Search PubMed⌕ Search

Biomedical subjects

T Kanno

Publications and source records attributed to T Kanno.

At least 217 records · Page 12Linked to original sources
PubMed1997

Valinomycin induces apoptosis of ascites hepatoma cells (AH-130) in relation to mitochondrial membrane potential.

Valinomycin is a potassium ionophore, and is well known to cause the collapse of the mitochondrial membrane potential. It has been reported that loss of mitochondrial membrane potential is observed in the early stages of apoptosis induced by various agents. Thus, the effects of valinomycin on tumor cells were examined. Valinomycin induced uncoupling of respiration and depolarization of isolated mitochondria. Depolarization of intact mitochondria in AH-130 rat ascites hepatoma cells was also induced by valinomycin. Valinomycin induced apoptosis revealing the typical apoptotic characteristics such as fragmentation and ladder formation of DNA, shrinkage of cells, and formation of pycnotic nucleus. There was a correlation between the depolarization of mitochondria and DNA fragmentation. After depolarization of mitochondria, the activity of caspase-3-like protease but not caspase-1-like protease increased markedly. In contrast, this apoptosis did not involve the release of reactive oxygen species from mitochondria, increase in intracellular calcium concentration, or protein synthesis. In addition, anti-apoptotic members of the Bcl-2 family (Bcl-xL and Bcl-2) were not correlated with apoptosis. These results indicate that valinomycin might induce apoptosis through degradation of the mitochondrial membrane potential. Taken together, these observations suggest that there may be a mechanism that transmits the signal from mitochondrial depolarization to subsequent apoptosis execution steps.

Animals↗
PubMed1997

Effects of quaternary ammonium compounds with 0.1% sodium hydroxide on swine vesicular disease virus.

The effects of quaternary ammonium compounds (QACs) with sodium hydroxide on swine vesicular disease virus (SVDV), an enterovirus were studied. Didecyldimethylammonium chloride (DDAC) with 0.1% NaOH showed a stronger effect against SVDV than other QACs with 0.1% NaOH. The effect of DDAC with 0.1% NaOH was strong at 40 degrees C. DDAC was effective against SVDV at pH values around 11.0, but not in the distilled water control. The effect of DDAC with 0.1% NaOH was already observed at 1 min after mixing of the DDAC with SVDV. Observation under an electron microscopy revealed that the probable mechanism of inactivation of DDAC with 0.1% NaOH is as follows: The virus particles were partially destroyed by 0.1% NaOH. DDAC gathered these affected particles and formed a micelle, then SVDV lost its infectivity. From these results, QACs with 0.1% NaOH are considered to be very effective against SVDV representing enteroviruses.

Animals↗
PubMed1997

GLP-I(7-36) amide augments Ba2+ current through L-type Ca2+ channel of rat pancreatic beta-cell in a cAMP-dependent manner.

The whole-cell patch-clamp method was used to examine the effect of glucagon-like peptide I (GLP-I)(7-36) amide on the activation process of L-type Ca2+ channels of rat pancreatic beta-cells. After depolarization, GLP-I (1-100 nmol/l) caused action potentials in cells exposed to a glucose-free solution for 10 min. The percentage of cells producing action potential depended on the concentration of GLP-I. In some cells, GLP-I caused action potentials without the prior depolarization of the membrane. In cells exposed to the glucose-free solution for longer than 30 min, or in cells that were deprived of ATP by a means of the conventional whole-cell configuration, GLP-I (20 nmol/l) did not cause the electrical excitation. Application of GLP-I augmented the maximum Ba2+ current (IBa) through L-type Ca2+ channels and shifted the current voltage curve to the left. Values of changes in the maximum IBa depended on GLP-I concentration. Application of dibutyryl cAMP (dbcAMP, 1 mmol/l) also augmented IBa. In cells pretreated with Rp-cAMP, dbcAMP did not change the magnitude of IBa. Also in cells pretreated with Rp-cAMP, GLP-I failed to augment IBa. These results suggest that in pancreatic beta-cells, GLP-I, by a cAMP-dependent mechanism, increases opening of L-type Ca2+ channels. cAMP-dependent augmentation of Ca2+ entry as well as cAMP production itself by GLP-I plays a crucial role in controlling insulin secretion.

Action Potentials↗
PubMed1997

[Determination of malondialdehyde-modified LDL(MDA-LDL) and its potential usefulness].

