An analysis of the brain weight of 196 rhesus monkeys and lateral X-rays of 91 more was made to determine and correct the effect of growth and development on stereotaxic variability. A comparison of body weight to brain weight shows that the brain grows rapidly initially in a linear relationship with body weight and can increase in weight even into adulthood, with a significant amount of variability found throughout its development. The examination of the cranial base and stereotaxic reference points indicates that the brain rotates during growth in a forward and downward direction in relation to the stereotaxic planes. The distance between the anterior clinoid process and AP-0 shows an increase of little variability from linearity during growth. This distance can be used to correct for the anterior-posterior plane found in standard stereotaxic atlases. The flattening out of the cranial base results in a horizontal plane readjustment during growth. A horizontal correction can be made by measuring the distance between the base of the pituitary fossa and H-10 plane.
The functional contribution of transient receptor potential vanilloid 4 (TRPV4) expression in maintaining human corneal endothelial cells (HCEC) homeostasis is unclear. Accordingly, we determined the effects of TRPV4 gene and protein overexpression on responses modulating the viability and survival of HCEC. Q‑PCR, Western blot, FACS analyses and fluorescence single-cell calcium imaging confirmed TRPV4 gene and protein overexpression in lentivirally transduced 12V4 cells derived from their parent HCEC‑12 line. Although TRPV4 overexpression did not alter the baseline transendothelial electrical resistance (TEER), its cellular capacitance (Ccl) was larger than that in its parent. Scanning electron microscopy revealed that only the 12V4 cells developed densely packed villus-like protrusions. Stimulation of TRPV4 activity with GSK1016790A (GSK101, 10 µmol/L) induced larger Ca2+ transients in the 12V4 cells than those in the parental HCEC‑12. One to ten nmol/L GSK101 decreased 12V4 viability, increased cell death rates and reduced the TEER, whereas 1 µmol/L GSK101 was required to induce similar effects in the HCEC‑12. However, the TRPV4 channel blocker RN1734 (1 to 30 µmol/L) failed to alter HCEC‑12 and 12V4 morphology, cell viability and metabolic activity. Taken together, TRPV4 overexpression altered both the HCEC morphology and markedly lowered the GSK101 dosages required to stimulate its channel activity.
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