Biomedical subjects

S Tsuruta

Publications and source records attributed to S Tsuruta.

At least 73 records · Page 4Linked to original sources

PubMed1994

[Age-delusion: (age-misidentification of chronic schizophrenic patients)].

I noted that some of the schizophrenic patients chronically institutionalized at our hospital mistook their age (age-delusion), and studied the primary symptoms and the psychodynamics of this schizophrenic phenomenon. The subjects were divided into a core group of 24 patients who had schizophrenia without any overt organic brain diseases and a peripheral group of 8 patients who had schizophrenia associated with organic brain diseases. I divided the core group patients into 3 categories. I. Underestimators: These patients insisted that they were much younger than their real age, and they could be divided into a dynamic subgroup (subjective age increased in parallel with time) and a static subgroup (subjective aging did not occur). II. Overestimators: these patients believed that they were much older than their real age. III. Vacillators: These patients sometimes underestimated and sometimes overestimated their age. They could be divided into a subgroup in which the age was decided on the basis of their systematic delusions and a subgroup in which one of two fixed and different ages was always given (one being over and the other under the real age). I compared these schizophrenic age-delusional patients to other organic brain disease patients without schizophrenia who also mistook their age. Organic brain disease patients had a temporal recognition disorder as their primary symptom, while the schizophrenic patients had abnormal time experience as the primary symptom. This abnormality of time experience, mixed with the patient's psychodynamics that they want to objectify and manipulate their age as a number, appeared as a discrepancy between the subjective length of hospitalization and the actual duration, which means the age-delusion. These schizophrenic age-delusional patients had lost the essential 'Zeitlichkeit' and shut themselves up in the unessential 'Zeitlichkeit' according to the concept of Heidegger. Believing in their subjective age seems to allow them to reunify or rewrite their own past history and gain some hope for the future.

Adult↗

PubMed1994

Angiotensin II receptor antagonist, TCV-116, prevents myocardial hypertrophy in spontaneously hypertensive rats.

Recently, it has been suggested that angiotensin II (AII) might be associated with cardiac hypertrophy and fibrosis. We investigated the preventive effect of an AII receptor antagonist, TCV-116, on the development of cardiac hypertrophy and fibrosis in spontaneously hypertensive rats (SHR) at 24 weeks of age through histopathological study and an AII receptor assay. Treatment with TCV-116, enalapril (an angiotensin-converting enzyme inhibitor, ACEI), and hydralazine for 20 weeks lowered systolic blood pressure (SBP) significantly (-39 mmHg, -45 mmHg, and -45 mmHg, respectively). The heart weight/body weight ratio, cardiac myocyte diameter, and percent cardiac fibrosis were significantly reduced by treatment with TCV-116 and enalapril as compared with hydralazine treatment or no treatment. The AII receptor density was significantly increased by treatment with TCV-116 and enalapril as compared with hydralazine treatment or no treatment. The results of this study suggest that AII receptors are involved in the development of cardiac hypertrophy and fibrosis in SHR. It was demonstrated that the AII receptor antagonist, TCV-116, was comparable to the ACEI, enalapril, in inhibiting the progression of cardiac hypertrophy and fibrosis via the AII receptor.

Angiotensin II↗

PubMed1993

Changes in the prevalence of hepatitis B and C infection in patients with hepatocellular carcinoma in the Nagasaki Prefecture, Japan.

The development of hepatocellular carcinoma (HCC) is very closely associated with chronic liver disease. In the present study, the prevalence of the hepatitis B virus (HBV) and hepatitis C virus (HCV) infection as a causative role in the development of HCC was analysed in 253 patients with HCC, who were admitted to our hospital during 1976-90. Among these patients, 68 (27%) were positive for HBsAg but negative for anti-HCV antibody (group I); in contrast, 147 (58%) were negative for HBsAg but positive for anti-HCV antibody (group II), 19 (7.5%) were both positive (group III), and 19 (7.5%) were both negative (group IV). To evaluate the serial changes in the prevalence of HBsAg and anti-HCV antibody, changes in the number of patients were compared between group I and group II. The number of group I patients reached a peak during 1982-84 and was thereafter followed by a decreasing trend, whereas the number of group II patients steadily increased and reached a plateau over 6 recent years. These results suggest that HCV infection recently seems to play a more important role in the development of HCC than chronic HBV infection, even in the Nagasaki Prefecture, where the HBV carrier rate is higher than elsewhere in Japan.

