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Biomedical subjects

Y Takiguchi

Publications and source records attributed to Y Takiguchi.

At least 91 records · Page 5Linked to original sources
PubMed1992

Genomic organization of the human homologue of the rat pancreatic elastase I gene.

The homologue of the rat pancreatic elastase I gene was found in the human genome, but its transcription was completely suppressed in the adult human pancreas as we reported previously. In this study, we characterized the complete structure of the eight putative exons of the silent gene for human elastase I. A genotype analysis of the exon 1 DNA sequence revealed that at least two allelic elastase I genes are present in human genomes. A primate-specific repetitive DNA element (MER1) was identified in the 3'-flanking region of the human elastase I gene. The primary structure of human preproelastase I, deduced from the sequences of the eight exons, showed an 89% identity with that of porcine or rat pancreatic preproelastase I. The amino acid residues of the serine protease catalytic triad and the eight cysteine residues conserved in the elastase family were present at positions equivalent to those observed in porcine and rat elastase I, suggesting that the gene product may function as an elastolytic enzyme if this gene is expressed in any tissue.

Amino Acid Sequence↗
PubMed1992

Characterization of the primate-specific repetitive DNA element MER1.

Computer analyses of the 3'-flanking DNA sequence of the human elastase I gene revealed a significant degree of similarity with seven human gene sequences in the GenBank and EMBL databases. Genomic Southern analysis indicates that the shared nucleotide sequences are a primate-specific family of short interspersed elements. These elements are members of MER1 sequences (medium reiteration frequency sequences). The consensus sequence of MER1 repeats spans 543 nucleotides and contains several inverted repeats. Since the copy number of MER1 elements seems to be much smaller than that of Alu and L1 repeats, MER1 elements may provide useful landmarks marks for human genome mapping.

Animals↗
PubMed1992

[Function, molecular structure and gene expression of interleukin-11 (IL-11/AGIF)].

Interleukin-11 (IL-11) is a novel cytokine that was identified in a medium conditioned by the primate bone marrow-derived stromal cell line PU-34. It was originally identified as a growth factor for the IL-6-dependent plasmacytoma cell line T1165. Adipogenesis inhibitory factor (AGIF) was cloned from the human bone marrow-derived cell line KM-102. The AGIF cDNA sequence was revealed to be identical to that of the IL-11 cDNA. AGIF inhibits the process of adipogenesis of the bone marrow-derived preadipocyte cell line H-1/A. Other biological activities of IL-11/AGIF, megakaryocytopoiesis, stem-cell proliferation, hepatic acute phase responses and antigen-specific antibody responses are also summarized.

Adipose Tissue↗
PubMed1992

[Correlation of signal intensity of blood flow in the pulmonary artery on MR images and clinical features of two cases of primary pulmonary hypertension].

ECG-gated spin-echo MR images of the chest were obtained in two patients with primary pulmonary hypertension (PPH). In transverse section at the level of the right main pulmonary artery (rPA), flow signals in the rPA were quantitatively evaluated, and the correlations with MR signal intensity of intravascular flow and data of routine clinical examinations and the severity of clinical manifestations were studied. In one case, the signal intensity of flowing blood markedly increased with exacerbation of hypoxemia and other clinical manifestations. However, in the other case with a stable course, the signal intensity of intravascular flow did not change significantly. Increase of flow signal in the rPA can reflect decrease of flow velocity that may be cause by a state of high pulmonary vascular resistance or low cardiac output. Therefore, it is suggested that MRI is a useful modality to evaluate the severity of disturbance of the pulmonary circulation in PPH.

Adolescent↗
PubMed1991

Adipogenesis inhibitory factor. A novel inhibitory regulator of adipose conversion in bone marrow.

Recombinant adipogenesis inhibitory factor (AGIF) was purified to homogeneity from the conditioned medium of COS-1 cells transfected with human AGIF cDNA. The amino-terminal sequence analysis of the mature AGIF revealed that AGIF was produced as a precursor consisting of 199 amino acids and processed into a mature form of 178 amino acids by a cleavage between Ala(-1) and Pro(+1). The purified AGIF inhibited the process of adipogenesis in mouse 3T3-L1 preadipocytes, indicating that AGIF directly acts on the cells. AGIF acted as an adipogenic antagonist not only on the extramedullary cell line 3T3-L1 but also on the mouse bone marrow stroma-derived cell line H-1/A, suggesting that this cytokine may regulate adipogenesis in bone marrow.

Adipose Tissue↗
PubMed1991

Effect of diabetes on photochemically induced thrombosis in femoral artery and platelet aggregation in rats.

