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Dive into the research topics where Martin Eichner is active.

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Featured researches published by Martin Eichner.


Nature Medicine | 2008

Simultaneous PET-MRI: a new approach for functional and morphological imaging

Martin S. Judenhofer; Danny F. Newport; Ciprian Catana; Stefan Siegel; Markus Becker; Axel Thielscher; Manfred Kneilling; Matthias P. Lichy; Martin Eichner; Karin Klingel; Gerald Reischl; Stefan Widmaier; Martin Röcken; Robert E. Nutt; Hans Jürgen Machulla; Kamil Uludag; Simon R. Cherry; Claus D. Claussen; Bernd J. Pichler

Noninvasive imaging at the molecular level is an emerging field in biomedical research. This paper introduces a new technology synergizing two leading imaging methodologies: positron emission tomography (PET) and magnetic resonance imaging (MRI). Although the value of PET lies in its high-sensitivity tracking of biomarkers in vivo, it lacks resolving morphology. MRI has lower sensitivity, but produces high soft-tissue contrast and provides spectroscopic information and functional MRI (fMRI). We have developed a three-dimensional animal PET scanner that is built into a 7-T MRI. Our evaluations show that both modalities preserve their functionality, even when operated isochronously. With this combined imaging system, we simultaneously acquired functional and morphological PET-MRI data from living mice. PET-MRI provides a powerful tool for studying biology and pathology in preclinical research and has great potential for clinical applications. Combining fMRI and spectroscopy with PET paves the way for a new perspective in molecular imaging.


Movement Disorders | 2007

Radicular and nonradicular back pain in Parkinson's disease: A controlled study

Doris Broetz; Martin Eichner; Thomas Gasser; Michael Weller; Joachim P. Steinbach

Postural abnormalities and increased muscle tone in Parkinsons disease (PD) may cause back pain. In this controlled study, we analyzed features of back pain in PD patients. The prevalence of back pain was 74% in PD patients (n = 101) when compared with 27% in control patients (n = 132; P < 0.0001, fishers exact test), but did not correlate with disease severity or duration. The mean back pain intensity (visual analog scale of 0–10) was 4.3 for PD patients, and 1.3 for controls. Both radicular and nonradicular types of back pain were more frequent, and back pain caused more impairment in PD patients. However, it is noteworthy that the PD patients in our study did not receive more pain medication than control patients. This suggests that back pain in PD patients is often neglected and insufficiently treated. Our results argue for the routine evaluation of back pain in every patient suffering from PD.


Proceedings of the National Academy of Sciences of the United States of America | 2015

IL-4 abrogates T(H)17 cell-mediated inflammation by selective silencing of IL-23 in antigen-presenting cells.

Emmanuella Guenova; Yuliya Skabytska; Wolfram Hoetzenecker; Günther Weindl; Karin Sauer; Manuela Tham; Kyu-Won Kim; Ji-Hyeon Park; Ji Hae Seo; Desislava Ignatova; Antonio Cozzio; Mitchell P. Levesque; Thomas Volz; Martin Köberle; Susanne Kaesler; Peter Thomas; Reinhard Mailhammer; Kamran Ghoreschi; Knut Schäkel; Boyko Amarov; Martin Eichner; Martin Schaller; Rachael A. Clark; Martin Röcken; Tilo Biedermann

Significance Interleukin 4 (IL-4) has been shown to be highly protective against delayed type hypersensitivity and organ-specific autoimmune and autoinflammatory reactions in mice and humans, but its mode of action has remained controversial and has failed to be explained solely by redirection of TH1/TH17 toward a TH2-type immune response. Here we uncovered that IL-4 selectively suppresses IL-23 transcription and secretion by cells of the innate immune system. We further describe a previously unidentified therapeutic mode of action of IL-4 in TH17-mediated inflammation, and a physiologically highly relevant approach to selectively target IL-23/TH17-dependent inflammation while sparing IL-12 and TH1 immune responses. Interleukin 4 (IL-4) can suppress delayed-type hypersensitivity reactions (DTHRs), including organ-specific autoimmune diseases in mice and humans. Despite the broadly documented antiinflammatory effect of IL-4, the underlying mode of action remains incompletely understood, as IL-4 also promotes IL-12 production by dendritic cells (DCs) and IFN-γ–producing TH1 cells in vivo. Studying the impact of IL-4 on the polarization of human and mouse DCs, we found that IL-4 exerts opposing effects on the production of either IL-12 or IL-23. While promoting IL-12–producing capacity of DCs, IL-4 completely abrogates IL-23. Bone marrow chimeras proved that IL-4–mediated suppression of DTHRs relies on the signal transducer and activator of transcription 6 (STAT6)-dependent abrogation of IL-23 in antigen-presenting cells. Moreover, IL-4 therapy attenuated DTHRs by STAT6- and activating transcription factor 3 (ATF3)-dependent suppression of the IL-23/TH17 responses despite simultaneous enhancement of IL-12/TH1 responses. As IL-4 therapy also improves psoriasis in humans and suppresses IL-23/TH17 responses without blocking IL-12/TH1, selective IL-4–mediated IL-23/TH17 silencing is promising as treatment against harmful inflammation, while sparing the IL-12–dependent TH1 responses.


