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"text": "\n114050\nAccuracy in melanoma detection: A 10-year multicenter survey.\n\nArgenziano, G\n\nCerroni, L\n\nZalaudek, I\n\nStaibano, S\n\nHofmann-Wellenhof, R\n\nArpaia, N\n\nBakos, RM\n\nBalme, B\n\nBandic, J\n\nBandelloni, R\n\nBrunasso, AM\n\nCabo, H\n\nCalcara, DA\n\nCarlos-Ortega, B\n\nCarvalho, AC\n\nCasas, G\n\nDong, H\n\nFerrara, G\n\nFilotico, R\n\nGmez, G\n\nHalpern, A\n\nIlardi, G\n\nIshiko, A\n\nKandiloglu, G\n\nKawasaki, H\n\nKobayashi, K\n\nKoga, H\n\nKovalyshyn, I\n\nLangford, D\n\nLiu, X\n\nMarghoob, AA\n\nMascolo, M\n\nMassone, C\n\nMazzoni, L\n\nMenzies, S\n\nMinagawa, A\n\nNugnes, L\n\nOzdemir, F\n\nPellacani, G\n\nSeidenari, S\n\nSiamas, K\n\nStanganelli, I\n\nStoecker, WV\n\nTanaka, M\n\nThomas, L\n\nTschandl, P\n\nKittler, H\n\nBeiträge in Fachzeitschriften\nISI:000305335900018\n21982636.0\n10.1016/j.jaad.2011.07.019\nNone\nEarly excision is the only strategy to reduce melanoma mortality, but unnecessary excision of benign lesions increases morbidity and healthcare costs.\n To assess accuracy in melanoma detection based on number-needed-to-excise (NNE) values over a 10-year period.\n Information was retrieved on all histopathologically confirmed cutaneous melanomas or melanocytic nevi that were excised between 1998 and 2007 at participating clinics. NNE values were calculated by dividing the total number of excised lesions by the number of melanomas. Analyses included changes in NNE over time, differences in NNE between specialized clinical settings (SCS) versus non-specialized clinical settings (NSCS), and patient factors influencing NNE.\n The participating clinics contributed a total of 300, 15 cases, including 17, 72 melanomas and 283, 43 melanocytic nevi. The overall NNE values achieved in SCS and NSCS in the 10-year period were 8.7 and 29.4, respectively. The NNE improved over time in SCS (from 12.8 to 6.8), but appeared unchanged in NSCS. Most of the effect on NNE in SCS was due to a greater number of excised melanomas. Higher NNE values were observed in patients younger than 40 years and for lesions located on the trunk.\n No data concerning the use of dermatoscopy and digital monitoring procedures were collected from the participating centers.\n Over the 10-year study period, accuracy in melanoma detection improved only in specialized clinics maybe because of a larger use of new diagnostic techniques such as dermatoscopy.\n Copyright © 2011 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.\n\nCerroni, Lorenzo\n\nHofmann-Wellenhof, Rainer\n\nZalaudek, Iris\n\n\n"
},
{
"text": "\n129654\nPrediction of Cancer Specific Survival After Radical Nephroureterectomy for Upper Tract Urothelial Carcinoma: Development of an Optimized Postoperative Nomogram Using Decision Curve Analysis.\n\nRoupret, M\n\nHupertan, V\n\nSeisen, T\n\nColin, P\n\nXylinas, E\n\nYates, DR\n\nFajkovic, H\n\nLotan, Y\n\nRaman, JD\n\nZigeuner, R\n\nRemzi, M\n\nBolenz, C\n\nNovara, G\n\nKassouf, W\n\nOuzzane, A\n\nRozet, F\n\nCussenot, O\n\nMartinez-Salamanca, JI\n\nFritsche, HM\n\nWalton, TJ\n\nWood, CG\n\nBensalah, K\n\nKarakiewicz, PI\n\nMontorsi, F\n\nMargulis, V\n\nShariat, SF\n\n\n\nBeiträge in Fachzeitschriften\nISI:000319262900012\n23103802.0\n10.1016/j.juro.2012.10.057\nNone\nPurpose: We conceived and proposed a unique and optimized nomogram to predict cancer specific survival after radical nephroureterectomy in patients with upper tract urothelial carcinoma by merging the 2 largest multicenter data sets reported in this population. Materials and Methods: The international and the French national collaborative groups on upper tract urothelial carcinoma pooled data on 3, 87 patients treated with radical nephroureterectomy for whom full data for nomogram development were available. The merged study population was randomly split into the development cohort (2, 71) and the external validation cohort (1, 16). Cox regressions were used for univariable and multivariable analyses, and to build different models. The ultimate reduced nomogram was assessed using Harrell's concordance index (c-index) and decision curve analysis. Results: Of the 2, 71 patients in the nomogram development cohort 510 (21.5%) died of upper tract urothelial carcinoma during followup. The actuarial cancer specific survival probability at 5 years was 73.7% (95% CI 71.9-75.6). Decision curve analysis revealed that the use of the best model was associated with benefit gains relative to the prediction of cancer specific survival. The optimized nomogram included only 5 variables associated with cancer specific survival on multivariable analysis, those of age (p = 0.001), T stage (p <0.001), N stage (p = 0.001), architecture (p = 0.02) and lymphovascular invasion (p = 0.001). The discriminative accuracy of the nomogram was 0.8 (95% CI 0.77-0.86). Conclusions: Using standard pathological features obtained from the largest data set of upper tract urothelial carcinomas worldwide, we devised and validated an accurate and ultimate nomogram, superior to any single clinical variable, for predicting cancer specific survival after radical nephroureterectomy.\n\nZigeuner, Richard\n\n\n"
},
{
"text": "\n132193\nSubclinical abnormalities in sarcoplasmic reticulum Ca(2+) release promote eccentric myocardial remodeling and pump failure death in response to pressure overload.\n\nSedej, S\n\nSchmidt, A\n\nDenegri, M\n\nWalther, S\n\nMatovina, M\n\nArnstein, G\n\nGutschi, EM\n\nWindhager, I\n\nLjubojević, S\n\nNegri, S\n\nHeinzel, FR\n\nBisping, E\n\nVos, MA\n\nNapolitano, C\n\nPriori, SG\n\nKockskämper, J\n\nPieske, B\n\nBeiträge in Fachzeitschriften\nISI:000334285900017\n24315909.0\n10.1016/j.jacc.2013.11.010\nNone\nThis study sought to explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca(2+) release through cardiac ryanodine receptors (RyR2) aggravate cardiac remodeling in mice carrying a human RyR2(R4496C+/-) gain-of-function mutation in response to pressure overload.\n RyR2 dysfunction causes increased diastolic SR Ca(2+) release associated with arrhythmias and contractile dysfunction in inherited and acquired cardiac diseases, such as catecholaminergic polymorphic ventricular tachycardia and heart failure (HF).