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"text": "\n2302\nSecondary prevention following coronary intervention. Survey of 13 intervention centers in Austria\n\nDrexel, H\n\nGaul, GB\n\nGrimm, G\n\nKlein, W\n\nKleemann, L\n\nLeisch, F\n\nMlczoch, J\n\nPichler, M\n\nSailer, S\n\nSlany, J\n\nSteinbach, K\n\nTragl, KH\n\nMori, M\n\nKühn, P\n\nBeiträge in Fachzeitschriften\nISI:000082580800006\n10510842.0\nNone\nNone\nRisk factor control has been shown to reduce the incidence of coronary events in patients with or without preceding infarction. Secondary prevention should therefore be borne in mind by every cardiologist. In order to test this concept and/or to promote secondary prevention in our country, the following survey was conducted by our working group for epidemiology and prevention. All interventional centres of the country (7 million inhabitants) were asked to report relevant data of 50 consecutive patients with PTCA in a structured questionnaire. Thirteen centres responded and we report the data of 650 patients. The mean proportion of women was 28%, the mean age 61.1 years and the mean stent rate 49.8%. The indications for PTCA varied widely: stable angina 10-74%, unstable angina 10-86%, primary PTCA 0-22%. The risk factor history was distributed as follows: diabetes 12-46% (mean 22.3%), hypertension 32-68% (mean 54.2%), current smoking 6-56% (mean 21.9%), and total cholesterol (TChol) > 200 mg/dl: 30-78% (mean 60.3%). Current lipid values were available for T chol. in 44-100% (mean 84.5%) and for LDL in 4-100% (mean 67.1%). Dietary counselling by a dietician was done in 4-100% of patients (mean 35.6%) Information concerning the hazards of smoking was given to 25-100% (mean 83.6%) of current smokers. Drug treatment at hospital discharge was as follows: 84-100% (mean 93.1%) received ASA, 24-74% (mean 49.8%) ticlopidine, 6-84% (mean 53.3%) nitrates, 34-82% (mean 60.2%) beta blockers, 10-70% (mean 39.5%) ACE inhibitors, 4-74% (mean 4 7.2%) lipid lowering drugs, 7-48% (mean 17.8%) calcium antagonists, 0-12% (mean 6.1%) digitalis and 0-28% (mean 13.6%) diuretics. Follow-up data were collected in 4 centres at 6 months post discharge and were available for 174 patients. Here we found an increase in the prescription of calcium antagonists, digitalis and statins. The following conclusions were drawn at a conference in which all centres participated: lipid values should be available for each patient at PTCA, dietary counselling should be initiated for every patient during hospitalisation (and continued by the family physician) and the national cardiac society should promote guidelines for the use of drugs in which the variation in use is too wide at present. It should be ensured that these guidelines are implemented not only in patients after AMI but also in those after PTCA.\n\n\n"
},
{
"text": "\n114329\nThe impact of tumor multifocality on outcomes in patients treated with radical nephroureterectomy.\n\nChromecki, TF\n\nCha, EK\n\nFajkovic, H\n\nMargulis, V\n\nNovara, G\n\nScherr, DS\n\nLotan, Y\n\nRaman, JD\n\nKassouf, W\n\nBensalah, K\n\nWeizer, A\n\nKikuchi, E\n\nRoscigno, M\n\nRemzi, M\n\nMatsumoto, K\n\nWalton, TJ\n\nPycha, A\n\nFicarra, V\n\nKarakiewicz, PI\n\nZigeuner, R\n\nPummer, K\n\nShariat, SF\n\nBeiträge in Fachzeitschriften\nISI:000298248700011\n21975249.0\n10.1016/j.eururo.2011.09.017\nNone\nBACKGROUND: The prognostic impact of multifocal upper-tract urothelial carcinoma (UTUC) is poorly understood. OBJECTIVE: To investigate the association between tumor multifocality and clinicopathologic features and outcomes of UTUC in patients managed by radical nephroureterectomy (RNU). DESIGN, SETTING, AND PARTICIPANTS: The study included 2492 patients treated with either open or laparoscopic RNU. Tumor and patient characteristics included tumor stage, tumor grade, lymph node status, lymphovascular invasion (LVI), tumor architecture, tumor location, unifocal or multifocal disease, gender, age, history of bladder cancer (BCa), Eastern Cooperative Oncology Group (ECOG) performance status (PS), and adjuvant chemotherapy. tumor multifocality of UTUC was defined as the synchronous presence of multiple tumors in the renal pelvis or ureter. INTERVENTION: All patients were treated with either open or laparoscopic RNU. MEASUREMENTS: Univariable and multivariable models tested the effect of tumor multifocality on disease progression and cancer-specific mortality. RESULTS AND LIMITATIONS: Five hundred ninety patients (23.7%) had tumor multifocality at the time of RNU. The median follow-up was 45 mo (interquartile range [IQR]: 0-101). Tumor multifocality was significantly associated with a history of previous BCa (p=0.032), lymph node involvement (p=0.036), tumor location in the ureter (p=0.003), higher tumor stage (p<0.001), higher tumor grade (p<0.001), sessile tumor architecture (p=0.003), and LVI (p=0.001). In organ-confined patients, tumor multifocality was an independent predictor of both disease progression (hazard ratio [HR]: 1.43; p=0.019) and cancer-specific mortality (HR: 1.46; p=0.027). When assessed in all patients, tumor multifocality was associated with both disease progression and cancer-specific mortality in univariable (p=0.005 and p=0.006, respectively) but not in multivariable analyses (p=0.468 and p=0.798, respectively). The main limitation is the retrospective design of the study. CONCLUSIONS: Tumor multifocality is an independent prognosticator of disease progression and cancer-specific mortality in patients with organ-confined UTUC treated with RNU. Multifocal organ-confined patients with UTUC may need closer follow-up. Integration of tumor multifocality with other factors may help identify those patients who would benefit from multimodal therapy. Copyright © 2011 European Association of Urology. Published by Elsevier B.V. All rights reserved.\n\nPummer, Karl\n\nZigeuner, Richard\n\n\n"
},
{
"text": "\n119563\nPharmacology of a selective cyclooxygenase-2 inhibitor, HN-56249: a novel compound exhibiting a marked preference for the human enzyme in intact cells.