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Biomedical subjects

S Ueda

Publications and source records attributed to S Ueda.

At least 433 records · Page 24Linked to original sources
PubMed1995

[Pulmonary tuberculosis complicated with tuberculosis of oral mucosa, mandible and cervical lymph nodes].

A case of pulmonary tuberculosis complicated with tuberculous of oral mucosa, mandible and cervical lymph nodes in 53-year-old man is reported. He was firstly treated for right side dental caries. He also received routinely an empiric antibiotic therapy, but discharge of pus continued. Then, pain of oral cavities spread to the right shoulder. The diagnosis of oral mucosa, osteomyelitis of mandible and lymph node tuberculosis was made by the histological examination of biopsy specimens and positive smear test for M. tuberculosis in granulation. The chest X-ray film showed multiple nodular shadows in bilateral lungs. The combination of INH, RFP and SM was applied initially and then SM was replaced by CS due to its side effect. Negative smear test for M. tuberculosis of oral mucosa was achieved five months after the initiation of treatment.

Humans↗
PubMed1995

Blocking measles virus infection with a recombinant soluble form of, or monoclonal antibodies against, membrane cofactor protein of complement (CD46).

Human membrane cofactor protein (MCP, CD46) functions as an inhibitor of the complement (C) cascade to protect host cells from C attack, and as a receptor for measles virus (MV). Normal human sera contains 10-60 ng/ml of naturally produced soluble forms of MCP, which is also a cofactor for the factor I-mediated inactivation of C3b. We produced monoclonal antibodies (mAb) against MCP and a recombinant soluble form of MCP similar to the natural soluble forms, and tested their ability to block MV infection. Vero cells and CHO cells expressing human MCP were the targets. Of the antibodies tested, M75 and M177, which blocked the C regulatory activity of MCP, efficiently blocked MV infection. More than 50 micrograms/ml of the soluble form moderately blocked MV infection of CHO cells expressing MCP, but barely blocked that of Vero cells. The two mAb and the soluble form also inhibited MV H protein-mediated green monkey erythrocyte rosette formation. A quantitative analysis suggested that 30 micrograms/ml of the soluble form functionally corresponded to 0.2 microgram/ml of M177 or M75. These data established that the C regulatory function and the MV receptor function of MCP were blocked simultaneously by the individual mAb, and that soluble forms of MCP could inhibit MV infection in cells expressing human MCP, although doses far higher than the natural concentration of soluble MCP were required.

Animals↗
PubMed1995

Regulation of ion transport by endothelins in rat colonic mucosa: effects of an ETA antagonist (FR139317) and an ETB agonist (IRL1620).

Rat colonic mucosa contains ETA and ETB receptors with Kd values for endothelin (ET)-1 of 32 and 11 pM and maximal binding capacities of 277 and 181 fmol/mg protein, respectively. In muscle-stripped rat colon without tonic nerve activity in Ussing chambers, the serosal addition of ET-1, ET-3 and IRL1620 inhibited amiloride-sensitive noncoupled Na+ entry and enhanced diphenylamine-2-carboxylate-sensitive Cl- secretion, producing a sustained decrease and a transient increase in the short-circuit current (Isc) and the transepithelial conductance, respectively. EC50 values of ET-1, ET-3 and IRL1620 and the maximal changes in Isc were 2.0, 10.2 and 10.9 nM and -12.7, -7.0 and -7.1 muA/cm2, respectively for the Na+ entry; these values were 50, 220 and 225 nM and +57.3, +47.3 and +21.3 muA/cm2, respectively, for the Cl- secretion. FR139317 (100 nM) inhibited ET-1-induced Na+ and Cl- movements, shifting the concentration-response curves to the right (EC50 = 25 nM and 1 microM, respectively), and inhibited ET-3 (> 100 nM)-induced Cl- movement, decreasing the maximal response to 35%, but it did not inhibit either ET-3-induced Na+ movement nor IRL1620-induced Na+ and Cl- movements. The removal of serosal Ca++ reduced 100 nM ET-1- and IRL1620-evoked changes in Isc by 50% and 70% for the Na+ entry and by 80% and 100% for the Cl- secretion, respectively. Indomethacin (1 microM) also reduced changes in Isc by 30% and 70% for the Cl- secretion but did not affect the Na+ entry. Our results show that ETA and ETB receptors regulate Na+ and Cl- transport by different mechanisms.

