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Biomedical subjects

T Masuda

Publications and source records attributed to T Masuda.

At least 343 records · Page 19Linked to original sources
PubMed1994

[Urachal cyst with stone: a case report].

A 52-year-old woman complained of persistent discharge from an umbilicus which she had for 18 years. Abdominal X-ray showed a stone-like shadow measuring 5 x 3 cm at the 5th lumbar spine. Cystoscopic examination revealed a hole at the dome of the bladder and a ureteral catheter was inserted approximately 3 cm through the hole. Computerized tomography scan and magnetic resonance imaging demonstrated a cyst communicating to the umbilicus and bladder. The preoperative diagnosis was a patient urachus associated with stone. Urachal cyst containing a stone was removed and partial cystectomy was performed. The stone was a mixture of magnesium ammonium phosphate and calcium phosphate. Pathological examination showed no evidence of malignancy. More than 210 cases of urachal cyst have been reported in Japan. About 10% of the cases were associated with stones.

Female↗
PubMed1993

Difference in plasminogen activator inhibitor activity between non-Q-wave infarction and Q-wave infarction.

We examined the plasma levels of tissue plasminogen activator antigen and plasminogen activator inhibitor activity in 14 patients with non-Q-wave infarction and in 27 patients with Q-wave infarction before the start of thrombolytic therapy and in 34 control subjects. The mean level of plasma tissue plasminogen activator antigen (ng/ml) was higher (P < 0.01) both in the patients with non-Q-wave infarction and in those with Q-wave infarction than in the control subjects (10.3 +/- 1.9, 9.5 +/- 0.8 vs. 5.8 +/- 0.3), and there was no difference in the level between the patients with non-Q-wave infarction and those with Q-wave infarction. The mean level of plasma plasminogen activator inhibitor activity (IU/ml) was lower (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (7.3 +/- 2.0 vs. 17.1 +/- 2.2), and there was no difference in the level between the patients with non-Q-wave infarction and the control subjects (7.3 +/- 2.0 vs. 4.1 +/- 2.6). The patency rate of infarct-related coronary artery before thrombolytic therapy was higher (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (54% vs. 15%). We conclude that plasminogen activator inhibitor activity was lower in non-Q-wave infarction than in Q-wave infarction and this may be related to the higher patency rate of infarct-related coronary artery in non-Q-wave infarction.

Aged↗
PubMed1993

A putative transcription factor binding to the upstream region of the puf operon in Rhodobacter sphaeroides.

Gel shift assays of the upstream region of the puf operon in Rhodobacter sphaeroides were performed using cell-free extracts from cells grown under various culture conditions. The results suggested that a protein binding to the upstream region functioned as a repressor-like substance of the expression of the operon by oxygen tension or light. The density of the shifted band of cell-free extracts from cells irradiated with blue light under semi-aerobic conditions was higher than that with red light. Phosphatase treatment of the cell-free extracts strongly increased the DNA-binding affinity of the protein.

Base Sequence↗
PubMed1993

Differential damage by hypoxia to dopamine and serotonin nerve terminals.

Serotonin and dopamine resemble each other in terms of their synthetic and degradative pathways, as well as in terms of structural features. However, responses to a low-oxygen environment differ between these two compounds. In this experiment, we studied the fluctuations of levels of serotonin, dopamine and their metabolites in the striatum of the rat brain under low-oxygen conditions using a microdialysis technique. Comparison of the extents of increases in extracellular levels of dopamine and serotonin, accompanied by decreases in levels of metabolites, indicates that the effects of hypoxia on the two types of neuronal terminal are different. This study suggests that dopamine plays a more important role than serotonin in the mechanism of irreversible destruction of neurons during moderate hypoxia.

Animals↗
PubMed1993

The post-translational processing of ras p21 is critical for its stimulation of mitogen-activated protein kinase.

The point-mutated active form of ras p21 is known to activate mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK) in intact mammalian cells and Xenopus oocytes, although the direct target molecule of ras p21 remains to be identified. To elucidate the role of the post-translational processing of ras p21 for the MAP kinase activation, we established the cell-free system in which ras p21 activated MAP kinase. The guanosine 5'-(3-O-thio)triphosphate (GTP gamma S) bound form of post-translationally processed Ki-ras 4B p21 activated MAP kinase in the cytosol fraction of Xenopus oocytes, but the GTP gamma S bound form of post-translationally unprocessed Ki-ras 4B p21 or the GDP bound form of processed or unprocessed Ki-ras 4B p21 was far less effective. The GTP gamma S bound form of processed Ki-ras 4B p21 activated recombinant ERK2 in the presence of the cytosol fraction of Xenopus oocytes, but the unprocessed protein was far less effective. These results provide a complete biochemical assay for ras p21 to activate MAP kinase in a cell-free system and indicate that all the elements downstream of ras p21 necessary for the MAP kinase activation are cytosolic and that the post-translational processing of ras p21 is important for the MAP kinase activation.

