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Biomedical subjects

A Abe

Publications and source records attributed to A Abe.

At least 109 records · Page 6Linked to original sources
PubMed1998

Enteropathogenic E. coli interactions with host cells.

Enteropathogenic E. coli (EPEC) interacts with intestinal epithelial cells, causing diarrhea and associated diseases. This pathogen binds to epithelial cells using sophisticated mechanisms that exploit existing epithelial signal transduction pathways and host cytoskeletal components, ultimately resulting in the bacterium resting upon a pedestal on host cell surfaces. Recent data indicates that similar mechanisms occur in vivo. EPEC interactions with host cells illustrate several principles of pathogenesis that are used by bacteria that interact with mammalian host cells.

Animals↗
PubMed1998

[Number of apolipoprotein(a) kringle IV repeats and mobility of isoforms in PAGE].

Serum apo(a) isoform sizes were determined by SDS-polyacryl amide gel electrophoretic (PAGE) method, followed by a high sensitive immunoblotting. The relation between the number of apo(a) kringle IV encoding sequences in the apo(a) gene, as assessed by pulsed field gel electrophoresis and genomic blotting (genotype), and the apo(a) isoforms (phenotype) in SDS-PAGE was evaluated in 78 individuals. The correlation of apo(a) allele number between phenotype and genotype method was high (r = 0.513) in 178 expressed apo(a) alleles. This nomenclature is achieved by using standard serum of kringle IV repeats. We conclude that this method is an approach to genotyping to designate the phenotypes by kringle IV repeats.

Adult↗
PubMed1998

[Actual situation and problems in the information office of clinical laboratories; questionnaire surveys of central laboratories of university hospitals].

The laboratory tests supplied by clinical laboratory comprise an increasing volume in most hospitals. Consultation and effective utilization of laboratory data are important aspects of evidence-based medicine. Effective utilization of laboratory data will also contribute to the efficiency of hospital practice. Questionnaire surveys were conducted to investigate the actual situation in the information office of clinical laboratories in national, public and private facilities of 80 medical universities in Japan. Few facilities demonstrated efficient functioning, although information offices had been opened in six national, one public, and four private universities. The office staff received many questions on specimen handling and analytical methods. In the future, the office will be expected to be actively involved in mutual communications with clinical physicians and an information system such as computerized web is anticipated. Furthermore, a full-time laboratory physician and technicians are expected to provide support as experts in patient diagnosis.

Clinical Laboratory Information Systems↗
PubMed1997

Fusion of the platelet-derived growth factor receptor beta to a novel gene CEV14 in acute myelogenous leukemia after clonal evolution.

Chromosomal translocations involving band 5q31-35 occur in several hematologic disorders. A clone with a t(5; 14)(q33; q32) translocation appeared at the relapse phase in a patient with acute myelogenous leukemia who exhibited a sole chromosomal translocation, t(7; 11), at initial diagnosis. After the appearance of this clone, the leukemia progressed with marked eosinophilia, and combination chemotherapy was ineffective. Southern blot analysis showed a rearrangement of the platelet-derived growth factor receptor beta (PDGFRbeta) gene at 5q33 which was not observed at initial diagnosis. This translocation resulted in a chimeric transcript fusing the PDGFRbeta gene on 5q33 with a novel gene, CEV14, located at 14q32. Expression of the 5' region of the PDGFRbeta cDNA, upstream of the breakpoint, was not detected. However, the 3' region of PDGFRbeta, which was transcribed as part of the CEV14-PDGFRbeta fusion gene, was detected. A partial cDNA for a novel gene, CEV14, includes a leucine zipper motif and putative thyroid hormone receptor interacting domain and is expressed in a wide range of tissues. The expression of a CEV14-PDGFRbeta fusion gene in association with aggressive leukemia progression suggests that this protein has oncogenic potential.

Amino Acid Sequence↗
PubMed1997

Complete remission in three patients with acute myeloblastic leukemia by administration of G-CSF without antileukemic agents.

We describe 3 patients with acute myeloblastic leukemia (AML), who received rhG-CSF for infections such as pneumonia or for prophylaxis of infection, and who achieved complete remission. They had not received any antileukemic therapy before or during the administration of rhG-CSF. These findings suggest the possibility that complete remission can be brought about by G-CSF itself in some patients with AML.

