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Hiroaki Matsuno

Publications and source records attributed to Hiroaki Matsuno.

At least 19 recordsLinked to original sources
PubMed2006

Rheumatoid nodulosis during methotrexate therapy in a patient with rheumatoid arthritis.

We report a 62-year-old man with rheumatoid arthritis (RA) who developed nodulosis after methotrexate (MTX) treatment. The epithelioid cells of nodules were positive for matrix metalloproteinases (MMP)-2, MMP-3, MMP-9, and Ki67. The synovial tissues obtained from the same patient were negative for MMP-3, MMP-9, and Ki67. This study demonstrated that MTX-induced nodules are different from synovial tissues in terms of MMP expression, suggesting the presence of different pathologic mechanisms and differential MTX susceptibility.

Antirheumatic Agents↗
PubMed2006

Sarcoidosis with acute recurrent polyarthritis and hypercalcemia.

A 45-year-old woman had bleary eyes and recurrent episodes of fever and arthritis in the knees and ankles. The patient had anterior uveitis, negative findings of the tuberculin test, and an increased serum lysozyme level, but bilateral hilar lymphadenopathy (BHL) was absent. During the course of her disease, the serum calcium and angiotensin-converting enzyme levels gradually increased to above the normal level, and the patient was clinically diagnosed as having sarcoidosis. The clinical features of arthritis were typical of those of Löfgrens syndrome although BHL and erythema nodosum were absent. The patient was successfully treated with 15 mg/day of prednisolone.

Acute Disease↗
PubMed2006

Trimethoprim-sulfamethoxazole-induced hypersensitivity syndrome associated with reactivation of human herpesvirus-6.

A 27-year-old man who had a history of bronchial asthma, eosinophilic enteritis, and eosinophilic pneumonia presented with fever, skin eruptions, cervical lymphadenopathy, hepatosplenomegaly, atypical lymphocytosis, and eosinophilia two weeks after receiving trimethoprim (TMP)-sulfamethoxazole (SMX) treatment. After the withdrawal of TMP-SMX and the administration of high-dose steroid, these systemic symptoms gradually resolved. During the disease course, the patient showed a transient increase in anti-human herpesvirus (HHV)-6 antibody titers and HHV-6 DNA in the peripheral blood, indicating the reactivation of a latent HHV-6 infection. This is the first case of TMP-SMX-induced hypersensitivity syndrome associated with the reactivation of a latent viral infection.

Adult↗
PubMed2006

Apoptosis of rheumatoid synovial cells by statins through the blocking of protein geranylgeranylation: a potential therapeutic approach to rheumatoid arthritis.

OBJECTIVE: To determine whether statins induce apoptosis in rheumatoid arthritis (RA) synoviocytes. METHODS: The effects of lipophilic and hydrophilic statins (fluvastatin and pravastatin, respectively) on the apoptosis of cultured RA synoviocytes were examined in vitro. Apoptosis was analyzed by flow cytometry after staining with JC-1 (to measure the mitochondrial transmembrane potential), active caspase 3, annexin V, and propidium iodide. Add-back experiments were conducted to determine which downstream products of the mevalonate pathway could suppress apoptosis. Modulation of various signaling pathways induced by statins, including protein prenylation, was also investigated. RESULTS: Fluvastatin, but not pravastatin, induced apoptosis in RA synoviocytes in a concentration-dependent (1-10 microM) and time-dependent (48-96 hours) manner. Another lipophilic statin, pitavastatin, displayed almost the same effects as fluvastatin. In sharp contrast, lipophilic statins did not significantly increase apoptosis in synoviocytes from patients with osteoarthropathy. Apoptosis induced by fluvastatin was mitochondrial- and caspase 3-dependent and was abrogated by mevalonate and geranylgeranyl pyrophosphate, but not by farnesyl pyrophosphate. In addition, the geranylgeranyl transferase inhibitor GGTI-298 mimicked the effect of fluvastatin on RA synoviocytes. Treatment of RA synoviocytes with the RhoA kinase inhibitor Y-27632 caused apoptosis. Fluvastatin decreased the amount of RhoA protein in the membrane fraction, but increased the amount in the cytosolic fraction. CONCLUSION: Fluvastatin induced apoptosis in RA synoviocytes through a mitochondrial- and caspase 3-dependent pathway and by the blockage of mevalonate pathways, particularly through the inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathways. These findings suggest that lipophilic statins have potential as novel therapeutic agents for RA.

Apoptosis↗
PubMed2006

Antibiotic-containing hyaluronic acid gel as an antibacterial carrier: Usefulness of sponge and film-formed HA gel in deep infection.

