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 & Virus. 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, Virus, Gene, Exciton, Photoluminescence
Papers published on a yearly basis
Papers
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TL;DR: By immunoelectron microscopy the podocyte foot processes of the rat and human kidney have been shown to contain three major proteins of the contractile apparatus in muscle, i.e., actin, myosin, and the Z-line protein, alpha-actinin, which suggests that these proteins constitute an important part of the total glomerular protein contents.
268 citations
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TL;DR: The functions of the mammalian semaphorin–plexin system as well as its role in diseases are summarized and emerging strategies to pharmacologically targetSemaphorins and plexins are discussed.
Abstract: Semaphorins are membrane-bound or diffusible factors that regulate key cellular functions and are involved in cell-cell communication. Most of the effects of semaphorins are mediated by plexins. Work over the past decade has revealed crucial functions of the semaphorin-plexin system in mammalian physiology. It has also become clear that semaphorins and plexins have important roles in many pathophysiological processes, including cancer, immunological diseases and bone disorders, and that they represent novel targets for drugs to prevent or treat various diseases. This Review summarizes the functions of the mammalian semaphorin-plexin system as well as its role in diseases and discusses emerging strategies to pharmacologically target semaphorin-plexin signalling.
268 citations
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TL;DR: It is shown that superimposed on an overall 1/Re scaling predicted and studied previously there are small, nonmonotonic variations reflecting folds in the edge of chaos, formed by the stable manifold of a unique flow field that is dominated by a pair of downstream vortices, asymmetrically placed towards the wall.
Abstract: The linear stability of pipe flow implies that only perturbations of sufficient strength will trigger the transition to turbulence. In order to determine this threshold in perturbation amplitude we study the edge of chaos which separates perturbations that decay towards the laminar profile and perturbations that trigger turbulence. Using the lifetime as an indicator and methods developed in Skufca et al., Phys. Rev. Lett. 96, 174101 (2006), we show that superimposed on an overall 1/Re scaling predicted and studied previously there are small, nonmonotonic variations reflecting folds in the edge of chaos. By tracing the motion in the edge we find that it is formed by the stable manifold of a unique flow field that is dominated by a pair of downstream vortices, asymmetrically placed towards the wall. The flow field that generates the edge of chaos shows intrinsic chaotic dynamics.
267 citations
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TL;DR: It is reported for the first time that CHILD syndrome (MIM 308050), an X-linked dominant, male-lethal trait characterized by an inflammatory nevus with striking lateralization and strict midline demarcation, as well as ipsilateral hypoplasia of the body is caused by mutations in the gene NSDHL located at Xq28 encoding a 3beta-hydroxysteroid dehydrogenase functioning in the cholesterol biosynthetic pathway.
Abstract: We report for the first time that CHILD syndrome (MIM 308050), an X-linked dominant, male-lethal trait characterized by an inflammatory nevus with striking lateralization and strict midline demarcation, as well as ipsilateral hypoplasia of the body is caused by mutations in the gene NSDHL located at Xq28 (NAD(P)H steroid dehydrogenase-like protein) encoding a 3β-hydroxysteroid dehydrogenase functioning in the cholesterol biosynthetic pathway. SSCA and genomic sequence analysis of NSDHL identified in 6 patients with CHILD syndrome, including one boy as well as a mother and her daughter, mutations potentially impairing protein function. This phenotype is distinct from, but shares various clinical and biochemical findings with chondrodysplasia punctata (CDPX2, MIM 302960). CDPX2 is due to mutations affecting a Δ8-Δ7 sterol isomerase (EBP, emopamil binding protein, at Xp11.22 - p11.23) that functions downstream of NSDHL in a later step of cholesterol biosynthesis. EBP was unaffected in the patients analyzed by us demonstrating that CHILD syndrome and CDPX2 are not caused by allelic mutations. Two mouse X-linked dominant male-lethal traits, bare patches (Bpa) and striated (Str) had previously been associated with mutations in Nsdhl. They provide animal models for the study of CHILD syndrome, a further human condition due to mutations in a gene of the cholesterol synthesis pathway. Am. J. Med. Genet. 90:339–346, 2000. © 2000 Wiley-Liss, Inc.
267 citations
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TL;DR: The knowledge about the neurotoxic mechanisms of MPTP such as mitochondrial dysfunction with breakdown of energy metabolism and free radical production will help to understand the underlying mechanisms of PD, which are not fully understood yet.
Abstract: Animal models are a very important approach to study the pathogenesis and therapeutic intervention strategies of human diseases. Since many human disorders do not arise spontaneously in animals, characteristic functional changes have to be mimicked by neurotoxic agents. For instance, the application of the dopaminergic neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is able to produce striking similarities to Parkinson's disease (PD) diagnosed in humans. MPTP is thought to selectively damage dopaminergic neurons predominantly those originating in the substantia nigra pars compacta (SNc) which leads to impaired dopaminergic neurotransmission accompanied by a loss of dopaminergic nerve terminals in the striatum. MPTP-induced neurochemical, behavioral, and histopathological alterations replicate very closely the clinical symptoms of PD patients, which will be discussed in this paper and render the MPTP model currently the most favored PD model to study therapeutic intervention strategies in an easy and reliable way in preclinical studies. We and many other research groups propose that the knowledge about the neurotoxic mechanisms of MPTP such as mitochondrial dysfunction with breakdown of energy metabolism and free radical production will help us to understand the underlying mechanisms of PD, which are not fully understood yet. In particular, the novel aspects of inflammatory processes and the involvement of reactive nitrogen species in addition to reactive oxygen species seem to be important milestones for a better understanding of the neurodegenerative effects of MPTP. In this review we focus on the MPTP mouse model which is easy practicable and widely used in neuroscience research and draw comparisons to the human pathology in PD.
267 citations
Authors
Showing all 23488 results
Name | H-index | Papers | Citations |
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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 |