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Institution

University of Duisburg-Essen

EducationEssen, Nordrhein-Westfalen, Germany
About: University of Duisburg-Essen is a education organization based out in Essen, Nordrhein-Westfalen, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 16072 authors who have published 39972 publications receiving 1109199 citations.


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Journal ArticleDOI
TL;DR: However, contrary to clinical doctrine, histological evidence does not support this concept, with inflammation rarely observed in chronic plantar fasciitis, despite an abundance of anecdotal evidence indicating a causal link between arch function and heel pain this article.
Abstract: Plantar fasciitis is a musculoskeletal disorder primarily affecting the fascial enthesis. Although poorly understood, the development of plantar fasciitis is thought to have a mechanical origin. In particular, pes planus foot types and lower-limb biomechanics that result in a lowered medial longitudinal arch are thought to create excessive tensile strain within the fascia, producing microscopic tears and chronic inflammation. However, contrary to clinical doctrine, histological evidence does not support this concept, with inflammation rarely observed in chronic plantar fasciitis. Similarly, scientific support for the role of arch mechanics in the development of plantar fasciitis is equivocal, despite an abundance of anecdotal evidence indicating a causal link between arch function and heel pain. This may, in part, reflect the difficulty in measuring arch mechanics in vivo. However, it may also indicate that tensile failure is not a predominant feature in the pathomechanics of plantar fasciitis. Alternative mechanisms including 'stress-shielding', vascular and metabolic disturbances, the formation of free radicals, hyperthermia and genetic factors have also been linked to degenerative change in connective tissues. Further research is needed to ascertain the importance of such factors in the development of plantar fasciitis.

234 citations

Journal ArticleDOI
TL;DR: Responses to alpha-adrenoceptor activation are augmented in the presence of coronary endothelial dysfunction and atherosclerosis, involving both alpha(1)- and alpha(2)- adrenoceptors in epicardial conduit arteries and microvessels, and it is powerful enough to induce myocardial ischemia and limit myocardIAL function.
Abstract: —The use of quantitative coronary angiography, combined with Doppler and PET, has recently been directed at the study of α-adrenergic coronary vasomotion in humans. Confirming prior animal experiments, there is no evidence of α-adrenergic coronary constrictor tone at rest. Again confirming prior experiments, responses to α-adrenoceptor activation are augmented in the presence of coronary endothelial dysfunction and atherosclerosis, involving both α1- and α2-adrenoceptors in epicardial conduit arteries and microvessels. Such augmented α-adrenergic coronary constriction is observed during exercise and coronary interventions, and it is powerful enough to induce myocardial ischemia and limit myocardial function. Recent studies indicate a genetic determination of α2-adrenergic coronary constriction.

234 citations

Journal ArticleDOI
TL;DR: It is demonstrated that genetically enforced expression of the anti-inflammatory cytokine interleukin (IL)-10 by macrophages attenuates the long-term behavioral and pharmacological consequences of prenatal immune activation in a mouse model of prenatal viral-like infection by polyriboinosinic–polyribocytidilic acid.
Abstract: Maternal infections during pregnancy increase the risk for schizophrenia and related disorders of putative neurodevelopmental origin in the offspring. This association has been attributed to enhanced expression of pro-inflammatory cytokines in the fetal environment in response to maternal immunological stimulation. In contrast, the specific roles of anti-inflammatory cytokines are virtually unknown in this context. Here, we demonstrate that genetically enforced expression of the anti-inflammatory cytokine interleukin (IL)-10 by macrophages attenuates the long-term behavioral and pharmacological consequences of prenatal immune activation in a mouse model of prenatal viral-like infection by polyriboinosinic-polyribocytidilic acid (PolyI:C; 2 mg/kg, intravenously). In the absence of a discrete prenatal inflammatory stimulus, however, enhanced levels of IL-10 at the maternal-fetal interface by itself also precipitates specific behavioral abnormalities in the grown offspring. This highlights that in addition to the disruptive effects of excess pro-inflammatory molecules, a shift toward enhanced anti-inflammatory signaling in prenatal life can similarly affect cognitive and behavioral development. Hence, shifts of the balance between pro- and anti-inflammatory cytokine classes may be a critical determinant of the final impact on neurodevelopment following early life infection or innate immune imbalances.

