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T Tokoro

Publications and source records attributed to T Tokoro.

At least 19 recordsLinked to original sources

Clinical course of newly developed or progressive patchy chorioretinal atrophy in pathological myopia.

Regional chorioretinal atrophy in the posterior fundus (patchy chorioretinal atrophy) in pathological myopia impairs vision severely when it covers the macula. The aim of this study was to assess the course of development and progression of patchy chorioretinal atrophy in pathological myopia. The location and progression of patchy chorioretinal atrophy that was either newly developed or had progressed during the follow-up period (mean 5.25 years) were analyzed. A total of 41 lesions of patchy atrophy were newly developed in 30 eyes of 25 patients. These lesions were more likely to occur in marginal regions of a posterior staphyloma but frequency per unit area was highest in the macula. There were 138 lesions of patchy chorioretinal atrophy that progressed in 75 eyes of 53 patients. Sixty percent of the lesions of patchy chorioretinal atrophy in marginal regions of a posterior staphyloma spread toward the center. Seventy percent of the lesions of patchy chorioretinal atrophy in the macula spread in all directions. Fluorescein angiography of newly developed patchy chorioretinal atrophy showed hyperfluorescence in 50% and hypofluorescence in 27%. Fluorescein angiography of progressive lesions of patchy chorioretinal atrophy showed hypofluorescence in 69%. Fluorescein angiography of some progressive areas of patchy chorioretinal atrophy, which showed a change from hyperfluorescence to hypofluorescence within several years, suggested that damage to the retinal pigment epithelium preceded the progression of the patchy chorioretinal atrophy. In conclusion, the patchy chorioretinal atrophy is most likely to occur in the macula and to enlarge in all directions. And it is suggested that the patchy chorioretinal atrophy which shows hyperfluorescence by fluorescein angiography should be kept under observation because our data suggest that this finding indicates progression in the future.

Adult

Apomorphine inhibits the growth-stimulating effect of retinal pigment epithelium on scleral cells in vitro.

Visual deprivation of the chicken eye causes axial elongation with high myopia. The cartilaginous layer of the myopic sclera shows an increase of mitotic activity. Previous studies reported that the in vivo administration of apomorphine, a dopamine nonselective agonist, effectively prevents visual-deprivation myopia. Because the retinal pigment epithelium (RPE) regulates growth of the sclera as we and others have shown previously, it is speculated that the RPE cells may play an important role in this preventive effect of apomorphine. In this study, to clarify the mechanism by which the administration of apomorphine inhibits the proliferation of scleral chondrocytes in vivo, we have investigated the effect of apomorphine on the proliferation of scleral chondrocytes with or without co-cultured RPE cells in vitro. We previously demonstrated that cell proliferation of scleral chondrocytes remarkably increases with co-cultured RPE cells. In this study, we found that apomorphine at concentrations of higher than 2 x 10(-5) M dramatically reduced the growth-stimulatory effect of RPE cells on the scleral chondrocytes, whereas the inhibitory effect of apomorphine on the proliferation of scleral chondrocytes without RPE cells was very little. Our results strongly suggest that apomorphine may reduce the production and/or release of some humoral factors from RPE cells, which stimulate the growth of scleral cells. There is also a possibility that apomorphine reduces the reactivity of scleral cells to the humoral factors released from RPE cells.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben

Regional scleral changes in form-deprivation myopia in chicks.

Similar neurochemical events appear to be involved in the development of myopia in chicks and mammals. The rapid post-hatching development of the chick is ideal for studying experimental myopia. In this investigation, one eye of 2-day-old chicks was deprived of form vision for 2 weeks and then compared to the fellow, non-deprived eye by immunohistochemistry and light and electron microscopy. All deprived eyes showed a high refractive error and ocular enlargement. In deprived eyes, the posterior cartilaginous sclera was thicker and the fibrous sclera of the same section was thinner than the control. Scleral morphological changes were restricted to a central button 6-7 mm in diameter (the posterior pole) within the posterior hemisphere, further divided into posterotemporal and posteronasal parts. The most enlarged, posterior cartilaginous structure of deprived sclera could be divided into an inner and an outer zone. The inner zone had many unevenly-arranged chondrocytes, each having a well-developed granular endoplasmic reticulum and Golgi complex and a very irregular cell surface. Numerous S-phase cells and isogenous groups were detected in the outer zone. Hypertrophic chondrocytes were often observed in the innermost region of the outer zone and the outermost region of the inner zone. The boundary between the outer fibrous sclera and the cartilaginous sclera was irregular and obscured in myopic eyes. Spindle-shaped chondrocytes were seen to be in contact with each other. Thick collagen fibrils, usually seen only in the outer fibrous sclera, were present among the chondrocytes. Results of this morphological study suggest an increased proliferation of chondrocytes and active synthesis of extracellular matrix in visually deprived eyes. The elongation of the ocular axis that accompanies myopia is caused primarily by an active remodeling and differentiation in a restricted section of the posterior scleral cartilage. These facts indicate the posterior scleral cartilage may be more immature than cartilage in anterior and lateral segments.

