PubMed Health⌕ Search

Biomedical subjects

S Urayama

Publications and source records attributed to S Urayama.

At least 37 records · Page 2Linked to original sources
PubMed1999

Induction of cyclooxygenase-2 in human synovial cells by beta 2-microglobulin.

BACKGROUND: Prostaglandins (PGs) are important mediators of inflammation in arthritis. We evaluated the role of the cycloxygenase-2 (COX-2) enzyme, which regulates PG biosynthesis, in osteoarthropathy associated with hemodialysis-associated amyloidosis (HAA) by characterizing COX-2 expression in beta 2-microglobulin-treated human synovial cells. METHODS: We examined the effects of beta 2-microglobulin (beta 2m), a major constituent protein of amyloid fibrils in HAA, on the COX-2 protein and mRNA expression in human synovial cells using Western blot and reverse transcriptase-polymerase chain reaction. RESULTS: beta 2m selectively increased the biosynthesis of COX-2 protein and induction of COX-2 mRNA in a dose-dependent manner. Immunoabsorption of beta 2m-containing media by anti-beta 2m-specific antibody abrogated beta 2m-mediated COX-2 expression on synovial cells. On the other hand, dexamethasone markedly suppressed the induction of COX-2 protein and mRNA in beta 2m-stimulated synovial cells. CONCLUSIONS: Our results suggest that induction of COX-2 expression by beta 2m may be an important component of the inflammatory process in hemodialysis-associated osteoarthropathy.

Blotting, Western↗
PubMed1998

Dexamethasone protection of rat intestinal epithelial cells against oxidant injury is mediated by induction of heat shock protein 72.

Although the therapeutic actions of glucocorticoids are largely attributed to their anti-inflammatory and immunosuppressive effects, they have been implicated in enhancing tissue and cellular protection. In this study, we demonstrate that dexamethasone significantly enhances viability of IEC-18 rat small intestinal cells against oxidant-induced stress in a dose-dependent fashion. This protective action is mediated by induction of hsp72, the major inducible heat shock protein in intestinal epithelial cells. Dexamethasone stimulates a time- and dose-dependent response in hsp72 protein expression that parallels its effects on cell viability. Furthermore, the induction of hsp72 is tissue dependent, as nonintestinal epithelioid HeLa cells show differential induction of hsp72 expression in response to the same dexamethasone treatment. Antisense hsp72 cDNA transfection of IEC-18 cells abolishes the dexamethasone-induced hsp72 response, without significantly affecting constitutive expression of its homologue, hsc73. Dexamethasone treatment also significantly induces hsp72 protein expression in rat intestinal mucosal cells in vivo. These data demonstrate that glucocorticoids protect intestinal epithelial cells against oxidant-induced stress by inducing hsp72.

Animals↗
PubMed1998

Night blindness secondary to vitamin A deficiency in a patient with bile duct strictures after liver transplantation.

Vitamin A deficiency and resulting night blindness have previously been reported in patients with chronic liver disease before undergoing liver transplantation. Because early identification of patients with vitamin A deficiency can lead to the relief of symptoms and the prevention of irreversible retinal degeneration, vitamin A deficiency should always be considered in the differential diagnosis of visual disturbances in patients with liver disease. We describe a case of night blindness due to vitamin A deficiency resulting from bile duct strictures in a post-orthotopic liver transplant patient and its successful resolution with vitamin A supplementation.

Cholestasis↗
PubMed1998

Insulin-like growth factor I stimulates proliferation and Fas-mediated apoptosis of human osteoblasts.

