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Biomedical subjects

Y Otsuka

Publications and source records attributed to Y Otsuka.

At least 145 records · Page 8Linked to original sources
PubMed1989

Cooperation between humoral factor(s) and Lyt-2+ T cells in effective clearance of Sendai virus from infected mouse lungs.

The mechanism of cooperation between the L3T4+ and Lyt-2+ T cell subsets in effective clearance of Sendai virus from infected mouse lungs was studied by adoptive cell transfer using nude mice. Simultaneous transfer of a long-term-cultured Sendai virus-specific L3T4+ T cell line with L3T4+ cell-depleted immune spleen cell (L3T4-) fraction to infected nude mice could result in viral clearance, although single injection with either of these cells was not effective. Instead of the L3T4+ T cells, culture supernatants of the L3T4- T cell line or concanavalin A-stimulated mouse spleen cells and mouse serum immunized with the virus were also active in the cooperative viral clearance with L3T4- fraction. The role of the Sendai virus-sensitized L3T4- cell fraction in cooperative viral clearance with humoral factors could be replaced by neither T cell-deprived immune spleen cell fraction nor normal spleen cells. The 1,500 units of recombinant mouse interleukin 2 (IL-2), which was more than 12 times the IL-2 activity present in the supernatants of the T cell line or concanavalin A-stimulated spleen cells, failed to clear the virus in combination with the L3T4- fraction. Monoclonal antibodies to Sendai or mouse hepatitis viruses were also effective in the cooperative antiviral activity. IL-2 activity was not detected in these monoclonal antibodies and the mouse immune serum. Single injection of any humoral factors failed to clear the virus. These results indicate that Sendai virus-sensitized Lyt-2+ subset of T cells acts cooperatively with humoral factor(s) other than IL-2 or Sendai virus-specific antibody present in supernatants of the T cell line, of concanavalin A-stimulated spleen cells or hybridomas, and in mouse serum immunized with the virus.

Animals↗
PubMed1989

Infection of rabbits with Sendai virus.

Rabbits were either inoculated with Sendai virus (SV), strain MN, or caged with virus-inoculated rabbits on the same day of the viral inoculation, and examined for viral shedding and detection of viral antigens in the respiratory tract, histopathologic changes, and serum antibodies. Infectious virus was recovered from nasal swabs at postinoculation day (PID) 3 and disappeared by PID 10. Viral antigens were detected by immunofluorescence in epithelial cells of the nasal cavities, but not of the trachea and lungs from PID 3 to PID 10, and antibodies were detected after PID 7. Rabbits had no clinical manifestations and only exhibited a moderate increase in goblet cells of the nasal epithelium. In the transmission study, virus was recovered from one of three uninoculated rabbits at postexposure day (PED) 10 and antibodies were detected at PED 15 in the same rabbit. These data suggest that, although viral multiplication was limited to the nasal epithelium, laboratory rabbits are susceptible to Sendai virus infection.

Animals↗
PubMed1989

[Cystine transport and glutathione metabolism in human erythrocytes].

Cystine was transported into human erythrocytes in the presence of tertiary-butyl hydroperoxide (t-BH) or 1-chloro-2, 4-dinitrobenzene (CDNB). The transport rate of cystine was dependent on the extracellular concentration of t-BH or CDNB, and on the incubation time. By Dowex-1 column chromatography, the transported cystine was incorporated into fractions of glutathione disulfide (GSSG) and glutathione-S (GSH-S) conjugate. Cystine was also transported into reconstituted erythrocyte ghost with GSSG. The transport of cystine was Na+ dependent and decreased in the presence of N-ethylmaleimide, and it was competitively inhibited by DL-homocystine and L-alanine. The inhibition rates by DL-homocystine and L-alanine were 75% and 68%, with similar Ki values of 0.7 mM and 0.6 mM, respectively. The Km value for cystine transport was 0.15 mM. The activity of GSH-cystine transhydrogenase was detected in the hemolysate and this enzyme is thought to catalyze the action of incorporation of cystine into GSH. This enzyme was partially purified from normal human erythrocytes. In the presence of CDNB, similar rates of cystine transport were observed among the diabetic patients (n = 11), hypoxemic patients (n = 10) and the control subjects (n = 20). It is suggested that cystine transport is induced for glutathione synthesis when human erythrocytes are exposed to oxidative stresses.

Biological Transport↗
PubMed1989

[A case report of rhinocerebral mucormycosis in hemodialysis patient receiving deferoxamine].