Numerous studies have indicated that oxidative modification of low-density lipoprotein(LDL) plays a critical role in the pathogenesis of atherosclerosis. Malondialdehyde-modified LDL(MDA-LDL) is one of the candidates which is the oxidative product of LDL. However, the existence of MDA-LDL in the circulation has been in dispute. Therefore, for the assessment of oxidized-LDL in human serum, we developed a sensitive enzyme-linked-immunosorbent assay(ELISA) for the detection of MDA-LDL. In our method, monoclonal antibody against MDA-LDL, ML25 was used. ML25 recognized MDA-LDL as well as MDA-modified proteins by a solid-phase competitive enzyme immunoassay. Therefore, to establish an ELISA method which is specific for detection of MDA-LDL, ML25 was combined with apoB-specific antibody (AB16) as the second antibody. Using this method, MDA-LDL was detectable in the sera of 314 healthy individuals. The concentration of MDA-LDL preferably ranged from 20 to 80 units/l when the absorbance with artificially prepared MDA-LDL at the concentration of 1 mg/l was defined as 1 unit/l. Furthermore, assays for lipoprotein subfractions separated by density-gradient ultracentrifugation revealed that MDA-LDL was mainly distributed in the LDL fraction as expected, and MDA-LDL/apoB ratio showed a peak at small, dense LDL fractions. This finding seems to be quite interesting since an elevated level of small, dense LDL has been reported to be associated with an increased risk of atherosclerosis. We concluded that our method is useful for specific detection of MDA-LDL in human serum and might be an elevation method for atherogenicity.

Arteriosclerosis↗
PubMed1997

[Complete cholesteryl ester transfer protein deficiency increases oxidized-LDL in plasma].

Malondialdehyde-modified LDL(MDA-LDL) is one of the major oxidative LDL. MDA-LDL was determined by enzyme immunoassay in patients with complete and partial cholesteryl ester transfer protein(CETP) deficiency. Significantly increased serum MDA-LDL levels and MDA-LDL/apoB ratios in the LDL fraction were observed in patients with complete CETP deficiency but not for those with partial CETP deficiency. The present results may indicate that patients with complete CETP deficiency have a higher risk for atherosclerosis than those with partial CETP deficiency and normal.

Arteriosclerosis↗
PubMed1997

Pitfalls in aneurysm surgery in acute stages.

Since the dawn of aneurysm surgery, many aneurysms present a more complex challenge. Large size, intimacy with critical perforator branches, deep location, atherosclerotic walls, ruptured aneurysms in the elderly and incorporation of afferent or efferent arteries in the dome represent factors that singly or in combination preclude safe clipping while high pressure circulation continues in the aneurysm. Despite the relative frequency of many class of aneurysms, there remains in the neurosurgical community some degree of confusion regarding the detailed anatomic features and the technical aspects of the treatment of these lesions in the acute stage. In our study of 1,433 cases, we have enumerated four aspects of the pitfalls in aneurysm surgery which should be considered when planning the operative approach to these lesions. These four aspects will be reviewed in relation to the aneurysm surgery: (1) inadequate pre-operative planning; (2) inappropriate response to unexpected premature rupture; (3) poor clipping techniques and clip selection; (4) unintentional occlusion or injury of perforating branches. This discussion will simply elaborate our own conceptual and microsurgical technical approach in dissecting the aneurysms. Minimal retraction was used during the whole surgical procedure. The intracranial brain tension was reduced through a ventricular tap for hydrocephalus or evacuation of hematoma prior to aneurysm surgery. A venous pathway was established for blood circulation. Sharp dissection, using our newly designed jet irrigation bipolar suction method was employed. Regarding the clipping of the aneurysm, we used the tentative clipping and the dome coagulation method thereby preventing the ischemic changes and shortening of the entire clipping procedure. Although the strategies, discussed represent simply our approach to this problem, the principles included have proven quite successful and have allowed safe and definitive treatment in the overwhelming majority of patients and also options to overcome the pitfalls in aneurysm surgery.

Acute Disease↗
PubMed1997

[Difference of blood cell counts with reference blood cell counters in different makers: Part II].

This is the second report of evaluation on the difference of blood cell counting among different automated blood cell counters in Japan. We tested reference blood cell counters of 6 different companies: Coulter, Sysmex, Bayer-Sankyo, Nihon Kohden, Horiba and Dainabot. Forty ml of whole blood were taken from 3 healthy persons and EDTA-2K anticoagulated blood samples (Sample 1, 2 and 3) were sent to each company to determine blood cell counts with a reference automated counter. As a result, the following items showed more than 10% difference among makers: RBC between Dainabot and Horiba in Sample 3, hematocrit values between Coulter and Dainabot in Sample 2, WBC between Nihon Kohden and each of three makers (Sysmex, Horiba and Dainabot) in all 3 samples and that between Bayer-Sankyo and each of two makers (Sysmex and Horiba) in Sample 3 and platelet count between Dainabot and each of 3 makers (Bayer-Sankyo, Nihon Kohden and Horiba) in all 3 samples. The following items showed difference between 5 and 10%: MCV between Coulter and each of two makers (Bayer-Sankyo and Horiba), WBC between each of two makers (Coulter and Nihon Kohden) and each of other 4 makers, and platelet count between each of two makers (Nihon Kohden and Horiba) and each of 3 makers (Coulter, Sysmex and Bayer-Sankyo). Recently Japanese Committee for Clinical Laboratory Standards proposed minimum clinical allowance of blood cell count as follows: hemoglobin 3%, RBC 4%, MCV 4%, WBC 7% and platelet count 10%. It is suggested that all of the items showing the difference more than above allowance among makers should be improved for clinical use to have good external quality control in blood cell counting by automated instruments.