\n\nBerg, J\n\nFellier, H\n\nChristoph, T\n\nKremminger, P\n\nHartmann, M\n\nBlaschke, H\n\nRovensky, F\n\nTowart, R\n\nStimmeder, D\n\nBeiträge in Fachzeitschriften\nISI:000086158700002\n10763850.0\n10.1007/s002109900192\nNone\nHN-56249 (3-(2, -dichlorothiophenoxy)-4-methylsulfonylamino-benzenesu lfonamide), a highly selective cyclooxygenase (COX)-2 inhibitor, is the prototype of a novel series of COX inhibitors comprising bicyclic arylethersulfonamides; of this series HN-56249 is the most potent and selective human COX-2 inhibitor. HN-56249 inhibited platelet aggregation as a measure of COX-1 activity only moderately (IC50 26.5+/-1.7 microM). In LPS-stimulated monocytic cells the release of prostaglandin (PG) F1alpha as a measure of COX-2 was markedly inhibited (IC50 0.027+/-0.001 microM). Thus, HN-56249 showed an approximately 1000-fold selectivity for COX-2 in intact cells. In whole blood assays HN-56249 showed a potent inhibitory activity for COX-2 (IC50 0.78+/-0.37 microM) only. COX-1 was only weakly inhibited (IC50 867+/-181 microM). Hence, HN-56249 exhibited a greater than 1000-fold selectivity for whole blood COX-2. HN-56249 surpassed the COX-2 selectivities of the COX-2 selective inhibitors 3-cyclohexyloxy-4-methylsulfonylamino-nitrobenzene (NS-398) and 6-(2, -difluorophenoxy)-5-methyl-sulfonylamino-1-indanone (flosulide) in the intact cell assays by eight- and threefold, respectively, and in the whole blood assays by approximately 40-fold. Following i.v. administration HN-56249 inhibited carrageenan-induced rat paw oedema only moderately (ID50 26.2+/-5.7 mg/kg, mean +/- SEM), approximately tenfold less potent than indomethacin (ID50 2.1+/-0.2 mg/kg, mean +/- SEM). After oral administration HN-56249 reversed thermal hyperalgesia in the carrageenan-induced rat paw oedema test, however, some 30-fold less potently than diclofenac. Comparing the inhibitory potency of HN-56249 against human COX-2 with that against murine COX-2 in intact cells revealed a 300-fold selectivity for the human enzyme. Similar effects were observed with other COX-2-selective arylethersulfonamides. In contrast, non-COX-2-selective arylethersulfonamides, including a highly selective COX-1 inhibitor, inhibited human and murine COX-2 approximately equipotently. In conclusion, HN-56249 is a novel potent and highly selective COX-2 inhibitor with a marked preference for the human COX-2 enzyme in vitro. Despite excellent bioavailability and the long plasma half-life of HN-56249, anti-inflammatory effects in rodents were only moderate. We suggest these differing in vitro-in vivo effects observed could be due to significant inflammatory prostaglandin synthesis by COX-1, or to the genetic differences between human and rodent COX-2, or to both.\n\n\n"
},
{
"text": "\n124629\nPrimary care management for optimized antithrombotic treatment [PICANT]: study protocol for a cluster-randomized controlled trial.\n\nSiebenhofer, A\n\nUlrich, LR\n\nMergenthal, K\n\nRoehl, I\n\nRauck, S\n\nBerghold, A\n\nHarder, S\n\nGerlach, FM\n\nPetersen, JJ\n\nBeiträge in Fachzeitschriften\nISI:000311623700001\n22929015.0\n10.1186/1748-5908-7-79\nPMC3499320\nBackground: Antithrombotic treatment is a continuous therapy that is often performed in general practice and requires careful safety management. The aim of this study is to investigate whether a best-practice model that applies major elements of case management and patient education, can improve antithrombotic management in primary healthcare in terms of reducing major thromboembolic and bleeding events. Methods: This 24-month cluster-randomized trial will be performed with 690 adult patients from 46 practices. The trial intervention will be a complex intervention involving general practitioners, healthcare assistants, and patients with an indication for oral anticoagulation. To assess adherence to medication and symptoms in patients, as well as to detect complications early, healthcare assistants will be trained in case management and will use the Coagulation-Monitoring List (Co-MoL) to regularly monitor patients. Patients will receive information (leaflets and a video), treatment monitoring via the Co-MoL and be motivated to perform self-management. Patients in the control group will continue to receive treatment as usual from their general practitioners. The primary endpoint is the combined endpoint of all thromboembolic events requiring hospitalization and all major bleeding complications. Secondary endpoints are mortality, hospitalization, strokes, major bleeding and thromboembolic complications, severe treatment interactions, the number of adverse events, quality of anticoagulation, health-related quality of life, and costs. Further secondary objectives will be investigated to explain the mechanism by which the intervention is effective: patients' assessment of chronic illness care, self-reported adherence to medication, general practitioners' and healthcare assistants' knowledge, and patients' knowledge and satisfaction with shared decision making. Practice recruitment is expected to take place between July and December 2012. Recruitment of eligible patients will start in July 2012. Assessment will occur at three time points: baseline and follow-up after 12 months and after 24 months. Discussion: The efficacy and effectiveness of individual elements of the intervention, such as antithrombotic interventions, self-management concepts in orally anticoagulated patients, and the methodological tool of case management, have already been extensively demonstrated. This project foresees the combination of several proven instruments, as a result of which we expect to profit from a reduction in the major complications associated with antithrombotic treatment.\n\nBerghold, Andrea\n\nSiebenhofer-Kroitzsch, Andrea\n\n\n"
},
{
"text": "\n156489\nFrom Mouth to Model: Combining <i>in vivo</i> and <i>in vitro</i> Oral Biofilm Growth.\n\nKlug, B\n\nSantigli, E\n\nWestendorf, C\n\nTangl, S\n\nWimmer, G\n\nGrube, M\n\nBeiträge in Fachzeitschriften\nISI:000383645900001\n27708626.0\n10.3389/fmicb.2016.01448\nPMC5030783\nBackground: Oral biofilm studies based on simplified experimental setups are difficult to interpret. Models are limited mostly by the number of bacterial species observed and the insufficiency of artificial media. Few studies have attempted to overcome these limitations and to cultivate native oral biofilm. Aims: This study aimed to grow oral biofilm in vivo before transfer to a biofilm reactor for ex situ incubation. The in vitro survival of this oral biofilm and the changes in bacterial composition over time were observed. Methods: Six human enamel-dentin slabs embedded buccally in dental splints were used as biofilm carriers. Fitted individually to the upper jaw of 25 non-smoking male volunteers, the splints were worn continuously for 48 h. During this time, tooth-brushing and alcohol-consumption were not permitted. The biofilm was then transferred on slabs into a biofilm reactor and incubated there for 48 h while being nourished in BHI medium. Live/dead staining and confocal laser scanning microscopy were used to observe bacterial survival over four points in time: directly after removal (T0) and after 1 (T1), 24 (T2), and 48 h (T3) of incubation. Bacterial diversity at T0 and T3 was compared with 454-pyrosequencing. Fluorescence in situ hybridization (FISH) was performed to show specific taxa. Survival curves were calculated with a specially designed MATLAB script. Acacia and QIIME 1.9.1 were used to process pyrosequencing data. SPSS 21.0 and R 3.3.1 were used for statistical analysis. Results: After initial fluctuations at T1, survival curves mostly showed approximation of the bacterial numbers to the initial level at T3. Pyrosequencing analysis resulted in 117 OTUs common to all samples. The genera Streptococcus and Veillonella (both Firmicutes) dominated at T0 and T3. They make up two thirds of the biofilm. Genera with lower relative abundance had grown significantly at T3. FISH analysis confirmed the pyrosequencing results, i.e., the predominant staining of Firmicutes. Conclusion: We demonstrate the in vitro survival of native primary oral biofilm in its natural complexity over 48 h. Our results offer a baseline for cultivation studies of native oral biofilms in (phyto-) pharmacological and dental materials research. Further investigations and validation of culturing conditions could also facilitate the study of biofilm-induced diseases.\n\nKlug, Barbara\n\nSantigli, Elisabeth\n\nWimmer, Gernot\n\n\n"
