8 research outputs found

    Effects of preoperative plasma exchange therapy with albumin replacement fluid on blood coagulation in patients undergoing ABO-incompatible living-donor kidney transplantation using rotational thromboelastometry

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    Abstract Background ABO-incompatible living-donor kidney transplantation (LDKT) requires immunotherapy and plasma exchange therapy (PEX). PEX with albumin replacement fluid reportedly decreases fibrinogen levels. However, no reports have described the effects of PEX with albumin replacement fluid on blood coagulation parameters and blood loss during the perioperative period. Therefore, we investigated the effects of preoperative PEX on blood coagulation parameters and blood loss during the perioperative period in patients undergoing ABO-incompatible LDKT as measured by rotational thromboelastometry (ROTEM®). Methods Twenty-eight patients undergoing LDKT were divided into the PEX group (ABO incompatible with PEX, n = 13) and non-PEX group (ABO compatible without PEX, n = 15). ROTEM® parameters, standard laboratory test parameters, bleeding volume, and transfusion volume were compared between PEX and non-PEX group. MCEplatelet, which represents platelet contribution to clot strength and where “MCE” stands for maximum clot elasticity, was calculated from the difference in MCE between EXTEM and FIBTEM. Results The bleeding volume during surgery and the intensive care unit (ICU) stay was significantly higher in the PEX than non-PEX group (p < 0.01). Maximum clot firmness (MCF) of EXTEM (MCFEXTEM), MCFFIBTEM, and MCEplatelet was significantly lower in the PEX than non-PEX group (p < 0.01). In the PEX group, the bleeding volume during surgery was very strongly correlated with the baseline MCFEXTEM and MCEplatelet, and the bleeding volume during the ICU stay was strongly correlated with the postoperative MCFEXTEM and MCEplatelet. Conclusions These results suggest that the increased blood loss in the PEX group during surgery and the ICU stay was associated with decreased platelet contribution to clot strength as measured by ROTEM®. Trial registration UMIN-Clinical Trial Registry UMIN000018355. Registered 21 July 2015

    <it>LIM only 4 </it>is overexpressed in late stage pancreas cancer

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    <p>Abstract</p> <p>Background</p> <p>LIM-only 4 (LMO4), a member of the LIM-only (LMO) subfamily of LIM domain-containing transcription factors, was initially reported to have an oncogenic role in breast cancer. We hypothesized that LMO4 may be related to pancreatic carcinogenesis as it is in breast carcinogenesis. If so, this could result in a better understanding of tumorigenesis in pancreatic cancer.</p> <p>Methods</p> <p>We measured <it>LMO4 </it>mRNA levels in cultured cells, pancreatic bulk tissues and microdissected target cells (normal ductal cells; pancreatic intraepithelial neoplasia-1B [PanIN-1B] cells; PanIN-2 cells; invasive ductal carcinoma [IDC] cells; intraductal papillary-mucinous adenoma [IPMA] cells; IPM borderline [IPMB] cells; and invasive and non-invasive IPM carcinoma [IPMC]) by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR).</p> <p>Results</p> <p>9 of 14 pancreatic cancer cell lines expressed higher levels of <it>LMO4 </it>mRNA than did the human pancreatic ductal epithelial cell line (HPDE). In bulk tissue samples, expression of <it>LMO4 </it>was higher in pancreatic carcinoma than in intraductal papillary-mucinous neoplasm (IPMN) or non-neoplastic pancreas (<it>p </it>< 0.0001 for both). We carried out microdissection-based analyses. IDC cells expressed significantly higher levels of <it>LMO4 </it>than did normal ductal epithelia or PanIN-1B cells (<it>p </it>< 0.001 for both) or PanIN-2 cells (<it>p </it>= 0.014). IPMC cells expressed significantly higher levels of <it>LMO4 </it>than did normal ductal epithelia (<it>p </it>< 0.001), IPMA (<it>p </it>< 0.001) and IPMB cells (<it>p </it>= 0.003).</p> <p>Conclusion</p> <p>Pancreatic carcinomas (both IDC and IPMC) expressed significantly higher levels of <it>LMO4 </it>mRNA than did normal ductal epithelia, PanIN-1B, PanIN-2, IPMA and IPMB. These results suggested that <it>LMO4 </it>is overexpressed at late stages in carcinogenesis of pancreatic cancer.</p
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