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  • 1
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 78 (1971), S. 127-138 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Acronycine  -  an alkaloid with antineoplastic activity against a wide range of experimental tumors  -  at concentrations of 0.5-12 μg/ml rapidly inhibits RNA synthesis in L5178Y mouse lymphoma and IRC rat monocytic leukemia cultures. Culture growth is arrested only at acronycine concentrations which markedly inhibit RNA synthesis. DNA synthesis is inhibited at rather higher concentrations but this is not a prerequisite of the arrest of growth. It is suggested that the arrest of growth may be a consequence of the inhibition of RNA synthesis.In both cultures arrest of growth coincides with the appearance of many cells with two apparently normal nuclei. Cells are not arrested in mitosis. It is shown these binucleated cells very probably arise from an inhibition of cell cleavage. Studies with synchronized cultures show that at low drug concentrations, more than one cell cycle may elapse before growth is arrested and binucleated cells appear, indicating the effect on cytokinesis is not immediate. The results suggest that the arrest of growth may be a result of a slow depletion of a component essential for cell cleavage. The disturbance at division is a major factor in arresting growth at low drug concentrations. At higher acronycine concentrations, when RNA synthesis may be inhibited by 80-90%, the cytotoxic effects appear earlier and are less specifically directed at cytokinesis; DNA synthesis is then also rapidly and markedly inhibited.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2014-07-25
    Description: Introduction Depressive symptoms are common and undermine the quality of life of people with Alzheimer's disease (AD). Cholinesterase inhibitors and antidepressants have all but no effect on the mood of patients, and their use increases adverse events. Cognitive bias modification (CBM) targets attentional and interpretative biases associated with anxiety, dysphoria and depression and may be useful to treat depression in AD (DAD). This trial aims to determine the effect of CBM on depression scores and the quality of life of people with DAD. Methods and analysis Randomised, double-blind, parallel, controlled trial of CBM (1:1 allocation ratio). Participants will be 80 adults with probable AD living in the Western Australian community who score 8 or more on the Cornell Scale for Depression in Dementia (CSDD). They will have mild to moderate dementia (Mini-Mental State Examination—MMSE score ≥15) and will be free of severe sensory impairment or suicidal intent. The intervention will consist of 10 40 min sessions of CBM delivered over 2 weeks using a high-resolution monitor using a local computer station at the Western Australian Centre for Health and Ageing. The primary outcomes of interest are the 2-week change, from baseline, in the severity of CSDD scores and the Quality of Life AD (QoL-AD) scores. Secondary outcomes include changes in the CSDD, QoL-AD after 12 weeks, and changes in MMSE scores, negative attentional and interpretative bias and the proportion of participants with CSDD 〈8 after 2 and 12 weeks. Ethics and dissemination The study will comply with the principles of the Declaration of Helsinki and participants will provide written informed consent. The Ethics Committee of the Royal Perth Hospital will approve and oversee the study (REG14-036). The results of this trial will provide level 2 evidence of efficacy for CBM as a treatment of DAD. Trial registration number Australian and New Zealand Clinical Trials Registry number ACTRN12614000420640, date registered 06/04/2014.
    Keywords: Open access, Geriatric medicine, Mental health, Neurology
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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