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Biomedical subjects

S Matsui

Publications and source records attributed to S Matsui.

At least 91 records · Page 5Linked to original sources
PubMed2000

[Acute eosinophilic pneumonia induced by cigarette smoking: positive lymphocyte stimulation test of a cigarette extract].

A 21-year-old man was admitted to our hospital with high fever, general fatigue and dyspnea. Chest radiography on admission showed diffuse bilateral infiltrate shadows with Kerley's B lines, and a CT scan showed patches of infiltrates with thickened interlobular septa in both lungs. Examination of the bronchoalveolar lavage fluid and the clinical course led to a diagnosis of acute eosinophilic pneumonia. The patient improved without steroid therapy. We suspected that the disease was related to smoking because the patient had started smoking seven days before the onset of the symptoms. Because a lymphocyte stimulation test gave a positive reaction to a cigarette extract, a challenge test was done. After this, the patient had fever and hypoxemia. These findings suggest that cigarette smoking induces acute eosinophilic pneumonia.

Acute Disease↗
PubMed2000

[A case of primary Sjögren's syndrome with interstitial pneumonia showing bronchiolitis obliterans organizing pneumonia pattern and lymphofollicular formation].

A 46-year-old woman with a 2-year history of xerostomia, who had had an episode of suspected Sjögren's syndrome in 1995, was admitted to our hospital because of a dry cough. Chest radiography on admission showed ground-glass infiltrates and reticular shadows in both lower lung fields. Primary Sjögren's syndrome was diagnosed by lip biopsy. Video-assisted thoracoscopic lung biopsies revealed the co-existence of interstitial pneumonia with the BOOP pattern and follicular bronchiolitis. Treatment with oral prednisolone improved the symptoms, and reduced the abnormal chest shadows. This was an interesting case of the BOOP pattern in a lung lesion associated with primary Sjögren's syndrome.

Administration, Oral↗
PubMed1999

Design of clinical trials for recurrent events with periodic monitoring.

This paper presents a design for randomized clinical trials in which incomplete data are collected on the occurrence of potentially recurrent events through periodic monitoring. In particular, events are assumed to arise according to a point process, but information is available at the times of monitoring only if one or more events has occurred since the preceding monitoring point. The event process is modelled via a piecewise Poisson process, and a proportional rates model is introduced to represent the difference in event rates between treatment groups. The design was developed on the basis of a Wald-type test derived from the generalized estimating equations of Liang and Zeger (Biometrika 73, 13-22 (1986)). Robustification of the variance of the estimator of the treatment effect was considered under a random effects model with a semi-parametric mixture distribution. The design was adopted to address issues which arose in an osteoporosis trial conducted in Japan.

Calcium↗
PubMed1999

A human homolog of Drosophila lethal(3)malignant brain tumor (l(3)mbt) protein associates with condensed mitotic chromosomes.

The lethal(3)malignant brain tumor (D-l(3)mbt) gene is considered to be one of the tumor suppressor genes of Drosophila, and its recessive mutations are associated with malignant transformation of the neuroblasts in the larval brain. The structure of D-l(3)mbt protein is similar to Drosophila sex comb on midleg (Scm) protein which is a member of Polycomb group (PcG) proteins. We have isolated here the first human homolog of the D-l(3)mbt gene, designated h-l(3)mbt. Radiation hybrid mapping and fluorescence in situ hybridization (FISH) analysis localized the h-l(3)mbt gene to chromosome 20q12. The h-l(3)mbt transcript is expressed in most of the human adult normal tissues and cultured cell lines. However, some cancer cells markedly reduce the h-l(3)mbt protein expression. Immunocytochemical study revealed that the h-l(3)mbt protein shows a speckled and scattered distribution in interphase nuclei and completely associates with condensed chromosomes in mitotic cells. This subcellular localization has been shown to be different from that of Bmi1 protein which is a component of PcG complex. Furthermore, overexpression of h-l(3)mbt protein by using a Cre-mediated gene activation system leads to failures of proper chromosome segregation and cytokinesis, which result in formation of multinuclei in U251MG cells. These observations suggest that h-l(3)mbt protein has functions distinct from those of PcG proteins and may play a role in proper progression of cell division.

Adult↗
PubMed1999

A model for CD8+ CTL tumor immunosurveillance and regulation of tumor escape by CD4 T cells through an effect on quality of CTL.

