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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Case Reports
Accelerated nodulosis during methotrexate therapy for refractory rheumatoid arthritis. A case report.
Accelerated nodulosis (AN) is a potential complication of methotrexate (MTX) therapy for rheumatoid arthritis (RA). We report on a 62-year old man affected by seropositive RA who developed AN after five months of MTX treatment. MTX-dose reduction was followed by rapid regression of the skin nodules. The Authors describe the typical features of AN and discuss on the pathogenetic mechanisms.
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Oxygen tension (pO2) in rat renal cortex and outer medulla was studied after an intravenous injection of mannitol or furosemide, followed 10 minutes later by an intravenous injection of the non-ionic X-ray contrast medium (CM) iopromide (370 mg iodine/ml). Ten minutes after mannitol injection, before injection of CM, pO2 in the medulla had decreased from a control level of 32 +/- 3 to 28 +/- 4 mm Hg. The addition of CM caused a further decrease, to 24 +/- 5 mm Hg, which was a significant reduction. ⋯ Injection of CM caused a significant decrease in pO2 to 37 +/- 3 mm. Ringer's solution (n = 6) caused no changes. We conclude that pretreatment with mannitol or furosemide does not prevent the CM-induced decrease in pO2 in the outer medulla.