Agency: European Commission | Branch: FP7 | Program: CSA | Phase: ICT-2007.8.0 | Award Amount: 797.38K | Year: 2008
One of the most important challenges of the emerging Information Age is to effectively utilise the immense wealth of information and data acquired, computed and stored by modern information systems. On the one hand, the appropriate use of available information volumes offers large potential to realize technological progress and business success. On the other hand, there exists the severe danger that users and analysts easily get lost in irrelevant, or inappropriately processed or presented information, a problem which is generally called the information overload problem. Visual Analytics is an emerging research discipline developing technology to make the best possible use of huge information loads in a wide variety of applications. The basic idea is to appropriately combine the strengths of intelligent automatic data analysis with the visual perception and analysis capabilities of the human user. We propose a Coordination Action to join European academic and industrial RandD excellence from several individual disciplines, forming a strong Visual Analytics research community. An array of thematic working groups set up by this consortium will focus on advancing the state of the art in Visual Analytics. Specifically, the working groups will join excellence in the fields of data management, data analysis, spatial-temporal data, and human visual perception research with the wider visualisation research community. This Coordination Action will (1.) form and shape a strong European Visual Analytics community, (2.) define the European Visual Analytics Research Roadmap, (3.) expose public and private stakeholders to Visual Analytics technology and (4.) set the stage for larger follow-up Visual Analytics research initiatives in Europe.
Zorowitz R.D.,Johns Hopkins University |
Gillard P.J.,Allergan, Inc. |
Brainin M.,Danube University Krems
Neurology | Year: 2013
Among the estimated 20% to 40% of stroke survivors who develop spasticity, the burden of this condition on patients, caregivers, and society is substantial. Stroke survivors with spasticity may experience reductions in their ability to perform activities of daily living and in their health-related quality of life. The occurrence of spasticity in stroke survivors may also result in an increased burden on their caregivers, who exhibit poorer physical and emotional health as compared with the general population. The responsibilities that caregivers have to the stroke survivor-in terms of providing medical care, protecting from falls, and assisting with feeding and hygiene, among other tasks of daily living-must be balanced with their responsibilities to other family members and to themselves. Caregivers of stroke survivors often report a feeling of confinement with little opportunity for relief, and although social support can be helpful, it is frequently limited in its availability. In terms of the socioeconomic burden of spasticity after stroke, recent data point to a 4-fold increase in health care costs associated with stroke survivors with spasticity compared with stroke survivors without spasticity. Thus, it is important to reduce the burden of spasticity after stroke. Consequently, effective spasticity treatment that reduces spasticity and the level of disability experienced by stroke survivors will likely increase their functioning and their health-related quality of life and will also result in a diminished burden on their caregivers. © 2013 American Academy of Neurology.
Finsterer J.,Danube University Krems
Heart Failure Reviews | Year: 2010
Left ventricular non-compaction, also known as left ventricular hypertrabeculation (LVHT), is a morphological abnormality of the left ventricular myocardium, characterised by a meshwork of myocardial strings, interlacing, and orderless in arrangement. LVHT is most frequently located in the apex and the lateral wall and may occur with or without other congenital or acquired cardiac abnormalities. LVHT is believed to be congenital in the majority of the cases but may develop during life in single cases (acquired LVHT). Congenital LVHT is believed to result from defective late-stage embryonic development of the myocardial architecture. The pathogenesis of acquired LVHT remains speculative. LVHT is most frequently found on transthoracic echocardiography and cardiac MRI but may be visualised also with other imaging techniques. In the majority of the cases, LVHT is associated with hereditary cardiac, neuromuscular, non-cardiac/non-muscle disease, or chromosomal aberrations. In the majority of the cases, LVHT is complicated by ventricular arrhythmias, systolic dysfunction, cardiac embolism, or sudden cardiac death. LVHT per se does not require a specific treatment. Only in case of complications, such as ventricular arrhythmias, cardioembolism, or systolic dysfunction, adequate therapy is indicated. Though initially assessed as poor, the prognosis of LVHT has meanwhile improved, most likely due to the increased awareness for the abnormality and the timely administration of adequate therapy. © 2010 Springer Science+Business Media, LLC.
