Search PubMed⌕ Search

Biomedical subjects

K Kaneda

Publications and source records attributed to K Kaneda.

At least 217 records · Page 12Linked to original sources

Biomechanical and histological changes in the patellar tendon after in situ freezing An experimental study in rabbits.

OBJECTIVE: The effects of freezing on the remodelling process of the patellar tendon were examined. DESIGN: An experimental study in rabbits. BACKGROUND: Patellar tendon weakens when grafted as a subsstitute for the anterior cruciate ligament. Fibroblast necrosis is considered to be one of the many factors contributing to this change. Therefore, the effect of freeze-induced necrosis on the patellar tendon has been studied. METHODS: Using a technique for freezing the patellar tendon in situ with liquid nitrogen to kill fibroblasts, we studied the biomechanical and histological changes in the patellar tendon up to 24 weeks after freezing. RESULTS: The cross-sectional area started to increase by week 3, reaching a plateau by week 12. The elastic modulus and tensile strength began decreasing by week 3. Although the maximum load decreased at weeks 12 and 24, the stiffness did not change. Histologically, cells were absent until week 2. Athough cells were apparently normal at week 24, there were none of the dense collagen bundles that are normally seen. CONCLUSIONS: The once-frozen patellar tendon weakens as tissue remodelling occurs. RELEVANCE: The study was designed to ascertain whether the remodelling process of the once-frozen patellar tendon coincides with its mechanical properties in different phases. The weakening of the patellar tendon occurred as new cells proliferated into the tendon and remodelled the tissue.

Journal Article↗

Lumbar trunk muscle endurance testing: an inexpensive alternative to a machine for evaluation.

OBJECTIVES: The goals of this study were to verify the reliability and safety of new methods for evaluating trunk muscle endurance, and to compare the differences between healthy subjects and patients with chronic low-back pain. DESIGN: Randomized and controlled study. SETTING: A referral center and institutional practice, and outpatient care. SUBJECTS: Ninety healthy subjects (37 men and 53 women average age 46.2 years) and 100 patients with CLBP (40 men and 60 women; average age 45.3 years) participated in this study. MAIN OUTCOME MEASURES: During trunk flexor and extensor endurance tests, the subjects were asked to maintain the original positions for as long as possible. The performance time (seconds) for which subject could maintain the position was compared between two groups. Test-retest correlation (r) was also analyzed. The degree of lumbar lordosis was compared in conventional and new methods. RESULTS: All test-retest correlations were significantly high in both groups (p < .01). The performance time was much longer in the healthy subjects than in the patients with CLBP during any procedures (p < .01). Lumbar lordosis was significantly less in our method than in the Kraus-Weber test (p < .01). CONCLUSIONS: This study demonstrated that our methods for measuring trunk flexor and extensor endurance had high reliability, reproducibility, and safety, and were easy to perform, with no need for special equipment. This study also showed that trunk muscles in patients with CLBP were more easily fatigued, compared with those in healthy subjects.

Adult↗

Identification of macrophage migration inhibitory factor in murine neonatal calvariae and osteoblasts.

Bone resorption and formation are dynamic processes that occur in both normal and injured bone tissues. Regulation of these processes is mediated at the local level by cytokines and growth factors. Macrophage migration inhibitory factor (MIF) is one of the proinflammatory cytokines that activates macrophages and regulates production of other cytokines, such as tumour necrosis factor-alpha and interleukin-1. We here demonstrate, by reverse transcription-polymerase chain reaction, high expression of MIF mRNA in murine osteoblasts obtained from mouse neonatal calvariae and murine osteoblastic MC3T3-E1 cells. The presence of MIF protein in the osteoblasts was confirmed by Western blot analysis using anti-rat MIF antibody. Moreover, the immunohistochemical study revealed that MIF was localized largely in the cytoplasm. The pathophysiological function of MIF remains undefined; however, the present results suggest that MIF takes part in the osseous metabolism as well as in immunological events.

Animals↗

Critical involvement of interferon gamma in the pathogenesis of T-cell activation-associated hepatitis and regulatory mechanisms of interleukin-6 for the manifestations of hepatitis.