},
{
"text": "\n161590\nHuman presence impacts fungal diversity of inflated lunar/Mars analog habitat.\n\nBlachowicz, A\n\nMayer, T\n\nBashir, M\n\nPieber, TR\n\nDe León, P\n\nVenkateswaran, K\n\nBeiträge in Fachzeitschriften\nISI:000405108600001\n28693587.0\n10.1186/s40168-017-0280-8\nPMC5504618\nAn inflatable lunar/Mars analog habitat (ILMAH), simulated closed system isolated by HEPA filtration, mimics International Space Station (ISS) conditions and future human habitation on other planets except for the exchange of air between outdoor and indoor environments. The ILMAH was primarily commissioned to measure physiological, psychological, and immunological characteristics of human inhabiting in isolation, but it was also available for other studies such as examining its microbiological aspects. Characterizing and understanding possible changes and succession of fungal species is of high importance since fungi are not only hazardous to inhabitants but also deteriorate the habitats. Observing the mycobiome changes in the presence of human will enable developing appropriate countermeasures with reference to crew health in a future closed habitat.\n Succession of fungi was characterized utilizing both traditional and state-of-the-art molecular techniques during the 30-day human occupation of the ILMAH. Surface samples were collected at various time points and locations to observe both the total and viable fungal populations of common environmental and opportunistic pathogenic species. To estimate the cultivable fungal population, potato dextrose agar plate counts method was utilized. The internal transcribed spacer region-based iTag Illumina sequencing was employed to measure the community structure and fluctuation of the mycobiome over time in various locations. Treatment of samples with propidium monoazide (PMA; a DNA intercalating dye for selective detection of viable microbial populations) had a significant effect on the microbial diversity compared to non-PMA-treated samples. Statistical analysis confirmed that viable fungal community structure changed (increase in diversity and decrease in fungal burden) over the occupation time. Samples collected at day 20 showed distinct fungal profiles from samples collected at any other time point (before or after). Viable fungal families like Davidiellaceae, Teratosphaeriaceae, Pleosporales, and Pleosporaceae were shown to increase during the occupation time.\n The results of this study revealed that the overall fungal diversity in the closed habitat changed during human presence; therefore, it is crucial to properly maintain a closed habitat to preserve it from deteriorating and keep it safe for its inhabitants. Differences in community profiles were observed when statistically treated, especially of the mycobiome of samples collected at day 20. On a genus level Epiccocum, Alternaria, Pleosporales, Davidiella, and Cryptococcus showed increased abundance over the occupation time.\n\nPieber, Thomas\n\n\n"
},
{
"text": "\n184407\nAcute Cardiovascular Manifestations in 286 Children With Multisystem Inflammatory Syndrome Associated With COVID-19 Infection in Europe.\n\nValverde, I\n\nSingh, Y\n\nSanchez-de-Toledo, J\n\nTheocharis, P\n\nChikermane, A\n\nDi Filippo, S\n\nKuciñska, B\n\nMannarino, S\n\nTamariz-Martel, A\n\nGutierrez-Larraya, F\n\nSoda, G\n\nVandekerckhove, K\n\nGonzalez-Barlatay, F\n\nMcMahon, CJ\n\nMarcora, S\n\nNapoleone, CP\n\nDuong, P\n\nTuo, G\n\nDeri, A\n\nNepali, G\n\nIlina, M\n\nCiliberti, P\n\nMiller, O\n\nAEPC COVID-19 Rapid Response Team*\n\nBeiträge in Fachzeitschriften\nNone\n33166189.0\n10.1161/CIRCULATIONAHA.120.050065\nNone\nThe aim of the study was to document cardiovascular clinical findings, cardiac imaging, and laboratory markers in children presenting with the novel multisystem inflammatory syndrome associated with coronavirus disease 2019 (COVID-19) infection.\n This real-time internet-based survey has been endorsed by the Association for European Paediatric and Congenital Cardiologists Working Groups for Cardiac Imaging and Cardiovascular Intensive Care. Children 0 to 18 years of age admitted to a hospital between February 1 and June 6, 2020, with a diagnosis of an inflammatory syndrome and acute cardiovascular complications were included.\n A total of 286 children from 55 centers in 17 European countries were included. The median age was 8.4 years (interquartile range, 3.8-12.4 years) and 67% were boys. The most common cardiovascular complications were shock, cardiac arrhythmias, pericardial effusion, and coronary artery dilatation. Reduced left ventricular ejection fraction was present in over half of the patients, and a vast majority of children had raised cardiac troponin when checked. The biochemical markers of inflammation were raised in most patients on admission: elevated C-reactive protein, serum ferritin, procalcitonin, N-terminal pro B-type natriuretic peptide, interleukin-6 level, and D-dimers. There was a statistically significant correlation between degree of elevation in cardiac and biochemical parameters and the need for intensive care support (P<0.05). Polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 was positive in 33.6%, whereas immunoglobulin M and immunoglobulin G antibodies were positive in 15.7% cases and immunoglobulin G in 43.6% cases, respectively, when checked. One child in the study cohort died.\n Cardiac involvement is common in children with multisystem inflammatory syndrome associated with the Covid-19 pandemic. The majority of children have significantly raised levels of N-terminal pro B-type natriuretic peptide, ferritin, D-dimers, and cardiac troponin in addition to high C-reactive protein and procalcitonin levels. In comparison with adults with COVID-19, mortality in children with multisystem inflammatory syndrome associated with COVID-19 is uncommon despite multisystem involvement, very elevated inflammatory markers, and the need for intensive care support.\n\nGrangl, Gernot\n\n\n"
},
{