\n Functional and structural properties of wild-type and catecholaminergic polymorphic ventricular tachycardia-associated RyR2(R4496C+/-) hearts were characterized under conditions of pressure overload induced by transverse aortic constriction (TAC).\n Wild-type and RyR2(R4496C+/-) hearts had comparable structural and functional properties at baseline. After TAC, RyR2(R4496C+/-) hearts responded with eccentric hypertrophy, substantial fibrosis, ventricular dilation, and reduced fractional shortening, ultimately resulting in overt HF. RyR2(R4496C+/-)-TAC cardiomyocytes showed increased incidence of spontaneous SR Ca(2+) release events, reduced Ca(2+) transient peak amplitude, and SR Ca(2+) content as well as reduced SR Ca(2+)-ATPase 2a and increased Na(+)/Ca(2+)-exchanger protein expression. HF phenotype in RyR2(R4496C+/-)-TAC mice was associated with increased mortality due to pump failure but not tachyarrhythmic events. RyR2-stabilizer K201 markedly reduced Ca(2+) spark frequency in RyR2(R4496C+/-)-TAC cardiomyocytes. Mini-osmotic pump infusion of K201 prevented deleterious remodeling and improved survival in RyR2(R4496C+/-)-TAC mice.\n The combination of subclinical congenital alteration of SR Ca(2+) release and pressure overload promoted eccentric remodeling and HF death in RyR2(R4496C+/-) mice, and pharmacological RyR2 stabilization prevented this deleterious interaction. These findings suggest potential clinical relevance for patients with acquired or inherited gain-of-function of RyR2-mediated SR Ca(2+) release.\n Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.\n\nBisping, Egbert Hubertus\n\nHolzer, Senka\n\nSchmidt, Albrecht\n\nSedej, Simon\n\n\n"
},
{
"text": "\n135160\nNeuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration\n\nWardlaw, JM\n\nSmith, EE\n\nBiessels, GJ\n\nCordonnier, C\n\nFazekas, F\n\nFrayne, R\n\nLindley, RI\n\nO'Brien, JT\n\nBarkhof, F\n\nBenavente, OR\n\nBlack, SE\n\nBrayne, C\n\nBreteler, M\n\nChabriat, H\n\nDeCarli, C\n\nde Leeuw, FE\n\nDoubal, F\n\nDuering, M\n\nFox, NC\n\nGreenberg, S\n\nHachinski, V\n\nKilimann, I\n\nMok, V\n\nvan Oostenbrugge, R\n\nPantoni, L\n\nSpeck, O\n\nStephan, BCM\n\nTeipel, S\n\nViswanathan, A\n\nWerring, D\n\nChen, C\n\nSmith, C\n\nvan Buchem, M\n\nNorrving, B\n\nGorelick, PB\n\nDichgans, M\n\nBeiträge in Fachzeitschriften\nISI:000322690600020\n23867200.0\n10.1016/S1474-4422(13)70124-8\nPMC3714437\nCerebral small vessel disease (SVD) is a common accompaniment of ageing. Features seen on neuroimaging include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. SVD can present as a stroke or cognitive decline, or can have few or no symptoms. SVD frequently coexists with neurodegenerative disease, and can exacerbate cognitive deficits, physical disabilities, and other symptoms of neurodegeneration. Terminology and definitions for imaging the features of SVD vary widely, which is also true for protocols for image acquisition and image analysis. This lack of consistency hampers progress in identifying the contribution of SVD to the pathophysiology and clinical features of common neurodegenerative diseases. We are an international working group from the Centres of Excellence in Neurodegeneration. We completed a structured process to develop definitions and imaging standards for markers and consequences of SVD. We aimed to achieve the following: first, to provide a common advisory about terms and definitions for features visible on MRI; second, to suggest minimum standards for image acquisition and analysis; third, to agree on standards for scientific reporting of changes related to SVD on neuroimaging; and fourth, to review emerging imaging methods for detection and quantification of preclinical manifestations of SVD. Our findings and recommendations apply to research studies, and can be used in the clinical setting to standardise image interpretation, acquisition, and reporting. This Position Paper summarises the main outcomes of this international effort to provide the STandards for ReportIng Vascular changes on nEuroimaging (STRIVE).\n Copyright © 2013 Elsevier Ltd. All rights reserved.\n\nFazekas, Franz\n\n\n"
},
{
"text": "\n137959\nIndependence of the blood pressure lowering effect and efficacy of the angiotensin receptor neprilysin inhibitor, LCZ696, in patients with heart failure with preserved ejection fraction: an analysis of the PARAMOUNT trial.\n\nJhund, PS\n\nClaggett, B\n\nPacker, M\n\nZile, MR\n\nVoors, AA\n\nPieske, B\n\nLefkowitz, M\n\nShi, V\n\nBransford, T\n\nMcMurray, JJ\n\nSolomon, SD\n\nBeiträge in Fachzeitschriften\nISI:000337470400013\n24692284.0\n10.1002/ejhf.76\nNone\nThe first in class angiotensin receptor neprilysin inhibitor, LCZ696 has been shown to reduce levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), reduce left atrial size and improve New York Heart Association (NYHA) class in patients with heart failure with preserved ejection fraction (HFpEF). We examined whether the effects of LCZ696 were independent of systolic blood pressure (SBP) lowering.\n In the Prospective comparison of ARNi (angiotensin receptor neprilysin inhibitor) with ARB (angiotensin receptor blocker) on Management Of heart failUre with preserved ejectioN fracTion (PARAMOUNT) trial 301 patients were randomly assigned to LCZ696 or valsartan. We examined the relationship between SBP lowering and LCZ696 on NT-proBNP level, left atrial size, NYHA class and estimated glomerular filtration rate (eGFR). By 12 weeks blood pressure was reduced by 9 mmHg (SD 15)/5 mmHg (SD 11) in patients receiving LCZ696 in comparison with 3 mmHg (SD 17)/2 mmHg (SD 12) in those receiving valsartan. The change in NT-proBNP was poorly correlated with change in SBP (LCZ696, r = 0.17, P = 0.06; valsartan, r = 0.05, P = 0.58) After adjustment for change in SBP, the ratio of change in NT-proBNP at 12 weeks for LCZ696 vs. valsartan was 0.76 (95% CI 0.63-0.93, P = 0.008), and similar to the ratio not adjusting for SBP (0.76, 95% CI 0.63-0.92, P = 0.006); P for interaction was 0.38). Similarly, reduction in left atrial volume index at 36 weeks, improvement in NYHA class and eGFR were all independent of the change in SBP.\n In patients with HFpEF, the effect of the angiotensin receptor neprilysin inhibitor LCZ696 on NT-proBNP, left atrial volume, functional class, and eGFR was independent of reduction in SBP.\n © 2014 The Authors. European Journal of Heart Failure © 2014 European Society of Cardiology.\n\n\n"
