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        {
            "text": "\n120366\nTransplantation and tracking of human-induced pluripotent stem cells in a pig model of myocardial infarction: assessment of cell survival, engraftment, and distribution by hybrid single photon emission computed tomography/computed tomography of sodium iodide symporter transgene expression.\n\nTemplin, C\n\nZweigerdt, R\n\nSchwanke, K\n\nOlmer, R\n\nGhadri, JR\n\nEmmert, MY\n\nMüller, E\n\nKüest, SM\n\nCohrs, S\n\nSchibli, R\n\nKronen, P\n\nHilbe, M\n\nReinisch, A\n\nStrunk, D\n\nHaverich, A\n\nHoerstrup, S\n\nLüscher, TF\n\nKaufmann, PA\n\nLandmesser, U\n\nMartin, U\n\nBeiträge in Fachzeitschriften\nISI:000306977200014\n22767659.0\n10.1161/CIRCULATIONAHA.111.087684\nNone\nEvaluation of novel cellular therapies in large-animal models and patients is currently hampered by the lack of imaging approaches that allow for long-term monitoring of viable transplanted cells. In this study, sodium iodide symporter (NIS) transgene imaging was evaluated as an approach to follow in vivo survival, engraftment, and distribution of human-induced pluripotent stem cell (hiPSC) derivatives in a pig model of myocardial infarction.\n                Transgenic hiPSC lines stably expressing a fluorescent reporter and NIS (NIS(pos)-hiPSCs) were established. Iodide uptake, efflux, and viability of NIS(pos)-hiPSCs were assessed in vitro. Ten (±2) days after induction of myocardial infarction by transient occlusion of the left anterior descending artery, catheter-based intramyocardial injection of NIS(pos)-hiPSCs guided by 3-dimensional NOGA mapping was performed. Dual-isotope single photon emission computed tomographic/computed tomographic imaging was applied with the use of (123)I to follow donor cell survival and distribution and with the use of (99m)TC-tetrofosmin for perfusion imaging. In vitro, iodide uptake in NIS(pos)-hiPSCs was increased 100-fold above that of nontransgenic controls. In vivo, viable NIS(pos)-hiPSCs could be visualized for up to 15 weeks. Immunohistochemistry demonstrated that hiPSC-derived endothelial cells contributed to vascularization. Up to 12 to 15 weeks after transplantation, no teratomas were detected.\n                This study describes for the first time the feasibility of repeated long-term in vivo imaging of viability and tissue distribution of cellular grafts in large animals. Moreover, this is the first report demonstrating vascular differentiation and long-term engraftment of hiPSCs in a large-animal model of myocardial infarction. NIS(pos)-hiPSCs represent a valuable tool to monitor and improve current cellular treatment strategies in clinically relevant animal models.\n\nReinisch, Andreas\n\n\n"
        },
        {
            "text": "\n140554\nMicronucleus assay with urine derived cells (UDC): a review of its application in human studies investigating genotoxin exposure and bladder cancer risk.\n\nNersesyan, A\n\nKundi, M\n\nFenech, M\n\nBolognesi, C\n\nMisik, M\n\nWultsch, G\n\nHartmann, M\n\nKnasmueller, S\n\nBeiträge in Fachzeitschriften\nISI:000347582000003\n25485594.0\n10.1016/j.mrrev.2014.04.004\nNone\nThe first micronucleus (MN) study with urine derived cells (UDC) appeared 30 years ago. So far, 56 investigations have been published with this method and it was shown that it can be used for the detection of chromosomal damage caused by environmental and lifestyle factors as well as by occupational exposures and certain diseases This approach may be also useful as a diagnostic tool for the detection and prognosis of bladder cancer. The test system has been improved in the last years, i.e., it was shown that, apart from MN also other nuclear anomalies can be evaluated in UDC which are found in other types of epithelial cells as well (e.g., in oral and nasal cells) and are indicative for acute toxicity (pyknosis, karyorrhexis, karyolysis, condensed chromatin) and genomic instability (nuclear buds, binucleates). Furthermore, an improved protocol with Carnoy I fixation and Papanicolaou stain was developed which enables the discrimination between cells which originate from the cervix and those from the urothelium. The evaluation of the currently available results indicates that exposures and health conditions which are associated with increased cancer rates in the bladder (and possibly also in other organs) lead to positive results in MN-UDC assays and a limited number of studies indicate that this method may be equally sensitive as other more frequently used human biomonitoring assays. The major shortcoming of the UDC-MN method is the lack of standardization; the evaluation of the current data shows that a variety of staining and fixation methods are used and that the numbers of evaluated cells vary over a broad range. These inconsistencies may account for the large inter-laboratory variations of the background frequencies. In order to improve the reliability of the method, further standardization and validation is required. Therefore an international program should be initiated in which a similar strategy could be used as in previous validation/standardization projects concerning MN-cytome assays with lymphocytes and buccal cells.\n                Copyright © 2014 Elsevier B.V. All rights reserved.\n\nWultsch, Georg\n\n\n"
        },
        {
            "text": "\n162596\n19th Workshop of the International Stroke Genetics Consortium, April 28-29, 2016, Boston, Massachusetts, USA: 2016.001 MRI-defined cerebrovascular genomics-The CHARGE consortium.\n\nDebette, S\n\nSaba, Y\n\nVojinovic, D\n\nJian, X\n\nAdams, H\n\nChauhan, G\n\nSargurupremraj, M\n\nKaffashian, S\n\nDing, J\n\nBis, JC\n\nNyquist, P\n\nMather, K\n\nVan Duijn, C\n\nLauner, LJ\n\nIkram, MA\n\nSchmidt, H\n\nLongstreth, WT\n\nFornage, M\n\nSeshadri, S\n\n\n\nPublizierte (zitierfähige) Beiträge für wissenschaftliche Veranstaltungen\nNone\n28428977.0\n10.1212/NXG.0000000000000100\nPMC5390739\nThe CHARGE consortium is an investigator-initiated collaboration to facilitate meta-analyses of genome-wide association studies (GWAS) and genomic analyses based on next generation sequencing (NGS), among multiple large and well-phenotyped population-based cohort studies around the world (http://www.chargeconsortium.com). Within the neuro-CHARGE working group, we are presenting an update of ongoing genomic studies on MRI-markers of cerebrovascular disease. Large population-based studies have shown that the burden of cerebrovascular disease extends far beyond that of clinical stroke. MRI-markers of cerebral small vessel disease, such as white matter hyperintensities (WMH), small subcortical brain infarcts, microbleeds, or dilated perivascular spaces, are particularly frequent in older community persons. These markers portend an increased risk of