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Biomedical subjects

K Takada

Publications and source records attributed to K Takada.

At least 379 records · Page 21Linked to original sources
PubMed1995

An interactive consultation multimedia software for orthodontic patients.

Presentation of diagnosis and treatment planning for orthodontic problems by orthodontists is often a hurdle and a nuisance to most patients. The reasons are that it has much content which may be hard to understand without having expert knowledge related to the temporal change in dentofacial structures known as the growth, development and physiological aspects of masticatory apparatus. To complement this, we have developed an interactive consultation multimedia software for orthodontic patients. he design concept of the current software has three aspects. Firstly, since the software is operated by orthodontic patients themselves or by their parents, it enhances the operational feasibility. Secondly, it helps the patients choose the information in which they are interested. Thirdly, it emphasizes audio-visual understanding of orthodontic practice, including terminology. e used a hypertext machine with a 240MB hard disk drive, an 8MB RAM and a 13 inch color monitor. In developing the current software, we also used a video camera, a video color board, a microphone, and an image scanner together with an image recorder, a movie and sound data editing system, image scanning and editing, an image changer, a spread sheet and mathematical software. he current software consists of various multimedia such as images, sounds, characters, and biosignals. The "stack" of the software consists of three parts: a) "General Understanding of Occlusion" b) "Understanding Specific Types of Occlusion Exhibited by the Patient" c) "Orthodontic Terminology" When card A is selected the patient can choose either "Good Occlusion" or "Malocclusion." If "Malocclusion" is chosen, respective occlusal types are shown. The next card provides pathological conditions caused by respective malocclusion, e.g., gingivitis. After selecting card B which asks the patient, "What do your teeth look like?" the following buttons are provided: "Maxillary Protrusion," "Reversed Occlusion," "Crowding," "Open Bite," and "Spaced Arch." After selecting one of these, the card with an explanation of the respective malocclusion is shown according to the patient's physiological age. Finally, after card C is selected, a new card which has a list of orthodontic terminology is presented. Patients can search any term according to their choice to open a new card which gives a detailed explanation. e confirmed that the current consultation multimedia software can provide a comfortable environment to the patients and their families to learn where the orthodontic problems lie and how they could be solved.

Audiovisual Aids↗
PubMed1995

Rilmenidine prevents epinephrine-induced arrhythmias in halothane-anesthetized dogs.

Stimulation of central alpha 2-adrenoceptors has been known to prevent epinephrine-induced arrhythmias in halothane-anesthetized dogs. Because recent studies suggested that several physiological processes that were traditionally attributed to activation of alpha 2-adrenoceptors, such as hypotensive action, are mediated through imidazoline receptors (IRs), it may be likely that IRs are involved in the antiarrhythmic action. We investigated the hypotensive effect of rilmenidine, a selective IR agonist (1, 3, and 10 micrograms/kg i.v.), and the antiarrhythmic effects of the drug on epinephrine-induced arrhythmias during halothane anesthesia in dogs. Although the hypotensive effect of rilmenidine was not remarkable in the dose range we tested, rilmenidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia, achieving statistical significance at 10 micrograms/kg, the highest dose we examined. These results suggest that rilmenidine prevents epinephrine-induced arrhythmias during halothane anesthesia and that this effect is more potent than its hypotensive action.

Adrenergic alpha-Agonists↗
PubMed1995

[Hepatic lesions in F344 rats treated orally with beta-cyclodextrin for 13 weeks].

A 13-week oral toxicity study of beta-cyclodextrin was carried out in F344 rats at the dose levels of 10, 5, 2.5, 1.25, 0.6 and 0% in powdered diet. Each group consisted of 10 males and 10 females. All animals survived at the end of the experiment, while a slight decrease in body-weight gain was observed in males of the 10%- and 5%-groups. Dose-dependent increases in serum levels of GOT, GPT and alkaline phosphatase were observed in treated animals of both sexes, and increases in serum levels of urea nitrogen and relative liver weights in treated males. Histopathologically, a dose-dependent increase in the severity of inflammatory cell infiltration was seen in the liver of treated animals, focal hepatocellular necrosis being detected in both sexes of the 10%-group and females of the 5%-group. These findings indicate that beta-cyclodextrin causes hepatocellular injury to rats when it is orally administered.