},
{
"text": "\n145093\nRed cell distribution width and other red blood cell parameters in patients with cancer: association with risk of venous thromboembolism and mortality.\n\nRiedl, J\n\nPosch, F\n\nKönigsbrügge, O\n\nLötsch, F\n\nReitter, EM\n\nEigenbauer, E\n\nMarosi, C\n\nSchwarzinger, I\n\nZielinski, C\n\nPabinger, I\n\nAy, C\n\nBeiträge in Fachzeitschriften\nISI:000347994900073\n25347577.0\n10.1371/journal.pone.0111440\nPMC4210186\nCancer patients are at high risk of developing venous thromboembolism (VTE). Red cell distribution width (RDW) has been reported to be associated with arterial and venous thrombosis and mortality in several diseases. Here, we analyzed the association between RDW and other red blood cell (RBC) parameters with risk of VTE and mortality in patients with cancer.\n RBC parameters were measured in 1840 patients with cancers of the brain, breast, lung, stomach, colon, pancreas, prostate, kidney; lymphoma, multiple myeloma and other tumor sites, that were included in the Vienna Cancer and Thrombosis Study (CATS), which is an ongoing prospective, observational cohort study of patients with newly diagnosed or progressive cancer after remission. Primary study outcome is occurrence of symptomatic VTE and secondary outcome is death during a maximum follow-up of 2 years.\n During a median follow-up of 706 days, 131 (7.1%) patients developed VTE and 702 (38.2%) died. High RDW (>16%) was not associated with a higher risk of VTE in the total study cohort; in competing risk analysis accounting for death as competing variable the univariable subhazard ratio (SHR) was 1.34 (95% confidence interval [CI]: 0.80-2.23, p = 0.269). There was also no significant association between other RBC parameters and risk of VTE. High RDW was associated with an increased risk of mortality in the total study population (hazard ratio [HR, 95% CI]: 1.72 [1.39-2.12], p<0.001), and this association prevailed after adjustment for age, sex, hemoglobin, leukocyte and platelet count (HR [95% CI]: 1.34 [1.06-1.70], p = 0.016).\n RDW and other RBC parameters were not independently associated with risk of VTE in patients with cancer and might therefore not be of added value for estimating risk of VTE in patients with cancer. We could confirm that high RDW is an independent predictor of poor overall survival in cancer.\n\nPosch, Florian\n\n\n"
},
{
"text": "\n157381\nPlacental DAPK1 and autophagy marker LC3B-II are dysregulated by TNF-α in a gestational age-dependent manner.\n\nProkesch, A\n\nBlaschitz, A\n\nBauer, T\n\nMoser, G\n\nHiden, U\n\nZadora, J\n\nDechend, R\n\nHerse, F\n\nGauster, M\n\nBeiträge in Fachzeitschriften\nISI:000401334200005\n28097431.0\n10.1007/s00418-016-1537-1\nPMC5429897\nAutophagy, a cell-survival process responsible for degradation of protein aggregates and damaged organelles, is increasingly recognized as another mechanism essential for human placentation. A substantial body of experiments suggests inflammation and oxidative stress as the underlying stimuli for altered placental autophagy, giving rise to placenta dysfunction and pregnancy pathologies. Here, the hypothesis is tested whether or not pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α are able to influence the expression profile of autophagy genes in human first-trimester villous placenta. Autophagy-focused qPCR arrays identified substantial downregulation of death-associated protein kinase 1 (DAPK1) in first-trimester placental explants in response to IL-6 and TNF-α, respectively. Immunohistochemistry of placental explants detected considerable DAPK1 staining in placental macrophages, villous cytotrophoblasts and less intense in the syncytiotrophoblast. Both immunohistochemistry and Western blot showed decreased DAPK1 protein in TNF-α-treated placental explants compared to control. On cellular level, DAPK1 expression decreased in SGHPL-4 trophoblasts in response to TNF-α. Observed changes in the expression profile of autophagy-related genes were reflected by significantly decreased lipidation of autophagy marker microtubule-associated protein light chain 3 beta (LC3B-II) in first trimester placental explants in response to TNF-α. Analysis of TNF-α-treated term placental explants showed decreased DAPK1 protein, whereas in contrast to first-trimester LC3B expression and lipidation increased. Immunohistochemistry of placental tissues from early-onset preeclampsia (PE) showed less DAPK1 staining, when compared to controls. Accordingly, DAPK1 mRNA and protein were decreased in primary trophoblasts isolated from early-onset PE, while LC3B-I and -II were increased. Results from this study suggest that DAPK1, a regulator of apoptosis, autophagy and programmed necrosis, decreases in human placenta in response to elevated maternal TNF-α, irrespective of gestational age. In contrast, TNF-α differentially regulates levels of autophagy marker LC3B in human placenta over gestation.\n\nGauster, Martin\n\nHiden, Ursula\n\nMoser, Gerit\n\nProkesch, Andreas\n\n\n"
},
{
"text": "\n162240\nCortical Bone Stem Cell Therapy Preserves Cardiac Structure and Function After Myocardial Infarction.\n\nSharp, TE\n\nSchena, GJ\n\nHobby, AR\n\nStarosta, T\n\nBerretta, RM\n\nWallner, M\n\nBorghetti, G\n\nGross, P\n\nYu, D\n\nJohnson, J\n\nFeldsott, E\n\nTrappanese, DM\n\nToib, A\n\nRabinowitz, JE\n\nGeorge, JC\n\nKubo, H\n\nMohsin, S\n\nHouser, SR\n\nBeiträge in Fachzeitschriften\nISI:000414934100012\n28912121.0\n10.1161/CIRCRESAHA.117.311174\nPMC5681384\nCortical bone stem cells (CBSCs) have been shown to reduce ventricular remodeling and improve cardiac function in a murine myocardial infarction (MI) model. These effects were superior to other stem cell types that have been used in recent early-stage clinical trials. However, CBSC efficacy has not been tested in a preclinical large animal model using approaches that could be applied to patients.\n To determine whether post-MI transendocardial injection of allogeneic CBSCs reduces pathological structural and functional remodeling and prevents the development of heart failure in a swine MI model.