Biomedical subjects
M Itoh
Publications and source records attributed to M Itoh.
[Isolated peripheral arterial aneurysm].
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Selenium distribution and metabolic profile in relation to nutritional selenium status in rats.
The disposition of selenium (Se) was investigated in Wistar rats of various Se status after an intravenous injection of 82Se-selenite. Various fractions of plasma, urine, and cytosols from liver and kidney were separated by high performance liquid chromatography (HPLC), coupled with an inductively coupled argon plasma-mass spectrometry (ICP-MS). The technique allowed simultaneous differentiation of the fate of injected and endogenous Se, and if it was influenced by the previous Se burden in the tissues. A broad Se-peak from plasma was resolved in two fractions by assessing the m/z 82/78 ratios. Urinary profiles indicated that the metabolism of Se was dose-dependent; monomethylselenol being the primary metabolite of Se in untreated animals, whereas noticeable amount of trimethylselenonium ion was detected after the injection of 82Se. Liver and kidney cytosols contained complex Se-enriched fractions, a positive identification of which was not done in this study. In most cases, the enrichment of tissue fractions with the stable isotope was altered by the dietary Se levels, the isotope nevertheless was exchanged with the endogenous Se in various macromolecules to a varying degree.
Inhibition of metastasis of Lewis lung carcinoma by urinary trypsin inhibitor in experimental and spontaneous metastasis models.
A purified human urinary trypsin inhibitor (UTI) and its related synthetic peptides were examined to determine whether they could inhibit production of experimental and spontaneous lung metastases by murine Lewis lung carcinoma (3LL) cells. Three peptides, peptide I, peptide 2 and peptide 3, representing the amino acid sequences within the UTI molecule, were synthesized. UTI and peptide 2 inhibited human leukocyte elastase (HLE). UTI and peptide 3 specifically inhibited human and murine plasmin activity. Peptide I had essentially no inhibitory activity. In an in vivo spontaneous metastasis model, multiple s.c. injections of UTI or peptide 3 for 7 days immediately after s.c. tumor cell inoculation significantly inhibited the formation of lung metastasis in C57BL/6 mice in a dose-dependent manner. UTI reduced lung tumor colonization more effectively than peptide 3. Peptides 1 and 2, however, did not affect the formation of lung metastasis. Inhibition of lung metastasis was not due to direct anti-tumor effects of UTI and peptide 3. In an in vivo experimental metastasis assay, multiple s.c. injections of UTI for 7 days after i.v. tumor cell inoculation inhibited metastatic lung tumor colonization, while peptide 3 did not affect metastasis. Peptides 1 and 2 did not affect the formation of lung metastasis. When examined with an in vitro assay system using a modified Boyden chamber, UTI and peptide 3 suppressed the invasion of tumor cells through Matrigel. UTI and peptide 3 inhibited neither cell proliferation nor the binding of tumor cells to Matrigel and showed no significant suppression of chemotactic migration of tumor cells to fibronectin. Our results suggest that UTI efficiently regulates the mechanism involved in not only the entry into vascular circulation of tumor cells (intravasation, though, at least in part, inhibition of the proteolytic enzyme plasmin) but also the extravasation step of the metastatic process.
Structure dependence of the ferromagnetic transition temperature in rhombohedral La1-xAxMnO3 (A=Na, K, Rb, and Sr).
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Human pancreatic phospholipase A2 stimulates the growth of human pancreatic cancer cell line.
Phospholipase A2 (PLA2) from human pancreas, designated hPLA2-I, functions as a digestive enzyme. Interestingly, the present study demonstrated that the mature form of hPLA2-I stimulated the growth of a human pancreatic cancer cell line MIAPaCa-2, whereas the pro-form was ineffective. PLA2s from Laticauda semifasciata fraction I, Crotalus adamanteus venom, Streptomyces violaceoruber and bee venom, showed no proliferative effect to the growth of MIAPaCa-2. The Scatchard plot analysis revealed that the MIAPaCa-2 cell had a specific binding site for the mature hPLA2-I. The equilibrium binding constant (Kd) and the maximum binding capacity (Bmax) were 2.6 nM and 0.4 fmol/10(6) cells, respectively. These results suggest that the mature hPLA2-I, but not the pro-form, may function as a growth factor of pancreas carcinoma via the specific binding site.
Suppression of influenza virus infection by an N-thioacetylneuraminic acid acrylamide copolymer resistant to neuraminidase.
