It is not clear if these changes are associated with an increased risk of significant symptoms. Fluid removal can reverse these abnormalities and their associated symptoms.”
“Restless legs syndrome (RLS) is a sleep-related movement disorder commonly involving an unpleasant urge to move the limbs, typically the legs. Dopaminergic agents represent the first-line therapy for RLS; however, long-term use of such drugs results in worsening symptoms due to “”augmentation”" or other adverse events. selleck Gabapentin, an analog of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), is an anticonvulsant/analgesic agent. Gabapentin is only mildly effective in relieving RLS symptoms,
perhaps a result of its poor absorption from the gastrointestinal (GI) tract. Gabapentin enacarbil is a prodrug of gabapentin specifically designed to enhance absorption via the GI tract, and hence provide improved circulating levels of gabapentin on metabolism. Clinical trials to date have demonstrated favorable safety and (compared to traditional gabapentin) improved pharmacokinetics and efficacy in treating RLS symptoms. Thus, gabapentin enacarbil may prove to be a useful
drug in treating RLS. An application of gabapentin enacarbil for treatment of RLS is currently pending Nirogacestat research buy with FDA for approval.”
“Ursodeoxycholic acid (UDCA) can prevent chemical and colitis-associated Dihydrotestosterone colon carcinogenesis by unknown mechanism(s). One of the processes underlying the chemopreventive action could be the inhibition of proliferation by UDCA. To clarify the antiproliferative
mechanism of UDCA, we used p53(wt) colon carcinoma cell lines HCT8 and HCT116. UDCA-induced inhibition of proliferation was reversible and was associated with a decrease of the S-phase and an increase of G1 phase population, but not with apoptosis or senescence. The treatment suppressed the expression of c-Myc protein and, as a consequence, of several cell cycle regulatory molecules, including CDK4 and CDK6. Using the HCT8 cell line as a model, we show that UDCA suppresses c-Myc at the protein level. The suppression of c-Myc alone or a simultaneous suppression of CDK4 and of CDK6 kinase is sufficient to inhibit cell proliferation. In sum, we identified c-Myc as a primary UDCA target in colon carcinoma cells. The degradation of c-Myc protein decreases the expression of the cell cycle regulators CDK4 and CDK6, which reversibly slows down the cell cycle. The suppression of these proproliferatory molecules is the likely initial mechanism of antiproliferatory action of UDCA on colon cancer cells. European Journal of Cancer Prevention 21:413-422 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Presurgical psychological screening of bariatric surgery candidates includes some form of standardized psychological assessment.