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Vienna, Austria

The Medical University of Vienna is a university located in Vienna, Austria. It is the direct successor of the faculty of medicine of the University of Vienna, founded in 1365 by Rudolf IV, Duke of Austria. Thus it is the oldest medical school in the German–speaking world, and it was the second medical faculty in the Holy Roman Empire, after the Charles University of Prague.The Medical University of Vienna is the largest medical organisation in Austria, as well as one of the top-level research institutions in Europe and provides Europe's largest hospital, the Vienna General Hospital, with all of its medical staff.It consists of 31 university clinics and clinical institutes, 12 medical-theoretical departments which perform around 48,000 operations each year. The Vienna General Hospital has about 100,000 patients treated as inpatients and 605,000 treated as outpatients each year.There have been seven Nobel prize laureates affiliated with the medical faculty, and fifteen in total with the University of Vienna. These include Robert Bárány, Julius Wagner-Jauregg and Karl Landsteiner, the discoverer of the ABO blood type system and the Rhesus factor. Sigmund Freud qualified as a doctor at the medical faculty and worked as a doctor and lecturer at the General Hospital, carrying out research into cerebral palsy, aphasia and microscopic neuroanatomy.In the 2014-15 Times Higher Education Rankings, Medical University of Vienna is listed among the top 15 medical schools in Europe and 49th in the world. .In 2014, there were 6,016 candidate applications for 660 places in medicine proper and 80 in dentistry, which corresponds to an admission rate of about 12 percent. Admission is based upon ranking in an admission test, called "MedAT", which is carried out every summer in conjunction with the two other public medical schools of Austria, Medical University of Graz and Innsbruck Medical University. Wikipedia.


Lassmann H.,Medical University of Vienna
GLIA | Year: 2014

Glia cells are mediators as well as targets of the chronic inflammatory process in the central nervous system of multiple sclerosis (MS) patients. They are involved in the control of autoimmunity, in the propagation and termination of the inflammatory reaction, in the induction of demyelination and neurodegeneration, and in remyelination and scaring. Demyelination, as well as neuronal and GLIA cell damage are induced by different immunological mechanisms including components of the adaptive and innate immune system. Oxidative injury resulting in mitochondrial dysfunction is one important mechanism of tissue injury. It is in part driven by the inflammatory response and the production of oxygen radicals mainly in microglia and macrophages. With increasing age of the patients and disease progression, oxidative injury is further amplified by additional mechanisms including central nervous system damage related microglia activation, progressive mitochondrial damage, and age-dependent iron accumulation within the human central nervous system. The inflammatory mechanisms associated with lesion formation in MS are to a large extent reflected in experimental models of inflammatory demyelination, such as autoimmune encephalomyelitis. This is not the case for the amplification mechanisms of oxidative injury, which mainly operate in the progressive stage of the disease. © 2014 Wiley Periodicals, Inc. Source


Holzer M.,Medical University of Vienna
New England Journal of Medicine | Year: 2010

A 62-year-old man collapses on the street, and emergency medical personnel who are called to the scene find that he is not breathing and that he has no pulse. The first recorded cardiac rhythm is ventricular fibrillation. Advanced cardiac life-support measures, including intubation, a total dose of 2 mg of epinephrine, and six defibrillation attempts, restore spontaneous circulation 22 minutes after the onset of the event. On admission to the emergency department, his condition is hemodynamically stable and he has adequate oxygenation and ventilation, but he is still comatose. A neurologic examination reveals reactive pupils and a positive cough reflex. The core body temperature is 35.5°C. A diagnosis of the post-cardiac arrest syndrome with coma is made. An intensive care specialist evaluates the patient and recommends the immediate initiation of targeted temperature management. Copyright © 2010 Massachusetts Medical Society. Source


Kovacs G.G.,Medical University of Vienna
Neuropathology and Applied Neurobiology | Year: 2015

Tauopathies are clinically, morphologically and biochemically heterogeneous neurodegenerative diseases characterized by the deposition of abnormal tau protein in the brain. The neuropathological phenotypes are distinguished based on the involvement of different anatomical areas, cell types and presence of distinct isoforms of tau in the pathological deposits. The nomenclature of primary tauopathies overlaps with the modern classification of frontotemporal lobar degeneration. Neuropathological phenotypes comprise Pick's disease, progressive supranuclear palsy, corticobasal degeneration, argyrophilic grain disease, primary age-related tauopathy, formerly called also as neurofibrillary tangle-only dementia, and a recently characterized entity called globular glial tauopathy. Mutations in the gene encoding the microtubule-associated protein tau are associated with frontotemporal dementia and parkinsonism linked to chromosome 17. In addition, further neurodegenerative conditions with diverse aetiologies may be associated with tau pathologies. Thus, the spectrum of tau pathologies and tauopathy entities expands beyond the traditionally discussed disease forms. Detailed multidisciplinary studies are still required to understand their significance. © 2014 British Neuropathological Society. Source


Seitz C.,Medical University of Vienna
European urology | Year: 2012

Incidence, prevention, and management of complications of percutaneous nephrolitholapaxy (PNL) still lack consensus. To review the epidemiology of complications and their prevention and management. A literature review was performed using the PubMed database between 2001 and May 1, 2011, restricted to human species, adults, and the English language. The Medline search used a strategy including medical subject headings (MeSH) and free-text protocols with the keywords percutaneous, nephrolithotomy, PCNL, PNL, urolithiasis, complications, and Clavien, and the MeSH terms nephrostomy, percutaneous/adverse effects, and intraoperative complications or postoperative complications. Assessing the epidemiology of complications is difficult because definitions of complications and their management still lack consensus. For a reproducible quality assessment, data should be obtained in a standardized manner, allowing for comparison. An approach is the validated Dindo-modified Clavien system, which was originally reported by seven studies. No deviation from the normal postoperative course (Clavien 0) was observed in 76.7% of PNL procedures. Including deviations from the normal postoperative course without the need for pharmacologic treatment or interventions (Clavien 1) would add up to 88.1%. Clavien 2 complications including blood transfusion and parenteral nutrition occurred in 7%; Clavien 3 complications requiring intervention in 4.1.%; Clavien 4, life-threatening complications, in 0.6%; and Clavien 5, mortality, in 0.04%. High-quality data on complication management of rare but potentially debilitating complications are scarce and consist mainly of case reports. Complications after PNL can be kept to a minimum in experienced hands with the development of new techniques and improved technology. A modified procedure-specific Clavien classification should be established that would need to be validated in prospective trials. Copyright © 2011 European Association of Urology. Published by Elsevier B.V. All rights reserved. Source


Lion T.,Medical University of Vienna
Clinical Microbiology Reviews | Year: 2014

Human adenoviruses (HAdVs) are an important cause of infections in both immunocompetent and immunocompromised individuals, and they continue to provide clinical challenges pertaining to diagnostics and treatment. The growing number of HAdV types identified by genomic analysis, as well as the improved understanding of the sites of viral persistence and reactivation, requires continuous adaptions of diagnostic approaches to facilitate timely detection and monitoring of HAdV infections. In view of the clinical relevance of life-threatening HAdV diseases in the immunocompromised setting, there is an urgent need for highly effective treatment modalities lacking major side effects. The present review summarizes the recent progress in the understanding and management of HAdV infections. © 2014, American Society for Microbiology. All Rights Reserved. Source

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