\n Female Göttingen swine underwent left anterior descending coronary artery occlusion, followed by reperfusion (ischemia-reperfusion MI). Animals received, in a randomized, blinded manner, 1:1 ratio, CBSCs (n=9; 2×107 cells total) or placebo (vehicle; n=9) through NOGA-guided transendocardial injections. 5-ethynyl-2'deoxyuridine (EdU)-a thymidine analog-containing minipumps were inserted at the time of MI induction. At 72 hours (n=8), initial injury and cell retention were assessed. At 3 months post-MI, cardiac structure and function were evaluated by serial echocardiography and terminal invasive hemodynamics. CBSCs were present in the MI border zone and proliferating at 72 hours post-MI but had no effect on initial cardiac injury or structure. At 3 months, CBSC-treated hearts had significantly reduced scar size, smaller myocytes, and increased myocyte nuclear density. Noninvasive echocardiographic measurements showed that left ventricular volumes and ejection fraction were significantly more preserved in CBSC-treated hearts, and invasive hemodynamic measurements documented improved cardiac structure and functional reserve. The number of EdU+ cardiac myocytes was increased in CBSC- versus vehicle- treated animals.\n CBSC administration into the MI border zone reduces pathological cardiac structural and functional remodeling and improves left ventricular functional reserve. These effects reduce those processes that can lead to heart failure with reduced ejection fraction.\n © 2017 American Heart Association, Inc.\n\nWallner, Markus\n\n\n"
},
{
"text": "\n163707\nVitamin D deficiency in critically ill children: a systematic review and meta-analysis.\n\nMcNally, JD\n\nNama, N\n\nO'Hearn, K\n\nSampson, M\n\nAmrein, K\n\nIliriani, K\n\nMcIntyre, L\n\nFergusson, D\n\nMenon, K\n\nBeiträge in Fachzeitschriften\nISI:000416060800002\n29169388.0\n10.1186/s13054-017-1875-y\nPMC5701429\nVitamin D deficiency (VDD) has been hypothesized not only to be common but also to represent a potentially modifiable risk factor for greater illness severity and clinical outcome during critical illness. The objective of this systematic review was to determine the frequency of VDD in pediatric critical illness and its association with clinical outcomes.\n MEDLINE, Embase, and CENTRAL were searched through December 12, 2016, with no date or language restrictions. The primary objective was to estimate the prevalence of VDD in the pediatric intensive care unit (PICU) and compare vitamin D status with healthy control populations. Secondary objectives were to evaluate whether VDD is associated with mortality, increased illness severity, PICU interventions, and patient clinical course. Random effects meta-analysis was used to calculate pooled VDD event rate, compare levels with those of control subjects, and evaluate for associations between VDD and clinical outcome.\n Among 2700 citations, 17 studies meeting study eligibility were identified. The studies reported a total of 2783 critically ill children and had a median sample size of 120 (range 12-511). The majority of studies used a 25-hydroxyvitamin D [25(OH)D] level less than 50 nmol/L to define VDD, and the pooled VDD prevalence was 54.8 (95% CI 45.4-63.9). Average 25(OH)D levels were significantly lower in PICU patients than in healthy control subjects (pooled difference -17.3 nmol/L, 95% CI -14.0 to -20.6). In a meta-analysis calculation, we found that VDD was associated with increased mortality (OR 1.62, 95% CI 1.11-2.36), illness severity, and need for PICU interventions.\n Approximately 50% of critically ill children have VDD at the time of PICU admission, defined as a blood total 25(OH)D concentration under 50 nmol/L. VDD was further determined to be associated with greater illness severity, multiple organ dysfunction, and mortality in the PICU setting. Clinical trials are required to determine if optimization of vitamin D status improves patient outcome.\n PROSPERO, CRD42016026617 . Registered on 11 January 2016.\n\nAmrein, Karin\n\n\n"
},
{
"text": "\n167681\nEffect of Vitamin D Supplementation on Markers of Vascular Function: A Systematic Review and Individual Participant Meta-Analysis.\n\nBeveridge, LA\n\nKhan, F\n\nStruthers, AD\n\nArmitage, J\n\nBarchetta, I\n\nBressendorff, I\n\nCavallo, MG\n\nClarke, R\n\nDalan, R\n\nDreyer, G\n\nGepner, AD\n\nForouhi, NG\n\nHarris, RA\n\nHitman, GA\n\nLarsen, T\n\nKhadgawat, R\n\nMarckmann, P\n\nMose, FH\n\nPilz, S\n\nScholze, A\n\nShargorodsky, M\n\nSokol, SI\n\nStricker, H\n\nZoccali, C\n\nWitham, MD\n\nBeiträge in Fachzeitschriften\nISI:000434979100015\n29848497.0\n10.1161/JAHA.117.008273\nPMC6015391\nLow 25-hydroxyvitamin D levels are associated with an increased risk of cardiovascular events, but the effect of vitamin D supplementation on markers of vascular function associated with major adverse cardiovascular events is unclear.\n We conducted a systematic review and individual participant meta-analysis to examine the effect of vitamin D supplementation on flow-mediated dilatation of the brachial artery, pulse wave velocity, augmentation index, central blood pressure, microvascular function, and reactive hyperemia index. MEDLINE, CINAHL, EMBASE, Cochrane Central Register of Controlled Trials, and http://www.ClinicalTrials.gov were searched until the end of 2016 without language restrictions. Placebo-controlled randomized trials of at least 4 weeks duration were included. Individual participant data were sought from investigators on included trials. Trial-level meta-analysis was performed using random-effects models; individual participant meta-analyses used a 2-stage analytic strategy, examining effects in prespecified subgroups. 31 trials (2751 participants) were included; 29 trials (2641 participants) contributed data to trial-level meta-analysis, and 24 trials (2051 participants) contributed to individual-participant analyses. Vitamin D3 daily dose equivalents ranged from 900 to 5000 IU; duration was 4 weeks to 12 months. Trial-level meta-analysis showed no significant effect of supplementation on macrovascular measures (flow-mediated dilatation, 0.37% [95% confidence interval, -0.23 to 0.97]; carotid-femoral pulse wave velocity, 0.00 m/s [95% confidence interval, -0.36 to 0.37]); similar results were obtained from individual participant data. Microvascular function showed a modest improvement in trial-level data only. No consistent benefit was observed in subgroup analyses or between different vitamin D analogues.\n Vitamin D supplementation had no significant effect on most markers of vascular function in this analysis.\n © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.\n\nPilz, Stefan\n\n\n"
