[Study of pancreatic duct pressure in the biliary tract and pancreatic diseases: endoscopic pressure determination of the pancreatic duct].
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Adult↗
Biomedical subjects
T Maeda
Publications and source records attributed to T Maeda.
Decidua is a possible source of serum mouse soluble interleukin-6 receptor (msIL-6R): gestational profile of serum msIL-6R concentration.
The serum concentration of msIL-6R of 10 weeks old virgin ICR mouse assessed by a RIA was 45.6 +/- 6.6 ng/ml. The serum msIL-6R concentration of the pregnant mouse mated at 10 weeks of age was 41.2 +/- 3.0 ng/ml on day 7 of pregnancy. The serum concentration gradually increased during gestation and reached peak on day 17 of pregnancy (149.1 +/- 13.7 ng/ml). On the third day of the puerperium, the serum msIL-6R concentration of the mother from which the pups had been removed on the day of delivery was decreased to the level of that on day 7 of pregnancy. IL-6R mRNA level in the decidua significantly increased during mid and late gestational stages. msIL-6R was detected in the medium of cultured decidual cells (8.03 +/- 0.28 ng/ml), but not placental cells. Western analysis for msIL-6R using the conditioned medium of the cultured decidual cells resulted in a single band at approximately 45 K. To find out a biological role of msIL-6R during gestation, placental cells were incubated with mIL-6 and msIL-6R, and mPL-I concentration in the medium was assessed by RIA. 2.5 nM mIL-6 did not affect the secretion of mPL-I in placental cells; however, addition of msIL-6R resulted in a significant stimulation of mPL-I secretion. These results suggest that serum msIL-6R, which is likely to be secreted from decidua, may play an important role during gestation.
Analysis of Variance↗
Cloning of an isoform of mouse TGF-beta type II receptor gene.
A variant of transforming growth factor-beta type II receptor (TGF-beta RII) cDNA was isolated from a mouse brain cDNA library. The predicted receptor is identical to previously reported mouse TGF-beta RII except that the isoform has an insertion sequence of 25 amino acids in the predicted ligand-binding domain. By the use of reverse transcription-polymerase chain reaction (RT-PCR), transcripts for both isoforms were detected in all tissues and developing embryos examined. The isoform transiently expressed in COS cells showed a similar ligand-binding specificity to authentic TGF-beta RII. These results suggest that the mouse TGF-beta RII gene generates multiple isoforms, possibly by alternative splicing, as reported for activin type IIB receptor; and an isoform which has the extra sequence in the ligand-binding domain is also involved in the TGF-beta signal transduction.
Alternative Splicing↗
Transforming growth factor-beta 1 post-transcriptionally inhibits mouse growth hormone releasing factor secretion in placenta.
The aim of this study was to investigate whether TGF-beta 1 regulates mouse GHRF secretion by primary cultures of placental cells from day 12 of pregnancy. Ten ng/ml TGF-beta 1 significantly inhibited mouse GHRF secretion by the third day of culture. The lowest concentration of TGF-beta 1 that significantly inhibited mouse GHRF secretion was 1 ng/ml. The inhibitory effect of TGF-beta 1 on mouse GHRF secretion was completely eliminated by addition of an anti-TGF-beta 1 antibody. Steady-state levels of mouse GHRF mRNA as assessed by Northern analysis was not reduced by incubation of placental cells from day 12 of pregnancy with 10 ng/ml TGF-beta 1 for 5 days. Both placenta and decidua expressed TGF-beta 1 mRNA, and the level of TGF-beta 1 mRNA in decidua increased during gestation while the level of TGF-beta 1 mRNA was constant throughout gestation. These findings suggest that TGF-beta 1 is one of the potent regulators of mouse GHRF secretion and that TGF-beta 1 regulates mouse GHRF secretion in an autocrine or paracrine manner in the mouse placenta in vivo.
Animals↗
Amelioration of acute graft-versus-host disease and re-establishment of tolerance by short-term treatment with an anti-TCR antibody.
