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Biomedical subjects

Y Honda

Publications and source records attributed to Y Honda.

At least 73 records · Page 4Linked to original sources

Comparison of three-dimensional computed tomography with rapid prototype models in the management of coronoid hyperplasia.

OBJECTIVES: To compare (1) the accuracy of 3DCT with rapid prototyping (RP) models and (2) their application in the management of coronoid hyperplasia. METHODS: An adult dry skull was used to compare 3DCT and a RP model for accuracy of reproduction; Polymerisation contraction and 17 distances between 27 anatomical points were measured. Two patients with coronoid process hyperplasia were assessed by means of 3DCT and plastic models. RESULTS: Differences in measurements with the RP model and the dried skull were smaller than those with 3DCT (P=0.04). Polymerisation contraction was greater than the errors in reproduction with the RP model and approximately equal to those with the 3DCT. The coronoid process was thick and prominent in the patients with coronoid process hyperplasia and the small space and early contact between zygomatic arch and the coronoid process demonstrated. The plastic model duplicated the exostosis of the inner surface of the malar bone facing the concavity of the elongated process. The coronoid process had an anterior tilt in one case. CONCLUSION: The plastic model duplicated the relationship between the maxillofacial deformity and the coronoid process with tolerable accuracy. Trismus may be due to the direction as well as the length of the enlarged coronoid process.

Adolescent↗

Production and chemiluminescent free radical reactions of glyoxal in lipid peroxidation of linoleic acid by the ligninolytic enzyme, manganese peroxidase.

Glyoxal is a key compound involved in glyoxal oxidase (GLOX)-dependent production of glyoxylate, oxalate and H2O2 by lignin-degrading basidiomycetes. In this paper, we report that glyoxal was produced from a metabolite of ligninolytic fungi, linoleic acid, by manganese peroxidase (MnP)-dependent lipid peroxidation. In the absence of the parent substrate of linoleic acid, the dialdehyde was oxidized by MnP and Mn(III) chelate to start free radical reactions with emission of chemiluminescence at 700-710 nm. The spectroscopic profile of the light emission is distinguishable from (a) singlet oxygen, (b) triplet carbonyls from dioxetane and alpha-hydroxyperoxyl radicals, and (c) biacyl triplet formed by the coupling of two acyl radicals. The photon emission of glyoxal by MnP was activated by co-oxidation of tartrate. The MnP-dependent oxidation of glyoxal in tartrate buffers continued for 10 days without addition of exogenous H2O2. The importance of these results is discussed in relation to the free radical chemistry of lignin biodegradation by wood rot fungi.

Biodegradation, Environmental↗

Haplotype analyses with the human leucocyte antigen and tumour necrosis factor-alpha genes in narcolepsy families.

Our previous study suggested that the tumour necrosis factor-alpha gene with thymine residue at position -857 in its promoter region [TNF-alpha(-857T)] could be associated with human narcolepsy independently of a strong association of the human leucocyte antigen (HLA)-DRB1*1501 with the disorder. To understand the relationship of DRB1*1501 with TNF-alpha(-857T) in narcoleptic patients, we investigated 28 members of four Japanese narcolepsy families and determined the haplotypes with the HLA-B, TNF-alpha(-857C/T) and HLA-DRB1 in the members. The resultant haplotypes indicated that not only the DRB1*1501-TNF-alpha(-857C) haplotype but also the DRB1*1501-TNF-alpha(-857T) haplotype, which is rare in healthy individuals and may have a strong predisposition to the disorder, were present in the affected members. From the chromosomal recombination observed in a few members, it is possible that chromosomal recombination could play a role in the generation of the rare DRB1*1501-TNF-alpha(-857T) haplotype.

Adult↗

H-, K-, and N-ras gene mutation in atypical fibroxanthoma and malignant fibrous histiocytoma.

