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Biomedical subjects

S Kikuchi

Publications and source records attributed to S Kikuchi.

At least 361 records · Page 20Linked to original sources

[CT evaluation of the anterior epitympanic recess--comparison among non-inflammatory ear, chronic otitis media with central perforation and cholesteatoma].

The structures of the anterior epitympanic recess and its surrounding tissues were examined among non-inflammatory ear, chronic otitis media with central perforation and cholesteatoma, using axial scans of high resolution computed tomography. The length and width of the recess, as well as the number of the slices where the cog was determined, had no significant differences among them. Thus, the bony structure of the recess was considered to be seldom influenced by inflammatory processes. In the non-inflammatory ear, the degree of pneumatization around the recess was similar to that of the petrous apex cells and lower than that of the mastoid cells. In the chronic otitis media with central perforation and cholesteatoma, the pneumatization of the whole temporal bones was suppressed and the tendency was also found that the cells around the recess were less pneumatized than the mastoid cells. When cholesteatoma invaded into the anterior epitympanic recess, the destruction of the bony protrusion of the lateral wall between the recess and the epitympanum was recognized, as well as the disappearance of the cog. The bony protrusion was considered to be an inferior extension of the cog toward the anterior tympanic spine.

Cholesteatoma↗

[Reevaluation of the diagnosis of placenta previa in midtrimester by means of transabdominal, transrectal and transvaginal ultrasonography].

The incidence of placenta previa in mid-pregnancy diagnosed by ultrasonography is abnormally high in comparison with its incidence during labor. The cause of this discrepancy has not been fully elucidated. Detection of the cervix is fundamental to the diagnosis of placenta previa. In the present study, the detection rates for three methods, abdominal, rectal and vaginal scanning were compared and the time course of mid-pregnancy placenta previa was traced. The cause of the above-mentioned discrepancy was thus elucidated. 1. Rate of cervix detection 1) In the 12-23 gestational week period, the cervix was successfully identified in 52.0-62.5% of cases by abdominal scanning, and in 85.7-87.5% by transrectal scanning. 2) The uterine isthmus was not identified by transabdominal scanning. 2. Changes in ultrasonographic findings with the passage of time 1) Transrectal scanning

Female↗

[Collins blood diluting reperfusion--an effective measure of controlled reperfusion for the heart hypothermically preserved for 24 hours in modified Collins solution].

Controlled reperfusion is assumed to provide an appropriate environment surrounding the ischemic cardiac tissue at the initial reperfusion phase. Hence, this procedure might play a key role in resuscitating the long term preserved hearts. This study was designed to assess the efficacy of the newly devised reperfusion method; namely Collins Blood Diluting Reperfusion (CBDR), for those hearts subjected to 24-hours cold (4 degrees C) storage in modified Collins (MC) solution. Coronary reperfusion is commenced with the MC solution, and the oxygenated blood is successively added to dilute this perfusate with gradual rewarming under controlled perfusion pressure. Initial reperfusate, therefore, is supposed to be a blood cardioplegia with low Ca2+ and high Mg2+ content. During this procedure, any difference in the ionic composition between the storage solution and the reperfusate is completely abolished and myocardium is free from hastiness of temperature elevation. Using an isolated isovolum contracting heart prepared with an ex vivo apparatus incorporating a support dog, each heart was reperfused by unmodified blood (Group I: n = 7) or CBDR method (Group II: n = 10) under equally controlled low perfusion pressure. There was no difference in the myocardial creatine phosphate level between the 2 groups. However, the adenosine triphosphate content, which had been depleted to 30% of the preischemic level during the 24-hour preservation period, was restored to 52.0% after CBDR procedure (p less than 0.01) and consequently to 57.9% of the control at 60 minutes after reperfusion. Group I showed a significantly lower repletion effect at this phase (41.2% control; p less than 0.05 versus group II).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

[Acquired coagulopathy caused by administration of parenteral broad-spectrum antibiotics].