Alanine Transaminase↗
PubMed1995

[A case of corticobasal degeneration--the usefulness of surface anatomy scatomy scanning image by MRI].

We experienced usefulness of surface anatomy scanning (SAS) image by weight-summation technique using MRI in corticobasal degeneration. The patient was a 73-year-old right-handed woman who had progressive dysarthria and clumsiness of the right hand. Neurological examination revealed mild dementia, dysarthria, buccofacial apraxia, rigidity and dystonic movement of the right upper limb. Dysarthria was guessed to be caused by buccofacial apraxia. Brain CT and MRI demonstrated atrophy of the left frontoparietal lobes, and hypoperfusion was shown in their areas by 123I-IMP SPECT. Clearly, SAS image disclosed the atrophy of the left pre- and post-central gyri that were surrounded by enlarged sulci. SAS was recently designed in Japan as a technique for visualization of brain surface structures. It is difficult to observe surface structures of cerebral gyri and sulci by conventional neuroradiological slice image, so SAS is useful for analysis of disorders affecting cerebral cortex as corticobasal degeneration.

Aged↗
PubMed1995

Structure and heterologous expression of the gene encoding the cell surface glycoprotein from Haloarcula japonica strain TR-1.

The gene encoding the cell surface glycoprotein (CSG) of Haloarcula japonica strain TR-1 was cloned and sequenced. The structural gene consisted from an open reading frame of 2,586 bp. A potential promoter sequence was found about 150 bp upstream of the ATG initiation codon. N-terminal amino acid sequence of the Ha. japonica CSG revealed that the mature CSG consisted of 828 amino acids. Five potential N-glycosylation sites were found in the mature sequence. The cloned CSG gene of Ha. japonica was expressed in closely-related halophilic archaea.

Amino Acid Sequence↗
PubMed1995

Effects of clonidine on intravenous sedation with midazolam.

The effect of clonidine, an alpha 2-adrenoceptor agonist, on intravenous (IV) sedation with midazolam was studied. Subjects were eight healthy adults; IV sedation was performed twice on each subject. In the control (CO) group, midazolam alone was administered. In the clonidine (CL) group, the subjects were given about 5 micrograms/kg of clonidine orally 2 hr before the initiation of sedation with midazolam. The following parameters were determined: dose of midazolam, changes in vital signs, recovery time, amnesia, and side effects. The average sedating dose of midazolam was 0.078 and 0.043 mg/kg in the CO and CL groups, respectively. Recovery times determined by stabilometry were 150 and 120 min in the CO and CL groups, respectively. Based on these results, the combined use of clonidine can reduce the dose of midazolam and shorten the recovery time. It is suggested that clonidine may be useful in IV sedation with midazolam.

Adrenergic alpha-Agonists↗
PubMed1994

Angiotensin II binding activity in cultured porcine arterial endothelial cells.

Angiotensin II (A II) binding activity was detected in the particulate fraction (100,000 g, 60 min precipitate) of cultured porcine aortic endothelial cells. Scatchard analysis of the binding activity indicated a single class of binding sites with a dissociation constant (Kd) of 1.1 nM and a total binding capacity (Bmax) of 125 fmol/mg protein. The binding of [125I]A II was inhibited by excess unlabelled A II, A II analogues ([Sar1, Ile8]A II and [Sar1, Ala8]A II), A I (angiotensin I) and A III (angiotensin III), but not by bradykinin. Type specific A II receptor antagonists, losartan (type 1 angiotensin II receptor) and PD123319 (type 2 angiotensin II receptor), did not inhibit the binding. These results suggest that the A II specific binding protein(s) or receptor(s) is present in arterial endothelial cells, and that it is different from typical type 1 and type 2 angiotensin II receptors.

Angiotensin II↗
PubMed1994

[Arterial infusion chemotherapy with human tumor necrosis factor (TNF): an experimental study using rabbits bearing VX2 tumor].

To evaluate the direct effects of TNF on tumor vessels, three groups of Japanese white rabbits bearing VX2 tumor received 5000 U, 25000, U, and 5000 U of TNF respectively. Angiograms were obtained before, and at 1, 15 and 30 minutes after arterial TNF injection. At 1 minute after TNF injection, dilated tumor vessels and dense tumor stains, depending on the dose of TNF, were demonstrated. At 30 minutes after injection these findings had disappeared However, there were no changes in normal vessels. It is suggested that arterial TNF injection influenced tumor vessels without damaging on normal vessels, indicating that it is effective as cancer therapy.

