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Biomedical subjects

T Kano

Publications and source records attributed to T Kano.

At least 73 records · Page 4Linked to original sources
PubMed1996

Novel designed enediynes: molecular design, chemical synthesis, mode of cycloaromatization and guanine-specific DNA cleavage.

The molecular design and chemical synthesis of novel enediyne molecules related to the neocarzinostatin chromophore (1), and their chemical and DNA cleaving properties are described. The 10-membered enediyne triols 16-18 were effectively synthesized from xylitol (10) in a short step, and found to be quite stable when handled at room temperature. The representative and acylated enediyne 16 was cycloaromatized by 1,8-diazabicyclo[5.4.0]undec-7-ene (DBU) in cyclohexa-1,4-diene-benzene to give the benzenoid product 21 through a radical pathway. On the other hand, the enediyne 16 was cycloaromatized by diethylamine in dimethyl sulfoxide-Tris-HCl, pH 8.5 buffer to afford another benzenoid product 22 as a diethylamine adduct through a polar pathway. Furthermore, the enediynes 16-18 were found to exhibit guanine-specific DNA cleavage under weakly basic conditions with no additive.

Alkynes↗
PubMed1996

Inhibition of purified human sucrase and isomaltase by ethanolamine derivatives.

Sucrase-isomaltase complex was purified from human intestinal mucosa. Immunostaining shows that sucrase-isomaltase is confined to the area of the striated cell borders of human small intestinal absorptive cells of the villus. Inhibition of sucrase and isomaltase activity by ethanolamine derivatives was investigated. Tris inhibits both types of enzyme activity and is the strongest inhibitor of the ethanolamine derivatives investigated. Bis-Tris inhibited sucrase more than isomaltase. On the other hand, mono-, di- and tri-ethanolamine were weak inhibitors of sucrase but not isomaltase.

Electrophoresis, Polyacrylamide Gel↗
PubMed1996

[Intraoperative use of plasma-derived activated factor VII (F VII a) in a hemophilia A patient with inhibitors].

We treated a 1-year 9-month-old boy with severe hemophilia A who developed high level of F VIII inhibitor. A placement of an implantable intravenous access device was scheduled under general anesthesia. After a slow induction using oxygen, nitrous oxide and sevoflurane, a peripheral venous line was placed and plasma-derived F VII a was infused. A catheter was inserted via the jugular vein to the SVC and it was connected to the device placed subcutaneously in his right chest wall. The peroperative blood loss was slight, and anesthesia and surgery went uneventfully.

Anesthesia, General↗
PubMed1996

[Primary amyloidosis complicated with chronic myelomonocytic leukemia].

A 79-year-old male was admitted to our hospital because of abnormal shadows in both lungs on chest X-ray film. He had a 5-year history of repeated bleeding episodes of unknown etiology before admission. Transbronchial lung biopsy revealed the alveolar septal type of lung amyloidosis. His serum contained a monoclonal IgA-lambda type protein but there was no evidence of multiple myeloma. A diagnosis of primary amyloidosis was made. On admission, his hematological findings revealed the coexistence of chronic myelomonocytic leukemia (CMML). Coexistence of primary amyloidosis and CMML is extremely rare. Because monocytes are known to play an essential role in the degenerative processes of serum amyloid precursor, it was suggested that his amyloidosis was accelerated by the onset of CMML through certain dysfunctions of pathological monocytes.

Aged↗
PubMed1995

Cocaine-induced CREB phosphorylation and c-Fos expression are suppressed in Parkinsonism model mice.

Cocaine exerts multiple neurochemical effects in the central nervous system through inhibition of the dopamine transporter at the synapse. Here we report that systemic administration of the drug induces rapid phosphorylation of CREB in the mouse striatum where expression of the nuclear proto-oncogene c-fos is observed. In MPTP-treated mice, in which dopaminergic neurones are degenerated and which show Parkinsonism-like behaviour, however, CREB phosphorylation is not induced by cocaine exposure and c-fos expression is significantly depressed in comparison with controls. These data suggest that CREB may play a major role in the dopaminergic activation of c-fos in the striatum and that the lack of a CREB-induced transcription cascade may have a critical relevance for long-lasting psychomotor disorders in Parkinsonism.

Animals↗
PubMed1995

Quantitative assessment of the autonomic nervous system activities during atropine-induced bradycardia by heart rate spectral analysis.

