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Biomedical subjects

H Taniguchi

Publications and source records attributed to H Taniguchi.

At least 451 records · Page 25Linked to original sources

Inhibition by putrescine of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.

Adenocarcinoma↗

Enhancement by methionine enkephalin of colon carcinogenesis induced by azoxymethane.

The effect of the opioid receptor agonist methionine enkephalin (Met-enkephalin) and the opioid receptor antagonist naloxone on colonic carcinogenesis induced by azoxymethane was investigated in Wistar rats. Rats received ten weekly injections of 7.4 mg/kg of body weight of azoxymethane and injections of Met-enkephalin (50 micrograms/kg of body weight), naloxone (2 mg/kg of body weight), or Met-enkephalin (50 micrograms/kg of body weight) plus naloxone (2 mg/kg of body weight) once every 2 days. In wk 40, the group treated with Met-enkephalin had a significantly increased incidence of colonic tumors. A combination of Met-enkephalin and naloxone attenuated the enhancing effect by Met-enkephalin on the development of colonic tumors. Administration of naloxone alone had no influence on colonic tumorigenesis. During and after administration of the carcinogen, the bromodeoxyuridine-labeling indices of the colon mucosa and/or cancers were significantly increased in rats treated with Met-enkephalin. However, a combination of Met-enkephalin and naloxone significantly decreased the labeling indices of the colon mucosa and/or cancers. These findings indicate that Met-enkephalin enhanced colon carcinogenesis and that naloxone attenuated this enhancement. Because naloxone is an opioid receptor antagonist, these findings also indicate that the enhancing effect of Met-enkephalin on colon carcinogenesis may be mediated through opioid receptors.

Adenocarcinoma↗

Enhancement by sulpiride of the inhibitory effects of cysteamine on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of sulpiride on cysteamine inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the BUdR labelling index of gastric mucosa were investigated in inbred Wistar rats. After 25 weeks of oral treatment with MNNG, rats received one of the following alternate-day injections: cysteamine (2 doses), cysteamine (2 doses) plus sulpiride or sulpiride. At week 52, prolonged administration of cysteamine significantly reduced the incidence of adenocarcinomas of the glandular stomach. Cysteamine at low dose had no effect on the incidence of gastric cancers, but a combination of low-dose cysteamine and sulpiride caused a significantly greater reduction in the incidence of gastric cancers. Administration of sulpiride alone had no influence on gastric carcinogenesis. The labelling index of the antral mucosa was significantly lower in rats treated with high but not low doses of cysteamine. However, a combination of low-dose cysteamine and sulpiride significantly decreased the labelling index of the antral mucosa. Our findings indicate that cysteamine suppressed gastric carcinogenesis and that sulpiride enhanced this inhibition. Because sulpiride is a dopamine antagonist, these findings also indicate that dopamine may play an important role in cysteamine inhibition of gastric carcinogenesis.

Animals↗

A case report of hepatocellular carcinoma within adenomatous hyperplasia: is adenomatous hyperplasia a precancerous lesion or not?

It is controversial whether adenomatous hyperplasia (AH) of the liver progresses to hepatocellular carcinoma. We experienced two hepatic lesions in a patient (73-yr-old male) with cirrhotic liver. One was diagnosed as HCC and the other was AH including a small HCC histologically. To investigate cell kinetics and the ploidy pattern of these lesions, Feulgen DNA-cytofluorometry analysis was performed. The result of this analysis suggested that AH developed into extremely well-differentiated HCC composed of mononuclear diploid cells at first and then was further transformed into clear cell type HCC composed of mononuclear tetraploid cells. The development of human HCC, at least in cirrhotic liver, may therefore be a multi-step process.

Aged↗

Mixed venous oxygen saturation as a guide to tissue oxygenation and prognosis in patients with acute myocardial infarction.