Deferoxamine (DFO) has been widely used in the treatment of aluminum toxicity in patients on chronic dialysis. Mucormycosis is an opportunistic infection caused by fungi of the Mucorales order and some reports suggested a role for DFO in the precipitation of this infection. A 50-year-old man had been on hemodialysis for 16 years. 6 weeks before admission, he was begun on DFO because of aluminum toxicity. 2 weeks before admission, general fatigue and fever developed and followed by headache and loss of vision. He was admitted to this hospital with disturbed consciousness. His clinical course and a CT scan of the head suggested cerebral infarction. Within 24 hours he required ventilatory support and died 5 days after the admission. On autopsy, rhino-cerebral mucormycosis was demonstrated with a mycotic thrombus involving the left middle cerebral artery. Dialysis-related mucormycosis has recently appeared in the literature. We feel that hemodialysis patients on DFO may be at risk for potentially fatal mucormycosis infections. With a possible relationship between DFO treatment and this fatal opportunistic infection, caution should be given before using this drug and the indications should be definitive.

Brain Diseases↗
PubMed1988

Some properties of the millimolar Ca2+-dependent proteinase from bovine cardiac muscle.

Three to six mg of the millimolar Ca2+-requiring proteinase (m-calpain) were obtained from 1 kg bovine cardiac muscle (fresh wt) and some enzymatic properties of this proteinase were determined. Activity of bovine cardiac m-calpain decreases as ionic strength increases from 75 to 1000 mM. Maximal activation of m-calpain by Ca2+, La3+, Ba2+, and Mn2+ occurs at 2 to 3 mM concentrations of each of these divalent cations, but La3+ activation is only 20 to 25% and Ba2+ and Mn2+ activation only 6 to 10% as great as Ca2+ activation. Maximum Sr2+ activation occurs at 20 mM Sr2+ and is 90 to 95% of maximum Ca2+ activation. Mg2+, Zn2+, Cr2+, and Cd2+ do not activate m-calpain when added alone; Mg2+ does not affect, but Zn2+ inhibits, Ca2+-stimulated activity. The nonionic detergents, Triton X-100 and Brij 35, activate m-calpain 1.6- to 2.0-fold but do not change its Ca2+ requirement. Sodium dodecyl sulfate and urea inhibit m-calpain completely at 0.045% and 2.0 M, respectively. Because they bind Ca2+ needed for activation, ATP, ADP, and ITP inhibit m-calpain. The trypsin inhibitors, phenylmethylsulfonyl fluoride, ovomucoid trypsin inhibitor, ovoinhibitor, aprotinin, alpha 1-antiproteinase inhibitor, soybean trypsin inhibitor, and lima bean trypsin inhibitor do not affect m-calpain activity; m-calpain does not release measureable quantities of acid-soluble peptides from a rabbit skeletal sarcoplasmic protein fraction but does degrade rabbit skeletal myofibrils and casein.

Ammonium Chloride↗
PubMed1988

T cells subsets responsible for clearance of Sendai virus from infected mouse lungs.

T cell subsets responsible for clearance of Sendai virus from mouse lungs determined by adoptive transfer of immune spleen cell fractions to infected nude mice. T cells with antiviral activity developed in spleens by 7 days after intranasal infection. Spleen cell fractions depleted of Lyt-2+, Lyt-1+, or L3T4+ cells showed antiviral activity in vivo, although the degree of the activity was lower than that of control whole spleen cells. The antiviral activity of the Lyt-2+ cell-depleted fraction was consistently higher than that of L3T4+ (Lyt-1+)-depleted cells. In vitro cytotoxic activity against Sendai virus-associated, syngeneic lipopolysaccharide-blast cells was detected in stimulated cells from intraperitoneally immunized mice but was lost after depletion of Lyt-2+ cells. Multiple injection of anti-Sendai virus antibody into infected nude mice had no effect on lung virus titer. These results indicate that L3T4+ (Lyt-1+) and Lyt-2+ subsets are cooperatively responsible for efficient clearance of Sendai virus from the mouse lung.

Animals↗
PubMed1988

Vascular relaxation and cGMP in hypertension.