Between October 1988 and May 1989, four cancer patients treated by broad-spectrum antibiotics developed a hemorrhagic diathesis induced by vitamin k (VK) deficiency. Activated partial thromboplastin time (APTT), prothrombin time (PT), factor II (FII) and protein induced by vitamin k absence of antagonist-II (PIVKA-II) were measured after administration of antibiotics and VK in all 4 patients. All these patients had been receiving intravenous hyperalimentation (IVH) and antibiotics for various infections. But all or them developed hemorrhagic diathesis within five days after the initiation of broad-spectrum cephem antibiotics (LMOX or CMNX). The abnormalities were 1) marked decrease of F II (6-18%), 2) prolongation of APTT (58.4-200 seconds), 3) prolongation of PT (7-21%), 4) marked increase of PIVKA-II (17-80 less than AU/ml). After being treated by intravenous administration of VK, hemorrhagic diathesis and abnormalities of coagulation tests except for PIVKA-II were corrected quickly in three evaluated patients. The measurement of PIVKA-II seemed to be useful to diagnose the hemorrhagic diathesis caused by VK deficiency in the patients during administration of antibiotics.

Aged↗

[Replacement of the aortic valve and ascending aorta for annuloaortic ectasia with severe tracheobronchial compression in an elderly patient].

A 74-year-old woman with severe tracheobronchial compression caused by annuloaortic ectasia was successfully operated upon. She was admitted to our hospital because of dyspnea with syncope and chest pain. Echocardiography and a computed tomographic scan of the chest showed annuloaortic ectasia. Broncho-fiberscopy found tracheo-bronchial stenosis caused by compression of an aneurysm of the ascending aorta. AVR and supracoronary graft replacement (separate graft/valve replacement) were performed because the coronary ostia were adjacent to the aortic annulus. Postoperatively compression of the airway subsided and dyspnea disappeared.

Aged↗

Effect of a thromboxane A2 synthetase inhibitor (OKY-046.HCl) on airway hyperresponsiveness in guinea pigs.

We studied the effect of (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate (OKY-046.HCl), a specific thromboxane (TX) A2 synthetase inhibitor, on airway hyperresponsiveness of guinea pigs. OKY-046.HCl (30-100 mg/kg, intraduodenally (i.d.) or orally (p.o.)) suppressed dose dependently the airway hyperresponsiveness to acetylcholine (ACh) induced by formyl-methionyl-leucyl-phenylalanine (FMLP), platelet activating factor (PAF) and repetitive antigen. OKY-046.HCl (100 mg/kg) also inhibited the increase in TXB2 in bronchoalveolar lavage fluid (BALF) induced by FMLP, PAF and antigen. Aspirin 10 or 30 mg/kg i.d. or p.o.) suppressed the airway hyperresponsiveness induced by FMLP and PAF but not by antigen. Azelastine (10 mg/kg i.d.) was ineffective on PAF- and antigen-induced airway hyperresponsiveness. TXA2 mimetic drugs caused airway hyperresponsiveness that was not inhibited by OKY-046.HCl (30 mg/kg i.v.). Furthermore, OKY-046.HCl showed no effect on propranolol- and physostigmine-induced airway hyperresponsiveness which did not accompany TXB2 generation in BALF. The number of eosinophils in BALF increased after FMLP exposure, an effect which was not inhibited by OKY-046.HCl. These results suggest that OKY-046.HCl inhibits airway hyperresponsiveness by suppressing TXA2 generation. We suggest that OKY-046.HCl will be a new antiasthmatic drug.

6-Ketoprostaglandin F1 alpha↗

Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone-10 in solution.

Kinetic study of the reaction between tocopheroxyl (vitamin E radical) and ubiquinol-10 (reduced ubiquinone, n = 10) has been performed. The rates of reaction of ubiquinol with alpha-tocopheroxyl 1 and seven kinds of alkyl substituted tocopheroxyl radicals 2-8 in solution have been determined spectrophotometrically, using a stopped-flow technique. The result shows that the rate constants decrease as the total electron-donating capacity of the alkyl substituents on the aromatic ring of tocopheroxyls increases. For the tocopheroxyls with two alkyl substituents at ortho positions (C-5 and C-7), the second-order rate constants, k1, obtained vary in the order of 10(2), and decrease predominantly, as the size of two ortho-alkyl groups (methyl, ethyl, isopropyl and tert-butyl) in tocopheroxyl increases. On the other hand, the reaction between tocopheroxyl and ubiquinone-10 (oxidized ubiquinone) has not been observed. The result indicates that ubiquinol-10 regenerates tocopherol by donating a hydrogen atom of the 1-OH and/or 4-OH group to the tocopheroxyl radical. For instance, the k1 values obtained for alpha-tocopheroxyl are 3.74 x 10(5) M-1.s-1 and 2.15 x 10(5) M-1.s-1 in benzene and ethanol solution at 25 degrees C, respectively. The above reaction rates, k1, obtained were compared with those of vitamin C with alpha-tocopheroxyl reported by Packer et al. (k2 = 1.55 x 10(6) M-1.s-1) and Scarpa et al. (k2 = 2 x 10(5) M-1.s-1), which is well known as a usual regeneration reaction of tocopheroxyl in biomembrane systems. The result suggests that ubiquinol-10 also regenerates the tocopheroxyl to tocopherol and prevents lipid peroxidation in various tissues and mitochondria.

