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Biomedical subjects

K Kaneda

Publications and source records attributed to K Kaneda.

At least 145 records · Page 8Linked to original sources

Photodynamic effect of a new photosensitizer ATX-S10 on corneal neovascularization.

In order to elucidate the mechanism by which a new photosensitizer ATX-S10 causes the photodynamic effect on neovasculature, we investigated the kinetics and localization of dye accumulation in the neovascular cornea of rats after systemic administration and the development of vascular injury induced by subsequent laser irradiation, compared to those in the normal iris. Under a fluorescence microscope, the neovascular cornea always exhibited more intense fluorescence than the iris between 0.5 and 4 hr after ATX-S10 administration, indicating the preferential deposit of dye in the former tissue. The fluorescence was found inside the vascular lumen at the earliest time period and thereafter in the vascular lining cells, interstitial tissue and infiltrating neutrophils until 6 hr. As observed using light and electron microscopy, laser irradiation performed 2.5 hr after ATX-S10 injection caused extensive vascular thrombosis with endothelial destruction, which persisted for at least 3 days. The proportion of thrombosed vessels at 6 hr after laser irradiation in the neovascular cornea (64+/-5%; n=3) was significantly (P<0.01) higher than that in the normal iris (44+/-8%; n=3). In the non-thrombosed vessels from heparinized rats, in which thrombosis-related ischemic effect was excluded, mitochondrial vacuolation was the pathologic change commonly seen in the endothelial cells, pericytes and neutrophils. Morphometric analysis revealed that the mitochondria of endothelial cells in the corneal new vessels were more severely injured than those in the iris vessels. The present results indicate that ATX-S10 is a potent photosensitizer which induces photodynamic occlusion particularly of new vessels probably due to the preferential biodistribution of dye in the neovascular tissue.

Animals↗

Imaging and modelling from serial microscopic sections for the study of anatomy.

A system is considered for segmenting noisy intensity images and consequent three-dimensional object reconstruction from a set of planar contours. A new semi-automatic method for the extraction of contours from a sequence of cross-sectional images based on an active contour model (ACM) is proposed. The dynamic ACM proceeds along the sequence of cross-sections following a non-rigid motion, in accordance with the organ boundary. Image texture information is also employed in the model. Problems associated with topological reconstruction from planar contours are addressed, and several criteria promoting semi-automatic topological reconstruction are introduced. The proposed system is successfully applied to the processing of real data related to animal embryonic organs, proving that the system allows detailed modelling of irregular objects. The reconstructed models can be observed in wire-frame, solid, transparent or stereoscopic semi-transparent format. The human-computer interaction implemented in the procedure assists with problems of feature identification and object manipulation about an arbitrary axis.

Anatomy↗

Establishment of chimerism in donor liver with recipient-type bone marrow cells prior to liver transplantation produces marked suppression of allograft rejection in rats.

In this study, we investigated whether establishment of chimerism in donor liver with recipient-type bone marrow cells (BMCs) prior to liver transplantation could prolong the liver allograft survival. Donor female ACI rats were inoculated with recipient-type BMCs of male LEW rats via the portal vein, with or without irradiation as cytoablation, followed by intramuscular administration of FK506 for 5 days. At 1-2 months later, livers were harvested and transplanted into naive female LEW rats. No immunosuppressants were used. Chimerism in donor rats was confirmed by primers specific for the sex determinant Y chromosome of rats. With livers from rats pretreated with recipient-type BMCs, survival of liver allografts was significantly extended, irrespective of irradiation. These results showed that modification of the donor liver by intraportal injection of recipient-type BMCs and concomitant administration of FK506 prior to liver transplantation prolonged liver allograft survival in rats.

Animals↗

Stimulation of bone formation in vivo by insulin-like growth factor-II in rats.

Insulin-like growth factor-II (IGF-II) plays an important role in skeletal remodeling, however, little is known about its effect on bone formation in vivo. In our study of the stimulation of bone formation in vivo by IGF II we injected recombinant human IGF-II into the parietal bones of neonatal rats once a day for 12 days. The bone mineral density measured by dual energy X-ray absorptiometry and the thickness of IGF-II-injected parietal bones increased in a dose-dependent manner. The layers of osteoblasts were observed along the IGF-II-injected side.