"text": "\n186692\nFurin Expression in Patients With Psoriasis-A Patient Cohort Endangered to SARS-COV2?\n\nGraier, T\n\nGolob-Schwarzl, N\n\nWeger, W\n\nBenezeder, T\n\nPainsi, C\n\nSalmhofer, W\n\nWolf, P\n\nBeiträge in Fachzeitschriften\nISI:000620988600001\n33644099.0\n10.3389/fmed.2021.624462\nPMC7902756\nBackground: SARS-Cov2 has raised concerns among dermatologists regarding psoriasis and its respective treatments. Comorbidities, which induce the expression of the proprotease furin have been associated with severe course of COVID-19. Furin and angiotensin converting enzyme 2 (ACE2) play a major role in viral host cell entry of SARS-Cov2. Objective: To evaluate mRNA expression of Furin and ACE2 from blood cells in psoriasis patients, and whether systemic or topical treatment reduces expression levels. Methods: This observational translational study analyzed blood samples from patients from a clinical trial and samples retrieved from the biobank of the Psoriasis Registry Austria (PsoRA). Furin and ACE2 expression levels were analyzed prior to as well as 3 and 12-24 months after start of biologic treatment with either ustekinumab or secukinumab. Additionally, the study analyzed expression levels prior to, 6 days after start of dithranol treatment and 4-6 weeks after end of dithranol treatment. Results: Furin mRNA expression was significantly increased at baseline in the biologic (4.9 ± 2.6 fold, p < 0.0001) and in the dithranol group (2.7 ± 1.4 fold, p < 0.001) compared to controls. There was a trend for arthritis patients to express more furin than patients with psoriatic skin involvement only (5.26 ± 2.30 vs. 3.48 ± 2.27, p = 0.078). Analyzing furin mRNA expression after treatment initiation with secukinumab or ustekinumab revealed a normalization of levels after 3 and 12 to 24 months. Similar findings were obtained for patients treated with dithranol, with significantly decreased expression levels 6 days after start of dithranol treatment and also at follow-up, (4-6 weeks after dithranol treatment had been terminated). ACE2 expression levels did not differ from controls at any timepoint, regardless of biologic or topical treatment. Conclusion: Significantly overexpressed levels of furin were observed in untreated patients, and, thus, these patients may be at risk for infection and a severe course of COVID-19. However, the data indicate that successful therapeutic intervention in psoriasis, by systemic biologic or topical treatment, can efficiently reduce furin levels in blood cells, possibly limiting the risk of psoriasis patients for a severe COVID-19 course. Clinical Trial Registration: ClinicalTrials.gov, identifier NCT02752672.\n Copyright © 2021 Graier, Golob-Schwarzl, Weger, Benezeder, Painsi, Salmhofer and Wolf.\n\nBenezeder, Theresa Helena\n\nGolob-Schwarzl, Nicole\n\nGraier, Thomas\n\nPainsi, Clemens\n\nSalmhofer, Wolfgang\n\nWeger, Wolfgang\n\nWolf, Peter\n\n\n"
},
{
"text": "\n187000\nThe Challenge to Decide between Pulmonary Hypertension Due to Chronic Lung Disease and PAH with Chronic Lung Disease.\n\nOlschewski, H\n\nBeiträge in Fachzeitschriften\nISI:000622451400001\n33671914.0\n10.3390/diagnostics11020311\nPMC7918977\nChronic lung diseases are strongly associated with pulmonary hypertension (PH), and even mildly elevated pulmonary arterial pressures are associated with increased mortality. Chronic obstructive pulmonary disease (COPD) is the most common chronic lung disease, but few of these patients develop severe PH. Not all these pulmonary pressure elevations are due to COPD, although patients with severe PH due to COPD may represent the largest subgroup within patients with COPD and severe PH. There are also patients with left heart disease (group 2), chronic thromboembolic disease (group 4, CTEPH) and pulmonary arterial hypertension (group 1, PAH) who suffer from COPD or another chronic lung disease as co-morbidity. Because therapeutic consequences very much depend on the cause of pulmonary hypertension, it is important to complete the diagnostic procedures and to decide on the main cause of PH before any decision on PAH drugs is made. The World Symposia on Pulmonary Hypertension (WSPH) have provided guidance for these important decisions. Group 2 PH or complex developmental diseases with elevated postcapillary pressures are relatively easy to identify by means of elevated pulmonary arterial wedge pressures. Group 4 PH can be identified or excluded by perfusion lung scans in combination with chest CT. Group 1 PAH and Group 3 PH, although having quite different disease profiles, may be difficult to discern sometimes. The sixth WSPH suggests that severe pulmonary hypertension in combination with mild impairment in the pulmonary function test (FEV1 > 60 and FVC > 60%), mild parenchymal abnormalities in the high-resolution CT of the chest, and circulatory limitation in the cardiopulmonary exercise test speak in favor of Group 1 PAH. These patients are candidates for PAH therapy. If the patient suffers from group 3 PH, the only possible indication for PAH therapy is severe pulmonary hypertension (mPAP ≥ 35 mmHg or mPAP between 25 and 35 mmHg together with very low cardiac index (CI) < 2.0 L/min/m2), which can only be derived invasively. Right heart catheter investigation has been established nearly 100 years ago, but there are many important details to consider when reading pulmonary pressures in spontaneously breathing patients with severe lung disease. It is important that such diagnostic procedures and the therapeutic decisions are made in expert centers for both pulmonary hypertension and chronic lung disease.\n\nOlschewski, Horst\n\n\n"
},
{
"text": "\n3404\nGamma knife surgery for epilepsy related to hypothalamic hamartomas.\n\nRégis, J\n\nBartolomei, F\n\nde Toffol, B\n\nGenton, P\n\nKobayashi, T\n\nMori, Y\n\nTakakura, K\n\nHori, T\n\nInoue, H\n\nSchröttner, O\n\nPendl, G\n\nWolf, A\n\nArita, K\n\nChauvel, P\n\nBeiträge in Fachzeitschriften\nISI:000165569900037\n11126905.0\n10.1097%2F00006123-200012000-00014\nNone\nOBJECTIVE: Drug-resistant epilepsy associated with hypothalamic hamartomas (HHs) can be cured by microsurgical resection of the lesions. Morbidity and mortality rates for microsurgery in this area are significant. Gamma knife surgery (GKS) is less invasive and seems to be well adapted for this indication. METHODS: To evaluate the safety and efficacy of GKS to treat this uncommon pathological condition, we organized a multicenter retrospective study. Ten patients were treated in seven different centers. The follow-up periods were more than 12 months for eight patients, with a median follow-up period of 28 months (mean, 35 mo; range, 12-71 mo). All patients had severe drug-resistant epilepsy, including frequent gelastic and generalized tonic or tonicoclonic attacks. The median age was 13.5 years (range, 1-32 yr; mean, 14 yr) at the time of GKS. Three patients experienced precocious puberty. All patients had sessile HHs. The median marginal dose was 15.25 Gy (range, 12-20 Gy). Two patients were treated two times (at 19 and 49 mo) because of insufficient efficacy. RESULTS: All patients exhibited improvement. Four patients were seizure-free, one experienced rare nocturnal seizures, one experienced some rare partial seizures but no more generalized attacks, and two exhibited only improvement, with reductions in the frequency of seizures but persistence of some rare generalized seizures. Two patients, now seizure-free, were considered to exhibit insufficient improvement after the first GKS procedure and were treated a second time. A clear correlation between efficacy and dose was observed in this series. The marginal dose was more than 17 Gy for all patients in the successful group and less than 13 Gy for all patients in the "improved" group. No side effects were reported, except for poikilothermia in one patient. Behavior was clearly improved for two patients (with only slight improvements in their epilepsy). Complete coverage of the HHs did not seem to be mandatory, because the dosimetry spared a significant part of the lesions for two patients in the successful group. CONCLUSION: We report the first series demonstrating that GKS can be a safe and effective treatment for epilepsy related to HHs. We advocate marginal doses greater than or equal to 17 Gy and partial dose-planning when necessary, for avoidance of critical surrounding structures.