Aim: To describe differences in the deep lateral orbital wall (specifically, trigone) between Chinese, Malay, Indian and Caucasian subjects
Methods: Single-centre retrospective Computed Tomogram (CT)-based study; 20 subjects of each ethnicity were used from existing databases, matched for gender, average age and laterality. Subjects below 16 years of age were excluded. DICOM image viewing software CARESTREAM Vue PACS (Carestream Health Inc., USA) and OsiriX version 7.5 (Pixmeo., Switzerland) were used to measure deep lateral wall length, thickness and volume, as well as orbital depth and statistical analyses performed using Statistical Package for Social Sciences version 21 (IBM, USA).
Results: In each group, there were 12 males (60%) and average age was not significantly different (p = 0.682–0.987). Using Chinese subjects as a reference, in Chinese, Malay, Indian and Caucasian subjects, mean trigone thickness was 13.68, 14.02, 11.60 (p < 0.001) and 13.80 mm, curved total wall length 45.23, 42.29 (p = 0.048), 41.91 (p = 0.020) and 45.00 mm, curved trigone length 23.03, 22.61, 17.19 (p = 0.011) and 18.76 mm (p = 0.030) and trigone volume 3120.97, 3221.01, 1613.66 (p < 0.001), 2498.46 mm3 (p = 0.059) respectively. Similarly, perpendicular orbital depth was 27.54, 24.97, 22.12 (p = 0.001) and 25.93 mm and diagonal orbital depth was 34.19, 33.27, 29.48 (p = 0.01) and 34.63 mm respectively.
Conclusions: Indian and, to a lesser extent, Caucasian subjects have smaller trigones compared to their Chinese and Malay counterparts. Indian subjects also have shallower orbits and due care should be taken during decompression surgery. 相似文献
Membrane trafficking processes are presumably vital for axonal regeneration after injury, but mechanistic understanding in this regard has been sparse. A recent loss-of-function screen had been carried out for factors important for axonal regeneration by cultured cortical neurons and the results suggested that the activity of a number of Rab GTPases might act to restrict axonal regeneration. A loss of Rab27b, in particular, is shown to enhance axonal regeneration in vitro, as well as in C. elegans and mouse central nervous system injury models in vivo. Possible mechanisms underlying this new finding, which has important academic and translational implication, are discussed. 相似文献
We investigated whether protein kinase C (PKC) is involved in trimethyltin (TMT)-induced neurotoxicity. TMT treatment (2.8 mg/kg, i.p.) significantly increased PKCδ expression out of PKC isozymes (i.e., α, βI, βII, δ, and ?) in the hippocampus of wild-type (WT) mice. Consistently, treatment with TMT resulted in significant increases in cleaved PKCδ expression. Genetic or pharmacological inhibition (PKCδ knockout or rottlerin) was less susceptible to TMT-induced seizures than WT mice. TMT treatment increased glutathione oxidation, lipid peroxidation, protein oxidation, and levels of reactive oxygen species. These effects were more pronounced in the WT mice than in PKCδ knockout mice. In addition, the ability of TMT to induce nuclear translocation of Nrf2, Nrf2 DNA-binding activity, and upregulation of γ-glutamylcysteine ligase was significantly increased in the PKCδ knockout mice and rottlerin (10 or 20 mg/kg, p.o. × 6)-treated WT mice. Furthermore, neuronal degeneration (as shown by nuclear chromatin clumping and TUNEL staining) in WT mice was most pronounced 2 days after TMT. At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. Rottlerin or PKCδ knockout significantly protected these changes in anti- and pro-apoptotic factors. Importantly, treatment of the PI3K inhibitor LY294002 (0.8 or 1.6 µg, i.c.v.) 4 h before TMT counteracted protective effects (i.e., Nrf-2-dependent glutathione induction and pro-survival phenomenon) of rottlerin. Therefore, our results suggest that down-regulation of PKCδ and up-regulations of Nrf2-dependent glutathione defense mechanism and PI3K/Akt signaling are critical for attenuating TMT neurotoxicity. 相似文献