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Biomedical subjects

Yasuo Tano

Publications and source records attributed to Yasuo Tano.

At least 127 records · Page 7Linked to original sources

Changes of ocular aberration with accommodation.

PURPOSE: To study the effect of accommodation on ocular aberrations. DESIGN: Observational case series. METHODS: The ocular aberrations in 33 eyes of 33 young adults were measured with a Hartmann-Shack wavefront aberrometer before and during 3 diopters of accommodation. RESULTS: The root mean square values of wavefront error did not change for a 4-mm and a 6-mm zone; however, spherical aberration changed significantly toward negativity for both the 4-mm zone (P <.001) and 6-mm zone (P =.022). CONCLUSIONS: During accommodation, the significant change in spherical aberration occurs without a change of image quality. Therefore, for customized aberration, it may not be advantageous to eliminate the physiologic spherical aberration for far vision.

Accommodation, Ocular↗

Pathologic myopia: where are we now?.

PURPOSE: To describe current concepts and available treatments for pathologic myopia. DESIGN: Review of experimental and clinical studies. METHODS: The demography, natural history, medical and surgical treatments for choroidal neovascular membrane, vitreoretinal interface disorders and future strategies for pathologic myopia are reviewed. RESULTS: Several medical and surgical modalities are currently available to treat various complications of pathologic myopia. Macular translocation appears to stabilize or improve visual function in many eyes with choroidal neovascularization. CONCLUSION: Newer strategies are emerging to better ameliorate or prevent the complications of pathologic myopia.

Animals↗

Wavefront aberrations measured with Hartmann-Shack sensor in patients with keratoconus.

OBJECTIVE: To compare the ocular wavefront aberrations of normal and keratoconic eyes and to describe the characteristics of the higher-order aberrations in eyes with keratoconus. DESIGN: Prospective case control and observational study. PARTICIPANTS: Thirty-five keratoconic eyes and thirty-eight normal controls. METHODS: Higher-order aberrations in refraction were measured with a wavefront sensor, and those aberrations resulting from the cornea were evaluated by videokeratographic data. MAIN OUTCOME MEASURES: Coma-like (S(3 + 5)), spherical-like (S(4 + 6)), and total (S(3 + 4 + 5 + 6)) higher-order aberrations in both refraction and the cornea. RESULTS: The mean +/- standard deviation of S(3 + 5) (1.88 +/- 1.16), S(4 + 6) (0.70 +/- 0.55), and S(3 + 4 + 5 + 6) (2.03 +/- 1.23) in refraction (6-mm diameter, root mean square, micro m) were significantly higher in the keratoconic eyes than in normal controls (0.26 +/- 0.10, 0.19 +/- 0.10, 0.34 +/- 0.11, respectively; Mann-Whitney U test, P = 0.001). Coma-like aberrations were 2.32 times larger than spherical-like aberrations in keratoconic eyes. CONCLUSIONS: The increase of ocular higher-order aberrations in keratoconic eyes results from an increase of corneal higher-order aberrations. Coma-like aberrations were dominant compared with spherical-like aberrations in keratoconic eyes. Wavefront sensing will enable us not only to evaluate the quality of vision but also to differentiate keratoconic eyes from normal eyes by analyzing the characteristics of the higher-order aberrations.

Adult↗

Topical administration of HSV gD-IL-2 DNA is highly protective against murine herpetic stromal keratitis.

PURPOSE: To evaluate the immunopreventive effect of eyedrops that contain gD-IL-2 DNA (a chimeric gene of the glycoprotein D gene of herpes simplex virus type I (HSV-1) and human interleukin-2 (IL-2) on murine herpetic keratitis. METHODS: A plasmid containing gD-IL-2 (pHDLneo1) was constructed. The eyedrops containing 90 microg/10 microL of the DNA was instilled bilaterally into the conjunctival sacs of BALB/c mice on days 0 and 7. Three weeks after the last administration, neutralizing antibody, delayed-type hypersensitivity (DTH), and 51Cr-release from infected targeted cells by lymphocytes from the cervical lymph nodes and spleen were determined. Immunized mice were challenged with HSV-1, after which the clinical signs of the corneal epithelia and stroma were scored. RESULTS: Specific neutralizing antibody was raised and prominent DTH reaction was elicited from immunized mice. Lymphocytes obtained from the local lymph nodes and spleen vigorously potentiated the cytotoxic activity against the virus-infected cells. Clinically, the development of stromal keratitis was completely inhibited, but prevention or reduction of HSV-1 epithelial lesions was not demonstrated statistically. CONCLUSION: Topical immunization with a DNA vaccine encoding gD-IL-2 totally prevented the development of herpetic stromal keratitis. This procedure is a simple and convenient method for possible clinical application in the future.