Finsterer J.,Danube University Krems
Acta Neurologica Scandinavica | Year: 2012
Among the various central nervous system (CNS) manifestations of mitochondrial disorders (MIDs), cognitive impairment is increasingly recognized and diagnosed (mitochondrial cognitive dysfunction). Aim of the review was to summarize recent findings concerning the aetiology, pathogenesis, diagnosis and treatment of cognitive decline in MIDs. Among syndromic MIDs due to mitochondrial DNA (mtDNA) mutations, cognitive impairment occurs in patients with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes syndrome, myoclonus epilepsy with ragged-red fibres syndrome, mitochondrial chronic progressive external ophthalmoplegia, Kearns-Sayre syndrome, neuropathy, ataxia and retinitis pigmentosa syndrome and maternally inherited diabetes and deafness. Among syndromic MIDs due to nuclear DNA (nDNA) mutations, cognitive decline has been reported in myo-neuro-gastro-intestinal encephalopathy, mitochondrial recessive ataxia syndrome, spinocerebellar ataxia with encephalopathy, Mohr-Tranebjaerg syndrome, leuko-encephalopathy; brain and spinal cord involvement and lactic acidosis, CMT2, Wolfram syndrome, Wolf-Hirschhorn syndrome and Leigh syndrome. In addition to syndromic MIDs, a large number of non-syndromic MIDs due to mtDNA as well as nDNA mutations have been reported, which present with cognitive impairment as the sole or one among several other CNS manifestations of a MID. Delineation of mitochondrial cognitive impairment from other types of cognitive impairment is essential to guide the optimal management of these patients. Treatment of mitochondrial cognitive impairment is largely limited to symptomatic and supportive measures. Cognitive impairment may be a CNS manifestation of syndromic as well as non-syndromic MIDs. Correct diagnosis of mitochondrial cognitive impairment is a prerequisite for the optimal management of these patients. © 2012 John Wiley & Sons A/S.
Finsterer J.,Danube University Krems
Open Neurology Journal | Year: 2012
Background: Though not obvious at a first glance, myopathies may be associated with ischemic stroke. Strokelike episodes resemble ischemic stroke only to some extent but are a unique feature of certain mitochondrial disorders with a pathogenesis at variance from that of ischemic stroke. Only limited data are available about ischemic stroke in primary myopathies and the management of stroke-like episodes in mitochondrial disorders. This review aims to summarize and discuss current knowledge about stroke in myopathies and to delineate stroke-like episodes from ischemic stroke. Methods: Literature review via PubMED using the search terms "stroke", "cerebrovascular", "ischemic event", "strokelike episode", "stroke-mimic", "mitochondrial disorder". Results: Stroke in myopathies is most frequently cardioembolic due to atrial fibrillation or atrial flutter, dilated cardio-myopathy, or left-ventricular hypertrabeculation (noncompaction). The second most frequent cause of stroke in myopathies is angiopathy from atherosclerosis or vasculitis, which may be a feature of inflammatory myopathies. Atherosclerosis may either result from classical risk factors, such as diabetes, arterial hypertension, hyperlpidemia, or smoking, associated with muscle disease, or may be an inherent feature of a mitochondrial disorder. In case of severe heart failure from cardiomyopathy as a manifestation of muscle disease low flow infarcts may occur. Thrombophilic stroke has been described in polymyositis and dermatomyositis in association with anti-phospholipid syndrome. Stroke-like episodes occur particularly in mitochondrial encephalopathy, lactacidosis and stroke-likeepisode syndrome but rarely also in Leigh-syndrome and other mitochondrial disorders. Stroke-like episodes are at variance from ischemic stroke, pathogenically, clinically and on imaging. They may be the manifestation of a vascular, metabolic or epileptic process and present with predominantly vasogenic but also cytotoxic edema on MRI. Differentiation between ischemic stroke and stroke-like episodes is essential in terms of management and prognosis. Management of ischemic stroke in patients with myopathy is not at variance from the treatment of ischemic stroke in non-myopathic patients. There is no standardized treatment of strokelike episodes but there is increasing evidence that these patients profit from the administration of L-arginine and consequent antiepileptic treatment if associated with seizure activity. Conclusions: Ischemic stroke may be a complication of myopathy and needs to be delineated from stroke-like episodes, which are unique to mitochondrial disorders, particularly mitochondrial encephalopathy, lactacidosis and stroke-likeepisode syndrome. Ischemic stroke in myopathies is most frequently cardioembolic and treatment is not at variance from non-myopathic ischemic stroke. Treatment of stroke-like episodes is not standardized but seems to respond to L-arginine and adequate antiepileptic treatment. © Josef Finsterer.
