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Biomedical subjects

S Koyama

Publications and source records attributed to S Koyama.

At least 145 records · Page 8Linked to original sources
PubMed1998

Primary gastric Burkitt's lymphoma presenting with c-myc gene rearrangement.

A 54-year-old man with primary gastric Burkitt's lymphoma is described. He was evaluated for appetite loss and intermittent midepigastric pain. Upper gastroduodenal endoscopy detected an ulcer in the lesser curvature of the body, and biopsy specimens revealed infiltration of medium-sized lymphoblasts with "starry sky" macrophages. The infiltrated cells were positive for a B-cell marker. Abdominal computed tomography scan demonstrated marked enlargement of the gastric wall, but no enlargement of lymph nodes. These findings led us to diagnose primary gastric Burkitt's lymphoma. The patient responded dramatically to CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy, but 6 months after his initial admission, the disease recurred in the stomach and bone marrow. Lymphoblastic cells were positive for B-cell markers (CD 10, 19, 20, and human leukocyte antigen [HLA]-DR) and showed an abnormal karyotype, 47, XY, t(8;14)(q24;q32), +12. In these cells, the Epstein-Barr virus genome was detected by polymerase chain reaction. Southern blot analysis revealed rearrangement of Ig heavy and light chain genes. In addition, c-myc gene rearrangement was detected. Eight months after the beginning of chemotherapy, the patient died of central nervous system involvement. To our knowledge, this is the first description of a genetic analysis of primary gastric Burkitt's lymphoma.

Blotting, Southern↗
PubMed1998

Mycotic abdominal aortic aneurysm associated with myelodysplastic syndrome (MDS): report of a case.

A 59-year-old man, who manifested lower back pain, was admitted with sepsis and disseminated intravascular coagulation (DIC). A computed tomographic scan showed a slight thickening of the abdominal aortic wall. A blood examination revealed pancytopenia. Myelodysplastic syndrome was diagnosed after bone marrow aspiration and a chromosome analysis. Sepsis due to a Staphylococcus aureus infection and DIC subsided after medical treatment; however, an aortobifemoral bypass was performed upon the detection of a localized rupture of a mycotic abdominal aortic aneurysm 1 month later. The patient is still alive 2 years after operation despite the presence of a hematological disorder.

Aneurysm, Infected↗
PubMed1998

Bradykinin stimulates type II alveolar cells to release neutrophil and monocyte chemotactic activity and inflammatory cytokines.

In the present study, we evaluated the potential of bradykinin (BK) to induce the release of neutrophil and monocyte chemotactic activity (NCA and MCA) and cytokines from an alveolar type II epithelial cell line, A549 cells. BK stimulated A549 cells to release NCA and MCA in a dose- and time-dependent manner (P < 0.001). Checkerboard analysis revealed that both NCA and MCA involved chemotactic and chemokinetic activity. Molecular sieve column chromatography showed three molecular weight masses (near 19 kd, 8 kd, and 400 d) for NCA and several molecular weight peaks (near 66 kd, 25 kd, 19 kd, 16 kd, and 400 d) for MCA. The release of NCA and MCA was inhibited by cycloheximide and lipoxygenase inhibitors (P < 0.01). The NCA and MCA were inhibited by leukotriene B4 (LTB4) receptor antagonist (P < 0.01), and the concentration of LTB4 was high enough for NCA and MCA. Antibodies to interleukin (IL)-8 and granulocyte colony-stimulating factor (G-CSF) attenuated NCA (P < 0.01), and antibodies to monocyte chemotactic protein-1 (MCP-1), G-CSF, and transforming growth factor (TGF)-beta attenuated MCA (P < 0.01). The levels of IL-8, G-CSF, MCP-1, and TGF-beta increased time dependently (P < 0.01). BK also stimulated the release of ILeukin-6 from A549 cells (P < 0.001). The receptors responsible for the release of NCA, MCA, and individual chemokines involved both BKB1 and BKB2 receptors. These data suggest that BK may stimulate alveolar type II pneumocytes to release inflammatory cytokines, which then may modulate the lung inflammation.

Antibodies↗
PubMed1998

Smoke extract stimulates lung epithelial cells to release neutrophil and monocyte chemotactic activity.

