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T Kanno

Publications and source records attributed to T Kanno.

At least 307 records · Page 17Linked to original sources
PubMed1994

[A today's trend of Japanese Council of Certification for Physicians--the current status in Japan].

Certification systems in Japanese medical associations basically involve review of educational background and experience by their own peers. The Japanese council for certification for physicians was built in 1981 to promote the understanding of certification for specialist and to ensure the system of certification. A tripartite commission, composed of Japan Medical Association, Japanese Council of Scientific Associations and Japanese Council for Certification for Physicians, was settled to promote the authorization of these certification systems. The commonly acceptable view is that certification has a number of valuable agreements including 1) examination may form a component of the certification system, 2) a renewal program is necessary, 3) the renewal program should be linked with an educational program of Japan Medical Associations, 4) post graduate education system should be included in the renewal program. Under these agreements, tripartite commission will be starting the authorization scheme of certified physicians in each medical association. Herein, we present a historical review of the Japanese councils of certification of physicians and authorization program of certified physicians including a brief discussion.

Certification↗
PubMed1994

Premature termination mutations in two patients with deficiency of lactate dehydrogenase H(B) subunit.

Two patients with low lactate dehydrogenase (LD) activity were discovered during healthcare examinations and were found to be homozygous for LD-H (heart) subunit deficiency by electrophoretic isoenzyme analysis of serum and erythrocyte hemolysate. The molecular nature of the genetic mutations was characterized by amplification by the polymerase chain reaction and DNA sequencing. In one case, a single-base substitution (T-->G transversion) at codon 147 of the LD-H(B) gene resulted in a nonsense mutation; in the other case, a deletion of 2 base pairs had occurred at codon 139, resulting in a frameshift translation and premature termination.

Adult↗
PubMed1994

[How to realize the concept--a reference intervals].

The concept of reference interval is basically different from that of decision making. However, the two are closely related and sometimes have been misunderstood to have the same meaning. Reference intervals are calculated as a statistical parameter of the values obtained from reference groups which as restricted with physiological situation. On the other hand, the values for diagnostic decision making, cut-off value or consensus values, are obtained from the idea of diagnostic sensitivity, specificity and predictive values of diagnosis. Today, the concept of diagnostic decision making has gradually permeated in medical practice and the laboratory. Herein, we define and discuss these two words.

Adult↗
PubMed1994

[Reestimation of aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio based on JSCC consensus method--changes of criteria for a differential diagnosis of hepatic disorders following the alteration from Karmen method to JSCC method].

We estimated clinical criteria of aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio that is measured by the consensus method of JSCC (Japan Society of Clinical Chemistry) for serum AST and ALT. The JSCC consensus method is closely correlated with both IFCC (International Federation of Clinical Chemistry) recommended method without pyridoxal phosphate and Karmen method recommended by the expert panel of liver function tests in Japanese Society of Gastroenterology. The slopes of the regression line is estimated to be 1.00 and 0.87 respectively. We propose that the decision making value of AST/ALT ratio to differentiate several types of liver diseases should be set to 0.87 measured by JSCC consensus method, instead of 1.0 measured by Karmen method.

Alanine Transaminase↗
PubMed1993

Inhibition by a receptor-mediated Ca2+ entry blocker, SK&F 96365, of Ca2+ and secretory responses in rat pancreatic acini.

The effect of a receptor-mediated Ca2+ entry blocker, 1-(beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl)-1H-imidazole hydrochloride (SK&F 96365), on a secretagogue-induced secretory response and Ca2+ dynamics was examined in isolated acini of rat pancreas. SK & F 96365 inhibited the secretory response induced by 100 pM cholecystokinin octapeptide (CCK-8) or 3 microM ethanaminium, 2-[(aminocarbonyl)oxy]-N,N,N-trimethyl,-chloride (carbachol) in isolated incubated acini up to 73.2 +/- 6.1% or 70.3 +/- 3.8% with IC50 of 47.7 microM or 42.0 microM, respectively. The inhibitory effect of SK&F 96365 on the time courses of CCK-8-induced amylase release and [Ca2+]c (cytoplasmic Ca2+ concentration) elevation was further examined in isolated perifused acini or isolated acini loaded with Fura-2. In the 100 pM CCK-8-stimulated preparation, 30 microM SK&F 96365 partly, and 100 microM SK&F 96365 completely, inhibited the sustained plateau phase, but did not inhibit the initial phase of the Ca2+ and secretory responses. In the 5 pM CCK-8-stimulated preparation; (a) 30 microM SK&F 96365 reduced the frequency of the [Ca2+]c oscillations, but caused little, if any, changes in the secretory response; (b) 100 microM SK&F 96365 transformed the oscillatory [Ca2+]c dynamics to a transient increase followed by a gradual decay and caused a significant inhibition of the sustained secretory response. These results indicate that the sustained responses to secretagogues are dependent on a receptor-mediated Ca2+ entry which can selectively be blocked by SK&F 96365 in rat pancreatic acini.

