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Biomedical subjects

T Sasaguri

Publications and source records attributed to T Sasaguri.

At least 37 records · Page 2Linked to original sources
PubMed1997

Solitary "amyloid ulcer" localized in the sigmoid colon without evidence of systemic amyloidosis.

In a 51-yr-old man, colonoscopy for heme-positive stools revealed a solitary "amyloid ulcer" localized in the sigmoid colon. There were no clinical symptoms suggesting amyloidosis, and additional examination revealed no findings characteristic of amyloidosis or any chronic inflammatory disease. Ischemic change as a result of amyloid infiltration into the vessel wall may lead to formation of an ulcer in the affected bowel. Although local resection can be considered for a symptomatic and well defined lesion, it should be kept in mind that amyloid can present in various forms and follow various courses, such as the spontaneous healing that occurred in our patient.

Amyloidosis↗
PubMed1996

Phorbol ester inhibits the phosphorylation of the retinoblastoma protein without suppressing cyclin D-associated kinase in vascular smooth muscle cells.

To elucidate the role of protein kinase C in vascular smooth muscle cell proliferation, we examined the effects of phorbol 12-myristate 13-acetate (PMA) on G1 events in human arterial cells. About 15 h after G0 cells were stimulated with fetal bovine serum and basic fibroblast growth factor, [3H]thymidine incorporation started. PMA (10 nM) inhibited the incorporation over 90% when added earlier than 3 h after stimulation, but had no effect when added 12 h or later. PMA inhibited the phosphorylation of the retinoblastoma protein (pRb), which normally began at about 9 h. PMA did not inhibit the gene expression of Cdk2, Cdk3, Cdk4, Cdk5, and cyclins G, C, and D, all of which began at 0-3 h. However, PMA reduced the expression of cyclins E and A, which usually began at 3-9 h and about 15 h, respectively. PMA inhibited the histone H1 kinase activity of Cdk2, which increased from about 9 h, whereas PMA did not inhibit the pRb kinase activities of cyclin D-associated kinase(s) and Cdk4, detectable from 0-3 h. These results suggested that the PMA-induced inhibition of pRb phosphorylation is not mediated by suppressing cyclin D-associated kinase(s) including Cdk4, but involves the suppression of Cdk2 activity that results from the reduced expression of cyclins E and A.

Cell Cycle↗
PubMed1996

[Characteristics and limitations of three-dimensional spiral CT--experimental evaluation].

We evaluated the image quality of three-dimensional (3D) spiral CT using a Somatom Plus CT scanner (Siemens, Germany). A T-shaped acrylate plastic model was made and scanning was performed with a table speed of 5 mm/sec for 24 seconds. The thickness of the X-ray beam was 5mm with one second per rotation. The various images of the model were created based on the shaded surface display (SSD) method and the effect of threshold and rotation (spin and tilt) on the quality of the 3D images was studied. The increase of threshold caused a rapid decrease in the diameter of the stick observed on the film, and this phenomenon was particularly remarkable on the transverse stick and the junctional portion of the longitudinal stick. The change of spin or tilt did not affect the diameter of the stick on the film. It was found that the depth perception of the stick could be achieved with the gray scale technique. We concluded that the interpretation of the 3D spiral CT image obtained with SSD needs caution and the diagnosis should not be made only on this image.

Humans↗
PubMed1996

Apoptosis of human kidney 293 cells is promoted by polymerized cadmium-metallothionein.

Transformed human kidney cells (293 cells) exposed to 12.5 to 37.5 microM CdCl(2) showed apoptosis as confirmed by characteristic electron microscopic features, a ladder on gel electrophoresis of extracted DNA, and fragmentation of nucleosomes as detected by enzyme linked immunosorbent assay (ELISA). Higher concentrations of Cd were less effective in inducing apoptosis. Furthermore, addition of the protein extract from the serum-free medium used for Cd-exposure promoted apoptosis exhibiting the same features as that after Cd-exposure. The apoptosis induced by the protein was dose-dependent. The molecular weight of the protein (Cd-protein) was shown to be 40 kDa by gel filtration. Two-dimensional electrophoresis revealed the Cd-protein as a single spot with a molecular weight of 6 kDa and pI of 4.5. Competitive ELISA showed that the Cd-protein reacted with anti-metallothionein antibody. The present findings suggest that apoptosis is induced not only by Cd itself but also by polymerized metallothionein molecules (MT) released from cells into the medium.

Animals↗
PubMed1996

Interleukin-4 stimulates rheumatoid synovial fibroblasts to express matrix metalloproteinase-1 (tissue collagenase) and histamine H1 receptor mRNA.