The relation of mixed venous oxygen saturation and the cardiac index to tissue oxygenation and prognosis was investigated in 119 patients with acute myocardial infarction. There was a positive correlation between mixed venous oxygen saturation and the cardiac index in 97 survivors and 22 nonsurvivors, but a significantly lower mixed venous oxygen saturation level at the same level of cardiac index was observed in nonsurvivors compared with survivors. Results of multivariate analysis with mixed venous oxygen saturation and the cardiac index indicated that only mixed venous oxygen saturation was significantly related to survival and to hyperlactacidemia. Oxygen delivery to tissues declined significantly in nonsurvivors because of a lower cardiac index and a lower hemoglobin concentration in these patients than in survivors. However, at the same level of oxygen delivery to tissues, nonsurvivors had a significantly higher rate of oxygen consumption leading to a correspondingly greater decrease in mixed venous oxygen saturation, suggesting that a greater increase in oxygen demand was also observed in nonsurvivors than in survivors. Thus mixed venous oxygen saturation after acute myocardial infarction is a better predictor of hyperlactacidemia and survival than the cardiac index, and this may be associated with an increased oxygen demand and an impaired oxygen transport system in seriously ill patients.

Aged↗

Effect of the cooling rate on insulin release from frozen-thawed In-111 cells.

Cultured cells derived from hamster insulinoma (In-111 R1 cells) were placed in 1.4 M dimethyl sulfoxide (Me2SO)-containing RPMI 1640 at 20 degrees C for 20 min. They were frozen to -40 degrees C at a cooling rate of 1.0 or 0.5 degrees C/min, subsequently to -80 degrees C at 3 degrees C/min with a programmable freezer. After being maintained at -80 degrees C, they were rapidly thawed to 37 degrees C. Thawed cells were washed with 0.75 M sucrose for removal of Me2SO. Recovered cells were cultured in 2 ml of RPMI 1640 with 1.3 mM theophylline under a gas phase of 95% air -5% CO2 at 37 degrees C for 2 days. In both cooling rates, frozen-thawed cells discharged more insulin than the thawed in the absence of theophylline. However, this released insulin level was higher in the cells frozen at a cooling rate of 0.5 degrees C/min than that at 1.0 degrees C/min. Moreover, insulin released from frozen-thawed hamster insulinoma cells increased significantly with the addition of 1.3 mM theophylline. Considering that the higher insulin release level at 11.1 mM glucose alone might indicate cellular damage, it is suggested that the cooling rate of 1 degree C/min may be better for cryopreservation of the dispersed cells under the present protocol for the assessment of the function of insulin release.

Animals↗

Simultaneous development of two cases of eosinophilia-myalgia syndrome with the same lot of L-tryptophan in Japan.

A newly recognized and well-described connective tissue disease, eosinophilia-myalgia syndrome, is thought to relate to L-tryptophan ingestion. The suspect L-tryptophan made in Japan has been distributed in Japan and in the United States. Different from many case reports of eosinophilia-myalgia syndrome in the United States, it has not been reported in Japan. We describe the first case reports of two Japanese patients. Eosinophilia-myalgia syndrome developed in these patients simultaneously, during L-tryptophan treatment by the same physician using the same lot of prescribed L-tryptophan. Furthermore, both patients had the following HLA types: HLA-Aw33(w19), -B44(12), and -DR6. These findings implicate the existence of another factor in the development of eosinophilia-myalgia syndrome in addition to the suspect L-tryptophan.

Aged↗

Effect of dexamethasone on uterine cell death.

Oestrogen, progesterone and androgen inhibit uterine cell death after the depletion of oestrogen. In the present study, we investigated effects of glucocorticoid on death of mouse uterine cells. Castrated female mice were given a daily injection of 17 beta-oestradiol (0.2 microgram/mouse/day) for 3 days, and then an injection of 5'-[125I]iodo-2'-deoxyuridine ([125I]IdUrd) to label DNAs of uterine cells with 125I. Mice were killed at intervals during subsequent treatments, and the retention of [125I]IdUrd incorporated into the whole uterus was determined. On subsequent injection of vehicle only, the 125I-radioactivity retained in the whole uterus rapidly decreased. Injections of dexamethasone (50 micrograms/mouse/day) reduced the loss of 125I-radioactivity slightly but significantly. Dexamethasone also showed synergistic effects on the retention of 125I-radioactivity when it was daily injected together with 17 beta-oestradiol, progesterone or 5 alpha-dihydrotestosterone. The present results suggest that glucocorticoid may affect the processes involved in the uterine cell death, in a manner such as inhibiting the uterine cell death or delaying the removal of DNAs of dead cells from the uterus.

