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"text": "\n63476\nDepressed ability of patients with melanoma or renal cell carcinoma to generate adherent lymphokine-activated killer cells.\n\nSedlmayr, P\n\nRabinowich, H\n\nElder, EM\n\nErnstoff, MS\n\nKirkwood, JM\n\nHerberman, RB\n\nWhiteside, TL\n\nBeiträge in Fachzeitschriften\nISI:A1991GH35800005\n1790141.0\n10.1097/00002371-199110000-00005\nNone\nAdherent lymphokine-activated killer (A-LAK) cells, selected from peripheral blood lymphocytes (PBL) of normal human donors by adherence to plastic, and cultured in the presence of interleukin 2 (IL-2), are highly enriched in CD3-CD56+ natural killer (NK) cells. These IL-2-activated NK cells proliferate extensively upon further culture in conditioned medium containing IL-2. In contrast, we previously found that with PBL of some patients with advanced cancer, the same procedure often failed to yield high enrichment of NK cells or substantial expansion in the numbers of these effector cells. To obtain sufficient numbers of A-LAK cells for adoptive immunotherapy in cancer patients, an improved method for generation of human A-LAK cells with irradiated mitogen-stimulated allogeneic PBL- or Epstein-Barr virus-transformed lymphoblastoid cell lines was introduced. In paired experiments, A-LAK cultures with feeder cells showed significantly enhanced IL-2-driven proliferation of A-LAK cells obtained from normal donors or patients with metastatic melanoma, renal cell carcinoma, and other types of solid cancers. The growth-promoting effect of feeders for A-LAK cells resulted in significantly improved expansion of CD3-CD56+ (NK) effector cells in A-LAK cultures established from normal donors. Cells in these cultures also had significantly higher levels of antitumor cytotoxicity against K562 and Daudi targets than did A-LAK cells grown in the absence of feeder cells. Enrichment in CD3-CD56+ cells and antitumor activity also occurred in patient A-LAK cultures supplemented with mitogen-stimulated feeder cells, but was not statistically significant. Overall, despite improved proliferation and CD3-CD56+ cell content of A-LAK cultures established in the presence of mitogen-activated feeder cells, only 39% (21/54) of patients tested generated A-LAK cells that would be judged acceptable for large-scale therapeutic use by criteria based on fold expansion and purity of A-LAK cells. These results suggest that in comparison to normal individuals, NK cells of many patients with advanced solid tumors are defective in their ability to respond by proliferation to IL-2 even in the presence of exogenously supplied growth factors.\n\nSedlmayr, Peter\n\n\n"
},
{
"text": "\n131489\nEffects of the depth of anesthesia on distortion product otoacoustic emissions.\n\nRopposch, T\n\nWalch, C\n\nAvian, A\n\nMausser, G\n\nSpary, M\n\nBeiträge in Fachzeitschriften\nISI:000343645200008\n24150547.0\n10.1007/s00405-013-2780-x\nNone\nTo analyze the effects of the depth of anesthesia on inner ear function measured with distortion product otoacoustic emissions (DPOAEs) at 2f 1 - f 2. Thirty patients who underwent tonsillectomy under general anesthesia (GA) were included. Patients were assigned randomly to one of two groups: group 1 (n = 15) received propofol, group 2 (n = 15) sevoflurane as anesthetic agent. The sedation level was assessed by the bispectral index system. DPOAE measurements were performed before premedication (T 1), 5 min after premedication (T 2), 3 min after induction of general anesthesia (T 3) and every 10 min (T 4, T 5) thereafter until the end of surgery at about 23 min post-anesthetic induction, while sedation levels were obtained starting at the beginning until the end of anesthesia. After premedication, both blood oxygen saturation and heart rate decreased. Following induction of anesthesia systolic and diastolic blood pressure decreased, while, as expected, the level of sedation increased. Analyzing the propofol and sevoflurane group separately, both groups showed comparable overall courses of DPOAE levels at higher frequencies (2.8 kHz p = 0.310, 4 kHz p = 0.193, 6 kHz p = 0.269, 8 kHz p = 0.223) and no changes of DPOAE levels compared with baseline values were observed. At T5 the 1 kHz DPOAE level increased in the propofol group and slightly decreased in the sevoflurane group (p < 0.001). While the 1.4 kHz DPOAE level in the propofol group did not change over time the 1.4 kHz DPOAE level decreased in the sevoflurane group (baseline to T 4 p = 0.045; Baseline to T 5 p = 0.004). While overall there were different courses between these two groups in the 2 kHz DPOAE level, in the post hoc analysis only a tendency in the change from baseline to T 4 could be observed (p = 0.082). These results indicate that while the amplitudes of certain DPOAEs were influenced by GA, the depth of anesthesia had no effect on this measure of cochlear function in clinical routine. Therefore, DPOAE measurements in sedation and during GA are useful but the effect of anesthetic agents on DPOAE levels needs to be taken into account when analyzing the test.\n\nAvian, Alexander\n\nWalch, Christian\n\n\n"
},
{
"text": "\n146683\nmiR-199a and miR-497 Are Associated with Better Overall Survival due to Increased Chemosensitivity in Diffuse Large B-Cell Lymphoma Patients.\n\nTroppan, K\n\nWenzl, K\n\nPichler, M\n\nPursche, B\n\nSchwarzenbacher, D\n\nFeichtinger, J\n\nThallinger, GG\n\nBeham-Schmid, C\n\nNeumeister, P\n\nDeutsch, A\n\nBeiträge in Fachzeitschriften\nISI:000366826100074\n26251897.0\n10.3390/ijms160818077\nPMC4581236\nMicro-RNAs (miRNAs) are short non-coding single-stranded RNA molecules regulating gene expression at the post-transcriptional level. miRNAs are involved in cell development, differentiation, apoptosis, and proliferation. miRNAs can either function as tumor suppressor genes or oncogenes in various important pathways. The expression of specific miRNAs has been identified to correlate with tumor prognosis. For miRNA expression analysis real-time PCR on 81 samples was performed, including 63 diffuse large B-cell lymphoma (DLBCL, 15 of germinal center B-cell like subtype, 17 non germinal center B-cell, 23 transformed, and eight unclassified) and 18 controls, including nine peripheral B-cells, 5 germinal-center B-cells, four lymphadenitis samples, and 4 lymphoma cell lines (RI-1, SUDHL4, Karpas, U2932). Expression levels of a panel of 11 miRNAs that have been previously involved in other types of cancer (miR-15b_2, miR-16_1*, miR-16_2, miR-16_2*, miR-27a, miR-27a*, miR-98-1, miR-103a, miR-185, miR-199a, and