Atypical fibroxanthoma (AFX) which is histologically similar to malignant fibrous histiocytoma (MFH), occurs in the sun-exposed skin. The presence of mutations at codons 12 and 13 of the H- and K-ras genes and in exons 1 and 2, which include codons 12, 13, and 61, of the N-ras gene was studied in 8 cases of AFX and 8 cases of storiform-pleomorphic-type MFH using polymerase chain reaction (PCR)-restriction fragment length polymorphism and PCR-single-conformation polymorphism. Two of the 8 cases of MFH showed ras mutations in the H-ras gene at codon 12 (GGC-AGC) and in the K-ras gene at codon 13 (GGC-GAC). H- and K-ras gene mutations were not seen in any of the cases of AFX (0 of 8). N-ras gene mutation was not detected in either the AFX (0 of 8) or MFH (0 of 8) cases. In conclusion, although the number of cases in this study was small, H- and K-ras genes were present in some of the MFH cases and accordingly may play an important role in the pathogenesis of MFH. In addition, the finding that H-, K-, and N-ras gene mutations are not present in AFX may indicate why AFX has a more favorable behavior than MFH.

Adult↗

Cerebral fat embolism after a nondisplaced tibial fracture: case report.

Fat embolism syndrome has been observed after traumatic or nontraumatic events. In traumatic cases, fat embolism syndrome is known to occur in patients with a fracture of a long bone. The case of a patient with a cerebral fat embolism associated with a nondisplaced fracture of the tibial shaft is reported.

Adult↗

Pulmonary fibrosis with intractable pneumothorax: new pulmonary manifestation of relapsing polychondritis.

Relapsing Polychondritis is a rare disease which causes the repetitive inflammation of cartilage and connective tissues. Although the large airway is sometimes involved and the stenosis of them often influences the prognosis of the patients, there have been few reports concerning the manifestation of the peripheral lung. A 60-year-old man with pulmonary fibrosis was admitted to a regional hospital due to sudden deafness, and then he suffered from relapsing polychondritis. During the steroid therapy, he also suffered from bilateral pneumothoraces. His computed tomogram revealed many bilateral bullae, emphysematous changes, and fibrotic changes in bilateral lungs. The mechanism of generating peripheral pulmonary manifestations is also discussed.

Blood Cell Count↗

Angiotensin II induces expression of the Tie2 receptor ligand, angiopoietin-2, in bovine retinal endothelial cells.

Recent studies have shown that angiopoietins (Angs) and their receptor, Tie2, play a role in vascular integrity and neovascularization. The renin-angiotensin system has been hypothesized to contribute to the development of diabetic retinopathy. In this study, we investigated the effect of angiotensin II (AII) on Ang1 and Ang2 expression in cultured bovine retinal endothelial cells (BRECs). AII stimulated Ang2 but not Ang1 mRNA expression in a dose- and time-dependent manner. This response was inhibited completely by angiotensin type 1 receptor (AT1) antagonist. AII increased the transcription of Ang2 mRNA, but did not change the half-life. Protein kinase C (PKC) inhibitor completely inhibited AII-induced Ang2 expression, and the mitogen-activated protein kinase (MAPK) inhibitor also inhibited it by 69.4+/-15.6%. In addition, we confirmed the upregulation of Ang2 in an AII-induced in vivo rat corneal neovascularization model. These data suggest that AII stimulates Ang2 expression through AT1 receptor-mediated PKC and MAPK pathways in BREC, and AII may play a novel role in retinal neovascularization.

Angiopoietin-1↗

Three-dimensional anisotropy contrast magnetic resonance axonography to predict the prognosis for motor function in patients suffering from stroke.

