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Abstract--After a temperature-dependent period when little dissolution occurs, the dissolution of rhyolitic glass can be described by dC/dt = k(Cs -C), where Cs is the concentration of dissolved silica at saturation, C is the instantaneous silica concentration, and k is a rate constant equal to 1.6 • 10 -5, 3.0 • 10 -s, and 4.5 • 10 -5 sec -1 at 115 ~ 130 ~ and 140~ respectively, in 2 M Na-K carbonate solution at 1 kbar pressure. At 130~ a C~ value of 0.177 M SiO2 is reached in 30 hr, and phillipsite, clinoptilolite, and mordenite begin forming at 34, 64, and 76 hr, respectively, in 2 M CO3, 1:1 NaJK. During glass dissolution and zeolite formation, the concentration of AI as AI(OH)4-is buffered at 3.7 x 10 -4 M by an unidentified phase. The ratio of SiO2 to AI(OH)4-at the onset of zeolite formation is 475. In 2 M CO3 solution, phillipsite crystallization begins at 144 hr at 115~ at 34 hr at 130~ and at 20 hr at 140~ Phillipsite crystallization begins at 48 hr in 1.5 M COz, at 168 hr in 1.0 M CO3, and in excess of 550 hr in 0.2 M CO3 at 140~ In addition to OH-catalysis, CO32-appears also to catalyze the glass-dissolution and zeolite-formation processes.Thermodynamically, phillipsite is unstable relative to clinoptilolite and mordenite in silica-rich alkaline hydrothermal solutions. Phillipsite forms first, followed by clinoptilolite, and then mordenite. Phillipsite formation is favored by runs of one-week duration, temperatures less than 150~ and K-rich fluids. Clinoptilolite formation is favored in runs of more than one week, temperatures less than 150~ and K-rich fluids. Mordenite formation is favored by runs of more than one week, temperatures greater than 140~ and Na-rich fluids. In 8-day runs at 140~ clinoptilolite formation was favored by liquid : solid reactant (volume : mass) ratios less than 1.0, mordenite by ratios from 0.85 to 1.5, and phillipsite by ratios greater than 1.5. The mechanism of formation of the different zeolites, particularly phillipsite, may involve silicacyclic tetramers which are abundant in concentrated solutions under alkaline hydrothermal conditions but which are almost absent in dilute low-temperature solutions. Thus, the results ofhydrothermal experiments may not be directly applicable to zeolite formation at low temperatures.

Summary Genomic studies have repeatedly associated variants in the gene encoding microRNA miR-137 with increased schizophrenia risk. Bioinformatic predictions suggest that miR-137 regulates schizophrenia-associated signaling pathways critical to neural development, but these predictions remain largely unvalidated. In the present study, we demonstrate that miR-137 regulates neuronal levels of p55γ, PTEN, Akt2, GSK3β, mTOR, and rictor. All are key proteins within the PI3K-Akt-mTOR pathway and act downstream of neuregulin (Nrg)/ErbB and BDNF signaling. Inhibition of miR-137 ablates Nrg1α-induced increases in dendritic protein synthesis, phosphorylated S6, AMPA receptor subunits, and outgrowth. Inhibition of miR-137 also blocks mTORC1-dependent responses to BDNF, including increased mRNA translation and dendritic outgrowth, while leaving mTORC1-independent S6 phosphorylation intact. We conclude that miR-137 regulates neuronal responses to Nrg1α and BDNF through convergent mechanisms, which might contribute to schizophrenia risk by altering neural development.