\n\n\n"
},
{
"text": "\n107101\nEffect of sex and bezafibrate on incorporation of blood borne palmitate into lipids of rat liver nuclei.\n\nGórski, J\n\nZendzian-Piotrowska, M\n\nWolfrum, C\n\nNawrocki, A\n\nSpener, F\n\nBeiträge in Fachzeitschriften\nISI:000165380700008\n11195790.0\n10.1023/A:1007189503183\nNone\nThe aim of the present study was to investigate whether lipid metabolism in the nuclei is affected by changes in the metabolism of free fatty acids in the liver. The experiments were carried out on 3 groups of rats: 1 - control-male, 2 - female, and 3 - male, treated with bezafibrate (a peroxisome proliferator). The rats received 14C-palmitic acid intravenously. Thirty min later liver samples and blood from the abdominal aorta were taken. The liver nuclei were isolated in sucrose gradient. Lipids were extracted from the nuclei and the liver homogenate and subsequently separated into the following fractions: phospholipids, mono, di- and triacylglycerols, free fatty acids, cholesterol and cholesterol esters. The radioactivity of each fraction was counted. Furthermore, the content of free fatty acids and the fatty acid binding proteins was measured. It was found that radioactivity was present in each lipid fraction obtained from the liver homogenate and from the nuclei. In the female group, the total radioactivity of lipids in the liver homogenate was lower, whereas in the nuclei it was higher in comparison to the male group. The reduction in the radioactivity in the liver was mostly accounted for by decreased radioactivity in the fraction oftriacylglycerols and phospholipids. In the nuclei, the radioactivity of the fraction of phospholipids, free fatty acids and diacylglycerols was elevated. Bezafibrate did not affect the total radioactivity of lipids in the liver and reduced it in the nuclei. In the liver, the drug increased radioactivity mostly in the fraction of phospholipids and reduced it mainly in the fraction of triacylglycerols. In the nuclei, the radioactivity of each lipid fraction examined was reduced. The content of the fraction of free fatty acids in the liver and in the nuclei in the female and in the bezafibrate-treated groups did not differ from the respective value in the control group. The content of fatty acid binding proteins in the nuclei of the female and bezafibrate-treated groups increased in parallel to the elevation in their content in the cytosol. It is concluded that the female sex hormones and bezafibrate influence the transport of selected lipids into the nuclei. The effects seem to be a consequence of the action of these factors directly on the nucleus.\n\n\n"
},
{
"text": "\n119050\nThe influence of timing on the functional and morphological result after nerve grafting: an experimental study in rabbits.\n\nRab, M\n\nKoller, R\n\nHaslik, W\n\nKamolz, LP\n\nBeck, H\n\nMeggeneder, J\n\nFrey, M\n\nBeiträge in Fachzeitschriften\nISI:000180679300005\n12550115.0\n10.1054/bjps.2002.3965\nNone\nClinical experience and experimental work in sheep have shown that a two-stage approach to restoring muscle function with a long nerve graft and free muscle grafting seems to be more beneficial than a one-stage approach. Based on a standardised experimental protocol, one-stage and two-stage nerve grafting approaches in rabbits were compared, and the actual differences in muscle force, together with morphological data, were calculated. In 20 rabbits the saphenous nerve was used as a 7 cm nerve graft. Animals were separated into two groups. In group 1, 10 rabbits underwent a one-stage approach to reinnervate the rectus femoris muscle. In the left hindlimb, the proximal end of the graft was coapted to the cut motor nerve branch of the vastus medialis muscle, and the distal end was coapted to the nerve branch of the rectus femoris muscle. In group 2, 10 rabbits underwent a two-stage approach, leaving the distal end of the nerve graft unconnected to the rectus femoris muscle in the first stage. In the second stage, this end was coapted to the freshly cut motor nerve branch of the rectus femoris muscle. After 15 months, the maximum tetanic tensions in the reinnervated rectus femoris muscle and the contralateral unoperated muscle were determined. The graft and the motor branch distal to the graft were biopsied in order to count the number of regenerated myelinated nerve fibres. The mean+/-s.d. maximum tetanic tensions in the reinnervated rectus femoris muscles were 10.6+/-4.9 N in group 1 and 21.4+/-1.1 N in group 2. Compared with the unoperated side, the muscle force following denervation and reinnervation was 38.3% in group 1 and 58.9% in group 2 (P=0.01). The mean+/-s.d. numbers of regenerated myelinated nerve fibres distal to the graft in the rectus femoris muscle branch were 737+/-340 in group 1 and 1487+/-1004 in group 2 (P=0.05). These results show that the neurotrophic effect of an immediately connected target organ is far outweighed by the adverse effect of the longer period of muscle denervation. Therefore, nerve grafting and muscle transplantation should not be performed in the same operation. Copyright 2002 The British Association of Plastic Surgeons. Published by Elsevier Science Ltd. All rights reserved.\n\nKamolz, Lars-Peter\n\n\n"
},
{