OBJECT: The purpose of this study was to assess how early wallerian degeneration in the corticospinal tracts of patients who had suffered from stroke was detected using three-dimensional anisotropy contrast (3D-AC) magnetic resonance (MR) axonography and to explore the possibility of predicting the prognosis for motor function in these patients. METHODS: Ten healthy volunteers and 16 stroke patients with hemiparesis were studied using MR images including 3D-AC MR axonography images obtained using a 1.5-tesla MR imaging system. The axonography was performed using an echoplanar imaging method. All patients underwent MR studies 2, 3, and 10 weeks after stroke onset. To detect wallerian degeneration, the diffusion anisotropy in the corticospinal tracts at the level of the upper pons was evaluated on axial images. These MR findings were compared with the patients' motor functions, which were classified according to the Brunnstrom criteria 12 weeks after the onset of stroke. In all patients with poor recovery (Brunnstrom Stages I-IV), wallerian degeneration, which was demonstrated as a reduction in diffusion anisotropy on axonography images, could be observed in the corticospinal tracts; this degeneration was not found in patients with good recovery (Stages V and VI). Axonography could be used to detect degeneration between 2 and 3 weeks after stroke onset. On conventional T2-weighted MR images, hyperintense areas indicating wallerian degeneration were not detected until 10 weeks after stroke onset. CONCLUSIONS: With the aid of 3D-AC MR axonography, wallerian degeneration can be detected in the corticospinal tracts during the early stage of stroke (2-3 weeks after onset), much earlier than it can be detected using T2-weighted MR imaging. The procedure of 3D-AC MR axonography may be useful in predicting motor function prognosis in stroke patients.

Adult↗

Isolation, and biological properties of a new cell cycle inhibitor, curvularol, isolated from Curvularia sp. RK97-F166.

A new cell growth inhibitor, curvularol, was isolated from the fermentation broth of Curvularia sp. RK97-F166. Curvularol showed no antibacterial activity, and very weak antifungal activity. However, curvularol inhibited the cell cycle progression of normal rat kidney (NRK) cells in G1 phase at 150 ng/ml. Curvularol induced the morphological reversion of srcts-transformed NRK cells at 100 ng/ml, and inhibited protein synthesis same as cycloheximide.

Animals↗

Effects of rho-associated protein kinase inhibitor Y-27632 on intraocular pressure and outflow facility.

PURPOSE: To elucidate the roles of Rho-associated protein kinase (ROCK) in regulating intraocular pressure (IOP) and outflow facility in the rabbit eye. METHODS: A specific ROCK inhibitor Y-27632 was used. The IOP, the outflow facility, and the pupil diameter were determined before and after the topical, intracameral, or intravitreal administration of Y-27632 in rabbits. Western blot analysis was used to identify specific ROCK isoform in human trabecular meshwork (TM) cells and bovine ciliary muscle (CM) tissues. The cell morphology and distribution of actin filaments and vinculin in TM cells were studied by cell biology techniques. Carbachol (Cch)-induced contraction of isolated bovine CM strips after administration of Y-27632 was measured in a perfusion chamber. RESULTS: In rabbit eyes, administration of Y-27632 resulted in a significant decrease in IOP in a dose-dependent manner. An increase of the outflow facility and pupil size dilation was also observed in Y-27632-treated eyes. Western blot analysis revealed the presence of p160ROCK in human TM cells and bovine CM tissues. In cultured human TM cells, exposure to Y-27632 caused retraction and rounding of cell bodies as well as disruption of actin bundles and impairment of focal adhesion formation. Y-27632 in addition inhibited Cch-induced contraction of isolated bovine CM strips. CONCLUSIONS: Administration of Y-27632 caused a reduction in IOP and an increase in the outflow facility. The in vitro experiments suggest that the IOP-lowering effects of Y-27632 may be related to the altered cellular behavior of TM cells and relaxation of CM contraction. These studies suggest that ROCK inhibitors may have great potential to be developed for treatment of glaucoma and other ocular diseases.

Actins↗

Inhibitory effects of antithrombin III against leukocyte rolling and infiltration during endotoxin-induced uveitis in rats.

