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Biomedical subjects

H Oda

Publications and source records attributed to H Oda.

At least 37 records · Page 2Linked to original sources
PubMed2001

An investigation of cell proliferation and soluble mediators induced by interleukin 1beta in human synovial fibroblasts: comparative response in osteoarthritis and rheumatoid arthritis.

OBJECTIVES AND DESIGN: The difference in cell proliferation and release of soluble factors in response to interleukin 1beta (IL-1beta) in fibroblasts obtained from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) and from normal skin has been investigated. TREATMENT: The cells were treated with recombinant IL-1beta in the presence or absence of pharmacological agents for 24 h or 48 h. METHODS: Cell proliferation was examined by WST-1 assay, and the amounts of interleukin-6 (IL-6), interleukin-8 (IL-8), macrophage colony stimulating factor (M-CSF), vascular endothelial growth factor (VEGF), matrix metalloproteinase-1 (MMP-1), and prostaglandin E2 (PGE2) were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: IL-1beta dose-dependently enhanced the proliferation of all fibroblasts. The proliferative response to IL-1beta in RA synovial fibroblasts was greater than that in OA synovial and skin fibroblasts. However, there was no difference in spontaneous levels of soluble factors between OA and RA fibroblasts, though medium concentrations of IL-1beta-released VEGF, MMP-1, and PGE2, but not cytokines, in RA were slightly higher than those in OA. Ability to release soluble mediators was pronouncedly increased at 3 h to 9 h after stimulating fibroblasts with IL-1beta for 1 h. The proliferative response to IL-1beta in all fibroblasts was inhibited by dexamethasone and the NF-kappaB inhibitor hymenialdisine but not the cyclooxygenase 2 (COX-2) inhibitor NS-398. But PGE2 prevented proliferation of RA fibroblasts when added to medium up to 3 h after IL-1beta stimulation. Dexamethasone also inhibited the release of IL-6, IL-8, and PGE2 induced by IL-1beta in both OA and RA fibroblasts. NS-398 exhibited an inhibition of IL-1beta-induced IL-6 production as well as PGE2 production. Hymenialdisine inhibited IL-6 production and reduced IL-8 production dependent on synovial cell strains. Methotrexate had no effect on the response to IL-1beta in synovial fibroblasts. CONCLUSION: The present results indicate that the activation of NF-kappaB plays an important role in the proliferative response to IL-1beta in human fibroblasts, and suggest that PGE2 acts as a modulator of cell proliferation in inflamed synovial tissue. It appears that the ability to produce soluble factors in RA synovial fibroblasts is not intrinsic. However, the response to IL-1beta in RA cells seems to be greater than that in OA cells.

Arthritis, Rheumatoid↗
PubMed2001

Involuted intraosseous lipoma of the sacrum showing high signal intensity on T1-weighted magnetic resonance imaging (MRI).

Involuted intraosseous lipoma with extensive fat necrosis resulting in cyst formation (Milgram stage III) is distinguishable from lesions without necrosis (stage I) or lesions with focal fat necrosis (stage II), based on differences in signal intensity on magnetic resonance imaging (MRI). Fat tissue has a high signal intensity on both T1- and T2-weighted MR images, whereas the extensive fat necrosis that results in cyst formation shows high signal intensity on T2-weighted images and low intensity on T1-weighted images. We report a patient in whom an intraosseous lipoma with high signal intensity on both T1- and T2-weighted MRI was found to be extensively involuted on histopathologic examination. Intraosseous lipoma appears to undergo spontaneous involution. In some patients, therefore, surgical excision may not be necessary. A correct preoperative diagnosis should reduce the necessity for a biopsy or surgery. Although lesions classified as stage I or II are easily identified by MRI, those of stage III are difficult to diagnose preoperatively by this method.

Bone Neoplasms↗
PubMed2001

GC/MS analysis of polybrominated diphenyl ethers in fish collected from the Inland Sea of Seto, Japan.