Animals

A possible role of endogenous inhibitor for nitric oxide synthesis in the bovine ciliary muscle.

The present experiments were designed to investigate the possible role of endogenous methylarginine derivatives such as NG-monomethyl-L-arginine, asymmetrical NG,NG-dimethyl-L-arginine and symmetrical NG,N'G-dimethyl-L-arginine for the nitric oxide synthesis in the bovine ciliary muscle. The contents of asymmetrical NG,NG-dimethyl-L-arginine and symmetrical NG,N'G-dimethyl-L-arginine in the bovine ciliary muscle were determined to be 370.2 +/- 27.6 (n = 5) and 182.4 +/- 22.9 (n = 5) pmoles g-1 wet weight, respectively by means of the automated high-performance liquid chromatography. NG-Monomethyl-L-arginine was below the assay limits. On the basis of the total tissue water content (0.792 +/- 0.006 ml g-1 wet weight, n = 14), the concentrations of asymmetrical NG,NG-dimethyl-L-arginine and symmetrical NG,N'G-dimethyl-L-arginine were tentatively estimated to be (4.7 +/- 0.3) x 10(-7) M (n = 5) and (2.3 +/- 0.3) x 10(-7) M (n = 5), respectively. A23187 (10(-7)-3 x 10(-4) M) produced a concentration-dependent relaxation of the ciliary muscle strips which had been contracted with 10(-5) M carbachol. Authentic asymmetrical NG,NG-dimethyl-L-arginine (3 x 10(-6)-3 x 10(-4) M), but not symmetrical NG,N'G-dimethyl-L-arginine (3 x 10(-4) M), inhibited the 10(-6) M A23187-induced relaxation in a concentration-dependent manner. The inhibition with asymmetrical NG,NG-dimethyl-L-arginine (10(-4) M) was reversed by an addition of 3 x 10(-3) M L-arginine, but not by 3 x 10(-3) M D-arginine. The A23187 (10(-6) M)-induced relaxation was enhanced by 3 x 10(-3) M L-arginine or superoxide dismutase (50 U ml-1), whereas it was inhibited by carboxy-PTIO (3 x 10(-4) M), a scavenger of nitric oxide, or methylene blue (10(-5) M), an inhibitor of guanylate cyclase. The carbachol-induced contraction was enhanced by asymmetrical, NG,NG-dimethyl-L-arginine (10(-5) M) and inhibited by 3 x 10(-3) M L-arginine. Any effect of prostanoid formation during the A23187-induced relaxation was ruled out by using indomethacin (10(-5) M). Sodium nitroprusside (10(-5) M), a donor of nitric oxide, also produced a relaxation, which was inhibited by methylene blue (10(-5) M) or carboxy-PTIO (3 x 10(-4) M) and was augmented by superoxide dismutase (50 U ml-1), but unaffected by asymmetrical NG,NG-dimethyl-L-arginine (3 x 10(-4) M) or L-arginine (3 x 10(-3) M). These results lead us to speculate that the nitric oxide synthesized endogenously from L-arginine may play a role for mediating relaxation of the bovine ciliary muscle and that the endogenous asymmetrical NG,NG-dimethyl-L-arginine may be involved in inhibiting the biosynthesis of nitric oxide when there are increased intracellular concentrations of the methylarginine under certain circumstances.

Animals

Indocyanine green angiography of retrobulbar vascular structures in severe myopia.

