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Satoshi Yamaji

Publications and source records attributed to Satoshi Yamaji.

At least 19 recordsLinked to original sources
PubMed2006

The gamma-parvin-integrin-linked kinase complex is critically involved in leukocyte-substrate interaction.

Leukocyte extravasation is an important step of inflammation, in which integrins have been demonstrated to play an essential role by mediating the interaction of leukocytes with the vascular endothelium and the subendothelial extracellular matrix. Previously, we identified an integrin-linked kinase (ILK)-binding protein affixin (beta-parvin), which links initial integrin signals to rapid actin reorganization, and thus plays critical roles in fibroblast migration. In this study, we demonstrate that gamma-parvin, one of three mammalian parvin family members, is specifically expressed in several lymphoid and monocytic cell lines in a complementary manner to affixin. Like affixin, gamma-parvin directly associates with ILK through its CH2 domain and colocalizes with ILK at focal adhesions as well as the leading edge of PMA-stimulated U937 cells plated on fibronectin. The overexpression of the C-terminal fragment containing CH2 domain or the depletion of gamma-parvin by RNA interference inhibits the substrate adhesion of MCP-1-stimulated U937 cells and the spreading of PMA-stimulated U937 cells on fibronectin. Interestingly, the overexpression of the CH2 fragment or the gamma-parvin RNA interference also disrupts the asymmetric distribution of PTEN and F-actin observed at the very early stage of cell spreading, suggesting that the ILK-gamma-parvin complex is essential for the establishment of cell polarity required for leukocyte migration. Taken together with the results that gamma-parvin could form a complex with some important cytoskeletal proteins, such as alphaPIX, alpha-actinin, and paxillin as demonstrated for affixin and actopaxin (alpha-parvin), the results in this study suggest that the ILK-gamma-parvin complex is critically involved in the initial integrin signaling for leukocyte migration.

Actinin↗
PubMed2006

Non-Hodgkin's lymphoma presenting as multiple bone lesions and hypercalcemia.

We report a rare case of a patient with non-Hodgkin's lymphoma who developed multiple bone lesions and hypercalcemia. A 50-year-old woman complained of drowsiness and multiple bone pain on admission. Radiographic examination revealed multiple bone fractures and osteolytic lesions. She was diagnosed with diffuse large B cell lymphoma by biopsy of an inguinal lymph node. Elevation of parathyroid hormone-related protein (PTHrP) and hypercalcemia were confirmed pretreatment, and those serum levels decreased during chemotherapy for lymphoma. However, the disease was resistant to chemotherapy combined with rituximab. These findings suggest that hypercalcemia is associated with PTHrP and the prognosis of patients with bone lymphoma in advanced stage is poor, although it is thought to be a relatively favorable prognosis in localized primary lymphoma of bone.

Antibodies, Monoclonal↗
PubMed2006

Does high-power computed tomography scanning equipment affect the operation of pacemakers?

BACKGROUND: Computed tomography (CT) is widely used in clinical practice, but there has not been a detailed report of its effect on the functioning of pacemakers. METHODS AND RESULTS: During CT, ECGs were recorded in 11 patients with pacemakers and the electromagnetic field in the CT room was also measured. The effect of CT on a pacemaker was also investigated in a human body model with and without shielding by rubber or lead. Transient malfunctions of pacemakers during CT occurred in 6 of 11 patients. The model showed that malfunctioning of the pacemaker was induced by CT scanning and this was prevented by lead but not by rubber. The alternating electrical field was 150 V/m on the CT scanning line, which was lower than the level influencing pacemaker functions. The alternating magnetic field was 15 muT on the CT scanning line, which was also lower than the level influencing pacemaker functions. CONCLUSIONS: Malfunctions of the pacemaker during CT may be caused by diagnostic radiant rays and although they are transient, the possibility of lethal arrhythmia cannot be ignored.

Cardiac Pacing, Artificial↗
PubMed2006

[Multiple myeloma presenting as cavernous sinus syndrome].