Inflammatory cells accumulate within the lungs of cigarette smokers. Current concepts suggest that these cells can induce protease-antiprotease and/or oxidant-antioxidant imbalance(s), which may damage the normal lung alveolar and interstitial structures. Because type II pneumocytes line the alveolar space, and because the inflammatory cells migrate and reside at the alveolus, we postulated that the type II pneumocytes might release chemotactic activity for neutrophils and monocytes in response to smoke extract. To test this hypothesis, A549 cells were cultured and the supernatant fluids were evaluated for the neutrophil and monocyte chemotactic activity (NCA and MCA) by a blind-well chamber technique. A549 cells released NCA and MCA in response to smoke extract in a dose- and time-dependent manner (P < 0.05). Checkerboard analysis showed that the activity was chemotactic. Partial characterization of NCA and MCA revealed that the activity was partly heat labile, trypsin sensitive, and ethyl acetate extractable. Lipoxygenase inhibitors and cycloheximide inhibited the release of NCA and MCA. Molecular sieve column chromatography showed multiple peaks for both NCA and MCA. NCA was inhibited by anti-human-interleukin (IL)-8 antibody, granulocyte colony-stimulating factor (G-CSF) antibody, or leukotriene (LT)B4 receptor antagonist. Monocyte chemoattractant protein (MCP)-1 antibody or LTB4 receptor antagonist inhibited MCA. Immunoreactive IL-8, G-CSF, MCP-1, and LTB4 significantly increased in the supernatant fluids in response to smoke extract. These data suggest that the type II pneumocytes may release NCA and MCA and modulate the inflammatory cell recruitment into the lung.

Antibodies↗
PubMed1998

Reading of Japanese Kanji (morphograms) and Kana (syllabograms): a magnetoencephalographic study.

Magnetoencephalograms were recorded from six healthy Japanese subjects in order to investigate the areas in the cortices which are involved in the recognition of Japanese characters (Kanji and Kana). Forty-four Kanji (morphograms), 44 Kana (syllabograms) and 20 alphabet letters were used as stimuli. They were presented randomly and the subjects were required to read each stimulus and count the number of letters. The magnetic responses were recorded with dual 37-channel SQUID (Superconducting Quantum Interference Device) gradiometers from the temporal, parietal and occipital areas of the brain. The magnetic responses to Kanji and Kana were similar and consequently the locations of equivalent current dipoles (ECDs) to Kanji and those to Kana did not differ at any recording site. In all the subjects, ECDs were found in the posterior inferior temporal (PIT) areas approximately corresponding to Brodmann area 37 in the latency range of 150-300 msec. These activities were found in both hemispheres without consistent laterality. The location of the ECD moved forward from posterior to anterior in the PIT area as the latency increased in all but one subject. Only one subject showed activities in the left angular gyrus. Since activities in PIT areas were also found in alphabet letters, the bilateral PIT areas are considered to play an essential role in reading.

Adult↗
PubMed1998

Electrophysiological evidence for the typicality effect of human cognitive categorization.

Event-related brain potentials (ERPs) were recorded from 14 normal subjects during a category verification task. Stimulus words were selected from 17 semantic categories (e.g. 'vegetables'). Half of the words were typical category members (e.g. 'carrot', 'spinach') and the other half were atypical (e.g. 'parsley', 'asparagus'). Subjects were required to judge whether each stimulus belonged to a target category ('vegetables' or 'sports') or a non-target category. For the non-target category, the typicality effect was neither found in ERPs nor in reaction times. For the target category, typical words were responded to more quickly than were atypical words and the ERP amplitudes between a 300-450 ms period were more negative after the atypical words than after the typical words (typicality effect). These results suggested that typical words of the target were more primed by a target category than were the atypical words of the target and thus that a concept is represented by a prototype, the central tendency of all members of the category.

Adult↗
PubMed1998

Effects of tactile interference stimulation on somatosensory evoked magnetic fields following tibial nerve stimulation.

We studied the effects of interfering tactile stimulation applied to the foot ipsilateral and contralateral to the stimulation on somatosensory evoked magnetic fields (SEFs) following tibial nerve stimulation at the ankle. Equivalent current dipoles (ECDs) of all 4 components, 1M-4M, in all sessions were estimated to be very close each other, around the foot area of the primary sensory cortex (SI). The 1M, 2M and 4M components were significantly reduced in amplitude by the ipsilateral-foot interference, and we consider that this phenomenon is due mainly to 'saturation' of the neurons in area 3b of the SI. In contrast, the 3M component was significantly enhanced in amplitude by the contralateral-foot interference. We suspect that this result was due to the effects of neuronal activities in areas 2, 5 and/or 7, which receive inputs from both sides of the body, i.e. to 'bilateral function'. Considering the various types of interference effects on SEFs and somatosensory evoked potentials (SEPs) observed in not only the present, but also in the previous studies, we conclude that both SEFs and SEPs following tibial nerve stimulation are generated mainly by ascending signals mediated by cutaneous fibers of the peripheral nerves rather than the muscle afferents.