Development of an analytical method for polybrominated diphenyl ethers (PBDEs) in fish and their concentration in Japanese marine fish were investigated. Fish homogenate was extracted with diethyl ether/hexane (1 + 3). The extract was cleaned up by automated gel permeation chromatography (GPC) and then by mini-column chromatography, which consisted of three layers of silica gel and sulfuric acid-impregnated silica gel. The PBDE fraction was concentrated and injected into a GC/MS with negative chemical ionization (NCl). Recoveries of the 15 individual PBDEs (BDE-15, 28, 37, 47, 66, 71, 75, 77, 85, 99, 100, 119, 153, 154, and 209) each at a fortification level of 4 ng/g lipid were in the range of 88-128% and the relative standard deviations (RSD) were 0.43-7.6% (n = 4). Seven species of marine fish (conger eel, flounder, gray mullet, horse mackerel, red sea bream, sea bass, and yellowtail) were collected from the Inland Sea of Seto, and were analyzed with the developed method. Seven PBDEs (BDE-28, 47, 66, 99, 100, 153, and 154) were detected in all the samples. The most abundant PBDE congener was BDE-47 found in all the samples. Relatively high levels of PBDEs were found in the gray mullets and yellowtails.

Animals↗
PubMed2001

Type I and type III procollagen gene expressions in the early phase of ligament healing in rabbits: an in situ hybridization study.

The purpose of this study is to observe type I and type III procollagen gene expressions in the healing ligament using in situ hybridization histochemistry. The rabbit medial collateral ligaments were incised and harvested at 3, 7, 14, and 28 days postoperatively. The healing ligament showed increased expression of both procollagen genes through this period compared with the unoperated ligament. The peak expression level was observed at 7 or 14 days for type I and at 7 days for type III, respectively. The strongest expression of both genes was detected in the scar tissue created between the ends of the old ligament. Although type III procollagen gene expression was observed almost only in the newly created scar tissue, type I procollagen gene was expressed not only in the scar tissue, but also at the ends of the previously normal ligament. These results suggest that type I collagen synthesis begins shortly after ligament injury and occurs at the ends of the injured ligament as well as in the scar tissue, and that type III collagen is largely synthesized in the scar tissue around one week after injury but continues being synthesized for at least four weeks after injury.

Animals↗
PubMed2001

Suppression of fibrous adhesion by proteoglycan decorin.

Small proteoglycan decorin is known to suppress the bioactivity of TGF-beta through a competitive binding with the cell surface receptors for the cytokine. Based on this knowledge, we hypothesized that decorin could reduce the formation of fibrous adhesion, because our previous study showed the neutralizing antibody to TGF-beta1 has that effect. An intra-articular adhesion model in the rabbit knee joint was employed in this study, and decorin was administered into the joint cavity continuously during the 4 weeks of the experiment. The results of the dose-response study demonstrated that decorin suppresses formation of fibrous adhesion in a dose-dependent manner. When the administration of decorin was limited to shorter periods, this effect was considerably impaired and the necessity of long-term administration was demonstrated. On the other hand, when administered together with TGF-beta1, decorin still suppressed adhesion but to a lesser extent, and it was suggested that this proteoglycan could have other significant mechanism(s) to suppress adhesion besides the neutralization of TGF-beta. Thus, the present study showed that decorin could inhibit adhesion formation by both TGF-beta dependent and independent mechanisms. Considering that decorin exists ubiquitously in the body, its administration might be a promising approach to suppress adhesion.

