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The subject of this paper is the buckling behavior of thin bar stiffeners attached to plates which are subjected to normal pressure loadings. The stiffeners are mathematically modeled by a nonlinear beam theory recently derived. An analytical solution is obtained to the beam buckling equations. The curvature of the centerline along the beam's base at the buckling load is expressed in terms of the beam's thickness, height, and rotational stiffness. Analytical results are compared with an experiment recently performed.
Experimental studies on the tripping behavior of narrow T-stiffened flat plates subjected to hydrostatic pressure and underwater shock
An experimental investigation was conducted to determine the static and dynamic responses of a specific stiffened flat plate design. The air-backed rectangular flat plates of 6061-T6 aluminum with an externally machined longitudinal narrow-flanged T-stiffener and clamped boundary conditions were subjected to static loading by water hydropump pressure and shock loading from an eight pound TNT charge detonated underwater. The dynamic test plate was instrumented to measure transient strains and free field pressure. The static test plate was instrumented to measure transient strains, plate deflection, and pressure. Emphasis was placed upon forcing static and dynamic stiffener tripping, obtaining relevant strain and pressure data, and studying the associated plate-stiffener behavior.
The Vascular Theory of Migraine‐Resuscitated or More Moribund?
Your decision to publish an important paper on cerebral blood flow (CBF) in migraine1 as the first in Headache for 1989 is to be applauded. But does it clarify or cloud the issue? After 20 years of CBF studies in migraine the results show 1) a reduction of at least 25 30% in classical migraine1, 2) an average increase of 31% in common and classical migraine2, 3) or no change in common migraine3. Now we learn that the measurements need modifying by 40% to allow for scattering of radiation the Compton scatter effect which has led to "an unbalanced interpretation of the data"1 So the results are as contradictory as they can be, the measurements require adjustment, and the interpretation is therefore doubly doubtful. From the clinical point of view the neurological aura, the enlarging scotoma, the scintillations, the migration of the paraesthesiae up the arm or visual disturbances across the visual field, have not been seen in cerebrovascular disease.4 The headache is throbbing in only 47% of 750 patients questioned during a migraine5; but even when the pain is pulsatlie, it throbs for only a portion of the time at the maximum of the headache (Blau unpublished observations). The evidence for a neurological aetiology has been examined6: the most potent argument against a vascular cause is that the common triggers stress, light and hunger go direct to the nervous system, not via blood vessels. No one denies that vascular changes occur in migraine but are they primary or secondary to a neurological disturbance? Sokoloff7 concluded that the stimulated rat and monkey cortex showed increased glucose uptake, and that the increased local blood flow occurred "in response (my italics) to changes in local functional activity". The evidence, therefore, points to an underlying neurological basis with secondary vascular responses. The vascular theory may need resuscitation but who is going to give it the kiss of life?