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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 937 records · Page 52Linked to original sources

Quantitation of tubotympanal mucociliary clearance in otitis media with effusion.

In an attempt to analyze the tubotympanal mucociliary function in otitis media with effusion (OME), human serum albumin labeled with technetium 99m was instilled into 36 ears with effusion and 16 without. The clearance function of the tubotympanum was measured quantitatively. The viscoelasticity of the effusions was measured and was compared with the clearance rate. The clearance rate was significantly lower in ears with effusion than in those without. A significant negative correlation was observed between clearance rate and dynamic viscosity at dynamic viscosities above 2 poise. It is concluded that ears with effusion have significantly lower mucociliary clearance than those without, and that the viscosity of the effusions plays an important role in the mucociliary dysfunction in OME.

Adolescent↗

Influences of stress on gastric alkaline secretion in rats.

Influences of restraint plus water-immersion stress on gastric alkaline response and mucosal blood flow were investigated in the rat. Under normal conditions, the stomach secreted alkali at the rate of approximately 1 microEq/15 min in the presence of omeprazole (60 mg/kg i.p.) and responded to mucosal acidification (1000 mM HCI for 10 min) by a significant rise of output (approximately 2.5 microEq/15 min), and the latter process was significantly blocked by indomethacin (5 mg/kg s.c.), quinacrine (100 mg/kg s.c.) and vasopressin (10 unit/kg/hr i.v.). Restraint alone decreased basal rates of HCO3- secretion but had no effect on acid-induced HCO3- output. Additional water-immersion stress further reduced alkaline secretion, totally abolished the increased HCO3- response to acid and significantly suppressed the increase of HCO3- output caused by 16,16-dimethyl prostaglandin E2 (3-30 micrograms/kg s.c.). During restraint stress mucosal blood flow was reduced only by 30% but after exposure to additional water-immersion, it further decreased to about 25% of normal values. Both indomethacin and quinacrine had no effect on mucosal blood flow, whereas vasopressin markedly reduced mucosal blood flow by about 80%. These results suggest that stress not only reduced basal rates of alkaline secretion in the stomach but also impaired the mucosal ability to increase HCO3- output in response to acid. These secretory disorders caused by stress may be attributed to both a decrease of mucosal blood flow and prostaglandin deficiency in the mucosa.

Animals↗

A cDNA fragment of hepatitis C virus isolated from an implicated donor of post-transfusion non-A, non-B hepatitis in Japan.

Recently, a cDNA from the hepatitis C virus (HCV) RNA genome has been isolated in the USA from a chronically infected chimpanzee. In order to isolate HCV cDNA derived from human material, RNA was extracted from plasma of a Japanese blood donor implicated in post-transfusion non-A, non-B hepatitis and HCV cDNA was synthesized and amplified by the PCR method using HCV-specific oligonucleotide primers. The cDNA fragment, 583 nucleotides long, showed 79.8% homology at the nucleotide level and 92.2% homology at the amino acid level compared with the prototype HCV cDNA. These results provides further evidence to show that HCV is closely associated with the development of post transfusion non-A, non-B hepatitis.

Amino Acid Sequence↗

[Cytological and histological effects of regional hyperthermia and radiation in cancer of the uterine cervix].

Hyperthermia is known to produce tumor-specific effect. Its combination with radiotherapy has been found to enhance antitumor effect and hyperthermia is a new modality of cancer treatment. Here, we report a cytological and histopathological study of the effects of hyperthermia on uterine cervical cancer. Our subject cases were 63 patients with cervical cancer (squamous cell carcinoma). Thirteen cases were treated with hyperthermia. Of these, the clinical stage was I b in 2, stage II in 10, stage III in 1. Before radical operation, external irradiation was given at 40Gy. with Lineac. During this period, the lesion was treated with hyperthermia at 42-45 degrees C for 30-60 min. with a 13.56 MHz RF capacitive heating system "Endoradiotherm 100A" (Kureha Chemical Industry CO. Ltd.) and an intraluminal applicator designed for uterine cervix. The control cases received radiotherapy alone before radical operation. There were 15 cases in Stage I b, 19 in stage II, and 16 in stage III. After the completion of radiotherapy, radical hysterectomy was performed in all cases. The effects of irradiation on the lesion were compared cytologically and histologically for different doses. The evaluation of the irradiation damage in cancer cells in the cytological study was based on findings such as intracytoplasmic vacuolation, the formation of giant nuclei, intranuclear vacuolation and formation of polynuclei. The degree of irradiation damage was classified into 5 grades from Do (little irradiation effect) to Dx (no viable cancer cells remaining), and the irradiation effect in the histopathological study was classified in to 8 grades from Grade 0 to Grade IVC according the Oboshi and Shimosato's classification. Cytological changes at 10Gy. were rated as D3 (relatively extensive irradiation damage in cancer cells) in 38.5% of the hyperthermia group, as compared to about 20% in the control groups. The cases rated Grade II B histologically made up 38.5% of the hyperthermia group: this grade was about 10% in the control groups. This suggests that radiation was more effective in the hyperthermia group than in the control groups, as was also suggested by the cytological results. With irradiation at 30Gy., cytological changes were rated as Dx in 61.5% of the hyperthermia group, as compared to 25.0-26.7% of the control groups. Histological results were Grade III, with only cancer cells regarded as non-viable observed, in 38.5% of the hyperthermia group and Grade IV, with no cancer cells, in another 23.1%. In the control groups, there were no cases with Grade IV, and those with Grade III totalled 12.5-26.7%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Quantitative determination of aqueous-phase ozone by chemiluminescence using indigo-5,5'-disulfonate.

