ANALYSIS OFVIBRATORY STRESS OF INTEGRAL SHROUD BLADE FOR MECHANICAL DRIVE STEAMTURBINE by Yasutomo Kaneko
The advanced integral shroud blade (ISB) structure has been developed to improve the reliability and thermal efficiency of mechanical drive steam turbines. This advanced ISB has been applied to not only the control stage blades but also the intermediate stage blades. Turbines using these advanced blades have been successfully operated. This paper presents the analysis method to calculate the vibratory stresses of the ISB caused by the stage interaction force and the shock load. The vibration response characteristics are explained and comparisons are made to the advanced ISB structure and the conventional grouped blade structure, using the calculated results. Additional verification test results to confirm the validity of the proposed analysis method are also shown.
Turbine blade vibration due to partial admission
Abstract A method is given for analyzing the vibrations of turbine blades during partial admission. The combined effects of shock loading as the blades enter and leave the arc of admission, and nozzle wake loading in the arc of admission are included. By separating these two effects, the dependence of blade stress on natural frequencies, running speed, number of nozzles, number of blades per row, number of blades per group and damping is illustrated. Apparatus for determining experimentally the exact nature of the steam loading acting on the blades is described.
Size-selective neuronal changes in the anterior optic pathways suggest a differential susceptibility to injury in multiple sclerosis.
Axonal damage is found in both acute and chronic lesions of multiple sclerosis. Direct axon counting in post-mortem tissue has suggested that smaller axons might have a greater susceptibility to damage, but methodological limitations have precluded unequivocal interpretation. However, as neuronal and axonal sizes are linked and neuronal changes would be expected with retrograde or transsynaptic degeneration following axon injury, we hypothesized that an alternative strategy for studying this phenomenon would be to define multiple sclerosis-associated changes in neurones. To test this hypothesis, we measured both axonal loss and neuronal size changes in the anterior optic pathway [including the optic nerve (ON), optic tract (OT) and lateral geniculate nucleus] of the brains of eight patients who died with multiple sclerosis and in eight control brains. The ONs and OTs in brains from the multiple sclerosis patients showed a trend to smaller mean cross-sectional areas (ON, multiple sclerosis = 6.84 mm(2), controls = 9.25 mm(2); and OT, multiple sclerosis = 6.45 mm(2), controls = 7.94 mm(2), P = 0.08) and had reduced axonal densities (ON, multiple sclerosis = 1.1 x 10(5)/mm(2), controls = 1.7 x 10(5)/mm(2); and OT, multiple sclerosis = 1.4 x 10(5)/mm(2), controls = 1.8 x 10(5)/mm(2), P = 0.006). Estimated total axonal counts were reduced by 32 (OT)-45% (ON) in the patients relative to controls (ON, multiple sclerosis = 8.1 x 10(5) axons, controls = 14.8 x10(5), P = 0.05; and OT, multiple sclerosis = 9.1 x 10(5), controls = 13.3 x 10(5), P = 0.02). The size distributions of the magnocellular cells in the lateral geniculate nucleus were similar for the two groups, but in multiple sclerosis brains the parvocellular cells were significantly smaller (mean sizes: multiple sclerosis = 226 microm(2), controls = 230 microm(2), P < 0.001) and had a larger variation in size, suggesting a greater proportion of atrophic neurones. Axon loss in the optic nerves of multiple sclerosis patients correlated strongly with measures of increased dispersion of cell sizes in the parvocellular layer (r = 0.8, P < 0.04). These data demonstrate that both atrophy and decreased density contribute to the substantial axonal loss in the anterior visual pathway of these patients. This appears related to a relatively selective atrophy of the smaller neurones of the parvocellular layer in the lateral geniculate nucleus, supporting the hypothesis that smaller axons may be preferentially susceptible to injury in multiple sclerosis.