PURPOSE: To evaluate angiographic findings of retrobulbar arteries and veins in severely myopic patients. METHODS: We examined 416 severely myopic eyes (213 patients) with refractive errors greater than -8.25 diopters using indocyanine green videoangiography. A control group of 74 eyes (37 patients) had refractive errors within plano +/- 3 diopters. Four severely myopic patients underwent computed tomographic angiography to identify the entire intraorbital course of retrobulbar veins. RESULTS: Of 416 severely myopic eyes, 231 (55.5%) exhibited retrobulbar arteries, which were tortuous and pulsatile behind the posterior pole of the globe. Retrobulbar arteries connected directly with choroidal arteries temporal to the macular area. In 17 of these 231 eyes, retrobulbar arteries were also observed nasal to the optic nerve head, continuous with the Zinn-Haller ring around the optic nerve head and directly connected with choroidal arteries. In 39 severely myopic eyes (31 patients), indocyanine green angiography disclosed retrobulbar veins, most of which coursed vertically just behind the posterior pole of the globe. These retrobulbar veins originated as an inferior vascular network of the inferior orbital vein and drained into the superior orbital vein in the upper orbit. CONCLUSION: Retrobulbar arteries observed in this study were temporal and nasal short posterior ciliary arteries. Only the lateral collateral vein, which was one of the collateral channels between the superior and inferior orbital veins, was visible in severely myopic eyes. Indocyanine green angiography is useful in evaluating retrobulbar vascular structure in severely myopic eyes.

Adolescent

Nitric oxide-induced ciliary muscle relaxation during contraction with endothelin-1 is mediated through elevation of cyclic GMP.

PURPOSE: Nitric oxide (NO) relaxes ciliary smooth muscle, and endothelin-1 (ET-1) is reported to regulate ciliary muscle tone. Despite the physiological significance of nitric oxide and ET-1, very few studies have attempted to characterize the mutual modes of action of these mediators in this tissue. Thus, the present experiments were designed to investigate a possible relaxation mechanism of nitric oxide in bovine ciliary muscle that has been contracted by ET-1. METHODS: The effects of sodium nitroprusside (SNP), as a nitric oxide donor, methylene blue, as an inhibitor of guanylate cyclase, and 8-bromo-cyclic GMP on the bovine ciliary muscle contracted with ET-1 were examined. The changes in cyclic GMP level and relaxation, in response to SNP alone or in combination with 3-isobutyl-1-methylxanthine (IBMX) as a nonselective inhibitor of phosphodiesterases, were also determined. RESULTS: Sodium nitroprusside (SNP) produced a concentration-dependent relaxation, which was significantly (p < 0.005) augmented by 10(-5) M 3-isobutyl-1-methylxanthine (IBMX) and significantly (p < 0.005) attenuated by 3 x 10(-5) M methylene blue as an inhibitor of guanylate cyclase. The relaxation in response to SNP was accompanied by an increase in the cyclic 3':5' guanosine monophosphate (cyclic GMP) level, which was again significantly (p < 0.05) augmented by 10(-5) M IBMX and significantly (p < 0.005) attenuated by 3 x 10(-5) M methylene blue. The exogenously applied 8-bromo-cyclic GMP relaxed the ciliary muscle strips during the contraction caused by ET-1. CONCLUSIONS: These results lead us to assume that NO generated from SNP is closely related to cyclic GMP production via the activation of guanylate cyclase and, in turn, causes a relaxation response in the bovine ciliary muscle contracted with ET-1.

1-Methyl-3-isobutylxanthine

The long-term follow-up of a highly myopic patient with a macular vortex vein.

We followed a highly myopic patient with a macular vortex vein for 11 years. His refraction was -12D OU at age 10 years when the vein was first observed ophthalmoscopically in the left eye. Eleven years later, his myopia had progressed (4 diopters OD; 8 diopters OS), and the axial lengths were elongated (+1.8 mm OD; +2.7 mm OS). The macular vortex vein was dilated and tortuous. Indocyanine green angiography revealed the outflow route of this vein in the posterior pole, where both nasal and temporal posterior choroidal venous blood collected. Computed tomography showed that the vein left the eyeball directly and coursed along the optic nerve 5 mm posterior to the optic disc. A major collecting channel of posterior choroid outflow in some highly myopic eyes, a macular vortex vein may be formed at a relatively early age, and continue to enlarge, with elongation of axial length and progression of myopia.