In the present study, we investigated the effect of interleukin-4 (IL-4) on metalloproteinase 1 (MMP-1/tissue collagenase) production in human rheumatoid synovial fibroblasts. Northern blot analysis revealed that addition of IL-4 with or without histamine stimulated the cells to increase the amount of proMMP-1 mRNA, and the IL-4 with histamine addition resulted in a 3.3-fold increase compared with histamine only. Furthermore, IL-4 itself stimulated the expression of histamine H1 receptor mRNA. These results suggest that IL-4 may play an important role in joint destruction in RA.

Arthritis, Rheumatoid↗
PubMed1996

Endometrial stromal sarcoma of the uterus with rhabdoid features.

A case of endometrial stromal sarcoma of the uterus with rhabdoid features, occurring in a 57 year old woman is reported. Electron microscopy and immunohistochemistry revealed that the rhabdoid cells contained intermediate filaments which were positive for vimentin, cytokeratin, alpha-smooth muscle actin, and muscle specific actin, but not for myoglobin and desmin. This indicated that the tumor in this case differed somewhat from the three rhabdoid tumors and an endometrial stromal sarcoma with rhabdoid differentiation previously reported and that, therefore, these tumors were heterogeneous.

Biomarkers, Tumor↗
PubMed1996

Cell cycle arrest in the G2 phase induced by phorbol ester and diacylglycerol in vascular endothelial cells.

The role of protein kinase C (PKC) in vascular endothelial cell proliferation was investigated using human umbilical vein endothelial cells released from the G1/S border. Phorbol 12-myristate 13-acetate (PMA) caused G2 arrest because 1) when added to G2 cells, PMA inhibited subsequent cell division; 2) these growth-arrested cells did not show morphological features of mitotic cells; and 3) PMA did not interrupt mitosis in cells released from nocodazole-induced M phase arrest. 1-Oleoyl-2-acetyl-sn-glycerol (OAG) added repeatedly from G2 also inhibited mitosis. The activation of cdc2 kinase around the G2/M transition was suppressed by PMA and OAG. Although cdc2 was expressed in the presence of PMA, dephosphorylation of its tyrosine residue was inhibited by PMA. In parallel, the expression of cdc25B was suppressed by PMA. The total and the cdc2-associated amount of cyclin B were both reduced by PMA. These data suggested that the PKC pathway negatively regulates the G2/M transition and that the inhibition of cdc2 kinase by the reduction in the levels of cdc25B and cyclin B may contribute to this effect.

CDC2 Protein Kinase↗
PubMed1995

Ovarian mucinous cystadenocarcinoma with sarcoma-like mural nodules.

A rare case of ovarian mucinous cystadenocarcinoma with sarcoma-like mural nodules is reported. Macroscopically, nodular or granular lesions were scattered over the inner surface of a huge, multilocular tumor in the left ovary. The histopathological features were consistent with those of previously documented cases, except significant squamous metaplasia in the present case. The pleomorphic sarcoma-like cells showed a positive reaction for vimentin and alpha-antichymotrypsin but were negative for carcinoembryonic antigen and common epithelial membrane antigen by immunohistochemistry. Electron microscopically, the tumor cells had neither desmosomes nor secretory granules, but they possessed abundant intermediate filaments. Both immunostaining and ultrastructure suggested that the sarcoma-like nodules were derived from reactive proliferation of fibrohistiocytic cells. The fibrohistiocytic reaction seemed to occur in response to hemorrhage, because hemorrhage was reported to be associated with the mural nodules in most of the previous cases as well as ours.

Cystadenocarcinoma, Mucinous↗
PubMed1995

Mild emphysema: a novel method using formalin-fixed lungs for computed tomography and pathological analyses.

We evaluated a novel method of computed tomography (CT) analysis using formalin-fixed lungs of autopsy cases with mild emphysema. Eight formalin-inflated lungs (FILs) obtained at autopsy were examined using CT after draining off the formalin and air inflation with an air pump, and subjected to pathological study including pathological scoring of emphysema and microscopic image analysis (MIA). Satisfactory CT examination was carried out within 5 h of lung fixation. The mean alveolar area determined by MIA correlated highly with the lung volume (r = 0.845) and CT score (r = 0.722). This method is simple compared with conventional polyethylene glycol fixation for CT and enables CT examination of resected lungs without anxiety about biohazards, Mild emphysema can be detected by MIA.

Aged↗
PubMed1994

Gene expression of monocyte chemoattractant protein-1 in human monocytes is regulated by cell density through protein tyrosine kinase and protein kinase C.