Animals↗

Morphometric and ultrastructural analyses of in vivo-activated murine Langerhans cells induced by administration of a streptococcal preparation (OK-432).

Langerhans cells (LCs) are activated in the epidermis by external and internal stimuli, such as antigens and cytokines, respectively. To reveal the morphologic and functional properties of in vivo-activated LCs during inflammation, we injected the streptococcal preparation OK-432 intradermally into the earskin of mice and performed time-course analyses by immunofluorescence and electron microscopy. Cellular infiltrate appeared in the dermis at 6 h after OK-432 injection and had progressively extended to the dermoepidermal junction at 12 and 24 h. Immunostaining for class II antigen revealed that LCs were enlarged and extended long dendrites during inflammation. Acidic compartments such as lysosomes and multivesicular bodies also increased in number and Golgi apparatuses developed as demonstrated by electron microscopy and morphometric analysis. Birbeck granules, although not showing numerical changes, were translocated from the Golgi area to the subplasmalemmal area. After epicutaneous application of cationic ferritin, LCs often contained endosomes as the result of engulfment by the cytoplasmic projections. The present results indicate that nonspecifically induced dermal inflammation is capable of inducing activation of LCs in vivo, and that in vivo-activated LCs have the capacity for active endocytosis and intracellular digestion or processing.

Animals↗

Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia.

PURPOSE: This study was carried out to examine the involvement of glutamate and nitric oxide neurotoxicity in ischemia/reperfusion-induced retinal injury in vivo. METHODS: We monitored glutamate release from in vivo cat retina during and after pressure-induced ischemia using a microdialysis technique. Morphometric studies were performed to study the effects of MK-801 (dizocilpine), L-NAME (N omega-nitro-L-arginine methyl ester), and D-NAME (N omega-nitro-D-arginine methyl ester) on the histological changes in the rat retina induced by ischemia or intravitreal injection of NMDA (N-methyl-D-aspartate; 200 nmol). RESULTS: A large release of glutamate occurred during ischemia, followed by a marked release after reperfusion. Histological changes occurred selectively in the inner part of the retina after ischemia as well as intravitreal injection of NMDA. Pretreatment with intravenous injection of MK-801 or L-NAME significantly inhibited the ischemic injury of the inner retina. Intravitreal injection of L-NAME inhibited NMDA-induced neurotoxicity in the retina. CONCLUSION: These findings indicate that nitric oxide mediates neurotoxic actions of glutamate which are responsible for ischemic injury in the retina.

Animals↗

Morphological and functional alterations to sinusoidal endothelial cells in the early phase of endotoxin-induced liver failure after partial hepatectomy in rats.

Liver failure following major hepatectomy is characterized pathologically by massive hepatic necrosis, which is thought to begin with injury of sinusoidal endothelial cells (SECs). To examine the early events of SECs leading to hepatic damage, we performed time-course analyses of the morphological and functional perturbation of SECs after endotoxin administration to hepatectomized rats. At 1.5 h after endotoxin injection, when hepatocellular damage was not yet evident, SECs showed augmented expression of intercellular adhesion molecule-1, with frequent adherence of infiltrating leucocytes and ultrastructural features of defenestration and hypertrophied cytoplasm enriched with cell organelles. The serum level of hyaluronate, as an indicator of the functional state of SECs, was significantly elevated. At 3 h, SECs underwent necrosis and disruption, accompanied by fibrin deposits with concomitant hepatocellular necrosis. The morphological and functional alterations of SECs precede necrotic changes in hepatocytes and SECs in endotoxin-induced liver failure after partial hepatectomy.

Animals↗

Occipitoatlantal instability associated with articular tropism.

The authors report the case of a patient with rotatory posterior subluxation of the occiput on the atlas associated with tropism of the O-C1 articulations. Lateral flexion-extension plain films demonstrated 5 mm of posterior translation of the occiput on the atlas. Tomographs revealed tropism of the O-C1 articulations, and CT scans on extension demonstrated posterior rotatory subluxation of the occiput on the atlas. The patient had no osseous abnormality caudally below the atlantoaxial joint, and underwent posterior occipitoatlantal fusion by wiring. At the 4-year follow-up, the grafted bone had been incorporated, and the patient was completely free from preoperative symptoms. In the present patient, occipitoatlantal instability is presumed to have derived from articular tropism.