Animals↗
PubMed1995

Endoscopic aspiration lumpectomy of esophageal leiomyomas derived from the muscularis mucosae.

OBJECTIVES: There is still much debate about the indications and best technique for endoscopy for the treatment of esophageal leiomyomas. We developed a novel technique for endoscopic aspiration lumpectomy and used it in patients with esophageal leiomyomas derived from the muscularis mucosae. METHODS: Nine patients with esophageal leiomyomas were treated with informed consent. The indication for intervention was based on the endosonographic confirmation of a tumor originating from the 2nd layer of the esophagus. We attached a transparent cylinder to the tip of an endoscope and a snare-guide tube to the outer axis of the scope. After endoscopic suction of the tumor into the cylinder, the snare was pushed open. The tumor was grabbed at its base with the entire surrounding mucosa, and removed. RESULTS: The overall procedure time averaged 18 minutes, and there were no complications in any of the subjects. The resected specimens were elliptical with a mean long diameter of 22 +/- 4 mm and a mean short diameter of 17 +/- 4 mm. Complete resection was possible in eight of the nine tumors that were under 2 cm in diameter. After a follow-up period of 4 to 27 months (mean 11 months), no recurrence was found in any of the completely resected cases. CONCLUSIONS: Endoscopic aspiration lumpectomy has been proven to be a safe, effective, and less invasive procedure for small esophageal leiomyomas derived from the muscularis mucosae.

Esophageal Neoplasms↗
PubMed1995

[Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells].

To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These date indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

Animals↗
PubMed1995

[Contribution of oxidative stress to pulmonary hypertension induced by chronic hypoxia].

Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with media wall thickening of pulmonary arteries in rats. Platelet-activating factor plays an important role in the pulmonary vascular remodeling induced by chronic hypoxia, and reactive oxygen species are involved in tissue injury induced by platelet activating factor. We therefore hypothesized that reactive oxygen species contribute to the pulmonary hypertension induced by chronic hypoxia, and examined the effect of N-acetyl-L-cysteine (NAC), a free radical scavenger and the precursor of glutathione sulfhydryl (GSH), on hypoxia-induced pulmonary hypertension. We used a chemiluminescence-HPLC assay to measure the levels of phosphatidylcholine hydroperoxide (PCOOH) in the rat lungs exposed to hypoxia. Three weeks of normobaric hypoxia (FiO2 = 0.1) with NAC significantly reduced pulmonary hypertension, right ventricular hypertrophy, and media wall thickening of the pulmonary arteries. NAC had no effect on the hematocrit of normoxic or chronically normobaric hypoxic rats. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. These results indicate that hypoxia induces oxidative stress in the lung tissue, and that oxidative stress may have a role in the development of pulmonary hypertension induced by chronic hypoxia in rats.

Acetylcysteine↗
PubMed1995

[Role of peptide leukotrienes in monocrotaline-induced lung disease].

Monocrotaline (MCT) causes lung inflammation and right ventricular hypertrophy associated with lung vascular thickening in rats. We hypothesized that peptide leukotrienes play a role in MCT-induced lung disease, and examined the effect of ONO 1078, a specific antagonist of LTC4, D4 and E4 receptors on MCT-induced right ventricular hypertrophy and on lung vascular thickening. Next, we measured leukotriene C4 (LTC4) levels in the lung tissue of MCT-treated rats. Within 3 weeks after the injection MCT had caused an increase in the ratio of right ventricular weight to left ventricle+septum weight (RV/(LV+S)) and an increase in media wall thickness of the muscular arteries of the lung. In rats given both ONO 1078 and MCT, these changes were significantly less severe than in rats given MCT only. The LTC4 levels in MCT-treated rats were significantly higher than in saline-treated control rats. These results indicate that this antagonist of peptide leukotriene receptors inhibits right ventricular hypertrophy induced by MCT, and suggest a role for peptide leukotrienes in the inflammatory process that contributes to lung vascular remodeling in MCT-treated rats.