A single intravenous injection of concanavalin A (Con A) induces T-cell activation and an acute hepatitis in mice. This study investigated the role of interferon gamma (IFN-gamma) in the pathogenesis of this hepatitis model. Striking increases in the plasma levels of various cytokines, including tumor necrosis factor (TNF), interleukin-2 (IL-2), and IFN-gamma, were detected before the increase in plasma aminotransferase levels induced by Con A injection. TNF levels peaked within 2 hours, whereas IFN-gamma levels peaked at 6 hours after Con A injection. In contrast to a sharp peak of TNF levels, high IFN-gamma levels were detected for a more prolonged period. Passive immunization with anti-IFN-gamma monoclonal antibody (MAb) conferred a dose-dependent protection against liver injury in this model. This protection was observed when anti-IFN-gamma MAb was administered at least 30 minutes before Con A injection but not when given 1 hour after Con A injection. The protection from Con A-induced hepatitis was also induced by administration of rIL-6 before Con A injection. rIL-6 treatment induced significant albeit incomplete inhibition of IFN-gamma and TNF production, whereas this regimen did not affect IL-2 production. Despite striking protective effects of rIL-6 or anti-IFN-gamma MAb, comparable levels of cellular (both T cell and polymorphonuclear cell) infiltration were detected in liver sections from animals untreated, or treated with either rIL-6 or anti-IFN-gamma MAb. Moreover, electron microscopic examination showed that infiltrating T cells exhibited a blastoid appearance in all groups. These results indicate that IFN-gamma plays a critical role in the development of Con A-induced acute hepatitis and suggest that IL-6 administration can regulate the manifestation of hepatitis through mechanisms including the reduced production of inflammatory cytokines such as IFN-gamma.

Animals↗

Identification of macrophage migration inhibitory factor in synovial membranes of loosened total joint replacement.

Endosteal bone resorption often occurs around loosened total joint replacements. In the process of the loosening, macrophages play an important role by releasing cytokines such as interleukin-1, tumor necrosis factor-alpha and prostaglandin E2. In this study, we investigated the involvement of macrophage migration inhibitory factor (MIF) in the pathological state of the loosening of a total hip replacement. Interface membranes were harvested from bone-cement or bone-implant interfaces of two patients during revision hip surgeries. The tissues were immunohistochemically examined with a polyclonal antibody against human recombinant MIF. This study detected MIF in the cytoplasm of the macrophages in all the tissues tested, though it was not detected in that of interstitial cells. The expression of MIF mRNA in the membrane was also examined by reverse transcription polymerase chain reaction, which demonstrated that expression of the MIF mRNA in the interface membranes was higher than that of the normal synovium. Considering these results, it is suggested that MIF is one of important cytokines mediating the inflammatory process during loosening of total joint replacements.

Antibodies↗

Development of angiosarcoma at the site of a bone infarct.

A 34-year-old man presented with angiosarcoma which developed at the site of a preexisting bone infarct in the metaphysis of the right tibia. A malignant bone tumor may develop at the site of bone infarct, and its histologic type is most frequently malignant fibrous histiocytoma or fibrosarcoma. Few patients with osteosarcoma have been reported: only 2 patients who had angiosarcoma that developed in a preexisting bone infarct have been reported in the English literature. Malignant transformation of bone infarct into angiosarcoma is extremely rare.

Adult↗

Presence of common antigenic epitope in outer surface protein (Osp) A and OspB of Japanese isolates identified as Borrelia garinii.

Japanese Borrelia strains FujiP2, AP83, NT24, NT29 and HT2 which had a 31-kilodalton protein non-reactive with monoclonal antibody (MAb) H5332 to outer surface protein A (OspA) were identified as B. garinii by the DNA hybridization method. MAb P3134 raised to strain NT24 reacted with OspA and the OspB-ranging protein of these isolates and cross-reacted with the OspB-ranging protein of some other isolates. Since the reactive protein was extracted by the Triton X-114 phase partitioning method, the MAb recognized the common epitope present in OspA and OspB. To our knowledge, this is the first report of an MAb reactive to both OspA and OspB.

Antibodies, Bacterial↗

Kinetics of organ-associated natural killer cells and intermediate CD3 cells during pulmonary and hepatic granulomatous inflammation induced by mycobacterial cord factor.