miR-497) were measured and correlated with clinical data. Furthermore, cell lines, lacking miR-199a and miR-497 expression, were electroporated with the two respective miRNAs and treated with standard immunochemotherapy routinely used in patients with DLBCL, followed by functional analyses including cell count and apoptosis assays. Seven miRNAs (miR-16_1*, miR-16_2*, miR-27a, miR-103, miR-185, miR-199, and miR-497) were statistically significantly up-regulated in DLBCL compared to normal germinal cells. However, high expression of miR-497 or miR-199a was associated with better overall survival (p = 0.042 and p = 0.007). Overexpression of miR-199a and miR-497 led to a statistically significant decrease in viable cells in a dose-dependent fashion after exposure to rituximab and various chemotherapeutics relevant in multi-agent lymphoma therapy. Our data indicate that elevated miR-199a and miR-497 levels are associated with improved survival in aggressive lymphoma patients most likely by modifying drug sensitivity to immunochemotherapy. This functional impairment may serve as a potential novel therapeutic target in future treatment of patients with DLBCL.\n\nBeham-Schmid, Christine\n\nDeutsch, Alexander\n\nFeichtinger, Julia\n\nNeumeister, Peter\n\nNinaus, Daniela\n\nPichler, Martin\n\n\n"
},
{
"text": "\n161553\nThe role of dopamine in positive and negative prediction error utilization during incidental learning - Insights from Positron Emission Tomography, Parkinson's disease and Huntington's disease.\n\nMathar, D\n\nWilkinson, L\n\nHoll, AK\n\nNeumann, J\n\nDeserno, L\n\nVillringer, A\n\nJahanshahi, M\n\nHorstmann, A\n\nBeiträge in Fachzeitschriften\nISI:000403029900013\n27751503.0\n10.1016/j.cortex.2016.09.004\nNone\nIncidental learning of appropriate stimulus-response associations is crucial for optimal functioning within our complex environment. Positive and negative prediction errors (PEs) serve as neural teaching signals within distinct ('direct'/'indirect') dopaminergic pathways to update associations and optimize subsequent behavior. Using a computational reinforcement learning model, we assessed learning from positive and negative PEs on a probabilistic task (Weather Prediction Task - WPT) in three populations that allow different inferences on the role of dopamine (DA) signals: (1) Healthy volunteers that repeatedly underwent [11C]raclopride Positron Emission Tomography (PET), allowing for assessment of striatal DA release during learning, (2) Parkinson's disease (PD) patients tested both on and off L-DOPA medication, (3) early Huntington's disease (HD) patients, a disease that is associated with hyper-activation of the 'direct' pathway. Our results show that learning from positive and negative feedback on the WPT is intimately linked to different aspects of dopaminergic transmission. In healthy individuals, the difference in [11C]raclopride binding potential (BP) as a measure for striatal DA release was linearly associated with the positive learning rate. Further, asymmetry between baseline DA tone in the left and right ventral striatum was negatively associated with learning from positive PEs. Female patients with early HD exhibited exaggerated learning rates from positive feedback. In contrast, dopaminergic tone predicted learning from negative feedback, as indicated by an inverted u-shaped association observed with baseline [11C]raclopride BP in healthy controls and the difference between PD patients' learning rate on and off dopaminergic medication. Thus, the ability to learn from positive and negative feedback is a sensitive marker for the integrity of dopaminergic signal transmission in the 'direct' and 'indirect' dopaminergic pathways. The present data are interesting beyond clinical context in that imbalances of dopaminergic signaling have not only been observed for neurological and psychiatric conditions but also been proposed for obesity and adolescence.\n Copyright © 2016 Elsevier Ltd. All rights reserved.\n\nHoll, Anna\n\n\n"
},
{
"text": "\n166460\nMolecular Epidemiology of Staphylococcus aureus in the General Population in Northeast Germany: Results of the Study of Health in Pomerania (SHIP-TREND-0).\n\nHoltfreter, S\n\nGrumann, D\n\nBalau, V\n\nBarwich, A\n\nKolata, J\n\nGoehler, A\n\nWeiss, S\n\nHoltfreter, B\n\nBauerfeind, SS\n\nDöring, P\n\nFriebe, E\n\nHaasler, N\n\nHenselin, K\n\nKühn, K\n\nNowotny, S\n\nRadke, D\n\nSchulz, K\n\nSchulz, SR\n\nTrübe, P\n\nVu, CH\n\nWalther, B\n\nWestphal, S\n\nCuny, C\n\nWitte, W\n\nVölzke, H\n\nGrabe, HJ\n\nKocher, T\n\nSteinmetz, I\n\nBröker, BM\n\nBeiträge in Fachzeitschriften\nISI:000386113200023\n27605711.0\n10.1128/JCM.00312-16\nPMC5078557\nPopulation-based studies on Staphylococcus aureus nasal colonization are scarce. We examined the prevalence, resistance, and molecular diversity of S. aureus in the general population in Northeast Germany. Nasal swabs were obtained from 3, 91 adults in the large-scale population-based Study of Health in Pomerania (SHIP-TREND). Isolates were characterized using spa genotyping, as well as antibiotic resistance and virulence gene profiling. We observed an S. aureus prevalence of 27.2%. Nasal S. aureus carriage was associated with male sex and inversely correlated with age. Methicillin-resistant S. aureus (MRSA) accounted for 0.95% of the colonizing S. aureus strains. MRSA carriage was associated with frequent visits to hospitals, nursing homes, or retirement homes within the previous 24 months. All MRSA strains were resistant to multiple antibiotics. Most MRSA isolates belonged to the pandemic European hospital-acquired MRSA sequence type 22 (HA-MRSA-ST22) lineage. We also detected one livestock-associated MRSA ST398 (LA-MRSA-ST398) isolate, as well as six livestock-associated methicillin-susceptible S. aureus (LA-MSSA) isolates (clonal complex 1 [CC1], CC97, and CC398). spa typing revealed a diverse but also highly clonal S. aureus population structure. We identified a total of 357 spa types, which were grouped into 30 CCs or sequence types. The major seven CCs (CC30, CC45, CC15, CC8, CC7, CC22, and CC25) included 75% of all isolates. Virulence gene patterns were strongly linked to the clonal background. In conclusion, MSSA and MRSA prevalences and the molecular diversity of S. aureus in Northeast Germany are consistent with those of other European countries. The detection of HA-MRSA and LA-MRSA within the general population indicates possible transmission from hospitals and livestock, respectively, and should be closely monitored.\n Copyright © 2016 Holtfreter et al.\n\nSteinmetz, Ivo\n\n\n"