Understanding immune mechanisms influencing cancer regression, recurrence, and metastasis may be critical to developing effective immunotherapy. Using a tumor expressing HIV gp160 as a model viral tumor Ag, we found a growth-regression-recurrence pattern, and used this to investigate mechanisms of immunosurveillance. Regression was dependent on CD8 T cells, and recurrent tumors were resistant to CTL, had substantially reduced expression of epitope mRNA, but retained the gp160 gene, MHC, and processing apparatus. Increasing CTL numbers by advance priming with vaccinia virus expressing gp160 prevented only the initial tumor growth but not the later appearance of escape variants. Unexpectedly, CD4 cell depletion protected mice from tumor recurrence, whereas IL-4 knockout mice, deficient in Th2 cells, did not show this protection, and IFN-gamma knockout mice were more susceptible. Purified CD8 T cells from CD4-depleted mice following tumor regression had more IFN-gamma mRNA and lysed tumor cells without stimulation ex vivo, in contrast to CD4-intact mice. Thus, the quality as well as quantity of CD8+ CTL determines the completeness of immunosurveillance and is controlled by CD4 T cells but not solely Th2 cytokines. This model of immunosurveillance may indicate ways to enhance the efficacy of surveillance and improve immunotherapy.

Animals↗
PubMed1999

Effective utilization of N2-ethyl-2'-deoxyguanosine triphosphate during DNA synthesis catalyzed by mammalian replicative DNA polymerases.

Acetaldehyde is produced by metabolic oxidation of ethanol after drinking alcoholic beverages. This agent reacts with nucleosides and nucleotides, resulting in the formation of N2-ethyl-guanine residues. N2-ethyl-2'-deoxyguanosine (N2-ethyl-dG) adduct has been detected in the lymphocyte DNA of alcoholic patients [Fang, J. L., and Vaca, C. E. (1997) Carcinogenesis 18, 627-632]. Thus, the nucleotide pool is also expected to be modified by acetaldehyde. N2-Ethyl-2'-deoxyguanosine triphosphate (N2-ethyl-dGTP) was chemically synthesized. The utilization of N2-ethyl-dGTP during DNA synthesis was determined by steady-state kinetic studies. N2-Ethyl-dGTP was efficiently incorporated opposite template dC in reactions catalyzed by mammalian DNA polymerase alpha and delta. When pol alpha was used, the insertion frequency of N2-ethyl-dGTP was 400 times less than that of dGTP, but 320 times higher than that of 7,8-dihydro-8-oxo-2'-deoxyguanosine triphosphate (8-oxo-dGTP), an oxidative damaged nucleotide. Using pol delta, the insertion frequency of N2-ethyl-dGTP was only 37 times less than that of dGTP. The chain extension from dC:N2-ethyl-dG pair occurred much more rapidly: the extension frequencies for pol alpha and pol delta were only 3.8 times and 6.3 times, respectively, lower than that of dC:dG pair. We also found that N2-ethyl-dG can be detected in urine samples obtained from healthy volunteers who had abstained from drinking alcohol for 1 week before urine collection. This indicates that humans are exposed constantly to acetaldehyde even without drinking alcoholic beverages. Incorporation of N2-ethyl-dG adducts into DNA may cause mutations and may be related to the development of alcohol- and acetaldehyde-induced human cancers.

Adult↗
PubMed1999

Initial and long-term results of angioplasty in unprotected left main coronary artery.

Angioplasty of the unprotected left main coronary artery (LMCA) has been controversial. Although recent single-center studies suggest that new devices may change the situation, many questions and problems remain. Therefore, the results of unprotected left main coronary angioplasty of 175 procedures in 107 patients were analyzed to evaluate its feasibility and effectiveness. The treatment of the initial 107 cases included balloon angioplasty (39 cases, 36%), directional coronary atherectomy (53 cases, 50%), and stents (15 cases, 14%). They were divided into 3 major subgroups: (1) acute group (n = 14), in which LMCA angioplasty was performed in patients with acute myocardial infarction; (2) emergency group (n = 10); and (3) elective group (n = 83). In-hospital mortality was higher in the acute (35.7%) and emergency (40.0%) groups than in the elective group (3.6%; p <0.0001). Angiographic follow-up was routinely performed and the restenosis rate including in-hospital restenosis was 70% in the acute group, 37.5% in the emergency group, and 40% in the elective group (p = NS). The mean clinical follow-up period was 2.9 years, and the estimated 5-year survival rates of the acute and emergency groups were 50% and 48.2%, respectively. However the 5-year survival rate of the elective group was higher than that seen in the acute or emergency group (77.5%; p <0.05). Repeat LMCA angioplasty was performed in 37 of 68 patients with 8.8% mortality (38.5% of acute and emergency cases and 1.8% of elective cases). The results indicated that elective unprotected LMCA angioplasty is relatively feasible and effective under scheduled angiographic follow-up.