stroke, dementia, and premature death, and were shown to have a high heritability, especially WMH burden. Interestingly recent work has revealed genetic risk variants between WMH burden and stroke. To account for the major role of high blood pressure in the occurrence of WMH, we are performing a GWAS of WMH burden stratified on hypertension status, as well as a joint meta-analysis to account for gene-environment interaction with hypertension. Moreover, based on prior epidemiologic and histologic data suggesting that the pathogenesis of WMH may differ according to their location, we are running separate GWAS for periventricular and deep WMH burden. A GWAS of cerebral microbleeds is being finalized. We are also exploring the role of vascular risk factors in the occurrence of dementia by examining the relation of genetic risk scores for these factors with MRI-markers of brain aging and cerebrovascular disease. Finally, several NGS projects are being conducted to identify rare variants associated with WMH burden and lacunar brain infarcts. Additional projects are also currently being designed, including GWAS of novel MRI phenotypes, such as composite measures of cerebral small vessel disease, as well as lifetime, and epigenomic approaches.\n\nSchmidt, Helena\n\n\n"
        },
        {
            "text": "\n167636\nArterial hypertension drives arrhythmia progression via specific structural remodeling in a porcine model of atrial fibrillation.\n\nManninger, M\n\nZweiker, D\n\nvan Hunnik, A\n\nAlogna, A\n\nPrassl, AJ\n\nSchipke, J\n\nZeemering, S\n\nZirngast, B\n\nSchönleitner, P\n\nSchwarzl, M\n\nHerbst, V\n\nThon-Gutschi, E\n\nHuber, S\n\nRohrer, U\n\nEbner, J\n\nBrussee, H\n\nPieske, BM\n\nHeinzel, FR\n\nVerheule, S\n\nAntoons, G\n\nLueger, A\n\nMühlfeld, C\n\nPlank, G\n\nSchotten, U\n\nPost, H\n\nScherr, D\n\nBeiträge in Fachzeitschriften\nISI:000442908500011\n29803020.0\n10.1016/j.hrthm.2018.05.016\nNone\nArterial hypertension (HT) contributes to progression of atrial fibrillation (AF) via unknown mechanisms.\n                We aimed to characterize electrical and structural changes accounting for increased AF stability in a large animal model of rapid atrial pacing (RAP)-induced AF combined with desoxycorticosterone acetate (DOCA)-induced HT.\n                Eighteen pigs were instrumented with right atrial endocardial pacemaker leads and custom-made pacemakers to induce AF by continuous RAP (600 beats/min). DOCA pellets were subcutaneously implanted in a subgroup of 9 animals (AF+HT group); the other 9 animals served as controls (AF group). Final experiments included electrophysiology studies, endocardial electroanatomic mapping, and high-density mapping with epicardial multielectrode arrays. In addition, 3-dimensional computational modeling was performed.\n                DOCA implantation led to secondary HT (median [interquartile range] aortic pressure 109.9 [100-137] mm Hg in AF+HT vs 82.2 [79-96] mm Hg in AF; P < .05), increased AF stability (55.6% vs 12.5% of animals with AF episodes lasting >1 hour; P < .05), concentric left ventricular hypertrophy, atrial dilatation (119 ± 31 cm2 in AF+HT vs 78 ± 23 cm2 in AF; P < .05), and fibrosis. Collagen accumulation in the AF+HT group was mainly found in non-intermyocyte areas (1.62 ± 0.38 cm3 in AF+HT vs 0.96 ± 0.3 cm3 in AF; P < .05). Left and right atrial effective refractory periods, action potential durations, endo- and epicardial conduction velocities, and measures of AF complexity were comparable between the 2 groups. A 3-dimensional computational model confirmed an increase in AF stability observed in the in vivo experiments associated with increased atrial size.\n                In this model of secondary HT, higher AF stability after 2 weeks of RAP is mainly driven by atrial dilatation.\n                Copyright © 2018 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.\n\nBrussee, Helmut\n\nHuber, Stefan\n\nLueger, Andreas\n\nManninger-Wünscher, Martin\n\nPlank, Gernot\n\nPrassl, Anton\n\nRohrer, Ursula\n\nScherr, Daniel\n\nTrummer-Herbst, Viktoria\n\nZirngast, Birgit\n\nZweiker, David\n\n\n"
        },
        {
            "text": "\n177266\nPelvic and lower extremity physiological cross-sectional areas: an MRI study of the living young and comparison to published research literature.\n\nLube, J\n\nFlack, NAMS\n\nCotofana, S\n\nÖzkurtul, O\n\nWoodley, SJ\n\nZachow, S\n\nHammer, N\n\nBeiträge in Fachzeitschriften\nISI:000408431700005\n28258300.0\n10.1007/s00276-016-1807-6\nNone\nMorphological data pertaining to the pelvis and lower extremity muscles are increasingly being used in biomechanical modeling to compare healthy and pathological conditions. Very few data sets exist that encompass all of the muscles of the lower limb, allowing for comparisons between regions. The aims of this study were to (a) provide physiological cross-sectional area (PCSA) data for the pelvic, thigh, and leg muscles in young, healthy participants, using magnetic resonance imaging (MRI), and (b) to compare these data with summarized PCSAs obtained from the literature.\n                Six young and healthy volunteers participated and were scanned using 3 T MRI. PCSAs were calculated from volumetric segmentations obtained bilaterally of 28 muscles/muscle groups of the pelvis, thigh, and leg. These data were compared to published, summarized PCSA data derived from cadaveric, computed tomography, MRI and ultrasound studies.\n                The PCSA of the pelvis, thigh, and leg muscles tended to be 20-130% larger in males than in females, except for the gemelli which were 34% smaller in males, and semitendinosus and triceps surae which did not differ (<20% different). The dominant and the non-dominant sides showed similar and minutely different PCSA with less than 18% difference between sides. Comparison to other studies revealed wide ranges within, and large differences between, the cadaveric and imaging PCSA data. Comparison of the PCSA of this study and published literature revealed major differences in the iliopsoas, gluteus minimus, tensor fasciae latae, gemelli, obturator internus, biceps femoris, quadriceps femoris, and the deep leg flexor muscles.\n                These volume-derived PCSAs of the pelvic and lower limb muscles alongside the data synthesised from the literature may serve as a basis for comparative and biomechanical studies of the living and healthy young, and enable calculation of muscle forces. Comparison of the literature revealed large variations in PCSA from each of the different investigative modalities, hampering comparability between studies. Sample size, age, post-mortem changes of muscle tone, chemical fixation of cadaveric tissues, and the underlying physics of the imaging techniques may potentially influence PCSA calculations.\n\nHammer, Niels\n\n\n"
