Krüger, Ullrich

[["dc.bibliographiccitation.firstpage","1085"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","1090"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Blankenburg, S."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Thoms, Kai Martin"],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Westphal, G."],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Volkenandt, Matthias"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Kraemer, Kenneth H."],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T10:29:15Z"],["dc.date.available","2018-11-07T10:29:15Z"],["dc.date.issued","2005"],["dc.description.abstract","Individuals with the rare DNA repair deficiency syndrome xeroderma pigmentosum (XP) are sensitive to the sun and exhibit a 1000-fold increased risk for developing skin cancers, including cutaneous melanoma. Inherited polymorphisms of XP genes may contribute to subtle variations in DNA repair capacity and genetic susceptibility to melanoma. We investigated the role of three polymorphic alleles of the DNA repair gene XPC in a hospital-based case-control study of 294 Caucasian patients from Germany who had cutaneous melanoma and 375 healthy cancer-free sex-matched Caucasian control subjects from the same area. We confirmed that the XPC intron 9 PAT+, intron 11 -6A, and the exon 15 2920C polymorphisms are in a linkage disequilibrium. Only 1.6% of the 669 donors genotyped were discordant for these three polymorphisms. The allele frequencies (cases: controls) were for intron 9 PAT+ 41.7%:36.9%, for intron 11 -6A 41.8%:37.0% and for exon 15 2920C 41.3%:37.3%. Using multivariate logistic regression analyses to control for age, skin type and number of nevi, the three polymorphisms were significantly associated with increased risks of melanoma: OR 1.87 (95% CI: 1.10-3.19; P = 0.022), OR 1.83 (95% CI: 1.07-3.11; P = 0.026), and OR 1.82 (95% CI: 1.07-3.08; P = 0.026), respectively. Exploratory multivariate analyses of distinct subgroups revealed that these polymorphisms were associated with increased risks for the development of multiple primary melanomas (n = 28). The results of our case-control study support the hypothesis that the intron 9 PAT+, intron 11 -6A and exon 15 2920C haplotype may contribute to the risk of developing cutaneous melanoma by increasing the rate of an alternatively spliced XPC mRNA isoform that skips exon 12 and leads to reduced DNA repair. Our results should be validated in independent samples in order to guard against false positive findings."],["dc.description.sponsorship","Intramural NIH HHS [Z01 BC004517-31]"],["dc.identifier.doi","10.1093/carcin/bgi055"],["dc.identifier.isi","000229700100008"],["dc.identifier.pmid","15731165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43601"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","Assessment of 3 xeroderma pigmentosum group C gene polymorphisms and risk of cutaneous melanoma: a case-control study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1432"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of the European Academy of Dermatology and Venereology"],["dc.bibliographiccitation.lastpage","1439"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Zutt, Markus"],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kretschmer, Lutz"],["dc.date.accessioned","2018-11-07T08:49:13Z"],["dc.date.available","2018-11-07T08:49:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Background Chronic venous leg ulcers (CVU) cause considerable burden of disease for the patients as well as enormous costs for health care systems. The pathophysiology of CVU is complex and not entirely understood. So far reliable pathogenic and/or prognostic parameters have not been identified. Objectives We studied the role of thrombophilia in patients referred to a University dermatology department for treatment of CVU. Patients and methods A cohort of 310 patients with active chronic venous leg ulcers (CEAP 6) was stratified into two comparably large groups according to the presence or absence of post- thrombotic syndrome (PTS+; PTS-) as determined using duplex scan and/or phlebography. In addition, several thrombophilia parameters were assessed. Results The prevalence of protein S deficiency and factor V Leiden mutation was significantly higher in PTS+ patients compared with the PTS- group. However, patients in both subgroups revealed high prevalences of thrombophilia (antithrombin deficiency, protein C deficiency, protein S deficiency, activated protein C resistance, factor V mutation or elevated homocysteine). Conclusion Based on these data, it is conceivable that thrombophilia contributes to the pathogenesis of CVU, possibly through induction of microcirculatory dysregulations."],["dc.identifier.doi","10.1111/j.1468-3083.2011.04001.x"],["dc.identifier.isi","000297952800011"],["dc.identifier.pmid","21392126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21406"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0926-9959"],["dc.title","Thrombophilia in patients with chronic venous leg ulcers-a study on patients with or without post-thrombotic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","319"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Dermatology"],["dc.bibliographiccitation.lastpage","324"],["dc.bibliographiccitation.volume","214"],["dc.contributor.author","Zutt, Markus"],["dc.contributor.author","Haas, Ellen"],["dc.contributor.author","Krueger, Ullrich"],["dc.contributor.author","Distler, Meike"],["dc.contributor.author","Neumann, Christine"],["dc.date.accessioned","2018-11-07T11:06:26Z"],["dc.date.available","2018-11-07T11:06:26Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Leg ulcers caused by vasculitis, small vessel occlusion or other rare conditions often prove to be very difficult to treat. Despite polypragmatic, systemic and localized therapy, many of these wounds are progressive and characterized by severe pain. Methods and Results: We here portray the cases of 5 patients with ulcers resistant to systemic