Effect of collisionality and diamagnetism on the plasma dynamo.
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Journal Article↗
Biomedical subjects
Y Hirano
Publications and source records attributed to Y Hirano.
A human temperature-sensitive p53 mutant p53Val-138: modulation of the cell cycle, viability and expression of p53-responsive genes.
A human p53 mutant, p53Val-138 (amino acid 138, Alanine-->Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression. p53Val-138 caused growth arrest in Saos-2 cell line and apoptosis in Jurkat cell line at 32.5 degrees C while it allowed both cell lines to grow continuously at 37.5 degrees C. p53Val-138 activated expression of p53-responsive genes including MDM2, GADD45 and WAF1/CIP1/SD11 in Saos-2 cell line upon the temperature shift-down from 37.5 degrees C to 32.5 degrees C. Thus, p53Val-138 acted as a temperature-sensitive p53 mutant. Taking advantage of these human cell systems, we demonstrated that p53-mediated cell cycle arrest occurred in G1 and G2/M phases of Saos-2 cell line but not in Jurkat cell line. The induced level of WAF1/CIP1/SDI1 mRNA by p53 was extremely lower in Jurkat cell line than that of Saos-2 cell line. However, MDM2 mRNA accumulated to the similar levels in these two cell lines. These results suggest that a factor(s) other than p53 may be involved in differential expression of WAF1/CIP1/SDI1 and MDM2 mRNA.
Apoptosis↗
Transcriptional inhibition of insulin by FK506 and possible involvement of FK506 binding protein-12 in pancreatic beta-cell.
FK506 (tacrolimus) is a strong immunosuppressant: it has been approved as a drug for liver transplantation in Japan, the United States, and the United Kingdom. One of its main adverse effects is hyperglycemia. Thus, in this study, we investigated the mechanism and the reversibility of the hyperglycemia caused by FK506. FK506 did not affect the glucose uptake by insulin into rat strio-muscle cell line, but suppressed insulin production in rat insulinoma cells. Two-week oral administration of FK506 at 10 mg/kg/day suppressed insulin production time-dependently at the transcriptional step in pancreatic beta-cells, while glucagon content in pancreatic alpha-cells was not affected. When FK506 administration was stopped in these rats, insulin mRNA transcription and insulin production returned to normal. This recovery indicates that the adverse effect of FK506 on the pancreas is reversible. A high content of FK506 binding protein-12 (FKBP-12) in the pancreatic beta-cells was confirmed by immunostaining with anti-human FKBP-12 mAb, but the content was less in the pancreatic alpha-cells and almost negligible in the acinar cells. In contrast, a high content of calcineurin in the pancreatic alpha-cells was confirmed by using anti-calcineurin polyclonal antibody, but this content was less in the pancreatic beta-cells and not found in the acinar cells. Thus, as in the case with NF-AT in T cells, these findings point to the reduction of unidentified nuclear factors for insulin mRNA transcription caused by the binding of FK506 to FKBP-12 and a subsequent inhibition of calcineurin in the beta-cells.
Animals↗
A temperature sensitive mutant of the human p53, Val138, arrests rat cell growth without induced expression of cip1/waf1/sdi1 after temperature shift-down.
To investigate functions of wild type p53 in human cells, we introduced a (Ala-->Val) mutation at the 138th codon of the human p53 (Val138), which corresponds to the Val135 mutation of the temperature sensitive mouse p53. The human Val138 mutant showed temperature-sensitive transformation of rat embryo fibroblasts (REFs) in collaboration assay with activated ras, and arrested cell proliferation of transformed clones in G1 at 32.5 degrees C. Transient CAT assay for transcriptional activation in human Saos2 cells revealed activity equivalent to that of wild type at 32.5 degrees C but undetectable at 37.5 degrees C. These results suggest that the human Val138 mutant also exhibited the wild type phenotype at the permissive temperature as is for the mouse Val135 mutant, although we observed differences between the two mutants such as in transactivational activities in CV-1 and HeLa cells. Further, the role of cip1/waf1/sdi1 in the cell growth arrest of the Val138/ras-transformed REFs and Val138-introduced Saos2 cells was studied by northern hybridization analysis. Although rapid induction of cip1/waf1/sdi1 mRNA was observed in the Saos2 cells, no detectable induction of mRNAs for cip1/waf1/sdi1 and gadd45 was observed in the transformed REFs upon temperature shift-down, while mdm2 mRNA was enhanced, suggesting that the p53 gene could arrest cell growth by a mechanism other than that with induced expression of the gene for p21 cdk-cycline inhibitor.
