Abstract: A biological fluid sampling transfer device adapted to receive a multi-component blood sample is disclosed. After collecting the blood sample, the biological fluid sampling transfer device is able to separate a plasma portion from a cellular portion. After separation, the biological fluid sampling transfer device is able to transfer the plasma portion of the blood sample to a point-of-care testing device. The biological fluid sampling transfer device also provides a closed sampling and transfer system that reduces the exposure of a blood sample and provides fast mixing of a blood sample with a sample stabilizer. The biological fluid sampling transfer device is engageable with a blood testing device for closed transfer of a portion of the plasma portion from the biological fluid sampling transfer device to the blood testing device. The blood testing device is adapted to receive the plasma portion to analyze the blood sample and obtain test results.

Abstract: The invention is directed to a piston skirt oil seal system comprising a piston with a skirt operating in a cylinder chamber between an oil sump and a combustion chamber in an internal combustion engine. A first retainer attaches to the piston skirt, and a second retainer attaches to a cylinder wall defining the cylinder chamber above the oil sump. A boot made of a flexible, impervious membrane extends between the first and second retainers. The boot serves as a barrier preventing the migration of oil from the oil sump into the combustion chamber reducing the amount of unburned hydrocarbons introduced to the catalyst. To overcome gas leakage and friction, at least one self-lubricating or gas lubricated ring attaches to the piston above the boot. In an alternative embodiment, the boot forms an oil migration barrier through the use of a series of concentric rings linked together in a telescoping arrangement.

Abstract: Cystic fibrosis (CF), a lethal genetic disease associated with a defect in Cl transport, is caused by mutations in the gene coding for cystic fibrosis transmembrane conductance regulator (CFTR). Surprisingly, not only wild type CFTR, but several naturally-occurring CFTR mutants carrying a defect in the first nucleotide binding fold (NFB1) all expressed cAMP-activatable Cl currents. Treatment of the CFTR mutants with appropriate concentrations of methylxanthine phosphodiesterase inhibitor (which increases cAMP levels) activated Cl conductance to near wild type levels. The present invention thus provides a new avenue for treating cystic fibrosis by the administration of therapeutically effective amounts of compounds which elevate cAMP levels. Dosage and patient responsiveness to treatment, as well as relative efficacies of the compounds being or to be administered can also be determined in accordance with the methods of present invention.