Indigo-5,5'-disulfonate (IDS) was found to be an efficient reagent for the determination of ozone by chemiluminescence (CL); hence it was applied to the continuous measurements of dissolved ozone (O3(aq]. The optimum reagent composition was determined as 10 mg L-1 IDS plus 2 mM phosphate (pH 7.2). The CL intensity was proportional to the O3(aq) concentration in the range of 0.025-410 ng mL-1. The detection limit was 0.006 ng mL-1, which is 3 orders of magnitude lower than that obtained by spectrophotometry using IDS as reported previously. The reduction of interferences from aldehydes and hydrogen peroxide was attempted. Furthermore, the mechanism of the CL was discussed from CL and fluorescence spectra measured.

Chemical Phenomena↗

Role of renal kallikrein in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure.

We studied urinary excretion of active and inactive kallikrein every day for 3 weeks in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) subjected to 5/6 nephrectomy (5/6), 1/2-nephrectomy (1/2) or sham-operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). In the SHR group, blood pressure was significantly elevated in 5/6-animals as compared with 1/2 or sham, whereas in the WKY group blood pressure was not changed after either operation. Urinary active and total kallikrein excretion were decreased in 5/6-SHR to 34% and 59%, respectively, as compared with values of sham-SHR, and in 1/2-SHR to 70% and 70%, respectively. Similarly, they were also decreased in 5/6-WKY to 36% and 55%, respectively, as compared with values of sham-WKY. In 1/2-WKY urinary active kallikrein excretion was decreased to 88% as compared with the value of sham-WKY, but urinary total kallikrein excretion was not different from that of sham-WKY. Thus, the suppressed renal kallikrein activity due to reduced renal mass was not associated with any significant change in blood pressure in WKY, although it induced an elevation of blood pressure in SHR. These results indicate that the decreased production of renal active kallikrein may not play a significant role in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure. In addition, it is suggested that the elevation of blood pressure in this model of SHR may be due to other factors than renal kallikrein.

Animals↗

Role of renal kallikrein in the increased fractional sodium excretion in the rat remnant kidney model of chronic renal failure.

To assess the potential role of renal kallikrein-kinin system in enhancing sodium excretion per nephron in chronic renal failure, we studied urinary excretion of active and inactive kallikrein for 3 weeks in Wistar-Kyoto rats subjected to 5/6 nephrectomy (5/6), 1/2 nephrectomy (1/2) or sham operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Fractional sodium excretion was significantly increased in 5/6-rats as compared with 1/2- or sham-rats. On the contrary, urinary active kallikrein excretion per nephron was not different in the three models whereas a significant rise in urinary inactive kallikrein excretion per nephron was found in 5/6-rats as compared with 1/2- or sham-rats. Urinary total kallikrein excretion per nephron was significantly increased in 5/6-rats as compared with sham-rats. In addition, no correlation was found between fractional sodium excretion and urinary active kallikrein excretion corrected for creatinine clearance (Ccr) in 5/6-rats. These results indicate that decreased excretion of renal active kallikrein may not play a significant role in the increased sodium excretion per nephron in the rat remnant kidney model of chronic renal failure. Furthermore, it is suggested that in this model of rat there might be impaired production of renal active kallikrein although its exact mechanism remains to be determined.

Animals↗

PGE2 synthesis in cultured renal papillary collecting tubule cells from young and aged spontaneously hypertensive rats.