In vitro studies have shown that insulin-like growth factor I (IGF-I) is a potent growth factor for osteoblasts, although both bone formation and resorption are upregulated by IGF-I in vivo. To understand the difference in the action of IGF-I observed in vitro and in vivo experiments, we examined the effect of IGF-I on the proliferation and Fas-mediated apoptosis of human osteoblasts in vitro. Human osteoblastic cell line MG63 and human primary osteoblast-like cells obtained from biopsy specimens were used as human osteoblasts. Cells were cultured with or without various concentrations of IGF-I followed by determination of the proliferative response and Fas-mediated apoptosis. IGF-I dose dependently stimulated the proliferation of cultured human osteoblasts. Both Fas expression and the degree of anti-Fas IgM-induced apoptosis of human osteoblasts was also augmented by IGF-I. Furthermore, the cytotoxicity of Fas ligand (FasL) cDNA transformants against human osteoblasts was increased when IGF-I-stimulated osteoblasts were used as target cells, indicating that stimulation of IGF-I increased functional Fas expression on human osteoblasts as well as their proliferation. The addition of DEVD-CHO, a specific inhibitor of CPP32, to the culture resulted in a significant inhibition of Fas-mediated apoptosis of both unstimulated and IGF-I-stimulated osteoblasts, although it did not affect the proliferative response or Fas expression. Our data suggest that activation of CPP32 is necessary for Fas-mediated apoptosis of human osteoblasts, and treatment of IGF-I increased this signaling pathway. In contrast, regulation of proliferation and Fas expression of the cells were probably not affected by CPP32 activation. Our results suggest that IGF-I acts on cultured human osteoblasts by increasing their proliferation and induction of Fas-mediated apoptosis by neighbouring FasL+ cells such as osteoclasts, thus probably functioning as a local coupling factor in the bone in vivo, stimulating both bone formation and resorption.

Apoptosis↗
PubMed1998

Expression and function of Fas and Fas ligand on peripheral blood lymphocytes in normal subjects.

We investigated the expression and function of Fas and Fas ligand (FasL) on peripheral blood lymphocytes (PBLs). The cells were stimulated with various cytokines or 12-0-tetradecanoyl phorbol 13-acetate (PMA) plus ionomycin. About 30% of unstimulated PBLs expressed Fas, and the expression was augmented by interleukin-1beta (IL-1beta), IL-2, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), or PMA plus ionomycin. Although only minimal FasL expression was detected on unstimulated PBLs, FasL expression was markedly induced by IL-2 or PMA plus ionomycin, suggesting that Fas and FasL were both expressed on IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs. Although IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs were positive for both Fas and FasL, no significant increase in apoptosis was demonstrated in these activated PBLs. In addition, treatment of PBLs with IL-2 or PMA plus ionomycin did not change anti-Fas-induced apoptosis, although these activated PBLs expressed Fas strongly when compared with unstimulated PBLs. Only IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs killed Fas+ target cells efficiently via the interaction of Fas on target cells with FasL of PBLs. Bcl-2 was constitutively expressed on unstimulated PBLs, but its expression was significantly augmented by IL-2 or PMA plus ionomycin. The expression of Bax was clearly induced only on IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs and that of other Bcl-2 family proteins such as Bcl-x and Bad could not be detected on human PBLs, including IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs. Our results suggest that PBLs activated by IL-2 or PMA plus ionomycin express both Fas and FasL and that they kill Fas+ target cells by using FasL on the surface. The resistance of these activated PBLs to Fas-mediated apoptosis may be due to the augmented Bcl-2 expression or the presence of Bcl-2:Bax heterodimers on these cells.

Adult↗
PubMed1998

CD4+ T-cell-mediated cytotoxicity against staphylococcal enterotoxin B-pulsed synovial cells.

Apoptosis of synovial cells in rheumatoid arthritis (RA) synovium determined in vivo is suggested to counteract the overgrowth of synovium. Immunohistological examination has revealed the infiltration of activated CD4+ T cells, which express Fas ligand (FasL), in RA synovium. The presence of a putative antigen (Ag) of autoimmune disorders in a target organ may induce the activation of specific T cells in the inflammatory region such as RA synovium. We examined the possible role of CD4+ T cells activated by synovial cells in a staphylococcal enterotoxin B (SEB)-dependent manner, inducing synovial cell apoptosis. Synovial cells were cultured with or without interferon-gamma (IFN-gamma) and further incubated with CD4+ T cells in the presence of SEB. After the cocultivation, both the cytotoxicity and FasL expression of CD4+ T cells were investigated. Constitutive Fas expression was detected on both unstimulated and IFN-gamma-stimulated synovial cells. CD4+ T cells did not kill SEB-pulsed unstimulated synovial cells efficiently. In contrast, when CD4+ T cells were incubated with IFN-gamma-stimulated synovial cells with SEB whose human leucocyte antigen (HLA)-DR and -DQ expression was markedly induced, significant cytotoxicity by these cells against synovial cells was detected. The addition of anti-HLA-DR and -DQ monoclonal antibodies (mAbs) or human Fas chimeric protein (hFas-Fc) reduced this cytotoxicity. FasL expression of CD4+ T cells cocultured with IFN-gamma-stimulated synovial cells with SEB was significantly induced. Furthermore, the addition of mAbs against CD54, CD58 and CD106 inhibited both the cytotoxicity and FasL expression of CD4+ T cells induced by IFN-gamma-stimulated synovial cells in the presence of SEB, indicating the importance of costimulatory molecules on synovial cells in activating CD4+ T cells. Our results suggest that CD4+ T cells are activated by synovial cells by an SEB-dependent manner and express FasL, inducing Fas-mediated apoptosis of the latter cells. These phenomena may regulate the overgrowth of synovial cells in RA synovium.