PURPOSE: This study was designed to investigate the suppressive effects of antithrombin (AT)III on inflammatory reactions during endotoxin-induced uveitis (EIU) in rats by studying leukocyte-endothelium interactions. METHODS: EIU was induced in Lewis rats by footpad injection of lipopolysaccharide (LPS). ATIII was administered immediately after or at 6 hours after LPS injection. Its suppressive effects on inflammatory leukocyte behavior were evaluated in vivo with acridine orange digital fluorography. Clinical signs of inflammation were also examined, and aqueous humor (AH) was collected to evaluate leukocyte infiltration and protein leakage. In a separate experiment, P-selectin mRNA expression was studied in the iris-ciliary body (ICB) and the retina. RESULTS: After treatment with ATIII, leukocyte rolling was substantially inhibited along the retinal veins, suppressing subsequent leukocyte infiltration into the vitreous cavity. Similarly, leukocyte infiltration and protein leakage into the AH were significantly reduced with ATIII treatment. The clinical grade of EIU was substantially lower in ATIII-treated rats. In addition, delayed administration of ATIII after EIU induction significantly attenuated these inflammatory reactions. The levels of P-selectin mRNA expression in both ICB and retina, which were upregulated after LPS injection, were substantially lower in the ATIII-treated rats. CONCLUSIONS: ATIII treatment significantly inhibited inflammatory reactions induced with LPS. Its suppressive effects on P-selectin expression could contribute to the attenuation of leukocyte infiltration, possibly by inhibiting leukocyte rolling. The current findings suggest that ATIII may have a role in the management of patients with uveitis.

Animals↗

Inhibitory effects of neurocan and phosphacan on neurite outgrowth from retinal ganglion cells in culture.

PURPOSE: Neurocan and phosphacan are nervous tissue-specific chondroitin sulfate proteoglycans (CSPGs) that are highly expressed in postnatal rat retina. To elucidate potential roles of neurocan and phosphacan on neurite outgrowth from retinal ganglion cells (RGCs), in vitro experiments were conducted with purified RGCs. METHODS: Neurocan and phosphacan were purified from postnatal rat brain by DEAE-column chromatography and subsequent gel chromatography. RGCs were obtained from postnatal rat retinas by a two-step immunopanning procedure using an anti-Thy 1,1 antibody and an anti-macrophage antibody. Neurite outgrowth from RGCs was examined on poly-L-lysine (PLL)-conditioned plates, and PLL-conditioned plates treated with neurocan or phosphacan. RESULTS: Compared with PLL-conditioned plates, neurocan and phosphacan inhibited neurite outgrowth from RGCs at 48 and 72 hours after seeding. When chondroitin sulfate side chains linked to the core proteins were digested by chondroitinase ABC, the inhibitory effect remained, indicating that the core proteins are related to the effect. Furthermore, the digestion of chondroitin sulfate side chains linked to phosphacan core protein significantly promoted the inhibitory effect of phosphacan on neurite outgrowth from RGCs. CONCLUSIONS: Neurocan and phosphacan, which are highly expressed in postnatal rat retina, inhibit neurite outgrowth from postnatal rat RGCs, indicating that these proteoglycans may be inhibitory factors against neurite outgrowth from RGCs during retinal development.

Animals↗

In vivo evaluation of platelet--endothelial interactions after transient retinal ischemia.