Animals↗
PubMed1994

[Embolization of varicocele with ethanol].

Embolization with ethanol was performed in 40 varicocele patients to prevent recurrence due to collateral formation. A prescribed amount of ethanol (0.5-4 ml) was injected slowly into the testicular vein with the catheter tip as close as possible to the inguinal region. Embolization with stainless steel coils was also performed in 15 of the 40 patients. Immediately after embolization, three varicoceles were reduced in size, and 37 disappeared. Recurrence was recognized in only two patients. These patients were embolized at a proximal site above lumbar vertebra IV. Spermatic data have improved for 13 patients but not for one azoospermatic patient. Serious complications were recognized in only one patient, who received an injection of 15 ml ethanol in one dose. Therefore, we conclude that embolization with ethanol is an useful treatment for varicocele.

Adolescent↗
PubMed1994

Opposite effects of midazolam and beta-carboline-3-carboxylate ethyl ester on the release of dopamine from rat nucleus accumbens measured by in vivo microdialysis.

This report describes the effects of midazolam and beta-carboline-3-carboxylate ethyl ester (beta-CCE) on extracellular concentrations of dopamine in the nucleus accumbens of freely moving rats measured by in vivo microdialysis. The two compounds had opposite effects, midazolam (0.075 and 0.15 mg/kg i.v.) dose dependently decreasing, and beta-CCE (3 and 10 mg/kg i.p.) dose dependently increasing, dialysate concentrations of dopamine. Flumazenil (6 micrograms/kg i.v.) did not affect the efflux of dopamine but it prevented the effects of both midazolam and beta-CCE on dopamine efflux. N6-Cyclohexyladenosine (0.1, and 1 mg/kg i.p.), a selective adenosine A1 agonist, dose dependently increased the efflux of dopamine. This effect was blocked by 8-cyclopentyl-1,3-dipropylxanthine (25 mg/kg i.p.), a selective adenosine A1 receptor antagonist, a dose which given alone did not affect dopamine efflux; responses to midazolam were not affected. 3,7-Dimethyl-1-propargylxanthine (1 and 3 mg/kg i.p.), a selective adenosine A2 receptor antagonist, did not mimic the effects of beta-CCE. The results suggest that midazolam and beta-CCE modulate dopamine release in the nucleus accumbens by an action at the benzodiazepine binding site associated with the GABAA receptor complex.

Adenosine↗
PubMed1994

Monoclonal proliferation of double-negative (CD4-CD8-) T-cells bearing T-cell receptor-alpha beta followed by subsequent development of Hodgkin's disease.

Expression of CD4 or CD8 on the cell surface is an important guide for discriminating the immunologic functions of T-cells. However, a minor T-cell subset lacking both CD4 and CD8 molecules but bearing the usual form of T-cell receptor (TCR)-alpha beta (CD4-CD8-TCR-alpha beta+ T-cells) has recently been found not only in mice but also in humans, and the clinical relevance of this newly defined subpopulation to human diseases is now of considerable interest. The authors present a patient in whom CD4-CD8-TCR-alpha beta+ T-cells showed monoclonal proliferation in the peripheral blood for more than 3 years, then disappeared spontaneously, followed by subsequent development of Hodgkin's disease. The pathologic roles of double-negative T-cell proliferation in this case are discussed from the viewpoint of premalignancy in lymphoproliferative diseases.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1994

Determination of a new immunosuppressant, mycophenolate mofetil, and its active metabolite, mycophenolic acid, in rat and human body fluids by high-performance liquid chromatography.

Mycophenolate mofetil, a new immunosuppressant, is a morpholinoethyl ester of mycophenolic acid. A new selective, sensitive and simple high-performance liquid chromatographic method was developed for the determination of mycophenolic acid and mycophenolate mofetil in biological samples. The preparation of samples was based on liquid-liquid extraction. The compounds were separated on a CN column using acetonitrile-0.01 M phosphate buffer (1:4, v/v) as the mobile phase. UV detection was used at wavelengths 215 and 304 nm. The detection limit was 5 ng per injection volume. This method enabled pharmacokinetic and pharmacodynamic studies in humans and rats.

Animals↗
PubMed1994

A novel heparin-binding protein, HBp15, is identified as mammalian ribosomal protein L22.