We report on a 70-year-old male who developed cavernous sinus syndrome as the initial symptom of multiple myeloma. He was admitted with diplopia and ptosis in October 2004. The diagnosis of multiple myeloma and cavernous sinus syndrome due to a gross mass at the sinus base were made. Cerebral computed tomography revealed that the lesion occupied the sphenoid sinus and involved the oculomoter nerve. He underwent local irradiation of the mass followed by systemic chemotherapy. The symptoms caused by the mass disappeared after the treatment. Clinicians need to be aware of the rare manifestation of multiple myeloma.

Aged↗
PubMed2005

Up-regulation of integrin-linked kinase activity in rat mesangioproliferative glomerulonephritis.

This study investigated whether integrin-linked kinase (ILK) is involved in the pathogenesis of chronic glomerulonephritis (GN) by analyzing the expression and activity of glomerular ILK in a chronic rat model of mesangioproliferative GN. Double immunostaining of kidneys obtained at different time points with glomerular cell-specific markers revealed that ILK was primarily expressed by glomerular epithelial cells, and weakly by mesangial cells (MCs) and endothelial cells in control rats, but dramatically increased in a typical mesangial pattern at days 21 and 28 of GN. Semiquantitative assessment indicated that the level of glomerular ILK expression closely parallels the level of accumulation of glomerular extracellular matrix (ECM) as well as fibronectin (FN). Immunoprecipitation and kinase activity assays using isolated nephritic glomeruli indicated a striking increase of ILK activity on days 21 and 28 of GN. Further, cultured rat MCs overexpressing kinase-deficient ILK diminished FN assembly and collagen matrix remodeling as compared with control transfectants. The results showed that glomerular ILK expression and activity are markedly increased in an experimental model of chronic GN. Increased activity of ILK in MCs may contribute to the development of chronic mesangial alterations leading to glomerular scarring.

Animals↗
PubMed2005

A possible association between the presence of interleukin-4-secreting cells and a reduction in the risk of acute graft-versus-host disease.

OBJECTIVE: We monitored cytokine-secreting cells using an enzyme-linked immunospot (ELISPOT) assay in a prospective study to assess the cytokine network after transplantation. PATIENTS AND METHODS: Peripheral blood mononuclear cells were collected from 23 patients who received allogeneic stem cell transplantation, from before the preconditioning regimen to 56 days after transplantation. The number of interleukin-4 (IL-4), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha)-secreting cells were measured by ELISPOT assay. For IL-4 and IFN-gamma, in vitro stimulation with phorbol 12-myristate 13-acetate and phytohemagglutinin was performed. RESULTS: The frequency of IL-4-secreting cells was significantly higher in five patients receiving peripheral blood stem cell transplantation (PBSCT) than that in 18 patients who received bone marrow transplantation (BMT). Based on IFN-gamma and TNF-alpha release, there was a trend toward a decrease in the number of cytokine-secreting cells in PBSCT compared with BMT. Furthermore, patients who did not develop acute graft-vs-host disease (GVHD, n=5) showed a significantly higher number of IL-4-secreting cells compared with those who developed acute GVHD (n=18). Both IFN-gamma-secreting cells and TNF-alpha-secreting cells showed a trend to increase in number in patients with acute GVHD. In patients who received reduced-intensity stem cell transplantation (n=7) compared with conventional stem cell transplantation (n=16), there was a large number of cytokine-secreting cells detected by IL-4 and IFN-gamma release. CONCLUSIONS: These results are consistent with the hypothesis that IL-4-producing cells inhibit the development of acute GVHD. In addition, the increased percentage of IL-4-secreting cells may be responsible for the unexpected low incidence of acute GVHD in PBSCT, despite the presence of large numbers of mature T cells in the donor infusion.

Adult↗
PubMed2005

Idiopathic thrombocytopenic purpura and myasthenia gravis after fludarabine treatment for chronic lymphocytic leukemia.