Adult↗
PubMed1998

Pain processing traced by magnetoencephalography in the human brain.

The temporal and spatial processing of pain perception in human was traced by magnetoencephalography (MEG). We applied a painful CO2 laser beam to the forearm of 11 normal subjects, and estimated the activated areas using a single equivalent current dipole (ECD) at each time point, and a brain electric source analysis (BESA) as a spatio-temporal multiple source analysis method. The four-source model was found to be the most appropriate; sources 1 and 2 at the secondary sensory cortex (SII) contralateral and ipsilateral to the stimulation, and sources 3 and 4 at the anterior medial temporal area (probably the amygdalar nuclei or hippocampal formation) contralateral and ipsilateral to the stimulation, respectively. Activities in all 4 areas were temporally overlapped. Activity in the primary sensory cortex (SI) contralateral to the stimulated site was not identified. Activity in the cingulate cortex was also not clearly identified. These results are probably due to one or more of the following factors; (1) the cingulate cortex is too deep, (2) the ECDs generated in the cingulate cortex are mainly oriented radially, and (3) the ECDs generated in bilateral hemispheres interfere with each other. No significant or consistent magnetic fields were recorded after 500 msec following the stimulation, probably due to the complicated spatial and temporal overlapping of activities in multiple areas.

Adult↗
PubMed1998

Detection of complement C3 and factor B gene expression in normal colorectal mucosa, adenomas and carcinomas.

Local secretion of complement components in the human intestine has been previously reported. However, the cellular source has not been identified. In this study, we demonstrate complement C3 and factor B mRNA expression in the normal colonic mucosa by in situ hybridization analysis. C3 and factor B genes were found to be expressed at high levels in the epithelial cells of the lower parts of the crypts in colonic mucosa, and this expression decreased gradually from the crypt base to the luminal surface. At the upper crypt and the luminal surface, these genes almost disappeared. C3 and factor B genes were expressed in all crypts at the same level. Furthermore, C3 and factor B gene expression was also identified in adenomas and carcinomas. In these neoplastic tissues, C3 and factor B genes were expressed uniformly, and the polarized distribution observed in the normal crypts was not detected. It is likely that complement components are locally synthesized in the intestine, and that these complement components may actively participate in normal immune and inflammatory responses over the enormous surface area of the intestinal mucosa.

Adenoma↗
PubMed1998

The role of endogenous nitric oxide in the sympathetic and hemodynamic response to platelet activating factor-induced hypotension in anesthetized dogs.

We previously demonstrated that platelet-activating factor (PAF) when injected intravenously decreases renal sympathetic nerve activity in anesthetized dogs. Recently, nitric oxide (NO) has been shown to inhibit renal sympathetic nerve activity. The present study was designed to determine, using the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), whether endogenous NO contributes to the PAF-induced renal sympatho-inhibition in anesthetized dogs. We also determined the role of NO in systemic and pulmonary hemodynamics during PAF-induced hypotension. In response to PAF (10 microg x kg(-1), intravenously), renal sympathetic nerve activity showed similar responses in animals pretreated with L-NAME (n = 7; 20 mg x kg(-1) bolus and .05 mg x kg(-1) x min[-1]), D-NAME (n = 7), and phenylephrine (n = 7), as characterized by an initial increase (230%) followed by a decrease (56%). The depressor response to PAF was also similar as early as 10 min after injection in all PAF-injected groups. In contrast, L-NAME pretreatment potentiated PAF-induced pulmonary hypertension. Pulmonary arterial pressure 10 min after PAF in the L-NAME group (25+/-2 mmHg) was significantly greater than that in the D-NAME group (12+/-3 mmHg). In conclusion, endogenously produced NO is not involved in PAF-induced renal sympathetic nerve response or hypotension but attenuates PAF-induced pulmonary hypertension at the early stage in anesthetized dogs.

Anesthetics↗
PubMed1998

Case report: Haemangioma of the small intestine complicated by protein-losing gastroenteropathy.

