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"text": "\n114126\nGenetic spectrum of hereditary neuropathies with onset in the first year of life.\n\nBaets, J\n\nDeconinck, T\n\nDe Vriendt, E\n\nZimoń, M\n\nYperzeele, L\n\nVan Hoorenbeeck, K\n\nPeeters, K\n\nSpiegel, R\n\nParman, Y\n\nCeulemans, B\n\nVan Bogaert, P\n\nPou-Serradell, A\n\nBernert, G\n\nDinopoulos, A\n\nAuer-Grumbach, M\n\nSallinen, SL\n\nFabrizi, GM\n\nPauly, F\n\nVan den Bergh, P\n\nBilir, B\n\nBattaloglu, E\n\nMadrid, RE\n\nKabzińska, D\n\nKochanski, A\n\nTopaloglu, H\n\nMiller, G\n\nJordanova, A\n\nTimmerman, V\n\nDe Jonghe, P\n\nBeiträge in Fachzeitschriften\nISI:000294959800022\n21840889.0\n10.1093/brain/awr184\nPMC3170533\nEarly onset hereditary motor and sensory neuropathies are rare disorders encompassing congenital hypomyelinating neuropathy with disease onset in the direct post-natal period and Dejerine-Sottas neuropathy starting in infancy. The clinical spectrum, however, reaches beyond the boundaries of these two historically defined disease entities. De novo dominant mutations in PMP22, MPZ and EGR2 are known to be a typical cause of very early onset hereditary neuropathies. In addition, mutations in several other dominant and recessive genes for Charcot-Marie-Tooth disease may lead to similar phenotypes. To estimate mutation frequencies and to gain detailed insights into the genetic and phenotypic heterogeneity of early onset hereditary neuropathies, we selected a heterogeneous cohort of 77 unrelated patients who presented with symptoms of peripheral neuropathy within the first year of life. The majority of these patients were isolated in their family. We performed systematic mutation screening by means of direct sequencing of the coding regions of 11 genes: MFN2, PMP22, MPZ, EGR2, GDAP1, NEFL, FGD4, MTMR2, PRX, SBF2 and SH3TC2. In addition, screening for the Charcot-Marie-Tooth type 1A duplication on chromosome 17p11.2-12 was performed. In 35 patients (45%), mutations were identified. Mutations in MPZ, PMP22 and EGR2 were found most frequently in patients presenting with early hypotonia and breathing difficulties. The recessive genes FGD4, PRX, MTMR2, SBF2, SH3TC2 and GDAP1 were mutated in patients presenting with early foot deformities and variable delay in motor milestones after an uneventful neonatal period. Several patients displaying congenital foot deformities but an otherwise normal early development carried the Charcot-Marie-Tooth type 1A duplication. This study clearly illustrates the genetic heterogeneity underlying hereditary neuropathies with infantile onset.\n\n\n"
},
{
"text": "\n119973\nThe archaeal halophilic virus-encoded Dam-like methyltransferase M. phiCh1-I methylates adenine residues and complements dam mutants in the low salt environment of Escherichia coli.\n\nBaranyi, U\n\nKlein, R\n\nLubitz, W\n\nKrüger, DH\n\nWitte, A\n\nBeiträge in Fachzeitschriften\nISI:000085625800018\n10712697.0\n10.1046/j.1365-2958.2000.01786.x\nNone\nThe genome of the archaeal virus phiCh1, infecting Natrialba magadii (formerly Natronobacterium magadii), is composed of 58.5 kbp linear ds DNA. Virus particles contain several RNA species in sizes of 100-800 nucleotides. A fraction of phiCh1 genomes is modified within 5'-GATC-3' and related sequences, as determined by various restriction enzyme digestion analyses. High performance liquid chromatography revealed a fifth base, in addition to the four nucleosides, which was identified as N6-methyladenosine. Genetic analyses and subsequent sequencing led to the identification of a DNA (N6-adenine) methyltransferase (mtase) gene. The protein product was designated M.phiCh1-I. By the localization of the most conserved motifs (a DPPY motif occurring before FxGxG), the enzyme was placed within the beta-subgroup of the (N6-adenine) methyltransferase class. The mtase gene of phiCh1 was classified as a 'late' gene, as determined by measuring the kinetics of mRNA and protein expression in N. magadii during the lytic cycle of phiCh1. After infection of cells, M.phiCh1-I mRNA and protein could be detected in lower amounts than in the situation of virus induction from lysogenic cells. Consequently, only about 5% of the phiCh1 progeny genomes after infection of N. magadii carry the M.phiCh1-I methylation in contrast to 50% of virus genomes generated by induction of phiCh1-lysogenic N. magadii cells. Heterologous expression of the mtase from a halophile with 3 M cytoplasmic salt concentration showed an unexpected feature: the protein was active in the low environment of Escherichia coli and was able to methylate DNA in vivo. Interestingly, it seemed to exhibit a higher sequence specificity in E. coli that resulted in adenine methylation exclusively in the sequence 5'-GATC-3'. Additionally, expression of M.phiCh1-I in dam- E. coli cells led to a complete substitution of the function of M. Dam in DNA mismatch repair.\n\n\n"
},
{
"text": "\n120551\nOsteoporosis in Children and Young Adults: A Late Effect After Chemotherapy for Bone Sarcoma.\n\nPirker-Frühauf, UM\n\nFriesenbichler, J\n\nUrban, EC\n\nObermayer-Pietsch, B\n\nLeithner, A\n\nBeiträge in Fachzeitschriften\nISI:000308737300031\n22806259.0\n10.1007/s11999-012-2448-7\nPMC3441998\nPremature bone loss after childhood chemotherapy may be underestimated in patients with bone sarcoma. Methotrexate (MTX), a standard agent in osteosarcoma protocols, reportedly reduces bone mineral density (BMD). The literature, however, has reported cases of BMD reduction in patients with Ewing's sarcoma treated without MTX. Thus, it is unclear whether osteoporosis after chemotherapy relates to MTX or to other factors. We therefore asked whether (1) young patients with a bone sarcoma had BMD reduction, (2) patients treated with MTX had lower BMD, and (3) other factors (eg, lactose intolerance or vitamin D deficiency) posed additional risks for low BMD. We retrospectively reviewed 43 patients with malignancies who had dual-energy x-ray absorptiometry (DEXA) (lumbar, femoral); 18 with Ewing's sarcoma (mean age, 26 +/- A 8 years), and 25 with an osteosarcoma (mean age, 27 +/- A 10 years). The mean time since diagnosis was 8 +/- A 4 years in the group with Ewing's