Aged↗

PubMed1993

Regulation of albumin and alpha-fetoprotein gene expression by colloid osmotic pressure in human hepatoma cells.

BACKGROUND: Colloid osmotic pressure has been thought to regulate albumin synthesis; however, the exact mechanism remains obscure. In the present study, the effect of colloid osmotic pressure on the albumin and alpha-fetoprotein gene expression in HuH-7 human hepatoma cells was analyzed. METHODS: HuH-7 cells were treated with albumin or dextran (mean mol wt, 70,000), and changes in the levels of albumin and alpha-fetoprotein messenger RNA (mRNA) were analyzed by Northern blotting. Furthermore, in transient chloramphenicol acetyltransferase (CAT) plasmid transfection experiments, effects of colloid osmotic pressure on CAT activities were studied. RESULTS: By Northern blot analysis, the levels of both albumin and alpha-fetoprotein mRNA were dose-dependently suppressed by the elevation of colloid osmotic pressure and returned to pretreatment levels 48 hours after the culture medium containing dextran was replaced with a dextran-free fresh medium. In transient CAT plasmid transfection experiments, the increased level of colloid osmotic pressure resulted in the repression of both albumin and alpha-fetoprotein promoter activities. In contrast, alpha-fetoprotein enhancer activity, which possibly regulates not only alpha-fetoprotein but also albumin gene expression, was not affected by changes in colloid osmotic pressure. CONCLUSIONS: These results suggest that colloid osmotic pressure regulates both albumin and alpha-fetoprotein gene transcription through the modulation of their promoter activities.

Carcinoma, Hepatocellular↗

PubMed1993

A physiological role of epidermal growth factor in cell kinetics of gastric epithelium.

Administration of epidermal growth factor (EGF) stimulates DNA synthesis in gut epithelial cells and inhibits gastric acid secretion. A physiological role of EGF in cell kinetics of gastric epithelium, however, has not been fully understood. In mature male mice, large amounts of EGF are produced in the submandibular glands, and sialoadenectomy (removal of the submandibular glands) causes a marked reduction of plasma EGF levels. For the evaluation of a biophysical function of EGF, sialoadenectomized mice and sham-operated mice were injected with 3H-thymidine to compare the proliferative activity and the cell-turnover of gastric epithelium between the two groups using the autoradiographic analysis. When mice were killed 90 min after a single injection of 3H-thymidine, the percentages of fundic gland mucosal cells radiolabeled in sialoadenectomized and sham-operated mice were 27.3 +/- 5.0% and 26.3 +/- 5.8% (mean +/- SD), respectively. The difference was not significant (p > 0.05). Similarly, the labeling indices of pyloric gland mucosal cells were not different between the two groups (26.7 +/- 4.3% vs 27.8 +/- 3.7%, p > 0.05). In contrast, when mice were given 17 repeated injections of 3H-thymidine at 6 hr intervals and killed 48 hr after the last injection, labeling indices in sialoadenectomized mice were significantly lower than those in sham-operated mice (35.3 +/- 4.3% vs 52.8 +/- 1.1% in the fundic gland area; 41.0 +/- 6.2% vs 55.1 +/- 5.9% in the pyloric gland area, p < 0.001, respectively). Treatment of sialoadenectomized mice with EGF (5 mg/mouse per day) completely restored the percentages of the radiolabeled cells to control levels. These findings suggest that endogenous EGF plays a major role in maintaining biological cell-turnover of the mouse gastric epithelium.

