Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
Volume 43, Issue 2
Displaying 1-23 of 23 articles from this issue
Contents
  • KO KAWAKITA
    1997 Volume 43 Issue 2 Pages 244-254
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    Objective : To investigate changes of the enthesis in rheumatoid knees, histopathological study of the tibial insertion of the anterior cruciate ligament (ACL) was carried out. Materials and methods : The tibial insertion of the ACL from 25 rheumatoid knees taken at total knee arthroplasty was stained with hematoxylin-eosin and pentachrome. The histopathological findings were compared with the radiographical findings of the knee joints as well as the macroscopic findings of the ACLs. The age of the subjects ranged from 36 to 71 years with an average of 57.4 years. As a control, the same kind of specimen was taken from 20 osteoarthritic (OA) knees. The ACLs were classified into three types; type I : almost normal, type II : elongated and type III : torn or disappeared. For pathological evaluation, a scoring system using five pathological parameters was designed for rheumatoid arthritis (RA). For roentgenological evaluation, Larsen' grading as well as a four type classification of the intercondylar eminence of the tibia were used. Results : There were four layers in the ACL insertion to the bone : a ligamentous layer, an unmineralized fibrocartilage layer, a mineralized fibrocartilage layer and a bony layer as described by Cooper. This structure showed more destruction in RA than in OA. The pathological findings in RA included irregularity and disappearance of the tidemark, lymphocyte infiltration, invasion of fibrous granulation into the bone, fibrin deposition and thinning of the bony trabeculae. The ligament became degenerative, and the insertion to the bone also showed greater destruction. However, there was no relationship between pathological and radiographical findings. Conclusion : Changes of the enthesis in rheumatoid knees were found to depend not only on age as in OA but also on ligamentous degeneration and resultant tension decrease caused by synovitis and bone absorption.
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  • MASUMI SATOH
    1997 Volume 43 Issue 2 Pages 255-265
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    To determine effective ways of repairing the disc after nucleotomy, a series of canine experiment were performed. Under intravenous pentobarbital anesthesia, the lumbar intervertebral discs were approached anteriorly and nucleotomy was performed. The animals were divided into five groups : the first group underwent simple discectomy without replacement as a sham surgery. The second group underwent insertion of an autologous nucleus pulposus taken from an other disc. The third group underwent injection of fibrin tissue adhesive sealant. The fourth group underwent insertion of autologous synovium taken from the right knee joint and the fifth group underwent injection of sodium hyaluronate. In each group except after the first group, the anterior defect was repaired after the annulus fibrosus was removed from the other disc and sealed with fibrin tissue adhesive. Animals were sacrificed at intervals up to 12 weeks following the procedure, and histological observations were made. Fifty-two discs of 18 mongrel dogs were studied. In the first group, degeneration of the disc appeared to have progressed further. In the other groups, disc degeneration appeared to have been arrested to some extent, but regeneration of the disc was not apparent. However, there was no difference in histological findings among groups two to five. The initial injury to the disc by the nucleotomy may have been too extensive to be repaired by regenerated chondrocytes although some fibrous cartilaginous tissue reappeared in the surrounding tissue. In the fifth group in which sodium hyaluronate had been injected, the end plate was destroyed by proliferative chondrocytes.
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  • --Ananimalexperiment--
    MASATOSHI MORITA
    1997 Volume 43 Issue 2 Pages 266-279
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    This study investigated spinal cord injury affects spinal cord evoked potentials (SCEPs) and spinal cord blood flow. Twenty-six young mongrel dogs and four monkeys were used. In 13 dogs, transection of the spinal cord was performed in three stages at T12 level and in the other dogs, lateral compression was applied to the spinal cord at T10 level until one of the SCEP amplitudes disappeared. SCEPs induced by transcranial electrical stimulation (TCES) and magnetic stimulation (TCMS) were recorded at T8 and T13 levels using bipolar wire electrodes immediately after the transection or compression. In monkeys, lateral compression was applied at T11 level and SCEPs were recorded at T10 and L1 levels. In dogs, blood flows in the dura mater and in the spinal cord were simultaneously measured using a laser Doppler flowmeter during SCEP measurements. The results obtained were as follows : 1) In dogs, amplitudes of the second component by TCES and the first component by TCMS significantly decreased immediately after posterior column transection. Anterior column transection resulted in a relatively greater decrease in the amplitude of the first component by TCES. In monkeys, amplitudes of the second component by TCES and the first component by TCMS were higher in the posterolateral column than in other columns. However, the amplitude of the first component by TCES was higher in the anterior column. The latencies of the second component by TCES and the first component by TCMS were similar in both animals. These findings suggest that the second component by TCES and the first component by TCMS would run through a similar tract, probably in the posterolateral column, whereas the first component by TCES would run in the anterior column. 2) Blood flow in the spinal cord was slightly higher than that in the dura mater under preinjury conditions. The spinal cord blood flow (SCBF) temporarily increased after transection and lateral compression of the spinal cord, but the pattern varied in individual animals. This would be due to differences in the spinal blood flow pattern of the animals. SCBF measured cranially to the transection increased more than that measured caudally to the transection of the spinal cord. These findings suggested that the spinal cord would be supplied not only from the segmental radicular arteries, but also from the anterior and posterior spinal arteries.