Amylases↗
PubMed1993

Mutual regulation of the transcriptional activator NF-kappa B and its inhibitor, I kappa B-alpha.

The NK-kappa B transcription factor complex is sequestered in the cytoplasm by the inhibitory protein I kappa B-alpha (MAD-3). Various cellular stimuli relieve this inhibition by mechanisms largely unknown, leading to NF-kappa B nuclear localization and transactivation of its target genes. It is demonstrated here with human T lymphocytes and monocytes that different stimuli, including tumor necrosis factor alpha and phorbol 12-myristate 13-acetate, cause rapid degradation of I kappa B-alpha, with concomitant activation of NF-kappa B, followed by a dramatic increase in I kappa B-alpha mRNA and protein synthesis. Transfection studies reveal that the I kappa B-alpha mRNA and the encoded protein are potently induced by NF-kappa B and by homodimers of p65 and of c-Rel. We propose a model in which NF-kappa B and I kappa B-alpha mutually regulate each other in a cycle: saturating amounts of the inhibitory I kappa B-alpha protein are destroyed upon stimulation, allowing rapid activation of NF-kappa B. Subsequently, I kappa B-alpha mRNA and protein levels are quickly induced by the activated NF-kappa B. This resurgence of I kappa B-alpha protein acts to restore an equilibrium in which NF-kappa B is again inhibited.

Blotting, Northern↗
PubMed1993

The oncoprotein Bcl-3 directly transactivates through kappa B motifs via association with DNA-binding p50B homodimers.

Bcl-3 is an I kappa B-related protein with ankyrin repeat motifs. Its gene is located at a site of recurrent translocations in a subset of B cell chronic lymphocytic leukemias. Bcl-3 associates tightly with p50B (NFKB2, p52) homodimers in cells, and together these proteins form a ternary complex with DNA at kappa B sites. Such an association functionally leads to a novel and potent form of transactivation through the kappa B motif: the tethering of Bcl-3 to DNA via the p50B homodimers allows Bcl-3 to transactivate directly, while p50B homodimers alone cannot. Transactivation mediated by Bcl-3 requires two cooperating domains located amino- and carboxy-terminal to the ankyrin domain. Bcl-3 is localized to the nucleus, and a Bcl-3-p50B complex is detected in certain lymphoid cells. Our data reveal a novel role for Bcl-3, distinct from that of the inhibitor I kappa B. The results have implications for tumorigenesis.

Animals↗
PubMed1993

The oncoprotein Bcl-3 can facilitate NF-kappa B-mediated transactivation by removing inhibiting p50 homodimers from select kappa B sites.

Previously we have proposed a role for Bcl-3 in facilitating transactivation through kappa B sites by counteracting the inhibitory effects of bound, non-transactivating homodimers of the p50 subunit of NF-kappa B. Such homodimers are abundant for example in nuclei of unstimulated primary T cells. Here we extend the model and provide new evidence which fulfills a number of predictions. (i) Bcl-3 preferentially targets p50 homodimers over NF-kappa B heterodimers since the homodimers are completely dissociated from kappa B sites at concentrations of Bcl-3 which do not affect NF-kappa B. (ii) Select kappa B sites associate very strongly and stably with p50 homodimers, completely preventing binding by NF-kappa B. Such kappa B sites are likely candidates for regulation by p50 homodimers and Bcl-3. (iii) Bcl-3 and p50 can be co-localized in the nucleus, a requirement for active removal of homodimers from their binding sites in vivo. (iv) The ankyrin repeat domain of Bcl-3 is sufficient for the reversal of p50 homodimer-mediated inhibition, correlating with the ability of this domain alone to inhibit p50 binding to kappa B sites in vitro. Our data support the model that induction of nuclear Bcl-3 may be required during cellular stimulation to actively remove stably bound p50 homodimers from certain kappa B sites in order to allow transactivating NF-kappa B complexes to engage. This exact mechanism is demonstrated with in vitro experiments.

