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Our hypothesis is that GPx1 concentration in breast cells is controlled by (i) factors that affect Se bioavailability (Se supply and polymorphisms in SEPP1) or the selenoprotein hierarchy (e.g
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Particular targets appeared for the beta-blockers, carbonic anhydrase inhibitors, alpha-adrenergic agonists (aqueous humor inflow inhibition) [35,36,37,38,39], muscarinic agonists, and rho kinase inhibitors (aqueous humor outflow stimulation) [36,37,38,39]