Antibodies, Monoclonal↗
PubMed1997

Fas/Fas ligand interaction regulates cytotoxicity of CD4+ T cells against staphylococcal enterotoxin B-pulsed endothelial cells.

Infiltration of activated CD4+ T cells and apoptosis of endothelial cells are present in the synovium of rheumatoid arthritis (RA). Using staphylococcal enterotoxin B (SEB) as an antigen, we examined the possible role of antigen (Ag)-dependent activation of CD4+ T cells by endothelial cells, in inducing endothelial cell apoptosis. The human endothelial cell line, EA.hy926 cells, was cultured with or without interferon-gamma (IFN-gamma) and further incubated with CD4+ T cells in the presence or absence of SEB. After this cocultivation, the cytotoxicity and Fas ligand (FasL) expression of CD4+ T cells were examined. A small percentage of EA.hy926 cells expressed HLA-DR and -DQ, and this expression was significantly augmented after IFN-gamma stimulation. Anti-Fas IgM-induced apoptosis was exhibited by both unstimulated and IFN-gamma-stimulated EA.hy926 cells. Cytotoxicity of CD4+ T cells toward SEB-pulsed unstimulated EA.hy926 cells was detected. Furthermore, when CD4+ T cells were incubated with IFN-gamma-stimulated, SEB-pulsed EA.hy926 cells with augmented HLA-DR and -DQ expression, this cytotoxicity was more significant. The addition of anti-HLA-DR and -DQ monoclonal antibodies (mAbs) or human Fas chimeric protein (hFas-Fc) reduced the cytotoxicity. FasL expression was induced in CD4+ T cells cocultured with SEB-pulsed EA.hy926 cells, especially when the EA.hy926 cells were IFN-gamma-stimulated. Furthermore, the addition of mAbs against CD54 and CD58 inhibited both the cytotoxicity and FasL expression of CD4+ T cells induced by SEB-pulsed EA.hy926 cells, indicating the importance of costimulatory molecules on EA.hy926 cells in activating CD4+ T cells. Our results suggest that CD4+ T cells are activated by endothelial cells in an Ag-dependent manner and subsequently express FasL, which induces Fas-mediated apoptosis of endothelial cells. This phenomenon may counteract the growth of RA synovium by inhibiting the proliferation of endothelial cells.

Antibodies, Monoclonal↗
PubMed1997

An improved computer method to prepare 3D magnetic resonance images of thoracic structures.

The mediastinal and cardiovascular anatomy is complex. We have developed a three-dimensional (3D) reconstruction system for the major mediastinal structures using magnetic resonance imaging data on a NeXT workstation. The program uses a combination of automatic and manual procedures to determine the contours of the cardiac structures. The geometric centers of the contours are connected by a 3D space curve, and the central axis of each cardiac structures is determined. The contours are projected on the perpendicular plane to the central axis and semiautomatically processed until the contours of one pixel are obtained. Then the surface rendering with transparency is performed. Compositing combines two images so that both appear in the composite, superimposed on each other. Demonstration of the various mediastinal lines and cardiovascular diseases by the composits of the partly transparent 3D images has promoted a better understanding of the complex mediastinal and cardiovascular anatomy and diseases.

Heart↗
PubMed1997

Modulation of Fas-mediated apoptosis of human thyroid epithelial cells by IgG from patients with Graves' disease (GD) and idiopathic myxoedema.