        },
        {
            "text": "\n1448\nIodine deficiency induces thyroid autoimmune reactivity in Wistar rats.\n\nMooij, P\n\nde Wit, HJ\n\nBloot, AM\n\nWilders-Truschnig, MM\n\nDrexhage, HA\n\nBeiträge in Fachzeitschriften\nISI:A1993LW94200031\n8103449.0\n10.1210/endo.133.3.8103449\nNone\nThe last 2 decades it has become clear that iodine deficiency has a modulating effect on the thyroid autoimmune response in humans. Also, in animals that spontaneously develop autoimmune thyroid disease, evidence is accumulating that a low iodine intake can modulate thyroid autoimmune reactivity. However, it is still not clear what the effect of a low iodine intake on thyroid autoimmune reactivity is in normal nonautoimmune animals. To study the relationship of a dietary low iodine intake on the thyroid autoimmune reactivity in nonautoimmune animals, normal Wistar rats (female) were kept on an enriched iodine diet (daily iodine intake of 100 micrograms iodine), a "for our area normal" (conventional) diet (COD; daily iodine intake of 7 micrograms iodine), a low iodine diet (LID; 2 days of 1% KCLO4, followed by iodine-deficient drinking water/pellets), or an extremely low iodine diet (LID+; 1% KCLO4 continuously in the drinking water and iodine-deficient pellets). The enriched iodine diet rats were euthyroid (T3, approximately 8 nM/liter: T4, approximately 50 nM/liter; TSH, approximately 2 ng/ml), had a normal thyroid weight (approximately 12.5 mg), and showed only minimal signs of local thyroid immune reactivity; low numbers of intrathyroidal dendritic cells (DC; approximately 35 DC/mm2), CD4+ cells (approximately 2 cells/mm2), and CD8+ cells (approximately 2.5 cells/mm2) were found in combination with low anticolloid antibody production (incidence of positive animals, 12.5%). The COD resulted in a normal thyroid function. The rats were euthyroid (range of T3, 1.6-1.2 nM/liter; T4, approximately 50 nM/liter; TSH, approximately 2 ng/ml) and had a normal thyroid weight (approximately 12.5 mg). However, some signs of thyroid autoimmune reactivity were found [number of intrathyroidal DC, approximately 40/mm2; approximately 3 CD4-positive (CD+) cells/mm2; approximately 3 CD8+ cells/mm2; together with a 30% incidence of anticolloid antibodies]. The LID and LID+ not only induced goiter formation [thyroid weight, 27.3 +/- 4.2 mg (mean +/- SD) after 12 weeks of LID and 38.4 +/- 5.3 mg after 4 weeks of LID+] and low production of T4 by the thyroid [28 +/- 3 nM/liter (mean +/- SD)] after 12 weeks of LID and 14 +/- 3 nM/liter after 2 weeks of LID+], but also induced various signs of thyroid autoimmune reactivity.(ABSTRACT TRUNCATED AT 400 WORDS)\n\n\n"
        },
        {
            "text": "\n4676\nVisual rating of age-related white matter changes on magnetic resonance imaging: scale comparison, interrater agreement, and correlations with quantitative measurements.\n\nKapeller, P\n\nBarber, R\n\nVermeulen, RJ\n\nAdèr, H\n\nScheltens, P\n\nFreidl, W\n\nAlmkvist, O\n\nMoretti, M\n\ndel Ser, T\n\nVaghfeldt, P\n\nEnzinger, C\n\nBarkhof, F\n\nInzitari, D\n\nErkinjunti, T\n\nSchmidt, R\n\nFazekas, F\n\nEuropean Task Force of Age Related White Matter Changes\n\nBeiträge in Fachzeitschriften\nISI:000180954600040\n12574557.0\n10.1161%2F01.STR.0000049766.26453.E9\nNone\nBACKGROUND AND PURPOSE: To provide further insight into the MRI assessment of age-related white matter changes (ARWMCs) with visual rating scales, 3 raters with different levels of experience tested the interrater agreement and comparability of 3 widely used rating scales in a cross-sectional and follow-up setting. Furthermore, the correlation between visual ratings and quantitative volumetric measurement was assessed. METHODS: Three raters from different sites using 3 established rating scales (Manolio, Fazekas and Schmidt, Scheltens) evaluated 74 baseline and follow-up scans from 5 European centers. One investigator also rated baseline scans in a set of 255 participants of the Austrian Stroke Prevention Study (ASPS) and measured the volume of ARWMCs. RESULTS: The interrater agreement for the baseline investigation was fair to good for all scales (kappa values, 0.59 to 0.78). On the follow-up scans, all 3 raters depicted significant ARWMC progression; however, the direct interrater agreement for this task was poor (kappa, 0.19 to 0.39). Comparison of the interrater reliability between the 3 scales revealed a statistical significant difference between the scale of Manolio and that of Fazekas and Schmidt for the baseline investigation (z value, -2.9676; P=0.003), demonstrating better interrater agreement for the Fazekas and Schmidt scale. The rating results obtained with all 3 scales were highly correlated with each other (Spearman rank correlation, 0.712 to 0.806; P< or =0.01), and there was significant agreement between all 3 visual rating scales and the quantitative volumetric measurement of ARWMC (Kendall W, 0.37, 0.48, and 0.57; P<0.001). CONCLUSIONS: Our data demonstrate that the 3 rating scales studied reflect the actual volume of ARWMCs well. The 2 scales that provide more detailed information on ARWMCs seemed preferential compared with the 1 that yields more global information. The visual assessment of ARWMC progression remains problematic and may require modifications or extensions of existing rating scales.\n\nEnzinger, Christian\n\nFazekas, Franz\n\nFreidl, Wolfgang\n\nKapeller, Peter\n\nSchmidt, Reinhold\n\n\n"
        },
        {
            "text": "\n119133\nRole of Vascular Endothelial Growth Factor Polymorphisms in the Treatment Success in Patients with Wet Age-related Macular Degeneration.\n\nBoltz, A\n\nRuiâ, M\n\nJonas, JB\n\nTao, Y\n\nRensch, F\n\nWeger, M\n\nGarhöfer, G\n\nFrantal, S\n\nEl-Shabrawi, Y\n\nSchmetterer, L\n\nBeiträge in Fachzeitschriften\nISI:000307080100019\n22521084.0\n10.1016/j.ophtha.2012.02.001\nNone\nPurpose: Along with environmental risk factors such as smoking, hypertension, and atherosclerosis, genetic susceptibility is a primary contributor to the development and progression of exudative age-related macular degeneration (AMD). Vascular endothelial growth factor (VEGF) is a central angiogenic regulator and there has been general agreement now that it is an important trigger for the progression of exudative AMD. In the present study, we tested the hypothesis that VEGF gene polymorphisms play a role in the treatment success with VEGF inhibitors in patients with exudative AMD. Design: Prospective cohort study. Participants: We included 185 eyes of 141 patients with exudative AMD who were scheduled for their first treatment with intravitreally administered bevacizumab in this trial. Methods: All patients were aged >50 years and had angiographically verified exudative AMD. Blood from the finger pad was collected on