Effect of diabetes on thrombogenesis was examined by using a thrombus model with photochemical reaction in the rat femoral artery. In streptozotocin-induced diabetic rats for 8 weeks, the formation of thrombus following endothelial injury was significantly slower than that in non-diabetic rats. Insulin treatment normalized the abnormality of thrombogenesis. Aggregation in washed platelets from rats with diabetes was enhanced. However, platelet aggregation in whole blood was reduced in diabetic rats, and plasma from diabetic rats attenuated platelet aggregation. These results suggest that plasma factor(s) and/or other blood cells modify the hyperaggregability of platelets per se in vivo in diabetic rats. Treatment with insulin improved the aggregation in whole blood and washed platelets. In conclusion, diabetes induces the prolongation of thrombogenesis in the rat femoral artery. Hypoaggregability of whole blood is likely to be partly involved in the abnormal thrombogenesis.

Animals↗
PubMed1991

Isolation and characterization of thermostable chitinases from Bacillus licheniformis X-7u.

Four kinds of thermostable chitinase were isolated from the cell-free culture broth of Bacillus licheniformis X-7u by successive column chromatographies on Butyl-Toyopearl, Q-Sepharose, and Sephacryl S-200. We named the enzymes chitinases I(89 kDa), II(76 kDa), III(66 kDa) and IV(59 kDa). Chitinases II, III and IV possessed extremely high optimum temperatures (70-80 degrees C), showing remarkable heat stability. Chitinases II, III and IV produced (GlcNAc)2 and GlcNAc from colloidal chitin and chitinase I predominantly produced (GlcNAc)2. The action pattern of chitinase I on PN-(GlcNAc)4 also showed a stronger propensity to cleave off the (GlcNAc)2 unit from the non-reducing end than the other three chitinases. Chitinases II, III and IV catalyzed a transglycosylation reaction that converted (GlcNAc)4 into (GlcNAc)6.

Amino Acids↗
PubMed1991

Molecular cloning of cDNA encoding adipogenesis inhibitory factor and identity with interleukin-11.

A cDNA encoding a novel adipogenesis inhibitory factor (AGIF) that inhibits the process of adipogenesis in mouse 3T3-L1 preadipocytes was cloned from a cDNA library of the human bone marrow-derived stromal cell line KM-102. The cloned cDNA contains an open reading frame coding for an AGIF precursor of 199 amino acids. Analysis of the sequence of this cDNA revealed identity of this factor with a recently reported novel cytokine, designated interleukin-11 (IL-11). AGIF/IL-11 may play an important role in stromal cell-associated hematopoeisis through its regulatory action on adipocyte differentiation in the bone marrow microenvironment.

Adipose Tissue↗
PubMed1991

Baroreflex and atrial natriuretic factor concentration correlate with myocardial infarct size and predict early death in rabbits: implications for drug studies.

The severity of myocardial infarction (MI) and its functional consequences are difficult to assess in small animals. We searched for criteria to achieve such an assessment in rabbits 1 week after MI. Thirteen large mongrel rabbits (3-4 kg) were anesthetized with pentobarbitone for ligating a branch of the circumflex coronary artery and 7 rabbits were subject to a sham operation without ligation. All sham-operated rabbits and 12 MI animals survived for 1 week, when blood was obtained for biochemical analyses and the baroreflex was tested. Six animals survived to the third week (survivors) and six died earlier (nonsurvivors). The MI size, measured immediately after death, was 42 +/- 3% of the left ventricular mass in nonsurvivors and 20 +/- 7% in survivors. The plasma atrial natriuretic factor (ANF) concentration was correlated linearly with MI size (r = 0.77) over the whole range of infarct sizes and, like the MI size itself, was associated with the risk of early death (critical limit: 80 pM). Plasma renin activity and catecholamines yielded less prognostic information. The baroreflex control of the heart rate (tested using phenylephrine and nitroprusside) of nonsurvivors was severely impaired and the slopes correlated with MI size (r = 0.90 for phenylephrine and r = 0.67 for nitroprusside). The plasma ANF concentration and the baroreflex both accurately reflected MI size and also correctly classified 11/12 rabbits into survivors and nonsurvivors. An ANF- and baroreflex-based stratification of animals for future studies on therapeutic interventions after MI will reduce the number of animals required by at least 65%, making such studies far more feasible than in the past.

Animals↗
PubMed1991

Altered effect of arachidonic acid on inner ear blood flow in rats with streptozotocin-induced diabetes.