PURPOSE: Accumulating evidence suggests that platelets play an important role in ischemia-reperfusion injury. To fulfill that role, platelets flowing in the bloodstream would have to interact with retinal endothelial cells and to accumulate in the postischemic retina. This study was designed to investigate quantitatively platelet-endothelial interactions in postischemic retina after transient retinal ischemia. METHODS: Transient retinal ischemia was induced in Long-Evans rats for 60 minutes by temporal ligation of the optic nerve. Isolated platelet samples labeled with carboxyfluorescein diacetate succinimidyl ester were administered intravenously to recipient rats after various reperfusion periods. Platelet-endothelial interactions in postischemic retina were evaluated in vivo with a scanning laser ophthalmoscope. Anti-P-selectin monoclonal antibody (mAb) was administered 5 minutes before the injection of labeled platelets. P-selectin gene expression in the postischemic retina was studied by semiquantitative polymerase chain reaction. RESULTS: Under basal conditions, infused platelets showed minimal interactions with retinal endothelial cells. In contrast, postischemic retinas showed active platelet-endothelial interactions. Many platelets were observed rolling along and adhering to the major retinal veins. The number of rolling and adhering platelets reached a peak (555 +/- 65/mm per min and 25.8 +/- 3.2/mm(2)) 12 hours after reperfusion. However, the interactions between platelets and postischemic retinal endothelial cells were substantially inhibited by neutralizing P-selectin expressed on endothelial cells. In addition, P-selectin gene expression in postischemic retina corresponded with the time course of platelet-endothelial interactions during the reperfusion period. CONCLUSIONS: This study demonstrated that platelets actively interacted with retinal endothelial cells in the postischemic retina through P-selectin expressed on the retinal endothelial cells.

Animals↗

[Surgery of anterior communicating artery aneurysms with the perforating artery branching from the dome].

The authors have treated two cases of anterior communicating artery aneurysms with the perforating artery branching from the top of the dome. Case 1 was a 32-year-old female. She developed sudden-onset of headache while sleeping. Angiography showed an anterior communicating artery aneurysm with its dome directed upward. The left pterional approach was utilized, and a rather thick perforating artery was found branching from the top of the dome and going upward. Neck clipping of the aneurysm was performed resulting in interruption of the blood flow of the perforating artery. The patient showed no neurological deficit postoperatively. Case 2 was a 67-year-old female. She suffered from sudden-onset of headache and was transferred from another hospital to the author's care. Three-dimensional CT angiography revealed an anterior communicating artery aneurysm with its dome directed in the anterior-superior direction. A rather thick perforating artery was coming off the top of the dome. Neck clipping was carried out, but permanent memory impairment appeared postoperatively. The perforating arteries coming off the anterior communicating artery have been called the hypothalamic arteries. In 1994, Serizawa et al divided these arteries into three groups. One is the subcallosal artery, which gives blood flow not only to the hypothalamus but also to the subcallosal area. The other two are the hypothalamic and chiasmatic arteries. The authors consider that this nomenclature of those arteries is suitable in practical use for surgery, because these arteries have different vessel sizes, they originate from the anterior communicating artery, and supply different territories with blood. Since the septal nuclei are in the subcallosal area, interruption of blood flow of the subcallosal artery by the clipping of an aneurysm may result in memory impairment caused by damage to the septal nuclei. Serizawa et al also reported that some branches are coming from the A2-segment to the subcallosal area as collateral circulation. In the author's two cases, the perforating arteries branching from the top of the domes were considered to be subcallosal arteries, because their size was rather thick and the arteries were going upward directed probably to the subcallosal area. Memory impairment in case 2 was considered a natural outcome due to the interruption of blood flow of the subcallosal artery by the clipping of the aneurysm. On the other hand, in case 1, sufficient collateral blood flow from A2 to the subcallosal area might have prevented damage to the septal nuclei, probably because of the insufficient size of the subcallosal artery. In these rare cases, dome clipping and coating should be the first choice of treatment, because prognosis after dome clipping of the aneurysm with coating was rather satisfactory.

Adult↗

Inhibitory effect of ischemic preconditioning on leukocyte participation in retinal ischemia-reperfusion injury.