Blood Cell Count↗
PubMed1997

[Decision support of clinical laboratory test by object-oriented data base].

We have constructed an object-oriented database system, using prescription, lab test result, and disease registry data, transmitted from the order entry system of Hamamatsu University Medical School Hospital. It serves not only numeric data but also semantics of laboratory results. The database system has a feature to categorize each data into structured hierarchies of attributes. By this, the user can retrieve abstract level descriptions such as "prescriptions of anti-inflammation medicines, suppository only", "any kind of gastric ulcer", etc., which is expected to be useful for researchers and students. In transferring order entry data from HIS, HL7-ASTM E1238 standard data formats using the Japan Association of Clinical Pathology lab test item code are utilized, proving this system's transferability to other hospitals. This is the first real use implementation of an object-oriented data base in a clinical setting, and results are promising in terms of providing an intelligent clinical database. Also discussed are future trends of clinical master files, hospital administrative tools, and multi vendor configurations of HIS.

Clinical Laboratory Techniques↗
PubMed1997

Genetic mutations of butyrylcholine esterase identified from phenotypic abnormalities in Japan.

We have identified 12 kinds of genetic mutations of butyrylcholine esterase (BCHE) from phenotypic abnormalities, showing that BCHE activities were deficient or diminished in sera. These genetic mutations, detected by PCR-single-strand conformation polymorphism analysis and direct sequencing, consisted of one deletion (BCHE*FS4), nine missense (BCHE*24 M, *1005, *250P, *267R, *330I, *365R, *418S, *515C, *539T), and two nonsense mutations (BCHE*119STOP, *465STOP). All of the individuals deficient in serum BCHE activity were homozygous for silent genes (6 of 6). Fifty-eight percent of the individuals (31 of 53) with slightly reduced serum BCHE activity were heterozygous for silent genes. They also showed a higher frequency (47% as allele frequency) of the K-variant than the general population (17.5%). Finally, we confirmed low serum BCHE activity in 10 of 23 individuals heterozygous for silent genes.

Butyrylcholinesterase↗
PubMed1996

Activation of nuclear factor-kappaB via T cell receptor requires a Raf kinase and Ca2+ influx. Functional synergy between Raf and calcineurin.

Signals transduced via the TCR activate the transcription factor nuclear factor-kappaB (NF-kappaB), which, in turn, is critical to the transcriptional induction of many genes important for the proliferation and expression of a differentiated phenotype. Treatment of T cells with the protein kinase C activator PMA in combination with Ca2+ ionophores mimics this process, and the two agents are often substituted for TCR stimulation, bypassing the TCR. Here we identify intracellular signaling components involved in activation of NF-kappaB following TCR stimulation. TCR signaling was triggered by treating Jurkat T cells with PHA or anti-CD3 Abs, and NF-kappaB activation was monitored by electrophoretic mobility shift assays and/or by kappaB-dependent reporter assays. Contrary to the idea that protein kinase C is involved in TCR-mediated activation of NF-kappaB, high doses of staurosporine did not interfere with activation of NF-kappaB by PHA, while the same dose of staurosporine completely blocked activation by PMA. PHA-induced kappaB-dependent reporter activity was, however, effectively blocked by a dominant negative form of Raf-1, suggesting a critical role for a Raf kinase. The TCR-mediated activation of NF-kappaB was also dependent on a Ca2+ influx, because the Ca2+ channel blocker, SK&F 96365, as well as other agents that prevented the Ca2+ influx, inhibited NF-kappaB activation. Cotransfection of a constitutively active form of calcineurin largely substituted for the Ca2+ requirement and reversed the blockade by SK&F 96365. Consistent with these observations, coexpression of constitutively active forms of Raf-1 and calcineurin synergistically induced kappaB-dependent reporter activity, suggesting a physiologically relevant functional interaction between the kinase and the phosphatase.

Calcineurin↗
PubMed1996

Effects of GABA on spontaneous [Ca2+]c dynamics and electrical properties of rat adrenal chromaffin cells.

