Behnes, Carl-Ludwig

[["dc.bibliographiccitation.artnumber","574"],["dc.bibliographiccitation.journal","SpringerPlus"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.description.abstract","Recent breakthrough therapies targeting androgen receptor signalling in castration resistant prostate cancer (CRPC) involve multifunctional androgen receptor (AR) blockade and exhaustive androgen deprivation. Nevertheless, limitations to an enduring effectiveness of new drugs are anticipated in resistance mechanisms occurring under such treatments. In this study we used CRPC cell models VCaP and LNCaP as well as AR-negative PC-3- and non-neoplastic epithelial BPH-1-cells treated with 5, 10 or 25 mu mol/L abiraterone hydrolyzed from abiraterone acetate (AA). The origin of CYP17A1 up-regulation under AA treatment was investigated in CRPC cell models by qRT-PCR and western-blot procedures. AA treatments of AR positive CRPC cell models led to decreased expression of androgen regulated genes such as PSA. In these cells diminished expression of androgen regulated genes was accompanied by an up-regulation of CYP17A1 expression within short-term treatments. No such effects became evident in AR-negative PC-3 cells. AR directed siRNA (siAR) used in VCaP cells significantly reduced mRNA expression and AR protein abundance. Such interference with AR signalling in the absence of abiraterone acetate also caused a marked up-regulation of CYP17A1 expression. Down-regulation of androgen regulated genes occurs in spite of an elevated expression of CYP17A1, the very target enzyme for this drug. CYP17A1 up-regulation already takes place within such short treatments with AA and does not require adaptation events over several cell cycles. CYP17A1 is also up-regulated in the absence of AA when AR signalling is physically eliminated by siAR. These results reveal an immediate counter-regulation of CYP17A1 expression whenever AR-signalling is inhibited adequately but not a persisting adaptation yielding drug resistance."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG)"],["dc.identifier.doi","10.1186/2193-1801-3-574"],["dc.identifier.isi","000359105300002"],["dc.identifier.pmid","25332874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32049"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","2193-1801"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Increased expression of CYP17A1 indicates an effective targeting of the androgen receptor axis in castration resistant prostate cancer (CRPC)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","23"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Blech, Manfred"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.date.accessioned","2018-11-07T09:28:08Z"],["dc.date.available","2018-11-07T09:28:08Z"],["dc.date.issued","2013"],["dc.description.abstract","Sertoliform cystadenoma of the rete testis represents an uncommon benign tumour. They appear in patients from 26 to 62 years of age. We describe a case of a 66-year-old man with a tumour in the area of the epididymal head. The tumour markers were not increased. Under the assumption of a malignant testicular tumour an inguinal orchiectomy was performed. The cut surface of this tumour was of grey/white color and showed small cysts. The tumour consisted of two compartments. The epithelial like tumour cells showed a sertoliform growth pattern and cystic dilatations. In between the tumour cells repeatedly actin expressing sclerotic areas could be recognized as the second tumour component. Proliferative activity was not increased. Immunohistochemically the tumour cells were positiv for inhibin, S-100, and CD 99. Alpha feto protein (AFP), human chorionic gonadotropin (beta-HCG) and placental alkaline phosphatase (PLAP) as well as synaptophysin, epithelial membrane antigene (EMA), and BCL-2 were not expressed. As far as we know this is the sixth reported case of this tumour. Because of the benign nature of this tumour the correct diagnosis is important for the intra-and postoperative management. Here we present a case of this rare tumour and discuss potential differential diagnosis."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2013"],["dc.identifier.doi","10.1186/1746-1596-8-23"],["dc.identifier.isi","000315783000001"],["dc.identifier.pmid","23406299"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8573"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30703"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Sertoliform cystadenoma: a rare benign tumour of the rete testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","64"],["dc.bibliographiccitation.journal","Urology Case Reports"],["dc.bibliographiccitation.lastpage","66"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Uhlig, Annemarie"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Uhlig, Johannes"],["dc.contributor.author","Leitsmann, Conrad"],["dc.date.accessioned","2019-07-09T11:45:15Z"],["dc.date.available","2019-07-09T11:45:15Z"],["dc.date.issued","2018"],["dc.description.abstract","Primary Bladder Adenocarcinoma is a rare malignancy that has been observed in a heterogeneous pa- tient population. This case report presents a 51 year old female with muscle-invasive primary bladder adenocarcinoma diagnosed in 2008. After transurethral resection and cystectomy with ileum neobladder adjuvant radi- ochemotherapy was administered. Two years later, a symptomatic fistula between neobladder and ileoileal anastomosis was excised, resulting in urinary incontinency. In 2016, the patient shows no signs of disease relapse but suffers from reduction of bladder capacity. This case report presents classical symptoms of adenocarcinoma of the bladder and a possible treat- ment