Institution
University of Erlangen-Nuremberg
Education•Erlangen, Bayern, Germany•
About: University of Erlangen-Nuremberg is a education organization based out in Erlangen, Bayern, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 42405 authors who have published 85600 publications receiving 2663922 citations.
Topics: Population, Immune system, Catalysis, Medicine, Computer science
Papers published on a yearly basis
Papers
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TL;DR: The focus of this work is on the coarse-grained MARTINI force field, for which mapping definitions are written to allow conversion to and from the higher-resolution force fields GROMOS, CHARMM, and AMBER, and to andFrom a simplified three-bead lipid model.
Abstract: The conversion of coarse-grained to atomistic models is an important step in obtaining insight about atomistic scale processes from coarse-grained simulations. For this process, called backmapping or reverse transformation, several tools are available, but these commonly require libraries of molecule fragments or they are linked to a specific software package. In addition, the methods are usually restricted to specific molecules and to a specific force field. Here, we present an alternative method, consisting of geometric projection and subsequent force-field based relaxation. This method is designed to be simple and flexible, and offers a generic solution for resolution transformation. For simple systems, the conversion only requires a list of particle correspondences on the two levels of resolution. For special cases, such as nondefault protonation states of amino acids and virtual sites, a target particle list can be specified. The mapping uses simple building blocks, which list the particles on the di...
540 citations
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TL;DR: The improved insulin sensitivity after 2 nights of treatment may reflect a decreasing sympathetic activity, indicating that sleep apnea is an independent risk factor for increased insulin resistance.
Abstract: The obstructive sleep apnea syndrome is typically associated with conditions known to increase insulin resistance as hypertension, obesity, and diabetes. We investigated whether obstructive sleep apnea itself is an independent risk factor for increased insulin resistance and whether continuous positive airway pressure (CPAP) treatment improves insulin sensitivity. Forty patients (apnea-hypopnea index > 20) were treated with CPAP. Before, 2 days after, and after 3 months of effective CPAP treatment, hyperinsulinemic euglycemic clamp studies were performed. Insulin sensitivity significantly increased after 2 days (5.75 +/- 4.20 baseline versus 6.79 +/- 4.91 micromol/kg.min; p = 0.003) and remained stable after 3 months of treatment. The improvement in insulin sensitivity after 2 days was much greater in patients with a body mass index less than 30 kg/m2 than in more obese patients. The improved insulin sensitivity after 2 nights of treatment may reflect a decreasing sympathetic activity, indicating that sleep apnea is an independent risk factor for increased insulin resistance. The effect of CPAP on insulin sensitivity is smaller in obese patients than in nonobese patients, suggesting that in obese individuals insulin sensitivity is mainly determined by obesity and, to a smaller extent, by sleep apnea.
539 citations
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TL;DR: The concept of noninvasive detection and characterization of coronary atherosclerotic lesions in patients with ACS by MDCT is introduced and differences in lesion morphology and plaque composition are identified, consistent with previous intravascular ultrasound studies.
538 citations
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TL;DR: Fifty percent of patients with acute chest pain and low to intermediate likelihood of ACS were free of CAD by computed tomography and had no ACS, suggesting early coronary CTA may significantly improve patient management in the emergency department.
537 citations
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TL;DR: Increased rates of sympathetic nerve firing and reduced neuronal NE reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin II appear to be excluded.
Abstract: There is growing evidence that essential hypertension is commonly neurogenic and is initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic, and sympathetic neuromodulation by angiotensin II. To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects. The NE transport inhibitor desipramine was infused to directly assess the potential role of impaired neuronal NE reuptake. To evaluate possible angiotensin sympathetic neuromodulation, the relation of arterial and coronary sinus plasma concentrations of angiotensin II to sympathetic activity was investigated. Hypertensive patients displayed increased muscle sympathetic nerve activity and elevated total systemic, cardiac, and renal NE spillover. Cardiac neuronal NE reuptake was decreased in hypertensive subjects. In response to desipramine, both the reduction of fractional transcardiac 3[H]NE extraction and the increase in cardiac NE spillover were less pronounced in hypertensive patients. DNA sequencing analysis of the NE transporter gene revealed no mutations that could account for reduced transporter activity. Arterial baroreflex control of sympathetic nerve traffic was not diminished in hypertensive subjects. Angiotensin II plasma concentrations were similar in both groups and were not related to indexes of sympathetic activation. Increased rates of sympathetic nerve firing and reduced neuronal NE reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin II appear to be excluded.
537 citations
Authors
Showing all 42831 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hermann Brenner | 151 | 1765 | 145655 |
Richard B. Devereux | 144 | 962 | 116403 |
Manfred Paulini | 141 | 1791 | 110930 |
Daniel S. Berman | 141 | 1363 | 86136 |
Peter Lang | 140 | 1136 | 98592 |
Joseph Sodroski | 138 | 542 | 77070 |
Richard J. Johnson | 137 | 880 | 72201 |
Jun Lu | 135 | 1526 | 99767 |
Michael Schmitt | 134 | 2007 | 114667 |
Jost B. Jonas | 132 | 1158 | 166510 |
Andreas Mussgiller | 127 | 1059 | 73778 |
Matthew J. Budoff | 125 | 1449 | 68115 |
Stefan Funk | 125 | 506 | 56955 |
Markus F. Neurath | 124 | 934 | 62376 |
Jean-Marie Lehn | 123 | 1054 | 84616 |