"text": "\n142570\nProgressive improvement in cutaneous and extracutaneous chronic graft-versus-host disease after a 24-week course of extracorporeal photopheresis--results of a crossover randomized study.\n\nGreinix, HT\n\nvan Besien, K\n\nElmaagacli, AH\n\nHillen, U\n\nGrigg, A\n\nKnobler, R\n\nParenti, D\n\nReddy, V\n\nTheunissen, K\n\nMichallet, M\n\nFlowers, ME\n\nUVADEX Chronic GVHD Study Group\n\nBeiträge in Fachzeitschriften\nISI:000300472700008\n21621629.0\n10.1016/j.bbmt.2011.05.004\nNone\nIn a prior multicenter randomized controlled trial, we found that a 12-week course of extracorporeal photopheresis (ECP) plus standard immunosuppressive therapy resulted in several beneficial outcomes in patients with corticosteroid-refractory/intolerant/dependent chronic graft-versus-host disease (GVHD). Here, we report the results of an open-label crossover ECP study in 29 eligible participants randomized initially to the standard of care non-ECP (control) arm. Eligible for the crossover ECP study were control arm patients who either (1) had progression of cutaneous chronic GVHD (cGVHD), defined as >25% worsening from baseline as measured by the percent change in the total skin score (TSS) at any time, or (2) had less than 15% improvement in the TSS, or had a ≤25% reduction in corticosteroid dose at week 12 of the initial study. ECP was administered 3 times during week 1, then twice weekly until week 12, followed by 2 treatments monthly until week 24. The median age of the study cohort was 43 (20-67) years and 90% had extensive cGVHD. The median months from onset of cGVHD to start of ECP were 26 (range: 4-79). Twenty-five of 29 patients (86%) completed the 24-week course of ECP. Complete or partial skin response at week 24 was noted in 9 patients (31%). The median percent of decrease in TSS from baseline to weeks 12 and 24 was -7.9 and -25.8, respectively. In 4 (17%) and 8 (33%) patients, a ≥50% reduction in corticosteroid dose at weeks 12 and 24 was observed. Extracutaneous cGVHD response was highest in oral mucosa with 70% complete and partial resolution after week 24. In conclusion, progressive improvement in cutaneous and extracutaneous cGVHD was observed after a 24-week course of ECP in patients who previously had no clinical improvement or exhibited worsening of cGVHD while receiving standard immunosuppressive therapy alone in a randomized study. These results confirm previous findings and support the notion that prolonged ECP appears to be necessary for optimal therapeutic effects in corticosteroid-refractory cGVHD patients.\n Copyright © 2011 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.\n\nGreinix, Hildegard\n\n\n"
},
{
"text": "\n164855\nResident cell lineages are preserved in pulmonary vascular remodeling.\n\nCrnkovic, S\n\nMarsh, LM\n\nEl Agha, E\n\nVoswinckel, R\n\nGhanim, B\n\nKlepetko, W\n\nStacher-Priehse, E\n\nOlschewski, H\n\nBloch, W\n\nBellusci, S\n\nOlschewski, A\n\nKwapiszewska, G\n\nBeiträge in Fachzeitschriften\nISI:000428213800012\n29359814.0\n10.1002/path.5044\nPMC5903372\nPulmonary vascular remodeling is the main pathological hallmark of pulmonary hypertension disease. We undertook a comprehensive and multilevel approach to investigate the origin of smooth muscle actin-expressing cells in remodeled vessels. Transgenic mice that allow for specific, inducible, and permanent labeling of endothelial (Cdh5-tdTomato), smooth muscle (Acta2-, Myh11-tdTomato), pericyte (Cspg4-tdTomato), and fibroblast (Pdgfra-tdTomato) lineages were used to delineate the cellular origins of pulmonary vascular remodeling. Mapping the fate of major lung resident cell types revealed smooth muscle cells (SMCs) as the predominant source of cells that populate remodeled pulmonary vessels in chronic hypoxia and allergen-induced murine models. Combining in vivo cell type-specific, time-controlled labeling of proliferating cells with a pulmonary artery phenotypic explant assay, we identified proliferation of SMCs as an underlying remodeling pathomechanism. Multicolor immunofluorescence analysis showed a preserved pattern of cell type marker localization in murine and human pulmonary arteries, in both donors and idiopathic pulmonary arterial hypertension (IPAH) patients. Whilst neural glial antigen 2 (chondroitin sulfate proteoglycan 4) labeled mostly vascular supportive cells with partial overlap with SMC markers, PDGFRα-expressing cells were observed in the perivascular compartment. The luminal vessel side was lined by a single cell layer expressing endothelial markers followed by an adjacent and distinct layer defined by SMC marker expression and pronounced thickening in remodeled vessels. Quantitative flow cytometric analysis of single cell digests of diverse pulmonary artery layers showed the preserved separation into two discrete cell populations expressing either endothelial cell (EC) or SMC markers in human remodeled vessels. Additionally, we found no evidence of overlap between EC and SMC ultrastructural characteristics using electron microscopy in either donor or IPAH arteries. Lineage-specific marker expression profiles are retained during pulmonary vascular remodeling without any indication of cell type conversion. The expansion of resident SMCs is the major underlying and evolutionarily conserved paradigm of pulmonary vascular disease pathogenesis. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.\n © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.\n\nCrnkovic, Slaven\n\nKwapiszewska-Marsh, Grazyna\n\nMarsh, Leigh\n\nOlschewski, Andrea\n\nOlschewski, Horst\n\n\n"
},
{
"text": "\n118816\nAdipose tissue engineering: three different approaches to seed preadipocytes on a collagen-elastin matrix.\n\nKeck, M\n\nHaluza, D\n\nSelig, HF\n\nJahl, M\n\nLumenta, DB\n\nKamolz, LP\n\nFrey, M\n\nBeiträge in Fachzeitschriften\nISI:000296563100013\n21956145.0\n10.1097/SAP.0b013e31822f9946\nNone\nBACKGROUND: Millions of plastic and reconstructive surgical procedures are performed each year to repair soft-tissue defects that result from significant burns, tumor resections, or congenital defects. Tissue-engineering strategies have been investigated to develop methods for generating soft-tissue. Preadipocytes represent a promising autologous cell source for adipose tissue engineering. These immature precursor cells, which are located between the mature adipocytes in the adipose tissue, are much more resistant to mechanical stress and ischemic conditions than mature adipocytes. To use preadipocytes for tissue-engineering purposes, cells were isolated from human adipose tissue and seeded onto scaffolds. Once processed, preadipocytes become subject to the human tissue act and require handling under much tighter regulations. Therefore, we intended to identify any influence caused by processing of preadipocytes prior to seeding on the reconstructed adipose tissue formation. MATERIAL AND METHOD: Human preadipocytes were isolated from subcutaneous adipose tissue obtained from discarded tissue during abdominoplasties of healthy men and women. Preadipocytes were divided into 3 groups. Cells of group I were seeded onto the scaffold directly after isolation, cells of group II were proliferated for 4 days before seeding, and cells of group III were proliferated and induced to differentiate before seeded onto the scaffold. A 3-dimensional scaffold (Matriderm, Dr. Otto Suwelack Skin and Health Care GmbH, Billerbeck, Germany) containing bovine collagen and elastin served as a carrier. Fourteen days after isolation, all scaffolds were histologically evaluated, using hematoxylin and eosin, anti-Ki-67 antibody, as well as immunofluorescence labeling with Pref-1 antibody (DLK (C-19), peroxisome proliferator-activated receptor gamma antibody, and DAPI (4', -diamidino-2-phenylindole). RESULTS: Cells of all groups adhered to the scaffolds on day 21 after isolation. Cells of groups I (freshly isolated preadipocytes) and II (proliferated preadipocytes) adhered well and penetrated into deeper layers of the matrix. In group III (induced preadipocytes), penetration of cells was primarily observed to the surface area of the scaffold. DISCUSSION/CONCLUSION: : The collagen-elastin matrix serves as a useful scaffold for adipose tissue engineering. Freshly isolated preadipocytes as well as proliferated preadipocytes showed good penetration into deeper layers of the scaffold, whereas induced preadipocytes attached primarily to the surface of the matrix. We conclude that there might be different indications for each approach.\n\nKamolz, Lars-Peter\n\nLumenta, David Benjamin\n\n\n"
