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22 results on '"Werner, Jens"'

4. Advanced Non-Destructive Ocular Visualization Methods by Improved X-Ray Imaging Techniques

Author

Enders, Christian, Braig, Eva-Maria, Scherer, Kai, Werner, Jens U., Lang, Gerhard K., Lang, Gabriele E., Pfeiffer, Franz, Noël, Peter, Rummeny, Ernst, and Herzen, Julia

Subjects
Histology, Imaging Techniques, Swine, Contrast Media, lcsh:Medicine, Surgical and Invasive Medical Procedures, Research and Analysis Methods, Eye, Permeability, Diagnostic Radiology, Ocular System, Diagnostic Medicine, Medicine and Health Sciences, Animals, Humans, lcsh:Science, Staining, Staining and Labeling, Radiology and Imaging, lcsh:R, Ophthalmic Procedures, Biology and Life Sciences, Optic Nerve, X-Ray Microtomography, Bone Imaging, X-Ray Radiography, Ophthalmology, Specimen Preparation and Treatment, Stent Implantation, Eyes, lcsh:Q, Anatomy, Head, Research Article, Iodine
Abstract

Due to limited X-ray contrast, the use of micro-CT in histology is so far not as widespread as predicted. While specific staining procedures-mostly using iodine-address this shortcoming, long diffusion times restrict its use in the often time-constrained daily routine. Recently, a novel staining protocol has been proposed using a biochemical preconditioning step, which increases the permeability of the cells for the staining agent. This could enable the imaging of entire organs of small mammals at a yet unmatched image quality with reasonable preparation and scan times. We here propose an adaptation of this technique for virtual ophthalmology and histology by volumetrically assessing both human and porcine eyes. Hereby, we demonstrate that (contrast-enhanced) micro-CT can outperform conventional histology in the assessment of tumor entities, as well as functioning as a supplementary tool for surgeons in the positioning of intraocular implants in-vitro and as a general assessment tool for ophthalmologic specimens.

Published
2017

5. Early conversion to a CNI-free immunosuppression with SRL after renal transplantation—Long-term follow-up of a multicenter trial.

Author

Andrassy, Joachim, Guba, Markus, Habicht, Antje, Fischereder, Michael, Pratschke, Johann, Pascher, Andreas, Heller, Katharina M., Banas, Bernhard, Hakenberg, Oliver, Vogel, Thomas, Meiser, Bruno, Dick, Andrea, Werner, Jens, and Kauke, Teresa

Subjects
IMMUNOSUPPRESSION, BLOOD sampling
Abstract

Introduction: Early conversion to a CNI-free immunosuppression with SRL was associated with an improved 1- and 3- yr renal function as compared with a CsA-based regimen in the SMART-Trial. Mixed results were reported on the occurrence of donor specific antibodies under mTOR-Is. Here, we present long-term results of the SMART-Trial. Methods and materials: N = 71 from 6 centers (n = 38 SRL and n = 33 CsA) of the original SMART-Trial (ITT n = 140) were enrolled in this observational, non-interventional extension study to collect retrospectively and prospectively follow-up data for the interval since baseline. Primary objective was the development of dnDSA. Blood samples were collected on average 8.7 years after transplantation. Results: Development of dnDSA was not different (SRL 5/38, 13.2% vs. CsA 9/33, 27.3%; P = 0.097). GFR remained improved under SRL with 64.37 ml/min/1.73m2 vs. 53.19 ml/min/1.73m2 (p = 0.044). Patient survival did not differ between groups at 10 years. There was a trend towards a reduced graft failure rate (11.6% SRL vs. 23.9% CsA, p = 0.064) and less tumors under SRL (2.6% SRL vs. 15.2% CsA, p = 0.09). Conclusions: An early conversion to SRL did not result in an increased incidence of dnDSA nor increased long-term risk for the recipient. Transplant function remains improved with benefits for the graft survival. [ABSTRACT FROM AUTHOR]

Published
2020
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7. Epithelial to Stromal Re-Distribution of Primary Cilia during Pancreatic Carcinogenesis

Author

Schimmack, Simon, Kneller, Sarah, Dadabaeva, Nigora, Bergmann, Frank, Taylor, Andrew, Hackert, Thilo, Werner, Jens, and Strobel, Oliver