Adult↗
PubMed1999

Herbimycin A inhibits both dephosphorylation and translocation of cofilin induced by opsonized zymosan in macrophagelike U937 cells.

We previously reported that a 21-kDa phosphoprotein may play an important role in superoxide production through dephosphorylation by neutrophillike differentiated HL-60 cells (Suzuki et al., 1995, Biochim Biophys Acta 1266: 261-267). The phosphoprotein was identified as cofilin, an actin-binding protein, and the activation-induced changes in its intracellular distribution have been described elsewhere (Suzuki et al., 1995, J Biol Chem 270:19551-19556). However, the physiologic roles of cofilin in phagocytes remain to be established, and the regulatory mechanisms for dephosphorylation and translocation of cofilin are unknown. In the present study, we investigated the roles of cofilin in the opsonized zymosan (OZ)-activated macrophagelike U937 cells by using herbimycin A, an inhibitor for protein tyrosine kinase. In the individual adherent phagocytes, OZ induced many events: 1) production of superoxide, 2) phagocytosis of the insoluble particles OZ, 3) dephosphorylation of cofilin, 4) translocation of cofilin from cytosol to plasma membrane regions, 5) decrease in intracellular pH from 7.4 to aprroximately 6.8, and 6) rapid and transient increase in filamentous actin at the cell periphery. All of these events were inhibited or reduced significantly by herbimycin A. OZ increased phosphorylation of tyrosine in 110-, 50-, 34-, and 29-kDa proteins, whereas herbimycin A inhibited it. These results suggest that tyrosine kinase plays an essential role upstream of these events through phosphorylation of such proteins. Furthermore, microinjection of anti-cofilin antibody to the differentiated U937 cells caused inhibition of the phagocytosis. These results suggest that cofilin plays critical roles in phagocytic functions through changes in cytoskeletal organization.

Actin Depolymerizing Factors↗
PubMed1999

Magic echo solid-state NMR imaging without a rapidly switchable field gradient

To relax the high-speed requirement imposed on the gradient system used in solid-state proton imaging, we propose two simple modifications of the magic echo imaging sequence, TREV-16TS. In the first modification, the applied gradient is inverted in the middle of the RF irradiation; the second modification utilizes a sinusoidal gradient synchronized with the RF sequence. It is estimated by experiments that as long as the RF amplitude is at least about 10 times stronger than the resonance offset induced by the gradient, the spatial resolution is not degraded significantly by the line narrowing deterioration due to the gradient applied during the on-resonance RF irradiation. The modifications allow commercially available standard gradients to be used for the magic echo imaging of solids. Copyright 1999 Academic Press.

Journal Article↗
PubMed1999

Autoantibodies against M2 muscarinic receptors in patients with cardiomyopathy display non-desensitized agonist-like effects.

Circulating autoantibodies against the human M2 muscarinic receptors have been previously shown in 38% of patients with idiopathic dilated cardiomyopathy. The functional properties of these autoantibodies are reported herein. They were able to decrease the cell beating frequency of myocytes in cultured neonatal rat heart cells in a dose-dependent manner without desensitization over a period of more than 5 hours whereas the non-specific muscarinic receptor agonist carbachol also inhibited the heart cell beating frequency but was desensitized within 1 hour. In the same cell culture, anti-M2 muscarinic receptor autoantibodies were not able to induce internalization of muscarinic receptor whereas carbachol did. These results demonstrate for the first time that anti-M2 muscarinic receptor autoantibodies from patients with idiopathic dilated cardiomyopathy have stimulatory muscarinic activity in vitro, which differ from normal muscarinic agonists by non-desensitization.

Animals↗
PubMed1999

Role of the endogenous prostaglandin E2 in human lung fibroblast interleukin-11 production.