The expression of two autoimmune thyroid diseases. GD and idiopathic myxoedema, is associated with antibodies to the thyroid-stimulating hormone (TSH) receptor. Thyroid stimulating antibodies (TSAb) in GD are TSH agonists and cause hyperthyroidism as well as goitre, whereas thyroid stimulation blocking antibodies (TSBAb) in idiopathic myxoedema are TSH antagonists and cause hypothyroidism and thyroid atrophy. We investigated the effect of antibodies to TSH receptor on Fas-mediated apoptosis of thyroid epithelial cells (thyrocytes). Human IgG was isolated from healthy donors, patients with GD and idiopathic myxoedema. Human thyrocytes were obtained from surgical specimens. Thyrocytes were cultured in the presence or absence of human IgG with or without interferon-gamma (IFN-gamma) or IL-1beta for a specified time. After incubation, we examined the level of cAMP in cultured supernatants and both Fas and Bcl-2 expression on thyrocytes. In addition, we examined anti-Fas-mediated apoptosis of thyrocytes. Fas expression on thyrocytes was significantly down-regulated by Graves' IgG and TSH, although idiopathic myxoedema IgG did not affect Fas expression on thyrocytes. Idiopathic myxoedema IgG abrogated the effect of TSH on both cAMP production and inhibition of Fas expression on thyrocytes. Treatment of thyrocytes with IL-1beta or IFN-gamma caused a marked augmentation of Fas expression on thyrocytes. The increase of Fas expression of thyrocytes induced by IL-1beta or IFN-gamma was significantly suppressed in the presence of TSH or Graves' IgG. Anti-Fas-induced apoptosis of thyrocytes was observed in thyrocytes treated with IL-1beta or IFN-gamma, but was markedly inhibited in the presence of TSH or Graves' IgG. Furthermore, idiopathic myxoedema IgG abrogated most of the inhibitory effect of TSH on Fas-mediated apoptosis of thyrocytes treated with IL-1beta or IFN-gamma. Bcl-2 expression of thyrocytes did not change after stimulation with TSH, Graves' IgG, idiopathic myxoedema IgG, IL-1beta or IFN-gamma. These results suggest that TSAb found in Graves' patients may be potentially involved in the development of goitre by inhibition of Fas-mediated apoptosis of thyrocytes. In addition, TSBAb inhibit the action of TSH and increase the sensitivity toward Fas-mediated apoptosis of thyrocytes, inducing thyroid atrophy seen in patients with idiopathic myxoedema.

Apoptosis↗
PubMed1997

Inhibitory effects of interleukin-10 on synovial cells of rheumatoid arthritis.

This paper describes the immunoregulatory effects of interleukin-10 (IL-10) on synovial cells in vitro. Synovial cells were cultured with IL-10 in the presence or absence of various cytokines. Following incubation, the costimulatory molecule expression on synovial cells and cytokine production in culture supernatants were analysed by an indirect immunofluorescence method and enzyme-linked immunosorbent assay, respectively. We also examined the effect of IL-10 on the function of synovial cells as antigen-presenting cells (APC). Synovial cells spontaneously express several kinds of costimulatory molecule and produce various kinds of cytokines. Stimulation of synovial cells with interferon-gamma (IFN-gamma), IL-1 beta, or 12-O-tetradecanoyl phorbol 13-acetate (TPA) markedly enhanced the expression of costimulatory molecules and cytokine production of these cells. Both spontaneous and up-regulated costimulatory molecule expression and cytokine production were significantly suppressed by the addition of IL-10. Autologous T-cell proliferation was stimulated by purified protein derivative (PPD) in IFN-gamma-treated synovial cells and treatment of these synovial cells with IL-10 also suppressed T-cell proliferation. Our results suggest that IL-10 has an inhibitory effect on synovial cells and is an important immunoregulatory component of the cytokine network in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1997

Fas and Fas ligand interaction is necessary for human osteoblast apoptosis.

