Pressure retarded osmosis (PRO) is a technology that can be utilized to recover energy from the mixing of freshwater with seawater. This source of renewable energy is sizeable and in the past decade several investigations analyzed its potential. The vast majority of studies focused on mass transfer problems across the membrane in order to improve membrane productivity and just recently studies started to look at membrane module efficiencies and parasitic loads within the PRO facility. In this article, the net specific energy production from a facility-scale PRO system was determined and optimized by using a novel simulation method that integrates parasitic loads and efficiencies of the PRO facility components and combines the model with an optimization software in a linked system optimization scheme. It was found that the overall net specific energy that may be recovered by a river-to-sea PRO facility is approximately 0.12 kWh per m 3 of permeate. Furthermore, a sensitivity analysis was performed to elucidate the relationship between net specific energy and power density as functions of membrane area, flow rates, and operating pressures. In general, in order to maximize resource recovery, a low power density, thus a low membrane productivity, must be accepted.

Fetal distal lung epithelial (FDLE) cells exposed to a postnatal O(2) concentration of 21% have higher epithelial Na(+) channel (ENaC) mRNA levels and Na(+) transport relative to FDLE cells grown in a fetal O(2) concentration of 3%. To investigate the mechanism of this process, FDLE monolayers were initially cultured in 3% O(2), and then some were switched to a 21% O(2) environment. Incubation of FDLE cells with the iron chelator deferoxamine, CoCl(2), NiCl(2), or an inhibitor of heme synthesis prevented or diminished the O(2) induction of amiloride-sensitive short-circuit current in FDLE cells. Similarly, defer- oxamine and cobalt prevented O(2)-induced ENaC mRNA expression. Exposure of FDLE cells grown under hypoxic conditions to carbon monoxide increased both ENaC mRNA expression and amiloride-sensitive short-circuit current. We therefore concluded that induction of ENaC mRNA expression and amiloride-sensitive Na(+) transport in FDLE cells by a physiological increase in O(2) concentration seen at birth requires iron and heme proteins.

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