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Biomedical subjects

R Kato

Publications and source records attributed to R Kato.

At least 181 records · Page 10Linked to original sources
PubMed1996

Guidance with real-time CT fluoroscopy: early clinical experience.

A recently developed real-time computed tomography (CT) fluoroscopy system, which provides effective real-time reconstruction and display of CT images, was used to monitor nonvascular interventional procedures performed in 57 patients. Biopsy of thoracic lesions (n = 38), biopsy or drainage of pelvic lesions (n = 6), drainage or aspiration of intracranial hematomas (n = 9), and other procedures (n = 4) were performed. CT fluoroscopy successfully depicted the entire procedure in all patients. In thoracic lesions, a mean 1.3 passes was necessary to gain access to the lesion. Sufficient cytologic samples were obtained in 32 of 33 pulmonary lesions with a mean diameter of 26 mm.

Adult↗
PubMed1996

Radiation dosimetry at CT fluoroscopy: physician's hand dose and development of needle holders.

The radiation dose to physicians' hands without and with use of needle holders was determined at 10 computed tomography (CT) fluoroscopy-guided transthoracic needle biopsies. As measured with ionization chambers (tube voltage, 80 kVp; tube current, 30 mA), the mean absorbed dose rate without and with holders was 1.14 mGy/sec +/- 0.02 (standard deviation) and 0.019 mGy/sec +/- 0.001, respectively. The mean duration of CT fluoroscopy was 59 seconds in 10 biopsies performed with a holder and 82 seconds in 10 biopsies performed without a holder (difference not statistically significant). The needle holders did not cause any artifacts that interfered with the biopsy procedure.

Biopsy, Needle↗
PubMed1996

Inhibitory effect of TMK688 on skin tumor initiation caused by 7,12-dimethylbenz[a]anthracene in relation to inhibition of aryl hydrocarbon hydroxylase activity and Cyp1a1 mRNA induction.

Oral administration of TMK688 (1-([5'-(3"-methoxy-4"-ethoxycarbonyloxyphenyl)-2',4'-pentadien oyl] aminoethyl)-4-diphenylmethoxypiperidine: 30 mg/kg) at 6 h and 30 min prior to and at 30 min after a single topical application of 7,12-dimethylbenz[a]anthracene (DMBA) to dorsal skins of mice reduced both tumor incidence and number of tumors per mouse in the DMBA-initiated and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage mouse skin carcinogenesis. TMK688 and its active metabolite TMK777 (1-([5'-(3"-methoxy-4"- hydroxyphenyl)-2',4'-pentadienoyl]-aminoethyl)-4-diphenylmethox y piperidine) inhibited 3-methylchol-anthrene (MC)-induced epidermal aryl hydrocarbon hydroxylase (AHH) activity in a concentration-dependent manner. IC50 of TMK688 and TMK777 was 0.18 and 0.01 mumol/l, respectively. Oral administration of TMK688 (30 mg/kg) almost completely suppressed Cyp1a1 mRNA levels in mouse epidermis induced by a topical application of MC (40 mg/kg) or benzo[a]pyrene (200 nmol) to mouse skin. Oral administration of TMK688 (30 mg/kg) also almost completely inhibited induction of epidermal AHH activity caused by a topical application of MC. These results indicate that oral administration of TMK688 inhibited DMBA-caused skin tumor initiation at least in part by inhibiting Cyp1a1 mRNA induction and epidermal AHH activity.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Nitric oxide in vascular remodeling.

Vascular remodeling is a series of structural changes in blood vessels. Therefore, it may be conceivable that any humoral factors and physical forces acting on the vascular wall are involved in the remodeling processes. Cells in the vascular wall respond to the humoral and physical factors and may induce extracellular matrix, cell adhesion molecules and other humoral factors. They even grow so that cellular and noncellular components deviate from the normal population. We discuss the relationship among nitric oxide (NO), pressure and growth of smooth muscles. Decreased NO may be a consequence as well as a cause of high pressure. Similarly, high pressure is a cause as well as a consequence of decreased NO. Remodeling could be a consequence of both high pressure and decreased NO. Thus, vascular remodeling is a complex dynamic state, where any causes and results are influenced by each other. Interaction of NO and pressure is one such complexity.