We report a patient with chronic lymphocytic leukemia (CLL) who developed idiopathic thrombocytopenic purpura (ITP) and myasthenia gravis (MG) after fludarabine therapy. ITP developed after 6 cycles of fludarabine treatment, and MG occurred 2 months after the onset of ITP. MG was successfully treated with immunosuppressive therapy and plasma exchange, while rituximab was effective for CLL and ITP. Fludarabine seemed to have an important role in the onset of ITP and MG in this case.

Antibodies, Monoclonal↗
PubMed2005

Dysferlin interacts with affixin (beta-parvin) at the sarcolemma.

The dysferlin gene is defective in Miyoshi myopathy (MM) and limb girdle muscular dystrophy type 2B (LGMD2B). Dysferlin is a sarcolemmal protein that is implicated in calcium-dependent membrane repair. Affixin (beta-parvin) is a novel, integrin-linked kinase-binding protein that is involved in the linkage between integrin and the cytoskeleton. Here we show that affixin is a dysferlin binding protein that colocalizes with dysferlin at the sarcolemma of normal human skeletal muscle. The immunoreactivity of affixin was reduced in sarcolemma of MM and LGMD2B muscles, although the total amount of the affixin protein was normal. Altered immunoreactivity of affixin was also observed in other muscle diseases including LGMD1C, where both affixin and dysferlin showed quite similar changes with a reduction of sarcolemmal staining with or without cytoplasmic accumulations. Colocalization of dysferlin and affixin was confirmed by immunofluorescence analysis using dysferlin-expressing C2 myoblasts. Wild-type and mutant dysferlin colocalized with endogenous affixin. The interaction of dysferlin and affixin was confirmed by immunoprecipitation study using normal human and mouse skeletal muscles. Using immunoprecipitation with deletion mutants of dysferlin, we have identified that C-terminal region of dysferlin is an apparent binding site for affixin. We also found N-terminal calponin homology domain of affixin as a binding site for dysferlin. Our results suggest that affixin may participate in membrane repair with dysferlin.

Actinin↗
PubMed2005

[Outcome of allogeneic stem cell transplantation for hematological disorders in patients older than 50].

We retrospectively evaluated the outcomes in patients older than 50 years of age who underwent allogeneic hematopoietic transplantation. Twenty-three patients received conventional stem cell transplantation (CST) and 9 patients received reduced intensity stem cell transplantation (RIST). Regimen-related toxicity was observed in 21 (91%) patients with CST and 4 (44%) patients with RIST. Early death occurred within 100 days after transplantation in 6 patients with CST and 2 patients with RIST. Among the patients with complete remission, the two-year probability rate of survival was 44% in patients with CST and 100% in patients with RIST (p=0.08). Among the patients without complete remission, the two-year probability rate of survival was 30% in patients with CST and 0% in those with RIST (p=0.08). For patients receiving RIST without complete remission, relapse and infection were the main causes of death. Our data suggest that patients without complete remission should receive CST to the degree possible.

Female↗
PubMed2005

[Triple secondary malignancy of gingiva, palate and esophagus after an allogeneic bone marrow transplantation for cutaneous T-cell lymphoma].

A 31-year-old man was diagnosed as having cutaneous T-cell lymphoma in January 1994. He received an allogeneic bone marrow transplantation (BMT) from an HLA-matched sibling donor in May 1995, because of refractoriness to chemotherapy. The patient had been treated with immunosuppressants including prednisolone and cyclosporin A for chronic graft-versus-host disease (GVHD) of the extensive type following acute GVHD. Five years after the BMT, he developed moderately differentiated squamous cell carcinoma (SCC) on the mandibular gingival mucosa and underwent surgical resection. Furthermore, 6 years after the BMT well differentiated SCC developed on his palate and was resected. Concurrently, he was diagnosed as having esophageal cancer (poorly differentiated SCC) and underwent a subtotal esophagotomy. One year later he had a recurrence of the esophageal cancer with dysphagia and was treated with radiation and chemotherapy. He remains free of triple cancer and lymphoma. It is suggested that total body irradiation, immunosuppressants, and chronic GVHD are associated with a risk of secondary malignancies following allogeneic BMT. These factors might have contributed to the onset of triple cancer in our patient.

