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  1. Article ; Online: Biomarkers of Neurodegenerative Diseases

    Dorota Koníčková / Kateřina Menšíková / Lucie Tučková / Eva Hényková / Miroslav Strnad / David Friedecký / David Stejskal / Radoslav Matěj / Petr Kaňovský

    Biomedicines, Vol 10, Iss 7, p

    Biology, Taxonomy, Clinical Relevance, and Current Research Status

    2022  Volume 1760

    Abstract: The understanding of neurodegenerative diseases, traditionally considered to be well-defined entities with distinguishable clinical phenotypes, has undergone a major shift over the last 20 years. The diagnosis of neurodegenerative diseases primarily ... ...

    Abstract The understanding of neurodegenerative diseases, traditionally considered to be well-defined entities with distinguishable clinical phenotypes, has undergone a major shift over the last 20 years. The diagnosis of neurodegenerative diseases primarily requires functional brain imaging techniques or invasive tests such as lumbar puncture to assess cerebrospinal fluid. A new biological approach and research efforts, especially in vivo, have focused on biomarkers indicating underlying proteinopathy in cerebrospinal fluid and blood serum. However, due to the complexity and heterogeneity of neurodegenerative processes within the central nervous system and the large number of overlapping clinical diagnoses, identifying individual proteinopathies is relatively difficult and often not entirely accurate. For this reason, there is an urgent need to develop laboratory methods for identifying specific biomarkers, understand the molecular basis of neurodegenerative disorders and classify the quantifiable and readily available tools that can accelerate efforts to translate the knowledge into disease-modifying therapies that can improve and simplify the areas of differential diagnosis, as well as monitor the disease course with the aim of estimating the prognosis or evaluating the effects of treatment. The aim of this review is to summarize the current knowledge about clinically relevant biomarkers in different neurodegenerative diseases.
    Keywords neurodegeneration ; cerebrospinal fluid ; biomarkers ; blood-based biomarkers ; neurodegenerative diseases ; Alzheimer’s disease ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Very late complications of oncotherapy in glioblastoma patients

    Ondrej Kalita / Lumir Hrabalek / Matej Halaj / Pavel Hok / David Franc / Yvona Klementova / Martin Dolezel / Eva Cechakova / Zuzana Sporikova / Jiri Drabek / Marian Hajduch / Lucie Tuckova

    Biomedical Papers, Vol 166, Iss 2, Pp 236-

    A case series

    2022  Volume 241

    Abstract: Background. Stroke-like syndrome is defined as a rare, delayed complication of brain oncotherapy. Cases with more favorable brain cancer diagnoses and longer life expectancy have been previously reported, but here we present, for the first time, three ... ...

    Abstract Background. Stroke-like syndrome is defined as a rare, delayed complication of brain oncotherapy. Cases with more favorable brain cancer diagnoses and longer life expectancy have been previously reported, but here we present, for the first time, three long-term survivors of glioblastoma with stroke-like syndromes. Methods and Results. Three young or middle-aged patients underwent tumor resection and chemoradiotherapy. They received regular clinical and imaging follow-up with stable neurological status and no signs of tumor recurrence. They exhibited varied signs and symptoms (motor and sensory deficits, aphasia, memory and cognitive disorders, seizures, and headache) accompanied by imaging abnormalities. Stroke-like syndromes developed within 2-5 days and resolved in 2-6 weeks. Diffusion-weighted MRI and T2 brain perfusion abnormalities were demonstrated in all patients. In addition, there was focal T1 MRI contrast enhancement due to blood-brain barrier disruption. In addition to tumor recurrence, classic stroke, encephalitis, metabolic and mitochondrial disorders, and post-seizure swelling should be excluded. The imaging indicated intensive MRI scanning and symptomatic medication (steroids supplemented by antiepileptics, vasoactive agents, etc.) for judicious management. With respect to the course, an invasive procedure was still considered an option. Conclusion. All stroke-like syndromes are diagnoses of exclusion. To avoid misinterpretation of imaging findings as glioblastoma recurrence and avert recall oncotherapy or redundant interventions, better understanding of delayed complications of brain tumor therapy is crucial.
    Keywords stroke-like syndrome ; glioblastoma ; oncotherapy ; corticosteroid ; Medicine ; R
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Palacký University Olomouc, Faculty of Medicine and Dentistry
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells

    Elisabeth Anne Adanma Obara / Diana Aguilar-Morante / Rikke Darling Rasmussen / Alex Frias / Kristoffer Vitting-Serup / Yi Chieh Lim / Kirstine Juul Elbæk / Henriette Pedersen / Lina Vardouli / Kamilla Ellermann Jensen / Jane Skjoth-Rasmussen / Jannick Brennum / Lucie Tuckova / Robert Strauss / Christoffel Dinant / Jiri Bartek / Petra Hamerlik

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 14

    Abstract: Cancer stem cells can evade treatment. Here, the authors perform an in vitro screen to identify proteins that are involved in protecting glioma cancer stem cells from therapy and find that SPT6 increases BRCA1 expression and drives error-free DNA repair, ...

    Abstract Cancer stem cells can evade treatment. Here, the authors perform an in vitro screen to identify proteins that are involved in protecting glioma cancer stem cells from therapy and find that SPT6 increases BRCA1 expression and drives error-free DNA repair, thereby ensuring the survival of the cells.
    Keywords Science ; Q
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Author Correction

    Rikke D. Rasmussen / Madhavsai K. Gajjar / Lucie Tuckova / Kamilla E. Jensen / Apolinar Maya-Mendoza / Camilla B. Holst / Kjeld Møllgård / Jane S. Rasmussen / Jannick Brennum / Jiri Bartek / Martin Syrucek / Eva Sedlakova / Klaus K. Andersen / Marie H. Frederiksen / Petra Hamerlik

    Nature Communications, Vol 9, Iss 1, Pp 1-

    BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

    2018  Volume 1

    Abstract: This Article contains an error in the spelling of the author Kjeld Møllgård, which is incorrectly given as Kjeld Møllgaard. The error has not been fixed in the original PDF and HTML versions of the Article. ...

    Abstract This Article contains an error in the spelling of the author Kjeld Møllgård, which is incorrectly given as Kjeld Møllgaard. The error has not been fixed in the original PDF and HTML versions of the Article.
    Keywords Science ; Q
    Language English
    Publishing date 2018-12-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Author Correction

    Rikke D. Rasmussen / Madhavsai K. Gajjar / Lucie Tuckova / Kamilla E. Jensen / Apolinar Maya-Mendoza / Camilla B. Holst / Kjeld Møllgård / Jane S. Rasmussen / Jannick Brennum / Jiri Bartek / Martin Syrucek / Eva Sedlakova / Klaus K. Andersen / Marie H. Frederiksen / Petra Hamerlik

    Nature Communications, Vol 9, Iss 1, Pp 1-

    BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

    2018  Volume 1

    Abstract: This Article contains an error in the spelling of the author Kjeld Møllgård, which is incorrectly given as Kjeld Møllgaard. The error has not been fixed in the original PDF and HTML versions of the Article. ...

    Abstract This Article contains an error in the spelling of the author Kjeld Møllgård, which is incorrectly given as Kjeld Møllgaard. The error has not been fixed in the original PDF and HTML versions of the Article.
    Keywords Science ; Q
    Language English
    Publishing date 2018-12-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  6. Article ; Online: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

    Rikke D. Rasmussen / Madhavsai K. Gajjar / Lucie Tuckova / Kamilla E. Jensen / Apolinar Maya-Mendoza / Camilla B. Holst / Kjeld Møllgaard / Jane S. Rasmussen / Jannick Brennum / Jiri Bartek / Martin Syrucek / Eva Sedlakova / Klaus K. Andersen / Marie H. Frederiksen / Petra Hamerlik

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 14

    Abstract: BRCA1 loss can result in collapse of replication forks into DNA double strand breaks that can contribute to malignant transformation. Here, the authors find that BRCA1 promotes the expression of RRM2 protecting glioblastoma cells from replication stress, ...

    Abstract BRCA1 loss can result in collapse of replication forks into DNA double strand breaks that can contribute to malignant transformation. Here, the authors find that BRCA1 promotes the expression of RRM2 protecting glioblastoma cells from replication stress, DNA damage and apoptosis.
    Keywords Science ; Q
    Language English
    Publishing date 2016-11-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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