Aged↗
PubMed1997

Induction of TNF-alpha mRNA in murine macrophages by virulent and avirulent strains of Salmonella choleraesuis serovar typhimurium and serovar Choleraesuis.

TNF-alpha mRNA induction in murine macrophages by virulent and avirulent Salmonella strains was measured in vitro by RT-PCR method. Virulence plasmid-cured strains of S. choleraesuis serovar Typhimurium and serovar Choleraesuis, and rpoS-defective mutant of S. choleraesuis serovar Typhimurium induced significantly higher level of TNF-alpha mRNA than their parent (virulent) strains in macrophages of C3H/HeN mice. When macrophages of LPS-low responder (C3H/HeJ) mice were used, the difference of the induction level was not observed, indicating that LPS was involved in the enhanced level of TNF-alpha mRNA induction by avirulent Salmonella strains. LPSs from virulent and avirulent strains were analysed, but no difference was found for cytokine-inducing activity, and chemical properties. Those results suggested that avirulent Salmonella strains were damaged more easily, and released more LPS in macrophages to enhance TNF-alpha induction.

Animals↗
PubMed1997

Ultrastructure of cholesterol gallstones as observed by electron microscopy after freeze-fracturing.

The ultrastructure of cholesterol gallstones (mixed type) was studied in detail for the first time under the transmission electron microscope after freeze-fracturing. Gallstones consisted essentially of cholesterol crystals, some impurities, and fluid. In accord with the theoretical 3.4 nm bilayered structure of cholesterol crystals, 3-4 nm periodicity of crystal layering was observed. However, gallstone cholesterol crystals were not perfect and often showed structural defects. Between crystals, complete edge-to-surface, edge-to-edge and surface-to-surface adhesions, and overall block-like aggregations were found. These may represent the structural basis for the stability of cholesterol crystal aggregation. The easy breakdown of cholesterol gallstones by extracorporeal shock wave lithotripsy is discussed in relation to their ultrastructure.

Aged↗
PubMed1997

Culture in the presence of sugars increases activity of multi-drug efflux transporter on Haloferax volcanii.

We found that when a growth medium contained glucose, wild-type cells of Haloferax volcanii were able to grow even in the presence of doxorubicin (DOX), an anti-cancer reagent, whereas they usually cannot grow in its presence. The reason was that cells grown in the presence of glucose (glucose-grown cells) showed high multi-drug efflux activity even though the growth medium contained no DOX or substrates of the transporter. This transporter was ATP-driven and the elevation of efflux activity was not due to an increase in intracellular ATP contents. The activity was increased not only by glucose but also by sugars that could be metabolized.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Experimental studies on three types of heparin-coated cardiopulmonary bypass circuits.

In cardiovascular operations, we have usually used heparin-coated cardiopulmonary bypass circuits with low systemic heparinization. Three types of heparin-coated cardiopulmonary bypass circuits are available in Japan: 2 of the 3 have covalent heparin bonding, and the other has ionic heparin bonding. We studied these circuits in ex vivo experiments to explore which were the best in terms of biocompatibility. In this study we compared the Carmeda system (Medtronic) and the Capiox system (Terumo) with covalent heparin bonding, and the Duraflo-II (Baxter) with ionic heparin bonding, evaluating them in ex vivo experiments. They were primed with fresh human blood, and we studied and compared the platelet counts, fibrinogen, D-dimmer, beta-thioguanine (TG), thrombin-antithrombin complex (TAT), and C3a and C4a of each of them. Additional research will be presented in the future.

Anticoagulants↗
PubMed1997

Morphological variation of nonreentrant idiopathic ventricular tachycardia originating from the right ventricular outflow tract and effect of radiofrequency lesion.