Administration, Topical↗

Recurrence of corneal dystrophy resulting from an R124H Big-h3 mutation after phototherapeutic keratectomy.

PURPOSE: The purpose of the study was to investigate the recurrence-free interval after phototherapeutic keratectomy (PTK) in patients with corneal dystrophies resulting from an Arg124His (R124H) mutation of the Big-h3 gene. METHODS: Patients with corneal dystrophy resulting from a genetically confirmed Big-h3 R124H mutation were examined with a slit lamp. The patients were divided into two groups on the basis of the mutation genotype, and the recurrence-free interval was analyzed. RESULTS: In the 4 eyes of 3 homozygous patients, the mean (+/- standard deviation [SD]) recurrence-free interval was 9.5 +/- 3.1 months, whereas in the 7 eyes of 4 heterozygous patients it was 38.4 +/- 6.2 months. The former interval was statistically shorter than the latter (Kaplan-Meier survival analysis with log-rank test, p = 0.004). CONCLUSIONS: These results strongly suggest that the mutation genotype of Big-h3 gene determined the recurrence-free interval as well as the clinical picture after PTK. Therefore, PTK should be considered for patients with Big-h3 R124H corneal dystrophy, on the basis of the expected recurrence-free interval deduced from molecular analysis of the zygosity of the Big-h3 R124H mutation.

Adult↗

Effect of herpes simplex virus-1 gD or gD-IL-2 DNA vaccine on herpetic keratitis.

PURPOSE: To evaluate the efficacy of DNA immunization using herpes simplex virus (HSV)-1 gD or gD-IL-2 (chimeric gene of gD and human IL-2) with reference to their immune responses and preventive effect on the development of murine herpetic stromal keratitis, based on our previous work. METHODS: Plasmids containing gD (pHSDneol) or gD-IL-2 (pHDLneol) were constructed, and gD or gD-IL-2 peptides were purified. BALB/c mice were immunized by hypodermal injection, subconjunctival injection, or topical eye drop twice at 7-day intervals. Attained anti-HSV immune reaction was estimated, including neutralizing antibody, delayed-type hypersensitivity (DTH) measured by the swelling of the ear pinna, and cytotoxic T lymphocyte (CTL) measured by 51Cr release from MHC-matched target cells by splenic and/or local lymph node cells. The corneas of a group of the immunized mice were challenged with CHR3 strain of HSV-1 (10 microL of 3 x 10(6) PFU/mL) 3 weeks after the last immunization. Clinical signs (stromal and epithelial keratitis) were scored. Results. All gD- or gD-lL-2-immunized mice developed specific neutralizing antibody. Delayed-type hypersensitivity and CTL were obtained in gD DNA- or gD-IL-2 DNA-immunized mice. Chimeric DNA vaccine gD-IL-2 elicited higher DTH and more vigorous CTL activity. The scores of stromal keratitis for all gD- or gD-IL-2-immunized mice were significantly suppressed, although those of epithelial keratitis were not. Conclusion. Immunization with gD or gD-IL-2 was effective against herpetic stromal keratitis. By focusing specifically on high induction of cell-mediated immunity, gD-IL-2 DNA could have possible clinical applications against HSV-1 in the future.

Animals↗

Math3 and NeuroD regulate amacrine cell fate specification in the retina.

The basic helix-loop-helix genes Math3 and NeuroD are expressed by differentiating amacrine cells, retinal interneurons. Previous studies have demonstrated that a normal number of amacrine cells is generated in mice lacking either Math3 or NEUROD: We have found that, in Math3-NeuroD double-mutant retina, amacrine cells are completely missing, while ganglion and Müller glial cells are increased in number. In the double-mutant retina, the cells that would normally differentiate into amacrine cells did not die but adopted the ganglion and glial cell fates. Misexpression studies using the developing retinal explant cultures showed that, although Math3 and NeuroD alone only promoted rod genesis, they significantly increased the population of amacrine cells when the homeobox gene Pax6 or Six3 was co-expressed. These results indicate that Math3 and NeuroD are essential, but not sufficient, for amacrine cell genesis, and that co-expression of the basic helix-loop-helix and homeobox genes is required for specification of the correct neuronal subtype.

