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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.

Valent P.,Medical University of Vienna
Allergy: European Journal of Allergy and Clinical Immunology | Year: 2013

Mast cell activation (MCA) occurs in a number of different clinical conditions, including IgE-dependent allergies, other inflammatory reactions, and mastocytosis. MCA-related symptoms may be mild, moderate, severe, or even life-threatening. The severity of MCA depends on a number of different factors, including genetic predisposition, the number and releasability of mast cells involved in the reaction, the type of allergen, presence of specific IgE, and presence of certain comorbidities. In severe reactions, MCA can be documented by a substantial increase in the serum tryptase level above baseline. When symptoms are recurrent, are accompanied by an increase in mast cell-derived mediators in biological fluids, and are responsive to treatment with mast cell-stabilizing or mediator-targeting drugs, the diagnosis of mast cell activation syndrome (MCAS) is appropriate. Based on the underlying condition, these patients can further be classified into i) primary MCAS where KIT-mutated, clonal mast cells are detected, ii) secondary MCAS where an underlying inflammatory disease, often in the form of an IgE-dependent allergy, but no KIT-mutated mast cells, is found, and iii) idiopathic MCAS, where neither an allergy or other underlying disease, nor KIT-mutated mast cells are detectable. It is important to note that in many patients with MCAS, several different factors act together to lead to severe or even life-threatening anaphylaxis. Detailed knowledge about the pathogenesis and complexity of MCAS, and thus establishing the exact final diagnosis, may greatly help in the management and therapy of these patients. © 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.

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.

Zellner M.,Medical University of Vienna
Acta neuropathologica communications | Year: 2014

Peripheral biomarkers play an indispensable role in quick and reliable diagnoses of any kind of disease. With the population ageing, the number of people suffering from age-related diseases is expected to rise dramatically over the coming decades. In particular, all types of cognitive deficits, such as Alzheimer's disease, will increase. Alzheimer's disease is characterised mainly by coexistence of amyloid plaques and neurofibrillary tangles in brain. Reliable identification of such molecular characteristics antemortem, however, is problematic due to restricted availability of appropriate sample material and definitive diagnosis is only possible postmortem. Currently, the best molecular biomarkers available for antemortem diagnosis originate from cerebrospinal fluid. Though, this is not convenient for routine diagnosis because of the required invasive lumbar puncture. As a consequence, there is a growing demand for additional peripheral biomarkers in a more readily accessible sample material. Blood platelets, due to shared biochemical properties with neurons, can constitute an attractive alternative as discussed here. This review summarises potential platelet Alzheimer's disease biomarkers, their role, implication, and alteration in the disease. For easy comparison of their performance, the Hedge effect size was calculated whenever data were available.

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.

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.

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