Antioxidants↗

Effect of dextran sulfate on renal accumulation of gentamicin.

The effect of dextran sulfate of three molecular weights (1000, 5000, and 90,000) on the accumulation of gentamicin in rat kidney was investigated using a continuous infusion technique. During the infusions of both gentamicin and gentamicin-dextran sulfate mixtures, the gentamicin plasma concentration was maintained at 10 microgram/ml. The renal cortical accumulation of gentamicin was significantly lower when dextran sulfate (1000, 5000) was coadministered. The inhibition of cortical gentamicin accumulation increased with increasing dextran sulfate dose, and it was proportional to the amount of dextran sulfate excreted into the urine. Analysis by electrophoresis on cellulose acetate membrane indicated that gentamicin binds to dextran sulfate in rat urine. Therefore, gentamicin-dextran sulfate binding within the lumen of the proximal tubules may reduce the renal reabsorption and possibly the renal toxicity of gentamicin.

Animals↗

Blood screening for non-A, non-B hepatitis by hepatitis C virus antibody assay.

Hepatitis C virus (HCV) antibody was detected in 1499 donor sera by radioimmunoassay using an antigen expressed in yeast from a cDNA clone of the HCV genome. Eighteen samples over 4200 counts per minute (cpm) were considered to contain infectious HCV because these recipients developed typical posttransfusion non-A, non-B hepatitis after transfusion. The antibody-positive sera were all within the normal range of ALT levels. This assay system is thus useful for the screening for blood transfusion.

Adult↗

Hepatitis C virus infection is associated with the development of hepatocellular carcinoma.

A possible causative role for the recently discovered hepatitis C virus (HCV) in the development of hepatocellular carcinoma (HCC) was investigated by assay of sera from HCC patients in Japan for antibodies to a recombinant HCV antigen and to hepatitis B virus (HBV) antigens. Among the 253 HCC patients examined, 156 (61.7%) had no serum markers of either a previous or a current HBV infection (group I), 46 (18.2%) were negative for HBV surface antigen but positive for anti-HBV surface and/or anti-HBV core antibody, indicating the occurrence of a previous, transient HBV infection (group II), and 51 (20.2%) were chronically infected HBV carriers as evidenced by positivity for HBV surface antigen (group III). The prevalence of HCV antibody in group I (68.6%) and II (58.7%) patients was significantly higher than for group III (3.9%) or in 148 additional patients with other (non-HCC) cancers (10.1%) (P less than 0.01). Thus, there appears to be a strong association between HCV infection and the development of HCC, particularly in patients for which HBV infection cannot be implicated as a causative factor. The data also suggest an additional mode of transmission for HCV other than blood transfusion, since a history of blood transfusion was shown in only about 30% of the HCV antibody-positive HCC patients in groups I and II. A high prevalence of HCV antibody was also shown among patients with HCC whose disease was originally thought to be due to very high ethanol consumption.

Blood Transfusion↗

Detection of antibody against antigen expressed by molecularly cloned hepatitis C virus cDNA: application to diagnosis and blood screening for posttransfusion hepatitis.

A cDNA clone has been derived from the plasma of a chimpanzee with chronic non-A, non-B viral hepatitis (NANBH). We have assayed for antibodies reacting with the encoded antigen in sera from posttransfusion hepatitis patients (643 samples from 23 patients) and their corresponding donors collected during the past 10 years in Japan. The antibody was detected in 15 out of 17 (88.2%) posttransfusion NANBH (PT-NANBH) patients whose sera over time displayed multiple alanine aminotransferase (ALT) peaks. In general, the antibody was detected after several peaks of serum ALT elevations and, once detected, it persisted for years. In contrast to the patients of chronic hepatitis, the antibody was barely detected in patients with a single episode of ALT elevation (1 out of 6). Of the 15 well-defined cases of PT-NANBH that showed multiple ALT peaks and hepatitis C virus seroconversions, 11 (73.3%) were shown to be transfused with at least one unit of blood positive for the antibody. The retrospective analysis showed that all tested donor blood found to be positive for the antibody had been transfused to recipients who afterwards developed NANBH. These data strongly suggest that the cloned cDNA originated from an etiological agent of NANBH termed the hepatitis C virus. Furthermore, the present study demonstrates that had the screening been done with the anti-hepatitis C virus assay, 11 out of 17 (64.7%) cases of chronic PT-NANBH and 1 out of 6 (16.6%) acute PT-NANBH would have been prevented. The antibody assay thus can be used for diagnosis and blood screening for PT-NANBH.