We have previously shown that alpha-2-O-methyl-5-N-thioacetylneuraminic acid (alpha-Neu5thioAc2Me) has a higher affinity to bromelain-treated hemagglutinin (HA) of influenza A virus than sialic acid from natural sources (Machytka et al., 1993, FEBS Lett. 334, 117-120). We have now compared the inhibitory effects of alpha-Neu5thioAc2Me and other sialic acid analogs on receptor binding and plaque formation of intact influenza A viruses. When alpha-Neu5thioAc2Me was polymerized by conjugation to polyacrylamide, its affinity to HA increased 10(3)-fold. When analyzed by plaque reduction, the alpha-Neu5thioAc2 polymer was about 10 times more efficient as an inhibitor of virus replication than the alpha-Neu5Ac2 polymer, stressing the importance of sulfur at C5. The S-glycoside alpha-2-S-methyl-5-N-thioacetylneuraminic acid (alpha-Neu5thioAc2SMe) had the same affinity to HA as alpha-Neu5thioAc2Me, but was resistant to neuraminidase. The alpha-Neu5thioAc2S polymer interfered with the replication of a wider spectrum of influenza A virus subtypes than the alpha-Neu5thioAc2 polymer. The results indicate that the alpha-Neu5thioAc2S polymer has the potential to be used as an inhibitor of influenza virus infection.
Structure and magnetic properties of Sr2-xAxIrO4 (A=Ca and Ba).
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Effects of dibutyryl guanosine 3',5'-cyclic monophosphate and sodium nitroprusside in pepsinogen secretion from guinea pig chief cells with respect to intracellular Ca2+.
Both Ca2+ and adenosine 3',5'-cyclic monophosphate act as intracellular second messengers in pepsinogen secretion from chief cells. However, the role of intracellular guanosine 3',5'-cyclic monophosphate (cGMP) in this process has not been defined. Although dibutyryl cGMP (dbcGMP), a membrane-permeable derivative of cGMP, has been shown to inhibit pepsinogen secretion only stimulated by cholecystokinin (CCK), the intracellular mechanism of this effect remains unclear. We evaluated the role of intracellular cGMP in pepsinogen secretion from monolayer cultured guinea pig chief cells using dbcGMP and sodium nitroprusside, both of which increase intracellular cGMP. Dibutyryl cGMP and sodium nitroprusside have now been shown to inhibit pepsinogen secretion induced by not only CCK octapeptide but also carbamylcholine chloride and ionomycin in a dose-dependent manner. Furthermore, dbcGMP reduced the increase in intracellular free Ca2+ concentration induced by carbamylcholine chloride, CCK octapeptide, and ionomycin. These results suggest that intracellular cGMP may inhibit pepsinogen secretion by reducing the intracellular free Ca2+ concentration.
Mediation of pepsinogen secretion from guinea pig chief cells by Ca2+/calmodulin-dependent protein kinase II.
In the presence of Ca2+ bound to calmodulin, Ca2+/calmodulin-dependent protein kinase II (CaMK II) exhibits an intramolecular autophosphorylation and modulates many cell functions. In this study, the role of CaMK II in pepsinogen secretion was investigated in cultured guinea pig chief cells by using a specific CaMK II inhibitor, 1-[N,O-Bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpipera zin e (KN-62), and an antibody for the Thr-286-autophosphorylated alpha subunit of CaMK II which specifically recognized the autophosphorylated form of CaMK II. KN-62 inhibited the pepsinogen secretion stimulated by carbamylcholine chloride, cholecystokinin octapeptide, and ionomycin in a dose-dependent manner without affecting intracellular Ca2+ concentrations, but had no effect on the secretion by 12-O-tetradecanoyl phorbol-13-acetate (TPA) and forskolin. Heavy staining with the antibody for autophosphorylated CaMK II was observed in the cytoplasm of chief cells treated with carbamylcholine chloride or ionomycin, but only light staining was seen in cells treated with TPA or forskolin. Thus, CaMK II and its autophosphorylation may be a critical step in the intracellular pathway in which Ca2+ causes pepsinogen secretion from guinea pig chief cells.
Enriched stable isotopes of elements used as tracers: methods of presenting high-performance liquid chromatographic-inductively coupled argon plasma mass spectrometric data.
