Biomedical subjects

E Sho

Publications and source records attributed to E Sho.

4 recordsLinked to original sources

PubMed2001

Molecular mechanisms of aortic wall remodeling in response to hypertension.

OBJECTIVE: The molecular basis of vascular response to hypertension is largely unknown. Both cellular and extracellular components are critical. In the current study we tested the hypothesis that there is a balance between vascular cell proliferation and cell death during vessel remodeling in response to hypertension. METHODS: A midthoracic aortic coarctation was created in rats to induce an elevation of blood pressure proximal to the coarctation. The time course was 1 and 3 days and 1, 2, and 4 weeks for the study of the proximal aorta. Ribonuclease protection assay and Western blot analysis were used to evaluate gene expression of growth and apoptosis-related cytokines with two sets of multiple probes, rCK-3 and rAPO-1. Cell proliferation was determined with BrdU (5-bromo-2'-deoxyuridine) incorporation. Apoptosis was examined with TUNEL (transferase-mediated dUTP nick end-labeling). Morphometry was performed on histologic sections. RESULTS: Coarctation produced hypertension in the proximal aorta, 118 +/- 9 mm Hg versus 94 +/- 6 mm Hg in controls (P <.002). Both messenger RNA and protein levels of transforming growth factor (TGF)-beta1 and TGF-beta3 were increased (P <.005 vs controls). Messenger RNA and protein of Bcl-xS and Fas ligand, known as proapoptotic factors, were both reduced after coarctation (P <.005 vs controls). There was increased BrdU incorporation at 3 days and 1 and 2 weeks (P <.001 vs controls). There were no remarkable changes in the apoptosis rate until 4 weeks later. CONCLUSION: Cell proliferation was stimulated at 3 days, and apoptosis was halted until 4 weeks. These changes were associated with upregulation of TGF-beta and downregulation of Bcl-xS and Fas ligand gene expression. These findings suggest that a coordinated regulation of cell proliferation and cell death contributes to arterial remodeling in response to acute sustained elevation of blood pressure. Cell proliferation precedes apoptosis by 2 weeks in this procedure.

Animals↗

PubMed2001

Blood flow decrease induces apoptosis of endothelial cells in previously dilated arteries resulting from chronic high blood flow.

We investigated apoptosis of endothelial cells during the arterial narrowing process in response to reduction in flow. The decrease in flow was created in the carotid artery by closure of an arteriovenous fistula (AVF), which had been established for 28 days in rabbits. The endothelial cell apoptosis in the carotid artery was studied at 1, 3, 7, and 21 days of flow reduction after closure of the AVF by use of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) with laser scanning confocal microscopy and transmission and scanning electron microscopy. After AVF closure, arterial lumen diameter was reduced by 36%, and compared with endothelial cells before the closure, the number of endothelial cells was decreased by 45% at 21 days. Endothelial cell apoptosis was observed at 1 day, peaked at 3 days (381.3+/-87.1 cells per square millimeter), and decreased at 7 days. These cells had irregular protrusions under scanning electron microscopy and were characterized by fragmented nuclei under transmission electron microscopy. Apoptotic cells were mainly beneath the endothelium and were occasionally within smooth muscle cells and endothelial cells. The results suggest that apoptosis of endothelial cells may play a role in the arterial remodeling in response to a reduction in flow.

Animals↗

PubMed1988

Degenerative spondylolisthesis. Pathophysiology and results of anterior interbody fusion.

With special attention to the articular facets, an inspection of dry human spinal columns, microradiographic studies of cadaveric specimens, and animal experiments revealed that development of degenerative spondylolisthesis is attributable to rotational strain on the facetal joints at the level of involvement. Disc degeneration predisposes to intersegmental instability and rotational strain, which result in secondary osteoarthritic change of the articular processes and segmental canal stenosis. Thirty-six patients with degenerative spondylolisthesis were treated with anterior interbody fusion (AIF) for segmental canal stenosis at the authors' hospital during 1958-1985. The surgical results of these patients reveal that AIF corrects malalignment of the lumbar spine by complete discectomy, reduces the slip and restores the disc height, and resolves nerve compression, both from the front and from behind, by enlargement of the stenosing canal. In addition, AIF has consistent and satisfactory clinical results at long-term follow-up evaluation because it resolves intersegmental instability, an important problem of degenerative spondylolisthesis. AIF is a reasonable and reliable treatment for patients younger than 60 years of age with segmental stenosis.

Adult↗

PubMed1984

Anterior discectomy and interbody fusion for lumbar disc herniation. A review of 350 cases.

Based on the follow-up evaluation of 350 patients in whom lumbar disc herniation was treated by anterior discectomy and interbody fusion from 1955 to 1982, 94.3% of the patients obtained bony union and justified the principle of interbody stabilization of the spine. The normalization of the myelographic pattern observed after surgery indicates that sufficient nerve decompression can be obtained by this procedure. The good clinical results may be attributed to the restoration of disc height and to the correction of spinal alignment. The good results observed in long-term follow-up evaluation of 223 patients and the fact that most of the patients resumed their former work after surgery provide further testimony of the value of interbody fusion. The procedure is indicated in young adults, physical laborers with low back pain and sciatica, and patients with spinal instability.

Adolescent↗