Child

Visual deprivation myopia with translucent and black goggles.

To study how different visual deprivation conditions influence the degree of myopia, chicks were reared under conditions of unilateral and bilateral visual deprivation with translucent and black goggles in environments of a 12-hour light/dark cycle and complete darkness. Two weeks after hatching, the refractive errors and axial lengths of the eyes were measured. The deprived eyes of the light/dark-reared chicks exhibited severe myopia both unilaterally and bilaterally as well as axial elongations. The dark-reared chicks exhibited slight myopia in the eyes with goggles and no significant axial elongation. The experiments suggest that different degrees of visual deprivation can also cause severe myopia, that myopia develops independently in each eye, and that a light/dark environment is required for severe myopia to develop.

Animals

Coexistence of an autonomously functioning thyroid nodule in a patient with Graves' disease: an unusual presentation of Marine-Lenhart syndrome.

A 44-year-old woman developed hyperthyroidism due to the coexistence of Graves' disease and an autonomously functioning thyroid nodule (AFTN). Anti-thyrotropin receptor antibody (TRAb) was strongly positive (83.2%), and a thyroid scan initially showed diffuse uptake of Tc-99m pertechnatate in both lobes and further increased uptake in accordance with the right lobe nodule. The nodule in the right lobe was histologically diagnosed as thyroid follicular adenoma. After she was maintained in a euthyroid state by treatment with Methymazole (MMI), thyroid uptake of Tc-99m in the nodule became lower and was slightly suppressed by T3 administrations probably due to its dependence on TSH. Subtotal thyroidectomy was performed and she subsequently became euthyroid with negative TBII activity. It is concluded that she had a coexisting functioning nodule with Graves' disease (Marine-Lenhart syndrome) and that the nodule changed from hot to cool along with the anti-thyroid treatment, unlike usual cases of this syndrome showing a cold nodule on the initial imaging under the hyperthyroid state. Repeated Tc-99m pertechnatate thyroid scans were helpful in evaluating the reaction of MMI and TSH in both lesions separately in the present case.

Adenoma

Simultaneous xenotransplantation of human Graves' thyroid tissue and autologous bone marrow cells in severe combined immunodeficient mice: successful reconstitution of human Graves' hyperthyroidism.

Human thyroid xenografts and the autologous bone marrow (BM) cells from five patients with Graves' disease (GD) were simultaneously xenografted into severe combined immunodeficient (SCID) mice to study the role of BM cells for the perpetuation of human GD autoimmunity and hyperthyroidism. All SCID mice engrafted with thyroid tissue (TH) alone, TH + autologous peripheral blood mononuclear cells, and TH + autologous BM cells produced similar amounts of human IgG; however, the production in TH + BM-engrafted mice peaked later than that of mice without BM. Production of thyroperoxidase antibody and thyroglobulin antibody in TH + BM-bearing SCID mice peaked in later weeks after xenografting than in those without BM. Moreover, human Graves' hyperthyroidism was actually reconstituted in TH + BM-transplanted mice; this was confirmed by (A) significantly higher levels and longer periods of secreting thyroid-stimulating antibody than those in mice without BM engraftment. (B) persistent hyperthyroxinemia up to the end of the experiment. (C) extremely high radioidine uptake of the xenografted thyroid tissue, and (D) histological findings of the maintenance of hyperplastic change of the xenografted thyroid epithelial cells. Human BM stem cells (CD34) were identified only in mice with TH + BM xenografts when analyzed by immunohistochemistry. In conclusion, (A) we have developed an animal model for human hyperthyroid GD by simultaneous xenotransplantation of GD thyroid tissue plus autologous BM cells into SCID mice, and (B) BM cells have a crucial role for perpetuating human GD autoimmunity and hyperthyroidism in this system.

Adult

In vivo and in vitro association of retinoic acid with form-deprivation myopia in the chick.

