In the northern Gulf of Alaska and Prince William Sound, we have used wide‐angle seismic reflection/refraction profiles, earthquake studies, and laboratory measurements of physical properties to determine the geometry of the Prince William and Yakutat terranes, the Aleutian megathrust, and the subducting Pacific plate. In this complex region, the Yakutat terrane is underthrust beneath the Prince William terrane, and both terranes are interpreted to be underlain by the Pacific plate. Wide‐angle seismic reflection/refraction profiles recorded along five seismic lines are used to unravel this terrane geometry. Modeled velocities in the upper crust of the Prince William terrane (to 18 km depth) agree closely with laboratory velocity measurements of Orca Group phyllites and quartzofeldspathic graywackes (the chief components of the Prince William terrane) to hydrostatic pressures as high as 600 MPa (6 kbar). A landward dipping reflector at depths of 16–24 km is interpreted as the base of the Prince William terrane. This reflector corresponds to the top of the Wadati‐Benioff zone seismicity and is interpreted as the megathrust. Immediately beneath the megathrust is a 4‐km‐thick 6.9‐km/s refractor, which we infer to be the source of a prominent magnetic anomaly and which is interpreted by us and previous workers to be gabbro in Eocene age oceanic crust of the underthrust Yakutat terrane. Wide‐angle seismic data, magnetic anomaly data, and tectonic reconstructions indicate that the Yakutat terrane has been underthrust beneath the Prince William terrane for at least a few hundred kilometers. Wide‐angle seismic data are consistent with a 9° to 10° landward dip of the subducting Pacific plate beneath the outer shelf and slope, distinctly different from the inferred average 3° to 4° dip of the overlying 6.9‐km/s refractor and the Wadati‐Benioff seismic zone beneath the inner shelf. Our preferred interpretation of the geophysical data is that one composite plate, composed of the Pacific plate of a fairly uniform thickness and the Yakutat plate of varying thickness, is subducting beneath southern Alaska.

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We studied the role of P-selectin, an adhesion molecule known to be important for neutrophil localization to sites of inflammation, in a model of inflammatory liver injury. Male C3Heb/ FeJ (ET-sensitive) mice treated with 700 mg/kg galactosamine and 100 g/kg Salmonella abortus equi endotoxin (Gal/ET), murine tumor necrosis factor ␣ (TNF-␣, 15 g/kg), or interleukin-1 (IL-1, 13-23 g/kg), showed increased P-selectin mRNA levels in the liver. In contrast, C3H/HeJ (ET-resistant) mice responded only to cytokines with P-selectin mRNA formation. Whereas no P-selectin expression was detectable in control livers, there was temporary staining of endothelium in large blood vessels but not in sinusoids between 3 and 5 h after ET, TNF-␣, or IL-1 treatment. Severe liver injury induced by Gal/ET at 7 h was not inhibited by an anti-P-selectin antibody in C3Heb/FeJ mice or in P-selectin-deficient animals. Sequestration of neutrophils in sinusoids, i.e. those neutrophils that have been identified as critical for the injury, was not affected by the antibody or in P-selectindeficient mice. However, the temporary margination in portal and post-sinusoidal venules was reduced by 75% in anti-P-selectin antibody-treated animals and by 51% in P-selectin-deficient mice. We conclude that hepatic P-selectin gene transcription in vivo involves cytokines. However, blocking P-selectin neither attenuated sinusoidal neutrophil sequestration nor prevented neutrophil-induced liver injury during endotoxin shock but attenuated neutrophil margination in larger vessels. Thus, our data demonstrate similarities and fundamental differences in the requirement for adhesion molecules to localize neutrophils in the liver vasculature compared to other organs during an inflammatory response.

A simple point score of historical features distinguishes syncope from seizures with very high sensitivity and specificity.