Using power spectral analysis of heart rate fluctuation, autonomic nervous system activities in bradycardia appearing in the initial phase of atropine administration were evaluated quantitatively in 16 healthy females. Atropine sulfate (10 micrograms/kg), diluted in 100 ml of 0.9% NaCl solution, was intravenously infused at a rate of 0.5 micrograms/kg per min. Electrocardiograms were sampled for 4 min for later analysis before and 0, 5, 10, 15 and 20 min after initiation of atropine infusion. Powers of low (LFC, 0.05-0.15 Hz) and high-frequency (HFC, 0.15-0.4 Hz) components in the power spectrum of R-R interval variations, and the LFC/HFC ratio were determined at each sampling point. HFC power at 0-4 min increased from 1.11 +/- 0.18 ms2 (mean) of baseline value to 1.37 +/- 0.19 ms2 (P < 0.05). The next 5-9-min value of 1.48 +/- 0.14 ms2 was the maximum, and the amount of atropine infused by 9 min was 4.5 micrograms/kg. The HFC powers following this point decreased. The 20-24-min value after 10 micrograms/kg atropine decreased to 0.21 +/- 0.03 ms2 (P < 0.01), which was lower than the previous 15-19-min value of 0.36 +/- 0.04 ms2 (P < 0.01). The LFC/HFC ratios showed no significant change for the initial 9 min of the atropine infusion. However, these ratios at 15-19 min and 20-24 min were increased from 0.50 +/- 0.04 (mean) of baseline value to 0.75 +/- 0.09 and 0.81 +/- 0.09, respectively (P < 0.01). A transient vagotonic state after atropine administration, followed by the well-known vagolytic state, was quantitatively detected by non-invasive spectral analysis of heart-rate fluctuation.

Adolescent↗
PubMed1995

The effects of pituitary adenylate cyclase-activating polypeptide on cerebral arteries and vertebral artery blood flow in anesthetized dogs.

We investigated and compared the effects of pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) on cerebral circulation in anesthetized dogs. The intracisternal administration of PACAP-27, PACAP-38, and VIP dilated canine cerebral arteries in a dose-dependent manner. A 10 nmol dose of PACAP-27, PACAP-38, and VIP dilated the basilar artery by 23 +/- 3, 27 +/- 3 and 30 +/- 3%, respectively. Rostrally located arteries tended to be more responsive to PACAP-27. Pretreatment with NG-monomethyl-L-arginine did not affect PACAP-27-induced vasodilation. Vertebral artery blood flow was also affected by intra-arterial injection of these peptides in a dose-dependent manner. A 100 pmol dose of PACAP-27, PACAP-38, and VIP increased the vertebral artery blood flow by 42 +/- 10, 29 +/- 4, and 62 +/- 11%, respectively. The VIP receptor antagonist, [Lys1,Pro2,5,Arg3,4,Tyr6]VIP, inhibited both the VIP- and PACAP-38-induced increase in vertebral artery blood flow. These findings suggest that PACAP plays a role in the regulation of cerebral circulation.

Anesthesia↗
PubMed1995

Needle track seeding after percutaneous ethanol injection therapy for small hepatocellular carcinoma.

We present two cases of patients experiencing needle track seeding after undergoing percutaneous ethanol injection therapy (PEIT) for small hepatocellular carcinoma, who were treated by surgical resection of the metastases. One patient demonstrated metastatic tumors due to needle track seeding 6 months after the beginning of PEIT (a total of 7 injection sessions for 2 tumors measuring < 20 mm in diameters), whereas the other developed a metastatic tumor 20 months after beginning PEIT (a total of 30 injection sessions for 3 tumors measuring < 20 mm in diameter). In the two cases, both the primary and metastatic tumors histologically revealed moderately differentiated hepatocellular carcinoma. Moreover, the histological findings of the metastatic foci did not always appear to be more aggressive than those of the primary tumors. Therefore, in order to detect such metastasis as early as possible, more careful attention should be paid to the appearance of needle track seeding after performing PEIT for hepatocellular carcinoma, even if the target of such PEIT is small HCC.

Aged↗
PubMed1995

Poly A-linked non-isotopic microtiter plate reverse transcriptase assay for sensitive detection of clinical human immunodeficiency virus isolates.

A colorimetric reverse transcriptase assay (cRT assay) was developed for quantitative detection of HIV-1. In this format, reverse transcriptase incorporates biotin-labeled dUTP onto oligo-dT primers hybridized to poly A templates. The templates are covalently bound to the surface of microtiter wells. The amount of incorporated biotin-labeled dUTP is measured by binding horseradish peroxidase conjugated streptavidin, washing away unbound peroxidase, adding colorimetric substrate and then reading with a standard colorimetric reader. The sensitivity of the assay is very good. As little as 3 x 10(5) molecules of recombinant HIV-RT can be detected after 20 h of reaction time. Direct comparison using 3 cultured clinical isolates indicates that this level of detection is equivalent to the commercially available p24 antigen capture assay and the HIV-RNA assay based on branched DNA signal amplification. Other retroviruses, such as HIV-2 and feline immunodeficiency virus (FIV), can also be detected in this format. This non-isotopic assay is easy to perform and could provide a convenient and quantitative method for HIV study by monitoring reverse transcriptase, an essential activity in the infection process.