We report a case of haemangioma of the small intestine complicated by protein-losing gastroenteropathy. A 32-year-old female had suffered from hypoproteinaemia for 6 years, but the cause of this condition had not been determined. On diagnosis and therapy for hypoproteinaemia, intra-operative endoscopy and histological examination were performed and she was subsequently diagnosed with capillary haemangioma of the small intestine. Angiography was not useful for the detection of capillary haemangioma of the small intestine in this case. Although intestinal haemangioma is an important cause of gastrointestinal bleeding, protein loss is an extremely rare complication and this case is the first to be reported in Japan.

Adult↗
PubMed1998

Axil, a member of the Axin family, interacts with both glycogen synthase kinase 3beta and beta-catenin and inhibits axis formation of Xenopus embryos.

Using a yeast two-hybrid method, we identified a novel protein which interacts with glycogen synthase kinase 3beta (GSK-3beta). This protein had 44% amino acid identity with Axin, a negative regulator of the Wnt signaling pathway. We designated this protein Axil for Axin like. Like Axin, Axil ventralized Xenopus embryos and inhibited Xwnt8-induced Xenopus axis duplication. Axil was phosphorylated by GSK-3beta. Axil bound not only to GSK-3beta but also to beta-catenin, and the GSK-3beta-binding site of Axil was distinct from the beta-catenin-binding site. Furthermore, Axil enhanced GSK-3beta-dependent phosphorylation of beta-catenin. These results indicate that Axil negatively regulates the Wnt signaling pathway by mediating GSK-3beta-dependent phosphorylation of beta-catenin, thereby inhibiting axis formation.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Acetylcholine stimulates alveolar macrophages to release inflammatory cell chemotactic activity.

Neurological transmitters including ACh, substance P (SP), and calcitonin gene-related peptide (CGRP) play an important role in regulating airway tone, and increased bronchial reactivity to cholinergic stimulation is a well-recognized phenomenon in patients with bronchial asthma. We postulated that ACh, SP, and CGRP might stimulate alveolar macrophages (AMs) to release neutrophil, monocyte, and eosinophil chemotactic activities. To test this hypothesis, bovine AMs were isolated by bronchoalveolar lavage and cultured. AMs released chemotactic activities in response to ACh in a dose- and time-dependent manner (P < 0.05). However, SP and CGRP did not stimulate bovine AMs. Checkerboard analysis revealed that these released activities were predominantly chemotactic. Partial characterization and molecular-sieve column chromatography revealed that low-molecular-weight lipid-soluble activity was predominant. Lipoxygenase inhibitors significantly blocked the release of chemotactic activities (P < 0.05). Leukotriene B4- and platelet-activating factor-receptor antagonists blocked the chemotactic activities. Immunoreactive leukotriene B4 significantly increased in supernatant fluids in response to ACh (P < 0.05), but platelet-activating factor did not. The receptor responsible for the release of the chemotactic activities was the muscarinic M3 receptor. These data demonstrate that ACh stimulates AMs to release lipoxygenase-derived chemotactic activities and plays a role in inflammatory cell recruitment into the airway.

Acetylcholine↗
PubMed1998

Human lung fibroblasts release chemokinetic activity for monocytes constitutively.

We determined whether human lung fibroblasts (HLFs) might release mediators that are responsible for monocyte chemokinetic activity (MCA) constitutively. HLF supernatant fluids showed MCA in a time-dependent manner (P < 0.001). Checkerboard analysis of 24- and 72-h supernatant fluids showed that the activity was chemokinetic. Partial characterization of 24- and 72-h supernatant fluids revealed that the mediators released after 24 h were predominantly composed of lipid-soluble activity, and MCA was blocked by lipoxygenase inhibitors. The mediators released after 72 h were predominantly trypsin sensitive and blocked by cycloheximide. Molecular-sieve column chromatography identified four peaks of MCA. A polyclonal antibody to monocyte chemoattractant protein-1 (MCP-1) inhibited MCA by 20% after 24 h and by 40% after 72 h. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor-beta (TGF-beta) antibodies attenuated MCA released after 72 h by 30 and 10%, respectively. These antibodies inhibited corresponding molecular-weight peaks separated by molecular-sieve column. The concentrations of MCP-1, GM-CSF, and TGF-beta were 4,698 +/- 242, 26.8 +/- 3.8, and 550 +/- 15 pg/ml, respectively. A leukotriene B4 (LTB4)-receptor antagonist attenuated the total MCA and the lowest molecular weight peak of MCA. The concentrations of LTB4 were 153.4 +/- 12.4 (24 h) and 212 +/- 16.6 (72 h) pg/ml. These findings suggest that HLFs may modulate the recruitment of monocytes into the lung by releasing MCP-1, GM-CSF, TGF-beta, and LTB4 constitutively.