The purpose of this study is to clarify the role of retinoic acid (RA) in the mechanism of form-deprivation myopia (FDM) in the chick. FDM was induced in two-day old chicks by placement of a translucent plastic goggle over one eye, with the contralateral eye used as a control. After 12 days, the chicks were euthanized. RNA was extracted from scleras in the posterior segments, transcribed into cDNA, and amplified by PCR with primers specific for retinoic acid receptor (RAR) beta. G3PDH was used as a reference gene for normalization. The effects of RA, with or without TGF-beta, on the proliferation of scleral chondrocytes and scleral fibroblasts from 17-day chick embryos were studied by use of a colorimetric assay, and the alkaline phosphatase activities of those cells also studied. Furthermore, RAR beta expression in response to RA in cultured scleral cells was studied. As a result, RT-PCR products of the expected sizes were obtained from scleras from the myopic and control eyes. Expression of RAR beta in the myopic scleras was significantly higher than that in the controls. The proliferation of scleral chondrocytes and scleral fibroblasts was inhibited by treatment with RA in a dose-dependent manner (in 10% FBS). In the presence of TGF-beta (in 0.5% FBS), RA treatment stimulated the proliferation of scleral chondrocytes but inhibited the proliferation of scleral fibroblasts. RA induced alkaline phosphatase activities in both the scleral chondrocytes and scleral fibroblasts. RAR beta expression was induced by RA in cultured scleral cells. These results demonstrate that RA appears to play a role in the mechanism of FDM in the chick. However, it is also possible that the changes in the expression of RAR beta were secondary events related to other mechanisms responsible for ocular enlargement.

Alkaline Phosphatase

Functional neuroanatomy of visual object naming: a PET study.

BACKGROUND: The ability to name objects depends partly on visual perception. We used positron emission tomography (PET) to measure activity-related changes in regional cerebral blood flow (r-CBF) in order to identify regions of the brain activated during visual object naming. METHODS: Four right-handed volunteers were recruited. Following an intravenous injection of 15O-labeled water, r-CBF was measured during visual object naming, counting numbers, and resting. PET and MRI images were coregistered, the size of the brain was proportionally adjusted in each axis to Talairach's and Tournoux's atlas, and the comparison of stimulated versus resting blood flow images revealed activated brain regions. RESULTS: In the subtraction of resting from naming, activation was observed in the bilateral primary visual cortex, bilateral fusiform gyrus, left lingual gyrus, bilateral inferotemporal cortex, bilateral inferior frontal gyrus, bilateral precentral gyrus, anterior cingulate gyrus, left parietal operculum, and left putamen. In the subtraction of counting from naming, most of the those areas were activated, but no significant activity was observed in the left lingual gyrus, left parietal operculum, or bilateral precentral gyrus (motor cortex). The areas activated with the paradigm included those dedicated to visual perception (primary and associate visual cortex), visual recognition (inferior temporal cortex), and phonological output (Broca's area). CONCLUSION: Our results indicated that the major neural network from occipital lobe to frontal cortex, which is mainly involved in the ventral visual pathway, demonstrated activation in these tasks. Result of this study will serve as base line data for analyzing the findings in patients with impaired visual perception.

Adult

Unilateral eyeball enucleation differentially alters AMPA-, NMDA- and kainate glutamate receptor binding in the newborn rat brain.

The aim of the present work was to evaluate the neurochemical effects of early unilateral visual deprivation as a model of impaired visual maturation. For this purpose, binding to the different ionotropic glutamate receptor subtypes was quantified in vision-related and vision-unrelated brain structures of control and unilaterally deprived newborn rats. At post-natal (PN) day 10, male Sprague-Dawley rats underwent either unilateral eyeball enucleation (enucleation group, n = 12) or sham operation (control group, n = 12). In each group, brains were obtained either at post-natal day 20 (n = 6) or post-natal day 30 (n = 6) and processed for quantitative in vitro autoradiography selective for NMDA, kainate, and AMPA glutamate-binding sites, as well as for the presynaptic adenosine A1 receptor as a control of the deafferentation efficacy. In control animals, quantitative autoradiography revealed an increase in NMDA (e.g. +45% in superior colliculus) and kainate receptor binding (e.g. +55% in visual cortex, layer IV) from post-natal day 20 to post-natal day 30, associated with stable levels of AMPA receptor binding, in the vision-related structures. In the deafferented visual structures, monocular enucleation induced a marked decrease in A1 site density (e.g. -38 to -52%, in the superficial layer of superior colliculi, at PN day 20 and PN day 30, respectively) in parallel with a mild increase in both NMDA (e.g. +8 to 9%, in superior colliculi and visual cortex, layer IV at PN day 30, respectively) and AMPA (e.g. +16%, in layer IV of the visual cortex at PN day 30). Superimposed on marked bilateral decreases at PN day 30 in the enucleated rats, kainate receptor binding also revealed a slight but significant decrease (-5%) in the deafferented superior colliculus as compared to the non-deafferented side. The present findings (different time-courses of, and differential effects of deafferentation on, the NMDA, kainate and AMPA glutamate receptor subtypes throughout the visual brain structures) further support the involvement of these receptors in distinctive roles during maturation of the visual system.

