Objective: To evaluate the efficacy, safety, and tolerability of combination therapy with intramuscular interferon beta-1a and oral doxycycline, a potent inhibitor of matrix metalloproteinases, in patients with relapsingremitting multiple sclerosis (RRMS) having breakthrough disease activity.

No abstract

Knowledge and recognition of the various metabolic and toxic causes of myelopathy is important for the practicing neurologist, as timely diagnosis and rapid initiation of therapy is essential to improve the chances for recovery.

Multiple sclerosis (MS) is a common immune-mediated progressive neurodegenerative disease of the CNS that typically manifests with periods of disease activity followed by intervals of remission. The etiology of MS remains unknown; however, existing evidence indicates that MS is a ‘whole-brain disease’ that is driven by a potent immune response against CNS antigen(s), particularly myelin peptide antigens. The immunopathogenesis of MS includes both the cell- and humorally-mediated arms of the immune system. Genetic and environmental factors play important roles in the development of MS. Application of various neuroimaging techniques to the world of MS have expanded our knowledge concerning its pathogenesis and assist us in the more accurate diagnosis of MS versus its imitators. Current treatments target acute attacks and aim to reduce future clinical relapses. A summary of the potential future therapies for MS is presented.

Pregnant ICR mice were administered single intraperitoneal injections of 300, 400, or 500 mg/kg of the thymidine analogue 5-bromodeoxyuridine during the period of major organogenesis (days 7-11, Witschi stages 12-25). All dosages were teratogenic. The spectrum of malformations present on day 18 followed a definite stagedependency. Exencephaly with associated micrognathia and open eyelid were produced only by treatment during the time the anterior neuropore is open (days 7 and 8) with a peak on day 7. Polydactyly was produced by treatment on days 7 through 10 with a peak on day 9; while cleft palate occurred after treatment on days 9 through 11 with a peak on day 10. Experiments with SH-BUDR demonstrated that label appeared in the DNA of embryos and maternal liver at a time when the embryo is susceptible to the teratogenic action of BUDR. Acid-soluble 1 DNA 2 Maternal liver 512 235.6 8.33 f 1.33 Embryo 10.52 3.9 15.33 r+ 2.40 1 dpm (mean k SE x 103); liver acid-soluble activity expressed as dpm/g wet weight; embryo acid-soluble activity expressed as dpm/embryo. edpm/&g DNA (mean k SE).