Interleukin-11 (IL-11) is known to be a member of the interleukin-6 (IL-6)-type cytokine family. IL-11 is likely to be a major determinant of immune regulation in acute and chronic inflammatory lung diseases, although it is not directly linked with specific disease processes. It has already been shown that although unstimulated human lung fibroblasts did not produce significant amounts of IL-11, the addition of interleukin-1 alpha (IL-1 alpha) and/or transforming growth factor-beta (TGF-beta) stimulated fibroblasts dose-dependently to produce IL-11. Northern blot analysis showed that these stimulators also upregulated IL-11 mRNA expression. As it has been previously reported that IL-1 and TGF-beta stimulate prostaglandin E2 (PGE2) release from lung fibroblasts, we investigate here the role of endogenous PGE2 and the direct effects of the two inhibitors of prostaglandin synthesis, indomethacin and dexamethasone, on IL-11 production by human lung fibroblasts. The addition of indomethacin, a cyclo-oxygenase inhibitor, resulted in significant suppression of IL-11 production and mRNA expression in lung fibroblasts. There was no detectable effect of PGE2 alone on IL-11 levels; however, the suppression of IL-11 production by indomethacin was almost completely reversed by addition of PGE2. In contrast, suppression of IL-11 production by indomenthacin was not reversed by addition of thromboxane B2 and carbocyclic thromboxane A2. In addition, dexamethasone completely suppressed IL-11 production and downregulated IL-11 mRNA. These results suggest that endogenous PGE2 acts as an autocrine stimulus for IL-11 production by human lung fibroblasts activated by IL-1 alpha and TGF-beta.

Anti-Inflammatory Agents↗
PubMed1999

Characterisation of a synergistic interaction between a thymidylate synthase inhibitor, ZD1694, and a novel lipophilic topoisomerase I inhibitor karenitecin, BNP1100: mechanisms and clinical implications.

We developed a combination protocol for inhibitors of thymidylate synthase (TS) and DNA topoisomerase I (Topo I) that can exert highly lethal effects in vitro against HCT-8 human colorectal cancer cells. The specific schedule was constructed so that a TS inhibitor could induce not only primary DNA damage but also cellular conditions optimal for the efficient action of a Topo I inhibitor. The initial drug treatment consisted of a brief exposure to a quinazoline-based antifolate, ZD1694. After an interval of approximately one cell-doubling time, cells were exposed for 8-24 h to BNP1100, a Karenitecin-class 7-thiomethyl-camptothecin, in the presence of 1-10 microM thymidine; the latter acted as a crucial factor to promote the collision of moving replication forks with the drug-stabilised DNA-Topo I cleavable complexes even under continuous TS inhibition. Clonogenic analyses confirmed that these mechanistically distinct drugs at clinically achievable concentrations worked in a highly synergistic manner, with a maximum effect abolishing the viability of virtually all cancer cells (> 99.9%). The pretreatment with ZD1694 increased the amount of DNA-bound Topo I by up to 4-fold and the DNA-damaging capability of BNP1100 by up to 15-fold. The possibility of at least four DNA-damaging pathways is proposed which might have resulted from the individual actions of TS and Topo I inhibitors as well as their concerted actions. Taken together, the present findings provided a logically permissible explanation as to why TS and Topo I inhibitors in concerted interactions induced a highly lethal effect which was more than a simple additive effect. Since these drugs are effective specifically on actively proliferating cancer cells, but not on non-cycling G0/G1 cells, this mechanism-based protocol may warrant consideration for clinical verification.

Antimetabolites, Antineoplastic↗
PubMed1999

Active immunization of combined beta1-adrenoceptor and M2-muscarinic receptor peptides induces cardiac hypertrophy in rabbits.