A large fraction of rat adrenal chromaffin cells (about 60%) shows spontaneous [Ca2+]c oscillations and spontaneous action potentials. In the present study the effects of gamma-aminobutyric acid (GABA) on the spontaneous [Ca2+]c oscillations and electrical properties of rat adrenal chromaffin cells were investigated using Fura-2 [Ca2+]c imaging and patch clamp techniques. GABA inhibited the spontaneous [Ca2+]c oscillations in a reversible manner. The effect of GABA was mimicked by the GABAA and GABAC receptor agonist, muscimol, but not by the GABAB receptor agonist, baclofen. Moreover, the effect was antagonized by the selective GABAA receptor antagonist, bicuculline. The mode of the inhibition was all-or-none, and the threshold concentration at which the inhibition occurred varied widely (50 microM to over 1 microM) from cell to cell. GABA (100 microM) elicited a transient burst of action potentials of diminished amplitude, which was followed by arrest of action potentials. Further analysis showed that GABA (100 microM) induced inward whole-cell currents in voltage-clamp experiments and produced depolarization and membrane conductance increase in current-clamp experiments. The effects appear to be due to an increase in chloride ion conductance since the degree of GABA-induced depolarization depended on the pipette [Cl-]. These results suggest that GABA, acting through GABAA receptor, may play a role in the physiological regulation of rat adrenal chromaffin cells by directly modifying the discharge of spontaneous action potentials and spontaneous [Ca2+]c oscillations.

Action Potentials↗
PubMed1996

Lipid secretory mechanisms in the mammalian harderian gland.

The mammalian Harderian glands are lipid-secreting glands. In an unstimulated condition, the glandular cells frequently exocytose the lipid materials; however, no intracellular calcium ion ([Ca2+]c) changes are detectable. Cholinergic (muscarinic) secretagogues induce secretory activity and increase of [Ca2+]c. A G-protein activator, sodium fluoride, enhances the secretory activity and increase of [Ca2+]c. Removal of extracellular calcium ions inhibits the secretion enhanced by cholinergic stimulation. Under pharmacologic stimulation, glandular cells may show an apocrine-like secretory pattern. Cholinergic stimulation also induces contraction of the myoepithelial cells covering glandular end pieces; however, the reduction in volume of glandular end pieces is not prominent. Catecholamines have no effect on the release of lipid materials. These results indicate the involvement of G-proteins linking with muscarinic receptors and Ca2+ dynamics (increase of [Ca2+]c and Ca2+ influx) in lipid secretion by glandular cells and in contraction of myoepithelial cells of mammalian Harderian glands. However, the increase of [Ca2+]c in Harderian glands was less when compared with other cells--for instance, those which secrete protein.

Animals↗
PubMed1996

An improved technique for low anterior resection using a PDS endoloop.

We describe herein the results of performing a new technique of low anterior resection of the rectum using a PDS endoloop, on ten patients with rectal cancer. This technique involves first preparing the rectosigmoid colon with an anvil as in the conventional low anterior resection; then, after the stapler is inserted transanally, two endoloops are solid over the colon and rectum. The rectum is ligated by pushing the knot of the endoloop and a second knot is applied 2 cm proximal to the first. Finally, the rectum is cut and the stapler is closed and fired to make a circular end-to-end anastomosis. The level of the anastomosis ranged from 2.5 to 6 cm with a mean of 4.7 cm in the ten patients, only one of whom developed a minor anastomotic leakage postoperatively. Moreover, no patient has developed local recurrence or distant metastasis to date. In summary, this technique offers certain advantages that allow the operation to be done with more skill and safety in a narrow pelvis.

Adenocarcinoma↗
PubMed1996

Synthesized surface anatomy scanning (SSAS) for surgical planning of brain metastasis at the sensorimotor region: initial experience with 5 patients.

Surface anatomy scanning (SAS) is a powerful technique that uses T2-weighted magnetic resonance images (MRI) to visualize brain surface structures, and to precisely localize subcortical lesions. To overcome technical limitations of this method, synthesized SAS (SSAS) superimposes MR angiography (MRA) data on the SAS images. We describe our initial experience with surgical planning for the resection of metastases at the sensorimotor region in 5 patients using SSAS. Neurological deficits were assessed before and after surgical resection. Although 4 of 5 patients had mild to severe neurological deficits before surgery, three became symptom-free and no patient had an increased deficit after surgery. Our results undoubtedly provide palliative surgery for sensorimotor metastases. As SSAS is non-invasive and requires a short scanning time, this method could become a useful technique for the routine pre-operative simulation for surgery on brain surface lesions such as sensorimotor metastases.

Adenocarcinoma↗