Animals↗
PubMed1995

Lack of association between angiotensin converting enzyme gene insertion/deletion polymorphism and stroke.

AIM: The human angiotensin converting enzyme (ACE) gene is a candidate genetic locus for stroke because of the importance of the renin-angiotensin system to the development of cardiovascular disease. In the present study, the association between ACE gene deletion/insertion (D/I) polymorphism and the presence or absence of ischaemic stroke was evaluated and possible associations between ACE gene polymorphism and certain subgroups of stroke were investigated. MATERIALS AND METHODS: DNA samples from 585 unselected suspected stroke patients admitted to the Acute Stroke Unit, Western Infirmary, Glasgow, and from 188 age- and sex-matched controls were genotyped by polymerase chain reaction. RESULTS: There was no evidence of any association between ACE gene polymorphism and the presence of ischaemic stroke except in the subgroup containing only hypertensive patients, where the odds ratio of a DD genotype for ischaemic stroke was just significantly greater than 1 (odds ratio 2.51, 95% confidence interval 1.06, 5.94). There was no significant association between ACE genotype and the stroke subgroups investigated. CONCLUSION: The DD genotype may not be a risk factor for stroke, particularly in the normotensive population. Further study in a strictly controlled population is required to test for the possibility of an increased risk of stroke in hypertensives with DD homozygotes.

Cerebrovascular Disorders↗
PubMed1994

Effects of glucocorticoid on neurones of rat dentate gyrus in dissociated culture.

This study was undertaken to evaluate the short-term effects of glucocorticoid on the morphological characteristics of cultured rat dentate gyrus (DG) cells using immunocytochemistry for a cytoskeletal protein, micro-tubule-associated protein 2 (MAP2). A selective cell culture system of DG neurons was successfully established. Synthetic glucocorticoid, dexamethasone (DEX) increased the total length of immunoreactive (IR) processes of the DG neurones in a dose-dependent manner. DEX also increased the ratio of multipolar neurones with more than three processes. The area of cell body of immunoreactive processes increased with 5 microM DEX treatment. Our results suggest that cytological features of DG cells are strongly influenced by the action of glucocorticoid.

Animals↗
PubMed1994

[A case of primary thyroid T-cell lymphoma with infiltration of lymphoma cells in peripheral blood: diagnosed by DNA analysis].

A 57-year-old woman came to our hospital with complaints of neck swelling and headache in 1991. She was diagnosed as having chronic thyroiditis in euthyroidism because she had a diffuse goiter with both antithyroglobulin antibody (TGHA) and antimicrosomal antibody (MCHA). In 1992, she complained of the rapid growth of her thyroid gland and a swallowing disturbance. Atypical lymphocytes were observed in 16.5% of leukocytes in peripheral blood and similar atypical cells were found in bone marrow. Although an ultrasound scan of the thyroid gland revealed a symmetrical enlargement without a pseudocystic appearance, cytological study with fine needle aspiration biopsy of the thyroid gland demonstrated an abundance of atypical lymphoid cells. A whole body scintigram with 67gallium citrate showed no significant accumulation except in the thyroid gland. With a diagnosis of suspected primary thyroid lymphoma, total thyroidectomy was performed. However the diagnosis of malignant lymphoma was not confirmed histologically. A study of lymphocytes subset with two-color flow cytometry, which was performed for both lymphocytes in peripheral blood and infiltrating lymphocytes in the resected thyroid gland, revealed abnormal increased CD4 positive T cells and decreased HLA-DR expression. Additionally, southern blot DNA analysis for abnormal lymphocytes using restriction enzymes, EcoRI and BamHI, demonstrated rearrangement of the T-cell antigen receptor, which indicates a monoclonal proliferation of lymphocytes. After total thyroidectomy, atypical lymphocytes in peripheral blood decreased, and circulating autoantibodies including TGHA and MCHA disappeared. From these data, this patient was finally diagnosed as having a primary T-cell lymphoma of the thyroid gland, which is a very rare type of thyroid lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1994

Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein.