Animals↗

PubMed1993

Effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes.

1. The effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes (PMN) induced by three different chemotactic stimulants, platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (FMLP) and an activated fragment of C5 (C5a) were investigated. 2. Adenosine and its analogues inhibited the actin polymerization induced by these three agents in a concentration-dependent manner and theophylline, a competitive antagonist at adenosine receptors, abolished these inhibitory effects. 3. The adenosine analogue 5'-N-ethylcarboxamideadenosine (NECA) was a more potent inhibitor of actin polymerization than either L-N6-phenylisopropyladenosine (PIA) or adenosine itself; the rank order of potency of these agonists was characteristic of adenosine A2 receptors. 4. Adenosine deaminase (ADA) abolished the inhibitory effect of adenosine and augmented PAF-induced actin polymerization. 5. It was concluded that, at physiological concentrations, adenosine inhibits actin polymerization in PMN via activation of PMN surface membrane adenosine A2 receptors and thus modulates chemotactic stimulus-induced PMN motility.

Actins↗

PubMed1992

Enhanced DNA synthesis in rat hepatoma cells by conditioned media from Kupffer cells incubated with supernatants of tumor necrosis factor-alpha-pretreated hepatocytes.

The effects of tumor necrosis factor-alpha (TNF-alpha) on DNA synthesis in AH66 rat hepatoma cells and rat hepatocytes were analysed by means of [3H]thymidine incorporation. DNA synthesis in AH66 cells was suppressed when AH66 cells were directly incubated with TNF-alpha. When primary culture of rat Kupffer cells was incubated with hepatocyte conditioned media pretreated with TNF-alpha (0-200 U/ml), and AH66 cells were then treated with these hepatocyte/Kupffer cell-conditioned media, TNF-alpha used in the pretreatment caused a dose-dependent increase in DNA synthesis in AH66 cells with a maximum effect amounting to a more than 10-fold increase. In contrast, DNA synthesis in primary culture of rat hepatocytes was not stimulated by the TNF-alpha-pretreated hepatocyte/Kupffer cell conditioned media. These results suggest that TNF-alpha-mediated hepatocyte-Kupffer cell interaction selectively promotes proliferation of rat hepatoma cells.

Animals↗

PubMed1992

Inhibitory effect of prostaglandin delta 12-PGJ2 on cell proliferation and alpha-fetoprotein expression in HuH-7 human hepatoma cells.

9-deoxy-delta 9,delta 12-13,14-dihydro-prostaglandin D2 (delta 12-PGJ2) is a potent inhibitor of proliferation of tumor cells. In the present study, the effect of delta 12-PGJ2 on the alpha-fetoprotein(AFP) and the albumin gene expression was analyzed in HuH-7 human hepatoma cells. delta 12-PGJ2 inhibited the cell growth and reduced the medium AFP concentrations dose-dependently. To determine whether this decline of AFP depends only on the relative decrease in cell numbers by delta 12-PGJ2, or is in part, due to the decrease in the cellular AFP synthesis by delta 12-PGJ2, Northern blot analysis was performed in this study. By Northern blotting, it was shown that delta 12-PGJ2 caused a marked reduction in the levels of the AFP mRNA and the albumin mRNA. In contrast, the level of the beta-actin mRNA was not changed by delta 12-PGJ2. In the transient chloramphnicol acetyltransferase plasmid transfection experiments, delta 12-PGJ2 did not suppress the AFP enhancer activity, which possibly regulates both the AFP and the albumin gene expression in HuH-7 hepatoma cells, but resulted in the selective repression of the AFP and the albumin promoter activity. These results suggest that delta 12-PGJ2 suppresses not only cell growth but also expression of the AFP gene and the albumin gene at the transcriptional level in human hepatoma cells.

Albumins↗

PubMed1992

Adenosine inhibits divalent cation influx across human neutrophil plasma membrane via surface adenosine A2 receptors.