blood cards for genotyping for the VEGF polymorphisms rs1413711, rs3025039, rs2010963, rs833061, rs699947, rs3024997, and rs1005230. At each follow-up visit, visual acuity was reassessed and an ophthalmic examination was carried out. Visual acuity outcome, number of retreatments, and overall time of treatment were analyzed in dependence of the VEGF polymorphisms. Main Outcome Measures: Mean change in visual acuity at the end of the treatment period. Results: The included patients were reinjected with bevacizumab 1 to 15 times, resulting in a total treatment period of 42 to 1182 days. In univariate analysis only the G/G genotypes of rs3024997 and rs2010963 compared with all other 5 single nucleotide polymorphisms (SNPs) showed a significantly lower visual acuity at the end of treatment. In multivariate analysis including parameters such as time, baseline visual acuity, and number of reinjections, none of the SNPs showed a significant correlation. Conclusions: The current study indicates that VEGF polymorphisms are not major predictors of anti-VEGF treatment success in patients with exudative AMD. Financial Disclosure(s): The authors have no proprietary or commercial interest in any of the materials discussed in this article. Ophthalmology 2012;119:1615-1620 (C) 2012 by the American Academy of Ophthalmology.\n\nEl-Shabrawi, Yosuf\n\nWeger, Martin\n\n\n"
        },
        {
            "text": "\n133465\nHypoxia increases membrane metallo-endopeptidase expression in a novel lung cancer ex vivo model - role of tumor stroma cells.\n\nLeithner, K\n\nWohlkoenig, C\n\nStacher, E\n\nLindenmann, J\n\nHofmann, NA\n\nGallé, B\n\nGuelly, C\n\nQuehenberger, F\n\nStiegler, P\n\nSmolle-Jüttner, FM\n\nPhilipsen, S\n\nPopper, HH\n\nHrzenjak, A\n\nOlschewski, A\n\nOlschewski, H\n\nBeiträge in Fachzeitschriften\nISI:000331090500001\n24460801.0\n10.1186/1471-2407-14-40\nPMC3905926\nHypoxia-induced genes are potential targets in cancer therapy. Responses to hypoxia have been extensively studied in vitro, however, they may differ in vivo due to the specific tumor microenvironment. In this study gene expression profiles were obtained from fresh human lung cancer tissue fragments cultured ex vivo under different oxygen concentrations in order to study responses to hypoxia in a model that mimics human lung cancer in vivo.\n                Non-small cell lung cancer (NSCLC) fragments from altogether 70 patients were maintained ex vivo in normoxia or hypoxia in short-term culture. Viability, apoptosis rates and tissue hypoxia were assessed. Gene expression profiles were studied using Affymetrix GeneChip 1.0 ST microarrays.\n                Apoptosis rates were comparable in normoxia and hypoxia despite different oxygenation levels, suggesting adaptation of tumor cells to hypoxia. Gene expression profiles in hypoxic compared to normoxic fragments largely overlapped with published hypoxia-signatures. While most of these genes were up-regulated by hypoxia also in NSCLC cell lines, membrane metallo-endopeptidase (MME, neprilysin, CD10) expression was not increased in hypoxia in NSCLC cell lines, but in carcinoma-associated fibroblasts isolated from non-small cell lung cancers. High MME expression was significantly associated with poor overall survival in 342 NSCLC patients in a meta-analysis of published microarray datasets.\n                The novel ex vivo model allowed for the first time to analyze hypoxia-regulated gene expression in preserved human lung cancer tissue. Gene expression profiles in human hypoxic lung cancer tissue overlapped with hypoxia-signatures from cancer cell lines, however, the elastase MME was identified as a novel hypoxia-induced gene in lung cancer. Due to the lack of hypoxia effects on MME expression in NSCLC cell lines in contrast to carcinoma-associated fibroblasts, a direct up-regulation of stroma fibroblast MME expression under hypoxia might contribute to enhanced aggressiveness of hypoxic cancers.\n\nGallé, Birgit\n\nGülly, Christian\n\nHrzenjak, Andelko\n\nLeithner, Katharina\n\nLindenmann, Jörg\n\nOlschewski, Andrea\n\nOlschewski, Horst\n\nPopper, Helmuth\n\nQuehenberger, Franz\n\nSmolle-Juettner, Freyja-Maria\n\nStiegler, Philipp\n\n\n"
        },
        {
            "text": "\n186822\nEffect of variations in tissue-level ductility on human vertebral strength.\n\nSadoughi, S\n\nVom Scheidt, A\n\nNawathe, S\n\nZhu, S\n\nMoini, A\n\nKeaveny, TM\n\nBeiträge in Fachzeitschriften\nNone\n32454256.0\n10.1016/j.bone.2020.115445\nNone\nAlthough the ductility of bone tissue is a unique element of bone quality and varies with age and across the population, the extent to which and mechanisms by which typical population-variations in tissue-level ductility can alter whole-bone strength remains unclear. To provide insight, we conducted a finite element analysis parameter study of whole-vertebral (monotonic) compressive strength on six human L1 vertebrae. Each model was generated from micro-CT scans, capturing the trabecular micro-architecture in detail, and included a non-linear constitutive model for the bone tissue that allowed for plastic yielding, different strengths in tension and compression, large deformations, and, uniquely, localized damage once a specified limit in tissue-level ultimate strain was exceeded. Those strain limits were based on reported (mean ± SD) values from cadaver experiments (8.8 ± 3.7% strain for trabecular tissue and 2.2 ± 0.9% for cortical tissue). In the parameter study, the strain limits were varied by ±1 SD from their mean values, for a combination of nine analyses per specimen; bounding values of zero and unlimited post-yield strain were also modeled. The main outcomes from the finite element analysis were the vertebral compressive strength and the amount of failed (yielded or damaged) tissue at the overall structure-level failure. Compared to a reference case of using the mean values of ultimate strain, we found that varying both trabecular and cortical tissue ultimate strains by ±1 SD changed the computed vertebral strength by (mean ± SD) ±6.9 ± 1.1% on average. Mechanistically, that modest effect arose because the proportion of yielded tissue (without damage) was 0.9 ± 0.3% of all the bone tissue across the nine cases and the proportion of damaged tissue (i.e. tissue exceeding the prescribed tissue-level ultimate strain) was 0.2 ± 0.1%. If the types of variations in tissue-level ductility investigated here accurately represent real typical variations in the population, the consistency of our results across specimens and the modest effect size together suggest that typical variations in tissue-level ductility only have a modest impact on vertebral compressive strength, in large part because so few trabeculae are damaged at the load capacity of the bone.\n                Copyright © 2020 Elsevier Inc. All rights reserved.\n\nvom Scheidt, Annika\n\n\n"