Isolated aortas from hypertensive rats have a decreased relaxation response to acetylcholine chloride (ACh), the calcium ionophore A23187, and sodium nitroprusside (SNP). Since the vascular relaxation responses to these vasodilators may be a result of increases in guanosine 3',5'-cyclic monophosphate (cGMP), we measured the cGMP response to these agents in isolated aortas from normotensive rats and rats with either mineralocorticoid-induced hypertension (DOCA), renovascular hypertension (1K1C), or coarctation-induced hypertension (Coarc). The aortas from the hypertensive rats had decreased basal levels of cGMP and attenuated increases in cGMP in response to ACh and A23187. Rises in cGMP in response to SNP were also attenuated in aortas from the hypertensive rats, even at concentrations that induced maximum relaxation of blood vessels from normotensive and hypertensive rats. The relaxation responses to atrial natriuretic factor (ANF) and the cGMP generated in isolated aortas by ANF were attenuated in hypertension. Removal of the endothelium markedly attenuated cGMP generation in response to ANF in vessels from normotensive and Coarc rats, but the relaxation responses to ANF were unaltered in vessels after the removal of the endothelium. The reversal of experimentally induced hypertension was associated with increases in cGMP levels following exposure of the isolated vessels to ACh. Also, vessels treated with methylene blue relaxed in response to SNP despite inhibition of cGMP accumulation. The decreased relaxation response to endothelium-dependent vasodilators is accompanied by decreases in cGMP accumulation; the decreased vascular cGMP content in response to endothelium-dependent vasodilators is not due to increases in phosphodiesterase activity of vascular smooth muscle; and SNP may relax blood vessels through "cGMP-dependent" and "cGMP-independent" mechanisms.

Animals↗
PubMed1988

Reactivities of 4 murine coronavirus antigens with immunized or naturally infected rat sera by enzyme linked immunosorbent assay.

Four murine coronavirus antigens, sialodacryoadenitis virus (SDAV) strain TG, Parker's rat coronavirus (PCV) strain 8190, mouse hepatitis virus (MHV) strains S and NuU, were examined for their reactivities to hyperimmunized and naturally infected rat sera by ELISA. With the immunized sera, SDAV and PCV antigens reacted best with respective homologous sera. MHV antigens reacted with all antisera, anti-SDAV, anti-PCV, and anti-MHV-S at approximately the same level, and MHV-S showed a slightly higher reactivity than MHV-NuU. The reactivities of the sera from various colonies to these antigens were in the order--from high to low--of SDAV, MHV-S, MHV-NuU, and PCV. None of sera negative for SDAV antigen reacted positively to the other antigens. Within the sera positive for SDAV, the positivities were in the order of MHV-S, MHV-NuU, and PCV. These results suggested that, although homologous antigens are best to detect SDAV or PCV infection by ELISA, MHV antigen can be used if highly cross-reactive viral strain is selected.

Animals↗
PubMed1987

Unit structure of the anti-complementary arabinogalactan from Angelica acutiloba Kitagawa.

Mild acid hydrolysis of an anti-complementary arabinogalactan (AGIIb-1), isolated from the roots of Angelica acutiloba Kitagawa, gave one neutral (N-I) and two acidic arabinogalactans (A-I and A-II) and one neutral arabinan (N-II). Likewise, the product (AF-AGIIb-1) of digestion with exo-alpha-L-arabinofuranosidase gave four carbohydrate units. Methylation analysis showed that N-I was a (1----6)-linked galactan with unbranched short side-chains of Araf attached at position 3 and that A-I and A-II contained, in addition, 4-linked Galp. Methylation analysis and oligosaccharide analysis showed that A-I and A-II also contained highly branched Ara chains possessing Araf side-chains attached at positions 3 of some 4- or 5-linked Ara and that a small proportion of Arap was present in each acidic unit. Base-catalysed beta-elimination and oligosaccharide analysis indicated that A-1 and A-II also contained a rhamnogalacturonan moiety in which 2,4-disubstituted Rha residues were attached to 4-substituted GalpA through position 2 of Rha. Methylation analysis, 1H- and 13C-n.m.r. studies, and enzymic hydrolysis showed N-II to be a highly branched arabinan containing a backbone of (1----5)-linked alpha-L-Araf with alpha-L-Araf side-chains attached to positions 3.

Carbohydrate Conformation↗
PubMed1987

Effect of recombinant human tumor necrosis factor on the induction of murine macrophage tumoricidal activity.