We investigated whether tolerance can be re-established in mice with graft-vs-host disease (GVHD) by using a short-term, T cell-depleting treatment with an anti-TCR-alpha beta mAb. GVHD was induced in 950-rad-irradiated AKR mice (H-2k, Mls-1a) by injecting 5 x 10(6) T cell-depleted bone marrow cells together with either 10(7) or 2 x 10(6) lymph node (LN) cells from BALB/c mice (H-2d, and Mls-1b). AKR mice that received 10(7) LN cells exhibited a severe form of acute GVHD, in which all mice died by day 60. In this severe form of GVHD, treatment with anti-TCR-alpha beta mAb completely ameliorated the induction of GVHD when initiated on day 0 (a total of 800 micrograms/mouse administered on days 0,5, and 10). When the same protocol was begun on day 10, it had no therapeutic effect. However, this delayed treatment with anti-TCR-alpha beta mAb was very effective in reversing a less severe form of GVHD that was induced by the injection of 2 x 10(6) donor LN cells. Recipient mice given prophylactic anti-TCR-alpha beta treatment achieved host-specific tolerance in association with clonal deletion of host Mls-1a-reactive V beta 6+ T cells. In contrast, spleen cells from recipient mice that recovered from the mild form of GVHD as a result of the delayed anti-TCR-alpha beta treatment contained a considerable proportion of the V beta 6+ T cells, despite the healthy appearance of these mice. A MLR assay revealed that the spleen cells from these mice responded well to Mls-1a Ag but not to H-2k Ag, in contrast with the apparent responses of spleen cells from untreated GVHD controls to both Ags. In addition, cells from the anti-TCR-alpha beta-treated mice exhibited a specific reduction in cytotoxicity against AKR blasts. Collectively, these data indicate that a short-term treatment of mice having GVHD with an anti-TCR-alpha beta mAb, starting even after disease onset, can re-establish host-specific tolerance, at least to the host-histo-compatibility Ag.
Acute Disease↗
Monozygotic twins of different apparent sex.
We report on twins of unlike sex who shared a 45,X/46,X,+mar karyotype. The mar chromosome was found to be Yq- by DNA analysis. Marker studies, including 8 VNTR loci, yielded a probability of monozygosity of 0.99999996.
Adolescent↗
Dopaminergic innervation of rat locus coeruleus: a light and electron microscopic immunohistochemical study.
Dopaminergic innervation of the rat locus coeruleus (LC) was immunohistochemically studied by using monoclonal antibody directed against dopamine (DA) at the light- and electron-microscopic levels. A dense plexus of DA-immunoreactive (IR) varicose fibers was found not only in the cell body area of the LC but also in the dendritic area. Three hundred and forty DA-IR terminal boutons were observed. They were distributed in a wide range of diameters of 0.1-1.8 microns but most of them were large (mean value: 0.98 micron). Sixty-nine percent formed an asymmetric synapse. There were many axo-spinous connections. Small dendrites less than 0.3 micron in diameter displaying synaptic specialization were mostly dendritic spines (75%). Most of the target dendrites seemed to be noradrenergic in nature. It is suggested that dopaminergic innervation may play a powerful role in control mechanisms of activity of NA-containing neurons of the LC.
Animals↗
Polyclonal uses of T-cell receptor (TCR)alpha and beta genes for cytotoxic T lymphocytes in human metastatic melanoma: possible involvement of TCR alpha in tumor-cell recognition.