RF catheter ablation was performed in 16 patients with nonreentrant idiopathic VT originating from the RVOT. All documented VT was monomorphic, but subtle morphological variation in the VT-QRS complex was observed in 10 (63%) of 16 patients. Through endocardial mapping, VT origin was determined within a narrow site (< 0.5 x 0.5 cm) in 4 of the 10 patients with the morphological variation. In the other 6 of 10 patients, the origin extended to an area of > 0.5 x 0.5 cm. In VT with morphological variation, the local electrogram at the site of VT origin also showed variation in morphology and activation sequence. For VT of narrow origin, RF application to the site eliminated the VT. However, in VT from a wide arrhythmogenic area, RF current had to be delivered to 3-7 distinct sites to cover the possible origin, and specific QRS configuration of VT and/or PVC was ablated at each of the earliest activation site. All but one VT were successfully ablated by RF current. Subtle morphological variation was frequent in this type of VT, and about half were associated with a wide arrhythmogenic area. Precise mapping and analysis of the efficacy of each RF application might be helpful to better understand the relationship between subtle changes of VT-QRS morphology and their origins.

Adult↗
PubMed1997

Enteropathogenic Escherichia coli protein secretion is induced in response to conditions similar to those in the gastrointestinal tract.

The pathogenicity of enteropathogenic Escherichia coli (EPEC) is associated with the expression and secretion of specific bacterial factors. EspB is one such secreted protein which is required to trigger host signaling pathways resulting in effacement of microvilli and cytoskeletal rearrangements. These events presumably contribute to the ensuing diarrhea associated with EPEC infections. EPEC encounters several environmental changes and stimuli during its passage from the external environment into the host gastrointestinal tract. In this paper we show that the secretion of EspB is subject to environmental regulation, and maximal secretion occurs under conditions reminiscent of those in the gastrointestinal tract. Thus, secretion is maximal at 37 degrees C, pH 7, and physiological osmolarity. In addition, maximal secretion requires the presence of sodium bicarbonate and calcium and is stimulated by millimolar concentrations of Fe(NO3)3. The secretion of the four other EPEC-secreted proteins appears to be modulated in a manner similar to that of EspB. Our results also show that secretion is not dependent on CO2, as originally reported by Haigh et al. (FEMS Microbiol. Lett. 129: 63-67, 1995), but that CO2 more likely acts as a component of the medium buffering system, since CO2 dependence was abolished by the use of alternative buffers.

Ammonium Chloride↗
PubMed1997

Characterization of two virulence proteins secreted by rabbit enteropathogenic Escherichia coli, EspA and EspB, whose maximal expression is sensitive to host body temperature.

Enteropathogenic Escherichia coli (EPEC) and rabbit EPEC (RDEC-1) cause unique histopathological features on intestinal mucosa, including attaching/effacing (A/E) lesions. Due to the human specificity of EPEC, RDEC-1 has been used as an animal model to study EPEC pathogenesis. At least two of the previously identified EPEC-secreted proteins, EspA and EspB, are required for triggering host epithelial signal transduction pathways, intimate adherence, and A/E lesions. However, the functions of these secreted proteins and their roles in pathogenesis have not been characterized. To investigate the function of EspA and EspB in RDEC-1, the espA and espB genes were cloned and their sequences were compared to that of EPEC O127. The EspA proteins showed high similarity (88.5% identity), while EspB was heterogeneous in internal regions (69.8% identity). However, RDEC-1 EspB was identical to that of enterohemorrhagic E. coli serotype O26. Mutations in RDEC-1 espA and espB revealed that the corresponding RDEC-1 gene products are essential for triggering of host signal transduction pathways and invasion into HeLa cells. Complementation with plasmids containing EPEC espA or/and espB genes into RDEC-1 mutant strains demonstrated that they were functionally interchangeable, although the EPEC proteins mediated higher levels of invasion. Furthermore, maximal expression of RDEC-1 and EPEC-secreted proteins occurred at their respective host body temperatures, which may contribute to the lack of EPEC infectivity in rabbits.

Amino Acid Sequence↗
PubMed1997

Microatelectasis in patients with secundum atrial septal defect and its relation to pulmonary hypertension.

