PURPOSE. We analyzed the symmetry and pointedness of the posterior segment of highly myopic eyes. METHODS.We studied 234 eyes of 117 patients with bilateral high myopia (refractive error À8.00 diopters [D]) and 40 eyes of 20 patients with emmetropia (refractive error between À1.0 and þ1.0 D). Volume renderings of high-resolution magnetic resonance (MR) images were performed to obtain 3D images of the eye. To analyze the symmetry and pointedness of the posterior surface, a software was developed to measure the area and angle of a fan-shaped segment formed by selected points on the MR images.RESULTS. All of the emmetropic eyes were symmetrical in the horizontal and sagittal planes with no deformity. In highly myopic eyes, the shape was symmetrical in the horizontal plane in 146 eyes (62.4%) and in the sagittal plane in 162 (69.2%). The shape of the posterior pole was pointed (angle of fan-shaped segment <1508) in 45.7% and blunted (angle ‡1508) in 54.3% of highly myopic eyes. The most common shape was symmetrical in the horizontal and sagittal planes, and the posterior surface was blunt. The shape of the two eyes of the same individual was the same in 61 of 117 patients (52.1%). In 56 patients whose two eyes had different shapes, the most frequent pattern was a difference in the pointedness (51.8%).CONCLUSIONS. Quantitative assessments of the shape of eyes were useful in determining the pattern of eye shape deformity specific to pathologic myopia. (Invest Ophthalmol Vis Sci.

Abstract. Parkinson's disease is characterized by dopaminergic neuronal death and the presence of Lewy bodies in the substantia nigra pars compacta (SNpc). a -Synuclein and ubiquitin are components of Lewy bodies, but the process of Lewy body formation and the relationship between inclusion formation and dopaminergic neuronal death have not been resolved. In this study, unilateral intranigral microinjection of 6-hydroxydopamine caused a significant loss of tyrosine hydroxylase-immunopositive neurons in both the substantia nigra and striatum and apomorphine-induced contralateral rotation. The co-administration of proteasome inhibitors, such as lactacystin or carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132), significantly prevented both dopaminergic neurodegeneration and apomorphine-induced rotational asymmetry. Proteasome inhibitors markedly formed intracellular protein inclusions labeled by thioflavin-S in the SNpc. Inclusion-like immunoreactivities for a -synuclein and ubiquitin were detected after 4 weeks. These results suggest that proteasome plays an important role in both the early phase of dopaminergic neuronal death and inclusion body formation.

Serofendic acid was recently identified as a neuroprotective factor from fetal calf serum. This study was designed to evaluate the neuroprotective effects of an intranigral microinjection of serofendic acid based on behavioral, neurochemical and histochemical studies in hemi-parkinsonian rats using 6-hydroxydopamine (6-OHDA). Rats were injected with 6-OHDA in the presence or absence of serofendic acid, or were treated with serofendic acid on the same lateral side, at 12, 24 or 72 h after 6-OHDA lesion. Intranigral injection of 6-OHDA alone induced a massive loss of tyrosine hydroxylase (TH)-immunopositive neurons in the substantia nigra pars compacta (SNpc). Either simultaneous or 12 h post-administration of serofendic acid significantly prevented both dopaminergic neurodegeneration and drug-induced rotational asymmetry. Immunoreactivities for oxidative stress markers, such as 3-nitrotyrosine (3-NT) and 4-hydroxy-2-nonenal (4-HNE), were markedly detected in the SNpc of rats injected with 6-OHDA alone. These immunoreactivities were markedly suppressed by the co-administration of serofendic acid, similar to the results in vehicle-treated control rats. In addition, serofendic acid inhibited 6-OHDA-induced a-synuclein expression and glial activation in the SNpc. These results suggest that serofendic acid protects against 6-OHDA-induced SNpc dopaminergic neurodegeneration in a rat model of Parkinson's disease. Keywords: 6-hydroxydopamine, neuroprotection, Parkinson's disease, reactive oxygen species, serofendic acid, substantia nigra. In a search for novel neuroprotective substances of mammalian origin, conditioned medium of striatal cultures and ether extract of fetal calf serum (FCS) both inhibited glutamate neurotoxicity (Kume et al. 1997). Recently, a sulfur-containing atisane-type diterpenoid (named serofendic acid) was purified from a lipophilic fraction of FCS based on its ability to protect rat primary cortical cultures against nitric oxide (NO) donor-induced neurotoxicity, and mass spectrometry and nuclear magnetic resonance spectroscopy have revealed the chemical structure of serofendic acid to be 15-hydroxy-17-methylsulfinylatisan-19-oic acid Terauchi et al. 2002;Osakada et al. 2004). Serofendic acid prevents NO-mediated acute glutamate neurotoxicity in cultured cortical neurons (Taguchi et al.