},
{
"text": "\n182073\nSelexipag for the treatment of children with pulmonary arterial hypertension: First multicenter experience in drug safety and efficacy.\n\nHansmann, G\n\nMeinel, K\n\nBukova, M\n\nChouvarine, P\n\nWåhlander, H\n\nKoestenberger, M\n\nEuropean Pediatric Pulmonary Vascular Disease Network (EPPVDN)\n\nBeiträge in Fachzeitschriften\nISI:000547362000013\n32362477.0\n10.1016/j.healun.2020.03.029\nNone\nThe European Pediatric Pulmonary Vascular Disease Network (EPPVDN) investigated the safety and efficacy of add-on selexipag, an oral prostacyclin receptor agonist approved for pulmonary arterial hypertension (PAH) in adults, in the largest, exploratory pediatric cohort to date.\n This is a prospective observational study of 15 consecutive children with PAH, treated with oral add-on selexipag at 3 centers. Most patients underwent cardiac catheterizations at baseline and median of 8 months follow-up. All patients had clinical, echocardiographic, and N-terminal pro b-type natriuretic peptide studies, including the EPPVDN pediatric pulmonary hypertension (PH) risk score.\n There was no death during the use of selexipag. Two of 15 patients ultimately underwent lung transplantation. One patient with heritable PAH died on intravenous treprostinil (off selexipag). The mean right atrial pressure, the ratio of pulmonary arterial pressure (PAP) to systemic arterial pressure (SAP) (mean PAP/mean SAP, diastolic PAP/diastolic SAP: -17%), and transpulmonary pressure gradients (TPG) (mean TPG: -17%; p < 0.01; diastolic TPG: -6 mm Hg; p < 0.05) were improved after the therapy (n = 10). Selexipag therapy was associated with a better right ventricular systolic function (tricuspid annular plane systolic excursion: +14.5%; p < 0.01) and functional class. Improvement was seen in non-invasive and combined invasive/non-invasive PH risk scores (lower risk: +18%-22%, higher risk: -35%-37%; p < 0.05). Overall, the efficacy of selexipag was variable, often with a better response in less sick patients.\n Oral selexipag use in children with PAH is well tolerated and safe when closely monitored. Add-on selexipag therapy improved several outcome-relevant variables in about 50% of patients and prevented disease progression in additional 27% of patients. The novel EPPVDN pediatric PH risk score indicated these drug effects properly, can be useful in clinical follow-up, and should be validated in larger prospective studies.\n Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.\n\nKoestenberger, Martin\n\nMeinel, Katharina\n\n\n"
},
{
"text": "\n183847\nResponse to tyrosine kinase inhibitors in myeloid neoplasms associated with PCM1-JAK2, BCR-JAK2 and ETV6-ABL1 fusion genes.\n\nSchwaab, J\n\nNaumann, N\n\nLuebke, J\n\nJawhar, M\n\nSomervaille, TCP\n\nWilliams, MS\n\nFrewin, R\n\nJost, PJ\n\nLichtenegger, FS\n\nLa Rosée, P\n\nStorch, N\n\nHaferlach, T\n\nHorny, HP\n\nFabarius, A\n\nHaferlach, C\n\nBurchert, A\n\nHofmann, WK\n\nCross, NCP\n\nHochhaus, A\n\nReiter, A\n\nMetzgeroth, G\n\nBeiträge in Fachzeitschriften\nISI:000529014100001\n32279331.0\n10.1002/ajh.25825\nNone\nWe report on 18 patients with myeloid neoplasms and associated tyrosine kinase (TK) fusion genes on treatment with the TK inhibitors (TKI) ruxolitinib (PCM1-JAK2, n = 8; BCR-JAK2, n = 1) and imatinib, nilotinib or dasatinib (ETV6-ABL1, n = 9). On ruxolitinib (median 24 months, range 2-36 months), a complete hematologic response (CHR) and complete cytogenetic response (CCR) was achieved by five of nine and two of nine patients, respectively. However, ruxolitinib was stopped in eight of nine patients because of primary resistance (n = 3), progression (n = 3) or planned allogeneic stem cell transplantation (allo SCT, n = 2). At a median of 36 months (range 4-78 months) from diagnosis, five of nine patients are alive: four of six patients after allo SCT and one patient who remains on ruxolitinib. In ETV6-ABL1 positive patients, a durable CHR was achieved by four of nine patients (imatinib with one of five, nilotinib with two of three, dasatinib with one of one). Because of inadequate efficacy (lack of hematological and/or cytogenetic/molecular response), six of nine patients (imatinib, n = 5; nilotinib, n = 1) were switched to nilotinib or dasatinib. At a median of 23 months (range 3-60 months) from diagnosis, five of nine patients are in CCR or complete molecular response (nilotinib, n = 2; dasatinib, n = 2; allo SCT, n = 1) while two of nine patients have died. We conclude that (a) responses on ruxolitinib may only be transient in the majority of JAK2 fusion gene positive patients with allo SCT being an important early treatment option, and (b) nilotinib or dasatinib may be more effective than imatinib to induce durable complete remissions in ETV6-ABL1 positive patients.\n © 2020 The Authors. American Journal of Hematology published by Wiley Periodicals, Inc.\n\nJost, Philipp\n\n\n"
},
{
"text": "\n185620\nVoiding recovery after radical parametrectomy in cervical cancer patients: An international prospective multicentre trial - SENTIX.\n\nZapardiel, I\n\nKocian, R\n\nKöhler, C\n\nKlat, J\n\nGermanova, A\n\nJacob, A\n\nBajsova, S\n\nBöhmer, G\n\nLay, L\n\nGil-Ibañez, B\n\nHavelka, P\n\nKipp, B\n\nSzewczyk, G\n\nToth, R\n\nStaringer, JC\n\nDe Santiago, J\n\nCoronado, PJ\n\nPoka, R\n\nLaky, R\n\nLuyckx, M\n\nFastrez, M\n\nDusek, L\n\nHernandez, A\n\nCibula, D\n\nBeiträge in Fachzeitschriften\nISI:000620805400014\n33419610.0\n10.1016/j.ygyno.2020.12.018\nNone\nVoiding dysfunctions represent a leading morbidity after radical hysterectomy performed in patients with early-stage cervical cancer. The aim of this study was to perform ad hoc analysis of factors influencing voiding recovery in SENTIX (SENTinel lymph node biopsy in cervIX cancer) trial.