},
{
"text": "\n168606\nDifferent Types of White Matter Hyperintensities in CADASIL.\n\nDuchesnay, E\n\nHadj Selem, F\n\nDe Guio, F\n\nDubois, M\n\nMangin, JF\n\nDuering, M\n\nRopele, S\n\nSchmidt, R\n\nDichgans, M\n\nChabriat, H\n\nJouvent, E\n\nBeiträge in Fachzeitschriften\nISI:000438095800001\n30042721.0\n10.3389/fneur.2018.00526\nPMC6048276\nObjective: In CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy), white matter hyperintensities (WMH) are considered to result from hypoperfusion. We hypothesized that in fact the burden of WMH results from the combination of several regional populations of WMH with different mechanisms and clinical consequences. Methods: To identify regional WMH populations, we used a 4-step approach. First, we used an unsupervised principal component algorithm to determine, without a priori knowledge, the main sources of variation of the global spatial pattern of WMH. Thereafter, to determine whether these sources are likely to include relevant information regarding regional populations of WMH, we tested their relationships with: (1) MRI markers of the disease; (2) the clinical severity assessed by the Mattis Dementia Rating scale (MDRS) (cognitive outcome) and the modified Rankin's score (disability outcome). Finally, through careful interpretation of all the results, we tried to identify different regional populations of WMH. Results: The unsupervised principal component algorithm identified 3 main sources of variation of the global spatial pattern of WMH, which showed significant and sometime inverse relationships with MRI markers and clinical scores. The models predicting clinical severity based on these sources outperformed those evaluating WMH by their volume (MDRS, coefficient of determination of 39.0 vs. 35.3%, p = 0.01; modified Rankin's score, 43.7 vs. 38.1%, p = 0.001). By carefully interpreting the visual aspect of these sources as well as their relationships with MRI markers and clinical severity, we found strong arguments supporting the existence of different regional populations of WMH. For instance, in multivariate analyses, larger extents of WMH in anterior temporal poles and superior frontal gyri were associated with better outcomes, while larger extents of WMH in pyramidal tracts were associated with worse outcomes, which could not be explained if WMH in these different areas shared the same mechanisms. Conclusion: The results of the present study support the hypothesis that the whole extent of WMH results from a combination of different regional populations of WMH, some of which are associated, for yet undetermined reasons, with milder forms of the disease.\n\nRopele, Stefan\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n174192\nAssociation of Improvement in Fractional Flow Reserve With Outcomes, Including Symptomatic Relief, After Percutaneous Coronary Intervention.\n\nFournier, S\n\nCiccarelli, G\n\nToth, GG\n\nMilkas, A\n\nXaplanteris, P\n\nTonino, PAL\n\nFearon, WF\n\nPijls, NHJ\n\nBarbato, E\n\nDe Bruyne, B\n\nBeiträge in Fachzeitschriften\nISI:000465123600012\n30840026.0\n10.1001/jamacardio.2019.0175\nPMC6484787\nWhether the improvement in myocardial perfusion provided by percutaneous coronary intervention (PCI) is associated with symptomatic relief or improved outcomes has not been well investigated.\n To investigate the prognostic value of the improvement in fractional flow reserve (FFR) after PCI (ΔFFR) on patients' symptoms and 2-year outcomes.\n This study is a post hoc analysis of data from patients undergoing FFR-guided PCI in the randomized clinical trials Fractional Flow Reserve vs Angiography for Multivessel Evaluation (FAME) 1 (NCT00267774; 2009) and FAME 2 (NCT01132495; 2012), with inclusion of 2 years of follow-up data. The FAME 1 trial included patients with multivessel coronary artery disease from 20 medical centers in Europe and the United States. The FAME 2 trial included patients with stable coronary artery disease involving up to 3 vessels from 28 sites in Europe and North America. Lesions from the group in the FAME 1 trial from whom FFR was measured and the group in the FAME 2 trial who received FFR-guided PCI plus medical therapy were analyzed. Data analysis occurred from May 2017 to May 2018.\n Measure of post-PCI FFR.\n Vessel-oriented clinical events at 2 years, a composite of cardiac death, target vessel-associated myocardial infarction, and target vessel revascularization.\n This analysis included 639 patients from whom pre-PCI and post-PCI FFR values were available. Of their 837 lesions, 277 were classified into the lowest tertile (ΔFFR≤0.18), 282 into the middle tertile (0.19≤ΔFFR≤0.31), and 278 into the highest tertile (ΔFFR>0.31). Vessel-oriented clinical events were significantly more frequent in the lowest tertile (n = 25 of 277 [9.1%]) compared with the highest tertile (n = 13 of 278 [4.7%]; hazard ratio, 2.01 [95% CI, 1.03-3.92]; P = .04). In addition, a significant association was observed between ΔFFR and symptomatic relief (odds ratio, 1.33 [95% CI, 1.02-1.74]; P = .02).\n In this analysis of 2 randomized clinical trials, the larger the improvement in FFR, the larger the symptomatic relief and the lower the event rate. This suggests that measuring FFR before and after PCI provides clinically useful information.\n\nToth-Gayor, Gabor\n\n\n"
},
{
"text": "\n174411\nThe new liver allocation score for transplantation is validated and improved transplant survival benefit in Germany but not in the United Kingdom.\n\nSchrem, H\n\nFocken, M\n\nGunson, B\n\nReichert, B\n\nMirza, D\n\nKreipe, HH\n\nNeil, D\n\nKaltenborn, A\n\nGoldis, A\n\nKrauth, C\n\nRoberts, K\n\nBecker, T\n\nKlempnauer, J\n\nNeuberger, J\n\nBeiträge in Fachzeitschriften\nISI:000377491500006\n26947766.0\n10.1002/lt.24421\nNone\nPrognostic models for the prediction of 90-day mortality after transplantation with pretransplant donor and recipient variables are needed to calculate transplant benefit. Transplants in adult recipients in Germany (Hannover, n = 770; Kiel, n = 234) and the United Kingdom (Birmingham, n = 829) were used for prognostic model design and validation in separate training and validation cohorts. The survival benefit of transplantation was estimated by subtracting the observed posttransplant 90-day mortality from the expected 90-day mortality without transplantation determined by the Model for End-Stage Liver Disease (MELD) score. A prognostic model called the liver allocation score (LivAS) was derived using a randomized sample from Hannover using pretransplant donor and recipient