Adenosine and its analogues inhibited increases in divalent cation influx stimulated by platelet-activating factor (PAF) and formyl-methionyl-leucyl-phenylalanine (FMLP) in a dose-dependent fashion. This effect was antagonized by theophylline, an adenosine receptor antagonist. When extracellular adenosine was removed by adenosine deaminase, the effect of adenosine was completely abolished. Two adenosine analogues with different affinities for adenosine receptor subtypes, 5'-N-ethylcarboxamideadenosine (NECA) and L-N6-phenylisopropyladenosine (PIA), also inhibited divalent cation influx, NECA being more potent than PIA. These results suggest that adenosine and its analogues inhibit divalent cation influx across neutrophil plasma membranes via surface adenosine A2 receptors. Adenosine had little effect on the initial peaks of intracellular free calcium rises induced by chemoattractants, but it inhibited the subsequent rise in free calcium. Since calcium influx through the divalent cation channels or neutrophil plasma membranes is responsible for maintaining free calcium concentration following the initial peaks, we suggest that adenosine modulates neutrophil function by interfering with this calcium influx.

Adenosine↗

PubMed1991

Differentiation of a human eosinophilic leukemia cell line (EoL-1) by a human T-cell leukemia cell line (HIL-3)-derived factor.

Differentiation of a human eosinophilic leukemia cell line, EoL-1, induced by the culture supernatant of a human ATL cell line, HIL-3 (HIL-3 sup) was compared with differentiation induced by defined cytokines. HIL-3 sup induced EoL-1 cells to express eosinophilic granules and segmented nuclei after 6 to 9 days of incubation. HIL-3 sup also induced the expression of Fc epsilon receptor II (Fc epsilon RII/CD23) and an eosinophil differentiation antigen EO-1 mainly on eosinophilic granule (+) cells. Furthermore, HIL-3 sup induced EoL-1 cells to respond to an eosinophil chemotactic factor, platelet activating factor. HIL-3 cells express messenger RNA (mRNA) of interleukin-5 (IL-5), macrophage colony-stimulating factor (M-CSF), and IL-3 but not granulocyte CSF (G-CSF). Granulocyte-macrophage CSF (GM-CSF) and tumor necrosis factor-alpha (TNF-alpha) were detected in the HIL-3 sup. Recombinant IL-2 (rIL-2), rIL-3, rIL-4, rIL-5, rM-CSF, and rGM-CSF did not induce eosinophilic granules. rG-CSF induced a few eosinophilic granule (+) cells, and TNF-alpha, which did not induce eosinophilic granules by itself, enhanced the ability of G-CSF to induce them. However, G-CSF and TNF-alpha did not induce the expression of Fc epsilon RII and EO-1 antigen. Moreover, anti-G-CSF, anti-TNF-alpha, anti-GM-CSF, anti-IL-3, and anti-IL-5 antibodies did not suppress the effect of HIL-3 sup on the differentiation of EoL-1 cells. All the data suggest that HIL-3 sup contains an unidentified factor that induces differentiation of EoL-1 cells, and that EoL-1 cells and HIL-3 sup provide an important model for the examination of differentiation mechanisms and functions of eosinophils.

Antibodies↗

PubMed1991

[Effect of fluconazole on Aspergillus infection associated with chronic granulomatous disease].