In patients with secundum atrial septal defect, pulmonary hypertension appears to be attributable to microatelectasis of the lung. To confirm this hypothesis, pulmonary arteries in surgical biopsy specimens from 72 patients with atrial septal defect and pulmonary hypertension were subjected to morphometric examination. Thirty eight of the 72 patients (53%) were found to have microatelectasis of the lung, which suggests that an even higher frequency would have been found if the entire organ had been examined. Atelectatic changes were found in 21 of 39 patients with plexogenic pulmonary arteriopathy (54%), 8 of 15 with musculoelastosis (53%), and 9 of 13 with both of these lesions (69%). No such changes were observed in 5 patients with atrial septal defect who showed thromboembolism-type lesions of the pulmonary arteries. On the other hand, microatelectasis was not observed in another 5 patients with atrial septal defect who did not exhibit pulmonary hypertension. The medial smooth muscles of pulmonary arteries in atelectatic areas were thicker (16.4 +/- 4.0 microns) than those in non-atelectatic areas (10.3 +/- 3.3 microns). The index of pulmonary vascular disease was not significantly different between atelectatic (2.0 +/- 0.6) and non-atelectatic areas (1.9 +/- 0.5). We conclude that in microatelectatic areas, which may tend to develop after respiratory infections in patients with atrial septal defect, hypoxic vasoconstriction of the small pulmonary arteries is liable to occur, which causes hypertrophy of the media. This is likely to lead to the elevation of pulmonary arterial pressure and sustained pulmonary hypertension.

Adolescent↗
PubMed1997

Effects of adrenergic, cholinergic and ganglionic blockade on acute depressor responses to metformin in spontaneously hypertensive rats.

Metformin lowers blood pressure in humans and in experimental animal models. To determine the mechanism of acute metformin-induced hypotension, we measured changes in mean arterial pressure (MAP) and heart rate (HR) during metformin alone (0, 10, 50, 100 mg/kg i.v.; n = 10) and during concomitant alpha adrenergic (phentolamine, 5 mg/kg; n = 5), beta adrenergic (propranolol, 3 mg/kg; n = 6), muscarinic (atropine, 200 micrograms/kg; n = 7), ganglionic (hexamethonium, 30 mg/kg; n = 11), nitric oxide synthase (NG-methyl-L-arginine acetate salt, 15 mg/ kg; n = 9) and combination ganglionic plus alpha adrenergic plus beta adrenergic (n = 6) blockade in spontaneously hypertensive rats (SHR). Responses to metformin alone were also assessed in normotensive Wistar-Kyoto rats (n = 6). In SHRs, metformin elicited depressor responses accompanied by tachycardia (100 mg/kg; delta MAP, -26 +/- 3 mm Hg; delta HR, +49 +/- 12 bpm). Depressor responses in Wistar-Kyoto rats were significantly attenuated (100 mg/kg; delta MAP, -9 +/- 4 mm Hg; P < .01). Hypotensive actions of metformin in SHRs were abolished and reversed into pressor responses by hexamethonium (100 mg/kg; delta MAP, +24 +/- 6 mm Hg), phentolamine (100 mg/kg; delta MAP, +62 +/- 10 mm Hg) and by combination ganglionic plus adrenergic (100 mg/kg; delta MAP, +62 +/- 10 mm Hg) blockade. Neither propranolol, atropine nor NG-methyl-L-arginine acetate salt affected hypotensive responses to metformin. We conclude that acute intravenous metformin administration decreases MAP by causing withdrawal of sympathetic activity. The increase in MAP uncovered by hexamethonium and phentolamine suggests that the original depressor response to metformin is buffered by mechanisms unrelated to the autonomic nervous system.

Adrenergic Antagonists↗
PubMed1997

Does mexiletine have a preferential action (versus healthy myocardium) on the reentrant circuit of ventricular tachycardia?

The preferential action (in diseased versus healthy myocardium) of class 1a antiarrhythmic but not class 1b agents has been demonstrated on the reentrant circuit. This study assessed the effect of mexiletine on the fragmented electrogram at the origin of ventricular tachycardia (VT) associated with underlying heart diseases. In 11 consecutive patients, VT of the same morphology was induced, and entrained with rapid pacing during, before, and after mexiletine. The width of the fragmented electrogram, VT cycle length, and the block cycle length (defined as the longest VT-interrupting paced cycle length during entrainment) were measured before and after mexiletine and the findings compared. The effective refractory period (ERP) was measured at the pacing site (normal myocardium) and at the VT origin. To assess the preferential action of mexiletine, changes in fragmented electrogram were examined in relation to QRS duration (defined as the index of global intraventricular conduction). After mexiletine, VT cycle length, block cycle length, and fragmented electrogram were prolonged significantly. The QRS duration was also prolonged significantly, but this change was significantly smaller than that in VT cycle length or in the width of the fragmented electrogram. There was no significant change in ERP either at the pacing site or at the VT origin. Mexiletine was confirmed to preferentially depress conduction in the diseased myocardium at the VT origin, and this action occurred at a higher rate during VT.

