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Thi Phuong Thao Hoang,1 Philipp Schindler,2 Nikolaus Börner,3 Max Masthoff,2 Mirjam Gerwing,2 Philippa von Beauvais,2 Enrico N De Toni,4 Christian M Lange,4 Jonel Trebicka,5 Haluk Morgül,6 Max Seidensticker,1 Jens Ricke,1 Andreas Pascher,6 Markus Guba,3 Michael Ingrisch,1 Moritz Wildgruber,1,* Osman Öcal1,* 1Department of Radiology, University Hospital, LMU Munich, Munich, Germany; 2Clinic for Radiology, University Hospital Muenster, Muenster, Germany; 3Department of General, Visceral and Transplantation Surgery, University Hospital, LMU Munich, Munich, Germany; 4Department for Internal Medicine II, University Hospital, LMU Munich, Munich, Germany; 5Department for Internal Medicine B, Universitätsklinikum Münster, Münster, Germany; 6Department of General, Visceral and Transplant Surgery, Universitätsklinikum Münster, Münster, Germany*These authors contributed equally to this workCorrespondence: Osman Öcal, Department of Radiology, University Hospital – LMU Munich, Marchioninistrasse 15, D-81377, München, Germany, Email osman.oecal@med.uni-muenchen.dePurpose: To investigate the prognostic value of computed tomography (CT) derived imaging biomarkers in hepatocellular carcinoma (HCC) recurrence after liver transplantation (LT) and develop a predictive nomogram model.Patients and Methods: This retrospective study included 178 patients with histopathologically confirmed HCC who underwent liver transplantation between 2007 and 2021 at the two academic liver centers. We evaluated dedicated imaging features from baseline multiphase contrast-enhanced CT supplemented by several clinical findings and laboratory parameters. Time-to-recurrence was estimated by Kaplan–Meier analysis. Univariable Cox proportional hazard regression and multivariable Least Absolute Shrinkage and Selection Operator (LASSO) regression were used to assess independent prognostic factors for recurrence. A nomogram model was then built based on the independent factors selected through LASSO regression, to predict the probabilities of HCC recurrence at one, three, and five years.Results: The rate of HCC recurrence after LT was 17.4% (31 of 178). The LASSO analysis revealed six independent predictors associated with an elevated risk of tumor recurrence. These predictors included the presence of peritumoral enhancement, the presence of over three tumor lesions, the largest tumor diameter greater than 3 cm, serum alpha-fetoprotein (AFP) levels exceeding 400 ng/mL, and the presence of a tumor capsule. Conversely, a history of bridging therapies was found to be correlated with a reduced risk of HCC recurrence. In addition, Kaplan-Meier curves showed patients with irregular margin, satellite nodules, or small lesions displayed shorter time-to-recurrence. Our nomogram demonstrated good performance, yielding a C-index of 0.835 and AUC values of 0.86, 0.88, and 0.85 for the predictions of 1-year, 3-year, and 5-year TTR, respectively.Conclusion: Imaging parameters derived from baseline contrast-enhanced CT showing malignant behavior and aggressive growth patterns, along with serum AFP and history of bridging therapies, show potential as biomarkers for predicting HCC recurrence after transplantation.Keywords: hepatocellular carcinoma, transplantation, imaging, recurrence

This study assessed the influence of liming and waste organic materials on the yield and nitrogen, phosphorus and potassium contents in cock’s-foot (Dactylis glomerata L.) grown on nickel-contaminated soil in the third year of a pot culture experiment. In the experiment, the following factors were taken into consideration: (1) nickel soil contamination (0, 75, 150 and 225 mg Ni·kg−1 of soil); (2) liming (0 Ca and Ca according to 1 Hh of soil) and (3) organic materials (no waste organic materials added, brown coal from a coal mine in Turów and rye straw). Introducing nickel into the soil, regardless of its amount, caused a significant decrease in the total yield of cock’s-foot and increased the nitrogen and potassium contents. Liming caused a significant increase in the yield of cock’s-foot and decrease its potassium content, but it did not clearly differentiate the nitrogen and phosphorus content. The used organic materials (straw and brown coal) caused a decrease in the phosphorus content in the grass biomass.

The aim of these studies was to determine the effect of soil contamination with nickel (0, 75, 150 and 225 mg Ni kg-1 soil) on the content of nickel in biomass of cocksfoot and fractions of this metal in the soil under different liming (0 Ca and Ca by 1 hydrolytic acidity) and fertilization with organic materials (without the use of organic materials, straw rye and brown coal from Turow Coal Mine). Four swaths of cocksfoot gathered in the third year of a pot experiment were analyzed and fractions of nickel in the soil after the last swath of test plants were determined. Total nickel content in the plant and in the soil was determined by ICP-AES after earlier mineralization. Fractions of nickel in the soil were determined by sequential fractionation according to BCR procedure. The introduction of nickel into the soil, regardless of amount, significantly increased concentration of this metal in the biomass of cocksfoot and soil in all fractions, in particular the soluble and easily exchangeable fraction (F1). Liming the soil and the application of organic materials decreased nickel content in the biomass of cocksfoot and its soluble fraction in soil, easy available for plants, causing the same time to increase its share in the residual fraction (liming) and oxidisable fraction (the application of organic materials).

Abstract Background Four and one half LIM domain protein 2 (FHL2) has been reported to be a key regulator in many cellular processes being associated with fibrogenesis such as cell migration and contraction. Moreover, hepatic FHL2 is involved in regulation pathways mediating proliferation and cell death machineries. We here investigated the role of FHL2 in the setting of experimental and clinical liver fibrosis. Methods FHL2−/− and wild type (wt) mice were challenged with CCl4. Fibrotic response was assessed by quantitative real time PCR (qRT-PCR) of fibrotic marker genes, measurement of hydroxyproline content and histological methods. Murine FHL2−/− and hepatic stellate cells (HSC) were isolated and investigated via immunofluorescence. Human fibrotic and normal liver samples were analysed immunohistochemically using antibodies directed against FHL2. Results FHL2−/− mice displayed aggravated liver fibrosis compared to wt mice. However, immunofluorescence revealed no significant morphological changes in cultured FHL2−/− and wt myofibroblasts (MFB). In human liver samples, FHL2 was strongly expressed both in the nucleus and cytoplasm in MFB of fibrotic livers. In contrast, FHL2 expression was absent in normal liver tissue. Conclusions Deficiency of FHL2 results in aggravation of murine liver fibrosis. In human liver samples, FHL2 is expressed in activated HSCs and portal fibroblasts in human fibrotic livers, pointing to a central role of FHL2 for human hepatic fibrogenesis as well.