A 15kDa-protein (HBp15) was purified from mouse submandibular gland and bovine brain by virtue of its heparin-binding property. The amino acid sequences of mouse and bovine HBp15 showed a high degree of homology to a sea urchin protein encoded by gene called "development specific protein 217." Using reverse transcription-polymerase chain reaction methods, cDNA clones for HBp15 were isolated from submandibular gland mRNA of mouse, human and pig, and sequenced. Database search of HBp15 showed that HBp15 also resembles yeast ribosomal protein YL31 in addition to the 217 protein. Using specific antibodies against HBp15, HBp15 was identified as mammalian ribosomal protein L22, for which no sequence information is available.

Amino Acid Sequence↗
PubMed1994

Purification and characterization of hepatocyte growth factor (HGF)-converting enzyme: activation of pro-HGF.

Hepatocyte growth factor (HGF) is a heterodimer protein, derived from an inactive single-chain precursor (pro-HGF) by the proteolytic cleavage at Arg-Val site. Using a fluorogenic substrate Ac-Lys-Thr-Lys-Gln-Leu-Arg-MCA corresponding to the sequence around the cleavage site of pro-HGF, HGF-converting enzyme was purified from fetal bovine serum. The enzyme is a heterodimer molecule with an apparent molecular weight of about 90-kDa and is composed of a 65-kDa heavy-chain and a 32-kDa light-chain. The enzyme belongs to the serine-protease family and has an optimal pH around 8. The enzyme preferentially cleaved MCA-substrates containing the processing site of pro-HGF. The purified enzyme converted pro-HGF to a two-chain mature form of HGF. The enzyme-treated pro-HGF had mitogenic activity on primary cultured hepatocytes. Thus, the enzyme is likely to be involved in pro-HGF activation in vivo. The enzyme activity in rat serum was 9-fold higher than that in the plasma. This, together with the heterodimeric structure of the enzyme, suggests that the HGF-converting enzyme is activated by another protease in response to a trigger such as blood coagulation or tissue injury.

Amino Acid Sequence↗
PubMed1994

Plasma pharmacokinetics and urinary and biliary excretion of a new potent tripeptide HIV-1 protease inhibitor, KNI-272, in rats after intravenous administration.

The pharmacokinetic (PK) characteristics of KNI-272, a potent and selective HIV-1 protease inhibitor, were evaluated in rats after intravenous (IV) administration. The effect of dose on KNI-272 plasma kinetics, and the urinary and biliary elimination kinetics of KNI-272, were examined. After IV administration of 10.0 mg kg-1 KNI-272, the mean terminal elimination half-life, t1/2 lambda zeta, was 3.49 +/- 0.19 (SE) h, the total plasma clearance, CLtot, was 15.1 +/- 1.2 mL min-1 and the distribution volume at steady state, Vd,ss, was 3790 +/- 280 mL kg-1. On the other hand, after 1.0 mg kg-1 IV administration, t1/2 lambda zeta was 3.04 +/- 0.11 h, CLtot was 15.9 +/- 0.2 mL min-1, and Vd,ss was 6950 +/- 600 mL kg-1. The PK parameters of KNI-272 after IV administration showed that the disposition of KNI-272 in the rat plasma is linear within the dose range from 1.0 to 10.0 mg kg-1. Using an equilibrium dialysis method, the plasma binding of KNI-272 was measured in vitro. The free fractions were 17.7 +/- 0.6%, 12.1 +/- 1.5%, and 13.8 +/- 1.4% at the total concentration ranges of 9.898 +/- 0.097 microgram mL-1, 0.888 +/- 0.008 microgram mL-1, and 0.470 +/- 0.55 microgram mL-1, respectively. The percentages of the dose excreted into the urine and bile as the unchanged form were 1.20 +/- 1.06% and 1.61 +/- 0.32% at 1.0 mg kg-1 dose, and 0.164 +/- 0.083% and 1.42 +/- 0.26% at 10.0 mg kg-1 dose, respectively. The renal clearance (CLR) and the biliary clearance (CLB) were calculated to be 0.191 and 0.256 mL min-1 for 1.0 mg kg-1, and 0.0248 and 0.215 mL min-1 for 10.0 mg kg-1, respectively. When comparing these values with the CLtot values, the urinary and biliary excretion of KNI-272 are minor disposition routes.

Animals↗