11 results on '"Geisel, Marie Henrike"'
Search Results
2. B-type natriuretic peptide for incident atrial fibrillation—The Heinz Nixdorf Recall Study
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Kara, Kaffer, Geisel, Marie Henrike, Möhlenkamp, Stefan, Lehmann, Nils, Kälsch, Hagen, Bauer, Marcus, Neumann, Till, Dragano, Nico, Moebus, Susanne, Jöckel, Karl-Heinz, Erbel, Raimund, and Mahabadi, Amir Abbas
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- 2015
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3. Prolongation of the QTc interval in HIV-infected individuals compared to the general population
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Reinsch, Nico, Arendt, Marina, Geisel, Marie Henrike, Schulze, Christina, Holzendorf, Volker, Warnke, Anna, Neumann, Till, Brockmeyer, Norbert H., Schadendorf, Dirk, Eisele, Lewin, Erbel, Raimund, Moebus, Susanne, Jöckel, Karl-Heinz, Esser, Stefan, and On behalf of HIV HEART Study Group and the Heinz Nixdorf Recall Investigative Group
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- 2017
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4. Cost-effectiveness of preoperative SPECT/CT combined with lymphoscintigraphy vs. lymphoscintigraphy for sentinel lymph node excision in patients with cutaneous malignant melanoma
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Stoffels, Ingo, Müller, Markus, Geisel, Marie Henrike, Leyh, Julia, Pöppel, Thorsten, Schadendorf, Dirk, and Klode, Joachim
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- 2014
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5. Air Pollution and Progression of Atherosclerosis in Different Vessel Beds-Results from a Prospective Cohort Study in the Ruhr Area, Germany.
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Hennig, Frauke, Geisel, Marie Henrike, Kälsch, Hagen, Lucht, Sarah, Mahabadi, Amir Abbas, Moebus, Susanne, Erbel, Raimund, Lehmann, Nils, Jöckel, Karl-Heinz, Scherag, André, Hoffmann, Barbara, and Heinz Nixdorf Recall Study Investigative Group
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AIR pollution , *ATHEROSCLEROSIS , *DISEASE progression - Abstract
OBJECTIVES: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC). METHODS: We used baseline (2000-2003) and 5-y follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2.5), (PM10), and nitrogen dioxide (NO2) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise. RESULTS: While no clear associations were observed in the full study sample (mean age 59.1 (±7:6) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a 1.5 μg/m³ higher exposure to PM2.5 (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%). CONCLUSION: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. [ABSTRACT FROM AUTHOR]
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- 2020
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6. Recalibration of the ACC/AHA Risk Score in Two Population-Based German Cohorts
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de las Heras Gala, Tonia, Geisel, Marie Henrike, Peters, Annette, Thorand, Barbara, Baumert, Jens, Lehmann, Nils, Jöckel, Karl-Heinz, Moebus, Susanne, Erbel, Raimund, Meisinger, Christine, Mahabadi, Amir Abbas, and Koenig, Wolfgang
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Male ,Cerebrovascular Diseases ,German People ,Medizin ,Cardiology ,Myocardial Infarction ,Cardiovascular Medicine ,Biochemistry ,Vascular Medicine ,Risk Assessment ,Geographical Locations ,Risk Factors ,Germany ,Medicine and Health Sciences ,Ethnicities ,Coronary Heart Disease ,Humans ,ddc:610 ,health care economics and organizations ,Biology and Life Sciences ,Middle Aged ,Atherosclerosis ,Lipids ,Europe ,Stroke ,Cholesterol ,Neurology ,Cardiovascular Diseases ,People and Places ,Population Groupings ,Female ,Algorithms ,Research Article - Abstract
Background The 2013 ACC/AHA guidelines introduced an algorithm for risk assessment of atherosclerotic cardiovascular disease (ASCVD) within 10 years. In Germany, risk assessment with the ESC SCORE is limited to cardiovascular mortality. Applicability of the novel ACC/AHA risk score to the German population has not yet been assessed. We therefore sought to recalibrate and evaluate the ACC/AHA risk score in two German cohorts and to compare it to the ESC SCORE. Methods We studied 5,238 participants from the KORA surveys S3 (1994-1995) and S4 (1999-2001) and 4,208 subjects from the Heinz Nixdorf Recall (HNR) Study (2000-2003). There were 383 (7.3%) and 271 (6.4%) first non-fatal or fatal ASCVD events within 10 years in KORA and in HNR, respectively. Risk scores were evaluated in terms of calibration and discrimination performance. Results The original ACC/AHA risk score overestimated 10-year ASCVD rates by 37% in KORA and 66% in HNR. After recalibration, miscalibration diminished to 8% underestimation in KORA and 12% overestimation in HNR. Discrimination performance of the ACC/AHA risk score was not affected by the recalibration (KORA: C = 0.78, HNR: C = 0.74). The ESC SCORE overestimated by 5% in KORA and by 85% in HNR. The corresponding C-statistic was 0.82 in KORA and 0.76 in HNR. Conclusions The recalibrated ACC/AHA risk score showed strongly improved calibration compared to the original ACC/AHA risk score. Predicting only cardiovascular mortality, discrimination performance of the commonly used ESC SCORE remained somewhat superior to the ACC/AHA risk score. Nevertheless, the recalibrated ACC/AHA risk score may provide a meaningful tool for estimating 10-year risk of fatal and non-fatal cardiovascular disease in Germany. CA extern
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- 2016
7. Comparison of coronary artery calcification, carotid intima-media thickness and anklebrachial index for predicting 10-year incident cardiovascular events in the general population.