Angiotensin II↗
PubMed1996

Efficacy of direct injection of ethanol into the myocardium to control aconitine-induced ventricular tachycardia in anesthetized dogs.

The effect of injecting ethanol directly into the myocardium to control aconitine-induced ventricular tachycardia (VT) was evaluated in anesthetized dogs. In 17 dogs, VT was induced by injecting aconitine (1.0 microgram, median dose) directly into the epicardium. After inducing persistent VT for up to 3 min, 0.6 ml (median volume) of 96% ethanol was injected into the same epicardial region. Regular sinus rhythm reappeared in 15 dogs with no change in systolic blood pressure; the other 2 dogs died of ventricular fibrillation (VF). In another 13 dogs, VT was induced by injecting aconitine directly into the endocardium using a Variocath needle catheter. After persistent VT for up to 3 min, a regular sinus rhythm was restored in 7 dogs by injecting 2.0 ml (median volume) of 96% ethanol; the remaining 6 dogs died of VF. Histology showed no transmural necrosis and the subendocardial necrotic areas were essentially the same in the dogs that recovered from VT as in those that died. There was no statistically significant relationship between doses of ethanol and VT duration. These preliminary results suggest that the injection of ethanol into the myocardium may efficiently terminate VT when other techniques fail.

Aconitine↗
PubMed1996

A case of myocarditis associated with IDDM.

We report a case of diabetic ketoacidosis (DKA) complicated by acute myocarditis, which was confirmed by cardiac biopsy. A 26-year-old man was hospitalized with severe DKA. On admission, nonspecific ST-T change was noted on the electrocardiogram (ECG). The patient's levels of creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase were slightly elevated, but he did not complain of chest discomfort or symptoms of heart disease. On the first day after admission, ST-T elevation was noted on ECG during treatment of DKA. By cardiac angiography and cardiac biopsy, coronary heart disease was ruled out and postmyocarditic change was histologically confirmed. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient suffered from viral-induced myocarditis and consequent development of IDDM. This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus.

Adult↗
PubMed1996

Prevention of cerebrovasospasm following subarachnoid hemorrhage in rabbits by the platelet-activating factor antagonist, E5880.

Recently, an important role of platelet-activating factor (PAF), an inflammation mediator, has been demonstrated in the genesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). In the current study, the authors examined whether intravenous administration of the novel PAF antagonist, E5880, can prevent vasospasm following SAH in rabbits. A vasospasm model was produced in three groups of rabbits using two subarachnoid injections of autologous arterial blood, followed by intravenous administration of distilled water (control), a low dose of E5880 (0.1 mg/kg in distilled water), or a high dose of E5880 (0.5 mg/kg in distilled water). Neurological deterioration was largely prevented in the rabbits that received E5880. Basilar artery constriction was also reduced by both doses of E5880. Histological examination at autopsy predominantly showed ischemic changes in the brain. Animals in each E5880-treated group exhibited ischemic changes less frequently than those in the control group. Plasma thromboxane B2 concentrations were reduced in rabbits treated with E5880. Platelet-activating factor was immunolocalized in the intima and media of the basilar artery in the control group. The PAF immunoreactivity demonstrated in the basilar artery was decreased in the E5880 groups in a dose-dependent manner. Thus, this study provides evidence that PAF may play a role in the pathogenesis of vasospasm after SAH and that intravenous administration of E5880 is a promising approach in preventing vasospasm.

Animals↗
PubMed1996

[Reconstruction of chest wall defects with autogenous ribs grafts].