Adult↗

Expression of cellular prion protein in activated hepatic stellate cells.

Suppression subtractive hybridization was used to clone genes associated with the activation of hepatic stellate cells and 13 genes were found to be dominantly expressed in activated stellate cells. Among them, one was identical to the 421-837th base pairs of cDNA sequence reported for rat prion-related protein (PrP). In cultured stellate cells, PrP mRNA expression increased in a time-dependent manner in parallel with smooth muscle (SM) alpha-actin mRNA expression. In situ hybridization demonstrated that PrP mRNA was localized in and around the fibrous septa of carbon tetrachloride (CCl4)-treated liver. Cellular PrP (PrPc) was produced by culture-activated stellate cells, and immunohistochemically detected in the fibrous septa of CCl4-damaged liver and sinusoidal linings of common bile duct-ligated liver, consistent with the localization of SM alpha-actin. Immunoelectron microscopy revealed that PrPc resided on the plasma membrane of stellate cells. These results indicate that PrP expression is closely related to stellate cell activation associated with fibrogenic stimuli.

Actins↗

Clinical features and management of traumatic posterior interosseous nerve palsy.

The clinical features and results of treatment were reviewed in 17 traumatic palsies of the posterior interosseous nerve. Variations in clinical features depended on whether the recurrent branch or descending branch of the posterior interosseous nerve was injured. Seven patients had nerve repair, and two were treated by tendon transfers. Eight patients were treated conservatively. Sixteen of 17 patients recovered to more than M4 motor power at final follow-up. Associated muscle damage worsened the functional result.

Adolescent↗

Force transmission through the wrist joint in Kienböck's disease: a two-dimensional theoretical study.

This study quantifies the changes in force and pressure distributions across the wrist joint in different stages of Kienböck's disease using a 2-dimensional computer simulation model. Twenty-four cases classified as Lichtman's stage II, IIIA, or IIIB (8 cases in each category) were analyzed using the rigid body spring model technique. A 2-dimensional model in the posteroanterior plane of the wrist was loaded through the metacarpals under a total force of 142 N. The joint forces, peak pressures, and ligament tensions calculated on the involved side were normalized against the contralateral normal side values of the same patient. The results demonstrated that significant changes of the force transmission across the wrist joint occurred only from stage IIIA to IIIB, in which scaphoid rotation was prominent. On the basis of this study, scaphoid rotation plays an important role in affecting the wrist joint contact pressure distribution. This may be responsible for the progression of Kienböck's disease.

Biomechanical Phenomena↗

Diagnosis of synovial sarcoma with the reverse transcriptase-polymerase chain reaction: analyses of 84 soft tissue and bone tumors.

The chimeric transcript SYT-SSX is generated as a result of reciprocal translocation t(X;18), which is the primary cytogenetic abnormality found in, and appears to be specific for, synovial sarcoma. We performed a reverse transcriptase-polymerase chain reaction (RT-PCR) for SYT-SSX transcripts in a series of 84 tumors (61 soft tissue tumors and 23 bone tumors), including a variety of histologic types, to assess its usefulness in molecular diagnosis. Ten synovial sarcomas, three tumors initially unclassified, and one malignant peripheral nerve sheath tumor contained the chimeric transcripts. A review of the original slides and additional examination showed that a diagnosis of synovial sarcoma was appropriate for these cases. Additionally, in situ hybridization with an SSX1 probe indicated that the chimeric transcripts exist not only in the cells of special components but also in cells showing a variety of histologic patterns. Therefore, RT-PCR can be considered a useful molecular biological technique that can provide objective evidence for diagnosis of synovial sarcoma. Northern blot analysis with an SSX1 probe also detected chimeric SYT-SSX transcripts in the synovial sarcoma cases. The additional smaller bands, however, were also detected in six peripheral primitive neuroectodermal tumors (pPNETs) and one embryonal rhabdomyosarcoma. In five of these pPNETs, other bands ranging in size from 2.0 to 2.2 kb were also found, and it seems possible that these bands might represent novel karyotypic aberrations and/or splicing variants of SSX.