therapy for the underlying disease, who were treated successfully using vacuum-assisted closure ( VAC) for wound management. We present the advantages and disadvantages of this method, as well as illustrating the essential and known therapeutic principles. Conclusions: Our experience shows VAC to be an excellent and effective alternative in the treatment of therapy-resistant chronic wounds caused by vasculopathy (small vessel occlusion or vasculitis). We did not observe any pathergy or proinflammatory effects caused by VAC. Copyright (c) 2007 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000100882"],["dc.identifier.isi","000246063700008"],["dc.identifier.pmid","17460403"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8318"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52309"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1018-8665"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Successful use of vacuum-assisted closure therapy for leg ulcers caused by occluding vasculopathy and inflammatory vascular diseases - A case series"],["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.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Anders, N."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Schmidt, D."],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Volkenandt, Matthias"],["dc.contributor.author","Kaiser, R."],["dc.contributor.author","Westphal, G."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:12:01Z"],["dc.date.available","2018-11-07T10:12:01Z"],["dc.date.issued","2006"],["dc.format.extent","198"],["dc.identifier.isi","000235370600041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40158"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","33rd Annual Meeting of the Arbeitsgemeinschaft-Dermatologische-Forschung (ADF)"],["dc.relation.eventlocation","Aachen, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Variations of the MC1R and the GSTM1 and T1 genes in cutaneous malignant melanoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","576"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.lastpage","582"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Schulz, U."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Middel, Peter"],["dc.contributor.author","Schinner, S."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:06:19Z"],["dc.date.available","2018-11-07T10:06:19Z"],["dc.date.issued","2002"],["dc.description.abstract","Peroxisome proliferator-activated receptor gamma is a member of the nuclear receptor superfamily involved in adipocyte differentiation and glucose homeostasis. There is evidence that peroxisome proliferator-activated receptor gamma may also act as a tumor suppressor. Here, we demonstrate expression of peroxisome proliferator-activated receptor gamma in benign melanocytic naevi, different variants of primary cutaneous melanomas, and melanoma metastases. Peroxisome proliferator-activated receptor gamma protein and peroxisome proliferator-activated receptor gamma1 mRNA were also detected in human melanoma cell lines. The peroxisome proliferator-activated receptor gamma specific agonists 15-deoxy-Delta(12,14)-prostaglandin J(2), troglitazone, and rosiglitazone dose-dependently inhibited cell proliferation in four melanoma cell lines, whereas a specific agonist of peroxisome proliferator-activated receptor alpha had no such effect. At a concentration of 50 muM rosiglitazone, the most potent peroxisome proliferator-activated receptor gamma agonist tested suppressed cell growth by approximately 90%. Apoptosis could be induced in melanoma cell lines by incubation with tumor-necrosis-factor-related apoptosis-inducing ligand. In contrast, the growth inhibitory effect of peroxisome proliferator-activated receptor gamma activation was independent of apoptosis and seemed to occur primarily through induction of cell cycle arrest. Our data indicate that melanoma cell growth may be modulated through peroxisome proliferator-activated receptor gamma."],["dc.identifier.doi","10.1046/j.1523-1747.2002.01861.x"],["dc.identifier.isi","000177951400006"],["dc.identifier.pmid","12230498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39070"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Inc"],["dc.relation.issn","0022-202X"],["dc.title","Agonists of peroxisome proliferator-activated receptor gamma inhibit cell growth in malignant melanoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal Of Oral Sciences"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Götz, Werner"],["dc.contributor.author","Lossdörfer, Stefan"],["dc.contributor.author","Krüger, Ullrich"],["dc.contributor.author","Braumann, Bert"],["dc.contributor.author","Jäger, Andreas"],["dc.date.accessioned","2018-11-07T10:41:13Z"],["dc.date.available","2018-11-07T10:41:13Z"],["dc.date.issued","2003"],["dc.description.abstract","So-called epithelial rests of Malassez are derived from the Hertwig's root sheath and are located in the periodontal ligament, with still unknown functions. Different pathological conditions may lead to proliferation of these otherwise non-proliferative cell clusters. The insulin-like growth factor (IGF) system is an important growth factor system controlling proliferation and differentiation. In our study on Malassez cells from extracted human deciduous teeth, we investigated their structure by means of light and electron microscopy. Although they appeared as cellular clusters with a uniform epithelial phenotype, immunohistochemical analyses of components of the IGF system revealed an unique pattern: weak immunoreactivity could be seen for IGF-II while among all IGF binding proteins (IGFBPs) only IGFBP-6 and weakly IGFBP-4 were detectable in epithelial cells of Malassez. Since IGFBP-6 has a very high affinity for IGF-II and can inhibit its functions, we discuss that, in the normal periodontal ligament, autocrine IGFBP-6 may function as an antiproliferative molecule suppressing mitogenic effects of IGFs on Malassez cells."],["dc.identifier.doi","10.1034/j.1600-0722.2003.00003.x"],["dc.identifier.isi","000180745000005"],["dc.identifier.pmid","12558805"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46485"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0909-8836"],["dc.title","Immunohistochemical localization of insulin-like growth factor-II and its binding protein-6 in human epithelial cells of Malassez"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Wussow, M."],["dc.contributor.author","Schmidt, D."