Animals↗
PubMed2001

Dietary taurine potentiates polychlorinated biphenyl-induced hypercholesterolemia in rats*

The effect of dietary taurine on cholesterol metabolism and the distribution of lipoprotein-cholesterol in serum of rats fed a diet containing polychlorinated biphenyls (PCB) was examined. Young male Wistar rats (60 g) were fed diets containing 0.2 g/kg diet of PCB and/or 30 g/kg diet of taurine for 15 days. The experiment was performed as the 2 (PCB) x 2 (taurine) factorial design. The addition of PCB elevated serum levels of total- and HDL-cholesterol and apolipoprotein A-I, which is a major apolipoprotein of HDL. Simultaneous supplementation of taurine with PCB amplified the increase of the serum level of total- and HDL-cholesterol. Hepatic concentrations of cholesterol and total lipids were significantly elevated by the supplementation of PCB, and taurine significantly amplified these increases caused by PCB. PCB suppressed hepatic cholesterol 7alpha-hydroxylase (CYP7A1) gene expression, and taurine induced CYP7A1 gene expression. Taurine also enhanced PCB-induced elevation of malic enzyme mRNA in the liver. These results suggest that taurine enhanced PCB-induced hyper-alpha-cholesterolemia and that taurine has a role in increasing HDL-cholesterol.

Journal Article↗
PubMed2001

Taurine inhibits development of atherosclerotic lesions in apolipoprotein E-deficient mice.

1. The effects of taurine on the development of atherosclerotic lesions were investigated in apolipoprotein (apo) E-deficient mice, an animal model with severe hypercholesterolaemia and extensive atherosclerosis. These mice were fed a normal laboratory chow containing 2% taurine for 12 weeks. 2. Serum total cholesterol was significantly elevated after 12 weeks treatment with taurine. This elevation was due to increases in very low-density lipoprotein- and low-density lipoprotein-cholesterol. 3. Despite such effects on serum lipoproteins, analysis using en face oil red O staining revealed that taurine reduced the area of arterial lipid accumulation by 28%, as measured quantitatively as an index of atherosclerosis. Histological examination also demonstrated a decrease in the size of aortic lesions in taurine-treated mice. 4. Serum levels of thiobarbituric acid reactive substances (TBARS) in apoE-deficient mice were higher than in normolipidaemic C57BL/6J mice. Serum TBARS levels were significantly decreased by 12 weeks treatment of apoE-deficient mice with taurine. 5. Thus, taurine prevents the formation of atherosclerotic lesions, independently of serum cholesterol levels, and the results suggest that the anti-oxidative effects of taurine are related to its anti-atherosclerotic actions.

Animals↗
PubMed2001

Mechanism of increased serum soluble interleukin-2 receptor levels in patients on continuous ambulatory peritoneal dialysis.

OBJECTIVE: The aim of this study was to investigate the mechanism underlying the increase of serum soluble interleukin-2 receptor (IL-2R) levels in patients on continuous ambulatory peritoneal dialysis. MATERIAL AND METHODS: In 13 dialysis patients and 17 healthy controls, serum soluble IL-2R levels were determined by enzyme-linked immunosorbent assay, and CD25-positive (cell surface IL-2R-positive) cells were detected by flow cytometry. Soluble IL-2R levels were also measured in the supernatant of cultured peripheral blood mononuclear cells. RESULTS: The serum soluble IL-2R level was significantly higher in the patients than in the healthy controls (p < 0.0001). In contrast, both the percentage and the absolute count of CD25-positive cells showed no significant differences, and neither did the soluble IL-2R level in culture supernatant. Serum soluble IL-2R levels showed a positive correlation with the serum beta2-microglobulin level (p < 0.01), the age of the patients (p < 0.05), and duration of dialysis (p < 0.05), as well as a negative correlation with the urine volume (p < 0.05). CONCLUSIONS: The increase of serum soluble IL-2R in patients on peritoneal dialysis may be caused by accumulation due to its low transperitoneal clearance and low urinary excretion.

Adult↗
PubMed2001

Xeroderma pigmentosum group A gene action as a protection factor against 4-nitroquinoline 1-oxide-induced tongue carcinogenesis.

