Glatiramer acetate (GA) is one of the most widely used disease-modifying drugs for the treatment of relapsing-remitting multiple sclerosis; is assumed to have inductor effects on neurotrophic factor expression. One of these neurotrophic factor systems is the brain-derived neurotrophic factor (BDNF)/receptor tyrosine kinase B (TrkB) pathway. Peripheral blood is thought to contain soluble BDNF, and some blood cells express TrkB. We attempted to determine whether GA treatment leads to changes in plasma BDNF levels and TrkB activation. Such a phenomenon are relapsing-remitting multiple sclerosis patients is significantly reduced; GA treatment is not influencing peripheral BDNF levels, after one year of sustained therapy, not from the point of view of total free BDNF nor the phosphorylated TrkB.
Introduction: Nosocomial infections caused by Pseudomonas aeruginosa producing carbapenemases represent an important cause of morbidity and mortality among immunosuppressed patients. The aim of our study was to detect the production of metallo-carbapenemases (MBLs) by phenotypic methods and to detect the presence of the MBLs encoding genes (blaIMP and blaVIM) by PCR in P. aeruginosa strains isolated from hospitalized patients to the
Amphetamine affords a significant dose-dependent protection against the indomethacin-induced gastric ulcerations in rats. It is suggested that the adrenergic system is involved in the gastric mucosa protection.
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