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:56:17Z"],["dc.date.available","2018-11-07T10:56:17Z"],["dc.date.issued","2005"],["dc.format.extent","A58"],["dc.identifier.isi","000231862600339"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49977"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","35th Annual Meeting of the European-Society-for-Dermatological-Research"],["dc.relation.eventlocation","Tubingen, GERMANY"],["dc.relation.issn","0022-202X"],["dc.title","Evidence for a PPARgamma agonist-induced proteasomal degradation of cyclin D1 in melanoma cell lines"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Platzer, Anja"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Stiens, G."],["dc.date.accessioned","2018-11-07T08:32:05Z"],["dc.date.available","2018-11-07T08:32:05Z"],["dc.date.issued","2009"],["dc.format.extent","324"],["dc.identifier.isi","000263520200311"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17262"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","36th Annual Meeting of the Arbeitsgemeinschaft-Dermatologishche-Forschung"],["dc.relation.eventlocation","Heidelberg, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Psychosocial distress in psoriatic out-patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","168"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Wound Repair and Regeneration"],["dc.bibliographiccitation.lastpage","172"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Zutt, Markus"],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Neumann, Christine"],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Kretschmer, Lutz"],["dc.date.accessioned","2018-11-07T08:58:36Z"],["dc.date.available","2018-11-07T08:58:36Z"],["dc.date.issued","2011"],["dc.description.abstract","Chronic venous leg ulcers are common and cause considerable burden of disease for affected patients with significant costs for health care systems worldwide. The complex pathophysiology of chronic venous leg ulcers is still not entirely understood. In addition, reliable pathogenic and/or prognostic parameters are not known. Published data suggest that patients with chronic venous leg ulcers reveal congenital or acquired thrombophilia. We examined the serum Lipoprotein (a) [Lp(a)] level, a proatherogenic and prothrombotic risk factor, in patients with chronic venous leg ulcers (n=210, stratified into patients with postthrombotic syndrome or without) and in a healthy control group (n=341). Forty-two percent of all patients, compared with 20% of healthy controls, revealed significantly increased Lp(a) serum concentrations above 0.3 g/L. Furthermore, 49% without postthrombotic syndrome but only 35% with postthrombotic syndrome showed increased Lp(a) levels. The increase of Lp(a) level was significantly different between all three groups (p < 0.001). There was no correlation of Lp(a) levels and CRP values in all groups. Based on these data, it is conceivable that Lp(a) plasma level is a novel pathogenic parameter for chronic venous leg ulcers. Elevated concentrations may contribute to the pathogenesis through induction of thrombogenic microcirculatory dysregulations, impaired extravascular fibrinolysis, or other mechanisms like proinflammatory effects."],["dc.identifier.doi","10.1111/j.1524-475X.2010.00657.x"],["dc.identifier.isi","000287878100225"],["dc.identifier.pmid","21362083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23682"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1067-1927"],["dc.title","Increased Lipoprotein (a) concentrations in patients with chronic venous leg ulcers: a study on patients with or without postthrombotic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","296"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Kaiser, R."],["dc.contributor.author","Matern, P."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Westphal, Goetz Alexander"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:48:15Z"],["dc.date.available","2018-11-07T10:48:15Z"],["dc.date.issued","2004"],["dc.description.abstract","The three peroxisome proliferator-activated receptor (PPAR) subtypes alpha, delta (beta), and gamma belong to the group of nuclear receptors that act as ligand-activated transcription factors. Recently, expression of PPARalpha and gamma in keratinocytes has been demonstrated, and ligands of PPARalpha and gamma have been found to enhance epidermal maturation and protect against cutaneous inflammation. There is evidence for a possible role of PPARs in psoriasis, as the expression of PPARalpha and gamma is decreased in lesional skin and treatment with PPARgamma agonists improves psoriatic keratinocyte pathology in vitro and in vivo. We performed a case-control study to search for possible associations between variations in the genes encoding PPARalpha and gamma and psoriasis. Seven variations in these genes were analyzed in 192 patients with chronic plaque-type psoriasis and 330 healthy controls by PCR-based methods. No association between any of the investigated PPAR variants and psoriasis was found. Our findings argue against a significant contribution of the investigated PPAR variations to the genetic basis of psoriasis."],["dc.identifier.doi","10.1007/s00403-004-0463-6"],["dc.identifier.isi","000222059400001"],["dc.identifier.pmid","15083308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48146"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.title","Variations in the genes encoding the peroxisome proliferator-activated receptors alpha and gamma in psoriasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]