[Immature trabecular meshwork in juvenile open-angle glaucoma].
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Biomedical subjects
Publications and source records attributed to H Inomata.
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A case of primary orbital hemangiopericytoma was reported. A 44-year-old woman was first seen at our clinic in June 1970, complaining of exophthalmos of the right eye. On examination, the right eye showed a 6-mm proptosis and an upward displacement. Cerebral angiography revealed a vascularized mass occupying the lower and mid orbit. The tumor was surgically removed and diagnosed histologically as hemangiopericytoma. After the initial surgery, recurrent tumors in the right orbit were resected twice, in June 1975 and December 1979. The purpose of this presentation is to discuss the clinicopathologic features of the tumor. In addition, it is emphasized that hemangiopericytomas originating from the orbit or brain may be histopathologically identical to angioblastic meningiomas.
This paper reports the occurrence of candidal chorioretinitis in a 78-year-old male patient with malignant lymphoma. Macroscopically there were multiple lesions observed in the posterior pole of the left fundus. A main lesion, white, elevated and associating with hemorrhage, was present laterally to the macula and small, white satellite lesions were found scattered. Histopathologically the lesions showed typical features of candidiasis including suppurative and granulomatous chorioretinitis. It seems this is only the second reported case of ocular candidiasis without other organ involvement in the literature. It was suggested that candidal infection possibly occurred only in the eye.
Experimental macular edema of commotio retinae was studied in rhesus monkeys. Clinically, opacification of the retina in these experimental animals closely resembled commotio retinae of man. No pigment epithelial damage was detected by ophthalmoscopy and fluorescein angiography showed no leakage from the retinal and choroidal circulations in the macular region. Histologically, macular swelling was apparent and was due primarily to changes of the outer plexiform layer. In this layer, swelling of the axons of the photoreceptor cells was prominent. Intracellular edema was also detected in the Müller cell processes in the inner retina and in the pigment epithelial cells. Prominent changes also occurred in the inner and outer segments of the photoreceptor cells. Disruption of the blood-retinal barrier was not found using horseradish peroxidase as a tracer. We concluded that retinal opacification was due to disagreement and intracellular edema of the cellular elements of the retina, perhaps a direct result of movement of intracellular fluid in response to mechanical injury.
Histopathology of a clinically observed pipestem sheathed vessel in the retina was studied by electron microscopy. This vessel was characterized by a marked increase and disarrangement of collagen fibrils in the media and adventitia, and invasion of the cytoplasmic processes of Müller cells into the adventitia. The lumen of the vessel was extremely narrow but was preserved with healthy endothelial cells. It is suggested that increased and disarranged collagen fibrils in the vessel wall is related mainly to the ophthalmoscopic appearance of the pipestem sheathing. The infiltration of glial cells in the vessel wall may be of less significance to the pipestem sheathing.
A case of sarcoidosis with ocular involvement, including uncommon tumorous mass formation on the bulbar conjunctiva, was reported. The patient was a 62-year-old woman who had been suffering from chronic bronchiolitis for several years. The conjuctival masses, yellowish brown in color with localized injection and follicles, were found in both eyes. In addition to the conjunctival masses, the common manifestations of sarcoidosis were observed in the eyes, showing nodules on the iris and trabeculum, discrete fluffy "snowball" opacities in the vitreous, and perivascular nodules on the retinal vessels. Microscopically, the biopsy specimen obtained from he conjunctival masses was composed of epithelioid tubercles with Langhans type and foreign body type giant cells. Ziehl-Neelsen stain revealed no tuberculous bacilli. Transbronchial lung biopsy also revealed epithelioid tubercles. Both ocular and pulmonary lesions were observed to respond well to treatment with corticosteroid hormone. We emphasized that patients with interstitial pneumonitis or pulmonary fibrosis should be examined ophthalmologically, and recommended conjunctival biopsy in patients with suspected sarcoidosis.
We presented a familial case of congenital microcoria associated with late onset congenital glaucoma. The proband, a 36-year-old man, had abnormally small pupils with diameters of 3.5 mm in the right eye and 1.5 mm in the left. Mydriatics, such as 1.25% epinephrine, 5% neosynephrine, 5% tyramine, and 1% atropine did not dilate the pupils fully. The iris showed poor development of collarettes and crypts, and lacked circular contraction folds bilaterally. Gonioscopic examination revealed developmental anomalies of the anterior chamber angles in both eyes. Abundant iris processes, which fused together partially in the right and circumferentially in the left, inserted from the iris root onto the scleral spur or further near to the Schwalbe's line. Applanation tonometry measured high intraocular pressure in both eyes. The anterior chamber angle tissues obtained by trabeculectomy were studied histopathologically. In the trabecular meshwork, a thick endothelial meshwork with many layers of cells embedded in prominent extracellular materials was observed on the canal side. On the anterior chamber side, there were several layers of trabecular sheet. These findings indicate underdevelopment of the trabecular meshwork. We examined three generations of his family and found that 5 members showed bilateral congenital microcoria, and another, deceased, was said also to have had congenital microcoria. All 5 surviving patients (3 males and 2 females) with microcoria were found to have bilateral goniodysgenesis also. Two of the 5 were affected with bilateral late onset congenital glaucoma. The congenital disorders in this family, congenital microcoria and goniodysgenesis, appeared in close relation, and were transmitted by autosomal dominant inheritance.