BMC Infectious Diseases | 2007

The influenza pandemic preparedness planning tool InfluSim

Martin Eichner; Markus Schwehm; Hans-Peter Duerr; Stefan O. Brockmann

BackgroundPlanning public health responses against pandemic influenza relies on predictive models by which the impact of different intervention strategies can be evaluated. Research has to date rather focused on producing predictions for certain localities or under specific conditions, than on designing a publicly available planning tool which can be applied by public health administrations. Here, we provide such a tool which is reproducible by an explicitly formulated structure and designed to operate with an optimal combination of the competing requirements of precision, realism and generality.ResultsInfluSim is a deterministic compartment model based on a system of over 1,000 differential equations which extend the classic SEIR model by clinical and demographic parameters relevant for pandemic preparedness planning. It allows for producing time courses and cumulative numbers of influenza cases, outpatient visits, applied antiviral treatment doses, hospitalizations, deaths and work days lost due to sickness, all of which may be associated with economic aspects. The software is programmed in Java, operates platform independent and can be executed on regular desktop computers.ConclusionInfluSim is an online available software http://www.influsim.info which efficiently assists public health planners in designing optimal interventions against pandemic influenza. It can reproduce the infection dynamics of pandemic influenza like complex computer simulations while offering at the same time reproducibility, higher computational performance and better operability.


Osong public health and research perspectives | 2011

Incubation Period of Ebola Hemorrhagic Virus Subtype Zaire

Martin Eichner; Scott F. Dowell; Nina Firese

Objectives Ebola hemorrhagic fever has killed over 1300 people, mostly in equatorial Africa. There is still uncertainty about the natural reservoir of the virus and about some of the factors involved in disease transmission. Until now, a maximum incubation period of 21 days has been assumed. Methods We analyzed data collected during the Ebola outbreak (subtype Zaire) in Kikwit, Democratic Republic of the Congo, in 1995 using maximum likelihood inference and assuming a log-normally distributed incubation period. Results The mean incubation period was estimated to be 12.7 days (standard deviation 4.31 days), indicating that about 4.1% of patients may have incubation periods longer than 21 days. Conclusion If the risk of new cases is to be reduced to 1% then 25 days should be used when investigating the source of an outbreak, when determining the duration of surveillance for contacts, and when declaring the end of an outbreak.


Parasitology | 2003

On the interpretation of age-intensity profiles and dispersion patterns in parasitological surveys

Hans-Peter Duerr; K. Dietz; Martin Eichner

The present paper describes how age-intensity profiles of macroparasite burdens are affected by processes underlying the distribution of the parasite numbers in host populations. In a comparative way, we consider the following 6 processes: (i) age-dependent exposure, (ii) parasite-induced host mortality, (iii) heterogeneity within, the host population, (iv) clumped infection, (v) density-dependent parasite mortality and (vi) density-dependent parasite establishment. For each of these processes, we show typical patterns in the age-intensity profile and provide, if possible, explicit and simple solutions for the age-dependent mean parasite burden and the corresponding dispersion patterns. Emphasis is given to density-dependent parasite establishment and to age-intensity profiles resulting from the superposition of different processes. By means of 2 examples we show that the interpretation of observed patterns can be ambiguous if more than 1 process takes place. These findings underline that age-intensity profiles should be interpreted on the basis of available a priori knowledge about the processes assumed to be involved. For purposes of testing different hypotheses, a simulation program is provided with which discrepancies between model prediction and data can be explored.


Transactions of The Royal Society of Tropical Medicine and Hygiene | 2003

Density-dependent parasite establishment suggests infection-associated immunosuppression as an important mechanism for parasite density regulation in onchocerciasis.

Hans-Peter Duerr; K. Dietz; H. Schulz-Key; D.W. Büttner; Martin Eichner

The modulation of human immune response by filarial parasites has yielded contradictory experimental findings and attracted much controversy. We address the unresolved question of acquisition, establishment and accumulation of Onchocerca volvulus by using a modelling approach that relates computer simulations to cross-sectional data concerning parasite burdens in 913 West African onchocerciasis patients. It is shown that the acquisition of O. volvulus is not constant with host age; instead, the analysis of age profiles of parasite burdens strongly indicate the operation of immunosuppressive processes within the human host, associated with the presence of adult parasites or microfilariae. It is suggested that these processes suppress immunity against incoming infective larvae (L3), which themselves act as an immune modulating component once they have successfully overcome the barrier of concomitant immunity. Suppression of parasite-specific immunity leads to parasite establishment rates which increase along with the parasite burden, but which hardly depend on hyperendemic annual transmission potentials. Children, still immunocompetent due to low parasite burdens, acquire 0.1-0.5 adult female parasites per year, whereas older people, immunosuppressed due to high burdens, acquire 2-4 adult female parasites per year. Differences in parasite establishment between the forest and the savannah strains of O. volvulus are quantified and dynamic aspects of density-dependent parasite establishment discussed.