Subjects
endocrine system diseases, Carcinogenesis, lcsh:Medicine, Endocrine System, Epithelium, Pancreatic Cancer, Exocrine Glands, Cell Signaling, Animal Cells, Pancreatitis, Chronic, Gastrointestinal Tumors, Medicine and Health Sciences, Humans, Hedgehog Proteins, Cilia, lcsh:Science, Pancreas, Cells, Cultured, Connective Tissue Cells, Pancreatic Stellate Cells, lcsh:R, Biology and Life Sciences, Cancers and Neoplasms, Epithelial Cells, Cell Biology, Smoothened Receptor, digestive system diseases, Patched-1 Receptor, Biological Tissue, Oncology, Microscopy, Fluorescence, Connective Tissue, Hedgehog Signaling, Disease Progression, lcsh:Q, Cellular Structures and Organelles, Anatomy, Cellular Types, Stromal Cells, Neoplasm Grading, Research Article, Signal Transduction, Carcinoma, Pancreatic Ductal
Abstract

Background The Hedgehog (HH) pathway is a mediator in pancreatic ductal adenocarcinoma (PDAC). Surprisingly, previous studies suggested that primary cilia (PC), the essential organelles for HH signal transduction, were lost in PDAC. The aim of this study was to determine the presence of PC in human normal pancreas, chronic pancreatitis, and during carcinogenesis to PDAC with focus on both epithelia and stroma. Methods PC were analyzed in paraffin sections from normal pancreas, chronic pancreatitis, intraductal papillary-mucinous neoplasia, and PDAC, as well as in primary human pancreatic stellate cells (PSC) and pancreatic cancer cell lines by double immunofluorescence staining for acetylated α-tubuline and γ-tubuline. Co-staining for the HH receptors PTCH1, PTCH2 and SMO was also performed. Results PC are gradually lost during pancreatic carcinogenesis in the epithelium: the fraction of cells with PC gradually and significantly decreased from 32% in ducts of normal pancreas, to 21% in ducts of chronic pancreatitis, to 18% in PanIN1a, 6% in PanIN2, 3% in PanIN3 and to 1.2% in invasive PDAC. However, this loss of PC in the neoplastic epithelium is accompanied by a gain of PC in the surrounding stroma. The fraction of stromal cells with PC significantly increased from 13% around normal ducts to about 30% around PanIN and PDAC. HH-receptors were detected in tumor stroma but not in epithelial cells. PC are also present in PSC and pancreatic cancer cell lines. Conclusion PC are not lost during pancreatic carcinogenesis but re-distributed from the epithelium to the stroma. This redistribution may explain the re-direction of HH signaling towards the stroma during pancreatic carcinogenesis.

Published
2016

9. Open Surgical versus Minimal Invasive Necrosectomy of the Pancreas—A Retrospective Multicenter Analysis of the German Pancreatitis Study Group

Author

Rasch, Sebastian, primary, Phillip, Veit, additional, Reichel, Stephanie, additional, Rau, Bettina, additional, Zapf, Christian, additional, Rosendahl, Jonas, additional, Halm, Ulrich, additional, Zachäus, Markus, additional, Müller, Martin, additional, Kleger, Alexander, additional, Neesse, Albrecht, additional, Hampe, Jochen, additional, Ellrichmann, Mark, additional, Rückert, Felix, additional, Strauß, Peter, additional, Arlt, Alexander, additional, Ellenrieder, Volker, additional, Gress, Thomas M., additional, Hartwig, Werner, additional, Klar, Ernst, additional, Mössner, Joachim, additional, Post, Stefan, additional, Schmid, Roland M., additional, Seufferlein, Thomas, additional, Siech, Marco, additional, Werner, Jens, additional, Will, Uwe, additional, and Algül, Hana, additional

Published
2016
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14. Diagnostic and Prognostic Impact of Circulating YKL-40, IL-6, and CA 19.9 in Patients with Pancreatic Cancer

Author

Schultz, Nicolai A., primary, Christensen, Ib J., additional, Werner, Jens, additional, Giese, Nathalia, additional, Jensen, Benny V., additional, Larsen, Ole, additional, Bjerregaard, Jon K., additional, Pfeiffer, Per, additional, Calatayud, Dan, additional, Nielsen, Svend E., additional, Yilmaz, Mette K., additional, Holländer, Niels H., additional, Wøjdemann, Morten, additional, Bojesen, Stig E., additional, Nielsen, Kaspar R., additional, and Johansen, Julia S., additional

Published
2013
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15. Somatic Mutations in Exocrine Pancreatic Tumors: Association with Patient Survival