Amacrine Cells↗

Differential expression patterns of claudins, tight junction membrane proteins, in mouse nephron segments.

As the first step in understanding the physiologic functions of claudins (tight junction integral membrane proteins) in nephrons, the expression of claudin-1 to -16 in mouse kidneys was examined by Northern blotting. Among these claudins, only claudin-6, -9, -13, and -14 were not detectable. Claudin-5 and -15 were detected only in endothelial cells. Polyclonal antibodies specific for claudin-7 and -12 were not available. Therefore, the distributions of claudin-1, -2, -3, -4, -8, -10, -11, and -16 in nephron segments were examined with immunofluorescence microscopy. For identification of individual segments, antibodies specific for segment markers were used. Immunofluorescence microscopic analyses of serial frozen sections of mouse kidneys with polyclonal antibodies for claudins and segment markers revealed that claudins demonstrated very complicated, segment-specific, expression patterns in nephrons, i.e., claudin-1 and -2 in Bowman's capsule, claudin-2, -10, and -11 in the proximal tubule, claudin-2 in the thin descending limb of Henle, claudin-3, -4, and -8 in the thin ascending limb of Henle, claudin-3, -10, -11, and -16 in the thick ascending limb of Henle, claudin-3 and -8 in the distal tubule, and claudin-3, -4, and -8 in the collecting duct. These segment-specific expression patterns of claudins are discussed, with special reference to the physiologic functions of tight junctions in nephrons.

Animals↗

PAX6 mutation as a genetic factor common to aniridia and glucose intolerance.

A paired homeodomain transcription factor, PAX6, is a well-known regulator of eye development, and its heterozygous mutations in humans cause congenital eye anomalies such as aniridia. Because it was recently shown that PAX6 also plays an indispensable role in islet cell development, a PAX6 gene mutation in humans may lead to a defect of the endocrine pancreas. Whereas heterozygous mutations in islet-cell transcription factors such as IPF1/IDX-1/STF-1/PDX-1 and NEUROD1/BETA2 serve as a genetic cause of diabetes or glucose intolerance, we investigated the possibility of PAX6 gene mutations being a genetic factor common to aniridia and diabetes. In five aniridia and one Peters' anomaly patients, all of the coding exons and their flanking exon-intron junctions of the PAX6 gene were surveyed for mutations. The results of direct DNA sequencing revealed three different mutations in four aniridia patients: one previously reported type of mutation and two unreported types. In agreement with polypeptide truncation and a lack of the carboxyl-terminal transactivation domain in all of the mutated PAX6 proteins, no transcriptional activity was found in the reporter gene analyses. Oral glucose tolerance tests revealed that all of the patients with a PAX6 gene mutation had glucose intolerance characterized by impaired insulin secretion. Although we did not detect a mutation within the characterized portion of the PAX6 gene in one of the five aniridia patients, diabetes was cosegregated with aniridia in her family, and a single nucleotide polymorphism in intron 9 of the PAX6 gene was correlated with the disorders, suggesting that a mutation, possibly located in an uncharacterized portion of the PAX6 gene, can explain both diabetes and aniridia in this family. In contrast, the patient with Peters' anomaly, for which a PAX6 gene mutation is a relatively rare cause, showed normal glucose tolerance (NGT) and did not show a Pax6 gene mutation. Taken together, our present observations suggest that heterozygous mutations in the PAX6 gene can induce eye anomaly and glucose intolerance in individuals harboring these mutations.

Adolescent↗

Spatiotemporal expression patterns of N-syndecan, a transmembrane heparan sulfate proteoglycan, in developing retina.