Animals↗

Increased extravascular lung water in patients with low pulmonary artery occlusion pressure after acute myocardial infarction.

OBJECTIVE: To evaluate the clinical characteristics of increased extravascular lung water (EVLW) in patients with low pulmonary artery occlusion pressure (PAOP) in the early phase of acute myocardial infarction. DESIGN: Consecutive sample for descriptions of the clinical features of medical disorders. SETTING: A general medicine group practice in a university hospital. PATIENTS: Sixteen patients with low PAOP (less than 18 mm Hg) on the initial measurement obtained within 12 hr of chest pain onset. MEASUREMENTS AND MAIN RESULTS: EVLW was measured by the thermal indocyanine green dye double-indicator dilution method. QRS score was obtained on hospital day 7 from the Selvester's QRS Scoring System. Eleven (69%) patients had increased EVLW greater than 7 mL/kg despite low PAOP. EVLW had no significant correlation with PAOP and the difference between plasma colloid osmotic pressure and PAOP, but did have a significant correlation with pulmonary vascular resistance index (r2 = .31, p less than .05), and QRS score (r2 = .45, p less than .005). CONCLUSIONS: Larger infarcts led to increased EVLW even with low PAOP, and the accumulation of increased EVLW around the small arterioles might have led to increased pulmonary vascular resistance.

Blood Pressure↗

Purification and characterization of a lecithin-dependent haemolysin from Escherichia coli transformed by a Vibrio parahaemolyticus gene.

Lecithin-dependent haemolysin (LDH) of Vibrio parahaemolyticus was purified from Escherichia coli C600 transformed with a plasmid (pHL591) ligated with a 1.5 kb DNA fragment of V. parahaemolyticus. The final preparation comprised two LDH proteins with different molecular masses which were immunologically cross-reactive and had the same enzymic activity. The LDH was a phospholipase hydrolysing both fatty acid esters of phospholipid, i.e. it hydrolysed phosphatidylcholine (PC) to lysophosphatidylcholine (LPC) and then LPC to glycerophosphorylcholine (GPC). From this point of view, LDH should be classified as a phospholipase B. Phospholipase B, however, does not usually show haemolytic activity, because the intermediate (LPC), which is the actual haemolytic agent, is immediately hydrolysed to the final product (GPC). On the other hand, LPC formed by LDH action was comparatively stable, because the rates of the two reactions catalysed by LDH, PC to LPC and LPC to GPC, are almost the same. This is the reason that LDH shows haemolytic activity. Therefore, LDH of V. parahaemolyticus is an atypical phospholipase to be designated as phospholipase A2/lysophospholipase.

Amino Acid Sequence↗

Protective effect by potassium chloride against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of oral potassium supplementation on the enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and the norepinephrine concentration in their gastric wall were investigated. The SHR and normotensive Wistar Kyoto rats (WKY) as controls were given a solution of the carcinogen for 25 weeks and then 1% KCl solution or tap water to drink. In Week 52, the incidence of gastric cancers and their number per rat and the norepinephrine concentration in the gastric wall were significantly greater in SHR than in WKY. Prolonged oral treatment of SHR with potassium significantly reduced the incidence of gastric cancers and their number per rat, as well as the blood pressure and the norepinephrine concentration in the antral portion of the gastric wall. These findings indicate that prolonged treatment with KCl attenuated the enhancement of gastric carcinogenesis by MNNG in SHR.

Animals↗

Pulmonary gas exchange in acute myocardial infarction with low pulmonary capillary wedge pressure.

To evaluate the clinical characteristic of pulmonary gas exchange in patients with low pulmonary capillary wedge pressure (PCW less than 18 mmHg) in the early phase of acute myocardial infarction, we investigated 48 patients admitted within 24h from the onset of chest pain. The alveolar-arterial oxygen tension difference (AaDO2) and arterial blood gas parameters were obtained while breathing room air on admission. The disturbance of pulmonary gas exchange, as revealed by the high value of AaDO2, existed without left ventricular dysfunction, and AaDO2 had no significant relationship with any of the hemodynamic parameters including the difference between plasma colloid osmotic pressure and PCW. Multiple regression analysis was performed using 9 variables related to pulmonary gas exchange, to identify those which were important. As a result, QRS score (p less than 0.01) and age (p less than 0.05) were identified as significant variables related to AaDO2. Thus, the disturbance of pulmonary gas exchange in patients with low PCW was caused by mechanisms other than left ventricular failure which may reflect the extent of ischemic myocardium.

