Contingency theories of leadership: how might we use them in clinical practice?

This article explores how contingency theories of leadership (pragmatic theories that note 'no one size fits all') can be used by multidisciplinary health-care teams to improve communication and patient care.

SSPE-BIKEN: a naturally arising hemagglutination-defective mutant of measles virus.

Biochemical and genetic methods have been used to investigate a defective variant of measles virus previously isolated from a patient with subacute sclerosing panencephalitis (SSPE). Since its isolation, this syncytiogenic strain (SSPE-BIKEN) has remained cell-associated; infected cells do not hemadsorb and do not release infectious virus. Immune precipitation and polyacrylamide gel electrophoresis were used to study the synthesis of measles virion proteins in SSPE-BIKEN-infected cells. All of the virion proteins were detected in immune precipitated whole cell extracts. However, the hemagglutinin (HA) protein was not detected on the cell surface by lactoperoxidase iodination. These results suggest that the failure of the HA protein to insert into the cell membrane accounts for the block in the release of infections virus. Radioactively labeled, noninfectious, virus-like particles have been purified from the media of SSPE-BIKEN-infected cells. These particles contain virus nucleocapsid, nucleocapsid-associated, and membrane proteins, but very little HA and hemolysin proteins. Genetic complementation between SSPE-BIKEN and a temperature-sensitive mutant of measles virus was observed and suggests that the SSPE isolate defect is due to a mutation. Additional evidence of a mutation is provided by the detection of low frequency revertant progeny in SSPE-BIKEN stocks. Our results support the hypothesis that genetic variants of measles virus are involved in the etiology of SSPE.

Variation in ability of measles virus plaque progeny to induce interferon.

Plaque progeny of three interferon (IF)-inducing strains of measles virus (Edmonston, Schwarz, and CC) were examined for ability to induce IF in BSC-1 cells. Only after passage in Vero cells did any of the Edmonston progeny induce IF. The vast majority of plaque progeny selected from the Schwarz strain induced IF, even though this virus was originally derived from the Edmonston strain. This property was retained even after serial plaque purification of the progeny. However, the Schwarz-derived CC strain consisted of a population generally unable to induce IF. Stocks grown from both Edmonston and CC plaques demonstrating the IF+ phenotype maintained this characteristic as a whole, but it was not a property that was inherited by all progeny in the stocks. Levels of IF induced were approximately the same for all strains, even though the proportion of inducing progeny varied markedly among them. These noninducing variants appeared to be normal, fully infectious measles virions. The results suggest that induction of IF by measles virus is at least partially under the genetic control of the virus.

Heterogeneity among flavivirus proteins separated in slab gels.

35S-methionine-labeled proteins specified in Vero cells by flaviviruses were analysed by SDS-phosphate electrophoresis in polyacrylamide slab gels. The clarity of the profile produced by Kunjin virus permitted designation of the nonstructural proteins, and confirmed the identity of NV21/2; the profile included a protein previously designated V2 (core protein) but now named NV11/2 because it migrates perceptibly faster than V2. Despite a varying background of labeled host proteins, identifiable profiles were obtained for 11 of 12 flaviviruses. The large non-structural proteins NV5 and NV4 migrated at apparently the same rates for all viruses. Profiles of the remaining proteins displayed varying amounts of heterogeneity, notably in the migration of the envelope protein V3 which showed no evidence of subgroup specificity.