Mandibular intraosseous carcinoma coexisting with ameloblastoma.
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Ameloblastoma↗
Biomedical subjects
T Sumida
Publications and source records attributed to T Sumida.
Acute ischemic hepatic failure resulting from intraaortic balloon pump malposition.
We describe a rare intraaortic balloon pump (IABP) vascular complication as a result of malpositioning of the IABP. A 61-year-old man with unstable angina underwent emergency coronary artery bypass grafting soon after the insertion of an IABP. Postoperative hemodynamics were stable, but acute hepatic dysfunction occurred on the second postoperative day. Doppler echography revealed the absence of hepatic arterial flow. The IABP was removed, and arterial flow was immediately restored. Thereafter, the hepatic function recovered rapidly. This is a rare case that demonstrates how IABP can cause mechanical abdominal arterial branch obstruction. Evaluations using Doppler echography are useful in detecting such IABP complications.
Coronary Artery Bypass↗
Characterization of a novel nonpeptide vasopressin V(2)-agonist, OPC-51803, in cells transfected human vasopressin receptor subtypes.
We discovered the first nonpeptide arginine-vasopressin (AVP) V(2)-receptor agonist, OPC-51803. Pharmacological properties of OPC-51803 were elucidated using HeLa cells expressing human AVP receptor subtypes (V(2), V(1a) and V(1b)) and compared with those of 1-desamino-8-D-arginine vasopressin (dDAVP), a peptide V(2)-receptor agonist. OPC-51803 and dDAVP displaced [(3)H]-AVP binding to human V(2)- and V(1a)-receptors with K(i) values of 91.9+/-10.8 nM (n = 6) and 3.12+/-0.38 nM (n = 6) for V(2)-receptors, and 819+/-39 nM (n = 6) and 41.5+/-9.9 nM (n = 6) for V(1a)-receptors, indicating that OPC-51803 was about nine times more selective for V(2)-receptors, similar to the selectivity of dDAVP. OPC-51803 scarcely displaced [(3)H]-AVP binding to human V(1b)-receptors even at 10(-4) M, while dDAVP showed potent affinity to human V(1b)-receptors with the K(i) value of 13.7+/-3.2 nM (n = 4). OPC-51803 concentration-dependently increased cyclic adenosine 3', 5'-monophosphate (cyclic AMP) production in HeLa cells expressing human V(2)-receptors with an EC(50) value of 189+/-14 nM (n = 6). The concentration-response curve for cyclic AMP production induced by OPC-51803 was shifted to the right in the presence of a V(2)-antagonist, OPC-31260. At 10(-5) M, OPC-51803 did not increase the intracellular Ca(2+) concentration ([Ca(2+)](i)) in HeLa cells expressing human V(1a)-receptors. On the other hand, dDAVP increased [Ca(2+)](i) in HeLa cells expressing human V(1a)- and V(1b)-receptors in a concentration-dependent fashion. From these results, OPC-51803 has been confirmed to be the first nonpeptide agonist for human AVP V(2)-receptors without agonistic activities for V(1a)- and V(1b)-receptors. OPC-51803 may be useful for the treatment of AVP-deficient pathophysiological states and as a tool for AVP researches.
Arginine Vasopressin↗
Fas-associated death domain protein is a Fas-mediated apoptosis modulator in synoviocytes.
OBJECTIVE: To understand the intracellular regulatory mechanisms in Fas-mediated apoptosis of synoviocytes, we examined the involvement of caspases [caspase-1/ICE (interleukin-1beta converting enzyme), caspase-3/CPP32, and caspase-8/FLICE] and Fas-associated death domain protein (FADD) forming a death-inducing signalling complex (DISC) in Fas-mediated apoptosis of synoviocytes. METHODS: Synoviocytes were obtained from rheumatoid arthritis (RA) and osteoarthritis (OA) patients. The number of dead cells was counted after treatment with anti-Fas monoclonal antibody in the presence of caspase-1-, -3-, or -8-specific inhibitors. The involvement of caspases and FADD in Fas-mediated apoptosis of RA synoviocytes was examined by immunoblot and immunoprecipitation analyses. RESULTS: RA synoviocytes expressed high levels of caspase-3, caspase-8, and FADD compared with OA synoviocytes. Interestingly, Fas ligation activated caspase-8 and caspase-3 with the cleavage of poly(ADP-ribose) polymerase (PARP), corresponding to apoptosis of RA synoviocytes. Furthermore, specific inhibitors for caspase-3 and caspase-8 but not caspase-1 suppressed Fas-induced apoptosis of RA synoviocytes in a dose- and time-dependent manner. Caspase-8-specific inhibitor suppressed the activation of caspase-3 after Fas ligation on RA synoviocytes. Importantly, FADD was selectively recruited to the Fas death domain during Fas-mediated apoptosis of RA synoviocytes, consistent with sensitivity to the Fas-mediated apoptosis. CONCLUSION: Our findings suggest that Fas-mediated apoptosis in synoviocytes may be regulated at the level of recruitment of FADD to the DISC, subsequently leading to the activation of the FADD/caspase-8/caspase-3 signalling pathway.