Adult↗
PubMed1996

The loss of recombinant human granulocyte colony-stimulating factor and recombinant human TNF-alpha priming effects on the superoxide-generating response in exudated neutrophils is associated with a decrease in their receptor affinities.

Several cytokines are known to enhance FMLP-stimulated superoxide generation in human circulating blood neutrophils through binding to their specific receptors, a process referred to as the priming effect. The priming effects produced by recombinant human granulocyte CSF (rhGCSF) and TNF-alpha (rhTNF-alpha) on FMLP-stimulated superoxide production in human and rabbit blood neutrophils were compared with their effects in their respective tissue neutrophils, i.e., human salivary and rabbit peritoneal neutrophils. The receptor binding characteristics of rhGCSF and rhTNF-alpha were also compared between the two types of neutrophils. Both rhGCSF and rhTNF-alpha produced dose-dependent priming effects on FMLP-stimulated superoxide production in human blood neutrophils, whereas they failed to produce any priming effects in human salivary neutrophils. Similar results were obtained for the priming effects by rhGCSF in rabbit blood and peritoneal neutrophils. A decrease in receptor binding affinity, but not in receptor density, in tissue neutrophils was demonstrated by analyzing the binding of [125I]rhGCSF and [125I]rhTNF-alpha. These findings suggest that tissue neutrophils are less responsive to rhGCSF and rhTNF-alpha in the modulation of FMLP-stimulated superoxide generation. This is due at least in part to the lower affinities of GCSF and TNF-alpha to their receptors in tissue neutrophils. This marked difference in priming effects by cytokines between blood and tissue neutrophils may represent an early step in the defensive responses against invading microorganisms or Ags.

Animals↗
PubMed1996

A novel enzyme that catalyzes the esterification of N-acetylsphingosine. Metabolism of C2-ceramides.

A unique transacylase that catalyzes esterification of a short chain ceramide, N-acetylsphingosine, was found in Madin-Darby canine kidney cell and mouse tissue homogenates. It esterified the hydroxyl group at the carbon-1 position of the ceramide. The enzyme has a pH optimum of 4.2 and a Km of 9.4 microM for N-acetylsphingosine at pH 4.5. The transacylase activity is independent of free fatty acid or acyl-CoA and instead uses the 2-acyl group of phosphatidylethanolamine or phosphatidylcholine. The transacylase activity in the homogenate was present in the 100,000 x g supernatant, and the lipid extracted from the membranous fraction could function as a donor of the acyl group. When liposomes consisting of dioleoylphosphatidylcholine:1-palmitoyl-2-[14C]arachidonoyl-phosphati dylethanolamine:sulfatide (70:0.2:30) were incubated with the supernatant and N-acetylsphingosine, the formation of free arachidonic acid and O-arachidonoyl-N-acetylsphingosine was observed. The ratio of the two products depended on the concentration of ceramide; only the free acid was formed if the truncated ceramide was absent. Both deacylase and transacylase activities were inhibited 50-60% by 20 microM D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, an inhibitor of several glucosphingolipid synthases. Neither activity was inhibited by nonadecyltetraenyl trifluoromethyl ketone, a potent inhibitor of cytosolic phospholipase A2. N-Acetyldihydrosphingosine and N-octanoylsphingosine were only 55 and 10%, respectively, as effective as N-acetylsphingosine as acyl acceptors. Oleoylsphingosine was only slightly reactive. An esterase that releases the truncated ceramide from its ester linkage appears to be membrane bound. Lecithin was less effective than phosphatidylethanolamine as an acyl donor in the transacylation. Madin-Darby canine kidney cell cultures treated with N-acetyl-[3-3H]sphingosine formed radioactive polar sphingolipids, long chain ceramide, free sphingosine, and O-acyl-N-acetylsphingosine. This suggests that the deacylation and transacylation reactions observed in vitro occur in growing cells as well.

Acyltransferases↗