Effects of isoproterenol treatment of isolated perfused rat hearts on myofibrillar phosphorylation and ATPase activity

Perfusion of isolated rat hearts with isoproterenol resulted in increases in the level of protein-bound phosphate of the myofibrils. After perfusion of the hearts with 32P, followed by SDS-polyacrylamide gel electrophoresis of the purified myofibrils, four major 32P-containing protein bands were identified. Most of the increased 32P incorporation produced by isoproterenol was localized on the troponin I and myosin light chain bands, and, to lesser extent, on the M-protein band. ATPase activity was tested in the purified myofibrils. No changes in Ca2+ requirement for activation were found after isoproterenol perfusion. However, maximal ATPase activity was markedly reduced in the myofibrils obtained from isoproterenol-treated hearts. It would appear that the myofibrillar protein phosphorylation induced by isoproterenol perfusion results in a decrease in actomyosin ATPase activity.     

A model of muscular control of upper airway geometry

Some disorders of the upper airway in humans are marked by decreased cross-sectional area and increased airway wall compliance. Based on our observations from studies performed in the isolated upper airway of dogs, we hypothesized that the size, and perhaps the geometry, of the airway was altered by changes in the relative activation levels of various muscle pairs. This could be accomplished either by altering the intensity of the neuromuscular input, or by activating muscle pairs which have different geometric orientation to the airway. We developed an analytic relationship to allow us to vary the stimulus level driving any one of six muscle pairs, each with a different anatomic orientation, to evaluate the relationship between those parameters and upper airway volume. With data generated from bilateral electrical stimulation of upper airway muscles, we described a shape factor which allowed us to predict the maximum force produced at optimal length. These findings were applied to a length/tension curve common to striated muscle to allow us to examine the muscle behavior at lengths other than optimal. The position of each muscle was described in spherical coordinates relative to an elastic cylinder, which represented the isolated, sealed upper airway. These coordinates defined the direction in which the force generated by each muscle pair would be applied. Three compliance constants determined the change in airway dimensions produced by the muscle force. This system and its variables were used to calculate the change in volume of the sealed upper airway chamber resulting from muscle contraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Release of pseudorabies virus from infected cells is controlled by several viral functions and is modulated by cellular components.

The role of the nonessential glycoproteins gI, gp63, and gIII in the release of pseudorabies virus from different cell lines was investigated. We show that these glycoproteins may have a beneficial or deleterious effect on virus release depending on the type of cell in which the virus is grown. Inactivation of the genes encoding either gI, gp63, or gIII has no detectable effect on virus release from rabbit kidney cells. Inactivation of gI or gp63 strongly promotes virus release from chicken embryo fibroblasts, whereas inactivation of gIII reduces virus release from these cells. A defect in both gI and gIII or in both gp63 and gIII diminishes virus release from rabbit kidney cells but improves release from chicken embryo fibroblasts. We demonstrate that all three nonessential glycoproteins contribute to one specific aspect of viral growth, namely, virus release, and that they affect virus release in conjunction with each other. Furthermore, our results show that the manifestation of the role of each of these viral functions in virus growth may differ in different cell types, i.e., that release is affected by these viral functions in conjunction with some unknown cellular function.