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Lübeck, Germany

Zimbelmann M.,UKSH | Cordes J.,University of Lubeck
Phlebologie | Year: 2015

There are no cases reported about endovascular varicosis therapy having an impact on the erectile function of the man. This case reports' patient had a stronger erection in the area of the glans penis after he underwent endovenous lasertherapy of the great saphenous vein. This effect could also be explained with the anatomy of the veins because some of the blood of the penis is drained by the external pudendal vein which leads into the saphenofemoral junction. If there is a manipulation on the veins of the saphenofemoral junction it might have an impact on the drainage of the penis. © Schattauer 2015. Source


Hefti M.,UKSH | Campe G.V.,Universittslinik Graz | Schneider C.,Kantonsspital Winterthur | Roelcke U.,Kantonsspital Aarau
Zentralblatt fur Neurochirurgie | Year: 2010

Objective: Improvements in microneurosurgical techniques, radiotherapy and chemotherapy for the treatment of high grade gliomas resulted in better local tumor control and longer progression-free survival. Multicentric (MC) lesions located distant from the initial resection area contribute to treatment failure in a growing number of patients. These MC lesions may develop within the course of the disease (metachronous) or may already be present at the time of first tumor manifestation (synchronous). To look for mechanisms and regular patterns behind MC glioma manifestations and to investigate whether they are a second primary tumor or the result of continuous diffuse glioblastoma cell invasion, we retrospectively analyzed the initial and all follow-up MR studies of our high grade glioma (HGG) patients. Patients and Methods: MR studies of 247 consecutive patients treated for HGG at a single institution were analyzed. MC tumor manifestation was defined as more than one gadolinium enhancing lesion within the brain on MRI without a connecting signal alteration in T2 sequences and/or without a connecting hypointense mass in T1 sequences. The minimal distance to define two solitary lesions was set at >10mm. According to these specifications 40 patients showed MC tumor manifestations in their MR studies on admission or during treatment of their disease. The MR studies of these cases were retrospectively analyzed for patterns in MC tumor manifestation and progression. Topographical specifications and delay in manifestation were used to explain possible pathways of development. Kaplan Meyer survival graphs for metachronous and synchronous MC disease were calculated. Results: 24 patients showed MC tumor manifestation at the time of admission. 16 cases developed MC manifestation within a follow-up period of 357 months. The location of all lesions could be categorized into one of three distinct patterns (white matter, subependymal, intraventricular). The patterns showed individual and location-specific time gaps to metachronous manifestation. Calculated from the time of first tumor diagnosis, the median survival was longer for patients with metachronous MC lesions (353 days, p<0.05) compared to patients with synchronous MC lesions (110 days) or patients without multicentricity (234 days). Patients with metachronous lesions showed a similar survival (72 days) as patients with synchronous MC lesions (110 days) once they developed MC disease. Conclusion: The topographical patterns and temporal characteristics of MC disease suggest that all manifestations share common mechanisms such as an active migratory process. Our data therefore do not support the concept of an independent MC development of multiple gliomas. © Georg Thieme Verlag KG Stuttgart New York. Source


Ungefroren H.,Clinic for Applied Cellular Medicine | Sebens S.,University of Kiel | Sebens S.,C o Laboratory of Molecular Gastroenterology and Hepatology | Groth S.,Clinic for Applied Cellular Medicine | And 2 more authors.
International Journal of Oncology | Year: 2011

Both transforming growth factor (TGF)-β and the non-receptor tyrosine kinase Src play major roles during tumorigenesis by regulating cell growth, epithelial-to-mesenchymal transition (EMT), migration/invasion and metastasis, but little is known about the signaling crosstalk between them. To interfere with Src function in vitro and in vivo many studies have employed the pharmacologic Src inhibitors PP2 and PP1. Both agents have recently been shown to be powerful inhibitors of TGF-β receptor type I/ALK5 and type II. As this situation prohibited any definite conclusions with respect to the relative contribution of TGF-β vs. Src signaling, we decided to reappraise a potential role of Src in TGF-β1-mediated cellular responses using RNA and dominant-negative (dn) interference to block Src expression and function, respectively. In TGF-β-responsive pancreatic ductal adenocarcinoma (PDAC) cells, we show that Src is activated by TGF-β1 and that its specific inhibition strongly attenuated basal proliferation and enhanced TGF-β1-mediated growth arrest. However, Src inhibition was unable to impair TGF-β1-controlled EMT as evidenced by cell morphology and regulation of the epithelial marker E-cadherin. Despite its dispensibility for TGF-β-induced EMT, specific inhibition of Src dramatically reduced basal and TGF-β1-induced cell migration in Panc-1 cells as measured with a novel real-time migration assay (xCELLigence DP system). Biochemically, dnSrc inhibition failed to block TGF-β1/ALK5-induced activation of Smad2 and Smad3, but partially inhibited transcriptional activation of TGF-β/Smad-responsive reporter genes, and effectively blocked basal and TGF-β1-induced activation of p38 MAPK. Together, the data provide evidence for a role of Src in the regulation of basal proliferation as well as in basal and TGFβ1-mediated cell motility but not EMT in TGF-β-responsive pancreatic (tumor) cells. Source