regimen with associated side effects."],["dc.identifier.doi","10.1016/j.eucr.2018.02.006"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59191"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2214-4420"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Primary bladder adenocarcinoma: Case report with long-term follow-up"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Clinical Pathology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2019-07-09T11:54:07Z"],["dc.date.available","2019-07-09T11:54:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Testicular germ cell tumours (TGCTs) are the most common malignancy in young men aged 18–35 years. They are clinically and histologically subdivided into seminomas and non-seminomas. Cadherins are calcium-dependent transmembrane proteins of the group of adhesion proteins. They play a role in the stabilization of cell-cell contacts, the embryonic morphogenesis, in the maintenance of cell polarity and signal transduction. N-cadherin (CDH2), the neuronal cadherin, stimulates cell-cell contacts during migration and invasion of cells and is able to suppress tumour cell growth. Methods Tumour tissues were acquired from 113 male patients and investigated by immunohistochemistry, as were the three TGCT cell lines NCCIT, NTERA-2 and Tcam2. A monoclonal antibody against N-cadherin was used. Results Tumour-free testis and intratubular germ cell neoplasias (unclassified) (IGCNU) strongly expressed N-cadherin within the cytoplasm. In all seminomas investigated, N-cadherin expression displayed a membrane-bound location. In addition, the teratomas and yolk sac tumours investigated also differentially expressed N-cadherin. In contrast, no N-cadherin could be detected in any of the embryonal carcinomas and chorionic carcinomas examined. This expression pattern was also seen in the investigated mixed tumours consisting of seminomas, teratomas, and embryonal carcinoma. Conclusions N-cadherin expression can be used to differentiate embryonal carcinomas and chorionic carcinomas from other histological subtypes of TGCT."],["dc.identifier.doi","10.1186/1472-6890-12-19"],["dc.identifier.fs","593171"],["dc.identifier.pmid","23066729"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60578"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-cadherin expression in malignant germ cell tumours of the testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3"],["dc.bibliographiccitation.journal","BMC Urology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Schlegel, Christina"],["dc.contributor.author","Shoukier, Moneef"],["dc.contributor.author","Magiera, Isabella"],["dc.contributor.author","Henschke, Frank"],["dc.contributor.author","Schwarz, Alexander"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Loertzer, Hagen"],["dc.date.accessioned","2018-11-07T09:29:10Z"],["dc.date.available","2018-11-07T09:29:10Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Papillary renal cell carcinoma is a rare cancer. Some cases can be attributed to individuals with hereditary renal cell carcinomas usually consisting of the clear cell subtype. In addition, two syndromes with hereditary papillary renal cell carcinoma have been described. One is the hereditary leiomyomatosis and renal cell carcinoma, which is characterized by cutaneous and uterine leiomyomas and renal cell carcinoma mostly consisting of the papillary renal cell carcinoma type II with a worse prognosis. Case presentation: We describe a case of a 30-year-old woman with hereditary leiomyomatosis and renal cell carcinoma syndrome with extensively metastasized papillary renal cell carcinoma, primarily diagnosed in a cervical lymph node lacking leiomyomas at any site. Conclusion: Papillary renal cell carcinoma in young patients should be further investigated for a hereditary variant like the hereditary leiomyomatosis and renal cell carcinoma even if leiomyomas could not be detected. A detailed histological examination and search for mutations is essential for the survival of patients and relatives."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2013"],["dc.identifier.doi","10.1186/1471-2490-13-3"],["dc.identifier.isi","000314924400001"],["dc.identifier.pmid","23320739"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2490"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Hereditary papillary renal cell carcinoma primarily diagnosed in a cervical lymph node: a case report of a 30-year-old woman with multiple metastases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e78137"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Becker, Frank"],["dc.contributor.author","Junker, Kerstin"],["dc.contributor.author","Parr, Martin"],["dc.contributor.author","Hartmann, Arndt"],["dc.contributor.author","Fuessel, Susanne"],["dc.contributor.author","Toma, Marieta"],["dc.contributor.author","Grobholz, Rainer"],["dc.contributor.author","Pflugmann, Thomas"],["dc.contributor.author","Wullich, Bernd"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Otto, Wolfgang"],["dc.contributor.author","Stoeckle, Michael"],["dc.contributor.author","Jung, Volker"],["dc.date.accessioned","2018-11-07T09:18:33Z"],["dc.date.available","2018-11-07T09:18:33Z"],["dc.date.issued","2013"],["dc.description.abstract","Collecting duct carcinoma (CDC) is a rare renal neoplasm that is associated with poor prognosis due to its highly aggressive course and limited response to immuno-or chemotherapy. Histologically, CDC is defined as a subtype of renal cell carcinomas, but in some cases, it is difficult to differentiate from urothelial carcinomas (UC). Therefore the aim of this study was to determine genetic alterations of CDC in comparison to that of