To examine the biological role of adenosine A1 receptors in bovine pulmonary artery endothelial cells, we measured intracellular Cl-concentration [Cl-]i, using 10mM 6-methoxy-N-(3-sulfopropyl) quinolinium monohydrate (SPQ). N6-cyclopentyladenosine (CPA), a selective A1 agonist, at 10(-8)M to 10(-5)M, rapidly decreased [Cl-]i by 30% to 51%, without a rapid elevation in [Ca2+]i and cyclic AMP. This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin (IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker). We conclude that an A1 receptor in endothelial cells activates Cl- efflux via a PTX-sensitive G protein.

Adenosine↗
PubMed1994

Modulation of complement regulatory function and measles virus receptor function by the serine-threonine-rich domains of membrane cofactor protein (CD46).

Three major membrane cofactor protein (MCP) phenotypes with different serine-threonine (ST)-rich regions, namely STc (L-phenotype), STBC (H or U phenotype) and STABC, and the MCP without the ST domain (delta ST) were expressed in Chinese hamster ovary (CHO) cells by transfecting the respective cDNAs. The expressed molecules migrated with a larger molecular mass on SDS/PAGE than those expected from their amino acid sequences. O-Glycanase digestion showed that this was due to O-linked sugar chains. The apparent sugar contents in each ST segment were compatible with their serine and threonine contents in the ST regions. The functional properties of these phenotypes as inhibitors of human complement (C) and receptors of measles virus (MV) were compared. The classical pathway-dependent CHO cell lysis by human C was more effectively suppressed by the expressed delta ST and STC than by the STABC and STBC phenotypes, although the difference was not so prominent. In contrast, alternative C pathway-dependent CHO-cell lysis was most effectively suppressed by the STABC phenotype and was only slightly blocked by the ST-deleted mutant. MV infection occurred with all of the phenotypes, but the infectious dose required to cause the same level of syncytium formation was 100-times higher in large ST (STABC and STBC) than in small ST (STC and delta ST) phenotypes. Thus, the ST domain serves as a functional modulator in MCP: MCP with a large ST domain having high O-linked sugar contents is favourable to the effective suppression of both the alternative C pathway-mediated cytolysis and MV infection, whereas MCP with a small ST domain is favourable to the suppression of the classical C pathway.

Animals↗
PubMed1994

Role of phospholipase A2 in expression of the scavenger pathway in cultured aortic smooth muscle cells stimulated with phorbol 12-myristate 13-acetate.

We have demonstrated that cultured intimal smooth muscle cells (SMC) from thickened intima can metabolize acetylated low-density lipoprotein (LDL) by a scavenger pathway, but medial SMC from normal arteries cannot. In this study we investigated the expression mechanism of the scavenger pathway in medial SMC using a phorbol ester. Medial SMC were incubated with 10(-10)-10(-7) M phorbol 12-myristate 13-acetate (PMA) for 1-24 h and then their degradation of 125I-labelled acetylated LDL was assayed. Unstimulated SMC degraded little acetylated LDL, but incubation for 24 h with PMA dose-dependently stimulated its degradation by SMC, the optimal PMA concentration being 1 x 10(-8) M. Induction of expression of the scavenger pathway required more than 4 h of incubation with PMA and was completely inhibited by cycloheximide. In addition expression of the scavenger pathway was not transient but stable. Induction of expression of the scavenger pathway by PMA was not inhibited by protein kinase C inhibitors, but was inhibited about 50% by phospholipase A2 inhibitors. The study, using various phorbol esters, indicated that induction of the scavenger pathway was well correlated with their ability to stimulate phospholipase A2 in medial SMC but not with their ability to activate protein kinase C. Moreover, incubation with exogenous phospholipase A2 (0.1-10 units/ml) or its product, lysophosphatidylcholine (0.01-100 micrograms/ml) dose-dependently increased degradation of 125I-labelled acetylated LDL in medial SMC. Lysophosphatidylcholine was most effective in various lysophospholipids. These results suggest that PMA induced the scavenger pathway in part by stimulating phospholipase A2 in medial SMC, and that a product, lysophosphatidylcholine, is a mediator of expression of the scavenger pathway.