Animals

Studies of retroorbital tissue xenografts from patients with Graves' ophthalmopathy in severe combined immunodeficient (SCID) mice: detection of thyroid-stimulating antibody.

The pathogenesis of Graves' ophthalmopathy (GO) is still unclear and the possible role of TSH receptor antibody in the development of GO is controversial. However, the recent availability of severe combined immunodeficient (SCID) mice has provided a means to study of human autoimmune thyroid disease in an in vivo environment. In the present study, we xenografted human retroorbital (RO) tissues from 9 patients with GO into 9 SCID mice and the autologous peripheral blood mononuclear cells (PBMC) from 5 of 9 GO patients were engrafted into 5 separate SCID mice to reconstitute the immunological environment of human GO. Mice blood samples were taken every 2 weeks for the measurements of human IgG, thyroglobulin antibody (Tg-Ab), thyroperoxidase (TPO)-Ab, thyroid-stimulating antibody (TSAb), and interferon-gamma (IFN-gamma). Eight weeks after xenografting, mice were killed; RO tissues were analyzed histologically, SCID mice with RO tissues from 2 of 9 GO patients produced human IgG peaking at 6-8 weeks after xenografting. TPO-Abs and TG-Abs were detectable in low titer in mice with RO tissue xenografts from 3/9 and 4/9 GO patients, respectively. The mean level of IFN-gamma in SCID mice with GO RO xenografts was higher than that of a control subject (RO tissue from a non-GO patient). TSAbs were actually produced from 7 of 9 mice xenografted with GO RO tissues, and reached their peaks at 2-8 weeks after xenografting; autologous PBMC (alone, without RO tissues)-engrafted SCID mice did not produce any detectable level of TSAb. The control mouse did not produce any detectable levels of human IgG, TPO-Ab, Tg-Ab, or TSAb. Immunohistochemical analysis of orbital mononuclear cell infiltrates revealed a predominance of T lymphocytes, with a small percentage of B lymphocytes in GO RO tissue graft. In conclusion, we have successfully reconstituted the SCID mice with human lymphocytes of RO tissues from patients with GO. Autoreactive B cell clones responsible for secreting TSAb exist in GO RO tissue and may be a key factor in the initiation and/or the progression of GO.

Adult

IFN-gamma has a protective role against thyroid-specific autoantibody production in severe combined immunodeficient (SCID) mice xenografted with Graves' thyroid tissue.

We studied the effects of exogenous human IFN-gamma or neutralizing monoclonal antibody (mAb) to IFN-gamma on xenografted human Graves' thyroid tissue in severe combined immunodeficient (SCID) mice to investigate a possible role of IFN-gamma in the pathogenesis of human Graves' disease. Human thyroid tissues from four patients with Graves' disease were xenografted into SCID mice. Two weeks after xenografting, mice were divided into three groups with human IgG levels similar to each other. Mice in the first group were treated with human IFN-gamma daily for 6 weeks; mice in the second (similar) group were treated with an mAb to IFN-gamma; mice in the third group were given mouse IgG only (control group). Blood samples were taken every 2 weeks for human IgG and thyroid-specific autoantibodies (Tg-Ab, TPO-Ab, and thyroid-stimulating antibody). After 6 weeks' treatment, mice were killed, and the thyroid xenograft was examined for thyrocyte HLA-DR expression. Human IgGs were produced equally in all three groups; mice treated with IFN-gamma showed significantly lower amounts of thyroid autoantibodies than those in the control group. Thyrocyte HLA-DR expression was markedly increased in xenografts from mice with IFN-gamma administration. On the other hand, anti-IFN-gamma mAb injection caused only slight suppression of HLA-DR expression on xenografted thyroid cells. In conclusion, IFN-gamma may down-regulate the production of thyroid-specific autoantibodies but not human IgG, at least under these circumstances; there thus may be specific inhibitory effects of IFN-gamma against thyroid-specific autoantibody production of intrathyroidal plasma cells, and this animal model may help to elucidate the possible role of cytokines in the pathogenesis of Graves' disease.