Animals↗
PubMed1993

A protein factor for ras p21-dependent activation of mitogen-activated protein (MAP) kinase through MAP kinase kinase.

To identify the direct target molecule of ras p21 in higher eukaryotes, we have recently developed the cell-free system in which ras p21 activates mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK). In this cell-free system, the guanosine 5'-[gamma-thio]triphosphate- bound form of Ki-ras p21, but not the GDP-bound form, activates endogenous Xenopus MAP kinase as well as recombinant ERK2 in the presence of the cytosol fraction of Xenopus oocytes. We separated two protein factors from the cytosol fraction of Xenopus oocytes by column chromatography: one was the inactive form of MAP kinase kinase and the other was a factor tentatively named ras p21-dependent ERK-kinase stimulator (REKS). The former and latter showed M(r) values of approximately 45,000 and 150,000-200,000, respectively, as estimated by gel filtration. Both factors were necessary for Ki-ras p21-dependent activation of MAP kinase/ERK2. These results indicate that an additional protein factor (REKS) is essential for Ki-ras p21 to activate MAP kinase through MAP kinase kinase.

Animals↗
PubMed1993

Effects of intrathymic injection of organ-specific autoantigens, parietal cells, at the neonatal stage on autoreactive effector and suppressor T cell precursors.

Thymectomy on day 3 after birth (3d-Tx) induces autoimmune gastritis (AIG) in 81%, and oophoritis (AIO) in 25% of BALB/c mice at the age of 2 to 3 months. Intrathymic, but not intraperitoneal injection of syngeneic parietal cells into sex-matched BALB/c mice within 24 h of birth resulted in almost complete prevention of the development of AIG in these mice in which 3d-Tx was performed. The prevention induced was parietal cell specific, since the development of AIO was not inhibited in female mice. Moreover, the injection of BALB/c liver cells, Mls-matched (BALB/c) and -disparate (DBA/2) B blasts which resulted in V beta 6 T cell deletion, as well as the injection of staphylococcal enterotoxin B failed to prevent the diseases. These findings suggested that recognition of an autoantigen in the thymus is necessary for the induction of tolerance, and that involvement of Mls-1 antigens in the pathogenesis of AIG, as has been suggested previously (Schwartz, R. H., Cell 1989. 57: 1073), was unlikely. T cells that suppress the development of organ-specific autoimmune diseases in 3d-Tx mice seem to maintain the unresponsiveness of autoreactive T cells at the periphery in normal mice. In agreement with our previous observations, we found that intraperitoneal (i.p.) injection of spleen cells from 3-month-old normal mice into 3d-Tx mice on day 10 after birth prevented the development of AIG, whereas spleen cells from age-matched AIG+ (mice with AIG) or AIG- (mice without AIG) 3d-Tx mice failed to do this. This implies that the suppressor cells probably affect the differentiation of effector-precursor to effector. In fact, these suppressor cells did not inhibit the adoptive transfer of AIG to nu/nu BALB/c mice by spleen cells from 3d-Tx mice manifesting AIG. By negative selection using monoclonal antibody and complement, it was confirmed that the phenotype of the suppressor cell was CD4. In contrast to 3d-Tx, 10d-Tx did not induce AIG, indicating the peripheralization of the suppressor cell by that time. On the other hand, intrathymic injection of parietal cells immediately after birth did not affect suppressor cell generation, implying that some T cells, including suppressor cells, escape thymus selection. We postulate that these cells correspond to the precursors of the autoreactive effector T cells and suppressor T cells that are present in normal mice.

Animals↗
PubMed1993

Prevention of type I diabetes with lymphotoxin in BB rats.

We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). Recently we have further reported that lymphotoxin (LT), a cytokine with functional and structural characteristics similar to those of TNF, also protected NOD mice from diabetes. In this study, we have extended our observation on the LT to BB rats. Male and female BB/Wor rats were treated intraperitoneally with recombinant human LT three times a week from 4 to 11 weeks of age. The cumulative incidence of diabetes by 14 weeks of age was 24/30 (80.0%) in nontreated control rats, whereas it was 10/26 (38.5% vs control, P < 0.01) and 4/29 (13.8% vs control, P < 0.0001) in the rats treated with 1 x 10(3) and 1 x 10(4) of LT, respectively. There was no significant difference in nonfasting blood glucose levels and body weights between nontreated control and LT-treated rats, which were nondiabetic. In the LT-treated rats, intensity of insulitis was significantly reduced in comparison with the nontreated rats. Concanavalin A-stimulated TNF/LT productivity of spleen cells was significantly lower in BB/Wor and BB/Sendai rats than in Wistar rats or other normal rat strains. On the other hand, there was no difference between BB/Sendai and Wistar rats in the in vivo TNF/LT productivity induced with LPS or with IFN-gamma plus LPS, and the TNF/LT productivity of these rats was lower on stimulation with LPS alone, but higher with IFN-gamma plus LPS than the other normal rats. These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT.