sarcoma and 7 +/- A 5 years in the group with osteosarcoma. At last followup we determined BMD (computing z-scores), fracture rate, and lifestyle, and performed serum analysis. BMD reduction was present in 58% of patients (37% had a z-score between -1 and -2 SD, 21% had a z-score less than -2 SD) in at least one measured site. Seven of the 43 patients (16%) had nontrauma or tumor-associated fractures after chemotherapy. Findings were similar in the Ewing and osteosarcoma subgroups. We found vitamin D deficiency in 38 patients (88%) and borderline elevated bone metabolism; lactose intolerance was present in 16 patients (37%). Doctors should be aware of the possibility of major bone loss after chemotherapy with a risk of pathologic fracture. Vitamin D deficiency, calcium malnutrition, and lactose intolerance may potentiate the negative effects of chemotherapy, and should be considered in long-term patient management. Level II, prognostic study. See Guidelines for Authors for a complete description of levels of evidence.\n\nFriesenbichler, Jörg\n\nLeithner, Andreas\n\nObermayer-Pietsch, Barbara\n\nUrban, Ernst-Christian\n\n\n"
},
{
"text": "\n121413\nCardiac metabolism and function in patients with multiple sclerosis: A combined P-31-MR-spectroscopy and MRI study\n\nBeer, M\n\nSandstede, J\n\nWeilbach, F\n\nSpindler, M\n\nBuchner, S\n\nKrug, A\n\nKostler, H\n\nPabst, T\n\nKenn, W\n\nLandschutz, W\n\nvon Kienlin, M\n\nToyka, KV\n\nErtl, G\n\nGold, R\n\nHahn, D\n\nBeiträge in Fachzeitschriften\nISI:000168991900003\n11414146.0\n10.1055/s-2001-13339\nNone\nObjective: Involvement of the autonomic system in multiple sclerosis (MS) may concur with dysfunction of the cardiovascular system. The introduction of potentially cardiotoxic immunosuppressive drugs like Mitoxantrone into the treatment of MS warrants proper assessment of preexisting heart disease. However, systematic analyses of functional and metabolic derangements in MS are missing. Using quantitative P-31-MR-spectroscopy (MRS) and MR-imaging (MRI) metabolic and functional parameters were analyzed in patients with MS in comparison to healthy volunteers. Subjects/Methods: 14/15 patients with MS could be included in the study, as the MRS examination of one patient had to be excluded from analysis due to movement during the examination. Using chemical shift imaging (CSI) and AMARES, phosphocreatine (PCr) to adenosine triphosphate (ATP) ratios, characterizing myocardial high-energy phosphate metabolism, were determined. Additionally, absolute concentrations of PCr and ATP were calculated by SLOOP (Spatial Localization with Optimal Pointspread Function). Analysis of functional changes was performed by Cine-MRI. 14 healthy volunteers matched for age and gender served as control. Results: A significant decrease of absolute PCr concentration was observed in patients with MS compared to matched volunteers (p <0.05), whereas ATP concentrations showed no significant changes (p=0.27). Metabolite ratios calculated by SLOOP or AMARES showed a tendency to be reduced in patients, however, did not reach significance (p=0.08, SLOOP; p=0.47, AMARES). Using volunteers' mean values +/- 2xSD as cut off value revealed PCr changes in 5 of 14 patients, whereas only 2 also had pathologic PCr/ATP ratios. Functional analysis by MRI depicted depressed left ventricular ejection fraction in 4 patients. Conclusions: The reduction in cardiac high-energy phosphates in some patients with MS; points to a subclinical involvement of the heart. This may be important for treatment with potentially cardiotoxic drugs. Longitudinal studies are need to understand the clinical relevance of our findings.\n\n\n"
},
{
"text": "\n137453\nEURObservational Research Programme: a worldwide registry on peripartum cardiomyopathy (PPCM) in conjunction with the Heart Failure Association of the European Society of Cardiology Working Group on PPCM.\n\nSliwa, K\n\nHilfiker-Kleiner, D\n\nMebazaa, A\n\nPetrie, MC\n\nMaggioni, AP\n\nRegitz-Zagrosek, V\n\nSchaufelberger, M\n\nTavazzi, L\n\nvan Veldhuisen, DJ\n\nRoos-Hesslink, JW\n\nShah, AJ\n\nSeferovic, PM\n\nElkayam, U\n\nvan Spaendonck-Zwarts, K\n\nBachelier-Walenta, K\n\nMouquet, F\n\nKraigher-Krainer, E\n\nHall, R\n\nPonikowski, P\n\nMcMurray, JJ\n\nPieske, B\n\nBeiträge in Fachzeitschriften\nISI:000335444200013\n24591060.0\n10.1002/ejhf.68\nNone\nThe EURObservational Research Programme is a rolling programme of cardiovascular registries and surveys of the European Society of Cardiology (ESC). These registries will provide information on the nature of cardiovascular disease and its management. This manuscript provides an update on new literature on peripartum cardiomyopathy (PPCM), published since the 2010 Position Statement from the Heart Failure Association of the European Society of Cardiology Working Group on PPCM, and describes a new registry on this under-recognized condition. Peripartum cardiomyopathy is an idiopathic cardiomyopathy presenting with heart failure secondary to left ventricular systolic dysfunction towards the end of the pregnancy, or in the months following delivery, where no other cause for heart failure is found.\n The PPCM Registry aims to describe disease presentation, comorbidities, diagnostic and therapeutic management of patients with PPCM, as well as information on their offspring. Centres not only from ESC and ESC-affiliated countries, but from around the world, are encouraged to participate.\n A prospective registry on patients presenting with PPCM. At the time of writing, approximately 100 patients have been enrolled from 20 countries. All data entry is online via secure passwords and is supported by well-trained information technology personnel.\n The EURObservational Research Programme will allow a comparison of women from around the world, from different ethnic backgrounds, presenting with PPCM and will report on their 6 month and 12 month outcomes. The study aims to include 1000 patients and follow them for 1 year. New centres volunteering to participate in the study will be welcomed.\n © 2014 The Authors. European Journal of Heart Failure © 2014 European Society of Cardiology.\n\n\n"
},
{