Identification of genetic structure and diversity of T-cell receptor (TCR)alpha and beta genes for cytotoxic T lymphocytes (CTLs) infiltrating human cancers is important for the better understanding of molecular mechanisms of host defense at tumor sites. cDNAs of TCR alpha and beta genes of 22 different melanoma-specific CTL clones established from the tumor-infiltrating lymphocytes of 2 patients were sequenced for analysis of their genetic structure and diversity. V alpha 7.2-J alpha 10-C alpha was found in 4 of 22 clones, 2 of which also used the same beta-chain. The other 20 clones showed different combinations of alpha and beta use. At deduced amino-acid levels, 7 of 9 clones from one patient used a threonine residue at the 26th position in the complementarity-determining region (CDR)1 of TCR alpha. Eight of 13 clones used a threonine at the 99th or a serine residue at the 100th position in CDR3 of TCR alpha CTL clones with the same or different TCR alpha showed the same or different patterns of cytotoxicity, respectively. These results suggest that CTLs usually do not demonstrate clonal expansion at tumor sites of metastatic melanoma's but rather that polyclonal T cells capable of binding to multiple melanoma determinants through CDR3 of TCR alpha accumulate in the tumor.
Base Sequence↗
Characterization of autologous tumor-specific T-helper 2 cells in tumor-infiltrating lymphocytes from a patient with metastatic melanoma.
Human autologous tumor-specific T-helper 2 (Th2) cells were investigated in melanoma tumor-infiltrating lymphocytes (TILs). Both a CD4+ T-cell line and its 5 potential T-cell clones established from TILs of a patient with metastatic melanoma produced significant levels of IL-4, IL-6, IL-10 and granulocyte-macrophage colony-stimulating factor (GM-CSF) in response to autologous, but not any of 12 allogeneic, melanoma cell lines. They also produced IL-3 and IL-8 but not IL-2, IFN-gamma, TNF-alpha or TNF-beta in response to autologous tumor cells. Furthermore, they showed autologous melanoma-specific cytotoxicity only in an 18-hr 51Cr-release assay. Specific IL-4, IL-6 or IL-10 production by the CD4+ M73 T-cell line and its clone was inhibited by anti-class II DR (but not anti-class I) MAb, whereas their specific cytotoxicity was inhibited by anti-class I (but not anti-class II) MAb. Anti-CD3 and -CD4 MAb (but not anti-CD8) abrogated both IL-4, IL6 and IL-10 production and cytotoxicity, while anti-IL-4 antibody did not inhibit cytotoxicity. CD4+ potential T-cell clones, but not CD8+ clones, that were established from freshly isolated TILs without in vitro sensitization by autologous tumor cells also produced IL-4, IL-6 and IL-10 but not IFN-gamma or tumor necrosis factor (TNF) alpha in an autologous tumor-specific fashion. These Th2 cells were neither reactive to EBV-B cells nor suppressive against CD8+ T-cell clones. PMA and PHA stimulated these potential T-cell clones, regardless of their specific lymphokine production, to produce IL-3, IL-4, IL-6, IL-8, IL-10, GM-CSF, TNF alpha and IFN-gamma. Our results demonstrate the presence of autologous tumor-specific Th2 cells at the melanoma sites.
B-Lymphocytes↗
D-amino-acid oxidase is confined to the lower brain stem and cerebellum in rat brain: regional differentiation of astrocytes.
Based on enzymatic activity, the localization and the identification of D-amino-acid oxidase-containing cells in rat whole brain was systematically studied in serial fixed sections. The oxidase activity was absent or scarce in the forebrain, was confined to the brain stem (midbrain, pons and medulla oblongata) and cerebellum, and its localization was extended to the spinal cord. In the brain stem the oxidase was mainly localized in the tegmentum, particularly in the reticular formation. The intense oxidase reactions were present in the red nucleus, oculomotor nucleus, trochlear nucleus, ventral nucleus of the lateral lemniscus, dorsal and ventral cochlear nuclei, vestibular nuclei, nuclei of posterior funiculus, nucleus of the spinal tract of the trigeminal nerve, lateral reticular nucleus, inferior olivary nucleus, and hypoglossal nucleus. In the cerebellum the activity in the cortex was much more intense than that in the medulla. In all the fields described above, the oxidase-containing cells were exclusively astrocytes including Bergmann glial cells, and neither neuronal components, endothelial cells, oligodendrocytes nor ependymal cells showed oxidase activity. These results indicated that the astrocytes regionally differentiated into two distinct types, one of which expressed oxidase in the midbrain, rhombencephalon and spinal cord, and the other which did not in the forebrain. The localization of the oxidase was inversely correlated with the distribution of free D-serine in mammalian brains (Nagata, Y., Horiike, K. and Maeda, T., Brain Res., 634 (1994) 291-295). Based on the characteristic localization of the oxidase-containing astrocytes, we discussed the physiological role of the oxidase.