Animals↗
PubMed1993

Modulation of host cell nuclear proteins that bind to HIV-1 trans-activation-responsive element RNA by phorbol ester.

The trans-activation-responsive (TAR) element located within the 5' untranslated region of HIV-1 mRNA is the cis-responsive element for Tat, the viral trans-activator protein. Several TAR RNA binding proteins (TRBPs) have been identified in the nuclear extract from HeLa cells as cellular factors required for a full Tat-mediated trans-activation. In this study, we have tried to identify TRBPs in human T cell line (MOLT-4) persistently infected with HIV-1. Nuclear extract from the infected MOLT-4 cells was analyzed by gel-retardation and uv cross-linking assays with radiolabeled TAR RNA probe. Two major complexes of TAR RNA with some cellular proteins were detected in the gel-retardation assay. As the components of these complexes, at least five TRBPs (p30, p37, p46, p50, and p56) showing specific binding to the TAR RNA were detected in the uv cross-linking assay. We also observed that the detectable levels of p37 and p50 in the infected MOLT-4 cells were greatly reduced after phorbol ester (TPA) treatment under the condition of which HIV-1 gene expression was increased by about fivefold. These results suggest that the modulation of TRBPs by some mitogenic stimuli such as TPA might have a role in the trans-activation of HIV-1 gene expression in vivo.

Binding Sites↗
PubMed1993

The efficacy of extracorporeal shock wave lithotripsy on single dense calcified gallstones according to computed tomography.

The efficacy and complications of extracorporeal shock wave lithotripsy (ESWL) for single gallstones were compared between 15 patients with a CT-lucent stone and 18 patients with a dense calcified stone. In all of five patients with a stone smaller than 10 mm in diameter, complete or sufficient clearance was observed, regardless of calcification. However, in 28 patients with a stone larger than 11 mm in diameter, the rates of complete or sufficient clearance were lower in those with a dense calcified stone (64%) than in those with a computed tomography (CT) lucent stone (93%). There was no difference in the rate of complications between patients with a CT-lucent stone and those with a dense calcified stone. These results thus suggest that extracorporeal shock wave lithotripsy may be safely employed for patients with a single calcified gallstone.

Adult↗
PubMed1993

Analysis of 3' terminals of human immunodeficiency virus type 1 transcripts in persistently infected cells.

To examine the 3' terminal processing of human immunodeficiency virus type 1 (HIV-1) transcripts and the effects of phorbol ester (TPA) on this processing, cellular RNAs from persistently infected T cells (MOLT-4) or promonocytes (U937), with or without TPA treatment, were analyzed. To map the 3' terminals of viral transcripts, the RNA samples were examined by RNase-protection assay with an HIV-1 long terminal repeat (LTR) antisense riboprobe. Without TPA treatment, the viral transcripts initiated at the cap site in 5' LTR and polyadenylated at poly(A) site in 3' LTR were dominantly detected in both types of cells. This analysis demonstrated that some occlusion mechanism inactivating the poly(A) site in 5' LTR might exist in these infected cells. After TPA treatment, we found a dramatic shift in the protected patterns of viral transcripts in MOLT-4 cells, while the shift in U937 cells was less dramatic. These results suggested that the primary factor(s) involved in the observed effect of TPA might be cellular. We also demonstrated that the shift in the protected patterns of viral transcripts was associated with increased steady-state levels of viral transcripts. These results indicated that the factors involved in the TPA-induced shift might have some relation to the trans-activation of HIV-1 by similar substances.

Base Sequence↗
PubMed1993

Elevated plasma interleukin-6 levels in patients with acute myocardial infarction.

Interleukin-6 (IL-6) plays a key role in the synthesis of human acute-phase protein and several acute-phase responses occur in patients with acute myocardial infarction (AMI). We examined the plasma levels of IL-6 in 23 consecutive patients with AMI over the course of 4 weeks and in 30 control subjects. In patients with AMI, the plasma IL-6 levels (in picograms per milliliter) were increased at all sampling points from admission to discharge (ranging from 28.5 +/- 6.6 to 46.5 +/- 7.8) compared with levels in control subjects (11.4 +/- 2.9; p < 0.01). Cardiac catheterization did not influence plasma IL-6 levels. The plasma IL-6 level reached its peak approximately 3 days (46.5 +/- 7.8) and approximately 1 week after admission in patients with AMI. There was a significant positive linear correlation between the peak level of plasma IL-6 minus the level on admission and the peak level of plasma C-reactive protein in patients with AMI. The peak IL-6 level did not correlate with the peak levels of creatine kinase, pulmonary capillary wedge pressure, or left ventricular ejection fraction at 4 weeks. We conclude that the plasma IL-6 level is increased over a time course of 4 weeks in patients with AMI.