We investigated here the kinetics of natural killer (NK) cells and extrathymic T cells, which include intermediate CD3 cells and gamma delta T cells, in the cord factor-induced granulomatous inflammation of the lungs and liver. In Balb/c mice, pulmonary inflammation elevated the proportion of NK cells and that of extrathymic T cells to mononuclear cells in the lungs. C3H/He mice exhibited shorter-term inflammation of the lungs than Balb/c mice and accordingly showed a smaller increase in the proportions of pulmonary NK cells and intermediate CD3 cells. In the liver of Balb/c mice, hepatic NK cells increased as well with the granulomatous changes, while intermediate CD3 cells exhibited a transient decrease before they increased. The present study has demonstrated that granulomatous inflammation is accompanied by the increase of lung-associated NK cells and extrathymic T cells and that there exists a difference between these two mouse strains in the induction of these lymphocyte subsets by cord factor.

Animals↗

Sinusoidal capillarization and arterial blood supply continuously proceed with the advance of the stages of hepatocarcinogenesis in the rat.

Hepatocellular carcinoma (HCC) is supplied only with arterial blood and has capillaries instead of sinusoids, unlike the normal hepatic tissue. In order to reveal the sequential changes of sinusoidal structure and blood supply during hepatocarcinogenesis, we examined hyperplastic nodules (HPN), atypical hyperplastic nodules (AHPN) and HCC in F344 rats fed with 2-acetylaminofluorene for 25-35 weeks. The extent of arterial blood supply and the degree of sinusoidal capillarization were assessed by the staining of hepatic nodules with arterially infused ink and by immunohistochemical and ultrastructural analyses of the sinusoids, respectively. The proportion of arterialized nodules was 47% in HPN, 57% in AHPN and 85% in HCC, which indicates that arterialization begins at the stage of HPN and a few HCC still receive portal venous blood. The proportion of Factor-VIII-related antigen (F-VIII)-positive nodules was 25% in HPN, 40% in AHPN and 100% in HCC. Non-arterialized nodules did not express F-VIII, while some F-VIII-negative nodules were already arterialized. Electron microscopically, non-arterialized HPN exhibited normal features of sinusoids, while arterialized HPN showed disappearance of Kupffer cells and partial defenestration of sinusoidal endothelial cells. In non-arterialized and arterialized AHPN, basement membrane became continuous and lipid droplet-containing stellate cells were no longer seen. In HCC, endothelial fenestrae were diminished and basement membrane became thick. The present study has demonstrated that sinusoids are altered in the following order as hepatocarcinogenesis advances from HPN to HCC; onset of arterialization and decrease of endothelial fenestrae, expression of F-VIII by endothelial cells, disappearance of Kupffer cells, diminution of lipid droplets in stellate cells and thickening of basement membrane.

Animals↗

Effects of restressing on the mechanical properties of stress-shielded patellar tendons in rabbits.

We studied the effects of restressing on the mechanical properties and morphology of stress-shielded rabbit patellar tendons. After completely unloading the patellar tendon for 1 to 3 weeks, tension was again applied to the tendon for subsequent 3 to 12 weeks. Although the stress shielding markedly decreased the tangent modulus and tensile strength of the tendon, restressing significantly increased them. However, the mechanical properties of the tendon were not completely recovered even after a prolonged period of restressing. The microstructure of the tendon was also restored by restressing, although the recovery was incomplete. These results indicate that the mechanical properties and morphology of tendinous tissue change in response to mechanical demands.

Animals↗

A mathematical expression of three-dimensional configuration of the scoliotic spine.

Three-dimensional configuration of the scoliotic spine was mathematically expressed by a spatial curve passing through each vertebral centroid ("vertebral body line"). Three-dimensional location of the vertebral centroid was determined from digitization on the frontal and sagittal roentgenograms. Cobb angle, which is clinically used for measuring scoliosis curvature, was calculated in space to evaluate scoliosis deformity three-dimensionally. In forty-five scoliotic spines, regardless of curvature and curve patterns, the spinal configurations were excellently approximated by vertebral body lines. Vertebral body lines swerved from the sagittal plane at the end vertebrae, but aligned on a certain plane within the scoliosis region. Three-dimensional Cobb angle, which was larger than that in the frontal plane, can be utilized to evaluate the scoliosis deformity.

Adolescent↗

[Association between abnormal sensation and increased microneurographic muscle sympathetic nerve activity of the peroneal nerve in patients with lumbar spinal problems].