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Geisel, Marie Henrike, Bauer, Marcus, Hennig, Frauke, Hoffmann, Barbara, Lehmann, Nils, Möhlenkamp, Stefan, Kröger, Knut, Kara, Kaffer, Müller, Tobias, Moebus, Susanne, Erbel, Raimund, Scherag, André, Jöckel, Karl-Heinz, and Mahabadi, Amir A.
- Abstract
Aims: To compare the predictive value of coronary artery calcification (CAC), carotid intima-media thickness (CIMT) and ankle-brachial index (ABI) in a primary prevention cohort depending on risk factor profile to determine which of the three markers improves cardiovascular (CV) risk discrimination best in which risk group. Methods and results: We quantified CAC, CIMT, and ABI in 3108 subjects (mean age 59.2 ± 7.7, 47.1% male) without prevalent CV diseases from the population-based Heinz Nixdorf Recall study. Associations with incident major CV events (coronary event, stroke, CV death; n = 223) were assessed during a follow-up period of 10.3 ± 2.8 years with Cox proportional regressions in the total cohort and stratified by Framingham risk score (FRS) groups. Discrimination ability was evaluated with Harrell's C. All three markers were associated with CV events (hazard ratio [95% confidence interval (CI)]: CAC: 1.31 (1.23-1.39) per 1-unit increase in log(CAC + 1) vs. CIMT: 1.27 (1.13-1.43) per 1 SD vs. ABI: 1.30 (1.14-1.49) per 1 SD, in FRS adjusted models). Considering reclassification, CAC lead to highest reclassification in the total cohort, while also for CIMT and ABI significant improvement in net-reclassification was observed [NRI (95% CI): CAC: 0.55 (0.42-0.69); CIMT: 0.32 (0.19-0.45); ABI: 0.19 (0.10-0.28)]. Conclusion: Coronary artery calcification provides the best discrimination of risk compared with CIMT and ABI, particularly in the intermediate risk group, whereas CIMT may be an alternative measure for reassurance in the low risk group. [ABSTRACT FROM AUTHOR]
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- 2017
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8. Linkage and Association Analysis Identifies TRAF1 Influencing Common Carotid Intima-Media Thickness.
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Heßler, Nicole, Geisel, Marie Henrike, Coassin, Stefan, Erbel, Raimund, Heilmann, Stefanie, Hennig, Frauke, Hoffmann, Barbara, Jöckel, Karl-Heinz, Moebus, Susanne, Moskau-Hartmann, Susanna, Nürnberg, Gudrun, Nürnberg, Peter, Vens, Maren, Klockgether, Thomas, Kronenberg, Florian, Scherag, André, and Ziegler, Andreas
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- 2016
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9. Quantitative Molecular Detection of Putative Periodontal Pathogens in Clinically Healthy and Periodontally Diseased Subjects.