Adaptor Proteins, Signal Transducing↗
Palmar fasciitis and polyarthritis associated with gastric carcinoma: complete resolution after total gastrectomy.
Palmar fasciitis and polyarthritis (PFA) is a rare paraneoplastic rheumatic syndrome characterized by flexion contractures of both hands and thickening of palmar fascia. Several reports have suggested that this syndrome is a tumor-associated autoimmune disorder. We report a 44-year-old Japanese man who presented with flexion contractures of both hands associated with thickening of palmar fascia and polyarthritis. These clinical pictures were suggestive of PFA associated with occult neoplasm. Upper gastrointestinal endoscopic examination revealed advanced gastric cancer. Resection of the cancer resulted in a gradual resolution of palmar fasciitis and polyarthritis. This clinical course suggests an underlying tumor-related immunologic process in this syndrome.
Adenocarcinoma↗
Clinical usefulness of telomerase assay for the detection of lymph node metastasis in patients with oral malignancy.
OBJECTIVE: Telomerase is considered a diagnostic marker of malignancy. We investigated the usefulness of telomerase assay for the detection of lymph node micrometastasis. METHODS: Sixteen cervical lymph nodes with metastasis of oral cancer and 20 benign lymph nodes were studied. The oral cancer cell line was used to estimate the sensitivity for telomerase assay. Telomerase activity was measured by semiquantitative telomeric repeat amplification protocol. RESULTS: There was a significant difference between malignant and benign lymph nodes. The telomerase activity of 50 mg of lymph nodes with 103 or more cancer cells differed from that of control lymph nodes. Lymph nodes with 102 or fewer tumor cells expressed similar levels as benign lymph nodes. CONCLUSIONS: In addition to routine histologic examination, telomerase assay is considered a useful tool for the detection of lymph node metastasis in patients with oral malignancy.
Biomarkers, Tumor↗
A single cell analysis of Fas ligand positive T cells in rheumatoid synovial fluid.
OBJECTIVE: To investigate the function of Fas ligand (Fas-L) positive T cells in rheumatoid synovium, we analyzed the T cell receptor (TCR) CDR3 region and examined the expression of cytokines in both Fas-L+ and Fas-L- single T cells. METHODS: Synovial fluid (SF) samples were collected from 2 patients with rheumatoid arthritis. TCR BV8+ T cells were sorted into a 96 well plate at a density of one cell per well. Expression of Fas-L, interferon-gamma, interleukin 2 (IL-2), IL-4, IL-6, and IL-10 was analyzed by reverse transcription-polymerase chain reaction and Southern blot and the TCR BV8 junctional region was sequenced. RESULTS: Twenty-two of 30 TCR BV8+ T cells from Patient 1 and 20 of 43 TCR BV8+ T cells from Patient 2 were Fas-L+ T cells, while the others were Fas-L-. Junctional sequence analysis showed the presence of some conserved amino acid motifs in the CDR3 region (SRQ, GFG, SSG, SGS, LGTSGTL, TLSS) in 13 clones of Fas-L+ T cells from Patient 1, whereas no conserved amino acid motif in Fas-L-T cells was found. In Patient 2, conserved amino acid motifs (PGQ, GQG, TTWGA) in the CDR3 region were found in 6 clones of Fas-L+ T cells, while only one was found in 2 clones of Fas-L-cells. In Fas-L+ T cells, 90-93% expressed both IL-2 and IL-10 mRNA. CONCLUSION: Fas-L+ TCR BV8+ T cells revealed the conserved amino acids motif in the CDR3 region, suggesting that Fas-L+ T cells might expand by antigen stimulation and play a crucial role as Th0-type T cells in triggering autoimmunity in rheumatoid synovium.