Nine patients with lumbar spinal problems (patient group) and four healthy volunteers as a control group were examined by the microneurographic technique. A tungsten microelectrode (impedance 2 approximately 5 M omega) was introduced into the peroneal nerve in the affected limb in the patient group. Muscle sympathetic nerve activities were rectified and integrated every 0.1 sec. Muscle sympathetic nerve activity was expressed as the burst number of integrated muscle sympathetic nerve activities per minute (burst rate) and the burst number per 100 heart beats (burst incidence). Statistical analyses were performed by ANOVA. The mean burst rate was 22.5 +/- 5.3 burst/min in the patient group, and 11.9 +/- 1.9 burst/min in the control group. The mean burst incidence was 31.7 +/- 8.2 burst/100 HB in the patient group and 17.1 +/- 4.3 burst/100 HB in the control group. Both the mean burst rate and mean burst incidence were higher in the patient group than in the control group (mean burst rate: p < 0.005, mean burst incidence: p < 0.01). In 62.5% of the patients with increased muscle sympathetic nerve activity, dysesthesia (tingling, and pin prick sensations) was complained of. There was a positive correlation between dysesthesia and increased basic activity of the muscle sympathetic nerve. This suggests the sympathetic nervous system may be involved in inducing abnormal sensations.

Adult↗

Development of intralobular bile ductules after spontaneous hepatitis in Long-Evans mutant rats.

Oval cell proliferation occurs during spontaneous hepatitis in Long-Evans cinnamon (LEC) rats. It has been reported that oval cells undergo differentiation into mature hepatocytes via small hepatocytes during carcinogenesis. This study was designed to demonstrate in vivo differentiation of oval cells into typical bile ductular cells in the liver lobule and the characteristic feature of intralobular bile ductule formation in LEC rats. We have examined kinetics, intralobular distribution, and morphology of oval cells, small hepatocytes, and bile ductular cells in LEC rat livers at prehepatitic, acute hepatitic, chronic hepatitic, and precancerous stages by conventional light and electron microscopy, immunostaining for cytokeratin, and 3-dimensional reconstruction analysis. Our results indicate that oval cells proliferated and extended into the periportal zone of the liver lobule during acute hepatitis at 20 to 23 weeks after birth. They exhibited tubular structures with a poorly defined lumen and incomplete basement membrane. After remission of the jaundice, small hepatocytes proliferated in association with oval cells and predominated in the periportal zone at 26 weeks. In a chronic hepatitic stage at 28 to 30 weeks, tubular structures were transformed into typical bile ductules, which had a well defined lumen and complete basement membrane, and small hepatocytes became a normal size. Intralobular bile ductules originated from the interlobular bile ducts, ran in the space of Disse, giving rise to several branches in the course, and were terminated at the hepatocytes. The present results indicate that oval cells that proliferate in the liver lobule of LEC rats after spontaneous hepatitis not only differentiate into small hepatocytes but also into typical bile ductular cells. This study suggests that intralobular bile ductules may play roles in maintaining the bile excretion during and after the disorganized proliferation of oval cells and small hepatocytes.

Animals↗

[A patient with Goodpasture's syndrome revealed a poor prognosis regardless of receiving intensive therapy from an early stage after onset].

Goodpasture's syndrome has been reported as a disease that has a favorable prognosis when the patient receives intensive immunosuppressive drug-therapy from an early stage after onset. The present report describes a 50-year-old woman, who exhibited progressive renal failure accompanied by pulmonary hemorrhage, and an increase in serum level of antiglomerular basement membrane (GBM) antibody. Initial histological examination of a renal specimen indicated a severe fibrocellular crescentic glomerulonephritis with a linear deposition of Ig-G and C3 along the glomerular capillary wall. The patient was thus diagnosed as having Goodpasture's syndrome. Therapy with pulse treatment of steroid (corticosteroid hormone), immunosuppressive agents, or plasma-exchange for the removal of anti-GBM antibody was adopted a week after the clinical onset. However, histological amelioration of the glomeruli did not occur with this treatment in the second biopsy, while glomerular damage advanced progressively. In contrast to other patients with Goodpasture's syndrome, our case revealed an unfavorable outcome regardless of receiving intensive therapy from an early period after onset, which suggests that more intensive therapy of another approach to this patient may have been necessary.

Anti-Glomerular Basement Membrane Disease↗

Mechanism that regulates nitric oxide production by lipopolysaccharide-stimulated rat Kupffer cells.

