly, desferrioxamine, a potent iron chelator significantly potentiated cytotoxic effects of PDT. Altogether our results indicate that HO-1 is involved in an important protective mechanism against PDT-mediated phototoxicity and administration of HO-1 inhibitors might be an effective way to potentiate antitumor effectiveness of PDT.

Although the risk of aneurysm rupture after EVAR is low, all patients treated endovascularly should be routinely monitored, in order to select cases with potential endoleaks or stentgraft migration which may lead to fatal complications. When rupture occurs open aneurysmectomy is feasible, although it requires careful management in these high-risk patients.

Living donor SPK can represent a successful alternative to cadaveric donor SPK. The procedure can be performed safely in the donor and with low morbidity in the recipient.

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BackgroundPre-procurement pancreas suitability score (P-PASS) and pancreas donor risk (PDRI) index are scoring systems believed to predict suitability of pancreatic grafts. Most European countries and the United States apply PDRI, while Poltransplant keeps using P-PASS: more than 16 points raises a red flag for graft use. Recent data discourage use of PDRI to predict pancreas graft survival. The aim of the present study was to assess PDRI and P-PASS as predictors of transplanted pancreas survival in a Polish population.Material/MethodsFrom February 1998 to September 2015, 407 pancreas transplantations were performed in Poland: 370 (90.9%) simultaneous pancreas-kidney transplantation and 37 (9.1%) pancreas transplantation alone or pancreas after kidney. The endpoint was death-uncensored 12-month graft survival with satisfactory glycemic control without insulin.ResultsAverage P-PASS was 15.9±2.66 and PDRI was 0.96±0.37. Recipients who survived 12 months with good graft function had an average P-PASS score of 15.7 and PDRI of 0.95. Recipients with death-uncensored graft loss had a mean P-PASS of 16.4 and PDRI of 0.99. Univariate analysis revealed donor age, body mass index (BMI), and P-PASS to be significant risk factors for 1-year pancreas graft survival.ConclusionsP-PASS, but not PDRI, is a reliable tool to predict pancreas graft survival in the Polish population.