Adult↗
PubMed2005

[Pulmonary MALT lymphoma with macroglobulinemia].

An 84-year-old man was diagnosed as having pulmonary MALT lymphoma in January 1997. Six years later, he was admitted to our hospital with coughing and dyspnea in November 2003. Dissemination of MALT lymphoma was confirmed by findings of pleural effusion and bone marrow aspiration. A FISH analysis of cells from the pleural effusion revealed t(11;18)(q21;q21) and the serum level of IgM was 8,600 mg/dl (M-protein). The diagnosis of secondary macroglobulinemia was made. The patient received rituximab monotherapy because he was very elderly. Pleural effusion has not been seen after the administration of rituximab, although there have been no changes in the lung mass and serum values of M-protein.

Aged, 80 and over↗
PubMed2004

Affixin interacts with alpha-actinin and mediates integrin signaling for reorganization of F-actin induced by initial cell-substrate interaction.

The linking of integrin to cytoskeleton is a critical event for an effective cell migration. Previously, we have reported that a novel integrin-linked kinase (ILK)-binding protein, affixin, is closely involved in the linkage between integrin and cytoskeleton in combination with ILK. In the present work, we demonstrated that the second calponin homology domain of affixin directly interacts with alpha-actinin in an ILK kinase activity-dependent manner, suggesting that integrin-ILK signaling evoked by substrate adhesion induces affixin-alpha-actinin interaction. The overexpression of a peptide corresponding to the alpha-actinin-binding site of affixin as well as the knockdown of endogenous affixin by small interference RNA resulted in the blockade of cell spreading. Time-lapse observation revealed that in both experiments cells were round with small peripheral blebs and failed to develop lamellipodia, suggesting that the ILK-affixin complex serves as an integrin-anchoring site for alpha-actinin and thereby mediates integrin signaling to alpha-actinin, which has been shown to play a critical role in actin polymerization at focal adhesions.

Actinin↗
PubMed2004

Long-term cytogenetic remission with ubenimex monotherapy in a case of chronic myeloid leukemia.

A 65-year-old man was diagnosed with chronic myeloid leukemia (CML) in February 1990, and was treated with busulfan and ubenimex. Cytogenetic analysis of the bone marrow revealed the Philadelphia (Ph) chromosome in 100% of cells of analyzed at diagnosis. Treatment with busulfan was stopped in March 1993 due to bone marrow suppression. The Ph chromosome was seen in 80% of cells in June 1993. He received ubenimex monotherapy after cessation of busulfan. Complete disappearance of the Ph chromosome was confirmed in May 1995 and has continued to date. This suggests that ubenimex might specifically affect the Ph chromosome and be useful as maintenance therapy for CML.

Aged↗
PubMed2004

The first CH domain of affixin activates Cdc42 and Rac1 through alphaPIX, a Cdc42/Rac1-specific guanine nucleotide exchanging factor.

Rho GTPases, Cdc42 and Rac1, play pivotal roles in cell migration by efficiently integrating cell-substrate adhesion and actin polymerization. Although it has been suggested that integrins stimulate these Rho GTPases via some of integrin binding proteins such as focal adhesion kinase (FAK) and paxillin, the precise molecular mechanism is largely unknown. In this study, we showed that the over-expression of RP1 corresponding to the first CH domain (CH1) of affixin, an integrin-linked kinase (ILK)-binding protein, induced a significant actin reorganization in MDCK cells by activating Cdc42/Rac1. Affixin full length and RP1 co-immunoprecipitated with alphaPIX, a Cdc42/Rac1-specific guanine nucleotide exchanging factor (GEF), and they co-localized at the tips of lamellipodia in motile cells. The involvement of alphaPIX in the RP1-induced Cdc42 activation was demonstrated by the significant dominant negative effect of a point mutant of alphaPIX, alphaPIX (L383R, L384S), lacking GEF activity. Our data strongly support that ILK and affixin provide a novel signalling pathway that links integrin signalling to Cdc42/Rac1 activation.

