METHODS: Sixteen computed tomography scan of SC patients (8 months-6 years old) were imported to Materialise Interactive Medical Image Control System (MIMICS) and Materialise 3-matics software. Three-dimensional (3D) OC models were fabricated, and linear measurements were obtained. Mathematical formulas were used for calculation of OC volume and surface area from the 3D model. The same measurements were obtained from the software and used as ground truth. Data normality was investigated before statistical analyses were performed. Wilcoxon test was used to validate differences of OC volume and surface area between 3D model and software.
RESULTS: The mean values for OC surface area for 3D model and MIMICS software were 103.19 mm2 and 31.27 mm2, respectively, whereas the mean for OC volume for 3D model and MIMICS software were 184.37 mm2 and 147.07 mm2, respectively. Significant difference was found between OC volume (P = 0.0681) and surface area (P = 0.0002) between 3D model and software.
CONCLUSION: Optic canal in SC is not a perfect conical frustum thus making 3D model measurement and mathematical formula for surface area and volume estimation not ideal. Computer software remains the best modality to gauge dimensional parameter and is useful to elucidates the relationship of OC and eye function as well as aiding intervention in SC patients.
EXPERIMENTAL APPROACH: 3H-deoxycytidine-labeled PGs (17 or 41 kDa) and 3H-deoxycytidine were administered intravenously to normal rats and streptozotocin-induced diabetic rats. The biodistribution of these compounds was determined over 24 h. Accumulation of PG in normal kidneys was also tracked using 5-(aminoacetamido) fluorescein (fluoresceinyl glycine amide)-labeled PG (PG-AF). To evaluate the potential of PGs in ferrying renal protective anti-oxidative stress compounds, the model drug 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride (AEBSF) was conjugated to 41 kDa PG to form PG-AEBSF. PG-AEBSF was then characterized and evaluated for intracellular anti-oxidative stress efficacy (relative to free AEBSF).
RESULTS: In the normal rat kidneys, 17 kDa radiolabeled PG (PG-Tr) presents a 7-fold higher, while 41 kDa PG-Tr shows a 15-fold higher renal accumulation than the free radiolabel after 24 h post injection. The accumulation of PG-AF was primarily found in the renal tubular tissues at 2 and 6 h after an intravenous administration. In the diabetic (oxidative stress-induced) kidneys, 41 kDa PG-Tr showed the greatest renal accumulation of 8-fold higher than the free compound 24 h post dose. Meanwhile, the synthesized PG-AEBSF was found to inhibit intracellular nicotinamide adenine dinucleotide phosphate oxidase (a reactive oxygen species generator) at an efficiency that is comparable to that of free AEBSF. This indicates the preservation of the anti-oxidative stress properties of AEBSF in the conjugated state.
CONCLUSION/IMPLICATIONS: The favorable accumulation property of 41 kDa PG in normal and oxidative stress-induced kidneys, along with its capabilities in conserving the pharmacological properties of the conjugated renal protective drugs, supports its role as a potential renal targeting drug carrier.