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Distribution of microglia cells was studied in the normal retina of Wistar rats kept in a specific-pathogen-free condition, using a combined technique of light and electron microscopy with the weak silver carbonate staining method of del Rio-Hortega. Typical microglia cells were found mainly in the inner plexiform layer. By electron microscopy these cells were easily identified by metallic deposition in the cells, and had a small oval nucleus with a prominent chromatin pattern, which was one of the most characteristic features of the cell. Based upon these fine structures, microglia cells were identified in the nonimpregnated, ordinarily prepared retina by electron microscopy. These cells contained lysosomes, lipofuscin granules, Golgi apparatus, and long, narrow cisternae of rough-surfaced endoplasmic reticulum mainly at both sides of the perikaryon. These features were identical with those of microglia cells in the central nervous system. Microglia cells were found to be widely distributed in the inner portion of the retina, most of the cells locating closely to ganglion cells or capillary walls, and occasionally in the inner plexiform layer. The nuclear feature of the cell was also recognizable by light microscopy in 1-micron-thick Epon sections stained with toluidine blue. Serially cut thick sections of the retinal ribbon revealed that microglia cells were widely distributed from the peripapillary to the ora serrata region. From the present study, it is concluded that the microglia cell can be considered a component of the normal retina. This is the first report on the precisely described fine structures of the retinal microglia cells.
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An 18-year-old Japanese boy with optic disk drusen associated with left central retinal artery occlusion was reported. Transient central blurred vision, possibly caused by central retinal artery spasm, was noticed as an initial symptom of optic disk drusen in the left eye. Prolonged and repeated spasm might have given rise to a central retinal artery occlusion followed by neovascular glaucoma. The relationship between drusen in the disk and intrapapillary circulation disturbances was discussed.
We examined nine specimens of anterior chamber angle tissue obtained by trabeculectomy from seven patients with early-onset congenital glaucoma and one patient with late-onset congenital glaucoma by light and electron microscopy and compared them with specimens of trabecular meshwork from normal human and monkey eyes. One eye with early-onset congenital glaucoma had no Schlemm's canal. In all cases of congenital glaucoma, we observed a thick subcanalicular tissue with a structure similar to that seen in the endothelial meshwork beneath the inner wall of Schlemm's canal. There were abnormal deposits of ground substances that resembled basement membrane. Additionally, histologic studies of eyes from premature infants obtained at autopsy showed that trabecular sheet-formation initially occurs on the anterior chamber side of the trabeculum and advances gradually toward Schlemm's canal and that the undifferentiated portion of the trabeculum remains as endothelial meshwork beneath the inner wall of Schlemm's canal. Our observations strongly suggest that the existence of the thick subcanalicular tissue, which is considered to be endothelial meshwork, indicates an immature stage of the trabecular meshwork and may be one of the primary causes of increased intraocular pressure in congenital glaucoma.
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The ionic mechanism of excitation in intestinal smooth muscles has been reviewed. Mammalian smooth muscles are a very important group of excitable cells. There exists a considerable number of reports on the electrical and mechanical properties of these muscles. But little work has been done on the analysis of ionic mechanism of this excitable process. The recent successful application of the voltage-clamp technique using the double sucrose gap method has opened a new path for the study of the ionic mechanism in smooth muscles. In intestinal smooth muscle cells, the fast inward current responsible for spike generation is carried principally by the influx of Ca ions and not by Na ions. The outward currents which participate in the rate of repolarization are mainly carried by efflux of K ions. Sr ions and Ba ions can carry the current through the Ca channel. That is, Sr and Ba can substitute for Ca in generation of the fast inward current. The inactivation curve of the inward current of intestinal smooth muscle cells deviates from that of nerve cells and skeletal muscle cells in its hyperpolarizing range. Such an inactivation observed in the hyperpolarizing range is referred to hyperpolarizing inactivation. It seems likely that hyperpolarizing inactivation in smooth muscles is mainly due to the fast outward current. The electrophysiology of smooth muscles has made a remarkable advance lately due to the introduction of the double sucrose gap method. There exist, however, some serious limitations on the voltage control in this method and more quantitative, more accurate information can be expected upon further improvements of the voltage-clamp technique.