Aspergillus infection is the most frequent fungal infection associated with chronic granulomatous disease (CGD), and often results in a life-threatening situation. This report describes the use of high-dose fluconazole, a new antifungal agent, for invasive Aspergillus infection in a patient with CGD. A 27-month-old boy was sent to our hospital because of unknown fever in October, 1988. He was then admitted for pneumonia and pleural effusion of the right lung in February, 1989. Treatment with antibiotics was ineffective, and cultures of throat and pleural fluid were negative. In May, 1989, Aspergillus fumigatus was cultured from a subcutaneous abscess at the point of pleural puncture. Therefore we speculated that Aspergillus might have been the cause of pneumonia. The patient was diagnosed as having CGD by NBT test. Treatment with miconazole, flucitocin and amphotericin-B syrup was ineffective. From July, 1989, he was given 100 mg/day fluconazole d.i.v., but the drug did not reach an effective serum concentration to combat Aspergillus. However, an effective concentration of fluconazole was reached at a dose of 250 mg/day, and the chest X-ray findings subsequently improved, despite occasional high fever and continued high CRP. In July, 1990, the route of fluconazole administration was changed from d.i.v. to p.o. at the same dose, resulting in a serum concentration of fluconazole higher than that achieved with d.i.v. treatment. Both the clinical and laboratory findings showed improvement thereafter. Therapy for Aspergillus infection associated with CGD was found to necessitate high doses of anti-fungal drugs over a long period, although treatment with previously employed anti-fungal drugs could not be continued due to their adverse side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspergillosis↗

PubMed1990

The effect of adenosine on the fluorescence responses of chlorotetracycline-loaded human polymorphonuclear leukocytes.

Chlorotetracycline has been used in human polymorphonuclear leukocytes as a probe to investigate the state of membrane-bound calcium. We examined the effect of adenosine on the fluorescence responses of CTC-loaded PMNs stimulated with the synthetic chemotactic peptide, formyl-methionyl-leucyl- phenylalanine. Adenosine inhibited the decrease in CTC fluorescence in a dose-dependent fashion and its effect was reversed by theophylline, an adenosine receptor antagonist. Removal of extracellular adenosine by incubating PMNs with adenosine deaminase abolished the effect of adenosine. These data suggest that adenosine inhibits the release of membrane-bound calcium in PMNs that normally occurs in response to chemotactic stimuli, acting via PMN surface adenosine receptors.

Adenosine↗

PubMed1990

Transforming growth factor beta and dexamethasone suppress the expression of Fc epsilon receptor 2 (CD23) on a human eosinophilic cell line EoL-3.

The effects of interferon-alpha (IFN-alpha), INF-gamma, transforming growth factor beta (TGF-beta) and dexamethasone on low-affinity Fc receptors for IgE (Fc epsilon R2/CD23) expression on a human eosinophilic leukemia cell line, Eol-3, were examined. Fc epsilon R2/CD23 expression was enhanced by both IFN-alpha and IFN-gamma, and suppressed by TGF-beta and dexamethasone. Northern blot analysis revealed that these reagents regulate the Fc epsilon R2/CD23 expression from mRNA level: both IFN-alpha and IFN-gamma increased the amount of Fc epsilon R2/CD23 mRNA, while both dexamethasone and TGF-beta decreased Fc epsilon R2/CD23 mRNA, where the effect of dexamethasone was much stronger than that of TGF-beta. In comparison with IFN-alpha, IFN-gamma seemed to enhance preferentially the release of surface Fc epsilon R2/CD23, which resulted in the increase of soluble Fc epsilon R2/CD23. These results suggest that these reagents may play important regulatory roles in allergy and in helminth infections via their effects on Fc epsilon R2/CD23 expression on eosinophils.

Antigens, CD↗

PubMed1990

Ketotifen inhibits PAF-induced actin polymerization in a human eosinophilic leukaemia cell line, EoL-1.

The inhibitory effect of ketotifen on platelet activating factor (PAF)-induced actin polymerization in a human eosinophilic leukaemia cell line, EoL-1, was examined by flow cytometry with the use of reagents specific for the filamentous form of actin (F-actin). Actin polymerization has been considered to be essential for locomotion of cells, chemotaxis and chemokinesis, and thus it reflects the chemotactic reaction of EoL-1 cells stimulated by PAF. Unstimulated EoL-1 cells showed little PAF-induced actin polymerization, whereas EoL-1 cells cultured for 9 days with the supernatant of a human ATL cell line, HIL-3 (HIL-3 sup), showed marked actin polymerization when stimulated with PAF. The actin polymerization in EoL-1 cells induced by PAF was seen in a dose-dependent manner at concentrations of 10(-10) M to 10(-6) M of PAF, and the maximum effect was seen at 10(-7) M of PAF. CV-3988, a specific antagonist of PAF, inhibited 80% of the actin polymerization in EoL-1 cells induced by PAF at a concentration of 10(-5) M. Ketotifen inhibited up to 40% of the PAF-induced actin polymerization of EoL-1 cells in a dose-dependent manner at concentrations of 10(-9) M to 10(-5) M. These results suggest that ketotifen may play an important role in the prevention of eosinophil-induced inflammation in allergic disorders by inhibiting PAF-induced chemotaxis of eosinophils.

