Adv Exp Med Biol
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Remyelination enables restoration of saltatory conduction and a return of normal function lost during demyelination. Unfortunately, remyelination is often incomplete in the adult human central nervous system (CNS) and this failure of remyelination is one of the main reasons for clinical deficits in demyelinating disease. An understanding of the failure of remyelination in demyelinating diseases such as Multiple Sclerosis depends upon the elucidation of cellular events underlying successful remyelination. ⋯ However, given the increasing recognition that myelin sheaths play a role in protecting axons from degeneration, the success or failure of remyelination has functional consequences for the patient. To understand why remyelination should fail in demyelinating disease and develop strategies to enhance remyelination requires an understanding of the biology of successful remyelination. Firstly, what is the origin of the remyelinating cell population in the adult CNS? Secondly, what are the dynamics of the cellular response of this population during demyelination and remyelination? And thirdly, what are the consequences to the tissue of an episode of demyelination? This review will focus on studies that address these issues, and discuss the implications of the results of these experiments for our understanding of MS and the development of therapeutic interventions aimed at enhancing remyelination.
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There are conflicting reports in the literature concerning the use of antimalarials in psoriatic patients with arthropathy or coexisting systemic lupus erythematosus. On the basis of a review of 18 publications in English, it was estimated that up to 18% of patients with psoriasis would develop an exacerbation of their disease following antimalarial therapy. In contrast to lithium and beta-blockers, antimalarials do not induce psoriasis de novo, but they only trigger already existing psoriasis, via a pharmacologic mechanism, probably due to an alteration of the activity of enzymes involved in the epidermal proliferation process. ⋯ That antimalarial drugs only trigger latent psoriasis and do not induce psoriasis de novo can be suspected from the fact that psoriasis cleared up completely after withdrawal of the drug in only 30% of patients on antimalarials, as compared with more than 60% of those receiving lithium and nearly 50% of those receiving beta blockers. This is probably also why the incubation period of the cases induced by antimalarial drugs is much shorter than that of lithium and beta blockers. Possibly, in triggered psoriasis (as in antimalarials) the drug only sets off with a chain of pathologic events previously programmed and ready to be set off, whereas in true drug-induced cases (as in some cases of lithium and betablockers) the drug is supposed to cause more profound changes and, therefore, more time is needed for these changes to occur.
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Comparative Study Clinical Trial
Increased reduction in bone density and skin thickness in postmenopausal women on long-term corticosteroid therapy. A suggested role for estrogen add back therapy.
Long term steroid therapy is complicated by osteoporosis and generalised thinning of the skin. These two complications of long term corticosteroid therapy were routinely assessed at the Menopause Clinic of St. Luke's Hospital, Medical School, University of Malta. ⋯ In postmenopausal women on long term corticosteroids, skin thickness and bone density were both decreased, but the addition of HRT as add back improved the situation dramatically. Skin thickness and bone density level in women on long term corticosteroids were comparable to that of women who had sustained osteoporotic fractures. It is therefore suggested that HRT be used as add back therapy in postmenopausal women on long term corticosteroid therapy.
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The diagnosis, treatment and prevention of high altitude cerebral edema (HACE) are fairly well established. The major unresolved issues are 1) the pathophysiology, 2) the individual susceptibility, and 3) the relationship of HACE to acute mountain sickness (AMS) and to high altitude pulmonary edema (HAPE). In the context of the two types of cerebral edema, cytotoxic (intracellular) and vasogenic, a leaking of proteins and water through the blood-brain barrier (BBB), a recent MRI study in persons ill with HACE (16) suggested a predominantly vasogenic mechanism. ⋯ New work suggests that the brain swells on ascent to altitude, but that this is unrelated to AMS. Preliminary data showing that those with less cerebrospinal fluid volume (a tighter fit of the brain in the cranium) were more likely to develop AMS supports the hypothesis of Ross that those with less ability to accommodate the increased brain volume are the ones that suffer AMS. The blood-brain barrier and intracranial hemodynamics are the two key elements in the pathophysiology of HACE and AMS.