Adult↗

Infectivity and arthritis induction of Borrelia japonica on SCID mice and immune competent mice: possible role of galactosylceramide binding activity on initiation of infection.

We investigated the relationship between the binding activity to galactosylceramide (GalCer) and the arthritis induction activity of Borrelia japonica. The B. japonica strains maintained the ability to induce arthritis in inbred C3H/HeN and immunodeficient SCID mice, but the ability was lower than that of Borrelia burgdorferi sensu stricto virulent strain 297. Histopathological changes were restricted to the joints, and a marked effusion of polymorphonuclear neutrophils into the joint space was found. The binding activity of B. japonica strains to GalCer was lower than that of the virulent strain 297 but higher than that of the high-passage strain 297. The lower infectivity and virulence of B. japonica may explain its lower binding ability to GalCer.

Animals↗

Suppressive effect of the angiogenesis inhibitor TNP-470 on the development of carcinogen-induced hepatic nodules in rats.

Tumor metastasis can be prevented by inhibiting angiogenesis. In the present study, we have demonstrated that the angiogenesis inhibitor TNP-470 also suppresses the development of primary hepatic nodules. Hepatocarcinogenesis was performed by the feeding of 2-acetylaminofluorene to hepatectomized rats during 8-14 weeks of age. Predominantly arterial-to-portal circulation and sinusoidal capillarization were determined by the staining of nodules with arterially infused ink and immunostaining for factor VIII-related antigen, respectively. Intraperitoneal administration of 30 mg/kg b.w. of TNP-470 twice a week significantly reduced the number of hepatic nodules. Among the nodules, hyperplastic nodules stained with ink, atypical hyperplastic nodules and hepatocellular carcinoma, all of which possess structurally altered sinusoidal endothelial cells or capillary-type endothelial cells, were dramatically decreased in number. Suppression was observed equally in nodules of all sizes. TNP-470 was more effective when administered during 8-20 weeks than during 14-26 weeks. In contrast, ink-non-stained hyperplastic nodules, which have normal sinusoidal endothelial cells, were not affected at all. The present results indicate that TNP-470 suppresses the development of primary hepatic nodules whose microvessels are capillaries or transitional forms from sinusoids to capillaries.

2-Acetylaminofluorene↗

Detrimental effect of a non-selective nitric oxide synthase inhibitor on the energy state of the liver following acute endotoxemia in rabbits.

BACKGROUND: The effect of nitric oxide synthase (NOS) inhibitors in septic shock is very controversial. It is known that the administration of NOS inhibitors to normal subjects itself increases pulmonary vascular resistance with a concomitant decrease of cardiac output. Therefore, the hypothesis was tested that the detrimental effects of a non-selective NOS inhibitor on liver energetics in a rodent model of endotoxemia are mediated by the adverse pulmonary circulatory effect of the drug itself. METHODS: Twenty anesthetized rabbits were instrumented and two separate experiments (a magnetic resonance spectroscopic study and a hemodynamic study) were performed under similar conditions. Animals were assigned randomly to either a control group (group 1; animals received lipopolysaccharide (LPS) at a dose of 400 microg/kg alone) or a treatment group (group 2; animals received NG-nitro-L-arginine methyl ester (L-NAME) at a dose of 7.5 mg/kg, 75 min after administration of LPS). RESULTS: In group 1, slight decreases in hepatic adenosine triphosphate (ATP) value were observed. In group 2, the decreases in ATP values were more prominent than those observed in group 1. LPS produced an acute drop in mean arterial pressure (MAP) with a concomitant increase in pulmonary vascular resistance (PVR) and a reduction in the cardiac output (CO) at 30 min after LPS. The administration of L-NAME caused a transient increase in MAP with a concomitant increase in systemic vascular resistance at 2 h after LPS. However, these changes in PVR and CO were more prominent than in group 1. CONCLUSION: These results suggest that alterations within the pulmonary circulation may be a contributing factor which was responsible for the non-selective NOS inhibitor-induced acute hepatic energy derangement after LPS.

Acute Disease↗