Aged↗
Synovial hyperplasia in HTLV-I associated arthropathy is induced by tumor necrosis factor-alpha produced by HTLV-I infected CD68+ cells.
OBJECTIVE: To investigate the pathogenic role of macrophage lineage (CD68+) cells in synovial proliferation in patients with human T cell leukemia virus I (HTLV-I) associated arthropathy (HAAP). METHODS: Synovial tissues obtained from 3 patients with HAAP and 3 patients with osteoarthritis (OA) were examined for the expression of tumor necrosis factor-alpha (TNF-alpha) mRNA, HTLV-I tax/rex mRNA, and number of CD68 by in situ reverse transcription assay and immunohistochemistry. Western blot and flow cytometric analyses were used to determine TNF-alpha production in HTLV-I infected synoviocytes. Changes in CD68+ cell population were examined by flow cytometric analysis. Proliferative effects of supernatants of HTLV-I infected synoviocytes on normal synoviocytes were also determined. RESULTS: TNF-alpha and HTLV-I tax/rex mRNA were preferentially expressed in CD68+ cells in HAAP synovia. Infection of OA synoviocytes by HTLV-I resulted in preferential expression in CD68+ cells, and these cells produced TNF-alpha. Supernatants of HTLV-I infected synoviocytes significantly enhanced the proliferation of normal synoviocytes through a TNF-alpha dependent pathway. CONCLUSION: Our results suggest HTLV-I viral tropism for CD68+ cells, and that HTLV-I infected synoviocytes were induced to produce TNF-alpha, which enhances synovial proliferation in HAAP.
Aged↗
The relationship between serum immunoglobulin levels and pulmonary involvement in systemic sclerosis.
OBJECTIVE: To examine the relationship between serum immunoglobulin (Ig) levels and pulmonary function in patients with systemic sclerosis (SSc). METHODS: Twenty-four patients with SSc who had at least 2 sets of pulmonary function tests (PFT) at intervals of more than one year were eligible. Multiple linear regression models were constructed for prediction of the annualized rates of change of forced vital capacity (FVC), carbon monoxide diffusing capacity (DL(CO)), and DL(CO) per unit alveolar volume (K(CO)). RESULTS: The rates of change of FVC and K(CO) correlated with the annualized rate of change of IgG (p < 0.001 and p = 0.005, respectively), and the rate of change of DL(CO) correlated with the serum IgM level at the first PFT (p = 0.020) and with the annualized rate of change of IgG (p = 0.007). CONCLUSION: The rates of change of serum Ig levels are associated with those of pulmonary function in SSc. Use of this model may assist investigation of pulmonary involvement.
Adult↗
Structural identification of phosphatidylcholines having an oxidatively shortened linoleate residue generated through its oxygenation with soybean or rabbit reticulocyte lipoxygenase.
Phosphatidylcholines (PCs) with platelet-activating factor (PAF)-like biological activities are known to be generated by fragmentation of the sn-2-esterified polyunsaturated fatty acyl group. The reaction is free radical-mediated and triggered by oxidants such as metal ions, oxyhemoglobin, and organic hydroperoxides. In this study, we characterized the PAF-like phospholipids produced on reaction of PC having a linoleate group with lipoxygenase enzymes at low oxygen concentrations. When the oxidized PCs were analyzed by gas chromatography-mass spectrometry, two types of oxidatively fragmented PC were detected. One PC had an sn-2-short chain saturated or unsaturated acyl group (C(8)-C(13)) with an aldehydic terminal; the abundant species were PCs with C(9) and C(13). The other PC had a short chain saturated acyl group (C(6)-C(9)) with a methyl terminal, and the most predominant species was PC with C(8). When the extracts of oxidation products were subjected to catalytic hydrogenation, PCs having saturated acyl groups (C(6)-C(14)) were detected; the most abundant was C(12) species. The less regiospecific formation of PAF-like lipids suggests that they were generated by oxidative fragmentation of PC hydroperoxides formed by non-stereoselective oxygenation of the alkyl radical of esterified linoleate that escaped from the active centers of lipoxygenases. One of the PAF-like PC with an aldehydic terminal was found to be bioactive; it inhibited the production of nitric oxide induced by lipopolysaccharide and interferon-gamma in vascular smooth muscle cells from rat aorta.
Animals↗
[Sjögren's syndrome].