The present study was undertaken to clarify the altered effect of arachidonic acid on inner ear blood flow in rats with streptozotocin-induced diabetes by use of the laser-Doppler flowmeter. Drugs were administered intraarterially via the subclavian artery in a dose range that did not affect the systemic blood pressure. Both arachidonic acid and papaverine hydrochloride increased inner ear blood flow dose-dependently. Diabetic rats at 12 weeks, but not at 8 weeks, after the induction of diabetes showed a significant decrease in arachidonic acid response. However, there were no differences in papaverine response between diabetic and control rats. Pretreatment with ONO-3708, a selective thromboxane A2 antagonist, reversed the attenuated response to arachidonic acid found in diabetic rats. An increased response to thromboxane A2, which decreased inner ear blood flow, was also found in 12-week diabetic rats. In electrocochleograms, the latency in 12-week diabetic rats was significantly delayed compared with that in control rats, and this prolonged latency improved with insulin treatment. These results suggest that the responsiveness of inner ear blood flow to prostaglandins may be altered in individuals with diabetes mellitus.

Animals↗
PubMed1991

[The role of gamma-interferon in blister formation of bullous pemphigoid].

Recently it has been reported that cell-mediated immune (CMI) reaction is related to the blister formation as well as the reaction of autoantibody against the basement membrane zone (BMZ-Ab) in bullous pemphigoid (BP). Previously we reported that T-cells infiltrated were producing gamma-interferon (IFN-gamma) and that high levels of IFN-gamma were detected in the blister fluids of BP. In the present study, in order to find the effect of IFN-gamma on the skin, we have done the organ culture of normal skin explants with IFN-gamma. The dermal-epidermal separation (DES) was histologically observed in skin explants which were incubated with high level of IFN-gamma after 24 hours. The DES was found to be located between the basal layer and the site of laminin and type IV collagen. It is considered that IFN-gamma alters the antigenicity and mediates to release some other cytokines in CMI reaction. In addition to these, IFN-gamma seems to directly work on the DES in normal skin. Around the DES of the skin explants, plasminogen activator was accelerated immunohistologically. The results suggest that IFN-gamma mediated by CMI response also plays an important role as well as the autoantibody in the blister formation of BP.

Adult↗
PubMed1990

Immunohistopathologic studies in the development of psoriatic lesion influenced by gamma-interferon and the producing cells.

Immunological studies on psoriasis have been done using monoclonal antibodies (MoAbs) to elucidate the relation between gamma-interferon (IFN-gamma) secreted from inflammatory infiltrate, and the expression of HLA-DR molecule on epidermal keratinocytes in the lesion. In highly inflamed psoriatic lesions, IFN-gamma producing cells were found in the inflammatory infiltrate of the dermal papillae, while keratinocytes located near IFN-gamma+ cells expressed HLA-DR molecules on the surface. In fully developed psoriatic lesions, HLA-DR+ keratinocytes were mainly found in the thin epidermis over the elongated dermal papillae where IFN-gamma deposited not only at infiltrates but also in teh dermal components. The IFN-gamma+ cells were activated T cells which exhibited HLA-DR and interleukin 2 receptor. Munro's microabscess under the horny layer also included IFN-gamma producing cells. A radioimmunoassay by the sandwich method with anti-human IFN-gamma and anti-recombinant IFN-gamma MoAbs found that extracts from psoriatic scales contained IFN-gamma. The results suggest that HLA-DR+ keratinocytes are due to the effect of IFN-gamma secreted by activated T cells in psoriatic lesions. The proliferation of keratinocytes over the dermal papillae in fully developed lesions seemed to be inhibited by IFN-gamma from the inflammatory infiltrate. We consider that cell-mediated immune reaction plays an important role in the development of psoriatic eruption.

Adult↗
PubMed1990

Effect of arachidonic acid on the inner ear blood flow measured with a laser Doppler flowmeter.

The present study was undertaken to clarify the effect of arachidonic acid (AA) on the inner ear blood flow of rats as measured with a laser Doppler flowmeter. With the rats under anesthesia with sodium pentobarbital, the middle ear was approached ventrally and a laser Doppler probe was positioned over the lateral wall of the cochlea. Drugs were administered via the subclavicular artery. The dose range of each drug was determined so as not to affect the systemic blood pressure. The AA (20 to 70 micrograms) increased the inner ear blood flow dose-dependently; this effect was abolished by indomethacin (5 mg orally). Both prostaglandin E2 (PGE2; 1 to 50 ng) and CS-570, a PGI2 analogue (12.8 to 25.6 ng) caused a dose-dependent increase in the inner ear blood flow. The response of PGI2 was shorter than that of PGE2. On the other hand, a stable thromboxane A2 (STA2; 30 to 80 ng) decreased the inner ear blood flow dose-dependently. Administration of PGF2 alpha (0.2 to 3 micrograms) showed no effect on the inner ear blood flow. These results indicated that the effect of AA was mediated mainly via PGI2 and PGE2.

