Biomedical subjects

P Woodford

Publications and source records attributed to P Woodford.

3 recordsLinked to original sources

PubMed1997

Remote electronic blood release system.

BACKGROUND: The Hunter Area Pathology Service provides transfusion services to 4 metropolitan and 11 rural hospitals in Australia. To improve blood availability, conserve blood stocks, and reduce crossmatch-to-transfusion ratios, a networked electronic blood release system (EBRS) has been developed for computer cross-matching within the laboratory and at sites remote from the transfusion laboratory. It is innovative, in that non-laboratory staffs have been trained to release computer-matched blood at remote hospitals without transfusion laboratories. STUDY DESIGN AND METHODS: The EBRS software was tested and validated according to the Australian software standards AS 3563.1 and 3563.2 (1991). Over 7000 units were released by the EBRS in a laboratory trial conducted in conjunction with the conventional immediate-spin crossmatch. A further, 12-month study was conducted within the laboratory before the staged implementation of the EBRS at the remote hospitals. RESULTS: The EBRS has resulted in 1) a 25-percent reduction in the number of units requested by the medical staff, resulting from the reduction in time needed to provide compatible blood due to the elimination of the serologic crossmatch; 2) better blood stock management (reducing outdated red cell units by 30%); and 3) significant savings in laboratory workload (savings of approximately 100 hours/month). In addition, the rapid availability of computer-crossmatched red cells in emergency situations has enhanced patient safety. CONCLUSION: The EBRS is a safe and efficient means of providing red cells within the laboratory and at remote hospitals without laboratory services.

Blood Banks↗

PubMed1995

Ligand-stimulated beta 2-adrenergic receptor internalization via the constitutive endocytic pathway into rab5-containing endosomes.

The small GTPase rab5 appears to be rate-limiting for the constitutive internalization of transferrin receptor and for fluid-phase endocytosis. However, it is unknown whether rab5 regulates receptors whose internalization is stimulated by the binding of ligand, and whether such receptors change the underlying rate of the endocytic pathways they utilize. As a model for ligand-stimulated endocytosis, we used transfected HEK293 cells expressing high levels of an epitope-tagged human beta 2-adrenergic receptor. Nearly all receptors were on the cell surface in the absence of agonist, but within ten minutes of agonist addition > 50% of receptors internalized and colocalized extensively with rab5. Hypertonic sucrose blocked beta 2-adrenergic receptor internalization, as well as that of transferrin receptor, suggesting a clathrin-mediated process. In contrast, an inhibitor of potocytosis had little effect upon beta 2-adrenergic receptor internalization, suggesting that this process did not require active caveolae. Consistent with this finding, caveolin was not detectable in the 12 beta 6 line, as assessed by western blotting with a polyclonal anti-caveolin antibody. Stimulated receptor internalization did not affect the rate or capacity of the constitutive endocytic pathway since there was no detectable increase in fluid-phase endocytosis after addition of beta-agonist, nor was there a significant change in the amount of surface transferrin receptor. Altogether, these data suggest that beta 2-adrenergic receptors internalize by a clathrin-mediated and rab5-regulated constitutive endocytic pathway. Further, agonist-stimulated receptor internalization has no detectable effect upon the function of this pathway.

Adrenergic beta-2 Receptor Agonists↗

PubMed1971

The foreign body.

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Anesthesia↗