We have developed a novel bioabsorbable antibacterial carrier using hyaluronic acid (HA) gel for prevention and treatment of orthopedic infections. In this study, we investigated the in vivo antibacterial effects of two forms of this new material, an HA gel sponge and an HA gel film. A titanium cylinder was inserted into the intramedullary cavity of each rabbit femur, along with an HA gel sponge or HA gel film containing antibiotics. The HA gel sponge contained gentamycin, vancomycin, tobramycin, or minomycin. The HA gel film contained gentamycin or vancomycin. After 0, 7, and 14 days, the rabbit bone marrow was collected, and the antibacterial activity of the HA gel was determined by agar diffusion test. As a control, we used Septocoll, a commercially available antibacterial carrier. Both the HA gel sponge and HA gel film exhibited antibacterial activity. The present results indicate that HA gel containing antibiotics is a clinically useful bioabsorbable antibacterial carrier.

Animals↗
PubMed2006

A new antibacterial carrier of hyaluronic acid gel.

BACKGROUND: Postoperative infection following total joint arthroplasty is thought to be one of the most serious and devastating complications. To develop an effective treatment for this complication, we tested a bioabsorbable antibacterial carrier that is made from novel cross-linked hyaluronic acid (HA) gel and gentamicin (GM). METHODS: Antibacterial activity of the carrier was evaluated by the agar diffusion test, direct contact test, in vivo mouse model, and in vivo rabbit osteomyelitis model. RESULTS: GM-containing HA gel suppressed bacterial growth both in vitro and in vivo. In the rabbit osteomyelitis model, beads coated with HA gel containing GM did not disturb bone ongrowth in the femoral stem. CONCLUSIONS: Our bioabsorbable carrier of antibiotic-containing HA gel is effective for prophylactic treatment or treatment of an actual deep infection following total joint arthroplasty.

Animals↗
PubMed2005

A case of necrotizing fasciitis caused by coagulase-negative staphylococcus: utility of magnetic resonance imaging for the preoperative diagnosis of necrotizing fasciitis.

A 70-year-old woman presented with fever and pain in the right lower extremity. Fat-suppressed gadolinium-enhanced T1-weighted magnetic resonance imaging (MRI) showed contrast-enhanced fascia, fluid accumulation, and hypointense signals in the muscles. Surgical interventions including incisions and insertion of drainage tubes were performed on the basis of the MRI findings. The histopathological examinations of surgically obtained biopsy specimens demonstrated suppurative fasciitis, widespread myonecrosis, and thromboses of the vessels, all of which were compatible with a diagnosis of necrotizing fasciitis. The bacterial cultures were positive for a coagulase-negative staphylococcus. Following the surgical interventions, the patient was successfully treated by aggressive antimicrobial therapy. MRI can thus be useful for differentiating necrotizing fasciitis from nonnecrotizing soft tissue infection and for planning the treatment of necrotizing fasciitis.

Anti-Infective Agents↗
PubMed2005

[Examination of rheumatoid factor and other serum markers in rheumatoid arthritis].

Rheumatoid factor (IgM-RF) has been widely used to diagnose rheumatoid arthritis (RA) in clinical practice. We investigated the RA diagnostic performances of anti-cyclic citrullinated peptide antibody (anti-CCP), matrix metalloproteinase-3 (MMP-3), anti-agalactosyl IgG antibody (CA*RF), and anti-calpastatin antibody (ACA) in comparison with IgM-RF. Among 68 RA patients, IgM-RF was positive in 31 (45.6%) and negative in 37 (54.4%). In the IgM-RF-positive group, positivity in anti-CCP, CA*RF, and ACA was 97%, 100%, and 97%, respectively, although that in MMP-3 (74%) was inferior to the others. On the other hand, in the IgM-RF-negative group, positivity in anti-CCP, MMP-3, and ACA was 73%, 81%, and 86%, respectively, although that in CA*RF was only 59%. We conclude that the combination of IgM-RF and anti-CCP/ACA will provide an accurate diagnosis of RA in clinical practice.

Arthritis, Rheumatoid↗
PubMed2005

Takotsubo (ampulla-shaped) cardiomyopathy associated with microscopic polyangiitis.

Recently, a cardiac disorder characterized by ballooning and hypokinesis at the apex has been described as takotsubo (ampulla-shaped) cardiomyopathy. We encountered a patient with a rare case of takotsubo cardiomyopathy associated with microscopic polyangiitis. A 70-year-old woman suddenly presented with ventricular dysfunction during the active phase of microscopic polyangiitis. The findings on echocardiograms and electrocardiograms were consistent with those of takotsubo cardiomyopathy. The ventricular dysfunction completely resolved after treatment with 40 mg/day of prednisolone and methylprednisolone pulse therapy. This unique type of cardiomyopathy can be a complication of microscopic polyangiitis.

