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141.
Sebastian Reuther Silke Szymczak Annette Raabe Kerstin Borgmann Andreas Ziegler Cordula Petersen Ekkehard Dikomey Ulrike Hoeller 《Strahlentherapie und Onkologie》2015,191(1):59-66
Background and purpose
The aim of this study was to determine the impact of functional single nucleotide polymorphism (SNP) pathways involved in the ROS pathway, DNA repair, or TGFB1 signaling on acute or late normal toxicity as well as individual radiosensitivity.Materials and methods
Patients receiving breast-conserving surgery and radiotherapy were examined either for erythema (n?=?83), fibrosis (n?=?123), or individual radiosensitivity (n?=?123). The 17 SNPs analyzed are involved in the ROS pathway (GSTP1, SOD2, NQO1, NOS3, XDH), DNA repair (XRCC1, XRCC3, XRCC6, ERCC2, LIG4, ATM) or TGFB signaling (SKIL, EP300, APC, AXIN1, TGFB1). Associations with biological and clinical endpoints were studied for single SNPs but especially for combinations of SNPs assuming that a SNP is either beneficial or deleterious and needs to be weighted.Results
With one exception, no significant association was seen between a single SNP and the three endpoints studied. No significant associations were also observed when applying a multi-SNP model assuming that each SNP was deleterious. In contrast, significant associations were obtained when SNPs were suggested to be either beneficial or deleterious. These associations increased, when each SNP was weighted individually. Detailed analysis revealed that both erythema and individual radiosensitivity especially depend on SNPs affecting DNA repair and TGFB1 signaling, while SNPs in ROS pathway were of minor importance.Conclusion
Functional pathways of SNPs may be used to form a risk score allowing to predict acute and late radiation-induced toxicity but also to unravel the underlying biological mechanisms.142.
High‐dose dobutamine stress steady‐state free precession (SSFP) cine MRI at 3T with patient adaptive local radiofrequency (RF) shimming using dual‐source RF transmission 下载免费PDF全文
143.
Is Implantation of a Left Ventricular Assist Device in Patients With Critical or Impending Cardiogenic Shock an Absolute Contraindication? Looking Back at Our Past Experience Trying to Identify Contraindicative Risk Factors 下载免费PDF全文
Angelo Maria Dell'Aquila Stefan R.B. Schneider Paolo Risso Henryk Welp David G. Glockner Sebastian Alles Jürgen R. Sindermann Mirela Scherer 《Artificial organs》2015,39(12):998-1004
Poor survival has been demonstrated after ventricular assist device (VAD) implantation for Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) profile 1 and 2 patients compared with more stable levels. However, risk factors within this high‐risk cohort have not been determined so far. The aim of the present study was to identify risk factors associated with this very high mortality rate. Between February 1993 and January 2013, 298 patients underwent VAD implantation in our institution. One hundred nine patients were in INTERMACS level 1 and 49 patients were in INTERMACS level 2 and were therefore defined as hemodynamically critical (overall 158 patients). Assist devices implanted were: HVAD HeartWare n = 18; Incor n = 11; VentrAssist n = 2; DeBakey n = 22; and pulsatile systems n = 105. After cumulative support duration of 815.35 months, Kaplan–Meier analysis revealed a survival of 63.9, 48.8, and 40.3% at 1, 6, and 12 months, respectively. Cox regression analyses identified age > 50 (P = 0.001, odds ratio [OR] 2.48), white blood cell count > 13.000/μL (P = 0.01, OR 2.06), preoperative renal replacement therapy (P = 0.001, OR 2.63), and postcardiotomy failure (P < 0.001, OR 2.79) as independent predictors of mortality. Of note, last generation VADs were not associated with significantly better 6‐month survival (P = 0.59). Patients without the aforementioned risk factors could yield a survival of 79.2% at 6 months. This single‐center experience shows that VAD implantation in hemodynamically unstable patients generally results in poor early outcome, even in third‐generation pumps. However, avoiding the aforementioned risk factors could result in improved outcome. 相似文献
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SDF‐1/CXCR4/CXCR7 is pivotal for vascular smooth muscle cell proliferation and chronic allograft vasculopathy 下载免费PDF全文
Michael N. Thomas Aivars Kalnins Martin Andrassy Anne Wagner Sven Klussmann Markus Rentsch Antje Habicht Sebastian Pratschke Manfred Stangl Alexandr V. Bazhin Bruno Meiser Michael Fischereder Jens Werner Markus Guba Joachim Andrassy 《Transplant international》2015,28(12):1426-1435
Chronic rejection remains a major obstacle in transplant medicine. Recent studies suggest a crucial role of the chemokine SDF‐1 on neointima formation after injury. Here, we investigate the potential therapeutic effect of inhibiting the SDF‐1/CXCR4/CXCR7 axis with an anti‐SDF‐1 Spiegelmer (NOX‐A12) on the development of chronic allograft vasculopathy. Heterotopic heart transplants from H‐2bm12 to B6 mice and aortic transplants from Balb/c to B6 were performed. Mice were treated with NOX‐A12. Control animals received a nonfunctional Spiegelmer (revNOX‐A12). Samples were retrieved at different time points and analysed by histology, RT‐PCR and proliferation assay. Blockade of SDF‐1 caused a significant decrease in neointima formation as measured by intima/media ratio (1.0 ± 0.1 vs. 1.8 ± 0.1, P < 0.001 AoTx; 0.35 ± 0.05 vs. 1.13 ± 0.27, P < 0.05 HTx). In vitro treatment of primary vascular smooth muscle cells with NOX‐A12 showed a significant reduction in proliferation (0.42 ± 0.04 vs. 0.24 ± 0.03, P < 0.05). TGF‐β, TNF‐α and IL‐6 levels were significantly reduced under SDF‐1 inhibition (3.42 ± 0.37 vs. 1.67 ± 0.33, P < 0.05; 2.18 ± 0.37 vs. 1.0 ± 0.39, P < 0.05; 2.18 ± 0.26 vs. 1.6 ± 0.1, P < 0.05). SDF‐1/CXCR4/CXCR7 plays a critical role in the development of chronic allograft vasculopathy (CAV). Therefore, pharmacological inhibition of SDF‐1 with NOX‐A12 may represent a therapeutic option to ameliorate chronic rejection changes. 相似文献
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Muhammad Ahsan Javed Georg Beyer Nha Le Alessio Vinci Helen Wong Daniel Palmer Robert D. Morgan Angela Lamarca Richard A. Hubner Juan W. Valle Salma Alam Sumsur Chowdhury Yuk Ting Ma Livia Archibugi Gabriele Capurso Patrick Maisonneuve Albrecht Neesse Malin Sund Sebastian Krug 《Pancreatology》2019,19(1):97-104