},
{
"text": "\n159930\nLow-grade inflammation and tryptophan-kynurenine pathway activation are associated with adverse cardiac remodeling in primary hyperparathyroidism: the EPATH trial.\n\nVerheyen, N\n\nMeinitzer, A\n\nGrübler, MR\n\nAblasser, K\n\nKolesnik, E\n\nFahrleitner-Pammer, A\n\nBelyavskiy, E\n\nTrummer, C\n\nSchwetz, V\n\nPieske-Kraigher, E\n\nVoelkl, J\n\nAlesutan, I\n\nCatena, C\n\nSechi, LA\n\nBrussee, H\n\nLewinski, DV\n\nMärz, W\n\nPieske, B\n\nPilz, S\n\nTomaschitz, A\n\nBeiträge in Fachzeitschriften\nISI:000403075100025\n28432842.0\n10.1515/cclm-2016-1159\nNone\nPrimary hyperparathyroidism (pHPT) is associated with low-grade inflammation, left ventricular hypertrophy and increased cardiovascular mortality, but the association between inflammatory markers and parameters of adverse cardiac remodeling is unknown. We investigated the relationship between C-reactive protein (CRP), the essential amino acid tryptophan and its pro-inflammatory derivatives kynurenine and quinolinic acid (QUIN) with echocardiographic parameters.\n Cross-sectional baseline data from the "Eplerenone in Primary Hyperparathyroidism" trial were analyzed. Patients with any acute illness were excluded. We assessed associations between CRP, serum levels of tryptophan, kynurenine and QUIN and left ventricular mass index (LVMI), left atrial volume index (LAVI) and E/e'.\n Among 136 subjects with pHPT (79% females), 100 (73%) had arterial hypertension and the prevalence of left ventricular hypertrophy was 52%. Multivariate linear regression analyses with LVMI, LAVI and E/e' as respective dependent variables, and C-reactive protein and tryptophan, kynurenine and QUIN as respective independent variables were performed. Analyses were adjusted for age, sex, blood pressure, parathyroid hormone, calcium and other cardiovascular risk factors. LVMI was independently associated with CRP (adjusted β-coefficient=0.193, p=0.030) and QUIN (β=0.270, p=0.007), but not kynurenine. LAVI was related with CRP (β=0.315, p<0.001), kynurenine (β=0.256, p=0.005) and QUIN (β=0.213, p=0.044). E/e' was related with kynurenine (β=0.221, p=0.022) and QUIN (β=0.292, p=0.006). Tryptophan was not associated with any of the remodeling parameters. [Correction added after online publication (22 April 2017: The sentence "Among 136 subjects with pHPT (79% females), 100 (73%) had left ventricular hypertrophy." was corrected to "Among 136 subjects with pHPT (79% females), 100 (73%) had arterial hypertension and the prevalence of left ventricular hypertrophy was 52%."] Conclusions: Cardiac remodeling is common in pHPT and is associated with low-grade inflammation and activation of the tryptophan-kynurenine pathway. The potential role of kynurenine and QUIN as cardiovascular risk factors may be further investigated in future studies.\n\nAblasser, Klemens\n\nBrussee, Helmut\n\nFahrleitner-Pammer, Astrid\n\nKolesnik, Ewald\n\nMärz, Winfried\n\nMeinitzer, Andreas\n\nPilz, Stefan\n\nTheiler-Schwetz, Verena\n\nTrummer, Christian\n\nVerheyen, Nicolas Dominik\n\nvon Lewinski, Dirk\n\n\n"
},
{
"text": "\n4698\nEffect of endotoxin treatment on the expression of cyclooxygenase-2 and prostaglandin synthases in spinal cord, dorsal root ganglia, and skin of rats.\n\nSchuligoi, R\n\nUlcar, R\n\nPeskar, BA\n\nAmann, R\n\nBeiträge in Fachzeitschriften\nISI:000181233200013\n12617945.0\n10.1016%2FS0306-4522%2802%2900783-2\nNone\nPeripheral inflammation causes upregulation of cyclooxygenase in the spinal cord and subsequent increase in prostaglandin biosynthesis. However, prostaglandin synthases, which are downstream of cyclooxygenase control the type of prostaglandin that is formed predominantly. Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats.Endotoxin (2 mg/kg i.p.) induced the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in spinal cord, dorsal root ganglia, and skin as determined by reverse transcription polymerase chain reaction. In contrast, basal expression of lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia was not significantly altered by endotoxin. Dexamethasone (1 mg/kg s.c. at -18 h and -1 h) attenuated the effect endotoxin on the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in all tissues investigated, but did not significantly influence expression of lipocalin prostaglandin D synthase mRNA in spinal cord and dorsal root ganglia. In situ hybridisation histochemistry showed endotoxin-induced expression of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA throughout gray and white matter of spinal cord sections. In dorsal root ganglia, expression of membrane bound prostaglandin E synthase seemed primarily located to non-neuronal cells, while cyclooxygenase-2 messenger RNA was not detectable.The results show that the immune response elicited by endotoxin induced cyclooxygenase-2 and membrane bound prostaglandin E synthase, but not lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia of rats. The distribution of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA expressing cells suggests major involvement of non-neuronal cells in spinal prostaglandin biosynthesis. Determination of the regulation of enzymes downstream of cyclooxygenase at the messenger RNA level may represent a valuable tool to investigate effects of analgesic/anti-inflammatory drugs on the regulation of spinal prostaglandin biosynthesis.\n\nPeskar, Bernhard\n\nSchuligoi, Rufina\n\n\n"
},
{