variables. This model could be validated in the German training and validation cohorts (area under the receiver operating characteristic curve [AUROC] > 0.70) but not in the English cohort (AUROC, 0.58). Although 90-day mortality rates after transplantation were 13.7% in Hannover, 12.1% in Kiel, and 8.3% in Birmingham, the calculated 90-day survival benefits of transplantation were 6.8% in Hannover, 7.8% in Kiel, and 2.8% in Birmingham. Deployment of the LivAS for limiting allocation to donor and recipient combinations with likely 90-day survival as indicated by pretransplant LivAS values below the cutoff value would have increased the survival benefit to 12.9% in the German cohorts, whereas this would have decreased the benefit in England to 1.3%. The English and German cohorts revealed significant differences in 21 of 28 pretransplant variables. In conclusion, the LivAS could be validated in Germany and may improve German allocation policies leading to greater survival benefits, whereas validation failed in England due to profound differences in the selection criteria for liver transplantation. This study suggests the need for national prognostic models. Even though the German centers had higher rates of 90-day mortality, estimated survival benefits were greater. Liver Transplantation 22 743-756 2016 AASLD.\n © 2016 American Association for the Study of Liver Diseases.\n\nSchrem, Harald Heinrich\n\n\n"
},
{
"text": "\n182178\nGenetically Elevated LDL Associates with Lower Risk of Intracerebral Hemorrhage.\n\nFalcone, GJ\n\nKirsch, E\n\nAcosta, JN\n\nNoche, RB\n\nLeasure, A\n\nMarini, S\n\nChung, J\n\nSelim, M\n\nMeschia, JF\n\nBrown, DL\n\nWorrall, BB\n\nTirschwell, DL\n\nJagiella, JM\n\nSchmidt, H\n\nJimenez-Conde, J\n\nFernandez-Cadenas, I\n\nLindgren, A\n\nSlowik, A\n\nGill, D\n\nHolmes, M\n\nPhuah, CL\n\nPetersen, NH\n\nMatouk Md, CN\n\nGunel, M\n\nSansing, L\n\nBennett, D\n\nChen, Z\n\nSun, LL\n\nClarke, R\n\nWalters, RG\n\nGill, TM\n\nBiffi, A\n\nKathiresan, S\n\nLangefeld, CD\n\nWoo, D\n\nRosand, J\n\nSheth, KN\n\nAnderson, CD\n\nInternational Stroke Genetics Consortium\n\nBeiträge in Fachzeitschriften\nISI:000530728900001\n32277781.0\n10.1002/ana.25740\nPMC7523882\nObservational studies point to an inverse correlation between low-density lipoprotein (LDL) cholesterol levels and risk of intracerebral hemorrhage (ICH), but it remains unclear whether this association is causal. We tested the hypothesis that genetically elevated LDL is associated with reduced risk of ICH.\n We constructed one polygenic risk score (PRS) per lipid trait (total cholesterol, LDL, high-density lipoprotein [HDL], and triglycerides) using independent genomewide significant single nucleotide polymorphisms (SNPs) for each trait. We used data from 316, 28 individuals enrolled in the UK Biobank to estimate the effect of each PRS on its corresponding trait, and data from 1, 86 ICH cases and 1, 61 matched controls to estimate the effect of each PRS on ICH risk. We used these estimates to conduct Mendelian Randomization (MR) analyses.\n We identified 410, 339, 393, and 317 lipid-related SNPs for total cholesterol, LDL, HDL, and triglycerides, respectively. All four PRSs were strongly associated with their corresponding trait (all p < 1.00 × 10-100 ). While one SD increase in the PRSs for total cholesterol (odds ratio [OR] = 0.92; 95% confidence interval [CI] = 0.85-0.99; p = 0.03) and LDL cholesterol (OR = 0.88; 95% CI = 0.81-0.95; p = 0.002) were inversely associated with ICH risk, no significant associations were found for HDL and triglycerides (both p > 0.05). MR analyses indicated that 1mmol/L (38.67mg/dL) increase of genetically instrumented total and LDL cholesterol were associated with 23% (OR = 0.77; 95% CI = 0.65-0.98; p = 0.03) and 41% lower risks of ICH (OR = 0.59; 95% CI = 0.42-0.82; p = 0.002), respectively.\n Genetically elevated LDL levels were associated with lower risk of ICH, providing support for a potential causal role of LDL cholesterol in ICH. ANN NEUROL 2020 ANN NEUROL 2020;88:56-66.\n © 2020 American Neurological Association.\n\nSchmidt, Helena\n\n\n"
},
{
"text": "\n184450\nCellular contribution to left and right atrial dysfunction in chronic arterial hypertension in pigs.\n\nJin, G\n\nManninger, M\n\nAdelsmayr, G\n\nSchwarzl, M\n\nAlogna, A\n\nSchönleitner, P\n\nZweiker, D\n\nBlaschke, F\n\nSherif, M\n\nRadulovic, S\n\nWakula, P\n\nSchauer, S\n\nHöfler, G\n\nReiter, U\n\nReiter, G\n\nPost, H\n\nScherr, D\n\nAcsai, K\n\nAntoons, G\n\nPieske, B\n\nHeinzel, FR\n\nBeiträge in Fachzeitschriften\nISI:000594678900001\n33251761.0\n10.1002/ehf2.13087\nPMC7835565\nAtrial contractile dysfunction contributes to worse prognosis in hypertensive heart disease (HHD), but the role of cardiomyocyte dysfunction in atrial remodelling in HHD is not well understood. We investigated and compared cellular mechanisms of left (LA) and right atrial (RA) contractile dysfunction in pigs with HHD.\n In vivo electrophysiological and magnetic resonance imaging studies were performed in control and pigs treated with 11-deoxycorticosterone acetate (DOCA)/high-salt/glucose diet (12 weeks) to induce HHD. HHD leads to significant atrial remodelling and loss of contractile function in LA and a similar trend in RA (magnetic resonance imaging). Atrial remodelling was associated with a higher inducibility of atrial fibrillation but unrelated to changes in atrial refractory period or fibrosis (histology). Reduced atrial function in DOCA pigs was related to reduced contraction amplitude of isolated LA (already at baseline) and RA myocytes (at higher frequencies) due to reduced intracellular Ca release (Fura 2-AM, field stimulation). However, Ca regulation differed in LA and RA cardiomyocytes: LA cardiomyocytes showed reduced sarcoplasmic reticulum (SR) [Ca], whereas in RA, SR [Ca] was unchanged and SR Ca2+ -ATPase activity was increased. Sodium-calcium exchanger (NCX) activity was not significantly altered. We used ORM-10103 (3 μM), a specific NCX inhibitor to improve Ca availability in LA and RA cardiomyocytes from DOCA pigs. Partial inhibition of NCX increased Ca2+ transient amplitude and SR Ca in LA, but not RA cells.\n In this large animal model of HHD, atrial remodelling in sinus rhythm in vivo was related to differential LA and RA cardiomyocyte dysfunction and Ca signalling. Selective acute inhibition of NCX improved Ca release in diseased LA cardiomyocytes, suggesting a potential therapeutic approach to improve atrial inotropy in HHD.\n © 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.\n\nAdelsmayr, Gabriel\n\nHöfler, Gerald\n\nManninger-Wünscher, Martin\n\nRadulovic, Snjezana\n\nReiter, Ursula\n\nSchauer, Silvia\n\nScherr, Daniel\n\nZweiker, David\n\n\n"