234 citations

Journal ArticleDOI
TL;DR: Experimental studies addressing long-term effects of adjunct cardioprotection beyond infarct size reduction, that is, on repair, remodeling, and mortality, are lacking and future trials must focus on interventions/agents with robust preclinical evidence, have solid phase II dosing and timing data, and recruit patients who have truly a chance to benefit from adjunct cardiprotection.
Abstract: The translation from numerous successful animal experiments on cardioprotection beyond that by reperfusion to clinical practice has to date been disappointing. Animal experiments often use reductionist approaches and are mostly performed in young and healthy animals which lack the risk factors, comorbidities, and comedications which are characteristics of patients suffering an acute myocardial infarction or undergoing cardiovascular surgery. Conceptually, it is still unclear by how much the time window for successful reperfusion is extended by preconditioning, and how long the duration of ischemia can be so that adjunct cardioprotection by postconditioning at reperfusion still protects. Experimental studies addressing long-term effects of adjunct cardioprotection beyond infarct size reduction, that is, on repair, remodeling, and mortality, are lacking. Technically, reproducibility and robustness of experimental studies are often limited. Grave faults in design and conduct of clinical trials have also substantially contributed to the failure of translation of cardioprotection to clinical practice. Cardiovascular surgery with ischemic cardioplegic arrest is only a surrogate of acute myocardial infarction and confounded by the choice of anesthesia, hypothermia, cardioplegia, and traumatic myocardial injury. Trials in patients with acute myocardial infarction have been performed on agents/interventions with no or inconsistent previous animal data and in patients who had either some reperfusion already at admission or were reperfused too late to expect any myocardial salvage. Of greatest concern is the lack of adequate phase II dosing and timing studies when rushing from promising proof-of-concept trials with surrogate end points such as infarct size to larger clinical outcome trials. Future trials must focus on interventions/agents with robust preclinical evidence, have solid phase II dosing and timing data, and recruit patients who have truly a chance to benefit from adjunct cardioprotection.

232 citations

Journal ArticleDOI
TL;DR: In relapsed DLBCL, the observed no difference between the control group and the rituximab maintenance group and do not recommend ritUXimab after ASCT, and the saaIPI was a significant prognostic factor.
Abstract: Purpose The standard treatment for relapsed diffuse large B-cell lymphoma (DLBCL) is salvage chemotherapy followed by high-dose therapy and autologous stem-cell transplantation (ASCT). The impact of maintenance rituximab after ASCT is not known. Patients and Methods In total, 477 patients with CD20+ DLBCL who were in their first relapse or refractory to initial therapy were randomly assigned to one of two salvage regimens. After three cycles of salvage chemotherapy, the responding patients received high-dose chemotherapy followed by ASCT. Then, 242 patients were randomly assigned to either rituximab every 2 months for 1 year or observation. Results After ASCT, 122 patients received rituximab, and 120 patients were observed only. The median follow-up time was 44 months. The 4-year event-free survival (EFS) rates after ASCT were 52% and 53% for the rituximab and observation groups, respectively (P = .7). Treatment with rituximab was associated with a 15% attributable risk of serious adverse events after day...

232 citations


Authors

Showing all 16364 results

NameH-indexPapersCitations
Rui Zhang1512625107917
Olli T. Raitakari1421232103487
Anders Hamsten13961188144
Robert Huber13967173557
Christopher T. Walsh13981974314
Patrick D. McGorry137109772092
Stanley Nattel13277865700
Luis M. Liz-Marzán13261661684
Dirk Schadendorf1271017105777
William Wijns12775295517
Raimund Erbel125136474179
Khalil Amine11865250111
Hans-Christoph Diener118102591710
Bruce A.J. Ponder11640354796
Andre Franke11568255481
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023117
2022496
20213,694
20203,449
20193,155
20182,761