Animals↗
PubMed1993

Restriction map of a virulence-associated plasmid of Rhodococcus equi.

The restriction cleavage map of a virulence-associated plasmid pREAT701 of Rhodococcus equi was constructed with EcoRI and HindIII by means of cloning the restriction fragments, cross Southern hybridization with each fragment, and hybridization with probes generated by modified inverse PCR. The genetic region responsible for expression of virulence-associated 15- to 17-kilodalton antigens was determined.

Blotting, Southern↗
PubMed1993

Hemadsorptive activity of transfected COS-7 cells expressing BHV-1 glycoprotein gIII.

Bovine herpesvirus 1 (BHV-1) glycoprotein gIII plays an important role in virus adsorption. The SR alpha promoter expression vector containing BHV-1 gIII gene was transfected into COS-7 cells. Fluorescent antibody staining using a panel of monoclonal antibodies demonstrated antigenic authenticity with regard to at least three nonoverlapping neutralization sites as well as surface expression of the glycoprotein. C57BL mouse erythrocytes were found to absorb onto the gIII-expressing cells. The hemadsorbing activity was specifically inhibited by the monoclonal antibody blocking virus adsorption. Heparin, analog of cellular receptor for BHV-1, also prevented the erythrocytes from adsorbing to the cells and heparinase-treated erythrocytes showed no adsorption. These findings indicate that the gIII binds to the erythrocytes and probably to the host cells independently of other viral components.

Animals↗
PubMed1993

Effects of calcium channel and H1-receptor blockers on the responses of slowly adapting pulmonary stretch receptors to histamine in vagotomized rabbits.

We studied the effects of calcium channel antagonists (verapamil and nifedipine) and H1-receptor blockers (mequitazine) on changes in the slowly adapting pulmonary stretch receptors (SARs) located below the carina in response to right atrial injections of histamine (60 and 80 micrograms/kg) in anesthetized artificially ventilated rabbits with bilateral vagotomy. After histamine was injected into the right atrium, the SARs became more active during expiration but decreased their activity during inspiration. These changes were more pronounced by increasing the dosage of histamine. However, administration of histamine had no significant effect on tracheal pressure (PT). Verapamil treatment (1 mg/kg) did not alter the SAR response to histamine, whereas the responses of SARs to histamine at different dosages were significantly diminished by treatment with nifedipine (1 mg/kg). Mequitazine (1 mg/kg), a potent H1-receptor blocker, blocked completely all the responses of SAR activity to histamine. These results suggest that the effect of histamine 60-80 micrograms/kg on SAR activity is mediated by the activation of H1-receptors of the peripheral airway smooth muscle and that this activation, at least in part, involves the opening of calcium channels of the airway smooth muscle.

Animals↗
PubMed1993

Analysis of a genetic mutation in an electrophoretic variant of the human lactate dehydrogenase-B(H) subunit.

An electrophoretic variant of the lactate dehydrogenase (LDH)-B(H) subunit was discovered in a patient with diabetes mellitus. His LDH activity in serum was slightly lower than normal and the LDH isozyme pattern showed an abnormal migration indicating an LDH-B subunit variant of the fast type. The LDH containing the variant subunit revealed a decreased heat stability. DNA analysis of the variant allele detected a base substitution, an A to G transition, at codon 6 (AAA-->GAA). The mutation resulted in the replacement of a lysine by a glutamic acid (K6E). The change may cause the heat instability and affect the net charge of the variant subunit, resulting in an electrophoretic LDH-B subunit variant of the fast type.

Aged↗
PubMed1993

Detection and characterization of new genetic mutations in individuals heterozygous for lactate dehydrogenase-B(H) deficiency using DNA conformation polymorphism analysis and silver staining.