Finsterer J.,Danube University Krems
European Journal of Neurology | Year: 2011
Central nervous system (CNS) manifestations of mitochondrial disorders (MIDs) are accessible to therapy. Therapy of CNS abnormalities may be categorized as acting on the pathogenic cascade or on the genetic level, which is experimental. Treatment acting on the pathogenic cascade may be classified as non-specific, including antioxidants, electron donors/acceptors, lactate-lowering agents, alternative energy providers, cofactors, avoidance of mitochondrion-toxic drugs, and physiotherapy, or as specific, including drugs against epilepsy, movement disorders, migraine, spasticity, psychiatric abnormalities, hypopituitarism, or bulbar manifestations, ketogenic diet, deep brain stimulation, or artificial ventilation. Stroke-like episodes need to be delineated from ischaemic stroke and require special management. Potentially, mitochondrion-toxic drugs and drug cocktails need to be avoided, seizures should be consequently treated even with mitochondrion-toxic drugs if necessary, and as few drugs as possible should be given. Effective treatment acting on the pathogenic cascade may increase the quality of life and outcome in patients with MID and may prevent a therapeutic nihilism occasionally upcoming with MIDs. © 2010 The Author(s). European Journal of Neurology © 2010 EFNS.
Finsterer J.,Danube University Krems
Movement Disorders | Year: 2011
In the majority of cases, mitochondrial disorders are multisystem conditions that most frequently affect the skeletal muscle, followed by the central nervous system. One of the clinical manifestations of central nervous system involvement is Parkinson's syndrome (PS). Evidence for an association of mitochondrial defects with PS comes from mitochondrial disorder patients who have developed Parkinson's syndrome and from Parkinson's syndrome patients who have developed a mitochondrial disorder. In addition, there are a number of patients with Parkinson's syndrome or Parkinson's disease (PD) who later develop subclinical immunohistological or biochemical indications of mitochondrial defects or accumulates mitochondrial DNA mutations within various cerebral regions. There are also Parkinson's syndrome patients who present with elevated cerebrospinal-fluid lactate by magnetic resonance spectroscopy. Furthermore, it has been shown that mutations in genes causing PD, such as PINK1, parkin, DJ1, alpha-synuclein, and LRRK2, also cause mitochondrial dysfunction, which is one of the reasons why they are called mitochondrial nigropathies. Parkinson's syndrome in patients with a mitochondrial disorder may also result from oxidative stress or exogenous toxins. Treatment of mitochondrial Parkinson's syndrome is not at variance with the treatment of Parkinson's syndrome due to other causes, but because of the multisystem nature of mitochondrial disorders, mitochondrial Parkinson's syndrome requires additional therapeutic support. © 2011 Movement Disorder Society.
Finsterer J.,Danube University Krems
Advances in Experimental Medicine and Biology | Year: 2012
Though inherited mitochondrial disorders (MIDs) are most well known for their syndromic forms, for which widely known acronyms (MELAS, MERRF, NARP, LHON etc.) have been coined, the vast majority of inherited MIDs presents in a non-syndromic form. Since MIDs are most frequently multisystem disorders already at onset or during the disease course, a MID should be suspected if there is a combination of neurological and non-neurological abnormalities. Neurological abnormalities occurring as a part of a MID include stroke-like episodes, epilepsy, migraine-like headache, movement disorders, cerebellar ataxia, visual impairment, encephalopathy, cognitive impairment, dementia, psychosis, hypopituitarism, aneurysms, or peripheral nervous system disease, such as myopathy, neuropathy, or neuronopathy. Non-neurological manifestations concern the ears, the endocrine organs, the heart, the gastrointestinal tract, the kidneys, the bone marrow, and the skin. Whenever there is an unexplained combination of neurological and non-neurological disease in a patient or kindred, a MID should be suspected and appropriate diagnostic measures initiated. Genetic testing should be guided by the phenotype, the biopsy findings, and the biochemical results. © 2012 Springer Science+Business Media B.V.