High-performance liquid chromatography (HPLC) of biological fluids and tissue cytosolic preparations was employed in conjunction with argon-induced inductively coupled plasma mass spectrometry (ICP-MS) to investigate the distribution of stable isotopes as tracers. The common way of presenting the data from the ICP-MS is by plotting the count rates versus the retention time of HPLC fractions. Additional information can be derived, e.g., the composite peaks can be further resolved, and the level of enrichment in various biological components can be expressed by alternative ways of presenting these data. The two additional approaches described here involve presenting the ratios of enriched tracer with a suitable naturally abundant mass number of the same element, and by expressing the extent of enrichment by the tracer isotope in a given fraction to that of the same mass number in the fraction derived from an untreated source. Each method of presentation has different merits and drawbacks. The data therefore may be best presented in more than one way to emphasize the conclusions from a given experiment. Observations are presented after simultaneously injecting stable isotopes of three essential elements, copper, selenium and zinc, into mice. Plasma and liver cytosolic fractions were analysed and data represented in different ways as indicated above.
Phase separation, oxygen composition, and a glass transition due to freezing-in of the oxygen rearrangement in La2NiO4.094 single crystals.
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63,65Cu NMR and NQR study of the Cu2+ electronic state and the spin dynamics in the spin-Peierls compound CuGeO3.
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Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.
Approximately 10% of peripheral CD4+ cells and less than 1% of CD8+ cells in normal unimmunized adult mice express the IL-2 receptor alpha-chain (CD25) molecules. When CD4+ cell suspensions prepared from BALB/c nu/+ mice lymph nodes and spleens were depleted of CD25+ cells by specific mAb and C, and then inoculated into BALB/c athymic nude (nu/nu) mice, all recipients spontaneously developed histologically and serologically evident autoimmune diseases (such as thyroiditis, gastritis, insulitis, sialoadenitis, adrenalitis, oophoritis, glomerulonephritis, and polyarthritis); some mice also developed graft-vs-host-like wasting disease. Reconstitution of CD4+CD25+ cells within a limited period after transfer of CD4+CD25- cells prevented these autoimmune developments in a dose-dependent fashion, whereas the reconstitution several days later, or inoculation of an equivalent dose of CD8+ cells, was far less efficient for the prevention. When nu/nu mice were transplanted with allogeneic skins or immunized with xenogeneic proteins at the time of CD25- cell inoculation, they showed significantly heightened immune responses to the skins or proteins, and reconstitution of CD4+CD25+ cells normalized the responses. Taken together, these results indicate that CD4+CD25+ cells contribute to maintaining self-tolerance by down-regulating immune response to self and non-self Ags in an Ag-nonspecific manner, presumably at the T cell activation stage; elimination/reduction of CD4+CD25+ cells relieves this general suppression, thereby not only enhancing immune responses to non-self Ags, but also eliciting autoimmune responses to certain self-Ags. Abnormality of this T cell-mediated mechanism of peripheral tolerance can be a possible cause of various autoimmune diseases.
High- and low-spin transition of Ru4+ in the perovskite-related layered system Srn+1RunO3n+1 (n=1, 2, and
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Determination of oxygen content and cation valences in superconducting Tl-based cuprates by a wet chemical method.
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Molecular cloning and chromosomal mapping of a bone marrow stromal cell surface gene, BST2, that may be involved in pre-B-cell growth.
Bone marrow stromal cells regulate B-cell growth and development through their surface molecules and cytokines. In this study, we generated a mAb, RS38, that recognized a novel human membrane protein, BST-2, expressed on bone marrow stromal cell lines and synovial cell lines. We cloned a cDNA encoding BST-2 from a rheumatoid arthritis-derived synovial cell line. BST-2 is a 30- to 36-kDa type II transmembrane protein, consisting of 180 amino acids. The BST-2 gene (HGMW-approved symbol BST2) is located on chromosome 19p13.2. BST-2 is expressed not only on certain bone marrow stromal cell lines but also on various normal tissues, although its expression pattern is different from that of another bone marrow stromal cell surface molecule, BST-1. BST-2 surface expression on fibroblast cell lines facilitated the stromal cell-dependent growth of a murine bone marrow-derived pre-B-cell line, DW34. The results suggest that BST-2 may be involved in pre-B-cell growth.
Detection of selenium-containing biological constituents by high-performance liquid chromatography-plasma source mass spectrometry.
Mass spectrometry with inductively coupled argon plasma excitation (ICP-MS) was used as a multi-element specific detection method for HPLC for the speciation of selenium (Se) in biological samples. Se-containing biological constituents were separated on a size-exclusion column and were detected Se-specifically at m/z 78 and 82 for natural abundance 78Se and 82Se, respectively. Se peaks not identical with known authentic samples were detected. Diets with different Se contents induced changes in the distributions Se-containing constituents more in urine, kidney and liver samples than in plasma and red blood cells samples. The results indicate that HPLC-ICP-MS is a specific and sensitive means for the speciation of Se-containing biological constituents.