        },
        {
            "text": "\n187103\nInfluence of tumor-infiltrating immune cells on local control rate, distant metastasis, and survival in patients with soft tissue sarcoma.\n\nSmolle, MA\n\nHerbsthofer, L\n\nGoda, M\n\nGranegger, B\n\nBrcic, I\n\nBergovec, M\n\nScheipl, S\n\nPrietl, B\n\nEl-Heliebi, A\n\nPichler, M\n\nGerger, A\n\nPosch, F\n\nTomberger, M\n\nLópez-García, P\n\nFeichtinger, J\n\nBaumgartner, C\n\nLeithner, A\n\nLiegl-Atzwanger, B\n\nSzkandera, J\n\nBeiträge in Fachzeitschriften\nISI:000629348000001\n33763294.0\n10.1080/2162402X.2021.1896658\nPMC7954425\nSoft tissue sarcomas (STS) are considered non-immunogenic, although distinct entities respond to anti-tumor agents targeting the tumor microenvironment. This study's aims were to investigate relationships between tumor-infiltrating immune cells and patient/tumor-related factors, and assess their prognostic value for local recurrence (LR), distant metastasis (DM), and overall survival (OS). One-hundred-eighty-eight STS-patients (87 females [46.3%]; median age: 62.5 years) were retrospectively analyzed. Tissue microarrays (in total 1266 cores) were stained with multiplex immunohistochemistry and analyzed with multispectral imaging. Seven cell types were differentiated depending on marker profiles (CD3+, CD3+ CD4+ helper, CD3+ CD8+ cytotoxic, CD3+ CD4+ CD45RO+ helper memory, CD3+ CD8+ CD45RO+ cytotoxic memory T-cells; CD20 + B-cells; CD68+ macrophages). Correlations between phenotype abundance and variables were analyzed. Uni- and multivariate Fine&Gray and Cox-regression models were constructed to investigate prognostic variables. Model calibration was assessed with C-index. IHC-findings were validated with TCGA-SARC gene expression data of genes specific for macrophages, T- and B-cells. B-cell percentage was lower in patients older than 62.5 years (p = .013), whilst macrophage percentage was higher (p = .002). High B-cell (p = .035) and macrophage levels (p = .003) were associated with increased LR-risk in the univariate analysis. In the multivariate setting, high macrophage levels (p = .014) were associated with increased LR-risk, irrespective of margins, age, gender or B-cells. Other immune cells were not associated with outcome events. High macrophage levels were a poor prognostic factor for LR, irrespective of margins, B-cells, gender and age. Thus, anti-tumor, macrophage-targeting agents may be applied more frequently in tumors with enhanced macrophage infiltration.\n                © 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.\n\nBaumgartner, Claudia\n\nBergovec, Marko\n\nBrcic, Iva\n\nEl-Heliebi, Amin\n\nFeichtinger, Julia\n\nGerger, Armin\n\nLeithner, Andreas\n\nLiegl-Atzwanger, Bernadette\n\nLopez Garcia, Pablo\n\nPichler, Martin\n\nPosch, Florian\n\nPrietl, Barbara\n\nScheipl, Susanne\n\nSmolle, Maria Anna\n\nSzkandera, Joanna\n\n\n"
        },
        {
            "text": "\n190\nDosimetry of intracavitary placements for uterine and cervical carcinoma: results of orthogonal film, TLD, and CT-assisted techniques.\n\nKapp, KS\n\nStuecklschweiger, GF\n\nKapp, DS\n\nHackl, AG\n\nBeiträge in Fachzeitschriften\nISI:A1992JL59000001\n1410567.0\n10.1016/0167-8140(92)90372-2\nNone\nA total of 720 192Ir high-dose-rate (HDR) applications in 331 patients with gynecological tumors were analyzed to evaluate the dose to normal tissues from brachytherapy. Based on the calculations of bladder base, bladder neck, and rectal doses derived from orthogonal films the planned tumor dose or fractionation was altered in 20.4% of intracavitary placements (ICP) for cervix carcinoma and 9.2% of ICP for treatment of the vaginal vault. In 13.8% of intracervical and 8.1% of intravaginal treatments calculated doses to both the bladder and rectum were greater than or equal to 140% of the initially planned dose fraction. Doses at the bladder base were significantly higher than at the bladder neck (p less than 0.001). In 17.5% of ICP the dose to the bladder base was at least twice as high as to the bladder neck. The ratio of bladder base dose to the bladder neck was 1.5 (+/- 1.19 SD) for intracervical and 1.46 (+/- 1.14 SD) for intravaginal applications. The comparison of calculated doses from orthogonal films with in-vivo readings showed a good correlation of rectal doses with a correlation coefficient factor of 0.9556. CT-assisted dosimetry, however, revealed that the maximum doses to bladder and rectum were generally higher than those obtained from films with ratios of 1-1.7 (average: 1.44) for the bladder neck, 1-5.4 (average: 2.42) for the bladder base, and 1.1-2.7 (average: 1.37) for the rectum. When doses to the specified reference points of bladder neck and rectum from orthogonal film dosimetry were compared with the corresponding points on CT scans, similar values were obtained for both methods with a maximum deviation of +/- 10%. Despite the determination of multiple reference points our study revealed that this information was inadequate to predict doses to the entire rectum and bladder. If conventional methods are used for dosimetry it is recommended that doses to the bladder base should be routinely calculated, since single point measurements at the bladder neck seriously underestimate the dose to the bladder. Also the rectal dose should be determined at several points over the length of the implant due to the wide range of anatomic variations possible.\n\n\n"
        },
        {
            "text": "\n2741\nTransplantation of related and unrelated umbilical cord blood stem cells in Austria. Austrian Working Party for Stem Cell Transplantation. Austrian Society of Hematology and Oncology.\n\nSchwinger, W\n\nUrban, C\n\nLackner, H\n\nKerbl, R\n\nSovinz, P\n\nGardner, H\n\nPeters, C\n\nNiederwieser, D\n\nFink, FM\n\nKögler, G\n\nBeiträge in Fachzeitschriften\nISI:000080322000003\n10407995.0\nNone\nNone\nAllogeneic bone marrow transplantation is limited by the availability of suitable HLA-matched donors and the risk of graft versus host disease (GvHD). In an attempt to overcome these limitations umbilical cord blood (UCB), has become a further alternative. UCB transplantations in Austria were started in 1991. As of September 31, 1998, six patients have been transplanted. Diagnoses were severe aplastic anaemia (SAA) (n = 2), acute lymphoblastic leukaemia (ALL) (n = 1), familial hemophagocytic syndrome (FHL) (n = 2) and chronic myelomonocytic leukaemia (CMML) (n = 1). Three patients received UCB grafts from HLA-identical siblings and three patients from unrelated donors, of whom two were disparate at two HLA loci (A/B) and one mismatched at one locus (C). Five patients were engrafted with complete donor hematopoiesis, with a median time of 26.5 days (range 14 to 