Animals↗
PubMed1994

Therapeutic effects of imidazolineoxyl N-oxide against endotoxin shock through its direct nitric oxide-scavenging activity.

We recently found a new class of nitric oxide (NO) antidote, i.e., 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide derivatives (PTIOs). It has a potent inhibitory action against endothelium-derived relaxing factor. Here, we report the effect of a water-soluble carboxy derivative of PTIO (carboxy-PTIO) on endotoxin shock. Endotoxin [lipopolysaccharide (LPS)] (10 mg/kg) was injected into Wistar rats, and the mean arterial blood pressure (MABP), heart rate and urinary parameters were continuously measured. The MABP and urine volume gradually decreased during 1 hr after LPS injection, and within 4 hr, both values decreased to 50-70%. When carboxy-PTIO at 0.056-1.70 mg/kg/min was infused for 1 hr beginning 90 min after the LPS injection, the hypotension, renal dysfunction and survival rate were much improved and the state of shock was avoided. Carboxy-PTIO administered to normal rats did not affect each parameter. Measurement of urinary output of carboxy-PTIO and carboxy-2-phenyl-4,4,5,5-tetramethylimidazole-1-oxyl (carboxy-PTI), which is a reaction product of carboxy-PTIO and NO, showed that conversion of carboxy-PTIO to carboxy-PTI was augmented by LPS treatment due to the increased production of NO, and that the enhanced conversion (PTIO-->PTI) was significantly inhibited by administration of N omega-monomethyl-L-arginine. This indicates that carboxy-PTIO exhibits a potent therapeutic value in endotoxin shock through the direct scavenging action against NO.

Animals↗
PubMed1994

Cloning of a brain-type aldolase cDNA and changes in its mRNA level during oogenesis and early embryogenesis in Xenopus laevis.

A full length cDNA clone (cXALD3) for Xenopus laevis aldolase mRNA, which exists abundantly in oocytes, was isolated from Xenopus laevis ovary cDNA library, and its nucleotide sequence was determined. The cDNA was 1.8 kb in length and encoded 363 amino acids. From the deduced amino acid sequence and the Northern blot analysis of the RNAs from several adult tissues, this clone was concluded to be a brain-type aldolase gene. The XALD3 mRNA level per egg or embryo was high during early oogenesis, but was markedly reduced during late oogenesis and was maintained at low level during early embryogenesis until it started to increase at the late neurula stage. The mRNA was also detected in testis. The characteristic change in the temporal pattern of expression and the distribution of XALD3 mRNA among different tissues suggest a possibility that brain type aldolase may play some important roles in gametogenesis and in neurulation.

Amino Acid Sequence↗
PubMed1994

Marek's disease virus type 1-specific phosphorylated proteins pp38 and pp24 with common amino acid termini are encoded from the opposite junction regions between the long unique and inverted repeat sequences of viral genome.

The nucleotide sequence of the junction region between the long unique (UL) and terminal inverted repeat (TRL) sequences of Marek's disease (MD) virus type 1 (MDV1) DNA revealed the presence of a rightward open reading frame of 155 amino acids. The ORF inserted into an eukaryotic expression vector transiently expressed an antigen in the cytoplasm of COS7 cells which reacted with the monoclonal antibody M21 against an MDV1-specific phosphorylated protein complex consisting of at least the proteins pp38 and pp24. In addition, RNA synthesized in vitro from the ORF under the control of the T7 promoter was translated in vitro using rabbit reticulocyte lysates. A polypeptide of about 24 kDa was immunoprecipitated with M21 antibody. Thus, the MDV1-specific phosphorylated proteins pp38 and pp24 with common amino termini are encoded in the opposite junction regions between the UL and IRL and between the UL and TRL, respectively, of the MDV1 genome. The pp38 gene is transcribed leftward from the viral genome, while the pp24 gene was shown here to be transcribed rightward in a MD tumor cell line as well as in cells productively infected with MDV1.

Amino Acid Sequence↗