The ability of recombinant human tumor necrosis factor (rH-TNF) alone or in combination with lymphokines (LK) to induce the in vitro activation of murine macrophages was evaluated. The treatment of C57BL/6 mouse resident peritoneal exudate cells (PEC) with rH-TNF and LK was found to induce the activation of macrophages to a tumoricidal state against P815 mastocytoma cells. Neither rH-TNF nor LK alone induced macrophage cytotoxic activity. Furthermore, the macrophage activation seen was not due to small amounts of contaminating lipopolysaccharide. The TNF plus LK-mediated macrophage activation could be totally ablated by rabbit antiserum to murine gamma-interferon, thus suggesting a role for gamma-interferon in this system. Since adherent cells (greater than or equal to 95% macrophages) only marginally responded to stimulation with rH-TNF plus LK and the addition of nonadherent PEC caused a marked augmentation of rH-TNF plus LK-mediated macrophage activation, the involvement of nonadherent PEC was suggested. In addition, using antibodies and complement to deplete subsets of cells from the nonadherent PEC, the requirement for cells bearing Thy 1.2 and asialo GM1 surface markers was demonstrated. These results suggest that TNF may play an autocrine regulatory role in concert with lymphokines in macrophage-mediated host defense against malignant neoplasia.

Animals↗
PubMed1987

Purification of the Ca2+-dependent proteinase inhibitor from bovine cardiac muscle and its interaction with the millimolar Ca2+-dependent proteinase.

A protein inhibitor of the Ca2+-dependent proteinase has been purified from bovine cardiac muscle by using the following steps in succession: salting out 17,600 X gmax supernatants from muscle homogenates in 50 mM Tris acetate, pH 7.5, 4 mM EDTA between 25 and 65% ammonium sulfate saturation; eluting between 25 and 120 mM KCl from a DEAE-cellulose column at pH 7.5; salting out between 30 and 60% ammonium sulfate saturation; Ultrogel-22 gel permeation chromatography at pH 7.5; heating to 80 degrees C followed by immediate cooling to 0 degree C; 6% agarose gel permeation chromatography in 4 M urea, pH 7.5; and elution from a phenyl-Sepharose hydrophobic column between 0.7 and 0.5 M ammonium sulfate. Approximately 1.16-1.69 mg of purified Ca2+-dependent proteinase inhibitor are obtained from 1 kg of bovine cardiac muscle, fresh weight. Bovine cardiac Ca2+-dependent proteinase inhibitor has an Mr of 115,000 as measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, a pI of 4.85-4.95, very little alpha-helical structure, a very low specific absorbance of 1.647 (A1% 280), and very low contents of histidine, tryptophan, phenylalanine, and tyrosine. Bovine cardiac Ca2+-dependent proteinase inhibitor probably contains a single polypeptide chain in nondenaturing solvents. One 115-kDa inhibitor polypeptide inactivates 10 110-kDa millimolar Ca2+-requiring proteinase (millimolar Ca2+-dependent proteinase) molecules in assays of purified proteins. Inhibition of millimolar proteinase by the proteinase inhibitor did not change in the pH range 6.2-8.6. The inhibitor requires Ca2+ to bind to millimolar Ca2+-dependent proteinase. The Ca2+ concentration required for one-half-maximum binding of millimolar Ca2+-dependent proteinase to the inhibitor was 0.53 mM, compared with a Ca2+ concentration of 0.92 mM required for one-half maximum activity of millimolar Ca2+-dependent proteinase in the absence of the proteinase inhibitor. Unless millimolar Ca2+-dependent proteinase is located subcellularly in a different place than the proteinase inhibitor or unless the proteinase/inhibitor interaction is regulated, millimolar proteinase could never be active in situ.

Amino Acids↗
PubMed1987

Structural characterisation of an anti-complementary arabinogalactan from the roots of Angelica acutiloba Kitagawa.

An anti-complementary arabinogalactan (AGIIb-1), isolated from the roots of Angelica acutiloba Kitagawa, has been subjected to methylation analysis, digestion with alpha-L-arabinofuranosidase, controlled Smith-degradation, and partial acid hydrolysis. AGIIb-1 consisted of arabinose, galactose, rhamnose, galacturonic acid, and glucuronic acid in the molar ratios 1.8-2.2:1.0:0.2-0.3:0.2-0.4:0.1. AGIIb-1 contained mainly an arabino-3,6-galactan moiety, and most of the Ara was present as alpha-L-arabinofuranosyl residues in the non-reducing terminals and the highly polymerised and branched side-chains which were attached mainly to positions 3 and 6 of (1----6)- and (1----3)-linked Gal, respectively. Some Ara-containing chains were also attached to (1----4)-linked Gal residues. The 13C-n.m.r. data for AGIIb-1 showed that the Galp was beta. Mild acid hydrolysis of AGIIb-1 yielded several linear and highly branched arabino-oligosaccharides, a neutral arabinogalactan, and two acidic arabinogalactans. Some arabino-oligosaccharides contained a (1----4)-linked Arap at the reducing terminal. The neutral arabinogalactan contained (1----3)-, (1----4)-, and (1----6)-linked and 3,6-di-O-substituted Gal, whereas the acidic arabinogalactans contained, in addition, non-reducing terminal GlcA, (1----4)-linked GalA, and 2,4-di-O-substituted Rha. The anti-complementary activity was decreased when AGIIb-1 was partially hydrolysed with mild acid (10mM HCl, 100 degrees, 10 min), but treatment with exo-alpha-L-arabinofuranosidase markedly enhanced the activity.