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Antibodies, Antinuclear↗
[Clonality of infiltrative T cells in tubular dysfunction caused by Sjogren's syndrome].
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Clone Cells↗
Microchimerism in Japanese women patients with systemic sclerosis.
To examine whether microchimerism occurs in Japanese women patients with systemic sclerosis, we analysed the Y-chromosome in DNA by PCR. There was no significant difference between patients and healthy people, suggesting that microchimerism may not be the sole pathogenesis in Japanese women with systemic sclerosis.
Chimera↗
Fas ligand-mediated exocrinopathy resembling Sjögren's syndrome in mice transgenic for IL-10.
Although IL-10 has been implicated in the pathogenesis of several autoimmune diseases, the mechanisms by which this cytokine mediates inflammatory lesions remain to be elucidated. Exocrine gland destruction is an important early step in the development of Sjögren's syndrome. To better understand the role of IL-10 in Sjögren's syndrome, we made transgenic mice in which the mouse IL-10 gene was regulated by the human salivary amylase promoter. Transgenic expression of IL-10 induced apoptosis of glandular tissue destruction and lymphocyte infiltration consisting primarily of Fas-ligand (FasL)+ CD4+ T cells, as well as in vitro up-regulation of FasL expression on T cells. These data suggest that overexpression of IL-10 in the glands and their subsequent Fas/FasL-mediated bystander tissue destruction is a causal factor in the development of this disease.
Animals↗
Telomerase components as a diagnostic tool in human oral lesions.
Telomerase activity is considered to be a diagnostic marker of malignancy since most malignant cells express this activity and most somatic cells do not. However, the detection of telomerase activity is rather complicated and is affected by many factors. Recently, human telomerase components were cloned and found to consist of 3 subunits. We assessed which component of telomerase best correlates with malignancy in order to study the possibilities for developing a new diagnostic marker. Telomerase activity was measured by a telomeric repeat amplification protocol (TRAP) assay, and the telomerase components hTR, hTRT-mRNA and TP1-mRNA were detected by the reverse transcriptase-polymerase chain reaction (RT-PCR). Twenty-five of 26 oral malignant lesions, 9 of 22 benign lesions and none of 19 normal control tissues exhibited distinct telomerase activity. hTR and TP1-mRNA expression levels were detected in all malignant lesions and normal control tissues and had no significant correlation with the telomerase activity results. In contrast, hTRT-mRNA expression was closely associated with telomerase activity. All lesions expressing hTRT were telomerase positive. In addition, some samples of dysplastic lesions, benign tumors, lichen planus and normal mucosa exhibiting poor telomerase activity revealed weak expression of hTRT. Expression levels of hTRT-mRNA positively correlated with clinical and pathological findings. Detection of hTRT-mRNA by RT-PCR appeared to be more sensitive for telomerase than measurement of telomerase activity by the TRAP assay. Detection of hTRT-mRNA may provide information useful in the diagnosis of oral malignancies.
Biomarkers, Tumor↗
Telomerase activation and cell proliferation during 7,12-dimethylbenz[a]anthracene-induced hamster cheek pouch carcinogenesis.
Telomerase is a ribonucleoprotein complex intimately involved in cell immortalization and carcinogenesis. This enzyme is activated and stabilizes telomere length in almost all types of cancer. Telomerase may be necessary for continuous cell proliferation. In this study, we analyzed telomerase activity in hamster experimental oral lesions (starting from epithelial hyperplasia through dysplasia, carcinoma in situ, and invasive carcinoma) evoked by 7,12-dimethylbenz[a]anthracene, and in normal mucosa. We also analyzed proliferative activity in these lesions by using immunohistochemical analysis and flow cytometry. Histologically normal epithelium expressed weak telomerase activity. The telomerase activity count increased rapidly in the early stage of carcinogenesis and gradually in the late stage. Cell-proliferative activity closely correlated with progression of disease. These findings indicate that telomerase activation is an early event and that increases in telomerase activity upregulate cell proliferation in chemically induced hamster oral carcinogenesis.
9,10-Dimethyl-1,2-benzanthracene↗
Tumor necrosis factor alpha regulation of the FAS-mediated apoptosis-signaling pathway in synovial cells.