urothelial carcinomas of the upper urinary tract (UUT-UC) to clarify the histological origin of this rare tumor entity. Twenty-nine CDC samples were obtained from seven different German centers and compared with twenty-six urothelial carcinomas of the upper urinary tract. Comparative genomic hybridization (CGH) was used to investigate the genetic composition of patients' tumors and allowed the detection of losses and gains of DNA copy numbers throughout the entire genome. The clinical data were correlated with CGH results. CGH analysis of CDC revealed DNA aberrations in many chromosomes. DNA losses were more frequently observed than gains, while high-level amplifications were not detected. The mean frequency of CDC chromosomal aberrations (4.9/case) was slightly lower than that in UUT-UC (5.4/case). Recurrent CDC DNA losses occurred at 8p (n=9/29), 16p (9/29), 1p (n=7/29) and 9p (n=7/29), and gains occurred in 13q (n= 9/29). In contrast to CDC, the most frequently detected UUT-UC DNA aberration was a loss at 9q (n=13/26). DNA losses at 9q, 13q and 8q as well as gains at 8p showed significant variations in UUT-UC compared to CDC. There was no correlation between the patients' clinical course and the presence or absence of these recurrent genetic alterations. CDCs are characterized by a different genetic pattern compared to UUT-UC. Regarding the published data on renal cell carcinoma, we conclude that CDC appears to be a unique entity among kidney carcinomas."],["dc.identifier.doi","10.1371/journal.pone.0078137"],["dc.identifier.isi","000326034500060"],["dc.identifier.pmid","24167600"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9433"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28430"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Collecting Duct Carcinomas Represent a Unique Tumor Entity Based on Genetic Alterations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","95"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Bremmer, Felix"],["dc.date.accessioned","2018-11-07T09:07:12Z"],["dc.date.available","2018-11-07T09:07:12Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: Papillary renal cell carcinoma (RCC) represents a rare tumor, which is divided, based on histological criteria, into two subtypes. In contrast to type I papillary RCC type II papillary RCC shows a worse prognosis. So far, reliable immunohistochemical markers for the distinction of these subtypes are not available. Methods: In the present study the expression of N(neural)-, E(epithelial)-, P(placental)-, und KSP(kidney specific)cadherin was examined in 22 papillary RCC of histological type I and 18 papillary RCC of histological type II (n = 40). Results: All papillary RCC type II displayed a membranous expression for N-cadherin, whereas type I did not show any membranous positivity for N-cadherin. E-cadherin exhibited a stronger, but not significant, membranous as well as cytoplasmic expression in type II than in type I papillary RCC. A diagnostic relevant expression of P- and KSP-cadherin could not be demonstrated in both tumor entities. Conclusion: Thus N-cadherin represents the first immunhistochemical marker for a clear cut differentiation between papillary RCC type I and type II and could be a target for therapy and diagnostic in the future."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.1186/1746-1596-7-95"],["dc.identifier.isi","000313263100001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25739"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-cadherin is differentially expressed in histological subtypes of papillary renal cell carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Disease Markers"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","2019"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Strauß, Arne"],["dc.contributor.author","Maatoug, Yasmine"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Oing, Christoph"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Balabanov, Stefan"],["dc.contributor.author","Honecker, Friedemann"],["dc.date.accessioned","2019-09-24T07:40:13Z"],["dc.date.available","2019-09-24T07:40:13Z"],["dc.date.issued","2019"],["dc.description.abstract","Malignant germ cell tumors (GCT) are the most common malignant tumors in young men between 18 and 40 years. The correct identification of histological subtypes, in difficult cases supported by immunohistochemistry, is essential for therapeutic management. Furthermore, biomarkers may help to understand pathophysiological processes in these tumor types. Two GCT cell lines, TCam-2 with seminoma-like characteristics, and NTERA-2, an embryonal carcinoma-like cell line, were compared by a quantitative proteomic approach using high-resolution mass spectrometry (MS) in combination with stable isotope labelling by amino acid in cell culture (SILAC). We were able to identify 4856 proteins and quantify the expression of 3936. 