Animals↗
What is the most appropriate variable for estimation of mean pulmonary capillary wedge pressure by transesophageal pulsed Doppler echocardiography?
UNLABELLED: Although left ventricular (LV) inflow and pulmonary venous (PV) flow variables estimated by transesophageal Doppler echocardiography (TEE) reflect pulmonary capillary wedge pressure (PCWP), they are also affected by changes in cardiac function. The purpose of the present study was to detect the most appropriate variable for the estimation of PCWP by TEE in patients (pts) with ischemic heart disease. Several variables of LV inflow and left upper PV flow were compared with PCWP in 36 pts (six with angina pectoris and 30 with old myocardial infarction). Early diastolic flow (E) and atrial contraction flow (A) were used as LV inflow, while systolic forward flow (X), diastolic forward flow (Y) and atrial contractile reversal flow (z) were used as PV flow. The peak velocity of each flow wave (Ep, Ap, Xp, Yp, and Zp) and the time-velocity integral (Ei, Ai, Xi, Yi, and Zi) were measured. The ratio of Ep to Ap (Ep/Ap), Ei to Ai (Ei/Ai), Xp to Yp (Xp/Yp), Xi to Yi (Xi/Yi), Zp to Ap (Zp/Ap), Zi to Ai (Zi/Ai) and the systolic fraction of PV forward flow were calculated. Among these variables, the Zi/Ai ratio was most strongly correlated with PCWP (R = 0.80). The Zi/Ai ratio may not be influenced by atrial function because the augmentation of atrial pump function increases Zi as well as Ai, and this may be one reason why the ratio correlated well with PCWP. CONCLUSION: The Zi/Ai ratio is a new useful variable for estimating PCWP by TEE.
Aged↗
Roles of p53 mutation in cell line establishment and identification of the minimum transactivation and transform suppression domains.
The mutation of the p53 tumour suppressor gene is the most frequently recognised genetic alteration in human cancer. We recently showed that the frequency of p53 gene mutations in oral squamous cell carcinomas (SCCs) from which cell lines were established (group A) did not significantly differ from that in SCCs from which cell lines could not be established (group B), suggesting that the presence of a p53 mutation by itself is not sufficient. To assess the relevance of p53 mutations to cell line establishment, we determined sequences of the mutated genes, constructed the expression plasmids, and compared biological and biochemical activities. Both groups contained typical mutant type mutations at a similar frequency. However, two mutations in group A had strong transforming activity. One of the mutants, codon 306 Stop mutant with C-terminal truncation, was found to have the transactivation and transform suppression activities similar to wild type. The minimum transactivation and transform suppression domains of p53 were thus determined based on analysis of various C-terminal deletions. Activity disappeared between codons 300 and 282, an interval which contains the C-terminal end of the sequence-specific DNA binding domain, which suggests that the DNA binding domain is essential for the above activities.
Base Sequence↗
Acute disseminated encephalomyelitis after treatment with Japanese B encephalitis vaccine (Nakayama-Yoken and Beijing strains).
Seven children with acute disseminated encephalomyelitis (ADEM) after treatment with Japanese B encephalitis vaccine (JBEV) (Nakayama-Yoken strain 1968-88 and Beijing strain 1989-93) were identified by mailed questionnaires and by compilation of previously published case reports. It was considered that encephalomyelitis might have been related to vaccine treatment as the vaccine is derived from mouse brain tissue infected with Japanese B encephalitis virus, a potentially cross reactive antigen. The incidence of severe neurological complications associated with the newer Japanese B encephalitis Beijing strain vaccine seemed to be less than one case per 1,000,000, which is similar to the incidence of neurological complications associated with the older Nakayama-Yoken strain vaccine.
Child↗
Dual effects of external magnesium on action potential duration in guinea pig ventricular myocytes.
Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.
Action Potentials↗
Arginine vasopressin-induced potentiation of unitary L-type Ca2+ channel current in guinea pig ventricular myocytes.
The effects of arginine vasopressin (AVP) on L-type Ca2+ channels were studied by recording single-channel activity from cell-attached patches on isolated guinea pig ventricular myocytes, with 100 mmol/L Ba2+ used as the charge carrier. Bath application of AVP (100 nmol/L) reversibly increased channel open probability by a factor of 2.92 +/- 1.43 (n = 15) because of the increased number of channel openings and increased open times. AVP did not change the amplitudes of single-channel currents (1.17 +/- 0.10 pA in the control condition and 1.12 +/- 0.11 pA after AVP, at +20 mV; n = 6). In our experimental conditions, in which myocytes were bathed in Ca(2+)-free high-potassium solutions, AVP-induced potentiation was observed without changes in [Ca2+]i measured by fura 2 fluorescence signals (estimated [Ca2+]i, approximately 80 nmol/L). The AVP-induced increase in channel open probability was abolished by OPC-21268 (8 mumol/L), a specific blocker of V1 receptor, but not by a V2 blocker, OPC-31260 (5 mumol/L). AVP-induced potentiation was also suppressed by a broad-spectrum protein kinase inhibitor, H7 (100 mumol/L, bath application), but not by H89 (1 mumol/L), a blocker with high specificity to protein kinase A. AVP application after the treatment by phorbol ester (phorbol 12-myristate 13-acetate, 100 nmol/L for 1 hour) failed to potentiate the channel activity. These results raised the possibility that protein kinase C might be involved during signal transduction. Our results provide direct evidence that AVP potentiates cardiac L-type Ca2+ currents via V1 receptor stimulation.
Animals↗
Computer-assisted reconstruction of enamel fissures and carious lesions of human premolars.
The origin of cariogenesis in occlusal fissures remains elusive because of limited information about both the fissure structure and the morphologic details of carious lesions occurring there. The present study was aimed at reconstructing the coronal structure of human premolars with the aid of computer-assisted image analysis and, on the basis of the reconstructed structures, investigating the configuration of fissures, their proximity to the enamel-dentin junction (EDJ), and the occurrence and extension of carious lesions around the fissure walls. The coronal portions of the teeth were embedded in polyester resin and then ground off stepwise by hand. Serial images of the enamel contour on successive ground planes were recorded by objective microscopy after it was distinctly demarcated with either 0.5 w/v% carbol fuchsin or 1 w/v% basic fuchsin. Usually, from 150 to 250 photoprints were collected from a single enamel crown to reproduce the details of the fissure structures. The enamel outline (the occlusal and lateral surfaces, fissure walls, and EDJ) and, if present, the outline of caries-attacked areas were traced accurately on those photoprints by means of a digitizing system. The enamel contour data in series were input into an image analyzing system (Nikon COSMOZONE, 2SA). Observation of the computer-drawn coronal enamel allowed us to view the morphologic features of the fissures (shape, divarication, and proximity to EDJ) and to scrutinize the pathway of enamel caries along fissure walls.(ABSTRACT TRUNCATED AT 250 WORDS)
Dental Enamel↗
Adsorption of saliva-coated and just-harvested Streptococcus sanguis to saliva-coated hydroxyapatite beads.
It is possible that salivary proteins on bacterial cells have some influence on the adsorption of oral bacteria to the surface of oral tissues. The aim of this study was to clarify the influence of salivary proteins attached to the surface of Streptococcus sanguis ATCC 10556 (S. sanguis) on bacterial adsorption to hydroxyapatite beads treated with salivary proteins (S-HA beads). Just-harvested cells (N-system) and saliva-coated cells (C-system) were used. The results showed that adsorption to S-HA beads was gradually reduced by a covering of salivary proteins. No influence was observed on the adsorption of cells due to the presence of divalent cations, phosphate or EDTA when the N-system and C-system were compared. Though it was evident that hydrophobic bonding was involved in adsorption in the N-system, few such effects were observed in the C-system. Adsorption was inhibited to varying degrees by sugars in both systems. Pretreatment of cells with heat affected adsorption differently in the N-system and C-system. These findings suggest that salivary proteins attached to the bacterial cell surface may influence its adsorption to oral tissues.