Adult↗

[Anti-allergic effects of (E)-3-[p-(1H-imidazol-1-lylmethyl) phenyl]-2-propenoic acid (OKY-046), a specific thromboxane (TX) A2 synthetase inhibitor: effects on type I allergic reactions].

We studied the effects of OKY-046 on type I allergic reactions. OKY-046 (100 mg/kg) given orally suppressed antigen-induced bronchoconstriction and TXB2 generation in broncho alveolar lavage fluid in rats passively sensitized with anti-DNP-As monoclonal IgE. At the dose of 30 mg/kg given intraduodenally, it also inhibited antigen-induced bronchoconstriction in guinea pigs passively sensitized with anti DNP-As serum and actively sensitized with ovalbumin. However, aspirin (30 mg/kg) didn't suppressed them significantly. Azelastine (10 mg/kg) inhibited bronchoconstriction in passively sensitized rats and actively sensitized guinea pigs. In 48 hour homologous PCA reactions of rats and mice, oral administration of OKY-046 (300 mg/kg) and tranilast (100 mg/kg) suppressed the extravasated dye in the skin. OKY-046 decreased histamine release from passively sensitized rat peritoneal exudate cells. There was no effect of OKY-046 on SRS-A and leukotriene release from actively sensitized guinea pig lungs and passively sensitized rats. In conclusion, we think that OKY-046 should be an useful asthmatic drug or anti-allergic drug by oral administration.

Acrylates↗

[Anti-allergic effects of (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoic acid (OKY-046), a specific thromboxane (TX) A2 synthetase inhibitor: effect of OKY-046 on II-IV type allergic reactions].

We studied the effects of OKY-046 on types II, III and IV allergic reactions, as classified by Coombs and Gell. In Type II, OKY-046 at 30-100 mg/kg intraduodenally (i.d.) and at 1-30 mg/kg intravenously (i.v.) inhibited the bronchoconstriction in a dose-dependent manner after Forssman antigen injection. Aspirin (3 mg/kg, i.v.) also suppressed it. OKY-046 (30-100 mg/kg, i.d.) suppressed the increase of TXB2 level in the plasma in a dose-dependent manner. However, there was no effect of OKY-046 and aspirin on the decrease in complement activity (CH50), platelets and leukocytes. Additionally, OKY-046 (300 mg/kg, p.o.) prolonged the survival time following Forssman antigen injection. However, the immune hemolysis reaction was not prevented by OKY-046 (10(-6)-10(-3) M). FUT-175 protected against the Forssman shock at 1 mg/kg, i.v. and the in vitro immune hemolysis reaction at 10(-5) M. In Type III, OKY-046 (300 mg/kg, p.o.) significantly suppressed the direct passive Arthus reaction and immune complex nephritis in rats. There was no effect of OKY-046 on the delayed-type hypersensitive response to picryl chloride in mice. We think that OKY-046 should be a beneficial drug for the treatment of types II and III allergic reactions.

Acrylates↗

[Inhibitory effects of OKY-046.HCl, a selective thromboxane (TX) A2 synthetase inhibitor, on platelet activating factor (PAF)-induced airway hyperresponsiveness in guinea pigs].