Thaler K.,Danube University Krems
Cochrane database of systematic reviews (Online) | Year: 2011
Seasonal affective disorder (SAD) is a seasonal pattern of recurrent depressive episodes that is often treated with second-generation antidepressants (SGAs), light therapy or psychotherapy. To assess the efficacy and safety of SGAs for the treatment of SAD in adults in comparison with placebo, light therapy, other SGAs or psychotherapy. We searched the Cochrane Depression, Anxiety and Neuorosis Review Group's specialised register (CCDANCTR) on the 26 August 2011. The CCDANCTR contains reports of relevant randomised controlled trials from The Cochrane Library (all years), EMBASE (1974 to date), MEDLINE (1950 to date) and PsycINFO (1967 to date). In addition, we searched pharmaceutical industry trials registers via the Internet to identify unpublished trial data. Furthermore, we searched OVID MEDLINE, MEDLINE In-process, EMBASE and PsycINFO to 27July 2011 for publications on adverse effects (including non-randomised studies). For efficacy we included randomised trials of SGAs compared with other SGAs, placebo, light therapy or psychotherapy in adult participants with SAD. For adverse effects we also included non-randomised studies. Two review authors screened abstracts and full-text publications against the inclusion criteria. Data abstraction and risk of bias assessment were conducted by one reviewer and checked for accuracy and completeness by a second. We pooled data for meta-analysis where the participant groups were similar and the studies assessed the same treatments with the same comparator and had similar definitions of outcome measures over a similar duration of treatment. For efficacy we included three randomised trials of between five and eight weeks duration with a total of 204 participants. For adverse effects we included two randomised trials and three observational (non-randomised) studies of five to eight weeks duration with a total of 225 participants. Overall, the randomised trials had low-to-moderate risk of bias, and the observational studies had a high risk of bias (due to small size and high attrition). The participants in the studies all met DSM (Diagnostic and Statistics Manual of Mental Disorders) criteria for SAD. The average age was approximately 40 years and 70% of the participants were female.Results from one trial with 68 participants showed that fluoxetine was not significantly more effective than placebo in achieving clinical response (risk ratio (RR) 1.62, 95% confidence interval (CI) 0.92 to 2.83). The number of adverse effects were similar between the two groups.We located two trials that contained a total of 136 participants for the comparison fluoxetine versus light therapy. Our meta-analysis of the results of the two trials showed fluoxetine and light therapy to be approximately equal in treating seasonal depression: RR of response 0.98 (95% CI 0.77 to 1.24), RR of remission 0.81 (95% CI 0.39 to 1.71). The number of adverse effects was similar in both groups.Two of the three randomised trials and three non-randomised studies contained adverse effect data on 225 participants who received fluoxetine, escitalopram, duloxetine, reboxetine, light therapy or placebo. We were only able to obtain crude rates of adverse effects, so any interpretation of this needs to be undertaken with caution. Between 22% and 100% of participants who received a SGA suffered an adverse effect and between 15% and 27% of participants withdrew from the studies because of adverse effects. Evidence for the effectiveness of SGAs is limited to one small trial of fluoxetine compared with placebo, which shows a non-significant effect in favour of fluoxetine, and two small trials comparing fluoxetine against light therapy, which suggest equivalence between the two interventions. The lack of available evidence precludes the ability to draw any overall conclusions on the use of SGAs for SAD. Further larger RCTs are required to expand and strengthen the evidence base on this topic, and should also include comparisons with psychotherapy and other SGAs.Data on adverse events were sparse, and a comparative analysis was not possible. Therefore the data we obtained on adverse effects is not robust and our confidence in the data is limited. Overall, up to 27% of participants treated with SGAs for SAD withdrew from the studies early due to adverse effects. The overall quality of evidence in this review is very low.
Edelmann N.,Danube University Krems
Cyberpsychology, Behavior, and Social Networking | Year: 2013
Little research focuses on lurking in the online environment or considers lurking as a valid and important form of online behavior. This may be due to the fact that there are a number of definitions, and most of them focus on a lack of participation or contribution or see it as a problematic behavior that needs to be changed. Such definitions have given lurkers a negative connotation. They need to be considered as an important factor in online research, starting with a clearer and more positive definition of lurking. It is also necessary to understanding why users decide to lurk, what activities lurkers engage in, and whether the online environment is more valuable by turning lurkers into posters. © Copyright 2013, Mary Ann Liebert, Inc. 2013.