},
{
"text": "\n1908\nParticipation of endothelium-derived nitric oxide but not prostacyclin in the gastric mucosal hyperaemia due to acid back-diffusion.\n\nLippe, IT\n\nHolzer, P\n\nBeiträge in Fachzeitschriften\nISI:A1992HG58400037\n1628157.0\n10.1111/j.1476-5381.1992.tb09043.x\nPMC1908440\n1. The possible participation of prostacyclin and nitric oxide (NO) in the gastric mucosal hyperaemic response to acid back-diffusion through a disrupted gastric mucosal barrier was examined. The experiments were carried out on anaesthetized rats in which acid back-diffusion was elicited by gastric perfusion with dilute ethanol in 0.15 M HCl and gastric mucosal blood flow (MBF) was measured by the hydrogen gas clearance technique. 2. Indomethacin (28 mumols kg-1, s.c.), an inhibitor of the formation of cyclo-oxygenase products including prostacyclin, failed to alter mean arterial blood pressure (MAP), basal MBF and the hyperaemic response to acid back-diffusion in urethane-anaesthetized rats. 3. NG-nitro-L-arginine methyl ester (L-NAME; 13 and 43 mumols kg-1, i.v.), an inhibitor of endothelium-derived NO formation, increased MAP in a dose-dependent manner. Whilst basal MBF in urethane-anaesthetized rats was not changed, the increase in MBF caused by gastric perfusion with dilute ethanol in acid was dose-dependently depressed by L-NAME. The loss of H+ ions from the gastric lumen, an indirect measure of acid back-diffusion, was significantly enhanced by 43 mumols kg-1 L-NAME. In contrast, D-NAME (13 and 43 mumols kg-1) was without effect on MAP, basal and stimulated MBF, and acid back-diffusion. 4. Unlike in urethane-anaesthetized rats, L-NAME led to a significant reduction of basal MBF in phenobarbitone-anaesthetized rats. MAP in the phenobarbitone-anaesthetized rats was significantly higher than in urethane-anaesthetized rats, and the hypertensive effect of L-NAME under phenobarbitone anaesthesia was significantly smaller than under urethane anaesthesia.5. The rise in MBF brought about by acid back-diffusion was blocked by L-NAME administered to phenobarbitone-anaesthetized rats. Infusion of L-arginine (120 pmol kg -1 min- ', i.v.) led to a partial, but significant, reversal of the effects of L-NAME on MAP and the hyperaemia due to acid back-diffusion.6. These findings indicate that endothelium-derived NO plays an important mediator role in the gastric mucosal vasodilatation caused by back-diffusion whilst vasodilator prostanoids such as prostacyclin are not involved.\n\nHolzer, Peter\n\nLippe, Irmgard\n\n\n"
},
{
"text": "\n4636\nMalignant non-Hodgkin's lymphoma of childhood and adolescence in Austria--therapy results between 1986 and 2000.\n\nAttarbaschi, A\n\nMann, G\n\nDworzak, M\n\nTrebo, M\n\nUrban, C\n\nFink, FM\n\nHorcher, E\n\nReiter, A\n\nRiehm, H\n\nGadner, H\n\nAustrian Cooperative Study Group\n\nBeiträge in Fachzeitschriften\nISI:000180423400006\n12635465.0\nNone\nNone\nBetween 1986 and 2000 183 Austrian children and adolescents with non-Hodgkin's lymphoma (NHL) and mature B-cell acute leukemia (B-ALL) were enrolled in 3 consecutive studies of the Berlin-Frankfurt-Münster (BFM) Group. In trial NHL-BFM 86, patients were stratified according to the histologic subtype and clinical stage. In the succeeding studies NHL-BFM 90 and 95, treatment stratification was additionally based on the speed of tumor response to therapy and for children with B-cell NHL/B-ALL also on the pre-therapeutic serum lactic dehydrogenase level. Event-free survival rates were 84% +/- 6% in trial NHL-BFM 86 (n = 39) and 86% +/- 4% in both trials NHL-BFM 90 (n = 67) and NHL-BFM 95 (n = 77). Patients with lymphoblastic lymphoma (mainly with T-cell phenotypes) had an excellent prognosis with an ALL-type chemotherapy regimen (n = 49; relapse, n = 1), whereas an intensive, short-pulse therapy delivered within a 2- to 4-month period was found to be highly efficacious in children with B-cell NHL/B-ALL (n = 114; relapse, n = 6; progression, n = 5). Patients with anaplastic large cell lymphoma (ALCL) who were treated with similar alternating short courses of multi-agent chemotherapy had a less good outcome (n = 20; relapse, n = 6, progression, n = 3). Children with B-cell NHL and B-ALL who failed initial therapy also had a dismal prognosis (10/11 patients died). Local radiotherapy as a part of lymphoma therapy was completely abandoned in study NHL-BFM 90 and surgical interventions were confined to specific situations such as complete resection in localized B-cell NHL and ALCL, diagnostic biopsy and second-look operation. In conclusion, our results showed that the BFM treatment strategy for lymphoblastic lymphoma and B-cell NHL/B-ALL was highly successful in the majority of patients; however, optimal treatment for children with ALCL has not yet been defined. As a consequence, larger trials at an international level are necessary to find new prognostic markers that might define more precisely those patients who need further intensification of first-line treatment or novel therapy.\n\nUrban, Ernst-Christian\n\n\n"
},
{
"text": "\n6882\nUse of recombinant tissue plasminogen activator in children with meningococcal purpura fulminans: a retrospective study.\n\nZenz, W\n\nZoehrer, B\n\nLevin, M\n\nFanconi, S\n\nHatzis, TD\n\nKnight, G\n\nMüllner, M\n\nFaust, SN\n\nInternational Paediatric Meningococcal Thrombolysis Study Group\n\nBeiträge in Fachzeitschriften\nISI:000223410800022\n15286558.0\n10.1097%2F01.CCM.0000133667.86429.5D\nNone\nOBJECTIVE: Meningococcal disease causes septic shock with associated disseminated intravascular coagulation and hemorrhagic skin necrosis. In severe cases, widespread vascular thrombosis leads to gangrene of limbs and digits and contributes to morbidity and mortality. Uncontrolled case reports have suggested that thrombolytic therapy may prevent some complications, and the use of tissue plasminogen activator (t-PA) has been widespread. Our aim was to summarize the clinical outcome and adverse effects where systemic t-PA has been used to treat children with fulminant meningococcemia. DESIGN: International, multiple-center, retrospective, observational case note study between January 1992 and June 2000. SETTING: Twenty-four different hospitals in seven European countries and Australia. PATIENTS: A total of 62 consecutive infants and children with severe meningococcal sepsis in whom t-PA was used for the treatment of predicted amputations and/or