Full-scale or the truth in “true-scale”

Before architecture is put into reality it is simulated, either by means of drafts, or plans, models, or videos etc. All these simulations represent anticipations of a later reality, instructions for action, sometimes they are no more than forecasts. Whether they hold true is up to the built object to prove. Only the full-scale throws light on spatial impact, the quality of design, the environmental compatibility, the value in use and finally, on the constructional accuracy regarding any decisions followed through with. The focus of working at the Department for Experimental Building Construction of the Graz University of technology is aimed at getting the students acquainted with these possibilities during their studies. Planning as well as building is carried out right on the spot and thus the process starting with the mere idea right down to the architectural reality, as well as the feedback, however in reverse, can be witnessed and perceived

Local osmotic gradients drive the water flux associated with Na(+)/glucose cotransport

It recently was proposed [Loo, D. D. F., Zeuthen, T., Chandy, G. & Wright, E. M. (1996) Proc. Natl. Acad. Sci. USA 93, 13367–13370] that SGLT1, the high affinity intestinal and renal sodium/glucose cotransporter carries water molecules along with the cosubstrates with a strict stoichiometry of two Na(+), one glucose, and ≈220 water molecules per transport cycle. Using electrophysiology together with sensitive volumetric measurements, we investigated the nature of the driving force behind the cotransporter-mediated water flux. The osmotic water permeability of oocytes expressing human SGLT1 (L(p) ± SE) averaged 3.8 ± 0.3 × 10(−4) cm⋅s(−1) (n = 15) and addition of 100 μM phlorizin (a specific SGLT1 inhibitor) reduced the permeability to 2.2 ± 0.2 × 10(−4) cm⋅s(−1) (n = 15), confirming the presence of a significant water permeability closely associated with the cotransporter. Addition of 5 mM α-methyl-glucose (αMG) induced an average inward current of 800 ± 10 nA at −50 mV and a water influx reaching 120 ± 20 pL cm(−2) ⋅s(−1) within 5–8 min. After rapidly inhibiting the Na(+)/glucose cotransport with phlorizin, the water flux remained significantly elevated, clearly indicating the presence of a local osmotic gradient (Δπ) estimated at 16 ± 2 mOsm. In short-term experiments, a rapid depolarization from −100 to 0 mV in the presence of αMG decreased the cotransport current by 94% but failed to produce a comparable reduction in the swelling rate. A mathematical model depicting the intracellular accumulation of transported osmolytes can accurately account for these observations. It is concluded that, in SGLT1-expressing oocytes, αMG-dependent water influx is induced by a local osmotic gradient by using both endogenous and SGLT1-dependent water permeability

Abscisic acid regulation of guard-cell K+ and anion channels in Gβ- and RGS-deficient Arabidopsis lines

In mammals, basal currents through G protein-coupled inwardly rectifying K+ (GIRK) channels are repressed by Gαi/oGDP, and the channels are activated by direct binding of free Gβγ subunits released upon stimulation of Gαi/o-coupled receptors. However, essentially all information on G protein regulation of GIRK electrophysiology has been gained on the basis of coexpression studies in heterologous systems. A major advantage of the model organism, Arabidopsis thaliana, is the ease with which knockout mutants can be obtained. We evaluated plants harboring mutations in the sole Arabidopsis Gα (AtGPA1), Gβ (AGB1), and Regulator of G protein Signaling (AtRGS1) genes for impacts on ion channel regulation. In guard cells, where K+ fluxes are integral to cellular regulation of stomatal apertures, inhibition of inward K+ (Kin) currents and stomatal opening by the phytohormone abscisic acid (ABA) was equally impaired in Atgpa1 and agb1 single mutants and the Atgpa1 agb1 double mutant. AGB1 overexpressing lines maintained a wild-type phenotype. The Atrgs1 mutation did not affect Kin current magnitude or ABA sensitivity, but Kin voltage-activation kinetics were altered. Thus, Arabidopsis cells differ from mammalian cells in that they uniquely use the Gα subunit or regulation of the heterotrimer to mediate Kin channel modulation after ligand perception. In contrast, outwardly rectifying (Kout) currents were unaltered in the mutants, and ABA activation of slow anion currents was conditionally disrupted in conjunction with cytosolic pH clamp. Our studies highlight unique aspects of ion channel regulation by heterotrimeric G proteins and relate these aspects to stomatal aperture control, a key determinant of plant biomass acquisition and drought tolerance