Human lactate dehydrogenase (LDH)--B(H) mutant genes were analyzed by polymerase chain reaction (PCR) and DNA conformation polymorphism. We used polyacrylamide gradient gel and silver staining procedures for DCP analysis, and observed abnormal migration patterns in individuals heterozygous for the LDH-B deficiency. Subsequent sequence determination of the mutant alleles consistently resulted in detection of three single base substitutions (transversions), viz., a C to A at residue "35" (GCG, Ala-->GAG, Glu), a T to G at residue "172" (TTT, Phe-->GTT, Val), and an A to T at residue "176" (ATG, Met-->TTG, Leu). Furthermore, mismatched PCR or amplification refractory mutation system was developed for the rapid screening and confirmation of these mutations. These amino acid replacements may cause conformational changes in neighboring residues; this probably affects the active site arrangement and results in the loss of enzyme activity.

Amino Acid Sequence↗
PubMed1993

Carbamylcholine-induced morphological changes and spatial dynamics of [Ca2+]c in Harderian glands of guinea pigs: calcium-dependent lipid secretion and contraction of myoepithelial cells.

To determine whether lipid-secreting cells have cytosolic Ca2+ concentration ([Ca2+]c)-related secretory mechanisms, morphological changes and intracellular calcium dynamics of Harderian glands of guinea pigs stimulated by secretagogue were studied by electron microscopy and Fura-2/AM digital image analysis. Control glandular cells contained large lipid vacuoles that were bordered by multi-layered membranes. Rough-surfaced endoplasmic reticulum, mitochondria, and smooth-surfaced endoplasmic reticulum may be involved in lipid vacuole formation. Myoepithelial cells surrounded alveoli. After carbamylcholine (CCh, 10(-6), 10(-5), and 10(-3) M) stimulation, lipid materials within the membranous structures were frequently discharged by an exocytotic mechanism. Conspicuous deformation of glandular cells caused by vigorous contraction of myoepithelial cells was observed in isolated alveoli after 10(-6) M CCh stimulation, whereas the deformities of glandular tissues perfused via vessels were small even after 10(-3) M CCh stimulation. Connective tissue between glandular alveoli inhibited unbridled myoepithelial-cell contraction. Fura-2/AM digital imaging analysis revealed that CCh stimulation caused an increase in [Ca2+]c in isolated alveoli. The morphological reactions and changes in [Ca2+]c were prevented by atropine. When extracellular calcium ions were absent, enhanced extrusion of lipid vacuoles, myoepithelial-cell contraction, and a rise in [Ca2+]c after CCh stimulation were not observed. Nicotine and catecholamines had no effect on the secretion or on the dynamics of [Ca2+]c. It can be concluded that acetylcholine elicits exocytosis in glandular cells and contraction of the myoepithelial cells of Harderian glands, accompanied by an increase in [Ca2+]c. The dynamics of [Ca2+]c of the gland alveoli are mostly dependent on extracellular Ca2+.

Animals↗
PubMed1993

Effect of unilateral motor cortex ablation on activity of choline acetyltransferase and levels of amino acid transmitter candidates in the spinal cord of adult monkeys.

Evidence that L-glutamate is a neurotransmitter of corticofugal fibers was sought by measuring changes in several biochemical markers of neurotransmitter function in discrete regions of spinal cord after ablation of sensorimotor cortex in monkeys. One and five weeks after unilateral cortical ablation, samples from six areas of spinal cord (ventral, lateral and dorsal regions of the left and right sides) were analysed for choline acetyltransferase (ChAT) activity and contents of amino acid transmitter candidates-glutamic acid (Glu), aspartic acid (Asp), glycine (Gly), taurine (Tau) and gamma-aminobutyric acid (GABA). During one to five weeks after unilateral cortical ablation of the monkey, prolonged hemiplegia in the contralateral side was observed. Histological examination of the spinal cord 5 weeks after unilateral (left) cortical ablation showed no apparent change in either control (ipsilateral, left) or affected (contralateral, right) sides of the cord as examined by the Klüver-Barrera method. The ChAT activity as a cholinergic marker was scarcely changed in any region of either left (control) or right (affected) side of the spinal cord at one and five weeks after unilateral (left side) ablation of the motor cortex. Amino acid levels in each region of the spinal cord were not significantly changed one week after unilateral ablation of the motor cortex. However, a significant decrease of Glu content was observed in the lateral column of the affected (right) side compared to the control (left) side of cervical and lumbar cord five weeks after cortical ablation of the left motor area. No concomitant alterations of other amino acids were detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