No abstract available.
Brachial Artery

Intraocular lens power was calculated from data of axial length, corneal curvature, and anterior chamber depth in 112 eyes which underwent IOL implant surgery. Postoperative refractions of 112 eyes were analyzed into three groups such as the group of which constant A is 116.2, the group of which constant A is 116.8, and TI-59 system group. The results were as follows; 1. The A constant derived from retrograde analysis in our 112 cases was 116.2. In the cases of the constant A 116.2, error of predicted required spectacle lens power was -0.16D +/- 0.89 in relative average, 0.67D +/- 0.57 in absolute average. Using the standard formula described by Hoffer, the accuracy of IOL power calculation by the constant 116.2 was 76.1% +/- 1.0D / 97.4% +/- 2.0D / +2.42 to -2.11D. 2. The specific constant A of intraocular lenses inserted in our hospital was 116.8. In the cases of the constant A 116.8, error of predicted required spectacle lens power was -0.39D +/- 0.88 in relative average, 0.75D +/- 0.60 in absolute average. Using the standard formula described by Hoffer, the accuracy of IOL power calculated by the constant A 116.8 was 72% +/- 1.0D / 96% +/- 2.0D / +2.34 to -2,50D. 3. In TI-59 system of IOL power calculation, error of predicted required spectacle lens power was -0.12D +/- 1.0D in relative average and 0.75D +/- 0.66 in absolute average. Using the staudard formula described by Hoffer, the accuracy of IOL power calculation in this method was 73% +/- 1.0D / 91.5% +/- 2.0D / +2.77 to -2.31D. 4. There was a significant difference between the error of the A constant 116.2 and that of 116.8(P. 0.05), but wasn't between the error of the A constant 116.2 and that of TI-59 system. 5. In the case of axial length 21mm +/- 0.5, the IOL power calculation by the A constant 116.2 was the most accurate among three groups.
Anterior Chamber ; Lenses, Intraocular*

PURPOSE: To evaluate the changes of clinical features after long-term follow-up observation on patients with partially accommodative esotropia who had undergone conventional surgery. METHODS: Thirty-five patients who maintained orthophoria for at least one year duration after surgery were evaluated. The amount of surgery was measured based on the near angle of deviation after full hyperopic correction. The comparison was made based on the best corrected visual acuity, refractive errors, degree of stereopsis and ocular positions before and after surgery. RESULTS: The mean spherical equivalent was +4.46 D before surgery and +3.66 D at the final examination. Among a total of 70 eyes, the best corrected visual acuity of 0.6 or less was seen in 16 before surgery, and in 12 at the final examination. The average angle of deviation was 50.14 PD before correction and 34.43 PD after correction. The Titmus stereotest after surgery was 80 sec of arc in 6, and even 40 sec of arc in 2 out of the 35 patients. At the final examination, 29 of the 35 patients revealed stable orthophoria, but exophoria, in a range of 15-25 PD, developed in 6 patients. Of these 6, 4 had anisometropic amblyopia, and 1 had bilateral high hyperopia of 8.0 D with refractive amblyopia. CONCLUSIONS: Long-term follow-up observation is essential after surgery for partially accommodative esotropia due to fear of the gradual development of consecutive exotropia, particularly in amblyopia cases, even though acceptable initial postoperative orthophoria has been achieved.
Amblyopia ; Depth Perception ; Esotropia* ; Exotropia ; Follow-Up Studies* ; Humans ; Hyperopia ; Refractive Errors ; Visual Acuity