Acute-Phase Reaction↗
PubMed1993

Surfactant apoprotein A secretion by human tracheobronchial epithelial cells.

To determine whether surfactant apoproteins are produced locally by the airway walls, we used a two-site simultaneous immunoassay with monoclonal antibodies and measured the surfactant apoprotein-A (SP-A) content in media cultured with human airway explants or cultured epithelial cells. Tracheobronchial explants were cultured for 2 successive periods (periods I and II). Significant SP-A concentrations were detected in both periods. Methacholine (MCh) or isoproterenol (ISP), added to the medium at the beginning of period II, reduced the ratio of SP-A concentration in period II to that in period I, compared to samples without treatment. The SP-A concentration in the medium at the confluent period of cultured epithelial cells was significantly higher than at the mid-period, indicating that SP-A secretion is dependent on the cell number. The supernatant from explants stimulated by MCh was capable of reducing SP-A secretion from cultured epithelial cells. Immunohistochemical study of SP-A using monoclonal antibody demonstrated positive immunoperoxidase staining in the cytoplasm of epithelial cells. Further, Western blots of electrophoresed proteins from epithelial cells showed the characteristic properties of SP-A. These findings indicate that tracheobronchial epithelium can secrete SP-A.

Apolipoproteins A↗
PubMed1993

Increased plasma plasminogen activator inhibitor activity after coronary spasm.

To examine whether ischemic attack induced by coronary spasm changes fibrinolytic activity, we examined plasma levels of tissue-plasminogen activator antigen and plasminogen activator inhibitor activity before and after hyperventilation test in patients with variant angina and in control subjects. In 12 patients with variant angina, ischemic attack associated with ST-segment elevation on the electrocardiogram was induced by hyperventilation and plasma plasminogen activator inhibitor activity levels increased significantly 15 min after the attacks (pre, 5.1 +/- 0.8; immediately after, 5.8 +/- 1.1; and 15 min after, 7.2 +/- 0.9 IU/ml, P < 0.01). In 12 control subjects, plasminogen activator inhibitor activity levels did not change. Plasma tissue-plasminogen activator antigen levels did not change in both two groups. We conclude that coronary artery spasm increases plasma plasminogen activator inhibitor activity and that it may thereby lead to the coronary thrombus formation.

Adult↗
PubMed1993

Effects of extensive oral surgery and hemorrhage on coagulation and fibrinolysis.

The changes in coagulation and fibrinolytic activity in 22 patients with oral cancer undergoing extensive surgical procedures were studied. The patients were divided into two groups: group I patients suffered blood loss of less than 2,000 mL and group II patients had blood loss of more than 2,000 mL. The platelet count decreased significantly during surgery, at the end of surgery and on the 1st postoperative day in both groups. Fibrinogen was decreased during and at the end of surgery in both groups, but increased significantly on the 3rd postoperative day and reached about two times the preoperative levels on the 7th postoperative day. Fibrin degradation products increased significantly after surgery and reached the maximum value on the 1st postoperative day in both groups. Plasmin inhibitor complex and plasminogen increased significantly on the 3rd and 7th postoperative days. There was no clear evidence regarding the influence of blood loss on coagulation and fibrinolytic factors except for platelets. It was concluded that coagulation and fibrinolysis are enhanced between the 3rd and 7th postoperative days.

Adult↗
PubMed1993

Platelet-derived growth factor is released into the coronary circulation after coronary spasm.

BACKGROUND: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells and is implicated in the vascular response to injury and the pathogenesis of atherosclerosis. It is also a potent vasoconstrictor. METHODS: To examine whether acute myocardial ischemia increases the level of PDGF in the coronary circulation, we measured plasma levels of PDGF in the coronary sinus and the aortic root simultaneously in 14 patients with coronary spastic angina. These measurements were performed before and after the left coronary artery spasm induced by intracoronary injection of acetylcholine, and measurements were also taken in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Eleven patients with chest pain but normal coronary arteries and no coronary spasm served as controls. RESULTS: Plasma PDGF levels increased significantly (P < 0.01) from 274 +/- 28 pg/mL to 364 +/- 27 pg/mL only in coronary sinus after anginal attacks in the patients with coronary spastic angina. However, plasma PDGF levels in coronary sinus remained unchanged after these attacks in the patients with stable exertional angina (from 230 +/- 27 pg/ml to 247 +/- 28 pg/mL) and after intracoronary injection of acetylcholine in the control subjects. Plasma PDGF levels in aortic root remained unchanged in all three patient groups. CONCLUSIONS: PDGF is released into the coronary circulation after coronary artery spasm, and this may exacerbate coronary artery spasm.

Aged↗