Institution
University of Graz
Education•Graz, Steiermark, Austria•
About: University of Graz is a education organization based out in Graz, Steiermark, Austria. It is known for research contribution in the topics: Population & Quantum chromodynamics. The organization has 17934 authors who have published 37489 publications receiving 1110980 citations. The organization is also known as: Carolo Franciscea Graecensis & Karl Franzens Universität.
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TL;DR: Emphasis is devoted to the integration of PHA-production based on selected raw materials into the holistic patterns of sustainability; this encompasses the choice of new, powerful microbial production strains, non-hazardous, environmentally benign methods for PHA recovery, and reutilization of waste streams from the PHA production process itself.
365 citations
University of Michigan1, Cornell University2, University of Pennsylvania3, University of Massachusetts Medical School4, University of Naples Federico II5, Baylor College of Medicine6, Spanish National Research Council7, Complutense University of Madrid8, New York University9, Boston Children's Hospital10, University of Rome Tor Vergata11, NewYork–Presbyterian Hospital12, University of Pittsburgh13, University of Paris14, French Institute of Health and Medical Research15, National University of Cuyo16, Albert Einstein College of Medicine17, University of New Mexico18, Goethe University Frankfurt19, Weizmann Institute of Science20, University of Turku21, Sapienza University of Rome22, Virginia Commonwealth University23, St. Jude Children's Research Hospital24, Discovery Institute25, University of Copenhagen26, University of Tromsø27, Eötvös Loránd University28, Merck & Co.29, University of Freiburg30, Babraham Institute31, University of Adelaide32, University of South Australia33, University of Oviedo34, University of Chicago35, University of Graz36, National Institutes of Health37, Queens College38, City University of New York39, University of Tokyo40, University of Zurich41, University of British Columbia42, Austrian Academy of Sciences43, University of California, San Francisco44, Russian Academy of Sciences45, University Medical Center Groningen46, University of Cambridge47, University of Glasgow48, Rutgers University49, University of Padua50, University of Bern51, Kazan Federal University52, University of Oxford53, University of Oslo54, Oslo University Hospital55, Foundation for Research & Technology – Hellas56, University of Crete57, Francis Crick Institute58, Osaka University59, Chinese Academy of Sciences60, Harvard University61, Icahn School of Medicine at Mount Sinai62, Shanghai Jiao Tong University63, Karolinska Institutet64
TL;DR: In this paper, preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.
Abstract: Autophagy is a core molecular pathway for the preservation of cellular and organismal homeostasis. Pharmacological and genetic interventions impairing autophagy responses promote or aggravate disease in a plethora of experimental models. Consistently, mutations in autophagy-related processes cause severe human pathologies. Here, we review and discuss preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.
365 citations
TL;DR: In this paper, the vector potentials are approximated by edge finite elements and the scalar potentials by nodal ones, leading, in most cases, to singular finite element equations systems.
365 citations
TL;DR: It is demonstrated that visual BCI feedback clearly modulates sensorimotor EEG rhythms, and the presentation form (abstract versus realistic) does not influence the performance in a BCI, at least in initial training sessions.
363 citations
TL;DR: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features, implying interaction with additional host factors.
Abstract: Objective: To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain–Barre syndrome (GBS) Methods: We tested pretreatment sera, 7 ± 3 (mean ± SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features Results: Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein–Barr virus in four (2%) Patients with C jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM 1 antibodies, pure motor GBS, lower CSF protein, and worse outcome Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R) Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM 1 antibodies Conclusions: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors Most patients had no identified infection
363 citations
Authors
Showing all 18136 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| David Haussler | 172 | 488 | 224960 |
| Russel J. Reiter | 169 | 1646 | 121010 |
| Frederik Barkhof | 154 | 1449 | 104982 |
| Philip Scheltens | 140 | 1175 | 107312 |
| Christopher D.M. Fletcher | 138 | 674 | 82484 |
| Jennifer S. Haas | 128 | 840 | 71315 |
| Jelena Krstic | 126 | 839 | 73457 |
| Michael A. Kamm | 124 | 637 | 53606 |
| Frances H. Arnold | 119 | 510 | 49651 |
| Gert Pfurtscheller | 117 | 507 | 62873 |
| Georg Kresse | 111 | 430 | 244729 |
| Manfred T. Reetz | 110 | 959 | 42941 |
| Alois Fürstner | 108 | 459 | 43085 |
| David N. Herndon | 108 | 1227 | 54888 |
| David J. Williams | 107 | 2060 | 62440 |