"text": "\n157790\nEuropean consensus conference on faecal microbiota transplantation in clinical practice.\n\nCammarota, G\n\nIaniro, G\n\nTilg, H\n\nRajilić-Stojanović, M\n\nKump, P\n\nSatokari, R\n\nSokol, H\n\nArkkila, P\n\nPintus, C\n\nHart, A\n\nSegal, J\n\nAloi, M\n\nMasucci, L\n\nMolinaro, A\n\nScaldaferri, F\n\nGasbarrini, G\n\nLopez-Sanroman, A\n\nLink, A\n\nde Groot, P\n\nde Vos, WM\n\nHögenauer, C\n\nMalfertheiner, P\n\nMattila, E\n\nMilosavljević, T\n\nNieuwdorp, M\n\nSanguinetti, M\n\nSimren, M\n\nGasbarrini, A\n\nEuropean FMT Working Group\n\nBeiträge in Fachzeitschriften\nISI:000396419800004\n28087657.0\n10.1136/gutjnl-2016-313017\nPMC5529972\nFaecal microbiota transplantation (FMT) is an important therapeutic option for Clostridium difficile infection. Promising findings suggest that FMT may play a role also in the management of other disorders associated with the alteration of gut microbiota. Although the health community is assessing FMT with renewed interest and patients are becoming more aware, there are technical and logistical issues in establishing such a non-standardised treatment into the clinical practice with safety and proper governance. In view of this, an evidence-based recommendation is needed to drive the practical implementation of FMT. In this European Consensus Conference, 28 experts from 10 countries collaborated, in separate working groups and through an evidence-based process, to provide statements on the following key issues: FMT indications; donor selection; preparation of faecal material; clinical management and faecal delivery and basic requirements for implementing an FMT centre. Statements developed by each working group were evaluated and voted by all members, first through an electronic Delphi process, and then in a plenary consensus conference. The recommendations were released according to best available evidence, in order to act as guidance for physicians who plan to implement FMT, aiming at supporting the broad availability of the procedure, discussing other issues relevant to FMT and promoting future clinical research in the area of gut microbiota manipulation. This consensus report strongly recommends the implementation of FMT centres for the treatment of C. difficile infection as well as traces the guidelines of technicality, regulatory, administrative and laboratory requirements.\n Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.\n\nHoegenauer, Christoph\n\nKump, Patrizia\n\n\n"
},
{
"text": "\n159954\nSymmetric dimethylarginine, high-density lipoproteins and cardiovascular disease.\n\nZewinger, S\n\nKleber, ME\n\nRohrer, L\n\nLehmann, M\n\nTriem, S\n\nJennings, RT\n\nPetrakis, I\n\nDressel, A\n\nLepper, PM\n\nScharnagl, H\n\nRitsch, A\n\nThorand, B\n\nHeier, M\n\nMeisinger, C\n\nde Las Heras Gala, T\n\nKoenig, W\n\nWagenpfeil, S\n\nSchwedhelm, E\n\nBöger, RH\n\nLaufs, U\n\nvon Eckardstein, A\n\nLandmesser, U\n\nLüscher, TF\n\nFliser, D\n\nMärz, W\n\nMeinitzer, A\n\nSpeer, T\n\nBeiträge in Fachzeitschriften\nISI:000401674200017\n28379378.0\n10.1093/eurheartj/ehx118\nNone\nThe vascular effects of high-density lipoproteins (HDL) differ under certain clinical conditions. The composition of HDL is modified in patients with chronic kidney disease (CKD). As a consequence, uremic HDL induces endothelial dysfunction. We have previously shown that accumulation of symmetric dimethylarginine (SDMA) in HDL causes these adverse effects of HDL in CKD. The aim of the study is to determine the impact of the accumulation of SDMA on the association between HDL and mortality.\n Mortality, renal function, serum SDMA and HDL-cholesterol (HDL-C) were assessed in the LURIC study including 3310 subjects undergoing coronary angiography. All-cause mortality was 30.0% during median follow-up of 9.9 years. Serum SDMA levels significantly predicted all-cause and cardiovascular mortality, and were significantly correlated with SDMA accumulation in HDL. Notably, higher serum SDMA was independently associated with lower cholesterol efflux (P = 0.004) as a measure of HDL functionality. In subjects with low SDMA levels, higher HDL-C was associated with significantly lower mortality. In contrast, in subjects with high SDMA, HDL-C was associated with higher mortality. These findings were confirmed in 1424 participants of the MONICA/KORA S3 cohort. Of note, we derived an algorithm allowing for calculation of biologically effective HDL-C' based on measured HDL-C and SDMA. We corroborated these clinical findings with invitro evidence showing that SDMA accumulation abolishes the anti-inflammatory and regenerative properties of HDL.\n The data identify SDMA as a marker of HDL dysfunction. These findings highlight on the pivotal role of SDMA accumulation in HDL as a mediator of pre-mature cardiovascular disease in patients with CKD.\n Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com.\n\nMärz, Winfried\n\nMeinitzer, Andreas\n\nScharnagl, Hubert\n\n\n"
},
{
"text": "\n161175\nProspective multicentre clinical study on inter- and intrapatient genetic variability for antimicrobial resistance of Helicobacter pylori.\n\nBilgilier, C\n\nStadlmann, A\n\nMakristathis, A\n\nThannesberger, J\n\nKastner, MT\n\nKnoflach, P\n\nSteiner, P\n\nSchöniger-Hekele, M\n\nHögenauer, C\n\nBlesl, A\n\nDatz, C\n\nHuber-Schönauer, U\n\nSchöfl, R\n\nWewalka, F\n\nPüspök, A\n\nMitrovits, N\n\nLeiner, J\n\nTilg, H\n\nEffenberger, M\n\nMoser, M\n\nSiebert, F\n\nHinterberger, I\n\nWurzer, H\n\nStupnicki, T\n\nWatzinger, N\n\nGombotz, G\n\nHubmann, R\n\nKlimpel, S\n\nBiowski-Frotz, S\n\nSchrutka-Kölbl, C\n\nGraziadei, I\n\nLudwiczek, O\n\nKundi, M\n\nHirschl, AM\n\nSteininger, C\n\nAustrian Helicobacter Study Group of the Austrian Society of Gastroenterology and Hepatology\n\nBeiträge in Fachzeitschriften\nISI:000426417300011\n28669844.0\n10.1016/j.cmi.2017.06.025\nNone\nWe report on a large prospective, multicentre clinical investigation on inter- and intrapatient genetic variability for antimicrobial resistance of Helicobacter pylori.\n Therapy-naive patients (n = 2004) who had undergone routine diagnostic gastroscopy were prospectively included from all geographic regions of Austria. Gastric biopsy samples were collected separately from antrum and corpus. Samples were analysed by histopathology and real-time PCR for genotypic resistance to clarithromycin and quinolones. Clinical and demographic information was analysed in relation to resistance patterns.