39 days) to an ANC count of > or = 0.5 x 10(9)/L and a median time of 42.5 days (range 24 to 67 days) to a platelet count of > or = 20 x 10(9)/L. One patient with FHL had partial engraftment and died due to reactivation of cytomegalovirus (CMV) infection and CMV pneumonia on day +25. Of the five patients surviving the post-transplant period, one with CMML had a relapse on day +128 and died after a HLA-matched bone marrow transplantation from the same sibling donor in the second relapse. Another patient with ALL relapsed on day +200 but is still alive under palliative treatment; one patient with SAA showed graft rejection and autologous hematopoietic reconstitution and later had a successful CD34(+)-selected allogeneic peripheral stem cell transplant from a C-locus mismatched unrelated donor. Two patients (one with SAA and one with FHL) are alive with complete remission of the underlying disease. This report reflects the experience and results of UCB transplantation in Austria and discusses the position of UCB transplantation in the context of the other stem cell alternatives available today.\n\nKerbl, Reinhold\n\nLackner, Herwig\n\nRitter-Sovinz, Petra\n\nSchwinger, Wolfgang\n\nUrban, Ernst-Christian\n\n\n"
        },
        {
            "text": "\n2868\nXenoreactive natural antibodies and induced antibodies--their effects of beating cardiomyocytes as a model of a xenograft.\n\nMüller-Werdan, U\n\nKoidl, B\n\nAutenrieth, A\n\nKlein, D\n\nWerdan, K\n\nHammer, C\n\nBeiträge in Fachzeitschriften\nISI:A1996VM24200042\n8901489.0\n10.1007%2FBF00240065\nNone\nXenotransplantation has been complicated by hyperacute rejection reactions, which are supposedly triggered by preformed natural antibodies (PNAb) of the recipient organism, whereas the role of antibodies specifically induced by previous antigen contact (IAb) is less clear. Primary cultures of spontaneously beating neonatal rat cardiomyocytes were used as a model of the heart to elaborate the effects of both PNAb and IAb from xenogeneic species and to investigate into their mechanisms of action. An experimental setup allowing for rapid medium exchange under continuous observation was employed. Sera containing PNAb reproducibly bring about a stereotype pattern of altered contractility including an initial increase in beating frequency followed by a temporary cessation of beating within the first minutes after administration. After recovery of spontaneous contractions, the cells within the monolayer exhibited a dissociation of the synchronicity of the beating persisting for several hours. The temporary pause in beating was prevented by a very high extracellular calcium concentration, but not by extracellular electrical stimulation sufficient to trigger contractions in control cells. Electrophysiological measurements carried out in adult ventricular guinea pig heart muscle cells under the same experimental conditions revealed an increase of the excitation threshold of the cells after application of sera containing PNAb due to an enhanced input resistance. These results indicate that the effect of PNAb is the consequence rather of a generally reduced excitability of the cell than of the inhibition of a singular ionic conductance. After specific absorption of PNAb directed against rat antigens beating of neonatal rate cardiomyocytes ensued without interruption. Sera specimens devoid of complement produced similar effects on contractility, although the duration of the standstill period was significantly shorter. The increase in input resistance visualized in guinea pig myocytes was absent after removing PNAb against guinea pig antigens but not after absorbing PNAb directed against rat epitopes. Signs of a permanent cytotoxicity after the administration of PNAb were lacking in all experiments. IAb against rat heart tissue raised in rabbits stopped the contractions of neonatal rat cardiomyocytes within 30 min after administration irreversibly and lead concentration-dependently to a destruction of the cells.\n\nKoidl, Bernd\n\n\n"
        },
        {
            "text": "\n20039\nCo-expression of ICAM-1, VCAM-1, ELAM-1 and Hsp60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins\n\nAmberger, A\n\nMaczek, C\n\nJürgens, G\n\nMichaelis, D\n\nSchett, G\n\nTrieb, K\n\nEberl, T\n\nJindal, S\n\nXu, QB\n\nWick, G\n\nBeiträge in Fachzeitschriften\nISI:A1997XG20000004\nNone\n10.1379/1466-1268(1997)002<0094:CEOIVE>2.3.CO;2\nNone\nT-cells and monocytes are the first cells infiltrating the arterial intima during the early stages of atherogenesis, Recently our laboratory has provided evidence that T-cells isolated from atherosclerotic intima reacts against heat shock protein 60 (Hsp60). Transmigration of activated T-cells into the intima is mediated by adhesion molecules (ICAM-1; VCAM-1; ELAM-1) expressed on activated endothelial cells, Here we studied the potential of cytokines (TNF-alpha, IFN-gamma, IL-l), Escherichia coli lipopolysaccharide (LPS), native and oxidized low-density lipoprotein (LDL; oxLDL) and high temperature to induce adhesion molecules as well as Hsp60 and Hsp70 expression in human endothelial cells (EC). On Northern blots, a strong signal for ICAM-1, VCAM-1 and ELAM-1 was detected after 4 h, which thereafter declined, but did not reach the basal level of untreated control cells, Heat shock induced the expression of Hsp60 and Hsp70 but not of adhesion molecules. EC were cultivated in serum-free medium, which led to the expression of adhesion molecule transcripts, Addition of LDL or oxLDL to these ECs did not alter the expression of these transcripts, The production of adhesion molecule proteins was analysed by flow cytometry. In human venous endothelial cells (HVEC) and human arterial endothelial cells (HAEC) ICAM-1 and VCAM-1 production was permanently highly induced, whereas the high level of ELAM-1 production at 4 h disappeared after 24 h, Furthermore, only HAEC, but not HVEC, produced ICAM-1, VCAM-1 and ELAM-1 after stress by moderately and highly oxLDL, LDL and oxLDL did not induce the production of Hsp60 and Hsp70. The present study demonstrates the co-expression of Hsp60 and adhesion molecules in arterial and venous EC in response to cytokine and LPS exposure, and that oxLDL is an efficient inducer of adhesion molecules in arterial EC and not in venous EC. These features provide the prerequisites for a cellular immune reaction against Hsp60 expressed by stressed EC in the inital stages of atherosclerosis.\n\nJürgens, Günther\n\n\n"
        },
        {