\n The SENTIX trial (47 sites, 18 countries) is a prospective study on sentinel lymph node biopsy without pelvic lymphadenectomy in patients with early-stage cervical cancer. Overall, the data of 300 patients were analysed. Voiding recovery was defined as the number of days from surgery to bladder catheter/epicystostomy removal or to post-voiding urine residuum ≤50 mL.\n The median voiding recovery time was three days (5th-95th percentile: 0-21): 235 (78.3%) patients recovered in <7 days and 293 (97.7%) in <30 days. Only seven (2.3%) patients recovered after >30 days. In the multivariate analysis, only previous pregnancy (p = 0.033) and type of parametrectomy (p < 0.001) significantly influenced voiding recovery >7 days post-surgery. Type-B parametrectomy was associated with a higher risk of delayed voiding recovery than type-C1 (OR = 4.69; p = 0.023 vs. OR = 3.62; p = 0.052, respectively), followed by type-C2 (OR = 5.84; p = 0.011). Both previous pregnancy and type C2 parametrectomy independently prolonged time to voiding recovery by two days.\n Time to voiding recovery is significantly related to previous pregnancy and type of parametrectomy but it is not influenced by surgical approach (open vs minimally invasive), age, or BMI. Type B parametrectomy, without direct visualisation of nerves, was associated with longer recovery than nerve-sparing type C1. Importantly, voiding dysfunctions after radical surgery are temporary, and the majority of the patients recover in less than 30 days, including patients after C2 parametrectomy.\n Copyright © 2020 Elsevier Inc. All rights reserved.\n\nLaky, Rene Walter\n\n\n"
},
{
"text": "\n628\nCutaneous involvement in lymphoblastic lymphoma.\n\nChimenti, S\n\nFink-Puches, R\n\nPeris, K\n\nPescarmona, E\n\nPütz, B\n\nKerl, H\n\nCerroni, L\n\nBeiträge in Fachzeitschriften\nISI:000083216900002\n10551409.0\n10.1111/j.1600-0560.1999.tb01861.x\nNone\nLymphoblastic leukemia/lymphoma (LBL) is a malignant neoplasm of precursor lymphocytes of B- or T-cell phenotype. Involvement of the skin is relatively uncommon. We examined retrospectively the clinicopathologic, immunophenotypic, and molecular genetic features of six patients with cutaneous involvement of LBL (B-LBL=5; T-LBL=1). Patients presented clinically with solitary, large tumors located on the head (3 cases) or the back (1 case), or with generalized tumors (2 cases). Ulceration was uncommon. In two patients the onset of skin lesions was concomitant to the diagnosis of lymphoblastic leukemia. Histopathologic examination showed in all cases a dense, diffuse, monomorphous infiltrate located in the entire dennis and subcutaneous fat. A typical "starry sky" pattern was observed in the majority of the lesions. In some areas neoplastic cells were aligned in a "mosaic-like" fashion. Cytomorphologically, medium sized lymphoid cells with round or convoluted nuclei, inconspicuous nucleoli and scant cytoplasm predominated. There were no significant differences in the histopathologic features of skin lesions in T- and B-LBL. In B-LBL, CD79a was more useful than CD20 in determining the phenotype of neoplastic cells (4/5 cases positive for CD79a as compared to 2/5 cases positive for CD20). TdT, CD10 and CD43 were positive in 4 cases, CD34 in 2. The case of T-LBL revealed positivity for CD1a, CD3, CD43 and TdT, and negativity for CD34 and for B-cell markers. All neoplasms were positive for CD99 and bcl-2, and showed a high proliferation rate. Molecular genetic analysis of J(H) and T-cell receptor (TCR) genes performed using a polymerase chain reaction technique revealed a monoclonal rearrangement of J(H) genes in all five B-LBLs. One of these cases showed also a concomitant TCR-gamma gene rearrangement. A monoclonal rearrangement of the TCR-gamma gene was detected in the case of T-LBL. Our study shows that skin lesions of LBL present characteristic clinicopathologic and molecular features allowing the differentiation from other cutaneous lymphomas, even in cases without clinical history of previous precursor lymphoblastic leukemia/lymphoma.\n\nCerroni, Lorenzo\n\nFink-Puches, Regina\n\nKerl, Helmut\n\n\n"
},
{
"text": "\n1336\nInfluence of age on the release of reactive oxygen species by phagocytes as measured by a whole blood chemiluminescence assay.\n\nKukovetz, EM\n\nBratschitsch, G\n\nHofer, HP\n\nEgger, G\n\nSchaur, RJ\n\nBeiträge in Fachzeitschriften\nISI:A1997VZ99100006\n8981034.0\n10.1016/S0891-5849(96)00334-6\nNone\nPolymorphonuclear and mononuclear phagocytes play an important role in host defense, but may also cause tissue injury through excessive inflammation. Reactive oxygen species (ROS) are not only directly ore indirectly involved in a wide variety of clinical disorders, such as atherosclerosis, reperfusion injury, pulmonary toxicity and cancer, but they are also important in the aging process. This process is associated with increasing susceptibility to infection. In this study we investigated the influence of age and sex on phagocyte activation by means of a whole blood chemiluminescence (CL) assay. Circulating phagocyte activity was measured in 55 healthy volunteers (24 females, 31 males) aged from 6 to 92 years. Using an automated luminescence system, phagocytes were stimulated by polystyrene beads and Luminol-enhanced CL was determined in terms of peak height and peak time in freshly withdrawn, peripheral venous whole blood. An extremely significant positive correlation (p < 0.0001) between the maximum of light emission after stimulation and increasing age was found. This finding is true for the total population of blood phagocytes as well as for a single cell. In contrast the time of the appearance of the maximum of light emission showed an extremely significant inverse correlation (p < 0.0003) with increasing age. The influence of sex on the CL-parameters showed no significant difference between women and men. It is concluded that the increased susceptibility of circulating phagocytes to oxidative burst in elderly subjects may be the consequence of several biological events. Senescent cells express more and also have new antigens on their surfaces that trigger an autoimmune response. Cellular senescence appears earlier in old organisms. Therefore phagocytes in aging individuals may be increasingly involved in their scavenger tasks that grow with the catabolic bias in cell turnover. Moreover, atherosclerotic alterations in the intima and endothelial lesions are physiologic concomitants of age and may lead to a stimulation of circulating phagocytes.\n\nBratschitsch, Gerhard\n\nHofer, Herwig\n\n\n"