\n H. pylori infection was detected in 514 (26%) of 2004 patients by histopathology and confirmed in 465 (90%) of 514 patients by real-time PCR. PCR results were discordant for antrum and corpus in 27 (5%) of 514 patients, indicating inhomogeneous infections. Clarithromycin resistance rates were 17% (77/448) and 19% (84/455), and quinolone resistance rates were 12% (37/310) and 10% (32/334) in antrum and corpus samples, respectively. Combination of test results per patient yielded resistance rates of 21% (98/465) and 13% (50/383) for clarithromycin and quinolones, respectively. Overall, infection with both sensitive and resistant H. pylori was detected in 65 (14%) of 465 patients.\n Anatomically inhomogeneous infection with different, multiple H. pylori strains is common. Prospective clinical study design, collection of samples from multiple sites and microbiologic methods that allow the detection of coinfections are mandatory for collection of reliable data on antimicrobial resistance patterns in representative patient populations. (ClinicalTrials.gov identifier: NCT02925091).\n Copyright © 2017 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.\n\nBlesl, Andreas\n\nHoegenauer, Christoph\n\n\n"
},
{
"text": "\n168058\nDrug-Coated Balloon Treatment of Femoropopliteal Lesions for Patients With Intermittent Claudication and Ischemic Rest Pain: 2-Year Results From the IN.PACT Global Study.\n\nMicari, A\n\nBrodmann, M\n\nKeirse, K\n\nPeeters, P\n\nTepe, G\n\nFrost, M\n\nWang, H\n\nZeller, T\n\nIN.PACT Global Study Investigators\n\nBeiträge in Fachzeitschriften\nISI:000432995400008\n29798770.0\n10.1016/j.jcin.2018.02.019\nNone\nThe IN.PACT Global Study is the largest prospective, multicenter, independently adjudicated trial to evaluate a paclitaxel drug-coated balloon in patients with lifestyle-limiting claudication and/or ischemic rest pain due to atherosclerotic disease of the femoropopliteal artery and includes complex lesions beyond what are typically included in randomized controlled trials.\n Randomized controlled trials have demonstrated the safety and efficacy of drug-coated balloons for the treatment of Trans-Atlantic Inter-Society Consensus Document II A and B lesions, but there is a need for large-scale prospective studies to evaluate a broader range of lesions.\n The IN.PACT Global Study enrolled 1, 35 subjects, and 1, 06 (1, 73 lesions) were included in the pre-defined clinical cohort analysis. Freedom from clinically driven target lesion revascularization was evaluated at 24 months. The safety composite endpoint was freedom from device- and procedure-related death through 30 days and freedom from target limb major amputation and clinically driven target vessel revascularization within 24 months.\n Mean lesion length was 12.1 cm, 35.5% were total occlusions, and 18.0% had in-stent restenosis. Freedom from clinically driven target lesion revascularization at 24 months was 83.3%, the composite safety endpoint was met in 81.7%, the 2-year all-cause mortality rate was 7.0%, and the major target limb amputation rate was 0.7%. Increased lesion length and the presence of de novo in-stent restenosis or coronary artery disease were associated with increased risk for clinically driven target lesion revascularization by 24 months.\n This real-world study of femoropopliteal artery disease treatment with drug-coated balloons confirmed positive findings reported from more strictly designed randomized controlled trials and showed that outcomes are durable in this population up to 2 years after treatment. (IN.PACT Global Clinical Study; NCT01609296).\n Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.\n\nBrodmann, Marianne\n\n\n"
},
{
"text": "\n170519\nEnhanced inter-compartmental Ca<sup>2+</sup> flux modulates mitochondrial metabolism and apoptotic threshold during aging.\n\nMadreiter-Sokolowski, CT\n\nWaldeck-Weiermair, M\n\nBourguignon, MP\n\nVilleneuve, N\n\nGottschalk, B\n\nKlec, C\n\nStryeck, S\n\nRadulovic, S\n\nParichatikanond, W\n\nFrank, S\n\nMadl, T\n\nMalli, R\n\nGraier, WF\n\nBeiträge in Fachzeitschriften\nISI:000459361500039\n30458321.0\n10.1016/j.redox.2018.11.003\nPMC6243020\nSenescence is characterized by a gradual decline in cellular functions, including changes in energy homeostasis and decreased proliferation activity. As cellular power plants, contributors to signal transduction, sources of reactive oxygen species (ROS) and executors of programmed cell death, mitochondria are in a unique position to affect aging-associated processes of cellular decline. Notably, metabolic activation of mitochondria is tightly linked to Ca2+ due to the Ca2+ -dependency of several enzymes in the Krebs cycle, however, overload of mitochondria with Ca2+ triggers cell death pathways. Consequently, a machinery of proteins tightly controls mitochondrial Ca2+ homeostasis as well as the exchange of Ca2+ between the different cellular compartments, including Ca2+ flux between mitochondria and the endoplasmic reticulum (ER).\n In this study, we investigated age-related changes in mitochondrial Ca2+ homeostasis, mitochondrial-ER linkage and the activity of the main ROS production site, the mitochondrial respiration chain, in an in vitro aging model based on porcine aortic endothelial cells (PAECs), using high-resolution live cell imaging, proteomics and various molecular biological methods.\n We describe that in aged endothelial cells, increased ER-mitochondrial Ca2+ crosstalk occurs due to enhanced ER-mitochondrial tethering. The close functional inter-organelle linkage increases mitochondrial Ca2+ uptake and thereby the activity of the mitochondrial respiration, but also makes senescent cells more vulnerable to mitochondrial Ca2+-overload-induced cell death. Moreover, we identified the senolytic properties of the polyphenol resveratrol, triggering cell death via mitochondrial Ca2+ overload exclusively in senescent cells.\n By unveiling aging-related changes in the inter-organelle tethering and Ca2+ communications we have advanced the understanding of endothelial aging and highlighted a potential basis to develop drugs specifically targeting senescent cells.\n Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.\n\nFrank, Sasa\n\nGottschalk, Benjamin\n\nGraier, Wolfgang\n\nKlec, Christiane\n\nMadl, Tobias\n\nMadreiter-Sokolowski, Corina\n\nMalli, Roland\n\nRadulovic, Snjezana\n\nWaldeck-Weiermair, Markus\n\n\n"