refractory shock (40 to treat severe ischemia, 12 to treat shock, and ten to treat both). INTERVENTIONS: t-PA was administered with a median dose of 0.3 mg.kg(-1).hr(-1) (range, 0.008-1.13) and a median duration of 9 hrs (range, 1.2-83). MAIN RESULTS: Twenty-nine of 62 patients died (47%; 95% confidence interval, 28-65). Seventeen of 33 survivors had amputations (11 below knee/elbow or greater loss; six less severe). In 12 of 50 patients to whom t-PA was given for imminent amputation, no amputations were observed. Five developed intracerebral hemorrhages (five of 62, 8%; 95% confidence interval, 0.5-16). Of these five, three died, one developed a persistent hemiparesis, and one recovered completely. CONCLUSIONS: The high incidence of intracerebral hemorrhage in our study raises concerns about the safety of t-PA in children with fulminant meningococcemia. However, due to the absence of a control group in such a severe subset of patients, whether t-PA is beneficial or harmful cannot be answered from the unrestricted use of the drug that is described in this report. Our experience highlights the need to avoid strategies that use experimental drugs in an uncontrolled fashion and to participate in multiple-center trials, which are inevitably required to study rare diseases.\n\nZenz, Werner\n\n\n"
},
{
"text": "\n14641\nLectin-like oxidized low-density lipoprotein (LDL) receptor (LOX-1)-mediated pathway and vascular oxidative injury in older-age rat renal transplants.\n\nBräsen, JH\n\nNieminen-Kelhä, M\n\nMarkmann, D\n\nMalle, E\n\nSchneider, W\n\nNeumayer, HH\n\nBudde, K\n\nLuft, FC\n\nDragun, D\n\nBeiträge in Fachzeitschriften\nISI:000227596500042\n15780115.0\n10.1111/j.1523-1755.2005.00240.x\nNone\nBACKGROUND: Older-age renal allografts are associated with inferior survival; however, the mechanisms are unclear. Reactive oxygen species participate in aging and in chronic vascular disease. We investigated how mediators of oxidative stress may increase allograft susceptibility to vascular injury. METHODS: We employed the low-responder allogeneic F344-to-Lew rat renal transplantation model. We used nonimmunosuppressed young (donors and recipients aged 12 weeks), old (donors and recipients aged 52 weeks), and old-to-young animal (donors aged 52 weeks and recipients aged 12 weeks) combinations. Grafts were transplanted after 2 hours cold preservation in University of Wisconsin solution and harvested 1, 2, 7 and 10 days later. Additionally, old animals receiving continuous 1.5 mg/kg cyclosporine (CyA) immunosuppression were included. Renal allograft pathology was scored according to Banff criteria. We studied intragraft vascular adhesion molecule-1 (VCAM-1), lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1), and hypochlorite-modified LDL expression as well as ED-1+ monocytes/macrophages and CD8+ lymphocyte infiltration. Intragraft in situ superoxide anion radical production was determined with dihydroethidium assay on cryosections. RESULTS: During the first 2 posttransplant days, old transplants demonstrated higher functional impairment and increased oxidative stress, while young transplant had higher ED-1+ monocytes/macrophage infiltration and VCAM-1 expression. The degree of VCAM-1 expression and ED-1+ monocytes/macrophage and CD8+ lymphocyte infiltration correlated at later time points directly with the transplant age. VCAM-1 and LOX-1 staining were localized predominantly on the endothelium of arterial vessels, shifting the distribution to vascular smooth muscle layer strongly dependent on donor age and the grade of vascular injury. LOX-1 staining colocalized with hypochlorite-modified epitopes in the media of injured arteries. We measured increased in situ superoxide anion radical production in corresponding areas. Immunosuppression with CyA had no protective effect on vascular injury and LOX-1 expression. CONCLUSION: Induction of LOX-1-related oxidation pathways and increased susceptibility to oxidative stress could play an important role in promoting vascular injury in old renal transplants independent of the recipient age.\n\nMalle, Ernst\n\n\n"
},
{
"text": "\n67151\nIntravenous and oral itraconazole versus intravenous amphotericin B deoxycholate as empirical antifungal therapy for persistent fever in neutropenic patients with cancer who are receiving broad-spectrum antibacterial therapy. A randomized, controlled trial.\n\nBoogaerts, M\n\nWinston, DJ\n\nBow, EJ\n\nGarber, G\n\nReboli, AC\n\nSchwarer, AP\n\nNovitzky, N\n\nBoehme, A\n\nChwetzoff, E\n\nDe Beule, K\n\nItraconazole Neutropenia Study Group (incl. Linkesch, W)\n\nBeiträge in Fachzeitschriften\nISI:000170972500003\n11560454.0\n10.7326/0003-4819-135-6-200109180-00010\nNone\nBACKGROUND: Amphotericin B deoxycholate is currently the standard empirical antifungal therapy in neutropenic patients with cancer who have persistent fever that does not respond to antibiotic therapy. However, this treatment often causes infusion-related and metabolic toxicities, which may be dose limiting. OBJECTIVE: To compare the efficacy and safety of itraconazole with those of amphotericin B as empirical antifungal therapy. DESIGN: An open randomized, controlled, multicenter trial, powered for equivalence. SETTING: 60 oncology centers in 10 countries. PATIENTS: 384 neutropenic patients with cancer who had persistent fever that did not respond to antibiotic therapy. INTERVENTION: Intravenous amphotericin B or intravenous itraconazole followed by oral itraconazole solution. MEASUREMENTS: Defervescence, breakthrough fungal infection, drug-related adverse events, and death. RESULTS: For itraconazole and amphotericin B, the median duration of therapy was 8.5 and 7 days and the median time to defervescence was 7 and 6 days, respectively. The intention-to-treat efficacy analysis of data from 360 patients showed response rates of 47% and 38% for itraconazole and amphotericin B, respectively (difference, 9.0 percentage points [95% CI, -0.8 to 19.5 percentage points]). Fewer drug-related adverse events occurred in the itraconazole group than the amphotericin B group (5% vs. 54% of patients; P = 0.001), and the rate of withdrawal because of toxicity was significantly lower with itraconazole (19% vs. 38%; P = 0.001). Significantly more amphotericin B recipients had nephrotoxicity (P < 0.001). Breakthrough fungal infections (5 patients in each group) and mortality rates (19 deaths in the itraconazole group and 25 deaths in the amphotericin B group) were similar. Sixty-five patients switched to oral itraconazole solution after receiving the intravenous formulation for a median of 9 days. CONCLUSIONS: Itraconazole and amphotericin B have at least equivalent efficacy as empirical antifungal therapy in neutropenic patients with cancer. However, itraconazole is associated with significantly less toxicity.\n\n\n"
