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- BookMarie-Christine Pardon, Mark W. Bondi, editors.Contents:
Epidemiology of Cognitive Aging and Alzheimer's Disease: Contributions of the Cache County Utah Study of Memory, Health and Aging / Kathleen M. Hayden and Kathleen A. Welsh-Bohmer
Successful Cognitive Aging / Colin A. Depp, Alexandria Harmell and Ipsit V. Vahia
Behavioral Neuroscience of Emotion in Aging / Alfred W. Kaszniak and Marisa Menchola
Studying the Impact of Aging on Memory Systems: Contribution of Two Behavioral Models in the Mouse / Aline Marighetto, Laurent Brayda-Bruno and Nicole Etchamendy
Functional Neuroimaging Studies in Normal Aging / Leslie M. Guidotti Breting, Elizabeth R. Tuminello and S. Duke Han
Functional Magnetic Resonance Imaging in Aging and Dementia: Detection of Age-Related Cognitive Changes and Prediction of Cognitive Decline / John L. Woodard and Michael A. Sugarman
Neuroanatomical Changes Associated with Cognitive Aging / Janice M. Juraska and Nioka C. Lowry. The Impact of Age-Related Ovarian Hormone Loss on Cognitive and Neural Function / Marissa I. Boulware, Brianne A. Kent and Karyn M. Frick
Neuropsychological Features of Mild Cognitive Impairment and Preclinical Alzheimer's Disease / David P. Salmon
Cerebrovascular Disease and Cognition in Older Adults / Gregory A. Seidel, Tania Giovannetti and David J. Libon
Psychiatric Disorders in Ageing / C. Wijeratne, S. Reutens, B. Draper and P. Sachdev
The Impact of Physical and Mental Activity on Cognitive Aging / Amy J. Jak
Potential Benefits and Limitations of Enriched Environments and Cognitive Activity on Age-Related Behavioural Decline / Rosa Redolat and Patricia Mesa-Gresa
Reproductive Experience may Positively Adjust the Trajectory of Senescence / Craig Howard Kinsley, R. Adam Franssen and Elizabeth Amory Meyer
Treatment Trials in Aging and Mild Cognitive Impairment / Jody Corey-Bloom.Digital Access Springer 2012 - ArticleHurd ER, Ziff M.Clin Exp Immunol. 1977 Jul;29(1):132-9.The effects of cyclophosphamide an antinuclear antibody levels, immune complex deposition in renal glomeruli, glomerular cell proliferation and glomerulosclerosis in the (NZB x NZW)F1 hybrid mouse have been investigated in order to better understand the mechanism of action of this drug on nephritis. Five groups of mice were injected daily with this agent (15 mg/kg) by the i.p. route over a 2-month period. Treatment periods began at 1, 3, 5, 7 and 9 months. Each group was killed at the end of the treatment period. During the last week [3H]Tdr(1 mu Ci/g) was injected daily i.p. Immune complex deposition was measured by quantification of glomerular immunofluorescent staining in both capillary loops and mesangium. Glomerular cell proliferation was quantified by measurement of the number of glomerular cells which incorporated [3H]Tdr during in vivo labelling. The number of [3H]Tdr-labelled cells in each of 100 glomeruli was counted using kidney autoradiographs of whole kidney slices. This technique provided a very reproducible and quantitative index of glomerular cell proliferation. Glomerulosclerosis was measured by determining percentage of PAS-positive material in each of 100 counted glomeruli. Immune complex deposition in the kidney preceded the glomerular cell proliferation. The proliferation reached a peak at 9 months of age. Glomerulosclerosis gradually increased with age until the animal's death. Cyclophosphamide significantly decreased antinuclear antibody levels, glomerular cell proliferation, and immunoglobulin staining in the glomeruli. Progression of glomerulosclerosis was significantly arrested. The present findings demonstrate a very significant effect of cyclophosphamide on three important pathological changes which occur in the nephritis of the (NZB x NZW)F1 hybrid mouse and provide information about possible mechanisms underlying these changes.