},
{
"text": "\n176380\nAir-fluidized therapy in the treatment of severe burns: A retrospective study from a burn intensive care unit in Austria.\n\nNickl, S\n\nFochtmann-Frana, A\n\nNedomansky, J\n\nHitzl, W\n\nKamolz, LP\n\nHaslik, W\n\nBeiträge in Fachzeitschriften\nISI:000512947600012\n31420263.0\n10.1016/j.burns.2019.07.026\nNone\nAir-fluidized therapy (AFT) has long been used in the treatment of severe burns. In patients with extensive burns involving the posterior trunk, we aim to keep affected posterior areas dry and to postpone their treatment, initially applying available split-thickness skin grafts in functionally more important regions. We retrospectively assessed the impact of AFT on the survival of patients treated in the burn intensive care unit (ICU) of the Medical University of Vienna, Austria, between 2003 and 2016.\n This retrospective single-center study included patients aged ≥18 years with burned total body surface area (TBSA) ≥20% and IIb-III° thermal injuries on the posterior trunk who received AFT. Survival rates were compared with those predicted by the abbreviated burn severity index (ABSI). Demographic, clinical, and surgical data were analyzed.\n Seventy-five of 110 patients with posterior trunk burns received AFT. Their survival rate exceeded that predicted by the ABSI score (mean ABSI, 10.0 ± 2.0; 73.3% (95% CI: 62-83%) survival rate vs. 20-40% predicted; p < 0.0001); no such difference was observed in the non-AFT group (mean, 8.8 ± 1.9; 65.7% (95% CI: 48-81%) survival rate vs. 50-70% predicted). Patients receiving AFT had significantly greater TBSA (median, 50% (35-60) vs. 30% (25-45) and longer ICU stays (median, 63 (36-92) vs. 18 (9-52) days; both p < 0.0001). Fifty-one (68.0%) patients in the AFT group and 26 (74.3%) patients in the non-AFT group underwent posterior trunk surgery (p = 0.66) a median of 16 (10-26) and 5 (2.5-9.5) days, respectively, after admission (p < 0.0001).\n Patients receiving AFT had significantly better survival than predicted by ABSI score in contrast to patients not receiving AFT although burn injuries in this group were more severe (greater TBSA, higher ABSI). As intensive care was similar in these groups aside from AFT, the better survival could be attributed to this additional therapy.\n Copyright © 2019 Elsevier Ltd and ISBI. All rights reserved.\n\nKamolz, Lars-Peter\n\n\n"
},
{
"text": "\n177076\nLower HbA1c in patients with type 1 diabetes and celiac disease who reached celiac-specific antibody-negativity-A multicenter DPV analysis.\n\nNagl, K\n\nBollow, E\n\nLiptay, S\n\nRosenbauer, J\n\nKoletzko, S\n\nPappa, A\n\nNäke, A\n\nFröhlich-Reiterer, E\n\nDöring, C\n\nWolf, J\n\nSalfeld, P\n\nPrinz, N\n\nBeiträge in Fachzeitschriften\nISI:000482608500001\n31430021.0\n10.1111/pedi.12908\nPMC6899993\nTo study celiac-specific antibody status over 3 years in patients with type 1 diabetes and biopsy-proven celiac disease (T1D + CD). Furthermore, to determine clinical differences after diagnosis between patients reaching constant antibody-negativity (Ab-neg) and staying antibody-positive (Ab-pos).\n A total of 608 pediatric T1D + CD patients from the multicenter DPV registry were studied longitudinally regarding their CD specific antibody-status. Differences between Ab-neg (n = 218) and Ab-pos (n = 158) patients 3 years after biopsy were assessed and compared with 26 833 T1D patients without CD by linear and logistic regression adjusted for age, gender, diabetes duration and migration background.\n Thirty-six percent of T1D + CD patients reached and sustained antibody-negativity 3 years after CD diagnosis. The median time until patients returned to Ab-neg was 0.86 (0.51;1.16) years. Three years after diagnosis, HbA1c was lowest in Ab-neg and highest in Ab-pos patients compared to T1D-only patients (adjusted mean (95%CI): 7.72 (7.51-7.92) % vs 8.44 (8.20-8.68) % vs 8.19 (8.17-8.21) %, adjusted P < 0.001, respectively). Total cholesterol, LDL-cholesterol and frequency of dyslipidemia were significantly lower in Ab-neg compared to T1D-only patients (167 (161-173) mg/dl vs 179 (178-179) mg/dl, P < .001; 90 (84-96) mg/dl vs 99 (98-99) mg/dl, P = .005; 15.7 (10.5-22.9) % vs 25.9 (25.2-26.6) %, P = .017). In longitudinal analyses over 6 years after diagnosis, a constantly higher HbA1c (P < .001) and a lower height-SDS (P = .044) was observed in Ab-pos compared to Ab-neg patients.\n Only one third of T1D + CD patients reached constant Ab-negativity after CD diagnosis. Achieving Ab-negativity after diagnosis seems to be associated with better metabolic control and growth, supposedly due to a higher adherence to therapy in general.\n © 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.\n\nFröhlich-Reiterer, Elke\n\n\n"
},
{
"text": "\n182708\nPeople with type 1 diabetes and impaired awareness of hypoglycaemia have a delayed reaction to performing a glucose scan during hypoglycaemia: a prospective observational study.\n\nMoser, O\n\nZiko, H\n\nElsayed, H\n\nHochfellner, DA\n\nPöttler, T\n\nMueller, A\n\nEckstein, ML\n\nSourij, H\n\nMader, JK\n\nHypo-RESOLVE Consortium\n\nBeiträge in Fachzeitschriften\nISI:000548727400001\n32638428.0\n10.1111/dme.14362\nPMC7689757\nConsidering that people with type 1 diabetes and impaired awareness of hypoglycaemia (IAH) have a delayed perception of hypoglycaemia, the question arises whether they perform scans later in case of hypoglycaemia than people without IAH. We assessed whether time to performing a scan after reaching hypoglycaemia while using a flash glucose monitoring (flash GM) system is different in people with IAH compared with people without IAH.