We investigated the cellular and humoral interactions between peripheral blood mononuclear cells (PBMCs) and human osteoblasts, leading to apoptosis of osteoblasts. Human osteoblastic cell line MG63 and human primary osteoblast-like cells obtained from biopsy specimens were used in this study. PBMCs were isolated from healthy donors and cultured with or without stimulation by recombinant interleukin-2 followed by 12-o-tetradecanoylphorbol 13-acetate with ionomycin. Fas was functionally expressed on MG63 and primary osteoblast-like cells. Activated PBMCs expressed Fas ligand (FasL) strongly on their surface and killed MG63 and primary osteoblast-like cells. Cultured supernatants of activated PBMCs also induced apoptotic cell death of MG63 and primary osteoblast-like cells. In contrast, both unstimulated PBMCs and cultured supernatants of unstimulated PBMCs did not induce apoptosis of these cells. Furthermore, the cytotoxic effect and induction of apoptosis against MG63 and primary osteoblast-like cells by activated PBMCs and cultured supernatants were inhibited significantly by human Fas chimeric protein. Our data showed that human osteoblasts expressed Fas fuctionally and both membrane-type and soluble form FasL from activated PBMCs induced apoptosis of these cells, providing the one possible mechanism of bone loss in inflammatory diseases such as rheumatoid arthritis.

Antigens, Surface↗
PubMed1996

Evaluation of per-procedure equipment costs in an outpatient endoscopy center.

BACKGROUND: As disposable endoscopes become available, we need baseline costs associated with reusable instruments to make financially intelligent choices. Accordingly, we analyzed the per-use cost of several types of gastrointestinal endoscopes at our institution. METHODS: Records of 44 gastrointestinal endoscopes were analyzed. Data defined included purchase price, repair and cleaning expense (labor and materials), and number of uses. The labor cost per-use associated with endoscope cleaning was estimated by taking an average time required to clean an endoscope multiplied by the technician's salary. RESULTS: The average number of years of endoscope use varied from 4.6 to 6.9 years contingent on the type of endoscope. For flexible sigmoidoscopes, the average total cost per use was $8.35, and for colonoscopes the cost was $21.81. For gastroscopes and diagnostic and therapeutic duodenoscopes, costs were $20.99, $49.15, and $45.16, respectively. CONCLUSIONS: (1) Excluding costs associated with the procedure itself (admit-recovery, drugs, disposable equipment, and procedural personnel), total peruse scope cost ranged from a low of $8.35 for the flexible sigmoidoscope to $49.15 for the diagnostic duodenoscope. (2) The most important variables associated with per-use endoscope cost included number of uses, initial purchase price, and repair costs. (3) Techniques such as the above can be used to define per-procedure costs for a particular practitioner or institution.

Costs and Cost Analysis↗
PubMed1996

Mycobacteria and glutaraldehyde: is high-level disinfection of endoscopes possible?

BACKGROUND: High-level disinfection of endoscopes has traditionally been undertaken by manual or automatic scope cleaning plus a 10 to 20 minute soak in 2% alkaline glutaraldehyde. Mycobacteria species are less sensitive to glutaraldehyde, and a 45-minute instrument soak has recently been recommended by the manufacturer. Because of concerns over endoscope damage, need for more endoscopes, and perception that the current cleaning method is adequate, we prospectively studied mycobacteria-contaminated endoscopes at various stages of the cleaning process. METHODS: All work was done under a laminar flow hood in a microbiology laboratory. Five gastrointestinal scopes were contaminated with 10(8) colony forming units per milliliter (CFU/mL) of Mycobacterium chelonei, an atypical mycobacterium similar in chemical resistance to Mycobacterium tuberculosis but with less infectious potential. Cultures of the sheath, biopsy channel, and elevator channel were taken at baseline, after manual cleaning, and after 10, 20, and 45 minutes to glutaraldehyde soak both before and after alcohol rinse. RESULTS: Manual cleaning resulted in a mean of 4.7 log10 reduction in viable mycobacterial colonies. Qualitative studies of the external endoscope surface as well as the air-water valve showed no detectable organisms after a 10-minute exposure to alkaline glutaraldehyde. Conventional quantitative culture techniques of the channels demonstrated one endoscope out of five with consistent growth after a 10-minute exposure to glutaraldehyde. Following alcohol treatment, there was no significant colony growth. In contrast, a quantitative membrane filter system showed the presence of at least one mycobacterial colony in four out of five scopes after a 45-minute glutaraldehyde exposure. CONCLUSIONS: Additional studies utilizing a standardized mycobacterial species, inoculum size, and suspension characteristics are recommended to delineate adequate duration of disinfectant exposure time.