Adult↗
PubMed1987

The endothelium and cyclic guanosine monophosphate in hyperthyroid-induced hypertension.

We investigated the role of endothelium derived relaxing factor (EDRF) and cyclic guanosine monophosphate (cGMP) in the altered vascular reactivity of hyperthyroidism (HT). Rats were given daily injections of triiodothyronine (T3), 50 micrograms/100 g body weight for two weeks, and they had significantly higher serum levels of T3 compared to untreated, control rats (493 +/- 82 vs. 58 +/- 7 ng/dl, p less than 0.05) and significant elevations in their systolic blood pressure (188 +/- 6 vs 126 +/- 3 mm Hg, p less than 0.05). Vascular reactivity was studied in isolated muscle baths; cGMP was measured by RIA. There were no differences in contractile responses to phenylephrine (PE) in isolated aortae from the HT and control rats, but aortae from the HT rats contracted with PE relaxed less to acetylcholine (Ach); the calcium ionophore, A23187; and sodium nitroprusside (SNP). Sensitivity to atrial natriuretic factor (ANF) and 8-Br cGMP was unaltered. Blood vessels from HT rats generated significantly less cGMP in response to Ach, SNP, and ANF. Treatment of the hypertension in the HT rats which hydralazine or propranolol restored the vascular relaxation response to Ach but not SNP; cGMP responses remained blunted. These data suggest that endothelium dependent vasodilators may induce relaxation independent of elevations of cGMP in aortae from HT rats.

Acetylcholine↗
PubMed1987

Anti-Bacteroides fragilis substance from rhubarb.

Extracts of 178 Chinese herbs were screened for their antibacterial activity against Bacteroides fragilis a major anaerobic microorganism in the intestinal flora of humans. Only rhubarb root (Rheum officinale) was found to have significant activity and the purified active substance was identified as rhein.

Anthraquinones↗
PubMed1987

Phorbol ester, vascular relaxation, and cyclic guanosine 3',5'-monophosphate.

The relaxation of phenylephrine-contracted blood vessels by acetylcholine, nitroprusside, or atrial natriuretic factor has been linked to elevations in cyclic guanosine 3',5'-monophosphate (cGMP). Also, 8-bromo-cGMP can induce vascular relaxation in isolated vascular smooth muscle contracted with phenylephrine. We determined whether these cGMP-dependent vasodilators could relax isolated rat aortas contracted with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate. cGMP was measured by radioimmunoassay. Acetylcholine, nitroprusside, and atrial natriuretic factor induced relaxation in vascular smooth muscle contracted by 12-O-tetradecanoylphorbol-13-acetate. These relaxation responses were accompanied by elevations of cGMP. However, the sensitivity to these vasodilators was markedly decreased in phorbol ester-contracted vessels compared to phenylephrine-contracted vessels. Nifedipine and superoxide dismutase induced small but significant relaxations in phorbol ester-contracted vessels; however, blood vessels contracted with phenylephrine and phorbol ester relaxed completely with papaverine. There was a marked decrease in sensitivity to 8-bromo-cGMP in phorbol ester-treated vessels compared to phenylephrine-contracted vessels. Contractions induced by phorbol ester were not inhibited by amiloride or chlorpromazine. Also, following incubation in potassium-free salt solution, vessels incubated with phenylephrine or phenylephrine and phorbol ester underwent similar relaxations when exposed to potassium chloride. The contractile state induced by phorbol ester has decreased sensitivity to cGMP-dependent vasodilators. This may be due to nonspecific effects of the phorbol ester or to the mechanism by which protein kinase C activation maintains vascular tone.

Animals↗