Mohamed S.A.,University of Lubeck | Noack F.,Institute of Pathology | Schoellermann K.,University of Lubeck | Karluss A.,University of Lubeck | And 5 more authors.
The Scientific World Journal | Year: 2012

Our aim is to investigate the elevation of matrix proteins in tissues obtained from distal, above the sinotubular junction (proximal), concave, and convex sites of aneurysms in the ascending aorta using a simultaneous multiplex protein detection system. Tissues were collected from 41 patients with ascending aortic aneurysms. A total of 31 patients had a bicuspid aortic valve (BAV), whereas 10 had a tricuspid aortic valve (TAV). Concave and convex aortic site samples were collected from all patients, whereas proximal and distal convexity samples were obtained from 19 patients with BAV and 7 patients with TAV. Simultaneous detection of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) was performed at each of the four aortic sites. MMP-2 levels were higher in the concave aortic sites than in the convex aortic sites. In contrast, MMP-8 levels were higher in the convex sites than in the concave sites, as were MMP-9 levels. In both BAV and TAV patients, TIMP-3 levels were higher in the concave sites than in the convex sites. However, TIMP-2 and TIMP-4 levels were significantly elevated in the sinotubular proximal aorta of BAV patients. Simultaneous detection of MMPs and TIMPs revealed different levels at different aortic sites in the same patient. Copyright © 2012 Salah A. Mohamed et al. Source


Ungefroren H.,Clinic for Applied Cellular Medicine | Sebens S.,University of Kiel | Sebens S.,Laboratory of Molecular Gastroenterology and Hepatology | Groth S.,Clinic for Applied Cellular Medicine | And 2 more authors.
Current Cancer Drug Targets | Year: 2011

Both the nonreceptor tyrosine kinase Src and the receptors for transforming growth factor (TGF)-β (TβRI, TβRII) play major roles during tumorigenesis by regulating cell growth, migration/invasion and metastasis. The common Src family kinase inhibitors PP2 and PP1 effectively block Src activity in vitro and in vivo, however, they may exert nonspecific effects on other kinases. In this study, we have evaluated PP2 and PP1 for their ability to inhibit TGFβ1-mediated responses in the TGF-β-responsive pancreatic adenocarcinoma cell line Panc1. We show that PP2 and PP1 but not the more specific Src inhibitor SU6656 effectively relieved TGF-β1-induced growth arrest and p21WAF1 induction, while basal growth was enhanced by PP2 and PP1, and suppressed by SU6656. PP2 and PP1 but not SU6656 also suppressed TGF-β1-induced epithelial-to-mesenchymal transition (EMT) as evidenced by their ability to inhibit downregulation of the epithelial marker E-cadherin, and upregulation of the EMT-associated transcription factor Slug. Likewise, PP2 and PP1 but not SU6656 effectively blocked TGF-β1-induced activation of Smad2 and p38 MAPK and partially suppressed Smad activation and transcriptional activity on TGF-β/Smad-responsive reporters of a kinase-active TβRI mutant ectopically expressed in Panc1 cells. Interestingly, PP2 and PP1 strongly inhibited recombinant TβRI in an in vitro kinase assay, with PP1 being more potent and PP2 being nearly as potent as the established TβRI inhibitor SB431542. PP2 but not PP1 also weakly inhibited the TβRII kinase. Together, these data provide evidence that PP2 and PP1 are powerful inhibitors of TβR function that can block TGF-β/Smad signaling in a Src-unrelated fashion. Both agents may be useful as dual TGF-β/Src inhibitors in experimental therapeutics of late stage metastatic disease. © 2011 Bentham Science Publishers Ltd. Source

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