Three methods of chest wall reconstruction using autogenous rib grafts were reported. Fresh non-vascularized autogenous rib graft, vascularized autogenous ribs with muscle-flap, and pasteurized autogenous rib grafts were the materials used in these techniques. They are less convenient than those with artificial materials but afterwards physiologically more natural chest wall will be reconstructed. The third method (pasteurized rib graft) was applied to 22-year-old female with large recurrent desmoid tumor. Six resected ribs were heated in the saline at 60 degrees C for 30 min. and three of them were returned to the former position. Though tumor cells and bacteria are killed under this condition, these heated bone can be revascularized and replaced by normal bone as early as fresh non-vascularized rib graft.

Adult↗
PubMed1995

Dopamine release in the medial preoptic area during male copulatory behavior in rats.

In vivo microdialysis was employed to measure the extracellular concentrations of dopamine (DA) in the medial preoptic area (MPOA) of rats during male sexual activity to look for a correlation with sexual activity. During copulation, the concentration of DA in the MPOA was significantly increased. A significant difference was detected in changes of DA between copulators and non-copulators. These findings were consistent with the assertion that DA neuron activity in the MPOA facilities male copulatory behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Suppression of clofibrate-induction of peroxisomal and microsomal fatty acid-oxidizing enzymes by growth hormone and thyroid hormone in primary cultures of rat hepatocytes.

Using primary cultures of rat hepatocytes on a matri-gel, effects of peroxisome proliferator and omega-hydroxydodecanoic acid on cellular levels of acyl-CoA oxidase and CYP4A have been studied to determine the hormonal influence in serum-free media. Peroxisomal acyl-CoA oxidation, microsomal CYP4A content and laurate omega-hydroxylation were increased in rat hepatocytes by the addition of 100 microM clofibrate or Wy14,643 for two days. omega-Hydroxydodecanoic acid (100 microM) also increased peroxisomal acyl-CoA oxidation, but had no clear effect on microsomal CYP4A level and laurate omega-hydroxylation. CYP4A-mediated laurate omega-hydroxylation in hepatocytes was suppressed by the addition of pituitary growth hormone (0.05 mU/ml), but was not altered by the addition of triiodothyronine (30 nM). In contrast, clofibrate-mediated induction of acyl-CoA oxidase activity was decreased by the addition of either one of the hormones in hepatocytes. Suppression by those hormones was also observed with omega-hydroxydodecanoic acid-mediated induction of acyl-CoA oxidase activity. These results indicate the possibility that GH and T3 exert the suppressive effects on peroxisomal acyl-CoA oxidation through plural mechanisms with and without the alteration of CYP4A levels in livers.

Acyl-CoA Oxidase↗
PubMed1995

Properties of omega conotoxin MVIIC receptors associated with alpha 1A calcium channel subunits in rat brain.

Solubilized 125I-omega conotoxin MVIIC receptors from rat cerebellum were immunoprecipitated by antibodies directed against the calcium channel alpha 1A subunit. Anti-alpha 1A antibodies recognized a 240-220, 180 and 160 kDa proteins in immunoblots of cerebellar membranes. Disuccinimidyl suberate cross-linked 125I-omega conotoxin MVIIC to an alpha 2 delta-like 200-180 kDa subunit, which migrated at 150-140 kDa after disulfide reduction. These observations are consistent with a heteromeric structure in which high affinity omega conotoxin MVIIC binding sites formed by alpha 1A subunits are located in close proximity to peripheral alpha 2 subunits.

Affinity Labels↗
PubMed1995

A new cytochrome P450 form belonging to the CYP2D in dog liver microsomes: purification, cDNA cloning, and enzyme characterization.