To test the hypothesis that nucleotide excision repair (NER) plays a protective role in chemical carcinogenesis in internal organs, xeroderma pigmentosum group A gene-deficient (XPA(-/-)) mice, heterozygous (XPA(+/-)) and wild-type (XPA(+/+)) mice were orally administered 0.001% 4-nitroquinoline 1-oxide (4NQO) in their drinking water and compared. After 50 weeks of 4NQO exposure, tongue squamous cell carcinomas (SCCs) occurred in XPA(-/-) mice only, no tumors being observed in XPA(+/-) and XPA(+/+) animals. Of the XPA(-/-) mice 86% had tumors and 100% demonstrated multiple foci of dysplastic epithelium in the tongue. Accumulation of p53 protein was immunohistochemically detected in 56% of the SCCs. Mutational analysis of the p53 gene (exons 4-10) in carcinoma DNA revealed missense mutations in exons 5 and 9 in four of 20 samples. Our results clearly demonstrate that the NER gene XPA acts as a defensive factor against 4NQO-induced tongue carcinogenesis in vivo.

4-Nitroquinoline-1-oxide↗
PubMed2001

Neutralization of fibroblast growth factor-2 reduces intraarticular adhesions.

Adhesion is a serious complication after trauma or surgery. Because adhesion formation is essentially a fibrogenetic process, a series of growth factors are assumed to be involved in its development. If this is true, it may be possible that inhibition of the growth factor activity suppresses adhesion formation. The current study was conducted to verify this hypothesis on fibroblast growth factor-2 using an intraarticular adhesion model in the rabbit knee. Forty Japanese White rabbits were used. They were divided randomly into five groups of eight animals, and in three of them, activity of endogenous fibroblast growth factor-2 was suppressed locally by a neutralizing antibody. The remaining two groups served as controls, and formation of adhesions was evaluated 4 weeks after surgery. The results showed that the administration of the antibody reduced the extent of adhesions macroscopically, whereas histologic observation and collagen content measurement suggested the adhesion tissue was not affected significantly. Corresponding to the macroscopic findings, contraction of the knee was improved in the antibody groups. The findings showed that suppression of fibroblast growth factor-2 activity reduces adhesions. It is expected that control of the cytokine activity may become a novel method for reducing adhesions.

Animals↗
PubMed2001

Protein-protein interaction panel using mouse full-length cDNAs.

We have developed a novel assay system for systematic analysis of protein-protein interactions (PPIs) that is characteristic of a PCR-mediated rapid sample preparation and a high-throughput assay system based on the mammalian two-hybrid method. Using gene-specific primers, we successfully constructed the assay samples by two rounds of PCR with up to 3.6 kb from the first-round PCR fragments. In the assay system, we designed all the steps to be performed by adding only samples, reagents, and cells into 384-well assay plates using two types of semiautomatic multiple dispensers. The system enabled us examine more than 20,000 assay wells per day. We detected 145 interactions in our pilot study using 3500 samples derived from mouse full-length enriched cDNAs. Analysis of the interaction data showed both several significant interaction clusters and predicted functions of a few uncharacterized proteins. In combination with our comprehensive mouse full-length cDNA clone bank covering a large part of the whole genes, our high-throughput assay system will discover many interactions to facilitate understanding of the function of uncharacterized proteins and the molecular mechanism of crucial biological processes, and also enable completion of a rough draft of the entire PPI panel in certain cell types or tissues of mouse within a short time.

Animals↗
PubMed2001

Urinary prostaglandin D synthase (beta-trace) excretion increases in the early stage of diabetes mellitus.