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Göhler, André, Hetzer, Adrian, Holtfreter, Birte, Geisel, Marie Henrike, Schmidt, Carsten Oliver, Steinmetz, Ivo, and Kocher, Thomas
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RISK factors of periodontal disease ,MOLECULAR biology ,PERIODONTITIS ,DISEASE prevalence ,POLYMERASE chain reaction ,RIBOSOMAL RNA - Abstract
Periodontitis is a multi-microbial oral infection with high prevalence among adults. Putative oral pathogens are commonly found in periodontally diseased individuals. However, these organisms can be also detected in the oral cavity of healthy subjects. This leads to the hypothesis, that alterations in the proportion of these organisms relative to the total amount of oral microorganisms, namely their abundance, rather than their simple presence might be important in the transition from health to disease. Therefore, we developed a quantitative molecular method to determine the abundance of various oral microorganisms and the portion of bacterial and archaeal nucleic acid relative to the total nucleic acid extracted from individual samples. We applied quantitative real-time PCRs targeting single-copy genes of periodontal bacteria and 16S-rRNA genes of Bacteria and Archaea. Testing tongue scrapings of 88 matched pairs of periodontally diseased and healthy subjects revealed a significantly higher abundance of P. gingivalis and a higher total bacterial abundance in diseased subjects. In fully adjusted models the risk of being periodontally diseased was significantly higher in subjects with high P. gingivalis and total bacterial abundance. Interestingly, we found that moderate abundances of A. actinomycetemcomitans were associated with reduced risk for periodontal disease compared to subjects with low abundances, whereas for high abundances, this protective effect leveled off. Moderate archaeal abundances were health associated compared to subjects with low abundances. In conclusion, our methodological approach unraveled associations of the oral flora with periodontal disease, which would have gone undetected if only qualitative data had been determined. [ABSTRACT FROM AUTHOR]
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- 2014
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10. Synergistic Effects of Nonthermal Plasma and Disinfecting Agents against Dental Biofilms In Vitro.
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Koban, Ina, Geisel, Marie Henrike, Holtfreter, Birte, Jablonowski, Lukasz, Hübner, Nils-Olaf, Matthes, Rutger, Masur, Kai, Weltmann, Klaus-Dieter, Kramer, Axel, and Kocher, Thomas
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Aim. Dental biofilms play a major role in the pathogenesis of many dental diseases. In this study, we evaluated the synergistic effect of atmospheric pressure plasma and different agents in dentistry on the reduction of biofilms. Methods and Results. We used monospecies (S. mutans) and multispecies dental biofilm models grown on titanium discs in vitro. After treatment with one of the agents, the biofilms were treated with plasma. Efficacy of treatment was determined by the number of colony forming units (CFU) and by live-dead staining. For S. mutans biofilms no colonies could be detected after treatment with NaOCl or H2O2. For multispecies biofilms the combination with plasma achieved a higher CFU reduction than each agent alone. We found an additive antimicrobial effect between argon plasma and agents irrespective of the treatment order with cultivation technique. For EDTA and octenidine, antimicrobial efficacy assessed by live-dead staining differed significantly between the two treatment orders (p < 0.05). Conclusions. The effective treatment of dental biofilms on titanium discs with atmospheric pressure plasma could be increased by adding agents in vitro. [ABSTRACT FROM AUTHOR]
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- 2013
11. Genetic variants associated with subjective well-being, depressive symptoms and neuroticism identified through genome-wide analyses