A new form of cytochrome P450 (P450 DUT2) was purified from untreated male dog liver microsomes. The final preparation (a specific content of 19.1 nmol P450/mg protein) showed a single band with an apparent monomeric molecular weight of 50,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, but was further separated into two apoproteins (P450 DUT2a and P450 DUT2b) by reverse-phase HPLC. Both proteins had identical NH2-terminal amino acid sequences, but the first three amino acids of P450 DUT2b were truncated in P450 DUT2a. Purified P450 DUT2 showed 5 to 18 times higher catalytic activities than did hepatic microsomes toward desipramine, metoprolol, and dextromethorphan. These activities in dog liver microsomes were strongly inhibited by anti-P450 DUT2-IgG. A 1.7-kilobase pair cDNA (cDUT2) encoding a male dog liver P450 of 500 amino acid residues (molecular weight 56,400) was isolated and sequenced. The first 35 NH2-terminal amino acid sequence of P450 DUT2b coincided with the deduced amino acid sequence of cDUT2 at 2-36. The deduced total amino acid sequence of cDUT2 shared high similarity with the reported 2D forms (with 2D6, 74.6%; 2D14, 75.4%; 2D1, 65.4%; and 2D9, 63.6%). Moreover, the expressed P450 DUT2 in COS-7 cells had catalytic activities similar to those of purified P450 DUT2. Therefore, this paper is the first report about dog CYP2D. Furthermore, Northern and Western blot analyses indicated that the expressed levels of mRNA and protein were almost equal between male and female dogs. Western blot analysis suggested that P450 DUT2 is a constitutive and major (approximately 20% of the total P450) form, indicating that the 2D subfamily P450 in dog liver is quite unique from CYP2D members of other species.

Amino Acid Sequence↗
PubMed1995

Transcriptional elements directing a liver-specific expression of P450/6 beta A (CYP3A2) gene-encoding testosterone 6 beta-hydroxylase.

The P450/6 beta A (CYP3A2) gene encoding a testosterone 6 beta-hydroxylase is expressed predominantly in liver and induced by the treatment of rats with various compounds. To understand the mechanism of the basal transcriptional activation of the CYP3A2 gene, the cis-acting elements in the proximal promoter region (-165 to -73) of the CYP3A2 gene were identified in this study. Nuclear extract from rat livers interacted with three sites, 6 beta A-A (-106 to -87), 6 beta A-B (-140 to -119) and 6 beta A-C (-163 to -145). These sites were detectable by DNase I footprinting and gel mobility shift assays and found to share nucleotide sequence similarity with each other (T(A/C)(A/C)N(A/G)AAG(G/T)(C/T)CA). Direct repeats of AGTTCA (-134 to -120) and AG(G/C)TCA (-162 to -148) are also detected in 6 beta A-B and 6 beta A-C sites, respectively. To elucidate the relationship of these sites with basal transcriptional activation of the CYP3A2 gene, varying lengths of the proximal promoter region (-164 to +41) fused to a CAT reporter gene were transfected in human hepatoma (HepG2) and mouse adrenal tumor (Y-1) cells. The relative level of CAT activity in HepG2 cells was slightly increased by the deletion of the 5'-portion from -164 to -111 bp, but was reduced to 14% of the control (the construct including from -110 to +41) by the deletion from -110 to -81 including the 6 beta A-A site. On the other hand, these deletions have no clear effect on the level of the activity in Y-1 cells. Substitution mutations at two nucleotides in the 6 beta A-A site resulted in the reduction of CAT activity in HepG2 cells to 12% of the activity in the wild-type construct. The interaction of an oligonucleotide corresponding to the 6 beta A-A site (-106 to -87) with liver nuclear factors was completely inhibited by the addition of a typical oligonucleotide for hepatocyte nuclear factor-4 (HNF-4) binding site (F. M. Sladek, W. Zhong, E. Lai, and J. E. Darnell, Jr., 1990, Genes Dev. 4, 2353-2365) but not of oligonucleotides corresponding to 6 beta A-B or 6 beta A-C sites. These results suggest an essential role of the binding of HNF-4 and/or HNF-4-related nuclear factors to the 6 beta A-A site on the basal transcriptional activation of the CYP3A2 gene in liver cells.

Animals↗