\n Ninety-two people with type 1 diabetes [mean (± sd) age 42 ± 14 years, HbA1c 57 ± 9 mmol/mol] using a flash GM system for 3 months were included. Flash GM data were assessed for time until scan after reaching hypoglycaemia level 1 (< 3.9 mmol/l) and level 2 (< 3.0 mmol/l) and compared for type 1 diabetes with vs. without IAH via unpaired t-test/Mann-Whitney U test (P < 0.05).\n Significant differences were found only for the delay between reaching hypoglycaemia and scan between people with and without IAH for Gold score [hypoglycaemia level 1: IAH 78 (51-105) min vs. without IAH 63 (42-89) min, P = 0.03; night-time hypoglycaemia level 2: IAH 140 (107-227) min vs. without IAH 96 (41-155) min, P = 0.004] and Pedersen-Bjergaard score [hypoglycaemia level 1: IAH 76 (52-97) min vs. without IAH 54 (38-71) min, P = 0.011; night-time hypoglycaemia level 1: IAH 132 (79-209) min vs. without IAH 89 (59-143) min, P = 0.011; night-time hypoglycaemia level 2: IAH 134 (66-212) min vs. without IAH 80 (37-131) min, P = 0.002). Data are shown as median (i.q.r.).\n Time until scan after reaching hypoglycaemia might be an objective assessment tool for IAH, but needs to be investigated comprehensively in future studies.\n This article is protected by copyright. All rights reserved.\n\nElsayed, Hesham\n\nHochfellner, Daniel\n\nMader, Julia\n\nMoser, Othmar\n\nMüller, Alexander\n\nPöttler, Tina\n\nSourij, Harald\n\nZiko, Haris\n\n\n"
},
{
"text": "\n186984\nRelation of dopamine receptor 2 binding to pain perception in female fibromyalgia patients with and without depression--A [¹¹C] raclopride PET-study.\n\nLedermann, K\n\nJenewein, J\n\nSprott, H\n\nHasler, G\n\nSchnyder, U\n\nWarnock, G\n\nJohayem, A\n\nKollias, S\n\nBuck, A\n\nMartin-Soelch, C\n\nBeiträge in Fachzeitschriften\nISI:000371844200014\n26708319.0\n10.1016/j.euroneuro.2015.12.007\nNone\nDopamine D2/D3 receptor availability at rest and its association with individual pain perception was investigated using the [(11)C] raclopride PET-method in 24 female Fibromyalgia (FMS) participants with (FMS+, N=11) and without (FMS-, N=13) comorbid depression and in 17 healthy women. Thermal pain thresholds (TPT) and pain responses were assessed outside the scanner. We compared the discriminative capacity, i.e. the individual׳s capacity to discriminate between lower and higher pain intensities and the response criterion, i.e. the subject׳s tendency to report pain during noxious stimulation due to psychological factors. [(11)C] raclopride binding potential (BP), defined as the ratio of specifically bound non-displaceable radioligand at equilibrium (BP(ND)) was used as measure of D2/D3 receptor availability. We found significant group effects of BP(ND) in striatal regions (left ventral striatum, left caudate nucleus and left nucleus accumbens) between FMS+ and FMS- compared to healthy subjects. Correlational analysis showed negative associations between TPT and D2/D3 receptor availability in the left caudate nucleus in FMS-, between TPT and D2/D3 receptor availability in the right caudate nucleus in FMS + and positive associations between TPT and D2/D3 receptor availability in the left putamen and right caudate nucleus in healthy controls. The response criterion was positively associated with D2/D3 receptor availability in the right nucleus accumbens in FMS - and negatively with D2/D3 receptor availability in the left caudate nucleus in healthy controls. Finally, no significant associations between D2/D3 receptor availability and discriminative capacity in any of the groups or regions were determined. These findings provide further support for a disruption of dopaminergic neurotransmission in FMS and implicate DA as important neurochemical moderator of differences in pain perception in FMS patients with and without co-morbid depression.\n Copyright © 2015 Elsevier B.V. and ECNP. All rights reserved.\n\nJenewein, Josef\n\n\n"
},
{
"text": "\n1391\nInterferon-gamma in the treatment of systemic sclerosis: a randomized controlled multicentre trial.\n\nGrassegger, A\n\nSchuler, G\n\nHessenberger, G\n\nWalder-Hantich, B\n\nJabkowski, J\n\nMacHeiner, W\n\nSalmhofer, W\n\nZahel, B\n\nPinter, G\n\nHerold, M\n\nKlein, G\n\nFritsch, PO\n\nBeiträge in Fachzeitschriften\nISI:000076603600012\n9892907.0\n10.1046%2Fj.1365-2133.1998.02460.x\nNone\nWe report the results of a randomized controlled multicentre study on interferon-gamma (IFN-gamma) treatment of systemic sclerosis as determined by skin sclerosis, renal and other organ involvement, global assessment, subjective symptoms and quality of life. Forty-four patients were enrolled into the trial, 27 in the treatment group and 17 in the control group. All patients presented with type I or type II scleroderma. Twenty-nine patients (64%) finished the study. The mean duration of Raynaud's phenomenon and skin sclerosis was 15.3 and 10.8 years, respectively. The skin scores tended to improve in the treatment group (P > 0.05). Mouth aperture increased significantly from 38.5 to 47.7 mm in the treatment group (P < 0.001). Subanalysis of IFN-gamma treated patients with normalized skin sclerosis scores >/=1 showed significant improvement in both skin involvement and subjective symptoms (P < 0.05). Organ involvement improved in eight of 18 treatment patients and in three of 11 control patients. It worsened in three of 18 treatment patients and in four of 11 control patients. One control patient died due to cardiorespiratory failure during the study. No deterioration of renal function occurred during IFN-gamma treatment. There was a significant improvement in quality of life parameters in the control group but not in the treatment group. Plasma levels of neopterin increased significantly during IFN-gamma treatment but not in the control group, whereas N-terminal procollagen III peptide levels did not change in either group. There was a high frequency of mild to moderate influenza-like adverse events during IFN-gamma treatment. Only four of nine drop-out patients, however, experienced symptoms most probably associated with IFN-gamma treatment. We conclude that IFN-gamma therapy has mild beneficial effects on skin sclerosis and disease-associated symptoms in type I and II scleroderma. IFN-gamma treatment was associated with acceptable tolerability and did not induce major renal dysfunction in our patients.\n\nSalmhofer, Wolfgang\n\n\n"