            "text": "\n26438\nArteries in the posterior cervical triangle in man.\n\nWeiglein, AH\n\nMoriggl, B\n\nSchalk, C\n\nKünzel, KH\n\nMüller, U\n\nBeiträge in Fachzeitschriften\nISI:000233026300001\n16187318.0\n10.1002/ca.20143\nNone\nDue to frequent changes in the anatomical nomenclature of the arteries in the posterior cervical triangle (lateral cervical region), anatomical and surgical papers relating to these topics are sometimes difficult to understand and are hard to compare. These changes, coupled with improper knowledge of the gross anatomy and nomenclature of the arteries in the posterior cervical triangle, have presented difficulties in musculocutaneous flap planning, especially in plastic and reconstructive surgery. As an illustration of this concern, the term, transverse cervical artery (A. transversa colli [cervicis]), and its associated branches, have been used frequently over the past several decades with different meanings. In an effort to address this nomenclature challenge and to offer a rational basis for arguing specific name changes, a total of 498 neck-halves were investigated in Graz, Innsbruck, and Munich. Lateral neck dissections were carried out to expose the subclavian artery and those branches destined for the posterior cervical triangle, specifically, the superficial cervical artery, the dorsal scapular artery, and the suprascapular artery. The course of these arteries and details of their origins and branching patterns were documented. Several arose either as direct branches or from trunks. The convention used in labeling trunks was similar to that described for other trunk formations in the body (e.g., linguo-facial trunk). Four trunks were observed and named according to the branches that arose from each. A cervico-dorsal trunk gave origin to the superficial cervical and dorsal scapular arteries, and was found in 30% of cases. A cervico-scapular trunk gave rise to the superficial cervical and suprascapular arteries in 22% of cases, and a dorso-scapular trunk provided origins for the dorsal scapular and suprascapular arteries in 4% of cases. A cervico-dorso-scapular trunk gave origin to the superficial cervical artery, the dorsal scapular artery, and the suprascapular artery, and was found in 24% of cases. Each of these trunks, in turn, arose from either the subclavian artery or from the thyrocervical trunk. This labeling convention necessitated omitting the term, transverse cervical artery, because this term has become inherently imprecise and variously used over the years. This study describes a simple, uniform, and rational basis for standardizing the nomenclature of the arteries in the posterior cervical triangle.\n\n\n"
        },
        {
            "text": "\n81171\nLipoaugmentation of the vocal folds: a survey on alternative donor sites for graft harvesting.\n\nProdinger, PM\n\nWindisch, G\n\nHammer, GP\n\nAnderhuber, F\n\nFriedrich, G\n\nBeiträge in Fachzeitschriften\nISI:000269735200017\n18479890.0\n10.1016/j.jvoice.2008.01.015\nNone\nLipoaugmentation is a treatment option for patients suffering from glottic insufficiency. Autologous fat is a nearly ideal material for vocal-fold augmentation from the view of biocompatibility and viscoelasticity, but there is still the problem of high graft resorption. As distribution and biological behavior of fatty tissue is very different in the human body, the aim of the study was to elucidate possible donor sites with respect to the quantity of harvested fat, the surgical accessibility to the region, the donor site morbidity and possibility of aesthetic defects and the quality of harvested tissue. Possible donor sites for harvesting were examined by magnetic resonance imaging in thirty-five patients with special emphasis to the buccal fat pad, the neck, the dorsolateral side of the proximal upper extremity, the subcutaneous layer of the abdominal wall, the superficial trochanteric region, the medial thigh, and the infrapatellar fat pad. Identified regions that failed to be chosen into consideration because of an elaborate surgical approach (superficial axillary's space, ischio-anal fossa, subcutaneous layer of buttock, popliteal fossa) were not taken into consideration. The mean volume of the buccal fat was 3.994 cm(3); the average thickness of the fat at the level of C7 was 1.721 cm, the mean value in the upper extremities was 1.913 cm laterally and 1.275 cm dorsally. The subcutaneous fat of the abdominal wall was divided into a superficial compartment (mean: 1.527 cm) and a deep one (average: 3.545 cm). In the superficial trochanteric region, the mean thickness was 2.536 cm, in the medial thigh 2.127 cm; the mean volume of the infrapatellar fat pad was 20.198 cm(3). All regions of interest showed reproducible and sufficient amounts of harvestable tissue, we found significant intersexual differences in dorsolateral side of the upper arm, subcutaneous layer of the abdominal wall and superficial trochanteric region. When harvesting subcutaneous tissue of the abdominal wall, grafts of the deep layer should be preferred, in the upper extremity the deep, muscle-neighbored parts. An alternative method is the surgically accessible fat of the neck. Solid fat pads could be harvested from the buccal region or the infrapatellar fat.\n\nFriedrich, Gerhard\n\nHammer, Georg\n\n\n"
        },
        {
            "text": "\n87624\nEndocrine therapy plus zoledronic acid in premenopausal breast cancer.\n\nGnant, M\n\nMlineritsch, B\n\nSchippinger, W\n\nLuschin-Ebengreuth, G\n\nPöstlberger, S\n\nMenzel, C\n\nJakesz, R\n\nSeifert, M\n\nHubalek, M\n\nBjelic-Radisic, V\n\nSamonigg, H\n\nTausch, C\n\nEidtmann, H\n\nSteger, G\n\nKwasny, W\n\nDubsky, P\n\nFridrik, M\n\nFitzal, F\n\nStierer, M\n\nRücklinger, E\n\nGreil, R\n\nABCSG-12 Trial Investigators\n\nMarth, C\n\nBeiträge in Fachzeitschriften\nISI:000263260500005\n19213681.0\n10.1056/NEJMoa0806285\nNone\nBackground Ovarian suppression plus tamoxifen is a standard adjuvant treatment in premenopausal women with endocrine- responsive breast cancer. Aromatase inhibitors are superior to tamoxifen in postmenopausal patients, and preclinical data suggest that zoledronic acid has antitumor properties. Methods We examined the effect of adding zoledronic acid to a combination of either goserelin and tamoxifen or goserelin and anastrozole in premenopausal women with endocrineresponsive early breast cancer. We randomly assigned 1803 patients to receive goserelin ( 3.6 mg given subcutaneously every 28 days) plus tamoxifen ( 20 mg per day given orally) or anastrozole ( 1 mg per day given orally) with or without zoledronic acid ( 4 mg given intravenously every 6 months) for 3 years. The primary end point was disease- free survival; recurrence- free survival and overall survival were secondary end points. Results After a median follow- up of 47.8 months, 137 events had occurred, with disease- free survival rates of 92.8% in the tamoxifen group, 92.0% in the anastrozole group, 90.8% in the group that received endocrine therapy alone, and 94.0% in the group that received endocrine therapy with zoledronic acid. There was no significant difference in disease- free survival between the anastrozole and tamoxifen groups ( hazard ratio for disease progression in the anastrozole group, 1.10; 95% confidence interval [ CI], 0.78 to 1.53; P = 0.59). The addition of zoledronic acid to endocrine therapy, as compared with endocrine therapy without zoledronic acid, resulted in an absolute reduction of 3.2 percentage points and a relative reduction of 36% in the risk of disease progression ( hazard ratio, 0.64; 95% CI, 0.46 to 0.91; P = 0.01); the addition of zoledronic acid did not significantly reduce the risk of death ( hazard ratio, 0.60; 95% CI, 0.32 to 1.11; P = 0.11). Adverse events were consistent with known drug- safety profiles. Conclusions The addition of zoledronic acid to adjuvant endocrine therapy improves disease- free survival in premenopausal patients with estrogen- responsive early breast cancer. (ClinicalTrials. gov number, NCT00295646.).