"text": "\n118681\nCommon variants at 12q14 and 12q24 are associated with hippocampal volume.\n\nBis, JC\n\nDeCarli, C\n\nSmith, AV\n\nvan der Lijn, F\n\nCrivello, F\n\nFornage, M\n\nDebette, S\n\nShulman, JM\n\nSchmidt, H\n\nSrikanth, V\n\nSchuur, M\n\nYu, L\n\nChoi, SH\n\nSigurdsson, S\n\nVerhaaren, BF\n\nDeStefano, AL\n\nLambert, JC\n\nJack, CR\n\nStruchalin, M\n\nStankovich, J\n\nIbrahim-Verbaas, CA\n\nFleischman, D\n\nZijdenbos, A\n\nden Heijer, T\n\nMazoyer, B\n\nCoker, LH\n\nEnzinger, C\n\nDanoy, P\n\nAmin, N\n\nArfanakis, K\n\nvan Buchem, MA\n\nde Bruijn, RF\n\nBeiser, A\n\nDufouil, C\n\nHuang, J\n\nCavalieri, M\n\nThomson, R\n\nNiessen, WJ\n\nChibnik, LB\n\nGislason, GK\n\nHofman, A\n\nPikula, A\n\nAmouyel, P\n\nFreeman, KB\n\nPhan, TG\n\nOostra, BA\n\nStein, JL\n\nMedland, SE\n\nVasquez, AA\n\nHibar, DP\n\nWright, MJ\n\nFranke, B\n\nMartin, NG\n\nThompson, PM\n\nEnhancing Neuro Imaging Genetics through Meta-Analysis Consortium\n\nNalls, MA\n\nUitterlinden, AG\n\nAu, R\n\nElbaz, A\n\nBeare, RJ\n\nvan Swieten, JC\n\nLopez, OL\n\nHarris, TB\n\nChouraki, V\n\nBreteler, MM\n\nDe Jager, PL\n\nBecker, JT\n\nVernooij, MW\n\nKnopman, D\n\nFazekas, F\n\nWolf, PA\n\nvan der Lugt, A\n\nGudnason, V\n\nLongstreth, WT\n\nBrown, MA\n\nBennett, DA\n\nvan Duijn, CM\n\nMosley, TH\n\nSchmidt, R\n\nTzourio, C\n\nLauner, LJ\n\nIkram, MA\n\nSeshadri, S\n\nCohorts for Heart and Aging Research in Genomic Epidemiology Consortium\n\nBeiträge in Fachzeitschriften\nISI:000303416300015\n22504421.0\n10.1038/ng.2237\nPMC3427729\nAging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9, 32) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2, 18), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7, 94). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1, 63). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.\n\nCavalieri, Margherita\n\nEnzinger, Christian\n\nFazekas, Franz\n\nSchmidt, Helena\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n136971\nCkd lab methods, progression and risk factors 1.\n\nHeisterkamp, M\n\nTitze, S\n\nLorenzen, J\n\nEckardt, KU\n\nKoettgen, A\n\nKielstein, JT\n\nBouquegneau, A\n\nVidal-Petiot, E\n\nVrtovsnik, F\n\nCavalier, E\n\nKrzesinski, JM\n\nFlamant, M\n\nDelanaye, P\n\nAnguiano, L\n\nRiera, M\n\nPascual, J\n\nBarrios, C\n\nBetriu, A\n\nValdivielso, JM\n\nFernández, E\n\nSoler, MJ\n\nDenys, MA\n\nViaene, A\n\nGoessaert, AS\n\nDelanghe, J\n\nEveraert, K\n\nKim, YS\n\nChoi, MJ\n\nDeok, JY\n\nKim, SG\n\nBevc, S\n\nHojs, N\n\nHojs, R\n\nEkart, R\n\nGorenjak, M\n\nPuklavec, L\n\nBevc, S\n\nHojs, N\n\nHojs, R\n\nEkart, R\n\nGorenjak, M\n\nPuklavec, L\n\nPiskunowicz, M\n\nHofmann, L\n\nZürcher, E\n\nBassi, I\n\nZweiacker, C\n\nStuber, M\n\nNarkiewicz, K\n\nVogt, B\n\nBurnier, M\n\nPruijm, M\n\nRusu, E\n\nZilisteanu, D\n\nAtasie, T\n\nCirciumaru, A\n\nCarstea, F\n\nEcobici, M\n\nRosca, M\n\nTanase, C\n\nMihai, S\n\nVoiculescu, M\n\nKim, YS\n\nJeon, YD\n\nChoi, MJ\n\nKim, SG\n\nPolenakovic, M\n\nPop-Jordanova, N\n\nHung, SC\n\nTarng, DC\n\nTuta, L\n\nStanigut, A\n\nMesiano, P\n\nRollino, C\n\nFerro, M\n\nBeltrame, G\n\nMassara, C\n\nQuattrocchio, G\n\nBorca, M\n\nBazzan, M\n\nRoccatello, D\n\nMaksudova, A\n\nUrasaeva, LI\n\nKhalfina, TN\n\nZilisteanu, D\n\nRusu, E\n\nAtasie, T\n\nEcobici, M\n\nCirciumaru, A\n\nCarstea, F\n\nRosca, M\n\nTanase, C\n\nMihai, S\n\nVoiculescu, M\n\nTekce, H\n\nKin Tekce, B\n\nAktas, G\n\nAlcelik, A\n\nSengul, E\n\nLindic, J\n\nPurg, D\n\nSkamen, J\n\nKrsnik, M\n\nSkoberne, A\n\nPajek, J\n\nKveder, R\n\nBren, A\n\nKovac, D\n\nKin Tekce, B\n\nTekce, H\n\nAktas, G\n\nDelgado, G\n\nDrechsler, C\n\nWanner, C\n\nBlouin, K\n\nPilz, S\n\nTomaschitz, A\n\nKleber, ME\n\nWillmes, C\n\nKrane, V\n\nMärz, W\n\nRitz, E\n\nVan Gilst, WH\n\nVan Der Harst, P\n\nDe Boer, RA\n\nScholze, A\n\nPetersen, L\n\nHocher, B\n\nRasmussen, LM\n\nTepel, M\n\nDe Paula, EA\n\nVanelli, CP\n\nCaminhas, MS\n\nSoares, BC\n\nBassoli, FA\n\nDa Costa, DM\n\nLanna, CM\n\nGalil, AG\n\nColugnati, FA\n\nCosta, MB\n\nBastos, MG\n\nDe Paula, RB\n\nSantoro, D\n\nZappulla, Z\n\nAlibrandi, A\n\nTomasello Andulajevic, M\n\nLicari, M\n\nBaldari, S\n\nBuemi, M\n\nCernaro, V\n\nCampennì, A\n\nPallet, N\n\nChauvet, S\n\nLevi, C\n\nMeas-Yedid, V\n\nBeaune, P\n\nThevet, E\n\nKarras, A\n\nSantos, S\n\nMalheiro, J\n\nCampos, A\n\nPedroso, S\n\nSantos, J\n\nCabrita, A\n\nMayor, MM\n\nAyala, R\n\nRamos, C\n\nFranco, S\n\nGuillén, R\n\nKim, JS\n\nYang, JW\n\nHan, BG\n\nChoi, SO\n\nTudor, MN\n\nNavajas Martinez, MF\n\nVaduva, C\n\nMaria, DT\n\nMota, E\n\nClari, R\n\nMongilardi, E\n\nVigotti, FN\n\nConsiglio, V\n\nScognamiglio, S\n\nNazha, M\n\nRoggero, S\n\nPiga, A\n\nPiccoli, G\n\nMukhopadhyay, P\n\nPatar, K\n\nChaterjee, N\n\nGanguly, K\n\nPublizierte (zitierfähige) Beiträge für wissenschaftliche Veranstaltungen\nNone\nNone\n10.1093/ndt/gfu145\nNone\nNone\n\nMärz, Winfried\n\nPilz, Stefan\n\n\n"
},
{
"text": "\n160604\nThe motor repertoire in 3- to 5-month old infants with Down syndrome.\n\nHerrero, D\n\nEinspieler, C\n\nPanvequio Aizawa, CY\n\nMutlu, A\n\nYang, H\n\nNogolová, A\n\nPansy, J\n\nNielsen-Saines, K\n\nMarschik, PB\n\nGenGM Study Group\n\nBeiträge in Fachzeitschriften\nISI:000405975900001\n28586709.0\n10.1016/j.ridd.2017.05.006\nPMC5515547\nEven though Down syndrome is the most common chromosomal cause of intellectual disability, studies on early development are scarce.\n To describe movements and postures in 3- to 5-month-old infants with Down syndrome and assess the relation between pre- and perinatal risk factors and the eventual motor performance.\n Exploratory study; 47 infants with Down syndrome (26 males, 27 infants born preterm, 22 infants with congenital heart disease) were videoed at 10-19 weeks post-term (median=14 weeks). We assessed their Motor Optimality Score (MOS) based on postures and movements (including fidgety movements) and compared it to that of 47 infants later diagnosed with cerebral palsy and 47 infants with a normal neurological outcome, matched for gestational and recording ages.\n The MOS (median=13, range 10-28) was significantly lower than in infants with a normal neurological outcome (median=26), but higher than in infants later diagnosed with cerebral palsy (median=6). Fourteen infants with Down syndrome showed normal fidgety movements, 13 no fidgety movements, and 20 exaggerated, too fast or too slow fidgety movements. A lack of movements to the midline and several atypical postures were observed. Neither preterm birth nor congenital heart disease was related to aberrant fidgety movements or reduced MOS.\n The heterogeneity in fidgety movements and MOS add to an understanding of the large variability of the early phenotype of Down syndrome. Studies on the predictive values of the early spontaneous motor repertoire, especially for the cognitive outcome, are warranted.\n The significance of this exploratory study lies in its minute description of the motor repertoire of infants with Down syndrome aged 3-5 months. Thirty percent of infants with Down syndrome showed age-specific normal fidgety movements. The rate of abnormal fidgety movements (large amplitude, high/slow speed) or a lack of fidgety movements was exceedingly high. The motor optimality score of infants with Down syndrome was lower than in infants with normal neurological outcome but higher than in infants who were later diagnosed with cerebral palsy. Neither preterm birth nor congenital heart disease were related to the motor performance at 3-5 months.\n Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.\n\nEinspieler, Christa\n\nKrieber-Tomantschger, Magdalena\n\nMarschik, Dajie\n\nMarschik, Peter\n\nPansy, Jasmin\n\nScheuchenegger, Anna Birgitta\n\nUrlesberger, Berndt\n\n\n"
}
]
}