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      Cell Proliferation/Cell Death Balance in Renal Cell Cultures after Exposure to a Static Magnetic Field


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          The effect of a static magnetic field (MF) of 0.5 mT of intensity on the cell proliferation/cell death balance was investigated in renal cells (VERO) and cortical astrocyte cultures from rats. Magnetic stimulation was delivered by magnetic disks at known intensities. The percentage of apoptotic and necrotic cells was evaluated using flow cytometry and morphological analysis following Hoechst chromatin staining. An index of cell proliferation was determined using sulfonated tetrazolium (WST-1). Control cultures were prepared without exposure to MFs. After 2, 4 and 6 days of exposure to a MF, we observed a gradual decrease in apoptosis and proliferation and a gradual increase in cells with a necrotic morphology with respect to the control group. In astrocyte cultures, over a 6-day exposure period. A gradual increase was observed in apoptotic, proliferating, and necrotic cells. Our findings suggest that the effect of exposure to MFs varies, depending on the cell type; MFs may also have a nephropathogenic effect.

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          Glial reaction in aging and Alzheimer's disease.

          It is well-established that glial cells play an important role during injury and neurodegenerative processes in the central nervous system. In normal aging, no global glia proliferation is found morphologically, but reactive gliosis has been described in specific areas of the limbic system and neocortex that undergo selective neuronal or synaptic degeneration in nondemented elderly persons. In addition, there is an age-associated increase in the metabolic turnover of cellular proteins, such as glial fibrillary acidic protein, in human brain tissue, even without detectable signs of neurodegeneration. In contrast to the relatively moderate overall glial changes in normal aging, the close association of activated astrocytes and microglial cells with neuritic plaques and cells undergoing neurofibrillary degeneration in Alzheimer's disease (AD), the expression of receptors for complement by glial cells, and the release of soluble cytokines strongly suggest that inflammatory processes may play an important part in the complex pathophysiological interactions that occur in AD. Understanding the role of glia in age-associated neurodegenerative disorders may provide new insights into the neurobiology of glia-neuronal interaction and may allow the development of strategies to alter the disease process. This review aims to summarize some of the important aspects of glial cells in aging and dementia.
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            Bcl-xl-specific antibody labels activated microglia associated with Alzheimer's disease and other pathological states.

            This report describes the production of a monoclonal antibody raised against Bcl-xl, and includes an initial study of bcl-xl expression in neuropathology including Alzheimer's disease (AD). Bcl-xl is a potent apoptotic inhibitor and is known to be the predominant Bcl-x isoform in brain. To examine the expression of bcl-xl in aged brain and neurodegenerative disease, we raised a Bcl-xl-specific monoclonal antibody. In aged human brain, the highest bcl-xl expression was observed in cerebellum. By immunohistochemistry, significant bcl-xl expression was detected in reactive microglia of patients with AD and other neurological diseases such as progressive supranuclear palsy. Bcl-xl-positive microglia frequently colocalized with beta-amyloid plaques in AD and with activated astrocytes in non-AD and AD brains, suggesting a general role for Bcl-xl in regions of pathology. High levels of Bcl-xl protein might render microglia more resistant to cytotoxic environments such as areas of neurodegeneration and astrogliosis.
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              Experimental evidence for 60 Hz magnetic fields operating through the signal transduction cascade


                Author and article information

                S. Karger AG
                16 March 2001
                : 87
                : 3
                : 269-273
                aDipartimento di Medicina Interna, Facoltà di Medicina e Chirurgia, bIstituto di Fisiologia Generale, Facoltà di MM.FF.NN., cDipartimento di Pediatria Medica, Preventiva e Sociale, Facoltà di Medicina e Chirurgia, e dDipartimento di Statistica, Università degli Studi di Messina, eDipartimento di Fisica della Materia e Tecnologie Fisiche Avanzate, Università di Messina, fCentro Siciliano per le Ricerche Atmosferiche e di Fisica dell’Ambiente, Università di Messina, Italia
                45925 Nephron 2001;87:269–273
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 2, References: 23, Pages: 5
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45925
                Self URI (text/html): https://www.karger.com/Article/FullText/45925
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
                Original Paper

                Cardiovascular Medicine,Nephrology
                Vero cells,Magnetic field,Cell Proliferation,Apoptosis
                Cardiovascular Medicine, Nephrology
                Vero cells, Magnetic field, Cell Proliferation, Apoptosis


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