},
{
"text": "\n1827\nNo evidence for leptin as an independent associate of blood pressure in childhood and juvenile obesity.\n\nSudi, KM\n\nGallistl, S\n\nWeinhandl, G\n\nTroebinger, M\n\nCartellieri, M\n\nReiterer, E\n\nBorkenstein, MH\n\nBeiträge in Fachzeitschriften\nISI:000086787400008\n10803869.0\nNone\nNone\nWe studied whether leptin is an independent associate of blood pressure in obese children and adolescence. 102 obese children (48 girls, age: 11.6 +/- 2.22 yr; body mass index [BMI]: 27.45 +/- 4.4; blood pressure: 122.5 +/- 11.1/64.7 +/- 10.6 mm Hg and 54 boys, age: 11.5 +/- 2.4 yr; BMI: 27.6 +/- 4.4; blood pressure: 122.5 +/- 13.2/60.9 +/- 8.1 mm Hg [mean +/- SD]) were investigated. Serum leptin and insulin were measured by RIA; glucose was determined enzymatically. Fat mass (FM) was calculated by bioelectrical impedance. Leptin was higher in girls than in boys (p=0.018) but no significant gender differences were found with respect to indices of adiposity and systolic blood pressure (SBP). Children were divided into three groups, according to pubertal stage (Group 1: prepubertal, 32 boys/13 girls; Group 2: pubertal, 17 boys/25 girls; Group 3: late/postpubertal, 5 boys/10 girls). SBP and DBP correlated with body weight in the whole group (r=0.49, p<0.0001, and r=0.27, p=0.004). In Group 1, BMI showed the highest correlation to SBP; in Group 3 no indices of adiposity were related to SBP. In no case was leptin significantly associated with SBP after adjustment for adiposity. In Group 2, glucose was significantly associated with SBP after adjustment for body weight. In Group 3, however, no correlations were found between SBP, DBP and metabolic characteristics, perhaps due to small sample size. Stepwise multiple regression revealed that body weight and glucose contributed to the variation in SBP in the whole group (R2=0.31, p<0.0001). Insulin accounted for almost 8% of the variation in DBP (R2=0.08, p=0.0034). Body weight contributed significantly to SBP in boys (R2=0.39, p<0.0001) and girls (R2=0.24, p< 0.001). The results imply that body weight contributes independently to the variation in blood pressure. Glucose and insulin contribute to mean blood pressure to some extent, but our data do not support the assumption that leptin per se serves as an independent predictor of blood pressure in obese children and adolescents.\n\nBorkenstein, Helmuth Martin\n\nFröhlich-Reiterer, Elke\n\nGallistl, Siegfried\n\n\n"
},
{
"text": "\n3511\nCooperation of NMDA and tachykinin NK(1) and NK(2) receptors in the medullary transmission of vagal afferent input from the acid-threatened rat stomach.\n\nJocic, M\n\nSchuligoi, R\n\nSchöninkle, E\n\nPabst, MA\n\nHolzer, P\n\nBeiträge in Fachzeitschriften\nISI:000166949300006\n11166470.0\n10.1016/S0304-3959(00)00357-2\nNone\nNoxious challenge of the rat gastric mucosa by hydrochloric acid (HCl) is signaled to the nucleus tractus solitarii (NTS) and area postrema (AP). This study examined the participation of glutamate and tachykinins in the medullary transmission process. Activation of neurons was visualized by in situ hybridization autoradiography of c-fos messenger RNA (mRNA) 45 min after intragastric (IG) administration of 0.5 M HCl or saline. IG HCl caused many neurons in the NTS and some neurons in the AP to express c-fos mRNA. The NMDA glutamate receptor antagonist MK-801 (2 mg/kg), the NK(1) tachykinin receptor antagonist GR-205, 71 (3 mg/kg) and the NK(2) receptor antagonist SR-144, 90 (0.1 mg/kg) failed to significantly reduce the NTS response to IG HCl, whereas the triple combination of MK-801, GR-205, 71 and SR-144, 90 inhibited it by 45--50%. Only in rats that had been preexposed IG to HCl 48 h before the experiment was MK-801 alone able to depress the NTS response to IG HCl. In contrast, the c-fos mRNA response in the AP was significantly augmented by MK-801, an action that was prevented by coadministration of GR-205, 71 plus SR-144, 90. Inhibition of neuronal nitric oxide synthase with 7-nitroindazole (45 mg/kg) was without effect on the IG HCl-evoked c-fos mRNA expression in the NTS and AP. Our data show that glutamate acting via NMDA receptors and tachykinins acting via NK(1) and NK(2) receptors cooperate in the vagal afferent input from the acid-threatened stomach to the NTS and participate in the processing of afferent input to the AP in a different and complex manner. These opposing interactions in the AP and NTS and the increase in NMDA receptor function in the NTS after a gastric acid insult are likely to have a bearing on the neuropharmacology of dyspepsia.\n\nHolzer, Peter\n\nPabst, Maria-Anna\n\nSchuligoi, Rufina\n\n\n"
},
{
"text": "\n70946\nNegative inotropy of the gastric proton pump inhibitor pantoprazole in myocardium from humans and rabbits: evaluation of mechanisms.\n\nSchillinger, W\n\nTeucher, N\n\nSossalla, S\n\nKettlewell, S\n\nWerner, C\n\nRaddatz, D\n\nElgner, A\n\nTenderich, G\n\nPieske, B\n\nRamadori, G\n\nSchöndube, FA\n\nKögler, H\n\nKockskämper, J\n\nMaier, LS\n\nSchwörer, H\n\nSmith, GL\n\nHasenfuss, G\n\nBeiträge in Fachzeitschriften\nISI:000247719000015\n17576869.0\n10.1161/CIRCULATIONAHA.106.666008\nNone\nBackground - Proton pump inhibitors are used extensively for acid-related gastrointestinal diseases. Their effect on cardiac contractility has not been assessed directly. Methods and Results - Under physiological conditions (37 degrees C, pH 7.35, 1.25 mmol/L Ca2+), there was a dose-dependent decrease in contractile force in ventricular trabeculae isolated from end-stage failing human hearts superfused with pantoprazole. The concentration leading to 50% maximal response was 17.3 +/- 1.3 mu g/mL. Similar observations were made in trabeculae from human atria, normal rabbit ventricles, and isolated rabbit ventricular myocytes. Real-time polymerase chain reaction demonstrated the expression of gastric H+/K+-adenosine triphosphatase in human and rabbit myocardium. However, measurements with BCECF-loaded rabbit trabeculae did not reveal any significant pantoprazole-dependent