BMC Infectious Diseases | 2007

Influenza pandemic intervention planning using InfluSim: pharmaceutical and non- pharmaceutical interventions

Hans P. Duerr; Stefan O. Brockmann; Isolde Piechotowski; Markus Schwehm; Martin Eichner

BackgroundInfluenza pandemic preparedness plans are currently developed and refined on national and international levels. Much attention has been given to the administration of antiviral drugs, but contact reduction can also be an effective part of mitigation strategies and has the advantage to be not limited per se. The effectiveness of these interventions depends on various factors which must be explored by sensitivity analyses, based on mathematical models.MethodsWe use the freely available planning tool InfluSim to investigate how pharmaceutical and non-pharmaceutical interventions can mitigate an influenza pandemic. In particular, we examine how intervention schedules, restricted stockpiles and contact reduction (social distancing measures and isolation of cases) determine the course of a pandemic wave and the success of interventions.ResultsA timely application of antiviral drugs combined with a quick implementation of contact reduction measures is required to substantially protract the peak of the epidemic and reduce its height. Delays in the initiation of antiviral treatment (e.g. because of parsimonious use of a limited stockpile) result in much more pessimistic outcomes and can even lead to the paradoxical effect that the stockpile is depleted earlier compared to early distribution of antiviral drugs.ConclusionPharmaceutical and non-pharmaceutical measures should not be used exclusively. The protraction of the pandemic wave is essential to win time while waiting for vaccine development and production. However, it is the height of the peak of an epidemic which can easily overtax general practitioners, hospitals or even whole public health systems, causing bottlenecks in basic and emergency medical care.


International Journal for Parasitology | 2011

Control of onchocerciasis in Africa: threshold shifts, breakpoints and rules for elimination.

Hans P. Duerr; Günter Raddatz; Martin Eichner

Control of onchocerciasis in Africa is currently based on annual community-directed treatment with ivermectin (CDTI) which has been assumed to be not efficient enough to bring about elimination. However, elimination has recently been reported to have been achieved by CDTI alone in villages of Senegal and Mali, reviving debate on the eradicability of onchocerciasis in Africa. We investigate the eradicability of onchocerciasis by examining threshold shifts and breakpoints predicted by a stochastic transmission model that has been fitted extensively to data. We show that elimination based on CDTI relies on shifting the threshold biting rate to a level that is higher than the annual biting rate. Breakpoints become relevant in the context of when to stop CDTI. In order for the model to predict a good chance for CDTI to eliminate onchocerciasis, facilitating factors such as the macrofilaricidal effect of ivermectin must be assumed. A chart predicting the minimum efficacy of CDTI required for elimination, dependent on the annual biting rate, is provided. Generalisable recommendations into strategies for the elimination of onchocerciasis are derived, particularly referring to the roles of vectors, the residual infection rate under control, and a low-spreader problem originating from patients with low parasite burdens.


Blood | 2009

Direct Crosstalk between Mast Cell-TNF and TNFR1-expressing Endothelia Mediates Local Tissue Inflammation

Manfred Kneilling; Reinhard Mailhammer; Lothar Hültner; Tanja Schönberger; Kerstin Fuchs; Martin Schaller; Daniel Bukala; Steffen Massberg; Christian A. Sander; Heidi Braumüller; Martin Eichner; Konrad Maier; Rupert Hallmann; Bernd J. Pichler; Roland Haubner; Meinrad Gawaz; Klaus Pfeffer; Tilo Biedermann; Martin Röcken

Signaling through tumor necrosis factor receptor 1 (TNFR1) controls bacterial infections and the induction of inflammatory Th1 cell-mediated autoimmune diseases. By dissecting Th1 cell-mediated delayed-type hypersensitivity responses (DTHRs) into single steps, we localized a central defect to the missing TNFR1 expression by endothelial cells (ECs). Adoptive transfer and mast cell knockin experiments into Kit(W)/Kit(W-v), TNF(-/-), and TNFR1(-/-) mice showed that the signaling defect exclusively affects mast cell-EC interactions but not T cells or antigen-presenting cells. As a consequence, TNFR1(-/-) mice had strongly reduced mRNA and protein expression of P-selectin, E-selectin, ICAM-1, and VCAM-1 during DTHR elicitation. In consequence, intravital fluorescence microscopy revealed up to 80% reduction of leukocyte rolling and firm adhesion in TNFR1(-/-) mice. As substitution of TNF(-/-) mice with TNF-producing mast cells fully restored DTHR in these mice, signaling of mast cell-derived TNF through TNFR1-expressing ECs is essential for the recruitment of leukocytes into sites of inflammation.

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Klaus Dietz

University of Tübingen

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