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Biomedical subjects

S A Wong

Publications and source records attributed to S A Wong.

4 recordsLinked to original sources

A mechanical function of myosin II in cell motility.

Myosin II mutant Dictyostelium amoebae crawl more slowly than wild-type cells. Thus, myosin II must contribute to amoeboid locomotion. We propose that contractile forces generated by myosin II help the cell's rear edge to detach from the substratum and retract, allowing the cell to continue forward. To test this hypothesis, we measured the speed of wild-type and myosin II null mutant Dictyostelium cells on surfaces of varying adhesivity. As substratum adhesivity increased, the speed of myosin II null mutant cells decreased substantially compared to wild-type cells, suggesting that the mutant is less able to retract from sticky surfaces. Furthermore, interference reflection microscopy revealed a myosin-II-dependent contraction in wild-type but not null mutant cells that is consistent with a balance of adhesive and contractile forces in retraction. Although myosin II null mutant cells have a defect in retraction, pseudopod extension does not cause the cells to become elongated on sticky surfaces. This suggests a mechanism, based possibly on cytoskeletal tension, for regulating cell shape in locomotion. The tension would result from the transmission of tractional forces through the cytoskeletal network, providing the myosin II null mutant with a limited means of retraction and cell division on a surface.

Animals↗

Characterization of mechanisms of quinolone resistance in Pseudomonas aeruginosa strains isolated in vitro and in vivo during experimental endocarditis.

Mechanisms of resistance to quinolones were characterized in Pseudomonas aeruginosa strains isolated after Tn5 insertional mutagenesis and in resistant strains that emerged during pefloxacin therapy of experimental aortic endocarditis. Quinolone resistance achieved in in vitro-selected mutants Qr-1 and Qr-2 was associated with cross-resistance to several groups of antimicrobial agents, including beta-lactams, tetracycline, and chloramphenicol. A significant reduction of norfloxacin uptake was also observed. After ether permeabilization of the cells, DNA synthesis of these two isolates was as susceptible to norfloxacin as DNA synthesis of the parent strain (PAO1). These results indicate that alteration of outer membrane permeability is the primary determinant of resistance in these isolates. This altered cell permeability was correlated with reduction of outer membrane protein G (25.5 kilodaltons) and loss of a 40-kilodalton outer membrane protein in strain Qr-1. Resistance to quinolones that emerged during experimental endocarditis therapy was associated with both modification of outer membrane permeability (decreased uptake of norfloxacin) and decreased susceptibility of DNA synthesis to norfloxacin. Resistance was limited to quinolones and chloramphenicol. For these strains, norfloxacin inhibitory doses (50%) for DNA synthesis were identical to the drug MICs, suggesting that despite the identification of a permeability change, perhaps due to changes of lipopolysaccharide, the alteration of the quinolone intracellular target(s) susceptibility constitutes the primary determinant of resistance. Also, two distinct levels of norfloxacin resistance of DNA synthesis were found in these isolates, indicating that at least two distinct alterations of the drug target(s) are possible in P. aeruginosa.

Anti-Infective Agents↗

Long-term care coverage: the need is now.

As the world population steadily ages, the future of America's long-term healthcare system is facing a major crisis. By the year 2050, approximately 22 percent of the United States population is expected to be over the age of 65 and more than 19 million Americans will require long-term care. Long-term care financing will be increasingly important, since nursing home care can lead to financial catastrophe. The key to preventing this catastrophe for the elderly is appropriate third-party coverage. Although more insurance companies are offering long-term care policies today, three major obstacles to the success of such insurance remain: lack of knowledge about the extent of public funding for long-term care, denial of the need for such insurance, and lack of public awareness of potential liabilities inherent in financing long-term care. Congress is supporting the development of long-term care insurance, and states are placing long-term care legislation at the top of their agendas. Tax incentives have been proposed in the form of tax-free individual retirement accounts to finance long-term care, individual medical accounts, tax credits for policyholders, and favorable tax treatment for employers who offer long-term care benefits. But only coordination of public and private financiers will ensure adequate protection for all consumers of long-term care services.

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