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Siebens H, Tucker J, Leander K. Use of Geriatrics At Your Fingertips , a pocket guide, to educate physiatrists in geriatric care. Arch Phys Med Rehabil 2004;85:1552–4. Objective To determine whether a geriatric pocket guide, Geriatrics At Your Fingertips , may be a useful tool in educating physiatrists about the care of their older patients. Design Geriatrics At Your Fingertips was distributed through the American Academy of Physical Medicine and Rehabilitation (AAPM&R) to physical medicine and rehabilitation (PM&R) residents and practicing physiatrists. Two questionnaires evaluated guide use. Setting Two academic PM&R departments and physiatrists in the United States. Participants Two PM&R residency programs, members of AAPM&R’s Geriatric Rehabilitation Special Interest Group (GR-SIG), and AAPM&R’s membership. Interventions Not applicable. Main Outcome Measures Identification of clinically useful information by residents and GR-SIG members and frequency of guide use among AAPM&R membership. Results Forty-five PM&R residents and 17 GR-SIG members reported examples of useful information. Geriatrics At Your Fingertips was requested by 483 AAPM&R members. Forty-six percent returned questionnaires (N=223). Seventy percent had used the guide at least once and 49% 4 or more times. Conclusions Geriatrics At Your Fingertips is a useful tool with which to educate PM&R residents and physiatrists about geriatric care.

We have investigated the structure, function, and expression of the rat eye sodium/calcium+potassium exchanger NCKX1. The sequence of independent rat NCKX1 clones and the analysis of rat eye mRNA by RT-PCR revealed a region of alternative splicing that comprised four exons and encoded a stretch of 113 amino acids near the beginning of the large cytosolic loop. In comparison with other NCKX1 molecules and the rat NCKX2 protein, rat NCKX1 was highly conserved within the hydrophobic regions but was quite divergent in the two large hydrophilic loops. The only exception was the region of the cytosolic loop encoded by the second alternatively spliced exon, which was ∼60% identical. Similar to bovine, but different from human, rat NCKX1 possessed an acidic motif that was repeated 14 times in the cytoplasmic loop. Analysis of NCKX1 expression in different rat tissues by Northern blot revealed a very high level of expression of a 7-kb transcript in the eye but also lower levels of transcripts of various lengths in other tissues. The recombinant rat NCKX1 protein was tagged in the extracellular loop with the FLAG epitope and expressed in HEK-293 cells. Surface delivery and potassium-dependent sodium/calcium exchange activity were observed for each spliced variant.

The effect of Ag+ on Ca2+ fluxes mediated by the retinal rod Na+/Ca2+/K+ exchanger was investigated in intact bovine rod outer segments (ROS). Intracellular Na+ concentration ([Na+]in)-dependent Ca2+ influx and extracellular Na+ concentration ([Na+]out)-dependent Ca2+ efflux were monitored by changes in cytosolic free Ca2+ measured with the fluorescent Ca(2+)-indicating dye fluo 3. Ag+ was the most effective inhibitor of Na+/Ca2+/K+ exchange fluxes described to date, with half-maximal inhibition observed at 2-8 microM Ag+. Inhibition by Ag+ could be reversed by addition of beta-mercaptoethanol but not by addition of cysteine. Reversal by beta-mercaptoethanol resulted in a marked acceleration of [Na+]out-dependent lowering of cytosolic free Ca2+ but not of [Na+]in-dependent Ca2+ influx. We suggest that Ag+ inhibits and accelerates Na+/Ca2+/K+ exchange fluxes by binding to cysteine residues on the cytosolic surface of the exchanger protein.

Ca(2+)-depleted rod outer segments (ROS) were purified from bovine retinal rod photoreceptors, and factors influencing Ca2+ influx into ROS via the plasma membrane Na+/Ca2+/K+ exchanger were analyzed. Intracellular alkali cation concentrations were manipulated by 1) previous loading via the ionophore monensin followed by removal of monensin and 2) addition of the channel ionophore gramicidin during Ca(2+)-influx measurements. Ca2+ influx was measured as a rise in cytosolic free Ca2+ with the Ca(2+)-indicating dye fluo 3. An absolute requirement for intracellular Na+ was observed with a Na+ dissociation constant of 30-40 mM, whereas intracellular K+ was a potent inhibitor of Ca2+ influx, apparently by competing with Na+ for a common site on the Na+/Ca2+/K+ exchanger. Half-maximal Ca2+ influx was observed at an external free Ca2+ concentration of 0.9 microM when no external Na+ was present and 3.5 microM when 10 mM external Na+ was present. Our observations are discussed in the context of 1) a three-site model for the Na+/Ca2+/K+ exchanger and 2) earlier experiments on light adaptation in rods, which depended on minimizing Ca2+ fluxes across the ROS plasma membrane.

The kinetics of symplastic transport in staminal hairs of Setcreasea purpurea was studied. The tip cell of a staminal hair was microinjected with carboxyfluorescein (CF) and the symplastic transport of this CF was videotaped and the digital data analyzed to produce kinetic curves. Using a finite difference equation for diffusion between cells and for loss of dye into the vacuole, kinetic curves were calculated and fitted to the observed data. These curves were matched with data from actual microinjection experiments by adjusting K (the coefficient of intercellular junction diffusion) and L (the coefficient of intracellular loss) until a minimum in the least squares difference between the curves was obtained. (a) Symplastic transport of CF was governed by diffusion through intercellular pores (plasmodesmata) and intracellular loss. Diffusion within the cell cytoplasm was never limiting. (b) Each cell and its plasmodesmata must be considered as its own diffusion system. Therefore, a diffusion coefficient cannot be calculated for an entire chain of cells. (c) The movement through plasmodesmata in either direction was the same since the data are fit by a diffusion equation. (d) Diffusion through the intercellular pores was estimated to be slower than diffusion through similar pores filled with water.

Allegations that stock dividends serve as a vehicle for deceptive financing, evasion of taxes, misleading financial reporting, and stock market manipulation resulted in legislation that prohibited their use in the United States in the latter part of the 19th century. In the 20th century, efforts of the Supreme Court to determine the economic substance and taxability of stock dividends catalyzed a pioneering effort by the Court to define income within the 16th Amendment. As early as 1930 market reactions to stock dividends were investigated; this may have been one of the earliest forms of capital market research. This paper examines the effects of stock dividends on the development of accounting.

Canada's biotech sector ranks within the top five globally, but its life sciences venture capital (VC) industry is among the worlds weakest. This makes for an interesting case study in understanding the disconnect between low levels of VC and a healthy innovation ecosystem in terms of R&D spending, skilled workforce and enterprise support. Three key provinces (Quebec, Ontario and British Columbia) that have taken significantly different approaches to attracting VC are large enough to attract as much government investment as whole emerging markets. The aim of this article is to present evidence from a Canadian natural economic experiment in order to evaluate the effectiveness of varying government policies in attracting VC investment, to illustrate how these policies need tailoring to individual sub-sectors of the life sciences sector, and to highlight potential policy mechanisms that may be applicable beyond Canada's borders. We employ VC returns on investment (ROI) and exit data as a proxy for our evaluation. Our results suggest that government biotechnology investment needs to be structured end-to-end from early to late stage in order to be successful, that prevalence of private and international VC flows is critical for generating market efficiency, and that there is an ‘optimal’ efficient amount of capital before ROI result in diminishing returns.