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the capacity of PGE2 synthesis in cultured renal papillary collecting tubule cells from young (4-week-old) and aged (16-week-old) SHR and control Wistar-Kyoto rats (WKY). Basal levels of PGE2 synthesis were lower in young SHR cells than in WKY cells (p less than 0.001). Arachidonic acid-stimulated PGE2 synthesis, however, had a slight tendency to be higher in SHR cells than in WKY cells. Bradykinin- and A23187-stimulated PGE2 synthesis were similar in both strains. Basal levels of cyclic AMP were also lower in young SHR cells than in WKY cells (p less than 0.001), but the cAMP response to exogenous PGE2 was equal between the strains. In papillary collecting tubule cells from aged rats, basal levels of PGE2 and cyclic AMP as corrected for cellular protein were significantly lower than those in young rats, but there was no difference between the strains. Urinary excretion of PGE2 and thromboxane B2 was equal in aged SHR and WKY. These results suggest that papillary collecting tubule of young SHR and WKY may differ in the metabolism of PGE2 and cyclic AMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.

1-Methyl-3-isobutylxanthine↗

Elevated plasma prostaglandin E2 levels in schizophrenia.

Plasma levels of prostaglandin E2 (PGE2) were determined with radioimmunoassay in 40 DSM-III schizophrenics, 15 patients with other mental disorders, and 23 normal controls. The mean value of plasma immunoreactivity of PGE2 was significantly higher in the schizophrenic patients than in the normal controls. Schizophrenic patients with high plasma PGE2 levels had more guilt feelings and hallucinatory behavior on BPRS, relatively successful heterosexual relations, and a higher incidence of birth complications.

Adolescent↗

Effects of mepirizole and basic antiinflammatory drugs on HCl-ethanol-induced gastric lesions in rats.

Mepirozole, a basic antiinflammatory drug and duodenal ulcerogen in laboratory animals, macroscopically protected the gastric mucosa of rats from HCl-ethanol-induced damage in a dose-dependent manner. These effects were evident when the agent was given orally, intraperitoneally, or subcutaneously at 3 or 10 mg/kg 0.5 hr before HCl-ethanol administration. Histologically, the surface epithelial and pit cells were not protected by mepirizole, but most of the mucosal cells located in the deeper portions were well preserved. Gastric acid secretion in the pylorus-ligated or acute fistula preparation was not affected by 10 mg/kg of mepirizole. Gastric motility determined by a balloon method was dose-dependently inhibited by the agent. Mepirizole protection was significantly reduced by pretreatment with subcutaneous indomethacin (5 mg/kg) and N-ethylmaleimide (10 mg/kg). The gastric motility inhibited by mepirizole was not reversed by indomethacin and N-ethylmaleimide treatment. These results suggest that the mechanism underlying mepirizole protection relates to both endogenous prostaglandins and sulfhydryl compounds present in the gastric mucosa, but does not relate to an inhibition of gastric motility. Dulcerozine and other basic antiinflammatory drugs (tiaramide, tinoridine, and benzydamine) given either orally or intraperitoneally at 10-100 mg/kg also dose-dependently prevented the development of HCl-ethanol-induced lesions. Mepirizole and other basic antiinflammatory drugs are cytoprotective in the rat stomach.

Animals↗

Role of prostaglandin deficiency in pathogenetic mechanism of gastric lesions induced by indomethacin in rats.

The present study was undertaken in rats using 2-deoxy-D-glucose (2DG) as a stimulator of gastric motility and a low dose of indomethacin as a prostaglandin (PG) synthesis inhibitor to investigate the roles of gastric motility and PG deficiency in the pathogenesis of indomethacin-induced gastric lesions. Subcutaneously administered indomethacin at 5 mg/kg did not induce any visible damage in the mucosa within 4 hr, but at 25 mg/kg produced linear hemorrhagic lesions along the long axis of the stomach. 2DG (100 mg/kg/hr), given intravenously, produced linear nonhemorrhagic lesions along the mucosal folds and, in the presence of 5 mg/kg of indomethacin, caused severe hemorrhagic lesions in the same areas of the stomach. Gastric motility was markedly enhanced by both indomethacin (25 mg/kg) and 2DG, while acid output and mucosal blood flow were increased only by the latter. Mucosal PGE2 levels were significantly reduced by indomethacin (25 mg/kg) but not by 2DG. Indomethacin at 5 mg/kg alone had no or little effect on any parameter except PG levels, which were reduced to similar degrees as caused by 25 mg/kg of the agent. Time-course development of the lesions was closely associated with those changes in gastric motility after administration of indomethacin (25 mg/kg) and 2DG. These results suggest that the enhanced gastric motility is, by itself, sufficient to induce damage (nonhemorrhagic) in the mucosa and that a PG deficiency alone does not induce any damage but is required for further extension to hemorrhagic lesions of nonhemorrhagic ones that are initially induced by enhanced gastric motility.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