Adsorption↗
Bacterial adsorption to fetuin and mucin pellicle.
The ability of Actinomyces viscosus (A. viscosus) WVU 627 to attach to hydroxyapatite (HA) beads treated with either bovine fetuin or bovine mucin was studied. All preparations used were blocked with bovine serum albumin prior to incubation with [3H] thymidine-labeled A.viscosus cells. The quantity of fetuin or mucin adsorbed on the HA beads was determined by use of [3H] fetuin or [3H] mucin. Approximately 6 micrograms protein of [3H] fetuin and 20 micrograms of protein of [3H] mucin adsorbed to 5 mg of HA beads at saturation, respectively. The presence of fetuin or mucin on HA beads promoted attachment of the organism. However, HA beads treated with human whole saliva as a positive control promoted A.viscosus attachment more effectively than HA beads treated with these glycoproteins. Attachment of two additional strains (B 236 and B 25) of A. viscosus to HA beads was also promoted by these glycoproteins. The number of A.viscosus cells which attached to fetuin-treated HA beads was dose-dependent, except for strain B 25. For all three A.viscosus strains tested, attachment to the experimental pellicle with mucin was dose-dependent. These findings suggest that the use of these newly developed bacterial adhesion assay systems may be effective for elucidating bacterial adhesion mechanisms.
Actinomyces↗
Inhibition of insulin production by FK 506 is caused at the transcriptional level in pancreatic beta cell when FK BP-12 content is relatively high.
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Animals↗
[Dobutamine stress echocardiography in the diagnosis of myocardial ischemia in patients with implanted pacemakers: report of two cases].
Dobutamine stress echocardiography was used in the diagnosis of myocardial ischemia in patients with implanted VVI pacemakers. A 69-year-old woman received a pacemaker for Mobitz II type AV block in October 1992. She had suffered from chest pain during effort since January 1993 and underwent dobutamine stress echocardiography in April 1993. Although the electrocardiogram failed to identify ischemia because of the pacemaker rhythm, ischemia of the anterior wall was revealed as a worsening of the wall motion on the echocardiogram. The coronary angiogram showed 99% stenosis of the left descending artery. A direct coronary atherectomy was performed on the lesion. A 68-year-old man received a pacemaker for sick sinus syndrome in August 1993. He had suffered from chest oppression during effort since May 1992 and underwent dobutamine stress echocardiography in October 1993. Spontaneous rhythm appeared with dobutamine infusion, but the electrocardiogram could not demonstrate ischemia because of incomparability with the rhythm at rest. Echocardiography detected a new wall motion abnormality of the inferior wall caused by dobutamine. The coronary angiogram showed 90% stenosis of the right coronary artery. PTCA was performed on the lesion. Dobutamine stress echocardiography is useful for the diagnosis of myocardial ischemia in patients with implanted pacemakers.
Adrenergic beta-Agonists↗
Cardiovascular effects of YM099, a novel K+ channel opener, in anesthetized and conscious dogs.
Cardiovascular effects of a newly synthesized benzoxadiazol derivative K+ channel opener, YM099, 2-(7,8-dihydro-6,6-dimethyl-6H-[1,4]oxazino[2,3- f][2,1,3]benzoxadiazol-8-yl) pyridine N-oxide, were evaluated in dogs. In pentobarbital-anesthetized dogs, YM099 (1-10 micrograms/kg i.v.), similarly to levcromakalim (1-10 micrograms/kg i.v.), dose dependently increased coronary artery blood flow, max.d p/dt and cardiac output, and decreased total peripheral resistance and mean blood pressure, with a small increase in heart rate. These vasodilator effects were antagonized by glibenclamide (3 mg/kg i.v.). Interestingly, YM099 selectively increased coronary artery blood flow, although it increased carotid, coronary, mesenteric and renal artery blood flows and cardiac output. In addition, YM099 (1-10 micrograms/kg i.v.) increased large conductive coronary artery vessel diameter as well as coronary artery blood flow. In conscious dogs, YM099 (100 micrograms/kg i.v.) also increased the diameter of large conductive and small resistive coronary arteries. In conclusion, YM099 is a potent vasodilator agent, with particularly pronounced effects on the coronary artery. These effects of YM099 may be mediated by the opening of ATP-sensitive K+ channels.
