Institution
University of Marburg
Education•Marburg, Germany•
About: University of Marburg is a education organization based out in Marburg, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 23195 authors who have published 42907 publications receiving 1506069 citations. The organization is also known as: Philipps University of Marburg & Philipps-Universität.
Topics: Population, Gene, Crystal structure, Laser, Catalysis
Papers published on a yearly basis
Papers
More filters
••
TL;DR: The data suggest that SOCS proteins induced by TLR stimulation limit the extent of TLR signaling by inhibiting type I IFN signaling but not the main NFκB pathway.
271 citations
••
TL;DR: According to the cytotoxicity results, PEG 5 kDa is superior for PEGylation when compared to PEG 550 Da at similar graft ratios, and PEG-g-TMC merits further investigations as a drug delivery vehicle.
271 citations
••
TL;DR: Cure of Hp infection results in CCR in most patients, and a watch-and-wait strategy is justified when close follow-up is guaranteed.
Abstract: Purpose Cure of infection induces remissions in most patients with early stage Helicobacter pylori- (Hp) positive gastric MALT (mucosa-associated lymphoid tissue) lymphoma (GML). We tracked the long-term stability of remissions in this prospective, multicenter trial. Patients and Methods In 120 patients with stage I1E disease, we performed sequential endoscopic-bioptic follow-up after Hp eradication and polymerase chain reaction of the rearranged immunoglobulin heavy chain gene. The status of t(11;18) was assessed in 65 patients. Results Median follow-up was 75 months (range, one to 116). Five-year survival was 90%. Eighty percent of patients (96 of 120) achieved complete histologic remission (CR). Eighty percent of CRs are in continuous complete histologic remission (CCR). Three percent of CR patients (three of 96) relapsed and were referred for alternative treatment. Seventeen percent of CR patients (16 of 96) showed histologic residual disease (RD) during follow-up; a watch-and-wait strategy was applie...
271 citations
••
TL;DR: The need to intensify therapeutic PD research is stressed and reasons why the translation of basic research to disease‐modifying therapies has been unsuccessful so far are pointed out.
Abstract: Over a period of more than 50 years, the symptomatic treatment of the motor symptoms of Parkinson disease (PD) has been optimized using pharmacotherapy, deep brain stimulation, and physiotherapy. The arsenal of pharmacotherapies includes L-Dopa, several dopamine agonists, inhibitors of monoamine oxidase (MAO)-B and catechol-o-methyltransferase (COMT), and amantadine. In the later course of the disease, motor complications occur, at which stage different oral formulations of L-Dopa or dopamine agonists with long half-life, a transdermal application or parenteral pumps for continuous drug supply can be subscribed. Alternatively, the patient is offered deep brain stimulation of the subthalamic nucleus (STN) or the internal part of the globus pallidus (GPi). For a more efficacious treatment of motor complications, new formulations of L-Dopa, dopamine agonists, and amantadine as well as new MAO-B and COMT inhibitors are currently tested in clinical trials, and some of them already yielding positive results in phase 3 trials. In addition, non-dopaminergic agents have been tested in the early clinical phase for the treatment of motor fluctuations and dyskinesia, including adenosine A2A antagonists (istradefylline, preladenant, and tozadenant) and modulators of the metabolic glutamate receptor 5 (mGluR5 - mavoglurant) and serotonin (eltoprazine) receptors. Recent clinical trials testing coenzyme Q10, the dopamine agonist pramipexole, creatine monohydrate, pioglitazone, or AAV-mediated gene therapy aimed at increasing expression of neurturin, did not prove efficacious. Treatment with nicotine, caffeine, inosine (a precursor of urate), and isradipine (a dihydropyridine calcium channel blocker), as well as active and passive immunization against α-synuclein and inhibitors or modulators of α-synuclein-aggregation are currently studied in clinical trials. However, to date, no disease-modifying treatment is available. We here review the current status of treatment options for motor and non-motor symptoms, and discuss current investigative strategies for disease modification. This review provides basic insights, mainly addressing basic scientists and non-specialists. It stresses the need to intensify therapeutic PD research and points out reasons why the translation of basic research to disease-modifying therapies has been unsuccessful so far.
The symptomatic treatment of the motor symptoms of Parkinson disease (PD) has been constantly optimized using pharmacotherapy (L-Dopa, several dopamine agonists, inhibitors of monoamine oxidase (MAO)-B and catechol-o-methyltransferase (COMT), and amantadine), deep brain stimulation, and physiotherapy. For a more efficacious treatment of motor complications, new formulations of L-Dopa, dopamine agonists, and amantadine as well as new MAO-B and COMT inhibitors are currently tested in clinical trials. Non-dopaminergic agents have been tested in the early clinical phase for the treatment of motor fluctuations and dyskinesia. Recent clinical trials testing coenzyme Q10, the dopamine agonist pramipexole, creatine monohydrate, pioglitazone, or AAV-mediated gene therapy aimed at increasing expression of neurturin, did not prove efficacious. Treatment with nicotine, caffeine, and isradipine – a dihydropyridine calcium channel blocker – as well as active and passive immunization against α-synuclein and inhibitors of α-synuclein-aggregation are currently studied in clinical trials. However, to date, no disease-modifying treatment is available for PD. We here review the current status of treatment options and investigative strategies for both motor and non-motor symptoms. This review stresses the need to intensify therapeutic PD research and points out reasons why the translation of basic research to disease-modifying therapies has been unsuccessful so far.
This article is part of a special issue on Parkinson disease.
270 citations
••
TL;DR: The utility of the periodic-orbit description of chaotic motion is demonstrated by computing from a few periodic orbits highly accurate estimates of a large number of quantum resonances for the classically chaotic three-disk scattering problem.
Abstract: We demonstrate the utility of the periodic-orbit description of chaotic motion by computing from a few periodic orbits highly accurate estimates of a large number of quantum resonances for the classically chaotic three-disk scattering problem. The symmetry decompositions of the eigenspectra are the same for the classical and the quantum problem, and good agreement between the periodic-orbit estimates and the exact quantum poles is observed
270 citations
Authors
Showing all 23488 results
Name | H-index | Papers | Citations |
---|---|---|---|
John C. Morris | 183 | 1441 | 168413 |
Russel J. Reiter | 169 | 1646 | 121010 |
Martin J. Blaser | 147 | 820 | 104104 |
Christopher T. Walsh | 139 | 819 | 74314 |
Markus Cristinziani | 131 | 1140 | 84538 |
James C. Paulson | 126 | 443 | 52152 |
Markus F. Neurath | 124 | 934 | 62376 |
Nicholas W. Wood | 123 | 614 | 66270 |
Florian Lang | 116 | 1421 | 66496 |
Howard I. Maibach | 116 | 1821 | 60765 |
Thomas G. Ksiazek | 113 | 398 | 46108 |
Frank Glorius | 113 | 663 | 49305 |
Eberhard Ritz | 111 | 1109 | 61530 |
Manfred T. Reetz | 110 | 959 | 42941 |
Wolfgang H. Oertel | 110 | 653 | 51147 |