Adult↗
PubMed1998

Alveolar type II-like cells release G-CSF as neutrophil chemotactic activity.

We evaluated the potential of A549 cells, an alveolar type II epithelial cell line, to release granulocyte colony-stimulating factor (G-CSF), in addition to interleukin (IL)-8 and leukotriene B4, as neutrophil chemotactic activity (NCA). Human recombinant IL-1beta stimulated A549 cells to release NCA in a time- and dose-dependent fashion. The released NCA was blocked by mouse anti-human G-CSF polyclonal antibody. Molecular-sieve column chromatography revealed that IL-1beta induced the release of a 19- to 20-kDa chemotactic mass that was inhibited by anti-human G-CSF antibody. IL-1beta stimulated the release of G-CSF in a dose-dependent fashion, but the time-dependent profile of G-CSF showed that the concentration of G-CSF declined after 48 h. Tumor necrosis factor (TNF)-alpha, Escherichia coli lipopolysaccharide (LPS), and bradykinin (BK) stimulated A549 cells to release NCA that was inhibited by anti-G-CSF antibody. The release of G-CSF in response to TNF-alpha, LPS, and BK was significantly increased. The similar concentrations of human recombinant G-CSF (10-1,000 pg/ml) as in the supernatant fluid induced neutrophil chemotaxis. G-CSF mRNA was expressed time and dose dependently at 4 h and declined after 4 h in response to IL-1beta as evaluated by RT-PCR. The expression of G-CSF mRNA was also observed by TNF-alpha, LPS, and BK stimulation. These data suggest that type II alveolar epithelial cells may produce G-CSF as NCA and may participate in the regulation of leukocyte extravasation.

Animals↗
PubMed1998

Acetylcholine and substance P stimulate bronchial epithelial cells to release eosinophil chemotactic activity.

We investigated a role of neuroregulation in the release of eosinophil chemotactic activity (ECA) from bovine bronchial epithelial cells (BBEC). BBEC were stimulated with acetylcholine (ACh) and substance P (SP), and the supernatant fluids were tested for ECA by a blind-well chemotactic chamber technique. BBEC released ECA in response to ACh and SP in a dose- and time-dependent manner. Checkerboard analysis showed that ECA in regard to ACh and SP was chemotactic rather than chemokinetic. Partial characterization revealed that ECA involved both lipids and peptides. The release of ECA in response to ACh and SP was inhibited by nonspecific and 5-specific lipoxygenase inhibitors and by cycloheximide (P < 0.01). Molecular-sieve column chromatography revealed that these mediators induced three molecular mass peaks (near 25 kDa, 9 kDa, and 400 Da, respectively). The lowest peak, which represented the predominant activity, was blocked by leukotriene B4-receptor antagonist (P < 0. 01) but not by platelet-activating factor-receptor antagonist. The release of leukotriene B4 in the supernatant fluids was increased in response to ACh and SP stimulation (P < 0.01). Platelet-activating factor was not detected. These results raise the possibility of a role of neuroregulation for the elaboration of ECA in the airway.

Acetylcholine↗
PubMed1998

Effects of low phosphate intake on bone and mineral metabolism in rats: evaluation by biochemical markers and pyridinium cross-link formation in bone.

We have investigated the changes in biochemical markers and in pyridinium cross-links in bone in hypophosphatemic rats. Six-week-old female Wistar rats were divided into two groups (normal diet and a phosphate-deficient diet) and fed for 8 weeks. A low phosphate intake caused a significant difference in the concentrations of osteocalcin and alkaline phosphatase with advancing rachitis as well as an increase in bone resorption marker concentrations in urine. Femur biochemical analysis revealed a significant (p < 0.005) increase in deoxypyridinoline per mole collagen in the phosphate-deficient group which suggested that urinary excretions of pyridinium cross-links might reflect not only bone resorption but also increased pyridinium cross-links in bone matrix collagen. Our results demonstrate that a low phosphate intake causes an increase of pyridinium cross-link formation as well as a discrepancy between the circulation levels of alkaline phosphatase and osteocalcin with advancing rachitis. These alterations induced by low phosphate intake should be considered when interpreting the values of biochemical markers.

Alkaline Phosphatase↗