No abstract available.
Radiosurgery* ; Trigeminal Neuralgia*

No abstract available.
Uterine Cervical Neoplasms*

PURPOSE: Taxol (Paclitaxel) is a new generation of chemotherapeutic drug proven to be effective in the treatment of many cancers. In this study, to further demonstrate the differential effect of the tumor suppressor gene, p53, on the Taxol-induced apoptosis in osteogenic sarcoma cell lines, we used p53-defected SaOS2 cells and wild type p53-expressed U2OS cells. MATERIALS AND METHODS: The cell viability was measured by the XTT assay. To examine whether the differential expressions of p53, in U2OS and SaOS2 cells, were associated with Taxol-induced apoptosis, DNA fragmentation assays were performed on both cytosolic and genomic DNA. Since the cleavage of poly (ADP-ribose) polymerase (PARP) is primarily responsible for apoptosis, the cleavage of PARP, and the expression of cyclin B1, polo-like kinase, Bax, Bcl-xL, Bcl-2 in U2OS and SaOS2 cells were compared by Western blot analyses. RESULTS: The cell viability of the p53-defected SaOS2 cells was markedly decreased with Taxol treatment. Whereas, the cell viabilities due to 6-mercaptopurine and adriamycin were no different between the U2OS and SaOS2 cells. Treatment with Taxol induced a ladder- like pattern of DNA fragments, which is a biochemical hallmark of apoptosis, consisting of multiples of approximately 180-200 base pairs, in a dose-dependent manner in the SaOS2 cells, but insignificantly with the U2OS cells. When the cells were treated with Taxol, the 89 kDa cleavage product of PARP clearly appeared as a function of time in the SaOS2 cells, but not in the U2OS cells. The Taxol-induced apoptosis in p53 defected-osteogenic sarcoma cells was associated with the PARP cleavage as a result of the increased activity of caspase 3, and the high expressions of cyclin B1 and PLK. Bax, as a proapoptotic factor, was increased in the SaOS2cells, but the Bcl-xL and Bcl-2 were decreased when the cells were exposed to 10miceoM Taxol. CONCLUSION: From these results, it was concluded that p53-defected SaOS2 cells are much more sensitive to Taxol-induced apoptosis than p53-expressed U2OS cells.
6-Mercaptopurine ; Apoptosis* ; Base Pairing ; Blotting, Western ; Caspase 3 ; Cell Line ; Cell Survival ; Cyclin B1 ; Cytosol ; DNA ; DNA Fragmentation ; Doxorubicin ; Genes, Tumor Suppressor ; Osteosarcoma* ; Paclitaxel ; Phosphotransferases ; Sarcoma

BACKGROUND: Alzheimer's disease is a neurodegenerative disorder characterized by the extracellular deposition of beta-amyloid peptide(Abeta) in the brain, presumed to play a pathogenic role. However, the precise molecular mechanisms of its neurotoxicity are not fully understood. METHODS: Abeta-mediated cytotoxicity in neuronal cell lines (PC12, SH-SY5Y, IMR32, and U87) was measured by an MTT assay. NF-kappaB activation by Abetawas examined by a luciferase assay and apoptosis induced by Abetawas measured by cytoplasmic DNA fragmentations. RESULTS: Abetacytotoxicity in the tested cell lines was more prominent in the absence of serum than in the presence of serum in culture media. PC12 cells showed the highest sensitivity to Abetacytotoxicity among the cell lines. The Abeta(25-35) cytotoxicity in PC12 cells was increased in a dose-dependent manner. For convincing oxidative stress involved in Abetacytotoxicity, antioxidants such as DTT, GSH, vitamin C, or NAC were pretreated. GSH protected PC12 cells from Abetacytotoxicity, but DTT or NAC did not. Abeta (25-35) treatment to PC12 cells increased the NF-kappaB activity in a dose-dependent manner. Cytoplasmic DNA fragmentations, one of the apoptotic indicators, were increased at lower concentrations of Abeta(25-35) from 0.01 to 0.1 microM, however, dose-dependent increments of DNA fragmentations were not observed at higher concentrations from 1 to 10 microM. CONCLUSIONS: From these results, Abeta-induced cytotoxicity in PC12 cells might be mediated by oxidative stress.
Alzheimer Disease ; Amyloid beta-Peptides ; Animals ; Antioxidants ; Apoptosis ; Ascorbic Acid ; Brain ; Cell Line ; Culture Media ; Cytoplasm ; DNA ; Luciferases ; Neurodegenerative Diseases ; Neurons ; NF-kappa B ; Oxidative Stress* ; PC12 Cells*