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Okbay, Aysu, Baselmans, Bart M.L., De Neve, Jan-Emmanuel, Turley, Patrick, Nivard, Michel G., Fontana, Mark Alan, Meddens, S. Fleur W., Linnér, Richard Karlsson, Rietveld, Cornelius A., Derringer, Jaime, Gratten, Jacob, Lee, James J., Liu, Jimmy Z., de Vlaming, Ronald, Ahluwalia, Tarunveer S., Buchwald, Jadwiga, Cavadino, Alana, Frazier-Wood, Alexis C., Furlotte, Nicholas A., Garfield, Victoria, Geisel, Marie Henrike, Gonzalez, Juan R., Haitjema, Saskia, Karlsson, Robert, van der Laan, Sander W., Ladwig, Karl-Heinz, Lahti, Jari, van der Lee, Sven J., Lind, Penelope A., Liu, Tian, Matteson, Lindsay, Mihailov, Evelin, Miller, Michael B., Minica, Camelia C., Nolte, Ilja M., Mook-Kanamori, Dennis, van der Most, Peter J., Oldmeadow, Christopher, Qian, Yong, Raitakari, Olli, Rawal, Rajesh, Realo, Anu, Rueedi, Rico, Schmidt, Börge, Smith, Albert V., Stergiakouli, Evie, Tanaka, Toshiko, Taylor, Kent, Wedenoja, Juho, Wellmann, Juergen, Westra, Harm-Jan, Willems, Sara M., Zhao, Wei, Amin, Najaf, Bakshi, Andrew, Boyle, Patricia A., Cherney, Samantha, Cox, Simon R., Davies, Gail, Davis, Oliver S.P., Ding, Jun, Direk, Nese, Eibich, Peter, Emeny, Rebecca T., Fatemifar, Ghazaleh, Faul, Jessica D., Ferrucci, Luigi, Forstner, Andreas, Gieger, Christian, Gupta, Richa, Harris, Tamara B., Harris, Juliette M., Holliday, Elizabeth G., Hottenga, Jouke-Jan, De Jager, Philip L., Kaakinen, Marika A., Kajantie, Eero, Karhunen, Ville, Kolcic, Ivana, Kumari, Meena, Launer, Lenore J., Franke, Lude, Li-Gao, Ruifang, Koini, Marisa, Loukola, Anu, Marques-Vidal, Pedro, Montgomery, Grant W., Mosing, Miriam A., Paternoster, Lavinia, Pattie, Alison, Petrovic, Katja E., Pulkki-Råback, Laura, Quaye, Lydia, Räikkönen, Katri, Rudan, Igor, Scott, Rodney J., Smith, Jennifer A., Sutin, Angelina R., Trzaskowski, Maciej, Vinkhuyzen, Anna E., Yu, Lei, Zabaneh, Delilah, Attia, John R., Bennett, David A., Berger, Klaus, Bertram, Lars, Boomsma, Dorret I., Snieder, Harold, Chang, Shun-Chiao, Cucca, Francesco, Deary, Ian J., van Duijn, Cornelia M., Eriksson, Johan G., Bültmann, Ute, de Geus, Eco J.C., Groenen, Patrick J.F., Gudnason, Vilmundur, Hansen, Torben, Hartman, Catharine A., Haworth, Claire M.A., Hayward, Caroline, Heath, Andrew C., Hinds, David A., Hyppönen, Elina, Iacono, William G., Järvelin, Marjo-Riitta, Jöckel, Karl-Heinz, Kaprio, Jaakko, Kardia, Sharon L.R., Keltikangas-Järvinen, Liisa, Kraft, Peter, Kubzansky, Laura D., Lehtimäki, Terho, Magnusson, Patrik K.E., Martin, Nicholas G., McGue, Matt, Metspalu, Andres, Mills, Melinda, de Mutsert, Renée, Oldehinkel, Albertine J., Pasterkamp, Gerard, Pedersen, Nancy L., Plomin, Robert, Polasek, Ozren, Power, Christine, Rich, Stephen S., Rosendaal, Frits R., den Ruijter, Hester M., Schlessinger, David, Schmidt, Helena, Svento, Rauli, Schmidt, Reinhold, Alizadeh, Behrooz Z., Sørensen, Thorkild I.A., Spector, Tim D., Steptoe, Andrew, Terracciano, Antonio, Thurik, A. Roy, Timpson, Nicholas J., Tiemeier, Henning, Uitterlinden, André G., Vollenweider, Peter, Wagner, Gert G., Weir, David R., Yang, Jian, Conley, Dalton C., Smith, George Davey, Hofman, Albert, Johannesson, Magnus, Laibson, David I., Medland, Sarah E., Meyer, Michelle N., Pickrell, Joseph K., Esko, Tõnu, Krueger, Robert F., Beauchamp, Jonathan P., Koellinger, Philipp D., Benjamin, Daniel J., Bartels, Meike, and Cesarini, David
- Abstract
We conducted genome-wide association studies of three phenotypes: subjective well-being (N = 298,420), depressive symptoms (N = 161,460), and neuroticism (N = 170,910). We identified three variants associated with subjective well-being, two with depressive symptoms, and eleven with neuroticism, including two inversion polymorphisms. The two depressive symptoms loci replicate in an independent depression sample. Joint analyses that exploit the high genetic correlations between the phenotypes (|ρ̂| ≈ 0.8) strengthen the overall credibility of the findings, and allow us to identify additional variants. Across our phenotypes, loci regulating expression in central nervous system and adrenal/pancreas tissues are strongly enriched for association.
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- 2016
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