Aged↗
PubMed2005

[Case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment].

A 92-year-old man with a history of bronchial asthma and allergic rhinitis received antibiotics for sepsis by methicillin-resistant Staphylococcus aureus and multidrug-resistant Enterococcus gallinarum. During the antibiotics treatment, skin eruptions, liver dysfunction, and hypereosinophilia developed, followed by dyspnea, congestive heart failure, electrocardiographic abnormalities, and diffuse mild myocardial hypokinesis. After the discontinuation of the antibiotics and the administration of steroid, skin eruptions, liver dysfunction, and hypereosinophilia improved parallel with the improvement of the congestive heart failure. Vancomycin hydrochloride and teicoplanin were suspected as the causative drugs on the basis of the treatment course. Although congestive heart failure is rare in the case of drug-induced hypereosinophilia, it is one of life-threatening complications. We describe herein a case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment, successfully treated with steroid after the discontinuation of the causative drug.

Aged, 80 and over↗
PubMed2004

The role of Fas-mediated apoptosis after traumatic spinal cord injury.

STUDY DESIGN: Functional recovery and histopathological change after spinal cord injury in the Fas-deficient mice and the wild-type mice were investigated. OBJECTIVES: To investigate the role of the Fas/Fas ligand (FasL) system as a signal transduction pathway leading to apoptosis after spinal cord injury. SUMMARY OF BACKGROUND DATA: [corrected] Apoptosis observed after spinal cord injury has recently gained widespread interest as a cause of collateral damage after the initial injury. Apoptosis mediated by the Fas antigen in the postischemic brain or spinal cord was reported. Recently, the upregulation of Fas after spinal cord injury was also reported. However, the influence of Fas-mediated apoptosis on the extent of the secondary spinal cord injury has not yet been clarified. METHODS: We investigated Fas-mediated apoptosis after spinal cord injury and examined the behavioral changes and the histopathological changes after spinal cord injury using MRL/Mp-lpr/lpr (MRL/lpr) mice, which were Fas-deficient mutant mice, and MRL/Mp-+/+ (MRL/+) mice, which were Fas-positive wild-type mice. RESULTS: Locomotor recovery after spinal cord injury in MRL/lpr mice was superior to that observed in MRL/+ mice. In addition, the damaged area in MRL/lpr mice was significantly smaller than that seen in MRL/+ mice. Further, the frequency of apoptotic cells in the injured spinal cord of MRL/lpr mice was significantly less than that in MRL/+ mice. CONCLUSION: We demonstrated the appearance of Fas-mediated apoptosis in the spinal cord after spinal cord injury. In addition, we elucidated for the first time that Fas-mediated apoptosis following spinal cord injury played an important role in the spinal cord damage and the ultimate neurologic injury.

Animals↗
PubMed2004

Interleukin-18 enhances monocyte tumor necrosis factor alpha and interleukin-1beta production induced by direct contact with T lymphocytes: implications in rheumatoid arthritis.