Both direct and indirect environmental stress to brain were increase the expression of transcription factor c-fos in various populations of neurons. In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsion within 10 min increased the level of c-fos mRNA and protein in forebrain areas. In situ hybridization using (35S)UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels though hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr. In parallel with the mRNA expression, c-FOS protein immunoreactivity was also observed in the same forebrain areas. In contrast to the seizure activity and widespread neuronal degeneration following a kainate treatment, injections of lidocaine did not produce neuronal death within 3 days. The present study indicates that lidocaine induces convulsion and c-fos expression without causing neuro-toxicity.
Adult* ; Amygdala ; Animals ; Brain* ; Hippocampus ; Humans ; In Situ Hybridization ; Injections, Intraperitoneal ; Kainic Acid ; Lidocaine* ; Neostriatum ; Neurons ; Prosencephalon ; Rats* ; RNA, Complementary ; RNA, Messenger* ; Seizures ; Transcription Factors

Primitive neuroectodermal tumors(PNETs) and medulloblastoma are common primary malignant brain tumors of childhood. Untreated patients are proven to be fatal, but the current treatment regimens may achieve 50% to 60% cures. However, the prognosis of each individual case can not be accurately determined, because exact prognostic factors have not been established. The aim of this study was to investigate whether various factors were correlated with clinical outcome, and to understand their roles in the oncogenesis. Twenty-five patients with medulloblastoma and nine patients with supratentorial PNETs were reviewed(mean follow-up periods: 25.6 months). We have investigated the prognostic value of p53 protein and other oncogene expression by immunohistochemistry and DNA analysis by flow cytometry on paraffin section of the specimen. We also studied the other prognostic factors such as clinical features, tumoral factors, and treatment modalities as well. The positive expressions of p53 protein, c-myc, and pan-ras were significantly high in these tumors. With DNA flow cytometry, 18 were aneuploid and 8 were diploid. There was no significant prognostic correlation between the immunoreactivity of p53, oncogene expression, and DNA ploidy. Only the stage of tumor(T, M stage; p=0.0002, 0.0418, respectively) and chemotherapy(p=0.0433) were correlated with their prognosis. We conclude that further special investigations should be added to justify the prognostic factors for these highly malignant tumors.
Aneuploidy ; Brain Neoplasms ; Carcinogenesis ; Diploidy ; DNA ; Flow Cytometry ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Medulloblastoma* ; Neural Plate ; Neuroectodermal Tumors, Primitive* ; Oncogenes ; Paraffin ; Ploidies ; Prognosis*

The optimal management of lesions located in the brainstem(BS) is problematic. As an alternative to microsurgical resection, stereotactic radiosurgery employing the Gamma unit has been used to manage BS lesions, and this can provide relatively safe and effective management. This study describes our experience with 17 patients who underwent Gamma Knife radiosurgery(GKR) for vascular lesions of the brainstem between June 1989 and May 1996. Six of these had BS arteriovenous malformations(AVMs). The minimal radiation dose to the margin of AVMs ranged from 15 to 25Gy(mean, 18.9Gy). Four of six cases were partially obliterated, and on follow-up angiography, one small AVM was seen to be completely obliterated. Twelve months after GKR, one patient experienced a temporary neurologic deficit due to the effects of radiation and another patient, who had a large AVM, showed a permanent deficit as a direct result of treatment. There have been no instances of hemorrhage after GKR and all the patients are still alive. GKR was used to manage 11 patients with angiographically occult vascular malformations (AOVMs) of the BS. The periphery of the lesions received a radiosurgical dose of between 12 and 20Gy(mean, 15.5Gy). In four patients, the lesions became smaller, but in one, an increase was seen. In the remaining six, size change was not documented. One patient's neurological deficit worsened, though that might be related not to GKR but to non-fatal post-GKR rebleeding. At seven months, one patient developed a temporary neurologic deficit in association with perilesional edema that resolved over time. Three patients experienced post-GKR rebleeding, and none died during the follow-up period. We believe that GKR is an excellent option for patients with BS AVMs: when the risks of microsurgery are deemed too high, it is a course of action which seems reasonable. GKR does not, though, appear to obliterate AOVMs as effectively as it does AVMs. To assess the long-term effectiveness of the technique on these lesions, longer follow-up intervals will, however, be required.
Angiography ; Arteriovenous Malformations ; Brain Stem* ; Edema ; Follow-Up Studies ; Hemorrhage ; Humans ; Microsurgery ; Neurologic Manifestations ; Radiosurgery* ; Vascular Malformations