Author

Rachakonda, P. Sivaramakrishna, primary, Bauer, Andrea S., additional, Xie, Huaping, additional, Campa, Daniele, additional, Rizzato, Cosmeri, additional, Canzian, Federico, additional, Beghelli, Stefania, additional, Greenhalf, William, additional, Costello, Eithne, additional, Schanne, Michaela, additional, Heller, Anette, additional, Scarpa, Aldo, additional, Neoptolemos, John P., additional, Werner, Jens, additional, Büchler, Markus, additional, Hoheisel, Jörg D., additional, Hemminki, Kari, additional, Giese, Nathalia, additional, and Kumar, Rajiv, additional

Published
2013
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16. Hypoxia Induces EMT in Low and Highly Aggressive Pancreatic Tumor Cells but Only Cells with Cancer Stem Cell Characteristics Acquire Pronounced Migratory Potential

Author

Salnikov, Alexei V., primary, Liu, Li, additional, Platen, Mitja, additional, Gladkich, Jury, additional, Salnikova, Olga, additional, Ryschich, Eduard, additional, Mattern, Jürgen, additional, Moldenhauer, Gerhard, additional, Werner, Jens, additional, Schemmer, Peter, additional, Büchler, Markus W., additional, and Herr, Ingrid, additional

Published
2012
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17. Diagnosis of Pancreatic Ductal Adenocarcinoma and Chronic Pancreatitis by Measurement of microRNA Abundance in Blood and Tissue

Author

Bauer, Andrea S., primary, Keller, Andreas, additional, Costello, Eithne, additional, Greenhalf, William, additional, Bier, Melanie, additional, Borries, Anne, additional, Beier, Markus, additional, Neoptolemos, John, additional, Büchler, Markus, additional, Werner, Jens, additional, Giese, Nathalia, additional, and Hoheisel, Jörg D., additional

Published
2012
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18. A Common Variant of PNPLA3 (p.I148M) Is Not Associated with Alcoholic Chronic Pancreatitis

Author

Rosendahl, Jonas, primary, Tönjes, Anke, additional, Schleinitz, Dorit, additional, Kovacs, Peter, additional, Wiegand, Johannes, additional, Ruffert, Claudia, additional, Jesinghaus, Moritz, additional, Schober, Robert, additional, Herms, Max, additional, Grützmann, Robert, additional, Schulz, Hans-Ulrich, additional, Stickel, Felix, additional, Werner, Jens, additional, Bugert, Peter, additional, Blüher, Matthias, additional, Stumvoll, Michael, additional, Böhm, Stephan, additional, Berg, Thomas, additional, Wittenburg, Henning, additional, Mössner, Joachim, additional, Morsche, Rene te, additional, Derikx, Monique, additional, Keim, Volker, additional, Witt, Heiko, additional, and Drenth, Joost P. H., additional

Published
2012
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19. Pancreatic Cancer Susceptibility Loci and Their Role in Survival

Author

Rizzato, Cosmeri, primary, Campa, Daniele, additional, Giese, Nathalia, additional, Werner, Jens, additional, Rachakonda, P. Sivaramakrishna, additional, Kumar, Rajiv, additional, Schanné, Michaela, additional, Greenhalf, William, additional, Costello, Eithne, additional, Khaw, Kay-tee, additional, Key, Tim J., additional, Siddiq, Afshan, additional, Lorenzo-Bermejo, Justo, additional, Burwinkel, Barbara, additional, Neoptolemos, John P., additional, Büchler, Markus W., additional, Hoheisel, Jörg D., additional, Bauer, Andrea, additional, and Canzian, Federico, additional

Published
2011
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20. Prognostic Significance of Erythropoietin in Pancreatic Adenocarcinoma

Author

Welsch, Thilo, primary, Zschäbitz, Stefanie, additional, Becker, Verena, additional, Giese, Thomas, additional, Bergmann, Frank, additional, Hinz, Ulf, additional, Keleg, Shereen, additional, Heller, Anette, additional, Sipos, Bence, additional, Klingmüller, Ursula, additional, Büchler, Markus W., additional, Werner, Jens, additional, and Giese, Nathalia A., additional

Published
2011
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21. Chondroitin Sulfate Proteoglycan CSPG4 as a Novel Hypoxia-Sensitive Marker in Pancreatic Tumors.

Author

Keleg, Shereen, Titov, Alexandr, Heller, Anette, Giese, Thomas, Tjaden, Christine, Ahmad, Sufian S., Gaida, Matthias M., Bauer, Andrea S., Werner, Jens, and Giese, Nathalia A.