changes of pH(i). Ca2+ transients recorded from field-stimulated fluo 3-loaded myocytes (F/F-0) were significantly depressed by 10.4 +/- 2.1% at 40 mu g/mL. Intracellular Ca2+ fluxes were assessed in fura 2-loaded, voltage-clamped rabbit ventricular myocytes. Pantoprazole (40 mu g/mL) caused an increase in diastolic [Ca2+](i) by 33 +/- 12%, but peak systolic [Ca2+](i) was unchanged, resulting in a decreased Ca2+ transient amplitude by 25 +/- 8%. The amplitude of the L type Ca2+ current (I-Ca, -L) was reduced by 35 +/- 5%, and sarcoplasmic reticulum Ca2+ content was reduced by 18 +/- 6%. Measurements of oxalate-supported sarcoplasmic reticulum Ca2+ uptake in permeabilized cardiomyocytes indicated that pantoprazole decreased Ca2+ sensitivity (K-d) of sarcoplasmic reticulum Ca2+ adenosine triphosphatase: control, K-d = 358 +/- 15 nmol/L; 40 mu g/mL pantoprazole, K-d = 395 +/- 12 nmol L (P < 0.05). Pantoprazole also acted on cardiac myofilaments to reduced Ca2+-activated force. Conclusions - Pantoprazole depresses cardiac contractility in vitro by depression of Ca2+ signaling and myofilament activity. In view of the extensive use of this agent, the effects should be evaluated in vivo.\n\n\n"
},
{
"text": "\n129023\nApproach to the upper body after massive weight loss.\n\nScharnagl, E\n\nKoch, H\n\nWiedner, M\n\nSpendel, S\n\n\n\nBeiträge in Fachzeitschriften\nISI:000318280900004\nNone\n10.1007/s10353-013-0203-2\nNone\nUpper and lower body lifts are key concepts in re-shaping the body after massive weight loss. Because of their mutual interaction, the whole body should be examined and evaluated before any contouring operation. Upper body contouring covers the arms, thoracic flanks, male or female breast and back. Before the operation, the excess tissue is determined by pinching and then marking the skin. These lines are supplemented by perpendicular orientation lines to help the surgeon to recognise corresponding wound edges and join them after resection of the skin. As the skin excess on the upper arms is often overestimated, the actual resection line is usually well within the line determined by the pinch test. After the fatty tissue is suctioned off, the deep subcutaneous layer is left undisturbed to protect lymphatic vessels and the nerves, and the excess skin is removed from the superficial subcutaneous layer. On the lateral thoracic wall, the skin is firmed up from the back and upper abdomen to the breast fold. The latter must be secured topographically in its typical position with sutures to the ribs, rib periosteum or fascia so that the breast is not skewed. Contouring operations on the breast always require pre-operative imaging studies. Besides breast lift and reduction, breast enlargement to correct involution is not uncommon. Pedicled, de-epithelialized subcutaneous flaps from the thoracic flank and upper abdomen are more suitable than implants. If needed, breast volume may be further enhanced with secondary lipofilling. The combination of a thoracic flank and lower body lift usually avoids separate lifts and scars on the back. If necessary, however, any folds or bulges are removed from their base after liposuction. The optical result correlates directly with the body mass index at the time of surgery. As almost all the patients are above the BMI norms, there are limits to what can be expected. The majority of the patients under consideration here considered the optical result of the upper body lift to be good to very good and were well satisfied.\n\nKoch, Horst\n\nSpendel, Stephan\n\n\n"
},
{
"text": "\n138990\nInfluence of different conditioning methods on immediate and delayed dentin sealing.\n\nFalkensammer, F\n\nArnetzl, GV\n\nWildburger, A\n\nKrall, C\n\nFreudenthaler, J\n\nBeiträge in Fachzeitschriften\nISI:000340343600020\n24787131.0\n10.1016/j.prosdent.2013.10.028\nNone\nData are needed to evaluate the effect of various conditioning methods on immediate and delayed dentin sealing.\n The purpose of this study was to test bond strength and surface configuration of immediate and delayed dentin sealing surfaces after applying different surface conditioning methods.\n A total of 96 premolars were allocated to the immediate and delayed groups. The groups differed in the timing of dentin sealing. The immediate-group specimens were sealed with a self-etching adhesive immediately after preparation. The delayed-group specimens were sealed before the final ceramic restoration bonding. Provisional restorations were cemented on immediate-group and delayed-group specimens for 1 week. Four conditioning methods were used: polishing with fluoride-free pumice paste, airborne-particle abrasion with silicoated aluminum oxide, glycin, or calcium carbonate. After 24-hour storage, the shear bond strength was tested. The fractured specimens were optically inspected with a stereomicroscope. An optical 3-dimensional surface analysis was performed for quantitative and qualitative evaluation. A 2-way ANOVA with post hoc Tukey honestly significant difference tests for significant effects was performed to investigate effects of the 2 factors, sealing and conditioning, and their interaction (α=.05).\n Two-way ANOVA found significant differences between the sealing and conditioning groups. The immediate group had significantly lower bond strengths than the delayed group. In all groups, surface polishing produced the highest bond strengths, and airborne-particle abrasion with calcium carbonate produced the lowest. Fracture analysis found more failures in the adhesive layers in the immediate groups and a prevalence of mixed failures in the delayed groups. The surface analysis found significant abrasion and roughness when airborne-particle abrasion with silicoated aluminum oxide was used for immediate and delayed dentin sealing surfaces.\n Polishing and airborne-particle abrasion with silicoated aluminum oxide or glycin are efficient methods in conditioning immediate and delayed dentin sealing surfaces. Airborne-particle abrasion with silicoated aluminum oxide leaves significant surface alterations on both types of surfaces.\n Copyright © 2014 Editorial Council for the Journal of Prosthetic Dentistry. Published by Elsevier Inc. All rights reserved.\n\nFalkensammer, Frank\n\n\n"
}
]
}