},
{
"text": "\n112593\nShort-term effects of high-dose oral vitamin D3 in critically ill vitamin D deficient patients: a randomized, double-blind, placebo-controlled pilot study\n\nAmrein, K\n\nSourij, H\n\nWagner, G\n\nHoll, A\n\nPieber, TR\n\nSmolle, KH\n\nStojakovic, T\n\nSchnedl, C\n\nDobnig, H\n\nBeiträge in Fachzeitschriften\nISI:000292506000028\n21443793.0\n10.1186/cc10120\nPMC3219377\nIntroduction: Vitamin D deficiency is encountered frequently in critically ill patients and might be harmful. Current nutrition guidelines recommend very low vitamin D doses. The objective of this trial was to evaluate the safety and efficacy of a single oral high-dose vitamin D3 supplementation in an intensive care setting over a one-week observation period. Methods: This was a randomized, double-blind, placebo-controlled pilot study in a medical ICU at a tertiary care university center in Graz, Austria. Twenty-five patients (mean age 62 +/- 16yrs) with vitamin D deficiency [25-hydroxyvitamin D (25(OH) D) <= 20 ng/ml] and an expected stay in the ICU >48 hours were included and randomly received either 540, 00 IU (corresponding to 13.5 mg) of cholecalciferol (VITD) dissolved in 45 ml herbal oil or matched placebo (PBO) orally or via feeding tube. Results: The mean serum 25(OH) D increase in the intervention group was 25 ng/ml (range 1-47 ng/ml). The highest 25(OH) D level reached was 64 ng/ml, while two patients showed a small (7 ng/ml) or no response (1 ng/ml). Hypercalcemia or hypercalciuria did not occur in any patient. From day 0 to day 7, total serum calcium levels increased by 0.10 (PBO) and 0.15 mmol/L (VITD; P < 0.05 for both), while ionized calcium levels increased by 0.11 (PBO) and 0.05 mmol/L (VITD; P < 0.05 for both). Parathyroid hormone levels decreased by 19 and 28 pg/ml (PBO and VITD, ns) over the seven days, while 1, 5(OH) D showed a transient significant increase in the VITD group only. Conclusions: This pilot study shows that a single oral ultra-high dose of cholecalciferol corrects vitamin D deficiency within 2 days in most patients without causing adverse effects like hypercalcemia or hypercalciuria. Further research is needed to confirm our results and establish whether vitamin D supplementation can affect the clinical outcome of vitamin D deficient critically ill patients.\n\nAmrein, Karin\n\nPieber, Thomas\n\nSourij, Harald\n\nWünsch, Gerit\n\n\n"
},
{
"text": "\n118000\nAre myocardial infarction--associated single-nucleotide polymorphisms associated with ischemic stroke?\n\nCheng, YC\n\nAnderson, CD\n\nBione, S\n\nKeene, K\n\nMaguire, JM\n\nNalls, M\n\nRasheed, A\n\nZeginigg, M\n\nAttia, J\n\nBaker, R\n\nBarlera, S\n\nBiffi, A\n\nBookman, E\n\nBrott, TG\n\nBrown, RD\n\nChen, F\n\nChen, WM\n\nCiusani, E\n\nCole, JW\n\nCortellini, L\n\nDanesh, J\n\nDoheny, K\n\nFerrucci, L\n\nGrazia Franzosi, M\n\nFrossard, P\n\nFurie, KL\n\nGolledge, J\n\nHankey, GJ\n\nHernandez, D\n\nHolliday, EG\n\nHsu, FC\n\nJannes, J\n\nKamal, A\n\nKhan, MS\n\nKittner, SJ\n\nKoblar, SA\n\nLewis, M\n\nLincz, L\n\nLisa, A\n\nMatarin, M\n\nMoscato, P\n\nMychaleckyj, JC\n\nParati, EA\n\nParolo, S\n\nPugh, E\n\nRost, NS\n\nSchallert, M\n\nSchmidt, H\n\nScott, RJ\n\nSturm, JW\n\nYadav, S\n\nZaidi, M\n\nBoncoraglio, GB\n\nLevi, CR\n\nMeschia, JF\n\nRosand, J\n\nSale, M\n\nSaleheen, D\n\nSchmidt, R\n\nSharma, P\n\nWorrall, B\n\nMitchell, BD\n\nGARNET Collaborative Research Group\n\nGENEVA Consortium\n\nInternationalStrokeGeneticsConsortium\n\nBeiträge in Fachzeitschriften\nISI:000302124200016\n22363065.0\n10.1161/STROKEAHA.111.632075\nPMC3622211\nBACKGROUND AND PURPOSE: Ischemic stroke (IS) shares many common risk factors with coronary artery disease (CAD). We hypothesized that genetic variants associated with myocardial infarction (MI) or CAD may be similarly involved in the etiology of IS. To test this hypothesis, we evaluated whether single-nucleotide polymorphisms (SNPs) at 11 different loci recently associated with MI or CAD through genome-wide association studies were associated with IS. METHODS: Meta-analyses of the associations between the 11 MI-associated SNPs and IS were performed using 6865 cases and 11 395 control subjects recruited from 9 studies. SNPs were either genotyped directly or imputed; in a few cases a surrogate SNP in high linkage disequilibrium was chosen. Logistic regression was performed within each study to obtain study-specific âs and standard errors. Meta-analysis was conducted using an inverse variance weighted approach assuming a random effect model. RESULTS: Despite having power to detect odds ratio of 1.09-1.14 for overall IS and 1.20-1.32 for major stroke subtypes, none of the SNPs were significantly associated with overall IS and/or stroke subtypes after adjusting for multiple comparisons. CONCLUSIONS: Our results suggest that the major common loci associated with MI risk do not have effects of similar magnitude on overall IS but do not preclude moderate associations restricted to specific IS subtypes. Disparate mechanisms may be critical in the development of acute ischemic coronary and cerebrovascular events.\n\nSchmidt, Helena\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n126141\nValidity and reproducibility of sensor contact lens profiles in comparison to applanation tonometry in healthy eyes].\n\nFaschinger, C\n\nMossböck, G\n\nKrainz, S\n\nBeiträge in Fachzeitschriften\nISI:000312549700007\n23172649.0\n10.1055/s-0032-1315380\nNone\nPurpose: The aim of this study was to check the validity of the profiles gained by a sensor contact lens in one eye. We compared these values with measurements done by applanation tonometry in the other eye. The measurements were done in different body postures and head positions. All examinations were repeated 2 to 8 weeks afterwards to check the reproducibility.\nPatients, Material and Methods: Five young healthy individuals with normal eyes had the intraocular pressure (IOP) of their right eye measured by applanation tonometry (Goldmann and Perkins) in different postures (45 minutes upright, 30 minutes supine, 20 minutes head-body down and 30 minutes upright). Simultanously the left eye had a sensor contact lens, which measured the changes of the corneal curvature due to changes of the IOP within intervals of 5 minutes. Within 2-8 weeks all examinations were repeated completely in the same manner.