Actinin↗
PubMed2003

Clinical significance of fragmented red cells after allogeneic bone marrow transplantation.

To clarify the clinical significance of the presence of fragmented red cells (FRC) after allogeneic bone marrow transplantation (BMT), we measured the incidence and degree of FRC and their relationships to clinical features. The percentages of FRC (%FRC) were measured in 50 patients on weeks -2, 0, 2, 4, 6, 8, 10, and 12. The %FRC in pre-BMT patients (mean, 0.52%; range, 0.04%-1.56%) was higher than in healthy control subjects (mean, 0.08%; range, 0.02%-0.27%). The highest %FRC (> or = 1.3%) were seen in 2 pre-BMT and 17 post-BMT patients. Eight patients who developed thrombotic microangiopathy (TMA) showed %FRC values that were significantly higher than those in patients without TMA. However, the timing of elevated %FRC was delayed until several days after the onset of intravascular hemolysis and/or a drop in platelet count. Of the patients who did not experience TMA, 5 patients with infection and 4 patients with acute graft-versus-host disease (GVHD) also showed significant elevation of %FRC during the clinical course. Furthermore, multivariate analysis results demonstrated that TMA and infection had a statistically significant effect on the high value of %FRC. These findings indicate that the appearance of FRC is a common phenomenon in patients undergoing BMT and is not a predictive factor for the early diagnosis of TMA, although FRC is one of the main laboratory findings in TMA. Furthermore, an increased %FRC is seen in other post-BMT clinical settings, such as infection and acute GVHD.

Adolescent↗
PubMed2003

Involvement of central nervous system in prolymphocytoid transformation of chronic lymphocytic leukemia.

We report a rare case of involvement of the central nervous system (CNS) by chronic lymphocytic leukemia (CLL). A 68-year-old man with prolymphocytic variant of B-CLL (CLL/PLL), develops CNS involvement with headache and vomiting. Computed tomography of the head showed no abnormalities. The cerebrospinal fluid (CSF) revealed numerous lymphocytoid cells of prolymphocytic appearance consistent with findings on the peripheral blood smear. Immunophenotypic analysis demonstrated that the leukemic B cells were positive for CD19, CD20, and HLA-DR, but CD5 was difficult to detect. The patient was treated with intrathecal methotrexate, cytarabine, and hydrocortisone and had improvement in symptoms and CSF findings. Although CNS involvement is an unusual manifestation in CLL, one should be aware of the possibility of this complication in cases presenting with neurological symptoms.

Aged↗
PubMed2003

Clinical features and outcome in HCV-positive aggressive non-Hodgkin's lymphoma.

The clinical features and outcome of 25 previously untreated aggressive non-Hodgidn's lymphoma (NHL) patients with hepatitis C virus (HCV) infection were evaluated retrospectively. The patients included 18 males and 7 females with a median age of 66 years. The median observation period for survivors was 32 months. Although there were no patients with hepatocellular carcinoma during the follow-up period, 7 patients had cirrhosis (LC) at the initiation of therapy for NHL. Seventeen patients (68%) had initial extranodal involvement including 2 cases with liver involvement. The 5-year overall survival (OS) rate in the whole group was 46%, and the 5-year relapse-free survival (RFS) rate of patients with complete response (CR) was 48%. Patients with non-cirrhosis (n = 18) showed better OS (P = 0.04) compared with patients with LC (n = 7) and 5-year OS rates were 55 and 21%, respectively. Fourteen patients died in the whole group; 4 of NHL and 2 of liver failure in the LC group and 8 of NHL in the non-cirrhotic group. Among the latter 8 patients, cumulative dose (CD) of doxorubicin (ADR) and cyclophosphamide (CPA) were significantly lower than those of survivors with non-cirrhosis. In conclusion, patients with HCV-positive aggressive NHL have a similar prognosis as HCV-negative aggressive NHL. In non-cirrhotic patients, attention should be paid to the CD of drugs required to cure the aggressive NHL.

Aged↗