BACKGROUND: The high prevalence of patients with dilated cardiomyopathy (DCM) with anti-beta1-adrenoceptor and/or anti-M2-muscarinic receptor autoantibodies in their sera has been observed. However, the pathophysiological role of these autoantibodies in the development of cardiomyopathy is unknown. We previously reported an experimental model of early-stage DCM-like cardiomyopathy induced by immunizing rabbits for 1 year with synthetic peptides corresponding to the sequence of the second extracellular loop of either beta1-adrenoceptor or M2-muscarinic receptor. Because approximately half the sera of patients with DCM that recognize one of the two receptor sequences also recognize the second sequence, a model was created in rabbits simultaneously immunized with the synthetic peptides corresponding to the second extracellular loop of the beta1-adrenoceptor and M2-muscarinic receptor. METHODS AND RESULTS: All rabbits (n = 8) immunized with both peptides had a high titer of both anti-beta1-adrenoceptor and anti-M2-muscarinic receptor autoantibodies in their sera, whereas none of the sera from control rabbits injected with saline (n = 9) was positive. No significant cross-reaction with peptides other than those used for immunization was found. The weight of the hearts of immunized rabbits increased significantly. The hearts of immunized rabbits showed marked concentric left ventricular hypertrophy with mild inflammatory cell infiltration. In these rabbits, mild or moderate interstitial fibrosis was also observed. In electron micrographs, immunized rabbits showed focal myofibrillar lysis, loss of myofilament, and a marked increase in the number of mitochondria and deposition of dense granules in both sarcoplasm and myofibrils. Conversely, one of the control rabbits showed scant mononuclear cell infiltration. However, in this control rabbit, no significant alteration was found by electron microscopy. CONCLUSION: Our results showed the coexistence of both anti-beta1-adrenoceptor and anti-M2-muscarinic receptor autoantibodies in the sera has pathophysiological importance, shown by their ability to induce cardiac hypertrophy in rabbits.

Amino Acid Sequence↗
PubMed1999

Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure.

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.

Aged↗
PubMed1999

Expression of E-cadherin and alpha-catenin in patients with colorectal carcinoma. Correlation with cancer invasion and metastasis.

Cadherins form complexes with groups of cytoplasmic proteins, such as alpha-, beta-, and gamma-catenins, that link the cadherin molecule to the cytoskeleton. In this study, we conducted an immunohistochemical investigation of E-cadherin and alpha-catenin expression in 100 tissue samples obtained from colorectal cancer patients undergoing surgical treatment. Reduced expression of alpha-catenin was observed in 56 (56%) of the cases and found to be significantly correlated with the depth of invasion of the patients' colorectal cancer and its metastasis to lymph nodes and liver. In contrast, E-cadherin expression was reduced in 29 (29%) of the cases and was not significantly correlated with either depth of invasion or metastasis. Although the levels of expression of these proteins were positively correlated, coexpression pattern analysis showed that invasion and metastasis were correlated with a reduction of alpha-catenin expression regardless of the status of E-cadherin staining. Thus, to predict tumor invasion and metastasis in colorectal adenocarcinoma, it is useful to investigate not just the expression of E-cadherin but also the expression of alpha-catenin.

Adenocarcinoma↗
PubMed1999

Enhanced expression of interleukin-6 in chronic hepatitis C.

AIMS/BACKGROUND: There is a possibility that proinflammatory cytokines such as interleukin-6 (IL-6) are involved in the inflammatory process of chronic hepatitis C. This study was undertaken to investigate the possible role of IL-6 in the pathophysiology of chronic hepatitis C. METHODS: Serum IL-6 levels in 63 patients with chronic hepatitis C and in 26 normal controls were measured. Light and electron immunostaining studies to localize IL-6 protein as well as in situ hybridization to localize IL-6 messenger RNA were performed on 10 liver biopsy specimens. RESULTS: Serum IL-6 levels were significantly (p<0.01) elevated in chronic hepatitis C compared to those in normal controls. Although no statistically significant correlation was found between serum IL-6 levels and hepatobiliary enzyme levels, a significant correlation (p<0.01) was found between serum IL-6 levels and category II of Knodell's histological activity index score. Non-parenchymal cells in hepatic sinusoids and the cells infiltrating enlarged fibrous portal tracts were definitely positive for IL-6 protein and mRNA by immunohistochemistry and in situ hybridization. In addition, immunoelectron microscopy revealed a weak and occasional positive reaction in the cytoplasm of hepatocytes. The majority of the positive cells in hepatic sinusoids showed CD68 immunoreactivity in consecutive sections indicating that these were Kupffer cells. Sinusoidal endothelial cells and hepatic stellate cells also exhibited a weak reaction. CONCLUSION: These results strongly suggest that Kupffer cells in liver parenchyma and macrophages infiltrating in portal tracts are the main producers of elevated IL-6 in serum. Moreover, there is a possibility that IL-6 produced by hepatocytes could also act as a regenerative stimulus to hepatocytes themselves in an autocrine fashion.

DNA Primers↗