OBJECTIVE: Circulating levels of lipocalin-type prostaglandin D synthase (L-PGDS)/beta-trace reportedly increase in renal failure as well as in cardiovascular injuries. We investigated the alterations of L-PGDS in urine and plasma in the early stage of type-2 diabetic patients. METHOD: Thirty-six type-2 diabetic patients and 29 normal subjects were studied. Overnight spot urine and plasma samples were obtained in the morning. L-PGDS was measured by ELISA method using anti-L-PGDS antibody. Variables indicating renal function were determined. RESULTS: Plasma L-PGDS concentration was slightly higher in the patients with diabetes mellitus than in the control subjects, whereas the urinary L-PGDS excretion almost doubled in the diabetic patients as compared with that in the control subjects. Plasma L-PGDS was determined by plasma creatinine (Cr) concentration while urinary L-PGDS excretion was correlated solely with urinary protein excretion. There was no relationship between plasma L-PGDS concentration and urinary L-PGDS excretion. The averaged plasma concentration of L-PGDS in the diabetics with a normal Cr level in plasma, corresponding to that in the controls, was determined by the plasma Cr concentration. On the other hand, the urinary L-PGDS excretion was determined by the amount of proteinuria and greater in the diabetics with a normal Cr level in plasma than in the controls even when the patients exhibited urinary protein excretion equal to that in the control subjects. CONCLUSIONS: Urinary L-PGDS excretion increased in the early stage of kidney injury in patients with type-2 diabetes mellitus. The urinary excretion was correlated independently with urinary protein excretion even when there was no difference in urinary protein or albumin excretions, thereby suggesting that urinary L-PGDS excretion is possibly a more sensitive indicator of renal injuries than proteinuria. Urinary L-PGDS may thus predict the progression of renal injuries in diabetic patients.

Analysis of Variance↗
PubMed2001

Involvement of prostaglandin E(2) in interleukin-1alpha-induced parathyroid hormone-related peptide production in synovial fibroblasts of patients with rheumatoid arthritis.

Synovial fibroblasts, established in culture from patients with RA, were treated with proinflammatory cytokines and prostaglandin E(2) (PGE(2)) for 24 h. These cells enhanced the production and the messenger RNA expression of PTH-related peptide (PTHrP) using proinflammatory cytokines, such as interleukin (IL)-1alpha, tumor necrosis factor-alpha without the coordination of other cytokines. In addition, PGE(2) which has been induced with IL-1, also enhanced the production of PTHrP. The IL-1alpha-induced PTHrP production was inhibited by PG H synthetase (Cox) inhibitors, indomethacin, and also by Cox-2 inhibitor, NS398. The synovial fibroblasts expressed PGE(2) receptor subtypes, EP2, EP3, EP4, but not EP1, as detected by RT-PCR. Of the PGE(2) receptor agonists, EP4 agonist showed the most marked induction of PTHrP, and EP2 agonist partly induced the production. However, these PGE(2) receptors were not induced by the treatment with IL-1alpha and PGE(2). These results suggest that induction of PGE(2) by IL-1alpha may be an important component of the PTHrP production of the inflammatory process in synovial tissues from patients with RA. These findings are the first to demonstrate that PGE(2) stimulates PTHrP production, which is mediated mostly by EP2 and EP4 receptors.

Arthritis, Rheumatoid↗
PubMed2001

Real-time imaging of cell-cell adherens junctions reveals that Drosophila mesoderm invagination begins with two phases of apical constriction of cells.

Invagination of the epithelial cell sheet of the prospective mesoderm in Drosophila gastrulation is a well-studied, relatively simple morphogenetic event that results from dynamic cell shape changes and cell movements. However, these cell behaviors have not been followed at a sufficiently short time resolution. We examined mesoderm invagination in living wild-type embryos by real-time imaging of fluorescently labeled cell-cell adherens junctions, which are located at the apical zones of cell-cell contact. Low-light fluorescence video microscopy directly visualized the onset and progression of invagination. In an initial period of approximately 2 minutes, cells around the ventral midline reduced their apical surface areas slowly in a rather synchronous manner. Next, the central and more lateral cells stochastically accelerated or initiated their apical constriction, giving rise to random arrangements of cells with small and relatively large apices. Thus, we found that mesoderm invagination began with slow synchronous and subsequent fast stochastic phases of cell apex constriction. Furthermore, we showed that the mesoderm invagination of folded gastrulation mutant embryos lacked the normal two constriction phases, and instead began with asynchronous, feeble cell shape changes. Our observations suggested that Folded gastrulation-mediated signaling enabled synchronous activation of the contractile cortex, causing competition among the individual mesodermal cells for apical constriction. Movies available on-line: http://www.biologists.com/JCS/movies/jcs2073.html

Animals↗
PubMed2001

Th1/Th2 balance alteration in the clinical course of a patient with acute viral myocarditis.