1-Propanol↗
PubMed1995

Three-dimensional display of cardiac structures using reconstructed magnetic resonance imaging.

It is sometimes difficult to understand the three-dimensional (3D) relationship of cardiac and mediastinal structures despite advances in magnetic resonance (MR) imaging techniques. We present a low-cost system for 3D reconstruction of the major mediastinal structures by processing the MR imaging data on a NeXT workstation. MR images of multisection, multiphase, spin-echo techniques stored in a picture archiving and communication system (PACS) data base were used for the reconstruction. The computer program obtained the contours of the multiple components of the mediastinal structures by the combination of automatic and manual procedure. The bundled software of a 3D kit was used for surface rendering of hidden surface removal, shading of the visible parts of the surfaces, perspective transformation, and motion parallax by rotation of the surfaces. 3D reconstruction was performed in 15 patients with cardiac diseases, and the 3D-reconstructed images were compared with the plain chest x rays of the patients. The 3D presentation clearly showed the complex anatomy of cardiovascular diseases and helped elucidate the misconceptions in the interpretation of the plain chest x rays. Our 3D images are used for education and should be viewed by medical students and beginners in radiology at an individual pace with plain chest radiographs, MR images, and legends. Although applied to the heart and the great vessels in this report, this system is also applicable to other structures.

Computer Graphics↗
PubMed1995

Presentation and treatment of annular pancreas in an adult population.

OBJECTIVE: To describe a series of adult patients with annular pancreas, their presentation, and treatment modalities. METHOD: A retrospective chart review of patients seen at a multispecialty referral center from 1977 to 1994. RESULTS: Seven adult patients (ages ranging from 33 to 77 yr, four females and three males) presented with various symptoms and signs: abdominal pain (six patients) gastric outlet obstruction (two), pancreatitis (two), pancreatic mass (two), gastric/duodenal ulcer (one), and/or postoperative obstructive jaundice (one). The duration of symptoms ranged from 1 wk to 16 yr before diagnosis (median 18 months). Upper GI radiography was consistent with annular pancreas in two cases, CT scan in two cases (neither of which actually depicted the annulus), and four of six successful endoscopic retrograde cholangiopancreatographies. Three patients were diagnosed during operative procedures. Five of the seven patients required therapeutic operative procedures that included transduodenal sphincteroplasty, duodenojejunostomy, gastrojejunostomy, subtotal gastrectomy, or Whipple procedure. Four of the five had significant symptomatic relief. In one case, endoscopic sphincterotomy and biliary stent placement was therapeutic. CONCLUSIONS: 1) Annular pancreas occasionally presents in the adult population. 2) Although gastric outlet obstruction was seen in two of seven patients, a plethora of additional presentations included pancreatic mass, pancreatitis, peptic ulcer disease, and post-operative obstructive jaundice. 3) Diagnosis of annular pancreas was most commonly suggested by upper GI series or endoscopic retrograde cholangiopancreatography. However, fully 40% of diagnoses required surgery for confirmation. 4) In contrast to the pediatric population in whom gastrojejunostomy or duodenojejunostomy is the treatment of choice, a variety of surgical as well as interventional endoscopic procedures were utilized for effective treatment in adults with annular pancreas.

Aged↗
PubMed1986

[Histological and ultrastructural study of degeneration of the lumbar intervertebral disc in the rabbit following nucleotomy, with special reference to the topographical distribution pattern of the degeneration].

The degenerative and repair processes of rabbit lumbar disc after nucleotomy were topographically followed by light and electron microscopy. Light microscopic studies showed a proliferation of cells with large pericellular matrices in the inner annulus. Electron microscopic changes of the inner annular cells showed an increase in the number of micropinocytotic vesicles in the first 8 weeks following nucleotomy, early appearance of lysosomes, and a reduction in the amount of rough endoplasmic reticula from 6 weeks after operation. 'Islet areas' consisting of small ruthenium red positive materials increased in number in the pericellular matrices. These changes were topographically similar to each of them. Activation of remnant notochordal cells was evident morphologically and autoradiographically. It seemed most likely that cells of the inner annulus were activated for a initial certain period following nucleotomy, while they degenerated rapidly after surgery. Light microscopy showed these changes of annular tissue following nucleotomy to be just like those after disc incision.

Animals↗