OBJECTIVE: At sites of inflammation, T cells exert pathologic effects through direct contact with monocyte/macrophages, inducing massive up-regulation of interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha). We examined the regulatory effects of IL-18 on monocyte activation by direct contact with T lymphocytes in rheumatoid arthritis (RA). METHODS: Activated T cells were isolated from RA synovial fluid. Resting T cells and monocytes were isolated from peripheral blood mononuclear cells. RA synovial T cells or phytohemagglutinin (PHA)-stimulated T cells were fixed by paraformaldehyde and then cocultured with monocytes at a ratio of 4:1. Levels of TNFalpha, IL-1beta, IL-10, and IL-18 were measured by enzyme-linked immunosorbent assay. Expression of adhesion molecules, IL-18 receptor, and TNF receptors was analyzed by flow cytometry. Expression of NF-kappaB p65, phosphorylated IkappaBalpha, and phosphatidylinositol 3-kinase (PI 3-kinase) p110 was analyzed by Western blotting. RESULTS: IL-18 dose-dependently enhanced the production of IL-1beta and TNFalpha, but not IL-10, by monocytes following contact with RA synovial T cells or PHA-prestimulated T cells. NF-kappaB inhibitors N-acetyl-L-cysteine and Bay 11-7085 and PI 3-kinase inhibitor LY294002 inhibited the enhancing effects of IL-18, but MAPK p38 inhibitor SB203580, ERK inhibitor PD98059, and JNK inhibitor SP600125 did not. Increased levels of NF-kappaB in the nucleus, phosphorylated IkappaB, and PI 3-kinase were confirmed in monocytes cocultured with PHA-prestimulated T cells, and the levels were further increased by stimulation with IL-18. Neutralizing antibody to IL-18 inhibited monocyte activation induced by direct contact with PHA-prestimulated T cells. Via cell-cell contact, PHA-prestimulated T cells increased autocrine production of IL-18 by monocytes, which was mediated by activation of the NF-kappaB and PI 3-kinase pathways, and up-regulated the expression of the IL-18 receptor in monocytes. IL-18 up-regulated the expression of the TNF receptors vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) on monocytes. Blocking the binding of the TNF receptors VCAM-1 or ICAM-1 on monocytes to their ligands on stimulated T cells suppressed the IL-18-enhanced production of TNFalpha and IL-1beta in monocytes induced by contact with PHA-prestimulated T cells. CONCLUSION: IL-18 augments monocyte activation induced by contact with activated T cells in RA synovitis, which is dependent on activation of the NF-kappaB and PI 3-kinase pathways. IL-18 up-regulates the expression of the TNF receptors VCAM-1 and ICAM-1 on monocytes, which mediate the enhancing effects of IL-18 on T cell-monocyte contact.

Arthritis, Rheumatoid↗
PubMed2004

High diagnostic value of anticalpastatin autoantibodies in rheumatoid arthritis detected by ELISA using human erythrocyte calpastatin as antigen.

OBJECTIVE: To develop a quantitative method of measuring autoantibodies against human calpastatin in rheumatoid arthritis (RA) and to determine their diagnostic value compared with other autoimmune and articular diseases. METHODS: We performed a highly sensitive ELISA for IgG and IgM anticalpastatin autoantibodies in human sera using human erythrocyte calpastatin as an antigen. Samples were diluted 1:2000 for the measurement of IgG and 1:400 for IgM. RESULTS: IgG anticalpastatin antibodies were found in the sera of 48 of 58 patients (82.8%) with RA. In contrast, IgG anticalpastatin antibodies were found in the sera of only 2 of 11 (8.3%) patients with osteoarthritis (OA). Compared to sera from patients with other autoimmune diseases, anticalpastatin antibody sensitivity for RA was better than that of systemic lupus erythematosus (5.6%), systemic sclerosis (0%), mixed connective tissue disease (0%), and Sjögren's syndrome (20%). IgG anticalpastatin antibodies also showed high specificity (96.1%) for RA. Almost 90% of patients with RA were positive for IgG or IgM anticalpastatin antibodies. CONCLUSION: We have developed a simple, sensitive, specific, and quantitative ELISA for anticalpastatin antibodies that may have a high diagnostic value for RA.

Adult↗
PubMed2003

Suppression of osteoclastogenesis in rheumatoid arthritis by induction of apoptosis in activated CD4+ T cells.

OBJECTIVE: To examine the suppressive effect of anti-human Fas monoclonal antibody (mAb) on osteoclastogenesis in rheumatoid arthritis (RA) both in vitro and in vivo. METHODS: For in vitro analysis, activated CD4+ T cells derived from peripheral blood mononuclear cells were left untreated or were treated with humanized anti-human Fas mAb (R-125224) and cocultured with human monocytes. On day 12, the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells was counted. For in vivo analysis, tissue derived from human RA pannus was implanted with a slice of dentin subcutaneously in the backs of SCID mice (SCID-HuRAg-pit model). R-125224 was administered intravenously once a week for 3 weeks. The implanted tissue and dentin slice were removed, and the pits formed on the dentin slice were analyzed. RESULTS: In vitro, coculture of activated CD4+ T cells and peripheral monocytes induced osteoclastogenesis. The number of TRAP-positive multinucleated cells was reduced when activated CD4+ T cells were treated with R-125224. We established a new animal model for monitoring osteoclastogenesis, SCID-HuRAg-pit. We found that with R-125224 treatment, the number of pits formed on the implanted dentin slices was significantly reduced and the number of lymphocytes in the implanted RA synovial tissue was dramatically reduced in this model. CONCLUSION: This is the first study to demonstrate the suppressive effect of anti-human Fas mAb on osteoclastogenesis in RA synovial tissues through the induction of T cell apoptosis. Induction of apoptosis of infiltrated lymphocytes could be a useful therapeutic strategy for RA, in terms of suppressing both inflammation and bone destruction.

Animals↗