Animals↗
PubMed1990

Comparative hemodynamic studies of isradipine and dihydralazine in atherosclerotic and normal rabbits.

The hemodynamic effects of the calcium antagonist isradipine (code name PN 200-110) and the arteriolar vasodilator dihydralazine were compared in atherosclerotic (cholesterol-fed) and normal conscious rabbits with implanted catheters. Regional blood flows were measured using the microsphere technique. Cardiac output and blood flow to several organs, especially to the gastrointestinal system, but not to the heart and brain, were lower in atherosclerotic rabbits than in normal ones. Intravenous isradipine (10 and 30 micrograms/kg) increased heart rate less in atherosclerotic than in normal rabbits. Isradipine had no effect on the surface electrocardiogram (ECG). In contrast, 0.4 mg/kg dihydralazine caused depression of the ST segment while decreasing blood pressure similarly. This was explained partly by an intramyocardial maldistribution of coronary blood flow (using microspheres). Isradipine increased and dihydralazine decreased flow to the brain. Isradipine redistributed cardiac output in atherosclerotic and normal animals in favor of the heart, brain, and skeletal muscle. However, in atherosclerotic animals, the high dose was less effective than the low dose in some vascular beds. Thus, isradipine is not a general vasodilator in either atherosclerotic or in normal animals, but favors the vital organs. This redistribution of cardiac output contrasts favorably with that induced by dihydralazine.

Animals↗
PubMed1990

Attenuation of endothelin-induced regional vasoconstriction by isradipine: a nonspecific antivasoconstrictor effect.

The modification of endothelin effects by the calcium antagonist isradipine was investigated by infusion of 1.0 nM/kg endothelin, a dose known to cause profound vasoconstriction, into eight anesthetized rabbits, followed by an infusion of 10 micrograms/kg isradipine or its vehicle into four rabbits each. In a second series of experiments, only isradipine (same dose) or its vehicle was infused into six rabbits each. Endothelin increased blood pressure and caused systemic vasoconstriction, marked bradycardia, and cardiodepression (measured with a strain guage), yet decreased central venous pressure. The regional vascular effects (measured with microspheres) encompassed widespread vasoconstriction (especially to the kidneys, adrenals, stomach, cecum, and heart), but also a tendency for vasodilatation (hepatic artery). Isradipine decreased blood pressure in endothelin-treated and normal animals. It increased cardiac output more in the endothelin group. The interaction between endothelin and isradipine in the peripheral circulation was generally additive. Isradipine blunts many, but not all, endothelin effects, thus resembling the antivasoconstrictor effects of calcium antagonists against a variety of vasoconstrictor agents such as angiotensin II (Ang II) or vasopressin. Similar to these, endothelin appears to cause vasoconstriction by several mechanisms, one of which apparently involves L-channel activation. A specific interaction of endothelin with the L-channel appears unlikely.

Animals↗
PubMed1990

Effect of an aldose reductase inhibitor on altered sympathetic nerve responsiveness of isolated right atria in diabetic rats.

1. To determine the effects of an aldose reductase inhibitor (ARI) on diabetes-induced cardiac sympathetic disturbance, the effects of (E)-3-carboxymethyl-5-[(2E)-methyl-3-phenylpropenylidene] rhodamine (ONO-2235), an aldose reductase inhibitor, as well as insulin on the responsiveness to the transmural sympathetic nerve stimulation (TNS) and norepinephrine (NE) of isolated right atria of streptozotocin-induced diabetic rats were investigated. 2. The responsiveness to TNS of 8-week diabetic rats decreased, and those of 12-week diabetic rats severely decreased. The responses to NE also decreased 8 weeks or more after the induction of diabetes. 3. In 8-week diabetic rats, the insulin treatment completely restored the responsiveness to TNS, while ARI treatment partially restored the responsiveness to TNS. In 12-week diabetic rats, the single treatment with insulin or ARI only slightly restored the responsiveness to TNS, while the combination treatment with insulin and ARI almost completely restored the responsiveness to TNS in 12-week diabetic rats. 4. From the present results, the following may be concluded: Sympathetic nerve responses of right atria decreases in diabetic rats, and these changes may be related to hypoinsulinemia and abnormal polyol pathway. Although a serious sympathetic disturbance was only slightly improved by insulin or ARI, the combination of insulin and ARI produced more remarkable improvement of this disturbance.

Aldehyde Reductase↗