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Biomedical subjects

Y Mukai

Publications and source records attributed to Y Mukai.

85 records · Page 5Linked to original sources
PubMed1983

Ultrastructure of the congenital epulis.

This report presents the ultrastructural features of a congenital epulis. The granular cells of the epulis were packed with numerous membrane bound cytoplasmic granules containing particles, small vesicles, and electron-dense materials. These granules were negative in immunohistochemical reaction for CEA (DAKO PAP KIT). Cytoplasmic organelles such as mitochondria, rough surfaced endoplasmic reticulum, and Golgi apparatus, were absent. Nuclei were markedly indented. Occasionally, banded intracellular collagen fibrils were observed within the cytoplasm. Some of these fibrils were surrounded by a limiting membrane, whereas others appeared to lie free in the cytoplasm. The collagen fibrils were also seen within a deep invagination of the cell surface. There was no basal lamina around the granular cells. Sporadically, mast cells with many granules containing lamellar formations were found between the granular cells. These observations support the idea that granular cells of the congenital epulis are derived from mesenchymal cells, probably fibroblasts.

Basement Membrane↗
PubMed1980

Ultrastructrual studies on choroidal vessels in streptozotocin-diabetic and spontaneously hypertensive rats.

Seven spontaneously hypertensive rats (SHR) and 14 Wistar inbred Kyoto strain rats (WKR) were used. Seven WKR were made diabetic by a single intravenous injection of streptozotocin (50 mg/kg body weight); the seven untreated WKR served as controls. The choroidal vessels of all rats were observed by electron microscopy after 12 months. The choroidal capillaries of control rats showed focal accumulation of basement (BM) in the subendothelial space. Two distinct types of BM lesions were noted: homogeneous thickening and sparse, interlacing branches, or ramifications, of BM. Increased BM caused indentations in the vascular wall. In diabetic rats, BM of capillaries, small arteries, and small veins showed arabesque ramification of BM which represented advanced forms of the sparse, interlacing ramifications seen in normal controls. Contiguous lesions of ramified BM, separated by narrow cytoplasmic processes projecting from the endothelial cells, resembled a scalloped border. In hypertensive rats, the arabesque ramifications were most conspicuous in the small veins. Homogeneous thickening of BM was noted in choroidal capillaries, small arteries, and small veins of SHR, although ramified BM was seen adjacent to it. Endothelial cell proliferation was seen in the small arteries of diabetic and hypertensive rats. The cytoplasm of endothelial cells at the lesion of proliferation was broadened, and cell nuclei appeared cubic or spherical. Consequently, the arterial lumina were narrowed. Complete occlusion was seldom seen in the choroidal arteries of diabetic rats, but it was observed in small arteries of SHR, accompanited by hypertrophy of medial smooth muscle cells and endothelial proliferation. Basement membrane accumulation and endothelial proliferation were common to both groups of rats, but the overall effect of pathological changes was more profound in hyptertension than in diabetes.

Animals↗
PubMedDate not supplied

Effect of a solution with high fluoride concentration on remineralization of shallow and deep root surface caries in vitro.

A root dentin single-section model was developed to compare the efficacy of different fluoride treatments on the remineralization of lesions. Shallow ( approximately 170 microm) and deep ( approximately 400 microm) lesions were produced in acetic acid buffer solutions (pH 5.0) with 0.1- and 0.5-ppm fluoride for 3 days and 2 weeks, respectively. Next, the sections were pH-cycled for 4 weeks. Following the pH cycling, all sections were first remineralized for 5 weeks, then subjected to 10 days of demineralization. The treatments were (1) no treatment (control), (2) daily 1,450-ppm NaF toothpaste, (3) weekly 4,000-ppm fluoride solution, (4) a combination of treatments 2 and 3. In the shallow lesions, the 4,000-ppm fluoride solution and the combination treatment enhanced mineral deposition at the lesion front, producing a second, slightly hyperremineralized layer. Similarly, in the deep lesions a second remineralized layer was detected. In all lesions, the fluoride solution treatment showed significantly more remineralization compared to the control and the toothpaste treatment (p<0.05), most of which was formed during the pH cycling. In the demineralization period, the control showed significantly higher mineral loss than all other treatments. These results indicate that a 4,000-ppm fluoride solution might be effective for remineralization of root dentin lesions even over 400 microm depth.

Acetates↗
PubMedDate not supplied

Remineralization of advanced root dentin lesions in vitro.

The possibility for remineralization of advanced root dentin lesions was investigated in vitro. Lesions were produced in acidic buffer solution with 0.1 and 0.5 ppm fluoride, for 3 and 5 weeks, respectively, using a single-section model. Next, the sections were immersed in a remineralization solution containing 0.1 ppm F (as NaF) for 20 weeks. Microradiographs were made after each 4-week-period. The lesions were around 500 micro m deep, with mineral loss values between 11,000 and 18000 vol%.microm. After 20 weeks of remineralization, the absolute amounts of deposited mineral ranged from 7500 to 10000 vol%. micro m, corresponding to a repair between 50 and 85%. Lesion depth was, on average, reduced by 199 micro m. This was not significantly different (at p < 0.05) between the four experimental groups. This study showed that remineralization of advanced dentinal lesions is possible in spite of the virtual absence of mineral in the lesion body after demineralization. The surface layer of the lesion was the preferred site for mineral deposition until mineral content values reached those of sound dentine. The mineral content in the lesion body increased with time, at a rate reflecting the initial severity of the lesion. We conclude that a remineralized surface layer does not inhibit transport of mineral ions to the body and that the remineralization in the lesion body reflected the number of sites for crystal growth.

Analysis of Variance↗