Animals↗
PubMed1995

Inhibition of the high-affinity glutamate uptake system facilitates the massive potassium flux during cerebral ischaemia in vivo.

During cerebral ischaemia, the extracellular concentration of K+ ([K+]e) increases abruptly to 50-60 mM following an initial slow increase to 6-10 mM. We have recently shown that the increase in [K+]e is significantly delayed by in situ administration of kynurenic acid, a broad spectrum antagonist of excitatory amino acids, suggesting that the catastrophic ionic fluxes occurring during ischaemia are initially mediated by EAA-coupled ion channels. In order to confirm further the role of EAAs, the changes in extracellular K+ ([K+]e) and glutamate ([Glu]e) during cerebral ischaemia were determined in the rat hippocampus by microdialysis in vivo, and the effect of dihydrokainate (DHKA), an inhibitor of the high-affinity uptake system of EAAs, was examined by in situ administration through the dialysis probe. DHKA induced a significant increase in baseline [Glu]e and facilitated the abrupt increase in [K+]e during cerebral ischaemia. These findings support the hypothesis that EAAs play a vital role in producing the rapid ionic shifts earlier during cerebral ischaemia.

Animals↗
PubMed1995

[Bupivacaine-fentanyl continuous infusion is superior to morphine bolus injection in postoperative epidural analgesia].

We compared bolus injection of morphine 51 +/- 9 micrograms.kg-1 (M-S group) with 48 h-continuous infusion of bupivacaine and fentanyl mixture (BF-C group) for postoperative epidural analgesia in 100 patients who had undergone upper abdominal laparotomy. The epidural analgesia was started about 60 min before completion of surgery. The mixed solution, consisting of bupivacaine 48 ml (240 mg), fentanyl 24 ml (1.2 mg) and 0.9% saline (24 ml), was administered at a rate of 2 ml.h-1 by using a 100 ml balloon infuser. Analgesic effects (determined by visual analogue scale, verbal pain scores at rest and with movement, additional requests of other analgesics), comfort and side effects of the epidural analgesia were examined. The evaluation based on postoperative analgesia and comfortable feeling rated higher in the BF-C group compared with the M-S group (P < 0.01 to of 0.05). There were fewer requests for other postoperative analgesics in the BF-C group (P < 0.01 to 0.05). There was no significant difference in side effects between the two groups. The plasma fentanyl concentration in the BF-C group (n = 5) was maintained almost constant for the period from 24 to 49 hours after the start of infusion and was approximately 1.6 ng.ml-1. We conclude that continuous infusion of bupivacaine (2.5 mg.ml-1) and fentanyl (12.5 micrograms.ml-1) at a rate of 2 ml.h-1 is superior to bolus injection of morphine for postoperative analgesia.

Adolescent↗
PubMed1994

Genomic analysis of a NF1-related pseudogene on human chromosome 21.

A neurofibromatosis type-1 (NF1)-related locus on human chromosome 21 has been characterized. A detailed genomic mapping performed by yeast artificial chromosome (YAC) dot-hybridization revealed that the NF1-related locus is close to the sequence-tagged site (STS), D21S329 (G52E12), which is located on the proximal region of 21q11.2. Sequence analysis showed that this locus seemed to be conserved to the NF1 gene only in several partial regions. Two exon-like segments corresponding to exons 8 and 9 of NF1 were found, in addition to two previously found fragments corresponding to exons 7 and 11. Other exon-like segments were not found in the region so far sequenced. Comparing these homologous segments with the NF1 cDNA, a 2-bp deletion appeared in exon 8 of the locus, resulting in the existence of stop codons in all reading frames. In addition, there were no amplified fragments derived from the related locus by reverse transcription-PCR. Thus, our results suggest that the NF1-related locus on chromosome 21 is a nonprocessed pseudogene.

Animals↗
PubMed1994

N-methyl-D-aspartate receptor-mediated, prolonged afterdischarges of CA1 pyramidal cells following transient cerebral ischemia in the rat hippocampus in vivo.