\nResults: After 45 minutes in upright position the mean IOP remained unchanged (14mmHg), increased after 30 minutes in supine position (20mmHg), increased again after 20 minutes in head-body-down position (22.4mmHg) and came back to 14mmHg after 30 minutes in upright position. A very similar profile was obtained in the repeat examinations. In contrast, the mean profiles gained by the sensor contact lens were not in a positive slope-like shape, but the mean values showed a flat or surprisingly, an even downward profile (head-body-down position). No statistical differences were found between all mean values of the first and repeat examinations.\nConclusions: Intraocular pressure measurements gained by applanation tonometry showed the expected physiological positive slope profile during changes of the body and head positions (upright, supine, head-body-down). None of the profiles simultaneously gained by the sensor contact lens had a slope-like shape, but were flat or even downward. The reasons for the lacking validity between applanation tonometry and sensor contact lens cannot be explained. Thismakes the interpretation of Triggerfish profiles uncertain and they should therefore be done with caution. The reproducibility of the applanation tonometry values as well as of the sensor contact lens values was good and showed no significant differences.\n\nFaschinger, Christoph\n\n\n"
},
{
"text": "\n141596\nClinical performance of the Nevisense system in cutaneous melanoma detection: an international, multicentre, prospective and blinded clinical trial on efficacy and safety.\n\nMalvehy, J\n\nHauschild, A\n\nCuriel-Lewandrowski, C\n\nMohr, P\n\nHofmann-Wellenhof, R\n\nMotley, R\n\nBerking, C\n\nGrossman, D\n\nPaoli, J\n\nLoquai, C\n\nOlah, J\n\nReinhold, U\n\nWenger, H\n\nDirschka, T\n\nDavis, S\n\nHenderson, C\n\nRabinovitz, H\n\nWelzel, J\n\nSchadendorf, D\n\nBirgersson, U\n\nBeiträge in Fachzeitschriften\nISI:000346600000003\n24841846.0\n10.1111/bjd.13121\nPMC4257502\nEven though progress has been made, the detection of melanoma still poses a challenge. In light of this situation, the Nevisense electrical impedance spectroscopy (EIS) system (SciBase AB, Stockholm, Sweden) was designed and shown to have the potential to be used as an adjunct diagnostic tool for melanoma detection.\n To assess the effectiveness and safety of the Nevisense system in the distinction of benign lesions of the skin from melanoma with electrical impedance spectroscopy.\n This multicentre, prospective, and blinded clinical study was conducted at five American and 17 European investigational sites. All eligible skin lesions in the study were examined with the EIS-based Nevisense system, photographed, removed by excisional biopsy and subjected to histopathological evaluation. A postprocedure clinical follow-up was conducted at 7 ± 3 days from the initial measurement. A total of 1951 patients with 2416 lesions were enrolled into the study; 1943 lesions were eligible and evaluable for the primary efficacy end point, including 265 melanomas - 112 in situ and 153 invasive melanomas with a median Breslow thickness of 0·57 mm [48 basal cell carcinomas (BCCs) and seven squamous cell carcinomas (SCCs)].\n The observed sensitivity of Nevisense was 96·6% (256 of 265 melanomas) with an exact one-sided 95% lower confidence bound estimated at 94·2% and an observed specificity of 34·4%, and an exact two-sided 95% confidence bound estimated at 32·0-36·9%. The positive and negative predictive values of Nevisense were 21·1% and 98·2%, respectively. The observed sensitivity for nonmelanoma skin cancer was 100% (55 of 48 BCCs and seven SCCs) with an exact two-sided 95% confidence bound estimated at 93·5-100·0%.\n Nevisense is an accurate and safe device to support clinicians in the detection of cutaneous melanoma.\n © 2014 The Authors. British Journal of Dermatology published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists.\n\nHofmann-Wellenhof, Rainer\n\n\n"
},
{
"text": "\n165435\nChanges of vitamin D levels and bone turnover markers after CPAP therapy: a randomized sham-controlled trial.\n\nTheorell-Haglöw, J\n\nHoyos, CM\n\nPhillips, CL\n\nYee, BJ\n\nHerrmann, M\n\nBrennan-Speranza, TC\n\nGrunstein, RR\n\nLiu, PY\n\nBeiträge in Fachzeitschriften\nISI:000438350700005\n28944524.0\n10.1111/jsr.12606\nNone\nThe aim was to investigate whether continuous positive airway pressure treatment could modulate serum vitamin D (25-hydroxyvitamin D) and bone turnover markers (collagen-type 1 cross-linked C-telopeptide, osteocalcin and N-terminal propeptide of type 1 collagen) in secondary analysis from a randomized controlled trial. Sixty-five continuous positive airway pressure-naïve male patients with obstructive sleep apnea (age = 49 ± 12 years, apnea-hypopnea index = 39.9 ± 17.7 events h-1 , body mass index = 31.3 ± 5.2 kg m-2 ) were randomized to receive either real (n = 34) or sham (n = 31) continuous positive airway pressure for 12 weeks. At 12 weeks, all participants received real continuous positive airway pressure for an additional 12 weeks. After 12 weeks of continuous positive airway pressure (real versus sham), there were no between-group differences for any of the main outcomes [Δ25-hydroxyvitamin D: -0.80 ± 5.28 ng mL-1 (mean ± SE) versus 3.08 ± 3.66 ng mL-1 , P = 0.42; Δcollagen-type 1 cross-linked C-telopeptide: 0.011 ± 0.014 ng mL-1 versus -0.004 ± 0.009 ng mL-1 , P = 0.48; Δosteocalcin: 1.13 ± 1.12 ng mL-1 versus 0.46 ± 0.75 ng mL-1 , P = 0.80; ΔN-terminal propeptide of type 1 collagen: 2.07 ± 3.05 μg L-1 versus -1.05 ± 2.13 μg L-1 , P = 0.48]. There were no further differences in subgroup analyses (continuous positive airway pressure-compliant patients, patients with severe obstructive sleep apnea or sleepy patients). However, after 24 weeks irrespective of initial randomization, vitamin D increased in patients with severe obstructive sleep apnea (9.56 ± 5.51 ng mL-1 , P = 0.045) and in sleepy patients (14.0 ± 4.69 ng mL-1 , P = 0.007). Also, there was a significant increase in osteocalcin at 24 weeks (3.27 ± 1.06 ng mL-1 , P = 0.01) in compliant patients. We conclude that 12 weeks of continuous positive airway pressure did not modulate vitamin D or modulate any of the bone turnover markers compared with sham. However, it is plausible that continuous positive airway pressure may have late beneficial effects on vitamin D levels and bone turnover markers in selected groups of patients with obstructive sleep apnea.\n © 2017 European Sleep Research Society.\n\nHerrmann, Markus\n\n\n"
}
]
}