[Studies on the alkaloids of magnoliaceous plants. XXXVII. Alkaloids of Magnolia obovata Thunb].
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Biomedical subjects
Publications and source records attributed to A Yoshida.
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Usual human livers contain two major ALDH isozymes, i.e., cytosolic ALDH1 and mitochondrial ALDH2, while approximately 50% of Orientals are "atypical" and have only the ALDH1 and are missing the ALDH2. Instead, the atypical livers contain an enzymatically inactive but immunologically cross-reactive material (CRM) corresponding to the ALDH2 component. Some Orientals are found to be atypical also in the ALDH1 locus, i.e., they are missing the enzymatically active ALDH1 but contain a large amount of CRM corresponding to the ALDH1 component. cDNA for ALDH1 and that for ALDH2 were cloned and their nucleotide sequences were determined. The amino acid sequences of ALDH1 and ALDH2 were deduced from their cDNA sequences. The molecular abnormality of the inactive ALDH2(2) is found to be the substitution of Glu at the 14th position from the COOH-terminal of the protein by Lys which resulted from G----A transition in the gene.
BACKGROUND: To report an Asian patient with branch retinal vein occlusion secondary to neurofibromatosis 1. CASE: A 64-year-old woman presented with a loss of vision in her right eye of 9-month duration. A diagnosis of neurofibromatosis 1 was made. A general medical examination showed no abnormalities except the signs of neurofibromatosis 1. OBSERVATIONS: Fundus examination of the right eye revealed irregularities of the venous caliber, partial sheathing of the corresponding vein and macular edema. Multiple dilated and tortuous collateral channels and an arteriovenous communication bridged the perfused and nonperfused retina. Fundus examination of the left eye showed a tortuous vein in the temporal region of the fovea. Fluorescein angiography of the right eye confirmed delayed filling in a superotemporal artery and in the corresponding vein. The temporal region of the fovea had large areas of capillary loss. The collaterals were tortuous and mimicked a neovascularization. Fluorescein angiography of the left eye confirmed that the vein in the temporal part of the fovea was tortuous and not leaking. A diagnosis of branch retinal vein occlusion of the superotemporal vein was made. CONCLUSIONS: Neurofibromatosis 1 should be considered in the differential diagnosis of retinal vascular occlusive disease without other risk factors.
To determine the mechanisms of vitreous liquefaction following vitreous hemorrhage, we investigated the effects of the free radicals produced by a bilirubin-sensitized photochemical reaction on collagen and hyaluronic acid (HA). Bovine vitreous collagen and HA were irradiated by visible light in the presence of bilirubin, which is produced from the degradation of hemoglobin, as a photosensitizer. Changes in molecular weight were monitored by sodium dodecyl sulfate-polyacrylamide gel electrophoresis for the collagen, and high-performance liquid chromatography for the HA. We found that free radicals caused an increase in high-molecular-weight components and insolubilization of the vitreous collagen, and a decrease in the molecular weight of HA. The changed molecular properties of the vitreous collagen could be attributed to the extensive cross-linking of the molecules. This cross-linking and the degradation of HA, both induced by the bilirubin-sensitized photochemical reaction, may contribute to vitreous liquefaction following vitreous hemorrhage.
A 37-year-old man presented with an optic nerve pit and serous macular detachment of the left eye. Scanning laser ophthalmoscopy revealed a cyst-like structure terminating at the pit in the premacular vitreous. During ocular movement, this structure moved vigorously and seemed to exert traction on the pit. We believe that it is part of an anomalous Cloquet's canal, and that traction on the pit may be a significant factor in the development of serous macular detachment in this patient.
PURPOSE: To investigate the vitreous findings in patients with cicatricial retinopathy of prematurity (ROP) who underwent retinal cryopexy and/or photocoagulation during the acute phase of the disease. METHODS: Vitreous findings were evaluated in 15 patients (29 eyes) with cicatricial ROP by slit-lamp biomicroscopy and indirect ophthalmoscopy. RESULTS: The ocular examination revealed that all eyes had extensive vitreous liquefaction that affected a large segment of the vitreous. A great deal of fibrillar condensation of the vitreous was present in membrane-like vitreous fibers that traversed the vitreous cavity to the periphery of the degenerating retina. These vitreous changes were most marked in the areas in which retinal cryopexy and/or photocoagulation had been performed. Despite advanced liquefaction, the posterior cortical vitreous was not separated from the retina in any eyes. CONCLUSION: In eyes with ROP that underwent retinal cryopexy and/or photocoagulation during the acute phase of the disease, the vitreous was abnormal, which may contribute to vitreoretinal traction that eventually leads to retinal breaks and detachment.
BACKGROUND: The pathogenesis of age-related macular degeneration (AMD) remains unknown. Genetic and environmental factors are thought to be associated with AMD. Although some studies have reported familial cases of AMD in the United States, as far as we know, familial cases of AMD have rarely been reported in Japan. CASES: We describe three families with two members of each family affected with AMD and one family with three affected members. OBSERVATIONS: In one family, two siblings were affected with AMD with choroidal neovascularization and two other siblings had retinal pigment epithelial abnormalities or drusen of the maculas, suggesting the heterogeneity of the maculas in the family. However, the other families did not show such heterogeneity of the fundus. Among the four families, six of nine affected individuals had a smoking habit, a risk factor for AMD. CONCLUSIONS: These findings suggest that the development and progression of AMD might be associated with genetic factors and environmental factors.
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Anterior capsular and ligamentous injuries occur frequently at initial traumatic shoulder dislocation. However, these injuries have not been considered to be one of the main causes of recurrent anterior dislocation, which is believed to heal spontaneously. We evaluated five joints of five patients in which tears in the middle portion of the anterior capsule including the inferior glenohumeral ligament were considered to be the main cause of recurrent dislocation. History of present illness and physical and plain x-ray results were not specific. The only specific finding was a diverticulum-like expansion at the anteroinferior portion of the joint on arthrographic computed tomography. Treatment consisted of anatomic repair of the capsule and concurrent injuries. The outcome of the three cases in which at least 2 years had passed after surgery was excellent. The point of emphasis is that tears of the anterior capsule are one of the primary lesions in recurrent anterior dislocation.
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