Adenosine Triphosphate↗
Dual modulation of unitary L-type Ca2+ channel currents by [Ca2+]i in fura-2-loaded guinea-pig ventricular myocytes.
1. Single-channel studies were performed to clarify how tonic changes in intracellular Ca2+ concentrations ([Ca2+]i) modulate cardiac L-type Ca2+ channels. Currents were recorded from fura-2-loaded guinea-pig ventricular myocytes in the cell-attached configuration. Fura-2 fluorescence signals were recorded simultaneously during pulses to elicit channel activity. 2. The myocyte [Ca2+]i was altered through changes in bath Ca2+ concentration during K+ depolarization. When [Ca2+]i exceeded approximately 2 times the resting level (estimated [Ca2+]i around 180-400 nM), the activity of Ca2+ channels was reversibly potentiated without changes in unitary current amplitudes. 3. Increased channel open probability during Ca(2+)-dependent potentiation resulted from increased availability and increased open probability during non-blank sweeps. Closed time analysis revealed a distribution best fitted with two exponentials. Increased [Ca2+]i reduced the longer time constant, but had no effect on the shorter time constant. The open time constant was unchanged in most cases. Current records occasionally included sweeps with long openings (approximately 10 ms or more), whose appearance increased during potentiation. 4. When [Ca2+]i was increased after cAMP-dependent upregulation of Ca2+ channels, the change in channel activity was diminished. Similar results were observed when Ca(2+)-dependent potentiation was examined in myocytes exposed to a membrane-permeant protein kinase inhibitor, H-89. This suggests that channel phosphorylation may be responsible for Ca(2+)-dependent potentiation. 5. When [Ca2+]i was further increased, but remained below the threshold for contraction (estimated [Ca2+]i above 600 nM), Ca2+ channel activity was suppressed. 6. Our results demonstrate directly at the single-channel level that [Ca2+]i modulates the activity of cardiac L-type Ca2+ channels, enhancing it with modest [Ca2+]i increases and decreasing it with greater [Ca2+]i increases.
Animals↗
Localization of blood-group-related linear poly-N-acetyllactosamine structure in different human tissues by Griffonia simplicifolia agglutinin-II staining following endo-beta-galactosidase digestion.
Endo-beta-galactosidase from Escherichia freundii cleaves polylactosaminyl structures as follows: R-GlcNAc beta I-3Gal beta I-4GlcNac beta I-R' + H2O-->R-GlcNAc beta I-3Gal + GlcNAc beta I-R'. By staining with Griffonia simplicifolia agglutinin-II following the enzyme digestion, the distribution of R-GlcNAc beta I-3Gal beta I-4GlcNAc can be demonstrated in tissue sections. This carbohydrate chain is one of the backbone structures carrying the blood-group-related antigens and, thus, localization of this structure may provide detailed information about the distribution of variants with different backbone structures. Various formalin-fixed, paraffin-embedded tissue sections were stained by Griffonia simplicifolia agglutinin-II with or without prior enzyme digestion and the reactivity of the agglutinin imparted by enzyme digestion was studied in the following tissues and cells: pancreatic acinar cells, gastric surface mucosae, duct cells and mucous cells of salivary glands and tracheal glands, surface epithelium of trachea, goblet cells of large intestine, columnar epithelium of uterine cervical glands, distal and collecting tubules of kidney, certain cells of anterior lobe and colloid of middle lobe of pituitary glands, epithelial reticular cells and Hassall's corpuscles of thymus and Kupffer cells of liver. In gastric surface mucosae, the reactivity of the agglutinin appeared in non-secretor individuals but not in the secretor individuals, and in mucous cells of salivary and tracheal glands the reactivity appeared in Le(a- b-) non-secretor individuals but not in Le(a + b-) non-secretor or secretor individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Four cases of acute liver damage following the ingestion of a sea hare egg.
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Adult↗