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| 1 | Assessment of hemostatic profile in patients with mild to advanced liver cirrhosis显示文摘BACKGROUND Hemostasis of patients suffering from liver cirrhosis is challenging due to both,pro-and anticoagulatory disorders leading to hemostatic alterations with distinct abnormalities of coagulation.Pathological changes in conventional coagulation analysis and platelet count are common manifestations of decreased liver synthesis of coagulation factors and reduced platelet count in these patients.However,conventional coagulation analysis and platelet count do not reflect invivo coagulation status or platelet function.The purpose of this present observational study was therefore to assess the haemostatic profile including plasmatic coagulation using thrombelastometry and impedance aggregometry for platelet function in patients suffering from liver cirrhosis.AIM To assess the hemostatic profile of cirrhotic patients according to model for endstage liver disease(MELD)score.METHODS Our study included both in-and outpatients suffering from liver cirrhosis attending the out-and inpatient care of the department of hepatology.Demographic and biochemical data as well as medical history including cause of liver cirrhosis,end stage kidney failure and medication with anticoagulants were recorded.To assess the hemostatic profile,platelet function was analyzed by multiple electrode aggregometry(MEA)using Multiplate^■(ADP-,ASPI-and TRAP-test)and thrombelastometry using ROTEM^■(EXTEM,INTEM,FIBTEM).Data were compared using Mann-Whitney U-or χ^2-test.Spearman correlation was performed to analyze the association between MELD Score and results of thrombelastometry and MEA.RESULTS A total of 68 patients attending the out-and inpatient care suffering from liver cirrhosis were screened.Of these,50 patients were included and assigned to groups according to MELD score 6 to 11(n=25)or≥17(n=25).Baseline patient characteristics revealed significant differences for MELD score(8 vs 22,P<0.0001)and underlying laboratory parameters(international normalized ratio,bilirubine,creatinine)as well as fibrinogen level(275 mg/dL vs 209 mg/dL,P=0.006)and aPTT(30 s vs 35 s,P=0.047).MEA showed a moderately impaired platelet function(medians:AUCADP=43U,AUCASPI=71U,AUCTRAP=92U)but no significant differences between both groups.Thrombelastometry using ROTEM?(EXTEM,INTEM,FIBTEM)revealed values within normal range in both groups.No significant correlation was observed between MELD score and results of MEA/thrombelastometry.CONCLUSION Our data demonstrate a partially impaired hemostatic profile in liver cirrhosis patients unrelated to MELD score.An individual assessment of a potential coagulopathy should therefore be considered. | Elisabeth Hannah Adam Madara Mohlmann Eva Herrmann Sonia Schneider Kai Zacharowski Stefan Zeuzem Christian Friedrich Weber Nina Weiler | 2020 | World Journal of Gastroenterology2020，26，17： | 5 |
| 2 | In vivo evaluation of riboflavin receptor targeted fluorescent USPIO in mice with prostate cancer xenografts显示文摘核黄素(Rf ) 受体绑并且 translocate Rf 和它的 phosphorylated 形式(例如黄素 mononucleotide,黄素单核甘酸) 进他们调停的房间各种各样的细胞的新陈代谢的小径。以前,我们证明黄素单核甘酸涂的 ultrasmall superparamagnetic 氧化铁(FLUSPIO ) nanoparticles 对在 vitro 把新陈代谢地活跃的癌症和 endothelial 房间标记合适。在这研究,我们集中了于在里面用前列腺癌症异种皮移植的 FLUSPIO 的 vivo 申请。FLUSPIO 的尺寸,充电,和化学作文被评估。我们探索了在里面为它用磁性的回声成像(MRI ) 和染色的普鲁士的蓝色的细胞的受体的 FLUSPIO 的 vitro 特性。竞争有约束力的实验被在过量注射免费黄素单核甘酸在 vivo 执行。FLUSPIO 的简历分发被用比色的试金在机关和肿瘤估计铁内容决定。AFM 分析和希腊语的第六个字母潜力大小揭示了微粒形态学在尺寸和一个否定希腊语的第六个字母潜力的近似 20-40 nm (-24.23 ??????????? | Jabadurai Jayapaul Susanne Ares Matt Bunker Marek Weiler Sandra Rutherford Peter Comba Fabian Kiessling | 2016 | Nano Research2016，9，5： | 3 |