347 were significantly differentially expressed between the two cell lines. For further validation, CD81, CBX-3, PHF6, and ENSA were analyzed by western blot analysis. The results confirmed the MS results. Immunohistochemical analysis on 59 formalin-fixed and paraffin-embedded (FFPE) normal and GCT tissue samples (normal testis, GCNIS, seminomas, and embryonal carcinomas) of these proteins demonstrated the ability to distinguish different GCT subtypes, especially seminomas and embryonal carcinomas. In addition, siRNA-mediated knockdown of these proteins resulted in an antiproliferative effect in TCam-2, NTERA-2, and an additional embryonal carcinoma-like cell line, NCCIT. In summary, this study represents a proteomic resource for the discrimination of malignant germ cell tumor subtypes and the observed antiproliferative effect after knockdown of selected proteins paves the way for the identification of new potential drug targets."],["dc.identifier.doi","10.1155/2019/8298524"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16378"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62439"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","0278-0240"],["dc.relation.issn","1875-8630"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Proteomic Comparison of Malignant Human Germ Cell Tumor Cell Lines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","537"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","World Journal of Urology"],["dc.bibliographiccitation.lastpage","542"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Bedke, Jens"],["dc.contributor.author","Stojanovic, Tomislav"],["dc.contributor.author","Kiss, Eva"],["dc.contributor.author","Behnes, Carl-Ludwig"],["dc.contributor.author","Proudfoot, Amanda E."],["dc.contributor.author","Groene, Hermann-Josef"],["dc.date.accessioned","2018-11-07T08:41:14Z"],["dc.date.available","2018-11-07T08:41:14Z"],["dc.date.issued","2010"],["dc.description.abstract","During rejection, leukocytes are recruited from the peripheral circulation into the graft leading to the damage of endothelial cells, capillary perfusion failure and graft loss. Chemokines play a pivotal role in the recruitment of leukocytes to the endothelium. Viral macrophage inflammatory protein-II (vMIP-II), a human herpes virus-8 DNA-encoded protein, is a broad-spectrum chemokine antagonist. The aim of the study was to prove the beneficial activity of vMIP-II treatment on acute rat kidney allograft damage. Heterotopic rat kidney transplantation was performed in the Fischer 344 to Lewis transplantation model and animals were treated with vMIP-II (2 x 15 A mu g or 100 A mu g/day) for 7 days. Rejection-induced damage was analyzed by histology, and microcirculatory changes within the graft were analyzed by in vivo microscopy. Viral macrophage inflammatory protein-II significantly improved acute glomerular damage and tubulointerstitial inflammation and lowered the extent of vascular and tubulointerstitial damage of the treated allografts. Functional microcirculation of peritubular capillaries was significantly improved in vivo, and the firm adherence of leukocytes was significantly reduced by vMIP-II treatment. The administration of the broad-spectrum antagonist vMIP-II improved acute renal allograft damage, mainly by a reduction in leukocyte recruitment with a subsequently improved renal cortical microcirculation in vivo."],["dc.description.sponsorship","[SFB 405]; [B10]"],["dc.identifier.doi","10.1007/s00345-010-0556-0"],["dc.identifier.isi","000280242600021"],["dc.identifier.pmid","20401660"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4983"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19422"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0724-4983"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Viral macrophage inflammatory protein-II improves acute rejection in allogeneic rat kidney transplants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","4"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Clinical Pathology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Schütze, Gunther"],["dc.contributor.author","Engelke, Christoph"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2019-07-09T11:54:11Z"],["dc.date.available","2019-07-09T11:54:11Z"],["dc.date.issued","2013"],["dc.description.abstract","Background The autosomal dominant tumor syndrome tuberous sclerosis complex is caused by the mutated TSC1 gene, hamartin, and the TSC2 gene, tuberin. Patients with this complex develop typical cutaneus symptoms such as peau chagrin or angiofibromas of the skin as well as other lesions such as astrocytomas in the brain and lymphangioleiomyomatosis in the lung. Only a few tuberous sclerosis patients have been described who showed a multifocal micronodular pneumocyte hyperplasia of the lung. Another benign tumor which often occurs together with tuberous sclerosis is the angiomyolipoma of the kidney. Furthermore, an increased incidence of renal cell carcinoma in connection with tuberous sclerosis has also been proven. Case presentation We report a 13-year-old white girl with epilepsy and hypopigmented skin lesions. Radiological studies demonstrated the typical cortical tubers leading to the diagnosis of tuberous sclerosis. In the following examinations a large number of angiomyolipomas were found in both kidneys. One lesion showed an increasing size and tumor like aspects in magnetic resonance imaging. The pathological examination of the following tumorectomy demonstrated an unclassified renal cell carcinoma. Four months postoperatively, a follow-up computer tomography revealed multiple bilateral pulmonary nodules. To exclude lung metastases of the renal cell carcinoma, multiple open-lung biopsies were performed. Conclusion Here we report a diagnostically challenging case of a 13-year-old patient with tuberous sclerosis and angiomyolipomas of the kidney who developed an unclassified renal cell carcinoma as well as multifocal micronodular pneumocyte hyperplasia."],["dc.identifier.doi","10.1186/1472-6890-13-4"],["dc.identifier.fs","591695"],["dc.identifier.pmid","23379654"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8532"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60582"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","13-year-old tuberous sclerosis patient with renal cell carcinoma associated with multiple renal angiomyolipomas developing multifocal micronodular pneumocyte hyperplasia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]