Mechanism that regulates nitric oxide (NO) production by stimulated Kupffer cells was studied. Lipopolysaccharide (LPS) stimulated NO production by primary-cultured Kupffer cells in a time- and dose-dependent manner. Twenty-four h after incubation with 1 microgram/ml of LPS, the nitrite concentration in the culture medium increased from 2.87 +/- 1.4 to 73.6 +/- 6.9 nmol/ml. NO production started to increase around 6 h after adding LPS and reached a maximum within 24 h. NO production was inhibited by 0.3 mM of NG-monomethyl-L-arginine and was reversed by adding 3 mM of L-arginine. When incubated with 1 microgram/ml of LPS for 24 h, NO synthase activity in Kupffer cells increased from 0.164 +/- 0.035 to 3.16 +/- 0.11 nmol/min/mg protein. Dexamethasone and prednisolone significantly inhibited the induction of NO synthase and NO production in Kupffer cells. Expression of mRNA for inducible type of NO synthase (iNOS) started to increase around 4 h after adding LPS (1 microgram/ml) and reached a maximum by about 20 h. The enhanced expression of iNOS mRNA was also suppressed by 1 microM dexamethasone. On the other hand, calcium ionophore A23187 significantly enhanced the induction of NO synthase and iNOS mRNA expression in LPS-stimulated Kupffer cells. In addition, a tyrosine kinase inhibitor, genistein (100 microM), significantly inhibited NO production by LPS-stimulated Kupffer cells. Neither phorbol 12-myristate 13-acetate, dibutyryl cAMP, indomethacin nor a protein kinase C inhibitor H-7 affected NO production by Kupffer cells. These results suggested that iNOS mRNA expression, NO synthase activity and NO production increased in LPS-stimulated Kupffer cells by a glucocorticoid-inhibitable mechanism and that Ca2+ and tyrosine phosphorylation might play important roles in LPS-dependent induction of NO synthase.

Animals↗

A three-dimensional structure model of the complex of glutamyl-tRNA synthetase and its cognate tRNA.

A docking model of glutamyl-tRNA synthetase (GluRS) and tRNAGlu was constructed, on the basis of the distinguished similarity between the X-ray crystallographic three-dimensional structures of the N-terminal halves of the Thermus thermophilus GluRS in the free state and the Escherichia coli glutaminyl-tRNA synthetase in a complex with tRNAGln. The modeled structure is energetically favorable and is also well consistent with the results of site-directed mutagenesis studies. The model indicates that the GluRS-specific insertions 2 and 3 fit and bind to the acceptor stem and the D arm, respectively, of the cognate tRNA without affecting other contacts. In particular, insertion 3 strongly interacts with the two D-stem base pairs that are essential for the tRNA-GluRS recognition.

Anticodon↗

Comparison of the type-2 insulin-like growth factor receptor in normal osteoblasts and osteosarcoma-derived osteoblast-like cells.

Insulin-like growth factor-II is known to stimulate the proliferation and differentiation of osteoblasts in part through activation of the type-2 insulin-like growth factor receptor. The present study examined the type-2 insulin-like growth factor receptors of three normal osteoblast-like cells and three osteosarcoma-derived osteoblast-like cells (OGA, SU, and IMAI) from humans. [125I]insulin-like growth factor-II was used for the binding studies. All of the cell types had high affinity binding sites for insulin-like growth factor-II (dissociation constants [Kd] < or = 1 nM). The concentration of these sites was 10 to 24-fold higher in normal osteoblasts than in the osteosarcoma cells studied. Unlabeled insulin-like growth factor-II inhibited the binding of [125I]insulin-like growth factor-II to the cells in a dose-dependent manner; however, unlabeled insulin-like growth factor-I and insulin were less effective. Covalent crosslinking of insulin-like growth factor-II binding sites gave molecular mass estimates of M(r) 250,000 in human osteoblast cells, 250,000 and 130,000 in OGA cells, 240,000 in SU cells, and 250,000 and 130,000 in IMAI cells. Unlabeled insulin-like growth factor-II inhibited all affinity labeling. In Northern blot analysis, the type-2 insulin-like growth factor receptor mRNA of normal osteoblasts was seen in greater abundance than it was in osteosarcoma cells. These results indicate that the numbers of type-2 insulin-like growth factor receptors differ between normal and transformed osteoblasts and that the differential expression of the receptor may be due to the differentiation of osteoblasts.

Adolescent↗