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Background: The aim of this study was to establish standards for determining sex from fragmentary and complete femurs in a Korean population. Materials and methods: The statistical analysis of 12 variables (6 about breadth and 6 about length) based on 100 Korean femurs (from 50 males and 50 females) showed that all variables have significant sex differences. Results: The most accurate discriminant variable was the condylar breadth parallel with epicondylar breadth (87.6% accuracy). In contrast, the transverse shaft diameter was not a discriminant variable for sex determination (67.0% accuracy). Breadth-related variables were generally more accurate than length-related variables. Three variables (vertical diameter of the neck [VDN], medial epicondylar length [MCL], and condylar breadth [CB]) were selected from stepwise analysis for discriminating sex (93.5% accuracy). The discriminating equation was as follows: 0.171 × VDN + 0.172 × MCL + 0.128 × CB2 – 21.471. Conclusions: The results of this study are helpful for determining sex, even if a femur is found in a fragmented condition in the field. (Folia Morphol 2014; 73, 3: 353–358)
Tottering mouse is an ataxic mutant that carries a mutation in a gene encoding for the α1A subunit of P/Q-type Ca2+ channel (Cav2.1). This study revisited to examine whether a Purkinje cell loss occurred in the cerebellum of tottering mice. In tottering mice, Calbindin D-28k negative gaps were apparent in the vermis but not in the hemisphere. Calbindin D-28k immunofluorescence with DAPI staining demonstrated the absence of Purkinje cells in the Calbindin D-28k negative gaps. The Purkinje cell loss seemed to be observed prominently in the zebrin II negative compartments of the anterior vermis, but in the zebrin II positive compartments of the posterior vermis. Quite consistent with the histopathological observations, quantitation of the density of Calbindin D-28k and zebrin II immunopositive Purkinje cells in the tottering cerebellum revealed that the Purkinje cells were selectively lost in the zebrin II immunonegative compartments of the lobules I and II but in the zebrin II immunopositive compartments in the lobule IX. Those results predict that the susceptibility to the Cav2.1 gene defect is different among Purkinje cell phenotypes of the tottering cerebellum rather than the expression pattern of mutated Cav2.1 channels. This may result in the reproducible parasagittal pattern of Purkinje cell loss.
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