OBJECTIVE: Fas-mediated apoptosis is observed in synoviocytes of patients with rheumatoid arthritis (RA), but not in those of patients with osteoarthritis (OA). The present study was conducted to elucidate the mechanisms that initiate induction of Fas-mediated apoptosis in RA synoviocytes. METHODS: Cultured OA synoviocytes, which are insensitive to Fas-mediated apoptosis in spite of Fas antigen expression, were used in these experiments. Synovial cell proliferation and cytotoxicity studies were performed using MTS and lactate dehydrogenase release assays. Surface expression of Fas antigen was analyzed by flow cytometry. The expression and function of apoptosis-signaling molecules, such as caspase 8 and caspase 3, were examined by immunoblot analysis. RESULTS: Tumor necrosis factor alpha (TNFalpha) induced proliferation of cultured OA synoviocytes. Fas ligation with anti-Fas monoclonal antibody (mAb) resulted in cytotoxic activity against cultured OA synoviocytes that had been pretreated with TNFalpha for 5 days, but not those pretreated for 2 days. In contrast, anti-Fas mAb did not show a cytotoxic effect against untreated cultured OA synoviocytes. A gradual up-regulation of caspase 8 and caspase 3, which played a role in the caspase cascade for Fas-mediated apoptosis, was observed in TNFalpha-treated cultured OA synoviocytes. In addition, Fas ligation to TNFalpha-treated cultured OA synoviocytes induced activation of caspase 8 and caspase 3, with subsequent cleavage of poly(ADP-ribose) polymerase (PARP), a substrate of activated caspase 3. More importantly, Z-IETD-FMK, a caspase 8 inhibitor, and Ac-DEVD-CHO, a caspase 3 inhibitor, almost completely inhibited Fas-mediated apoptosis of TNFalpha-treated cultured OA synoviocytes, whereas Ac-YVAD-CHO, a caspase 1 inhibitor, did not. CONCLUSION: Our results clearly demonstrate that TNFalpha stimulates synovial cells to proliferate as well as sensitizes the cells for Fas-mediated apoptosis, at least in part by up-regulation and activation of caspase 8 and caspase 3. These findings suggest that TNFalpha may be one of the factors providing sensitization of synovial cells to Fas-mediated apoptosis in RA.
Apoptosis↗
Differential regulation of rheumatoid synovial cell interleukin-12 production by tumor necrosis factor alpha and CD40 signals.
OBJECTIVE: To investigate the roles of tumor necrosis factor alpha(TNFalpha) and the CD40-CD154 interaction in interleukin-12 (IL-12) production by rheumatoid synovial cells (SC). METHODS: Levels of IL-12 (p40 and p70) in synovial tissue and culture supernatants of SC from patients with rheumatoid arthritis (RA), osteoarthritis (OA), and ankylosing spondylitis (AS) were assayed by enzyme-linked immunosorbent assay. Effects of anti-CD154 and anti-TNFalpha antibody on spontaneous and lipopolysaccharide (LPS)-stimulated IL-12 production by SC were examined. Effects of immobilized anti-CD3 treatment and depletion of CD4+ T cells on IL-12 production were also tested. CD154 expression by synovial T cells and intracellular IL-12 production during culture were analyzed by flow cytometry. RESULTS: IL-12 p40 and p70 levels in RA synovial tissue and spontaneous IL-12 p40 production by SC from RA patients were significantly higher than the levels in OA and AS patients. Spontaneous IL-12 production by SC from RA patients significantly decreased after depletion of CD4+ T cells from SC or after application of anti-CD154 antibody, but not by treatment with anti-TNFalpha antibody. Anti-CD3 antibody stimulation increased spontaneous IL-12 p40 production and CD154 expression by synovial T cells. The increment of IL-12 p40 production by anti-CD3 was abrogated by anti-CD154 antibody. IL-12 p40 production was also increased by LPS stimulation. LPS-stimulated IL-12 production was inhibited by anti-TNFalpha antibody, but not by T cell depletion and anti-CD154 antibody treatment. The TNFalpha inhibitor rolipram inhibited LPS-stimulated IL-12 p40 production by RA SC more strongly than spontaneous production. TNFalpha restored LPS-stimulated IL-12 production that had been inhibited by rolipram. CONCLUSION: IL-12 production in RA is regulated by 2 different pathways. One pathway is T cell dependent, predominantly through a CD40-CD154 interaction, while the other is T cell independent, mediated through TNFalpha. Inhibition of IL-12 production by interference with CD40-CD154 interaction and TNFalpha production may be a potential therapeutic strategy for treating RA.
Adjuvants, Immunologic↗