Improving the U.S. health care system requires simultaneous pursuit of three aims: improving the experience of care, improving the health of populations, and reducing per capita costs of health care. Preconditions for this include the enrollment of an identified population, a commitment to universality for its members, and the existence of an organization (an "integrator") that accepts responsibility for all three aims for that population. The integrator's role includes at least five components: partnership with individuals and families, redesign of primary care, population health management, financial management, and macro system integration.

The concept of the Triple Aim is now widely used, because of IHI's work with many organizations and also because of the adoption of the Triple Aim as part of the national strategy for US health care, developed during the implementation of the Patient Protection and Affordable Care Act of 2010. Even those organizations working on the Triple Aim before IHI coined the term found our concept to be useful because it helped them think about all 3 dimensions at once and organize their work around them.

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Proton fluxes were measured non-invasively on patch-clamped protoplasts isolated from wheat roots using an external H + electrode to measure the electrochemical gradient in the external solution. Under voltage clamp in the whole-cell configuration, the H + fluxes across the plasma membrane could be measured as a function of voltage and time and correlated with the simultaneous measurements of membrane current. Protoplasts could exist in three states based on the current–voltage (I–V) curves and the flux–V curves. In the pump-state where the membrane voltage (Vm) was more negative than the electrochemical equilibrium potential for potassium (E K ), a net efflux of H + occurred that was voltage-dependent such that the efflux increased as Vm was clamped more positive. In the K-state, where Vm was close to E K , similar flux–V curves were observed. In the depolarised state where Vm was greater than E K the proton flux was characterised by a net influx of H + (H + -influx state) that reversed direction at more positive values of Vm. The inhibitory effect of DCCD and stimulatory effect of fusicoccin were used to correlate current and H + flux through the H + -ATPase for which there was reasonably good agreement within the limits of the flux measurements. Some protoplasts were kept in the whole-cell configuration for up to 3 h revealing slow sustained oscillations (period about 40 min) in H + flux that were in phase with oscillations in free-running Vm. These oscillations were also observed under voltage clamp, with membrane current in phase with H + flux, but which became damped out after a few cycles. The oscillations encompassed the pump-state, K + -state and H + -influx-state. The H +- flux–V curves and I–V curves were used to model the electrical characteristics of the plasma membrane with H + -ATPase, inward and outward K + rectifiers, a linear conductance, and a passive H + influx possibly through gated proton channels.

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Detached internodes of Chara corallina survived in solutions containing 100 mol m~^ NaCI when the external concentration of Ca^^ was greater than 1 mol m~^. Na^ influx was roughly proportional to external Na^ up to 100 mol m"^ NaCI. Na+ influx involved two components: a Ca^^-insensitive influx which allowed the passage of Na^ independently of external Ca^^; and a Ca^^-rnhibitable mechanism where Na+ influx was inversely proportional to external Ca^+. The Ca^^-inhibJtable Na^ influx was similar to the Ca^^-inhibitable K* influx. Mg^+ and Ba^^ were able to substitute for Ca^^ in partially inhibiting Na^ influx in the absence of external Ca^^. The effect of Ca^* appears specific to Na+ and K+ influx since the effects of a Ca^^-free solution on the influx of some other cations, anions and neutral compounds is small. It is suggested that Na^ influx via the Ca^^-inhibitable mechanism represents Na^ leakage through K^ channels and that cell death at high salinity occurs due to a cytotoxic Na+ influx via this mechanism.

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