PURPOSE: N-syndecan is a transmembrane heparan sulfate proteoglycan, that is highly expressed in neural tissues. In the current study, changes in N-syndecan expression during retinal development were examined. METHODS: Localization of N-syndecan in developing rat retina was examined by immunohistochemistry and in situ hybridization. The amount of the core protein was evaluated by immunoblot analysis, using retinal homogenates at various developmental stages. In addition, mRNA expression was semiquantified by reverse transcription-polymerase chain reaction (RT-PCR). To understand better the localization of N-syndecan in retinal neuronal cells, we performed immunocytochemistry using retinal ganglion cells in culture. RESULTS: N-syndecan is highly expressed in nerve fiber-rich layers of the retina at early postnatal stages (between postnatal day [P]0 and P14). In contrast, immunoreactivity was faint during embryonic stages and late postnatal stages. In addition, in retinal flatmounted sections, N-syndecan immunoreactivity was observed on the axons of retinal ganglion cells. Intense signals were observed in the ganglion cell layer during in situ hybridization. Immunoblot analyses demonstrated that the amount of N-syndecan core protein reached a peak at approximately P14. The RT-PCR analyses using N-syndecan primers showed that an intense amplified band was observed in the cDNA derived from P14 retinas, whereas only faint bands were detected in the embryonic day (E)16 and P42 retinas. In retinal ganglion cells in culture, N-syndecan was located on the long, extended neurites. CONCLUSIONS: The data show that N-syndecan is transiently expressed, primarily in retinal neural fibers, during retinal development, indicating that it may be involved in formation of the retinal neural network.

Animals↗

ABCA4 gene mutations in Japanese patients with Stargardt disease and retinitis pigmentosa.

PURPOSE: To evaluate photoreceptor cell-specific adenosine triphosphate (ATP)-binding cassette transporter (ABCA4) gene mutations in Japanese patients with Stargardt disease (STGD) and the correlation of these mutations to clinical phenotypes. METHODS: Serum was obtained from 10 unrelated Japanese patients with STGD and 96 unrelated Japanese patients with autosomal recessive retinitis pigmentosa (arRP). All 50 ABCA4 gene exons of the patients with STGD were screened for mutations by a combination of single-strand conformation polymorphism analysis and polymerase chain reaction (PCR) direct-sequencing techniques. By restriction enzyme digestion, primer extension analysis, and PCR direct sequencing techniques, the patients with arRP were screened for three segregated, presumably null ABCA4 gene mutations observed in Japanese patients with STGD. RESULTS: Three novel, presumably null mutations of the ABCA4 gene, IVS7-45_952delinsTCTGACC, IVS12+2T-->G, and 1894delA, were identified. The Arg2149stop mutation that had been found in a white patient with STGD in a prior study was also found in a Japanese patient. Two arRP-affected siblings and two unrelated patients with STGD were found to be homozygous for the same IVS12+2T-->G mutation, and three other arRP-affected siblings were carriers of the IVS12+2T-->G mutation and/or the IVS7-45_952delinsTCTGACC mutation. These three siblings with arRP showed only atrophic degeneration in the macula early after the onset of the disease, and STGD had been diagnosed. CONCLUSIONS: Three novel ABCA4 gene mutations were identified in Japanese patients with STGD and arRP. Mutations in the ABCA4 gene can cause panretinal degeneration that changes its clinical appearance from STGD to arRP over time.

ATP-Binding Cassette Transporters↗

[Ocular complications in systemic lupus erythematosus--choroidal and retinal pigment epithelial changes].

PURPOSE: Cotton wool patch and retinal hemorrhage are common ocular findings in systemic lupus erythematosus(SLE). Immunosuppressive treatment with corticosteroids may modify choroidal and retinal findings. We examined ocular complications, mainly choroidal and retinal pigment epithelium (RPE) changes in patients with SLE. MATERIALS AND METHODS: Fifty SLE cases[3 males, 47 females, 41 +/- 15 (mean +/- standard deviation) year-old] were examined and treated in the departments of Internal Medicine and Ophthalmology of Osaka University Medical Hospital. RESULTS: Complications included cataract in 16 cases, glaucoma or ocular hypertension in 9 cases, and choroidal and retinal changes in 15 cases. Occlusive retinal vasculitis, retinal pigment epithelial dysfunction, such as pigment epithelial detachment, choroidal neovascularization and multiple posterior pigment epitheliopathy, in 6 cases, and branch retinal vein occlusion in 2 cases were detected as fundus complications. Average time period from the first detection of SLE was 13 years in patients with RPE changes. CONCLUSION: Long term corticosteroid therapy is probably responsible for the RPE complications.

Adult↗

The clinical role of N-isopropyl-p-[123I]-iodoamphetamine single photon emission computed tomography in the follow-up of choroidal melanoma after radiotherapy.