},
{
"text": "\n1941\nPerinatal motor behaviour and neurological outcome in spina bifida aperta.\n\nSival, DA\n\nBegeer, JH\n\nStaal-Schreinemachers, AL\n\nVos-Niël, JM\n\nBeekhuis, JR\n\nPrechtl, HF\n\nBeiträge in Fachzeitschriften\nISI:000071384400003\n9467691.0\n10.1016%2FS0378-3782%2897%2900090-X\nNone\nAIM OF THE STUDY: In the present longitudinal study we investigated the relationship between prenatal motor behaviour and the postnatal neurological sequelae of infants with spina bifida aperta. METHODS AND PATIENTS: Prenatal isolated leg movements and general movements of 13 fetuses/infants with spina bifida aperta were assessed by means of ultrasound recordings, and were compared with: 1. the spinal level of morphological defect (meningo-myelocele), 2. the postnatal motor behaviour, 3. the postnatal sensory function, and 4. the final motor outcome. RESULTS: In all 13 cases studied, the spinal defect was either at thoracic (n = 8) or at lumbal (n = 5) level. All fetuses displayed active leg movements corresponding to the functioning of low lumbal myelum segments (L4-5 in two cases or L5-S1 in 11 cases), despite vertebral defects at high localisation. These leg movements were of normal quality (normal in appearance) and endogenously generated, since no external stimulus was exerted to elicit them. This implies that in fetuses with spina bifida aperta active leg movements can be generated at spinal segments which are located at (n = 1), or under (n = 12) the meningo-myelelocele. Postnatally, for a short period of time (mostly during the first few hours), leg movements related to myelum function at (n = 1) or lower than (n = 7) the spinal defect were detected. However, only in two infants these early leg movements were of normal quality and corresponded with the final motor outcome. In contrast to these early neonatal leg movements, early sensory function was strongly related to the spinal defect (r = 0.76; P = 0.005) and to the final motor outcome (sensory function predicted outcome in all infants of whom follow-up was performed). CONCLUSION: These data on fetuses/infants with spina bifida aperta strongly indicate that a discrepancy exists between the occurrence of prenatal leg movements and the spinal localisation of the meningo-myelocele on the one hand, and between the occurrence of pre- and postnatal leg movements on the other hand (quantity and quality).\n\n\n"
},
{
"text": "\n2616\nThe role of lecithin: cholesterol acyltransferase for lipoprotein (a) assembly. Structural integrity of low density lipoproteins is a prerequisite for Lp(a) formation in human plasma.\n\nSteyrer, E\n\nDurovic, S\n\nFrank, S\n\nGiessauf, W\n\nBurger, A\n\nDieplinger, H\n\nZechner, R\n\nKostner, GM\n\nBeiträge in Fachzeitschriften\nISI:A1994PV81000024\n7989589.0\n10.1172/JCI117598\nPMC330062\nThe composition of lipoproteins in the plasma of patients with LCAT deficiency (LCAT-D) is grossly altered due to the lack of cholesteryl esters which form the core of normal lipoproteins. When plasma from LCAT-D patients and their relatives was examined we found that nine heterozygotes had plasma Lp(a) levels of 2-13 mg/dl whereas none of 11 affected homozygous individuals from different families contained detectable amounts of Lp(a) in their plasma. Therefore, the binding of apo(a) to LDL density particles was studied in vitro using LDL density fractions prepared from patients, and recombinant apo(a) [r-apo(a)], which was expressed and secreted by transfected COS-7 cells. The LDL from heterozygotes were chemically indistinguishable from normal LDL and homogeneous with regard to morphology, whereas the crude LDL floating fraction from homozygotes consisted of a heterogeneous mixture of large vesicles, and small spheres resembling normal LDL. The LDL density fraction from the LCAT-D patient lacked almost completely cholesteryl esters. Incubation of LCAT-D plasma with active LCAT caused a substantial augmentation of the original subfraction which morphologically resembled normal LDL. Using r-apo(a) and normal LDL or LDL of heterozygous individuals, apoB:r-apo(a) complexes were formed when incubated at 37 degrees C in vitro for 20 h. In contrast, the total LDL floating fraction from a homozygous LCAT-D patient failed to form apoB:r-apo(a) complexes. After treatment with active LCAT, a significant apoB:r-apo(a) association was observed with LCAT-D LDL-density particles. Our data emphasize the importance of the integrity of LDL structure and composition for the formation of Lp(a). In addition, we demonstrate that the absence of LCAT activity has a fundamental impact on the regulation of plasma Lp(a) levels.\n\nFrank, Sasa\n\nKostner, Gerhard\n\nSteyrer, Ernst\n\n\n"
},
{
"text": "\n73950\nExtended adjuvant therapy with anastrozole among postmenopausal breast cancer patients: results from the randomized Austrian Breast and Colorectal Cancer Study Group Trial 6a.\n\nJakesz, R\n\nGreil, R\n\nGnant, M\n\nSchmid, M\n\nKwasny, W\n\nKubista, E\n\nMineritsch, B\n\nTausch, C\n\nStierer, M\n\nHofbauer, F\n\nRenner, K\n\nDadak, C\n\nRuecklinger, E\n\nSamonigg, H\n\nBeiträge in Fachzeitschriften\nISI:000251928200007\n18073378.0\n10.1093/jnci/djm246\nNone\nBACKGROUND: Clinical trial data have shown that among breast cancer patients who were disease free after 5 years of adjuvant treatment with tamoxifen, further extended treatment with the nonsteroidal aromatase inhibitor letrozole reduces breast cancer recurrence. We examined the efficacy and tolerability of extended adjuvant therapy with another aromatase inhibitor, anastrozole, for 3 years among women who had completed 5 years of adjuvant therapy. METHODS: Austrian Breast and Colorectal Cancer Study Group (ABCSG) Trial 6a is an extension of ABCSG Trial 6, in which hormone receptor-positive postmenopausal patients received 5 years of adjuvant tamoxifen, with or without the aromatase inhibitor aminoglutethimide, for the first 2 years of therapy. For ABCSG Trial 6a, patients who were disease free at the end of Trial 6 were randomly assigned to receive either 3 years of anastrozole or no further treatment. Efficacy data were analyzed with the use of a Cox proportional hazards regression model with two-sided