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  • MASAHIRO ONOUE
    1997 Volume 43 Issue 2 Pages 280-292
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    Objective : To identify predictors influencing the response to interferon (IFN) therapy in children with chronic hepatitis C (CH-C) and to assess histological findings of the liver long after IFN therapy. Patients and Methods : Twenty-six children with CH-C who received natural IFN alfa therapy for 6 months (total dose : 8MU/kg), were divided into two groups : 12 patients showing a complete response (CR) and 14 patients with a partial response (PR). “CR” was defined as normalization of serum alanine aminotransferase (s-ALT) and the disappearance of hepatitis C virus ribonucleic acid (HCV RNA) from serum within 6 months after the cessation of therapy and continuing for at least 6 months thereafter. “PR” was defined as any other pattern of s-ALT and serum HCV RNA. Liver biopsies were performed within 6 months before IFN therapy in all 26 children, and again 2 years after therapy in 9 of the children. Liver histology was categorized according to the standard criteria and Knodell's index of histological activity with some modifications (Modified HAI). Moreover, the frequency of five histological features (bile duct damage, lymphoid follicles and/or aggregates, acidophil bodies, steatosis and iron deposition) were examined. Results : There were no significant differences on conventional histological diagnosis or in modified HAI for total, necroinflammation and fibrosis between the CR group and the PR group. Bile duct damage, acidophil bodies and steatosis were frequently observed in the PR group, while lymphoid follicles and/or aggregates were frequently recognized in the CR group. However, there were no significant differences in each of the four histological features between the two groups. However, there was a significant difference (p=0.009) in the frequency of liver iron deposition between the CR group (8%) and the PR group (58%). Significantly fewer patients in the CR group showed more than three of these five histological features compared to those in the PR group (0% vs 36%, p=0.021). There were also significantly fewer children in the CR group showing more than two of these four histological features excluding lymphoid follicles and/or aggregates compared to those in the PR group (8% vs 71%, p=0.001). Of the 9 children (CR : 7 cases, PR : 2 cases) who underwent liver biopsies 2 years after the cessation of IFN therapy, 8 (CR : 7 cases, PR : 1 case) showed an improved histological diagnosis. Conclusions : These results suggest that the response to IFN therapy in children with CH-C is influenced by hepatic iron deposition and a combination of several histological features. A period of more than 2 years after the cessation of therapy was necessary to determine histological remission in the CR group.
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  • KWANGSEOK YANG, YI JIANG, YOSHITOMO HAMANO, HIROMlCHI TURUI, HIROSHI H ...
    1997 Volume 43 Issue 2 Pages 293-303
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    The Fas/Fas ligand (FasL) system has been shown to participate in activation induced apoptotic cell death (AICD) of mature B cells. To determine whether any abnormalities in this system are involved in the autoreactive B cells, we examined levels of Fas expression and sensitivity to apoptosis of and-DNA antibody-producing B cells from autoimmune disease-prone NZB×NZW (NZB/W) F1 mice. Unstimulated B cells from the spleen and the peritoneal cavity of 2-month-old NZB/W Fl and normal healthy Balb/c mice expressed no, if any, Fas and were not prone to apoptosis when stimulated with anti-Fas mAb. When stimulated in vitro with agonistic anti-CD40mAb, but not LPS or anti-μ, these B cells from Balb/c and NZB/WF1 mice expressed Fas. However, the patterns of Fas expression differed between CD5+B (B1) cells and conventional B2 cells, in which all B2 cells expressed a high level of Fas, but the Bl cell population was divided into two levels of big and low Fas expression. Although all B cells with high levels of Fas were highly sensitive to Fasmediated apoptosis, Bi cells with low Fas expressior were virtually apoptosis-resistant. Because low Fas expression and apoptosis insensitivity remained unchanged in vitro, even in the presence of larger amounts of and-CD40 or following restimulation with anti-CD40, these properties of low Fas B1 cells seemed to be intrinsic and restricted to the low Fas Bl cell subpopulation. An intriguing finding was that such anti-CD40-induced low Fas B1 cell subpopulation from 2-month-old NZB/W Fl spleens was almost totally responsible for the in vitro IgM and-DNA antibody production. The spleen, but not the peritoneal cavity, from aged NZB/W F1 mice with overt autoimmune disease contained B cells with a spontaneous low Fas expression. These B cells were also apoptosis-resistant and were almost totally responsible for in vitro IgG and-DNA antibody synthesis. Thus, although such B cells lacked a CD5 phenotype, they were thought to be derived from low Fas Bl cells in young mice. Possibilities that autoantibody-producing B cells in autoimmune disease originate from a restricted subpopulation of apoptosis-resistant B1 cells, and that the selection and affinity maturation of certain clones from such a subpopulation may lead to the development of pathogenic autoantibodies are discussed.
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  • YUTAKA TAKAHASHI
    1997 Volume 43 Issue 2 Pages 304-311
    Published: September 16, 1997
    Released on J-STAGE: November 18, 2014
    JOURNAL FREE ACCESS
    It is widely assumed that glomerular mesangial cell proliferation and mesangial expansion represent major pathological mechanisms underlying progression to glomerulosclerosis. More recent findings in various animal models of focal glomerulosclerosis showed that failure of podocytes was a decisive step in sclerosis development. The present study evaluated podocyte density, a good morphometric marker of podocyte damage, to predict the outcome in patients with IgA nephropathy. Thirty-six patients whose renal function had been followed for at least 5 years after renal biopsy were selected and divided into two groups (mild/moderate group and advanced group) according to widely used pathological criteria based on the degree of mesangial lesions and formation of adhesion, crescents, and sclerosis. Progression to end-stage renal failure was encountered in both groups indicating the inability of these criteria to predict the outcome. However, podocyte density was significantly lower in patients who progressed to end-stage renal failure (17.0±4.2 in mild/moderate group and 13.7±3.8 in advanced group) compared with those who did not (24.1±4.2 in mild/moderate group, p<0.02; 23.7±7.8 in advanced group, p<0.01). It appears that podocyte density is a good marker for evaluating renal biopsy specimens to predict the outcome in patients with IgA nephropathy.
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