PURPOSE: Recent reports have shown that ischemic preconditioning induces strong protection against retinal damage by subsequent prolonged ischemia and that this protection is mediated by mechanisms involving the adenosine A1 receptor. This study was designed to evaluate quantitatively the effects of ischemic preconditioning on leukocyte-mediated reperfusion injury after transient retinal ischemia and to define the role of the adenosine A1 receptor in these effects. METHODS: Transient retinal ischemia was induced in male rats by temporary ligation of the optic nerve. Ischemic preconditioning (5 minutes of ischemia) was induced 24 hours before 60 minutes of ischemia. The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) was administered intramuscularly immediately after ischemic preconditioning. Leukocyte behavior in the retina after 60 minutes of ischemia was evaluated in vivo with acridine orange digital fluorography. RESULTS: Ischemic preconditioning inhibited leukocyte rolling. The maximum number of rolling leukocytes was reduced to 3.0% at 12 hours after reperfusion (P < 0.01). Subsequent leukocyte accumulation was also decreased with ischemic preconditioning. The maximum number of accumulated leukocytes was reduced to 22.6% at 24 hours after reperfusion (P < 0.01). These inhibitory effects were suppressed by administration of DPCPX (P < 0.0001). The numbers of rolling leukocytes at 12 hours after reperfusion and accumulated leukocytes at 24 hours after reperfusion were 102.7% (NS) and 83.4% (P < 0.01), respectively, compared with the number without ischemic preconditioning. CONCLUSIONS: The present study demonstrates the inhibitory effects of ischemic preconditioning on leukocyte rolling and subsequent leukocyte accumulation during retinal ischemia-reperfusion injury. Furthermore, the adenosine A1 receptor may play an important role in these inhibitory effects.

Acridine Orange↗

Monoclonal antibody-mediated drug targeting to choroidal neovascularization in the rat.

PURPOSE: Active drug targeting mediated by monoclonal antibodies (mAbs) of vascular endothelial cells in tumors is a new concept in cancer therapy. Integrin alphavbeta3 has been reported to be strongly expressed in vascular endothelial cells of surgically excised choroidal neovascular membranes and is thought to be a potential antigen for mAb-mediated drug targeting of choroidal neovascularization (CNV). The objective of this study was to evaluate the efficacy of drug targeting mediated by anti-integrin alphavbeta3 mAbs in a laser-induced CNV rat model. METHODS: The mitomycin C (MMC)-dextran (MMCD) conjugate was synthesized with a carbodiimide-catalyzed reaction. The mAb was conjugated with MMCD (MMCD-mAb). To evaluate the feasibility of mAb-mediated drug targeting in vitro, we investigated the effect of the immunoconjugates involving dextran-binding MMC on the proliferation of human umbilical vein endothelial cells (HUVECs). CNV was induced by laser photocoagulation in male Brown Norway rats. Immunolocalization of integrin alphavbeta3 in CNV lesions was assessed immunohistochemically with the anti-von Willebrand factor antibody as an endothelial cell marker. Intravenous administration of saline (n = 7), 1 mg/day mAb (n = 7), 100 microg/kg per day free MMC (n = 7), MMCD with irrelevant Ab (n = 7), unconjugated MMCD with unconjugated mAb (MMCD+mAb; n = 7), or MMCD with mAb (MMCD-mAb; n = 8) containing an equal amount of free MMC, was performed daily for 3 days from day 14 after CNV induction. CNV was assessed by fluorescein angiography 2 weeks after treatment. Fluorescein leakage was scored on a four-grade scale. The animals were killed 2 weeks after treatment, and the lesions were evaluated histologically. RESULTS: The inhibition of immunoconjugates on the proliferation of HUVECs was enhanced specifically by the mediatory effect of the mAb. Endothelial cells demonstrated strong immunoreactivity of integrin alphavbeta3 in the CNV. In the vehicle-treated group, fluorescein leakage equal to that before treatment was observed 2 weeks after treatment, with an average score of 2.00 +/- 0.17 (mean +/- SEM). MMCD-mAb significantly inhibited the development of CNV in rats (P < 0.01). Moreover, the thickness of the lesions was significantly reduced in the MMCD-mAb-treated group (P < 0.01). CONCLUSIONS: Immunoconjugates effectively inhibited progression of CNV in this model. The results suggest that mAb-mediated drug targeting may be beneficial in the treatment of CNV.

Animals↗