P values and Kaplan-Meier curves, and tolerability data were estimated using logistic regression analysis with odds ratios and 95% confidence intervals (CIs). RESULTS: ABCSG Trial 6a included 856 patients. At a median follow-up of 62.3 months, women who received anastrozole (n = 387) had a statistically significantly reduced risk of recurrence (locoregional recurrence, contralateral breast cancer, or distant metastasis) compared with women who received no further treatment (n = 469; hazard ratio = 0.62; 95% CI = 0.40 to 0.96, P = .031). Anastrozole was well tolerated, and no unexpected adverse events were reported. CONCLUSIONS: These data confirm the benefit of extending adjuvant tamoxifen therapy beyond 5 years with anastrozole compared with no further treatment. Further research is required to define the optimum length of extended adjuvant therapy and to investigate the possibility of tailoring this period to suit different disease types.\n\nSamonigg, Hellmut\n\n\n"
},
{
"text": "\n77009\nOutcome in borderline disorders. A literature review\n\nRothenhäusler, HB\n\nKapfhammer, HP\n\nBeiträge in Fachzeitschriften\nISI:000080521100002\n10367212.0\n10.1055/s-2007-993997\nNone\nThis paper reviews the current state of research results on borderline disorders in terms of course and outcome, variables predisposing to good or poor outcome, suicide rates and the influence of psychotherapeutical and pharmacotherapeutical strategies. It turned out that course and outcome of borderline disorders depend on the applied diagnostic criteria and on the length of the follow-up period. The outcome of the follow-up studies of borderline schizophrenia and of the borderline syndrome according to Grinker was on the whole worse compared to those of borderline personality disorder defined by DSM-III/III-R or DIB according to Gunderson or Kernberg's criteria. Further, it could be shown that the GAS or HSRS values of the short-term follow-up studies (up to five years) ranged from 46.4 to 59.2 points whereas those of the long-term studies with an average period of 13.6 till 20 years were measured in the lower and in the mid-60 s that reflects only mild difficulties in psychosocial functioning. However, the high rate of completed suicide in BPD was to be respected: The most extensive follow-up investigation with the highest trace-rate (PI-500) revealed a suicide rate of 9% till now, and the most lethal combination of circumstances was BPD x MAD x alcohol abuse (suicide rate of 38%). Prognostic factors predisposing to poor outcome were substance abuse, admixture with antisocial and schizotypal elements, chronic hostility and affective instability with depressive and anxious features. Prognostic factors predisposing to good outcome were high IQ, extraordinary talent, high attractiveness, likeability and regular appointments with the Alcoholics Anonymous. Finally, the influence of psycho- and pharmacotherapeutical interventions were controversially debated. Several psychodynamic therapy studies resulted in satisfactory outcome scores concerning a subgroup of patients with personality traits like warmth, likeability, reliability, talent. Behavioral treatment strategies such as dialectical behavior therapy by Linehan significantly diminished parasuicidality and impulsiveness. Psychopharmacotherapy should target predominating psychopathological features: Low-dose antipsychotics against micropsychosis and prolonged severe dissociative symptoms, SSRIs and MAOIs against affective instability, and, lithium, carbamazepine or valproate against severe impulsiveness and aggressiveness.\n\nKapfhammer, Hans-Peter\n\nRothenhäusler, Hans-Bernd\n\n\n"
},
{
"text": "\n106777\nEffects of subthalamic stimulation on speech of consecutive patients with Parkinson disease.\n\nTripoliti, E\n\nZrinzo, L\n\nMartinez-Torres, I\n\nFrost, E\n\nPinto, S\n\nFoltynie, T\n\nHoll, E\n\nPetersen, E\n\nRoughton, M\n\nHariz, MI\n\nLimousin, P\n\nBeiträge in Fachzeitschriften\nISI:000285682800016\n21068426.0\n10.1212/WNL.0b013e318203e7d0\nPMC3262409\nObjective: Subthalamic nucleus deep brain stimulation (STN-DBS) is an effective treatment for advanced Parkinson disease (PD). Following STN-DBS, speech intelligibility can deteriorate, limiting its beneficial effect. Here we prospectively examined the short-and long-term speech response to STN-DBS in a consecutive series of patients to identify clinical and surgical factors associated with speech change. Methods: Thirty-two consecutive patients were assessed before surgery, then 1 month, 6 months, and 1 year after STN-DBS in 4 conditions on-and off-medication with on-and off-stimulation using established and validated speech and movement scales. Fifteen of these patients were followed up for 3 years. A control group of 12 patients with PD were followed up for 1 year. Results: Within the surgical group, speech intelligibility significantly deteriorated by an average of 14.2% +/- 20.15% off-medication and 16.9% +/- 21.8% on-medication 1 year after STN-DBS. The medical group deteriorated by 3.6% +/- 5.5% and 4.5% +/- 8.8%, respectively. Seven patients showed speech amelioration after surgery. Loudness increased significantly in all tasks with stimulation. A less severe preoperative on-medication motor score was associated with a more favorable speech response to STN-DBS after 1 year. Medially located electrodes on the left STN were associated with a significantly higher risk of speech deterioration than electrodes within the nucleus. There was a strong relationship between high voltage in the left electrode and poor speech outcome at 1 year. Conclusion: The effect of STN-DBS on speech is variable and multifactorial, with most patients exhibiting decline of speech intelligibility. Both medical and surgical issues contribute to deterioration of speech in STN-DBS patients. Classification of evidence: This study provides Class III evidence that STN-DBS for PD results in deterioration in speech intelligibility in all combinations of medication and stimulation states at 1 month, 6 months, and 1 year compared to baseline and to control subjects treated with best medical therapy. Neurology (R) 2011; 76:80-86\n\nHoll, Etienne\n\n\n"
}
]
}