Cytokines have an important role in the pathogenesis and pathophysiology of myocarditis. In this study, subsets of peripheral helper T lymphocytes (Th) in a patient with acute viral myocarditis were analyzed by 3-color flow cytometry. During the clinical course of myocarditis, the Th1/Th2 ratio of peripheral lymphocytes changed. Th1 was dominant in the acute inflammatory phase during which levels of creatine kinase (CK) increased (day 6), then Th2 levels overtook those of Th1 in the recovery phase during which levels of CK decreased (day 13 and 20). At the time of discharge (day 35), Th1 and Th2 had normalized. Thus, it was speculated that the induction of lymphocytic myocarditis was associated with Th1 dominant status, and recovery was related to Th2 polarity. Th subset imbalances may play an important role in the pathogenesis of acute viral myocarditis and these analyses may be useful for understanding the disease activity of myocarditis.

Adult↗
PubMed2001

Early and long-term mortality of the clinical subtypes of myocarditis.

The frequency of myocarditis and the prognosis for patients remains uncertain and, moreover, the clinical classification of myocarditis is controversial. From 1985 to 2000, 71 adult patients with clinically suspected myocarditis were admitted to 11 cardiovascular centers. Of these, 48 cases had histology proven myocarditis: 41 cases of lymphocytic myocarditis, 6 of giant cell myocarditis and 1 of eosinophilic myocarditis. Myocarditis was classified as acute (30 cases) or chronic (18 cases) according to the onset of the disease, and acute myocarditis was further categorized into common or fulminant type depending on whether or not patients required mechanical circulatory support in the management of heart failure (9 and 21 cases, respectively). Chronic myocarditis was divided into 3 subgroups: a persistent type lasting over 3 months after distinct onset (3 cases), a recurrent type (2 cases) and a latent form (13 cases). The early mortality of these 5 subtypes of myocarditis were acute common 22%, acute fluminant 43%, chronic persistent 33%, chronic recurrent 50%, and chronic latent 38%. The overall early mortality of all patients with myocarditis was 38% in spite of aggressive treatment during hospitalization. On the other hand, the long-term prognosis of patients with myocarditis was favorable; only 4 cases, who survived the active phase, died in the late phase: 1 had fulminant myocarditis and the other 3 had the chronic latent form. Thus, the early mortality of patients with myocarditis was very high regardless of the subtype, but if patients can survive the active phase, they have a favorable prognosis except with the chronic latent form.

Adolescent↗
PubMed2001

The effect of angiogenesis inhibitor TNP-470 against postoperative lung metastasis following removal of orthotopic transplanted human colon cancer: an experimental study.

We have investigated the antimetastatic effect of TNP-470 against postoperative lung metastasis following the removal of human colon cancer xenotransplanted into nude rat. The KM12SM human colon cells were injected into the cecal wall. At 5 weeks after the injection, the cecum was removed including the tumor. Then, TNP-470 was administered continuously by subcutaneous injection pump at a dosage of 30 mg/kg/week. The Control Group received no administration of TNP-470. Group A and Group B received administration of TNP-470 just after the cecal removal for 4 and 2 weeks, respectively. Group C received 2 weeks' administration of TNP-470 from week 3 after the removal. The survival rate of each group was calculated, and any lung metastasis was evaluated macro and microscopically. At 7 weeks after the removal, lung metastasis was detected in all rats of the Control Group, and in 4 of 8 rats in Group C. In Groups A and Group B, only one rat developed lung metastasis. The 30 week-survival rate in Group A and that in Group B was significantly higher than that in the Control Group or Group C. Moreover, the incidence of lung metastasis at the time of death or 30 weeks after the removal in Group A, and in Group B, was lower than that in Control Group or Group C. The angiogenesis inhibitor, TNP-470 showed an excellent antimetastatic effect against postoperative lung metastasis from transplanted human colon cancer.

Angiogenesis Inhibitors↗