Subjects
CHONDROITIN sulfate proteoglycan, HYPOXEMIA, BIOMARKERS, PANCREATIC tumors, GENE expression, CYSTADENOMA
Abstract

CSPG4 marks pericytes, undifferentiated precursors and tumor cells. We assessed whether the shed ectodomain of CSPG4 (sCSPG4) might circulate and reflect potential changes in CSPG4 tissue expression (pCSPG4) due to desmoplastic and malignant aberrations occurring in pancreatic tumors. Serum sCSPG4 was measured using ELISA in test (n = 83) and validation (n = 221) cohorts comprising donors (n = 11+26) and patients with chronic pancreatitis (n = 11+20) or neoplasms: benign (serous cystadenoma SCA, n = 13+20), premalignant (intraductal dysplastic IPMNs, n = 9+55), and malignant (IPMN-associated invasive carcinomas, n = 4+14; ductal adenocarcinomas, n = 35+86). Pancreatic pCSPG4 expression was evaluated using qRT-PCR (n = 139), western blot analysis and immunohistochemistry. sCSPG4 was found in circulation, but its level was significantly lower in pancreatic patients than in donors. Selective maintenance was observed in advanced IPMNs and PDACs and showed a nodal association while lacking prognostic relevance. Pancreatic pCSPG4 expression was preserved or elevated, whereby neoplastic cells lacked pCSPG4 or tended to overexpress without shedding. Extreme pancreatic overexpression, membranous exposure and tissuehigh/seralow-discordance highlighted stroma-poor benign cystic neoplasm. SCA is known to display hypoxic markers and coincide with von-Hippel-Lindau and Peutz-Jeghers syndromes, in which pVHL and LBK1 mutations affect hypoxic signaling pathways. In vitro testing confined pCSPG4 overexpression to normal mesenchymal but not epithelial cells, and a third of tested carcinoma cell lines; however, only the latter showed pCSPG4-responsiveness to chronic hypoxia. siRNA-based knockdowns failed to reduce the malignant potential of either normoxic or hypoxic cells. Thus, overexpression of the newly established conditional hypoxic indicator, CSPG4, is apparently non-pathogenic in pancreatic malignancies but might mark distinct epithelial lineage and contribute to cell polarity disorders. Surficial retention on tumor cells renders CSPG4 an attractive therapeutic target. Systemic ‘drop and restoration’ alterations accompanying IPMN and PDAC progression indicate that the interference of pancreatic diseases with local and remote shedding/release of sCSPG4 into circulation deserves broad diagnostic exploration. [ABSTRACT FROM AUTHOR]

Published
2014
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22. In Vivo Activity and Pharmacokinetics of Nemorosone on Pancreatic Cancer Xenografts.

Author

Wolf, Robert J., Hilger, Ralf A., Hoheisel, Jörg D., Werner, Jens, and Holtrup, Frank

Subjects
PANCREATIC cancer, XENOGRAFTS, PHARMACOKINETICS, ANTINEOPLASTIC agents, LEAD compounds, BIOAVAILABILITY
Abstract

Pancreatic cancer is one of the leading cancer-related causes of death in the western world with an urgent need for new treatment strategies. Recently, hyperforin and nemorosone have been described as promising anti-cancer lead compounds. While hyperforin has been thoroughly investigated in vitro and in vivo, in vivo data for nemorosone are still missing. Thus, we investigated the growth-inhibitory potential of nemorosone on pancreatic cancer xenografts in NMRI nu/nu mice and determined basic pharmacokinetic parameters. Xenograft tumors were treated with nemorosone and gemcitabine, the current standard of care. Tumor sections were subjected to H&E as well as caspase 3 and Ki-67 staining. Nemorosone plasma kinetics were determined by HPLC and mass spectrometry. Induction of CYP3A4 and other metabolizing enzymes by nemorosone and hyperforin was tested on primary hepatocytes using qRT-PCR. At a dose of 50 mg/kg nemorosone per day, a significant growth-inhibitory effect was observed in pancreatic cancer xenografts. The compound was well tolerated and rapidly absorbed into the bloodstream with a half-life of approximately 30 min. Different metabolites were detected, possibly resembling CYP3A4-independent oxidation products. It is concluded that nemorosone is a potential anti-cancer lead compound with good bioavailability, little side-effects and promising growth-inhibitory effects, thus representing a valuable compound for a combination therapy approach. [ABSTRACT FROM AUTHOR]

Published
2013
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