Animals↗
Formation of sheared G:A base pairs in an RNA duplex modelled after ribozymes, as revealed by NMR.
The thermal stability and structure of an RNA duplex, r(GGACGAGUCC)2, the base sequence of which was modelled after both a hammerhead ribozyme and a lead ribozyme, were studied by CD and NMR. We previously demonstrated that the corresponding DNA duplex, d(GGACGAGTCC)2, formed unique 'sheared' G:A base pairs, where an amino proton, instead of an imino proton, of G is involved in the hydrogen bonding, and G and A bases are arranged 'side by side' instead of 'head to head' (Nucleic Acids Res. (1993) 21, 5418-5424). CD melting profiles showed that the RNA duplex is thermally more stable than the corresponding DNA duplex. NMR studies revealed that sheared G:A base pairs are formed in the RNA duplex, too, although the overall structure of the RNA is the A form, which differs from the B form taken on by the corresponding DNA. A model building study confirmed that sheared G:A base pairs can be accommodated in the double helical structure of the A form. A difference between the RNA and DNA duplexes in the stacking interaction involving G:A mismatch bases is also suggested. The demonstration that sheared G:A base pairs can be formed not only in DNA but also in RNA suggests that this base pairing plays an important role regarding the RNA structure.
Adenine↗
[Usefulness and safety of segmental-subsegmental TAE for hepatocellular carcinoma in cases of liver hypofunction].
We analyzed the safety of the segmental-subsegmental TAE for hepatocellular carcinoma in 18 cases of liver hypofunction by checking total bilirubin change after TAE. The TAE was performed safely in all of the cases. The highest value of total bilirubin before TAE was 5.1 mg/dl in the 1-2 subsegment TAE group, 3.8 mg/dl in the 3-4 subsegment TAE group and 2.0 mg/dl in the 6 subsegment TAE group. We conclude that segmental TAE is safe even in the patient of liver hypofunction.
Aged↗
A two-component system that regulates an osmosensing MAP kinase cascade in yeast.
In the prokaryotic two-component signal transduction systems, recognition of an environmental stimulus by a sensor molecule results in the activation of its histidine kinase domain and phosphorylation of a histidine residue within that domain. This phosphate group is then transferred to an aspartate residue in the receiver domain of a cognate response regulator molecule, resulting in the activation of its output function. Although a few eukaryotic proteins were identified recently that show sequence similarity to the prokaryotic sensors or response regulators, it has not been clear whether they constituted a part of a 'two-component' system. Here we describe a two-component system in Saccharomyces cerevisiae that regulates an osmosensing MAP kinase cascade.
Amino Acid Sequence↗
Protein induced by vitamin K absence or antagonist II as a prognostic marker in hepatocellular carcinoma. Comparison with alpha-fetoprotein.