We studied the inhibitory effects of OKY-046.HCl on PAF-induced airway hyperresponsiveness (AHR) in guinea pigs. 1) Inhalation of PAF (1 or 10 micrograms/ml) caused AHR to acetylcholine (ACh) aerosol and increased TXB2 generation in broncho-alveolar lavage fluid (BALF) at 30 min and 60 min, but the AHR and the TXB2 generation disappeared at 2 hr. OKY-046.HCl (100 mg/kg, intraduodenally) inhibited the AHR, which was accompanied by its inhibition of the TXB2 generation. However, no changes of 6-keto-PGF1 alpha in BALF were found. 2) There were no changes in the number of leukocytes; the activities of alkaline phosphatase, N-acetyl-beta-D-glucosaminidase, and lactate dehydrogenase; and the LTC4/D4/E4 in BALF. 3) In bronchus-lung preparations, PAF (1 microgram/min) also caused the AHR and increased TXB2 generation. OKY-046.HCl (100 micrograms/min) inhibited the AHR and TXB2 generation. 4) PAF (1 microgram/ml) evoked TXB2 generation in BALF from normal guinea pigs. OKY-046.HCl (10(-4)M) inhibited its increase. 5) Stable TXA2 (STA2, 1 ng/ml) inhalation also caused AHR to ACh at 30 min. STA2 (0.45 ng/min) also caused the AHR in bronchus-lung preparations. These results suggest that OKY-046.HCl can inhibit PAF-induced AHR by suppressing the generation of TXA2. We also supposed that TXA2 is released from lung parenchyma, airway epithelium and cell components in BALF.

Acrylates↗

Inhibitory action of OKY-O46.HCl, a specific TXA2 synthetase inhibitor, on platelet activating factor (PAF)-induced airway hyperresponsiveness of guinea pigs: role of TXA2 in development of PAF-induced nonspecific airway hyperresponsiveness.

We studied a role of TXA2 in the development of PAF-induced nonspecific airway hyperresponsiveness in guinea pigs using a TXA2 synthetase inhibitor (OKY-O46.HCl) and a stable TXA2 mimetic agent (STA2). Inhalation of PAF (1 microgram/ml) and STA2 (1 or 10 ng/ml) increased the airway response to acetylcholine (ACh), histamine, leukotriene D4 and electrical vagal stimulation. Intraduodenal administration (i.d.) of OKY-O46.HCl (100 mg/kg) inhibited PAF-induced airway hyperresponsiveness. However, OKY-046.HCl (30 mg/kg, i.v.) did not suppress STA2-induced airway hyperresponsiveness. Neither hexamethonium (1 mg/kg, i.v.) nor hemicholinium-3 (10 mg/kg, i.v.) prevented the increase in the airway response to ACh after inhalation of PAF and STA2. In the presence of atropine (0.5 mg/kg, i.p.), PAF-induced airway hyperresponsiveness to histamine did not change. OKY-046.HCl (100 mg/kg, i.d.) inhibited the increase in ACh (10(-8) M)-induced 45Ca uptake into the lung tissue from PAF-inhalated guinea pigs. Inhalation of STA2 increased the number (Bmax) of muscarinic and H1-histaminergic receptors in the lung tissue from guinea pigs, but no changes were found on beta-adrenoceptors. These results suggest that TXA2 should act on the smooth muscle cells or alter functions of muscarinic and H1-histaminergic receptors, except beta-adrenoceptors, and then increase the membrane permeability to extracellular Ca2+. We also assume that OKY-046.HCl can inhibit PAF-induced nonspecific airway hyperresponsiveness by suppressing the generation of TXA2.

Acrylates↗

Gallium-67 citrate uptake in experimental tumors and inflammatory lesions--an histo-autoradiographic correlation.

In a DAB-hepatoma organic tumor, Ga-67 accumulated markedly in the hepatocellular carcinoma with scant stroma but not in the cholangioma that was rich in connective tissue. No granulation tissue was formed around the tumor. In transplanted tumors (Ehrlich's tumor and Sarcoma 180), Ga-67 accumulated in the granulation tissue within the fibroblasts, leukocytes and capillaries surrounding the tumor, rather than in the tumor. In inflammatory lesions, Ga-67 uptake was similar in granulation tissue with large numbers of phagocytes, such as leukocytes and histiocytes, and capillaries. There was a very good correlation between the degree of Ga-67 uptake and of cellular infiltration and the proliferation of capillaries. Ga-67 uptake, both in inflammatory lesions and in transplanted tumors, was observed in the granulation tissue. This result implies that the mechanisms of Ga-67 uptake in tumor and inflammatory tissues are not the same, because Ga-67 accumulated in the DAB-hepatoma that had no inflammatory granulation tissue. This study indicates that a non-transplanted tumor is required to study Ga-67 accumulation in tumors, as different results may occur in tumors with and without inflammatory granulation tissue.

Animals↗