To further understand the neuroanatomy, neurochemistry and neuropathology of the normal and diseased human brain, it is essential to have access to human brain tissue where the biological and chemical nature of the tissue is optimally preserved. We have established a human brain bank where brain tissue is optimally processed and stored in order to provide a resource to facilitate neuroscience research of the human brain in health and disease. A donor programme has been established in consultation with the community to provide for the post-mortem donation of brain tissue to the brain bank. We are using this resource of human brain tissue to further investigate the basis of normal neuronal functioning in the human brain as well as the mechanisms of neuronal dysfunction and degeneration in neurodegenerative diseases. We have established a protocol for the preservation of post-mortem adult human brain tissue firstly by snap-freezing unfixed brain tissue and secondly by chemical fixation and then storage of this tissue at -80 degrees C in a human brain bank. Several research techniques such as receptor autoradiography, DNA and RNA analysis, are carried out on the unfixed tissue and immunohistochemical and histological analysis is carried out on the fixed human tissue. Comparison of tissue from normal control cases and from cases with neurodegenerative disorders is carried out in order to document the changes that occur in the brain in these disorders and to further investigate the underlying pathogenesis of these devastating neurological diseases.
It has recently been reported that the Beta-adrenergic receptor-blocker acebutolol accelerates the development of antinuclear antibodies (ANAs) in hypertensive patients. We examined data from over 1500 hypertensive patients to determine whether this effect is associated with other beta blockers. Groups of patients treated with acebutolol, atenolol, labetalol, and pindolol all displayed increased development of ANAs relative to patients on other medication. When patients taking methyldopa (a drug associated with a high ANA incidence) were excluded from the analysis, only acebutolol retained an association (P less than 0.001) with ANA production. Sequential studies to assess the development of ANAs in patients during the course of beta-blocker treatment revealed a similar pattern. With methyldopa patients excluded, the fraction of patients developing ANAs was less then 10% for all but atenolol (10.9%), labetalol (13.8%), and acebutolol (33%). Thus, although some of the beta blockers may be associated with an increase in ANA incidence, the dramatic effects of acebutolol do not appear to be a group property.
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