Animals

The progression of lacquer cracks in pathologic myopia.

PURPOSE: Lacquer cracks are found in the posterior fundus of 4.3% of highly myopic eyes. They represent healed and mechanical breaks of the retinal pigment epithelium, Bruch's membrane, and choriocapillaris complex. This prospective study examined the progressive course and angiographic characteristics of transitional changes in highly myopic eyes with lacquer cracks. METHODS: The authors studied 66 eyes (53 patients with lacquer cracks, using general ocular examinations and fluorescein angiography once every 3 to 12 months. Follow-up ranged from 7 to 243 months (average, 72.8 months). RESULTS: The lacquer cracks progressed in 37 eyes (56.1%). Of these 37 eyes, the number of lacquer cracks increased in 14 eyes and turned into other myopic fundus changes in 25 eyes. These changes included patchy atrophy, diffuse atrophy, and choroidal hemorrhage with neovascular membrane (Fuchs' spot). Fluorescein angiography showed patchy atrophy beginning with a small hypofluorescent area at the peripheral end of the lacquer cracks. CONCLUSION: A high incidence of lacquer cracks progressed into advanced fundus changes during a mean follow-up period of 6 years. Even faint lacquer cracks may characterize an unfavorable prognostic course, leading to macular pathology in patients with pathologic myopia.

Adolescent

Subretinal bleeding without choroidal neovascularization in pathologic myopia. A sign of new lacquer crack formation.

PURPOSE: The clinical significance of subretinal bleeding without choroidal neovascularization in pathologic myopia is unclear. Only two reports in the ophthalmic literature have demonstrated the clinical course of subretinal bleeding and have indicated that it might be a precursor of lacquer cracks. In this study, the authors observed the clinical course of subretinal bleeding in highly myopic eyes and studied this condition in relation to new lacquer crack formation. METHODS: The authors examined consecutively and prospectively 22 highly myopic eyes (19 patients) with subretinal bleeding. Indirect ophthalmoscopy and fluorescein fundus angiography were performed in all patients. Indocyanine green (ICG) angiography could be performed in three patients. The follow-up period ranged from 6 to 198 months (mean, 61.3 months). RESULTS: In 17 of 22 eyes, lacquer cracks appeared at the site of previous subretinal bleeding. The period for the formation of new lacquer cracks after the onset of the bleeding ranged from 2 to 6 months (mean, 4.0 months). In one patient, ICG angiography revealed linear hypofluorescence, indicating a ruptured Bruch's membrane at the onset of subretinal bleeding. CONCLUSION: A rupture of Bruch's membrane and choriocapillaris complex results in subretinal bleeding, which is the first process of new lacquer crack formation. Atrophy of the overlying pigment epithelium and further scar formation results in the development of a lacquer crack.

Adolescent

Posterior routes of choroidal blood outflow in high myopia.

PURPOSE: A few reports in the ophthalmic literature have described choroidal blood outflow through posterior routes. Most of the patients reported were highly myopic; therefore, a correlation between such posterior routes and high myopia has been suspected. The authors examined highly myopic eyes using indocyanine green (ICG) videoangiography and investigated the prevalence and clinical significance of posterior routes in them. METHODS: The authors examined 255 highly myopic eyes (146 patients) using ICG videoangiography. All had refractive errors greater than--8.25 diopters (D). They also examined a control group consisting of 42 eyes (26 patients) that had refractive errors within +/- 3D. RESULTS: Of 255 highly myopic eyes, 61 (23.9%) had choroidal blood outflow through posterior routes. These routes were classified by type of vein according to its penetration site. One drained into the margin of the optic nerve head, and the other penetrated the sclera near the macula. However, only 1 of the 42 eyes (2.4%) in the control group showed choroidal outflow by a posterior route. The prevalence of posterior routes was significantly higher in the highly myopic eyes than in the control group (P < 0.05). CONCLUSION: Posterior routes of choroidal blood outflow were observed in nearly 25% of highly myopic eyes. These vessels appear to be one of the major routes of posterior choroidal outflow in highly myopic eyes.

Adolescent