Showing 81 - 100 results of 904 for search 'B well development dysfunction', query time: 0.16s Refine Results
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    2BALANCE: a cognitive-motor dual-task protocol for individuals with vestibular dysfunction by Maya Danneels, Ruth Van Hecke, Laura Leyssens, Sofie Degeest, Dirk Cambier, Raymond van de Berg, Vincent Van Rompaey, Leen Maes

    Published 2020-07-01
    “…Ultimately, this project could enable individualised and holistic clinical care in these patients, taking into account single as well as dual-task performance.Ethics and dissemination The current study was approved by the ethics committee of Ghent University Hospital on 5 July 2019 with registration number B670201940465. …”
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    Risk Factors for Postoperative Neurologic Dysfunction in Patients with Spinal Tuberculosis: A Retrospective Study by Shao P, Wang Y, Dong M, Fan H, Gao Y, Gao Y, Hao Z, Lv J, Bai J, Wu Z, Feng Y

    Published 2025-07-01
    “…We also compared the patients’ pre- and postoperative changes in relevant inflammatory indicators, such as the ESR and PCT.Results: Postoperatively, one patient developed paraplegia with an ASIA grade of A; 29 patients developed incomplete paraplegia with an ASIA score of grade B in 5 patients, grade C in 7 patients, and grade D in 17 patients. …”
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    The role of endosarcomeric cytoskeleton proteins in the mechanisms of left ventricular diastolic dysfunction: focus on titin by V. V. Kalyuzhin, A. T. Teplyakov, I. D. Bespalova, E. V. Kalyuzhina, G. E. Chernogoryuk, N. N. Terentyeva, E. V. Grakova, K. V. Kopeva, V. Yu. Usov, N. P. Garganeeva, I. K. Livshits, I. V. Petrova, T. V. Lasukova

    Published 2023-10-01
    “…Impairment of myocardial relaxation and deterioration of its wall compliance under a wide range of pathological conditions (pressure overload, ischemia, inflammation, cardiotoxic effects, oxidative stress, etc.) underlying DD can be explained by a shift in titin expression toward its more rigid N2B isoform, hypophosphorylation by protein kinases A and G or dephosphorylation by serine / threonine phosphatase 5 of its molecule in the extensible protein segment containing a unique N2B sequence, hyperphosphorylation of PEVK regions of titin by protein kinase C, as well as inhibition of the Ca2+-dependent titin – actin interaction.The results of deciphering these mechanisms can become a tool for developing new approaches to targeted therapy for diastolic heart failure that currently does not have effective treatment, on the one hand, and the key to understanding the therapeutic effects of drugs already used to treat chronic heart failure with preserved LV ejection fraction, on the other hand.…”
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