BACKGROUND: Single photon emission computed tomography (SPECT) images with N-isopropyl-p-[123I]-iodoamphetamine (123I-IMP) have recently been used for the sensitive and specific detection of melanoma. CASES: Using 123I-IMP SPECT, we observed three patients over a period of 18 months in whom choroidal melanoma had been diagnosed. Two underwent radiotherapy (cyber knife) in our clinic; the other patient was referred to us after 8 months of proton beam irradiation at another clinic. OBSERVATIONS: In two of the three cases, no metastasis or tumor recurrence has been observed up to the present time. In these individuals, the average 123I-IMP uptake in the pathological eye gradually and progressively decreased after radiotherapy to levels seen in the fellow eye. One eye of the three patients examined here, however, exhibited tumor recurrence in the ciliary body as well as hepatic metastasis 12 months after radiation treatment. In the pathological eye of this patient, the average 123I-IMP uptake gradually decreased, but never reached the levels in the fellow eye during the observation period. CONCLUSIONS: 123I-IMP SPECT is a useful examination method not only for diagnosis but also for the follow-up of patients with choroidal melanoma.

Adult↗

Development of bilateral, nonarteritic anterior ischemic optic neuropathy in an eye with diabetic papillopathy.

BACKGROUND: Diabetic papillopathy and anterior ischemic optic neuropathy are different clinical entities with different prognoses. We describe a case of diabetic papillopathy that developed into bilateral nonarteritic anterior ischemic optic neuropathy (AION). CASE: A 58-year-old woman with diabetes mellitus had bilateral disc elevation. Goldmann perimetry showed altitudinal hemianopsia in the left eye. The early phase of fluorescein angiography showed hypoperfusion in the superior segment of the left optic disc indicating AION in the left eye. OBSERVATIONS: During the follow-up period, the visual field of the left eye was further constricted and that of the right eye also developed signs of AION, suggesting that bilateral anterior ischemic optic neuropathy had developed. After steroid pulse therapy, her vision recovered slightly, but the visual field remained constricted in both eyes. The optic discs had a low cup/disc ratio. CONCLUSIONS: Our findings demonstrated that diabetic papillopathy can precede the development of nonarteritic anterior ischemic optic neuropathy.

Diabetes Complications↗

Transretinal electrical stimulation with a suprachoroidal multichannel electrode in rabbit eyes.

PURPOSE: Several approaches for placing an electrode device for visual prosthesis have been previously proposed. In this study, we investigated if transretinal stimulation from the suprachoroidal space can elicit an electrical evoked potential (EEP) in albino rabbits. METHODS: A flat electrode array (polyimide plate, platinum electrode) was developed and used for this study. After performing a scleral incision at 2-2.5 mm from the limbus and placing an anchoring suture, the array was inserted into the suprachoroidal space in the posterior portion of the eye by direct observation under a microscope. A platinum wire was implanted into the vitreous space as a reference electrode. For electrical stimulation, a biphasic pulse was used. When the electrode was stimulated, the EEP was recorded. RESULTS: When the electrical stimulation from the suprachoroidal space was applied, the EEP could be recorded with an epidural electrode, and the threshold was 66.0 +/- 32.1 micro A (420 micro C/cm(2)) [corrected]. placement of the array and the electrical stimulation. CONCLUSIONS: Transretinal electrical stimulation from the suprachoroidal space could elicit EEP, suggesting that this approach may be useful for a retinal prosthesis system.

Animals↗

Electrical stimulation with a needle-type electrode inserted into the optic nerve in rabbit eyes.

PURPOSE: To investigate whether electrical stimulation of the optic nerve can elicit an electrical evoked potential (EEP) in rabbits and to determine whether such stimulation is a useful approach for the placement of a visual prosthesis. METHODS: Two needle-type electrodes were inserted into the optic nerve using a transvitreal approach. For electrical stimulation, monophasic and biphasic pulses were used. By stimulating the optic nerve, the EEP was elicited. After evaluation of the EEP, a histological study was carried out. RESULTS: When electrical stimulation was applied, the EEP could be recorded. The threshold with monophasic and biphasic stimulation was 10 +/- 0 microA and 20 +/- 8.2 microA, respectively. Histological examination revealed no major complications, such as bleeding or degeneration, which might have resulted from the insertion of electrodes or the electrical stimulation. CONCLUSIONS: Electrical stimulation of the optic nerve can elicit an EEP, suggesting that this approach may be useful for a visual prosthesis system.

Animals↗