| 3 | Concise review: Interferon-free treatment of hepatitis C virus-associated cirrhosis and liver graft infection显示文摘Chronic hepatitis C is a major reason for development of cirrhosis and hepatocellular carcinoma and a leading cause for liver transplantation. The development of direct-acting antiviral agents lead to(pegylated) interferon-alfa free antiviral therapy regimens with a remarkable increase in sustained virologic response(SVR) rates and opened therapeutic options for patients with advanced cirrhosis and liver graft recipients. This concise review gives an overview about most current prospective trials and cohort analyses for treatment of patients with liver cirrhosis and liver graft recipients. In patients with compensated cirrhosis Child-Pugh-Turcotte(CTP) class A, all approved agents are safe and SVR rates do not significantly differ from patients without cirrhosis in general. In patients with decompensated cirrhosis CTP class B or C, daclastasvir, ledipasvir, velpatasvir, and sofosbuvir are approved, and SVR rates higher than 90% can be achieved. Especially for patients with a model of end stage liver disease score higher than 15 and therefore eligible for liver transplantation, data is scarce. Reported SVR rates in patients with cirrhosis CTP class C are lower compared to patients with a less severe liver disease. In liver transplant recipients with a maximum of CTP class A, SVR rates are comparable to patients without LT. Patients with decompensated graft cirrhosis should be treated on an individual basis. | Nina Weiler Stefan Zeuzem Martin-Walter Welker | 2016 | World Journal of Gastroenterology2016，22，41： | 2 |
| 4 | Early Steroid-Free Immunosuppression With FK506 After Liver Transplantation: Long-Term Results of a Prospectively Randomized Double-Blinded Trial显示文摘 | Nina Weiler Ina Thrun Maria Hoppe-Lotichius Tim Zimmermann Irene Kraemer Gerd Otto | 2010 | Transplantation2010，，12： | 2 |
| 5 | Individual patterns of functional reorganization in the human cerebral cortex after capsular infarction显示文摘 | Weiler C Ramsay S Wise R | 1993 | Ann Neurol1993，33，： | 2 |
| 6 | Characterization of a mouse model for thrombomodulin deficiency1 显示文摘 | Weiler H Lindner V Kerlin B | 2001 | Arterioscler Thromb Vasc Biol2001，21，： | 1 |
| 7 | Limb-girdle muscular dystrophy type 2H associated with mutation in TRIM32, a putative E3-ubiquitin-ligase gene 显示文摘 | Frosk P Weiler T Nylen E | 2002 | Am J Hum Genet2002，70，3： | 1 |
| 8 | Edge-based data structures for solid modeling in curved-surface environments显示文摘 | WEILER K J | 1985 | Institute of Electrical and Electronic Engineers Computer Graphics and Applications1985，5，1： | 1 |
| 9 | Epidemiology of posterior cruciate ligament injuries显示文摘 | SCHULZ M S RUSSE K WEILER A | 2003 | Arch Orthop Trauma Surg2003，123，： | 1 |
| 10 | Enhancement of the mechanical properties ofpolyiactides by solidstate extrusion显示文摘 | Walter Weiler Sylwester Gogolewski | 1996 | Biomaterials1996，17，： | 1 |
| 11 | How to sharpen virtual business显示文摘 | Weiler R | 2001 | Information Week2001，，12： | 1 |
| 12 | Influence of protein kinase C on transcription of the tight junction elements ZO-1 and occludin 显示文摘 | Weiler F Marbe T Scheppach W | 2005 | J Cell Physiol2005，204，1： | 1 |
| 13 | High-frequency oscillatory ventilation in adultacute respiratory distress syndrome显示文摘 | David M Weiler N Heinriehs W et ai | 2003 | Intensive Care Med2003，29，10： | 1 |
| 14 | Expression of major matrix metal oproteinases is associated with intervertebral disc degradation and resorption显示文摘 | Weiler C Nerlich AG Zipperer J | | 0，，： | 1 |
| 15 | Altered pharmacokinetics of voriconazole in a patient with liver cirrhosis显示文摘 | Weiler S Zoller H Graziadei I | 2007 | Antimicrob Agents Chemother2007，51，9： | 1 |
| 16 | The Adaptive MarketsHypothesis: Evidence from the Foreign Exchange Market 显示文摘 | Neely C J Weiler P A and Ulrioh J M | 2009 | Journalof financial and Quantitative analysis2009，44，2： | 1 |
| 17 | Eco- nomics of Disaster Risk, Social Vulnerability, and Mental Health Resilience显示文摘 | Zahran S Peek L Snodgrass J G Weiler S Hempel L | 2011 | Risk Analysis2011，31，7： | 1 |
| 18 | A Model for Short-term Institutional Enrollment Foreeasting显示文摘 | Weiler William C | 1980 | The Journal of Higher Education1980，51，3： | 1 |
| 19 | Simulating surface and subsurface initiation of macropore flow显示文摘 | WEILER M NAEF F | 2003 | Journal of Hydrology2003，273，14： | 1 |
| 20 | Skoura-a genetic island for congenital insensitivity to pain and anhidrosis among Moroccan Jews, as determined by a novel mutation in the NTRK1 gene 显示文摘 | Suriu C Khayat M Weiler M | 2009 | Clin Genet2009，75，3： | 1 |
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