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Biomedical subjects

H Oda

Publications and source records attributed to H Oda.

535 records · Page 30Linked to original sources

Enlargement of the lumbar vertebral canal in lumbar canal stenosis.

A new surgical technique, enlargement of the spinal canal, was carried out on eight patients with lumbar canal stenosis. The conditions of all the patients have improved, and there have been no complications so far. A laminectomy is performed in which both sides of the pars interarticularis are cut out with an osteotome to eliminate the cause of the stenosis. The ventral side of the removed lamina is then ground with a surgical air drill to enlarge the posterior area of the lumbar canal. The lamina is subsequently replaced and fixed with screws. This method makes it possible to remove the cause of the stenosis. By replacing the removed lamina, the additional advantage of avoiding weakening vertebral stability is afforded.

Constriction, Pathologic↗

Substratum-bound elastin peptide inhibits aortic smooth muscle cell migration in vitro.

Migration of smooth muscle cells (SMCs) of the media through the internal elastic lamina to the intima in response to various chemoattractants is considered to be an important event in the development of atherosclerosis. We evaluated the influence of elastin peptides prepared from normal aorta on migration of cultured rat aortic SMCs in vitro. Studies with filters coated with elastin peptides in a modified Boyden's chamber showed that the migratory response of cultured rat aortic SMCs in response to platelet-derived factors was impeded by filter-bound elastin peptides. The inhibitory effect appeared to be relatively specific for elastin peptides and for SMCs, as other matrix components (Types I, III, IV, and V collagens and fibronectin) did not impede SMC migration, and polymorphonuclear leukocytes were not impeded by elastin peptides. Elastin peptides in solution in the lower well caused the migratory response, and this response was also inhibited by filter-bound elastin peptides. Attractants such as platelet-derived factors and elastin peptides are likely to be present in the matrix around migrating SMCs. These studies suggest that elastin peptides adhering to the substratum or elastin, a major component of elastic fiber, may be one of the natural inhibitors of vascular SMC migration in response to chemoattractants in the fluid phase.

Animals↗

Role of transforming growth factor-beta 1 and -beta 2 in ddY mouse nephropathy.

We investigated the glomerular distribution of transforming growth factor-beta (TGF-beta 1 and TGF-beta 2) protein and the expression of its mRNA, and related factors, in ddY mice, aged 5-60 weeks, before and after the onset of nephropathy, TGF-beta 1 protein expression was observed from the age of 20 weeks onwards, peaking at 50 weeks, and then declining. Expression of TGF-beta 2 protein gradually increased from 5 to 60 weeks. TGF-beta 1 and TGF-beta 2 mRNA were both detected from 5 to 60 weeks. The mesangial matrix expansion index (MMEI) was significantly higher in mice with nephropathy than in those without nephropathy, as was the expression of TGF-beta 1 and TGF-beta 2 proteins (P < 0.05). TGF-beta 2 was significantly positively correlated with the MMEI (P < 0.05). Infiltration of CD68-positive monocytes/macrophages gradually increased until 60 weeks, and was significantly correlated with the expression of TGF-beta 1 (P < 0.05) and TGF-beta 2 (P < 0.01). These findings indicate that TGF-beta 1 and TGF-beta 2 were overexpressed in ddY mice with overt nephropathy compared with pre-nephropathic mice. TGF-beta 2 may be an important mediator of mesangial matrix expansion in ddY mouse nephropathy.

Aging↗

[Indications for percutaneous transvenous mitral commissurotomy: evaluation according to the Sellors classification].

Fifty-eight consecutive patients underwent percutaneous transvenous mitral commissurotomy (PTMC) for mitral stenosis from August 1987 to June 1990. Patients were divided by echocardiographic characteristics of the mitral valve according to the Sellors classification into three groups: group 1 (mobile cusps, 20 patients), group 2 (thickened cusps, 34 patients), group 3 (rigid cusps, 4 patients). Immediately after PTMC, the mitral valve area increased significantly from 1.41 +/- 0.37 to 2.07 +/- 0.38 cm2 (p < 0.01) in group 1 and from 1.09 +/- 0.21 to 1.64 +/- 0.25 cm2 (p < 0.01) in group 2. The mitral valve area did not increase significantly in group 3 (from 0.82 +/- 0.27 to 1.10 +/- 0.22 cm2). Mitral regurgitation developed or increased in severity in four patients (100%) in group 3 (p < 0.01 vs group 1, 20% and group 2, 21%). The symptomatic improvement was 0% for group 3 (p < 0.01 vs group 1, 90% and group 2, 91%). At follow-up period (mean 24.6 months), symptomatic improvement was maintained in 44 patients (76%) of the total patient population. The mitral valve area was maintained well in group 1 and group 2, but three patients in group 2 showed recurrence of symptoms due to valvular restenosis. PTMC is an effective nonsurgical treatment for patients with mobile or with thickened cusps. Surgical method is preferable for patients with rigid cusps.

Adult↗