We previously reported the post-ischemic potentiation (PIP) of synaptic efficacy in hippocampal Schaffer collateral/CA1 responses of the rat beginning at 6-8 h following 12 min transient cerebral ischemia in vivo. The present study demonstrated that repetitive stimulation with a relatively low frequency (5 Hz, 6 s), which produced short-lasting afterdischarges (ADs; duration, 4.49 +/- 4.26 s; n = 7) in sham-controls, resulted in prolonged ADs (duration, 26.33 +/- 12.63 s; n = 6; P < 0.001) at the same period after ischemia. The PIP was not affected by 2-amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia. The prolonged ADs in response to repetitive stimulation were, however, reversed to short-lasting ADs (duration, 7.13 +/- 1.44 s; n = 4; P < 0.02) by the same procedure, leaving the response to single stimulation unaffected. These findings suggest that, during the reperfusion period, Ca2+ influx into the CA1 pyramidal cells can be greatly increased through N-methyl-D-aspartate (NMDA) receptor-coupled ion channels if appropriately timed multiple synaptic inputs bombard these cells. Such Ca2+ influx may contribute to delayed death of CA1 pyramidal cells after transient cerebral ischemia if synaptic activity is maintained at relatively high levels during the reperfusion period.

Animals↗
PubMed1994

Propentofylline administered by microdialysis attenuates ischemia-induced hippocampal damage but not excitatory amino acid release in gerbils.

Systemic administration of propentofylline (PPF), an adenosine uptake inhibitor, has been demonstrated to protect CA1 pyramidal cells from death following transient cerebral ischemia in gerbils. In order to examine the direct effects of this inhibitor, we tested whether or not PPF administered into the hippocampus in situ through a microdialysis probe could attenuate ischemia-induced excitatory amino acid (EAA) release and prevent subsequent death of CA1 pyramidal cells in the gerbil. The EAA release and death of CA1 pyramidal cells observed in the hippocampus were compared with those in the contralateral hippocampus of the same animal into which vehicle alone was administered. The results indicated that pre- as well as post-treatments with PPF inhibited the death of CA1 pyramidal cells after 5-min ischemia in a dose-dependent manner, but did not significantly alter the EAA release during ischemia and reperfusion in the same animals. While the neuroprotective effect of PPF against ischemic damage has commonly been ascribed to attenuation of EAA release during ischemia, other actions of adenosine such as those influencing the synaptic responses, neuronal excitation, and local cerebral circulation, or as yet unidentified actions may be involved in the observed neuroprotective effects of PPF.

Amino Acids↗
PubMed1994

Homogeneous fluorescence detection method for human leukocyte antigen-DR typing following polymerase chain reaction amplification with sequence-specific primer.

A fluorescent homogeneous method for the detection of sequence-specific amplification of human leukocyte antigen (HLA) alleles has been developed. In this approach, polymerase chain reaction sequence-specific primers (PCR-SSP) are used to amplify DRB1, DRB3, and DRB4 alleles. Lambda exonuclease and Exonuclease I are added to reduce background by digesting template DNA, partial primer dimer, and primer. PCR amplicons are then detected following the addition of a fluorescent dye (thiazole yellow dimer) which binds to double-stranded DNA. No transfer or wash steps are required. Thus, the risk of sample contamination, which is a major source of inaccuracy for DNA amplification methods, is greatly reduced. This approach is also faster and more easily automated than the standard approach using gel electrophoresis and ethidium bromide staining. Speed and automation are important considerations for HLA typing since the number of possible alleles for each HLA type is substantial. A homogeneous HLA-SSP typing method may be especially useful for clinical labs doing large numbers of samples and for the eventual automation of HLA DNA typing.

Alleles↗
PubMed1994

Attenuation of hemispheric swelling associated with acute subdural hematomas by excitatory amino acid antagonist in rats.

Acute subdural hematoma (ASDH) gives rise to a mass effect not only by itself but also through unilateral hemispheric swelling. The present study tested the hypothesis that hemispheric swelling is mediated by mechanisms which involve excitatory amino acids (EAAs). After removal of the subdural clot, introduced by homologous blood (0.1-0.2 ml), the % brain water was determined from the formula: ((wet weight--dry weight)/wet weight) x 100. The % brain water of the left hemisphere was significantly greater than that of the right hemisphere during the initial 6 hours after induction of ASDH in animals injected with 0.2 ml blood. A less marked but significant increase was observed in the animals injected with 0.1 ml blood. Systemic pretreatment with kynurenic acid (KYN; 800 mg/kg, i.p.), a broad-spectrum EAA antagonist, attenuated the increase in % brain water in the animals injected with 0.2 ml blood. In order to determine the changes in cerebral metabolism induced by the model of ASDH employed in the present study, we measured the cortical cytochrome oxidase (CYO) activity, a marker of mitochondrial respiration, in a separate group of animals. The CYO activity estimated densitometrically from the histochemical staining was not significantly altered in the animals injected with either 0.1 or 0.2 ml blood, suggesting absence of ischemia. These results indicated that the hemispheric swelling associated with thin ASDHs may be partially mediated by mechanisms other than ischemia, in which EAAs appear to be involved.

Animals↗