Aged↗

Erythromycin reduces the severity of bronchial hyperresponsiveness in asthma.

It has been demonstrated that bronchial hyperresponsiveness is a characteristic feature of bronchial asthma, and airway inflammation plays an important role in bronchial hyperresponsiveness. Erythromycin is an antibiotic extensively used worldwide which is also reported to have anti-inflammatory action. This study was designed to clarify whether erythromycin could favorably alter bronchial responsiveness in patients with bronchial asthma. To estimate bronchial responsiveness, histamine challenge was performed in 23 patients with bronchial asthma (atopic type, 11; nonatopic type, 12). All patients were treated for ten weeks with erythromycin, 200 mg three times daily, orally. After ten weeks' treatment, PC20, an index of bronchial sensitivity, was increased significantly. There was no difference between atopic and nonatopic patients in the improvement of PC20. It was concluded that erythromycin reduces the severity of bronchial responsiveness in patients with bronchial asthma.

Adult↗

Purification and properties of a xylanase from Cellvibrio gilvus that hydrolyzes p-nitrophenyl cellooligosaccharides.

An enzyme component that hydrolyzes pNP-G2 but not CMC has been isolated from a culture broth of Cellvibrio gilvus by a multi-step procedure involving Butyl-Toyopearl, DEAE-Toyopearl, and CM-Toyopearl chromatographies. The purified enzyme gave a single protein band on native, SDS-, and IEF-PAGE. The enzyme had a molecular weight of 40,000, an isoelectric point of 5.0, an optimum pH of 6.5, and an optimum temperature of 55 degrees C. It was stable from pH 4.0 to 9.0 at 37 degrees C for 1 hr and below 50 degrees C for 30 min. It hydrolyzed agluconic bonds not only of pNP-G2 but also of pNP-G3, pNP-G4, and pNP-G5. Cellooligosaccharides with D.P. of 3 to 5 were not hydrolyzed at all. Instead, the enzyme hydrolyzed xylan 4 times as fast as pNP-G2. Both HgCl2 and p-chloromercuribenzoic acid inhibited the two activities completely. Xylan inhibited the hydrolysis of pNP-G2 competitively. From these results, the purified enzyme was considered to be a unique xylanase that hydrolyzed the agluconic bonds of pNP-Gn.

Amino Acid Sequence↗

[Primary myelofibrosis transforming into multiple subcutaneous monoblastoma--a case report].

A 83-year-old man was diagnosed with primary myelofibrosis based on the presence of leukoerythroblastosis, splenomegaly, chromosome 46 XY, a dry tap bone marrow aspiration and fibrosis on bone marrow biopsy, when he was admitted for herpes zoster in June 1987. He was admitted for a second time with multiple subcutaneous tumors over his entire body in July, 1989. He had mild splenomegaly, but no hepatomegaly nor lymphadenopathy. Laboratory tests were as follows: RBC 214 x 10(4)/microliters, Hb 5.1 g/dl, Ht 17.7%, WBC 3,200/microliters with leukoerythroblastosis, platelets 11.6 x 10(4)/microliters, s-lysozyme 251 micrograms/ml, u-lysozyme 770 micrograms/ml, NAP ratio 98%, score 278. Bone marrow aspiration resulted in a dry tap. Bone marrow biopsy showed marked fibrosis. Histologic examination of subcutaneous tumor biopsy specimens revealed a diffuse infiltration of monocytes with flexuous nuclei. These cells were positive for alpha-naphtyl butyrate esterase stain, and negative for peroxidase, alpha-naphtol ASD chloroacetate esterase stain and platelet glycoprotein IIb/IIIa stain (APAAP). Ultrastructurally, these cells were mostly monocytes and promonocytes, while phenotypically, CD11b, CD13, CD14, CD33 and HLA-DR were positive. These date indicated that the subcutaneous tumors originated from monocytes.

Aged↗