The present study investigated the signal transduction pathways leading to the gene expression for monocyte chemoattractant protein-1 (MCP-1) in human monocytes. By Northern blot analysis, MCP-1 mRNA was undetectable in freshly isolated monocytes, but was induced and reached a maximal level at 4 h during culture. The level of accumulated mRNA altered with cell density of the monocytes and was highest at a density of 1 x 10(6) cells/ml. Nuclear run-on assay demonstrated that this cell density-dependent expression of MCP-1 mRNA was regulated at the transcriptional level, and protein tyrosine kinase (PTK) inhibitors, genistein and herbimycin A, completely abrogated this gene transcription. Immunoblot analysis for phosphotyrosine in whole cell lysates demonstrated gradual increases in tyrosine phosphorylation of 55-, 60-, and 70-kDa proteins during culture. Cell density regulated tyrosine phosphorylation of 70-kDa protein in parallel with alterations in MCP-1 mRNA expression. The protein kinase C (PKC) inhibitor H-7 also abrogated the gene transcription and suppressed tyrosine phosphorylation of 70-kDa protein, whereas HA1004, a structural analogue of H-7, did not. These results suggest that MCP-1 gene expression in cultured monocytes is regulated by the cell density at the transcriptional level and that the signaling pathways leading to the gene transcription are mediated through PTK and PKC. It is also suggested that PKC activity plays a critical role in tyrosine phosphorylation of 70-kDa protein, which may mediate signals regulating the cell density-dependent expression of the MCP-1 gene.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Protein tyrosine kinase inhibitors inhibit chemotaxis of vascular smooth muscle cells.

The effects of protein tyrosine kinase inhibitors on platelet-derived growth factor (PDGF)-induced chemotaxis in cultured rat aortic smooth muscle cells (SMCs) were investigated to elucidate the role of tyrosine phosphorylation in the chemotaxis of vascular SMCs. Two tyrosine kinase inhibitors, methyl 2,5-dihydroxycinnamate and genistein, inhibited PDGF-induced chemotaxis, the IC50 being 5 and 150 mumol/L, respectively. Methyl cinnamate and genistein partly inhibited the adhesion of SMC to collagen-coated dishes. A chemotaxis assay using double-well culture dishes revealed that both agents also inhibited cell migration after adhesion. H-7, a C kinase inhibitor, did not inhibit either chemotaxis or SMC adhesion at 100 mumol/L. Western blot analysis using anti-phosphotyrosine revealed that the tyrosine kinase inhibitors inhibited the tyrosine phosphorylation of at least two proteins of molecular weight 85 and 95 kD under our experimental conditions. An immunocytochemical study revealed that these inhibitors eliminated tyrosine phosphorylation along the cell margins; these agents also inhibited the reorganization of microtubules and stress fibers, both of which are involved in directional cell locomotion. These findings suggest that tyrosine kinases may play an important role in SMC chemotaxis.

Animals↗
PubMed1994

Bidirectional regulation of smooth muscle cell proliferation by IFN-gamma.

We studied the effects of interferon gamma (IFN-gamma), a T-cell lymphokine, on the proliferation and chemotaxis of vascular smooth muscle cells (SMC). Recombinant human IFN-gamma dose-dependently inhibited the proliferation of SMC cultured in the presence of 20% fetal calf-serum. It also inhibited PDGF-induced chemotaxis of SMC. Similar concentrations of IFN-gamma induced DNA-synthesis of SMC cultured in mitogen-depleted medium for 5 days. The inhibition and the stimulation of SMC proliferation were accompanied by concomitant decrease and increase in the number of PDGF receptors. Our study indicated that IFN-gamma is a bidirectional regulator of SMC proliferation.

Cell Division↗
PubMed1993

Protein kinase C-mediated inhibition of cyclin A expression in human vascular endothelial cells.

Proliferation of cultured human vascular endothelial cells may be negatively regulated by the protein kinase C (PKC) pathway, because phorbol 12-myristate, 13-acetate (PMA) inhibits DNA synthesis and cell population doubling in PKC-retaining cells, but not in cells depleted of PKC by a long-term exposure to PMA. We investigated the mechanism through which PKC arrests the cell cycle with regard to cyclin A, which has been reported to play a key role in G1/S progression activating CDK2. Cyclin A mRNA was elevated from late G1 in accordance with the protein expression, which reached the maximal level during the S phase. PMA added at late G1 potently reduced the levels of cyclin A mRNA and the protein in concentration-dependent manners parallel to its effect on the proliferation. However, it failed to inhibit the expression in PKC-depleted cells. The mRNA reduction by PMA was due to inhibition of the transcription. The PMA effects were mimicked by multiple doses of 1,2-dioctanoylglycerol. These findings suggest that PKC inhibits G1/S progression through suppression of cyclin A gene transcription in endothelial cells.

Blotting, Western↗