\n\nBauernhofer, Thomas\n\nBjelic-Radisic, Vesna\n\nHofmann, Guenter\n\nLuschin-Ebengreuth, Gero\n\nSamonigg, Hellmut\n\nSchippinger, Walter\n\n\n"
        },
        {
            "text": "\n114207\nDrug-induced torsade de pointes arrhythmias in the chronic AV block dog are perpetuated by focal activity.\n\nBoulaksil, M\n\nJungschleger, JG\n\nAntoons, G\n\nHoutman, MJ\n\nde Boer, TP\n\nWilders, R\n\nBeekman, JD\n\nMaessen, JG\n\nvan der Hulst, FF\n\nvan der Heyden, MA\n\nvan Veen, TA\n\nvan Rijen, HV\n\nde Bakker, JM\n\nVos, MA\n\nBeiträge in Fachzeitschriften\nISI:000293898900031\n21622813.0\n10.1161/CIRCEP.110.958991\nNone\nBackground-The electrically remodeled canine heart after chronic AV block (CAVB) has a high susceptibility for drug-induced torsade de pointes (TdP) arrhythmias. Although focal mechanisms have been considered for initiation, there is still controversy about whether reentry is the dominant mechanism for perpetuation of TdP. In this animal model with known nonuniform prolongation of repolarization, the mechanism of perpetuation of TdP arrhythmia was explored. Methods and Results-Seventeen TdP-sensitive CAVB and 10 sinus rhythm (SR) dogs were studied. In 6 animals, 66 needle electrodes were evenly distributed transmurally to record 240 unipolar local electrograms simultaneously. Activation times and activation recovery intervals were determined before and during ibutilide-induced TdP. In 12 CAVB and 9 SR dogs, left ventricular (LV) and right ventricular (RV) epicardial electrograms were recorded with a 208-point multiterminal grid electrode allowing conduction velocity (CV) and ventricular effective refractory period (VERP) measurements. Biopsy specimens were processed for connexin43 (Cx43) expression and collagen content. Ventricular myocytes were isolated to determine sodium current (I(Na)) density and cell dimensions. Computer simulations were used to assess the effects of changes therein. In CAVB, VERP and ARI were increased, whereas CV was unaltered in LV. Transversal but not longitudinal CV was increased in RV. I(Na) was reduced by 37% in LV but unaltered in RV. LV and RV cell size were increased, but collagen and Cx43 content remained unchanged. Simulations showed increase in CV of RV as a consequence of increased cell size at normal I(Na). Ibutilide increased ARI, ERP, and maximal transmural dispersion of ERP (45 +/- 25 to 120 +/- 65 ms; P<0.05). Twenty-eight of 47 episodes of self-terminating TdP (43 +/- 72 beats) were analyzed. The majority (>90%) of beats were focal; reentry was observed only occasionally. Conclusions-Focal activity is the dominant mechanism involved in perpetuation of ibutilide-induced TdP in CAVB dogs based on detailed 3D mapping. This conclusion is in line with unaltered conduction and documented increase in VERP. (Circ Arrhythm Electrophysiol. 2011;4:566-576.)\n\n\n"
        },
        {
            "text": "\n145229\nCharacteristics and Outcomes of Granulomatosis With Polyangiitis (Wegener) and Microscopic Polyangiitis Requiring Renal Replacement Therapy: Results From the European Renal Association-European Dialysis and Transplant Association Registry.\n\nHruskova, Z\n\nStel, VS\n\nJayne, D\n\nAasarød, K\n\nDe Meester, J\n\nEkstrand, A\n\nEller, K\n\nHeaf, JG\n\nHoitsma, A\n\nMartos Jimenéz, C\n\nRavani, P\n\nWanner, C\n\nTesar, V\n\nJager, KJ\n\nBeiträge in Fachzeitschriften\nISI:000361820100017\n25975963.0\n10.1053/j.ajkd.2015.03.025\nNone\nThis study describes the incidence and outcomes of European patients requiring renal replacement therapy (RRT) for kidney failure due to antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).\n                Cohort study.\n                12 renal registries providing individual RRT patient data to the European Renal Association-European Dialysis and Transplant Association (ERA-EDTA) Registry in 1993-2012 participated.\n                Cause of primary kidney disease: AAV (ie, granulomatosis with polyangiitis [Wegener] and microscopic polyangiitis) versus 3 separate matched control groups without AAV: (1) primary glomerulonephritis, (2) diabetes mellitus, and (3) disease other than diabetes mellitus as the cause of primary kidney disease, including glomerulonephritis (termed "nondiabetes").\n                Incidence, causes of death, and survival.\n                ERA-EDTA primary renal disease codes.\n                2, 11 patients with AAV (1, 55, granulomatosis with polyangiitis; 756, microscopic polyangiitis) were identified, representing an incidence of 1.05 per million population (pmp) for granulomatosis with polyangiitis (predominating in Northern Europe) and 0.45 pmp for microscopic polyangiitis (prevailing in Southern Europe). Kidney transplantation was performed in 558 (22.2%) patients with vasculitis. The 10-year probability for survival on RRT after day 91 was 32.5% (95% CI, 29.9%-35.1%) in patients with vasculitis. Survival on RRT after day 91 did not differ between AAV and matched nondiabetes patients. Patient and transplant survival after kidney transplantation, adjusted for time period and country, was better in AAV than in matched nondiabetes patients (HRs of 0.81 [95% CI, 0.67-0.99] and 0.82 [95% CI, 0.69-0.96], respectively).\n                No data for extrarenal manifestations, treatment, and relapses.\n                Geographical differences in the incidence of RRT for kidney failure due to granulomatosis with polyangiitis and microscopic polyangiitis copied their distribution in the general population. Overall survival on RRT after day 91 for patients with AAV was similar to that for patients with nondiabetes diagnoses. Our results suggest that patients with AAV are suitable candidates for kidney transplantation with favorable survival outcomes.\n                Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.\n\nEller, Kathrin\n\n\n"
        }
    ]
}