BACKGROUND: Protein induced by vitamin K absence or antagonist II (PIVKA-II) was widely used as a diagnostic marker for hepatocellular carcinoma (HCC), however, its prognostic value is unclear. The authors evaluated PIVKA-II clinicopathologically as a prognostic marker for HCC. METHODS: The relationship between pathologic prognostic factors and plasma PIVKA-II and alpha-fetoprotein (AFP) was investigated in 72 patients with resectable HCC measuring less than 6 cm in greatest dimension. RESULTS: PIVKA-II shows significantly lower sensitivity, but higher specificity than AFP, and the use of these two complementary markers appears to be useful in the diagnosis of HCC. The frequencies of intrahepatic metastasis, portal vein tumor thrombus, hepatic vein tumor thrombus, and capsular infiltration were significantly higher in patients with positive PIVKA-II than in those with negative-PIVKA-II, and the recurrence-free rate was significantly lower in patients with positive rather than with negative PIVKA-II. However, there were no significant differences between the patients who were AFP positive and those who were AFP negative in pathologic prognostic factors and the recurrence-free rate. From univariate and multivariate analyses, the authors find that PIVKA-II is one of the risk factors for recurrence of HCC after hepatectomy. CONCLUSIONS: PIVKA-II may be a useful marker for the prediction of intrahepatic spread and for the prognosis of HCC. In addition, PIVKA-II-positive patients, thus, need aggressive postoperative adjuvant therapy for undetectable residual tumors and careful postoperative monitoring to enable the early recognition of recurrence.
Adult↗
Effects of dipyridamole on left ventricular systolic and diastolic function in healthy young and elderly subjects as assessed by radionuclide angiography.
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Adult↗
Cloning of the pka1 gene encoding the catalytic subunit of the cAMP-dependent protein kinase in Schizosaccharomyces pombe.
We have isolated Schizosaccharomyces pombe genes that confer sterility to the fission yeast cell when expressed from a multicopy plasmid. One of these genes strongly hybridized to a probe carrying the open reading frame of Saccharomyces cerevisiae TPK1, which encodes a catalytic subunit of the cAMP-dependent protein kinase (protein kinase A). This S. pombe gene, named pka1, has a coding potential of 512 amino acids, and the deduced gene product is 60% identical with the S. cerevisiae Tpk1 protein in the C-terminal 320 amino acids. Disruption of pka1 slows cell growth but is not lethal. The resultant cells, however, are highly derepressed for sexual development, readily undergoing conjugation and sporulation in the absence of nitrogen starvation. They are, thus, phenotypically indistinguishable from the adenylyl cyclase-defective (cyr1-) cells previously characterized, except that the pka1- spores are retarded in germination, whereas the cyr1- spores are not. Disruption of pka1 is epistatic to a defect in cgs1, which encodes the regulatory subunit of protein kinase A. These results strongly suggest that the product of pka1 is a catalytic subunit of protein kinase A and, furthermore, that S. pombe has only one gene encoding it. This situation contrasts with the case of S. cerevisiae, in which three genes encode the catalytic subunits.
Amino Acid Sequence↗
A mouse TGF-beta type I receptor that requires type II receptor for ligand binding.
A cDNA for a serine/threonine kinase receptor was isolated from a mouse brain cDNA library. The receptor transiently expressed on COS cells bound TGF-beta 1 not by itself but only when TGF-beta type II receptor was coexpressed. The molecular mass of the ligand-receptor complex was estimated to be 75 kDa. The type II receptor-dependent binding and the molecular mass of the complex suggest that the receptor is a TGF-beta type I receptor.
Amino Acid Sequence↗
Inhibition of the early phase of free fatty acid liberation during cerebral ischemia by excitatory amino acid antagonist administered by microdialysis.
In order to determine the role of excitatory amino acids (EAAs) in free fatty acid (FFA) liberation during cerebral ischemia, we examined the effect of in situ administration of kynurenic acid, a broad-spectrum antagonist of EAA receptors, by microdialysis on the increase in FFA levels during ischemia in the rat hippocampus. A transient rapid increase in FFA levels, superimposed on a continued slow increase, was observed beginning at 1-2 min after ischemia induction. The early rapid increase in FFAs was profoundly inhibited by kynurenic acid, suggesting that EAAs are critically involved in the early phase of FFA liberation. Development of massive ionic shifts during cerebral ischemia can be delayed for several minutes by kynurenic acid administered by the same procedure, suggesting a vital role for EAAs in the early appearance of anoxic depolarization. The observed inhibition of early FFA liberation may thus be attributable to the delay in development of massive ionic shifts and resultant neurotransmitter release which may activate phospholipase A2 and C.
Amino Acids↗