Actins↗

PubMed1990

[Application of gypsum-bonded investment containing niobium carbide on casting of alloy for metal-ceramic restoration].

Experimental gypsum-bonded investments containing 0.5-5.0 wt% NbC were prepared by mechanical mixing of each powder. Setting and thermal expansion measurement, compressive strength and casting accuracy for Ni-Cr alloy for metal-ceramic restoration were investigated. Analysis of NbC during heating was carried out by X-ray diffraction, TG-DTA and SEM. NbC was oxidized to Nb2O5 with a volume change between 300-600 degrees C, as in the following equation: 2NbC + 4 1/2O2----Nb2O5 + 2CO2 The theoretical volume of 1/2Nb2O5 calculated from the lattice constants according to JCPDS file was approximately 4 times larger than that of NbC. The experimental investments of 70 wt% cristobalite and 30 wt% gypsum containing 2.0, 3.0 and 5.0 wt% NbC showed large thermal expansion of 7.0, 10.0 and 13.0% respectively. The investment containing 2.0 wt% NbC showed nearly the same casting accuracy for Ni-Cr alloys for metal-ceramic restoration as the commercial phosphate-bonded investment.

Calcium Sulfate↗

PubMed1989

Cell cycle related change of Ara-C transport in HL-60 cells after differentiation induction.

Using a promyelocytic leukemia cell line, HL-60, we studied the membrane transport of Ara-C before and after differentiation induced by retinoic acid (RA). In RA-treated cells, Ara-C transport was reduced and there was a concomitant increase of the ID50 values of Ara-C in comparison with the controls. By three different procedures to synchronize untreated cells, i.e. density arrest G1 phase enrichment, aphidicolin-induced S phase accumulation and the double isoleucine block method, we found that Ara-C transport was 30-50% higher in the S phase than in the G1 phase. Therefore, the observed decrease in Ara-C transport is, in part, due to the retarded growth accompanied by an accumulation of cells in the G1 phase after differentiation induction.

Aphidicolin↗

PubMed1989

The effect of cell synchronization on the efficiency of stable gene transfer by electroporation.

We synchronized thymidine kinase deficient mouse Ltk-cells by two different methods, hydroxyurea double-block treatment or aphidicolin single-block treatment and transformed them with the cloned herpes simplex virus thymidine kinase gene at various time intervals by the electroporation technique. Marked enhancement of stable transformation efficiency was observed at the time corresponding to the peak of G2/M phase. These results suggest that the G2/M phase is the most efficient period for stable gene transfer by electroporation.

Animals↗

PubMed1989

Occurrence of an anti-peplomycin IgE antibody cross-reacting with bleomycin in a patient with cervical uterine cancer.

An allergic reaction to peplomycin was observed in a patient with cervical uterine cancer who had previously been treated with peplomycin. A positive Prausnitz-Küstner test and its elimination after heat treatment of the serum showed the production of anti-peplomycin IgE antibody. Peplomycin was coupled to a paper disc and a sensitive radioallergosorbent test for peplomycin was developed to quantitate the antibody. Patient serum IgE and IgG were purified by DE52 column chromatography; the IgE fraction contained binding activity to peplomycin. A competition test revealed that the antibody bound to both peplomycin and bleomycin. DNA, RNA, and mononucleotides had no effect on antibody binding, but the antibody inhibited peplomycin's activity.

Aged↗