A Perceptual Bias for Accelerated Intensity Change: An Evolved Mechanism?

2002 ◽  
Author(s):  
John G. Neuhoff ◽  
Kimberly Fukai ◽  
John Preston ◽  
Kate Willaman
2020 ◽  
Vol 39 (3) ◽  
pp. 231-241
Author(s):  
Jin-Won Kang ◽  
Jae-Won Yang

Atmosphere ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 284
Author(s):  
Evan A. Kalina ◽  
Mrinal K. Biswas ◽  
Jun A. Zhang ◽  
Kathryn M. Newman

The intensity and structure of simulated tropical cyclones (TCs) are known to be sensitive to the planetary boundary layer (PBL) parameterization in numerical weather prediction models. In this paper, we use an idealized version of the Hurricane Weather Research and Forecast system (HWRF) with constant sea-surface temperature (SST) to examine how the configuration of the PBL scheme used in the operational HWRF affects TC intensity change (including rapid intensification) and structure. The configuration changes explored in this study include disabling non-local vertical mixing, changing the coefficients in the stability functions for momentum and heat, and directly modifying the Prandtl number (Pr), which controls the ratio of momentum to heat and moisture exchange in the PBL. Relative to the control simulation, disabling non-local mixing produced a ~15% larger storm that intensified more gradually, while changing the coefficient values used in the stability functions had little effect. Varying Pr within the PBL had the greatest impact, with the largest Pr (~1.6 versus ~0.8) associated with more rapid intensification (~38 versus 29 m s−1 per day) but a 5–10 m s−1 weaker intensity after the initial period of strengthening. This seemingly paradoxical result is likely due to a decrease in the radius of maximum wind (~15 versus 20 km), but smaller enthalpy fluxes, in simulated storms with larger Pr. These results underscore the importance of measuring the vertical eddy diffusivities of momentum, heat, and moisture under high-wind, open-ocean conditions to reduce uncertainty in Pr in the TC PBL.


2021 ◽  
pp. 030098582110021
Author(s):  
Yuta Takaichi ◽  
James K. Chambers ◽  
Moeko Shiroma-Kohyama ◽  
Makoto Haritani ◽  
Yumi Une ◽  
...  

Canavan disease is an autosomal recessive leukodystrophy caused by mutations in the gene encoding aspartoacylase (ASPA), which hydrolyses N-acetylaspartate (NAA) to acetate and aspartate. A similar feline neurodegenerative disease associated with a mutation in the ASPA gene is reported herein. Comprehensive clinical, genetic, and pathological analyses were performed on 4 affected cats. Gait disturbance and head tremors initially appeared at 1 to 19 months of age. These cats eventually exhibited dysstasia and seizures and died at 7 to 53 months of age. Magnetic resonance imaging of the brain revealed diffuse symmetrical intensity change of the cerebral cortex, brainstem, and cerebellum. Gas chromatography–mass spectrometry analysis of urine showed significant excretion of NAA. Genetic analysis of the 4 affected cats identified a missense mutation (c.859G>C) in exon 6 of the ASPA gene, which was not detected in 4 neurologically intact cats examined as controls. Postmortem analysis revealed vacuolar changes predominantly distributed in the gray matter of the cerebrum and brain stem as well as in the cerebellar Purkinje cell layer. Immunohistochemically, these vacuoles were surrounded by neurofilaments and sometimes contained MBP- and Olig2-positive cells. Ultrastructurally, a large number of intracytoplasmic vacuoles containing mitochondria and electron-dense granules were detected in the cerebral cortex. All 4 cats were diagnosed as spongy encephalopathy with a mutation in the ASPA gene, a syndrome analogous to human Canavan disease. The histopathological findings suggest that feline ASPA deficiency induces intracytoplasmic edema in neurons and oligodendrocytes, resulting in spongy degeneration of the central nervous system.


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