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Biomedical subjects

T Shinohara

Publications and source records attributed to T Shinohara.

At least 217 records · Page 12Linked to original sources
PubMed1992

Cerebral microcirculatory changes during and following transient ventricular tachycardia in cats.

Although reduced cerebral perfusion is believed to be the cause of syncope due to cardiac arrhythmias, investigations on the cerebral microcirculation during cardiac arrhythmias have been rare. We therefore studied the effects of transient ventricular tachycardia on the local cerebral blood volume and blood flow. Experimental ventricular tachycardia was induced in cats by electrically stimulating the ventricle of the heart at a rate of 300/min for 1 min. Using our photoelectric method, the local cerebral blood volume, mean transit time of blood, and cerebral blood flow in the parieto-temporal region were measured during and for 3 h after ventricular tachycardia. Transient ventricular tachycardia of as short as 1 min caused cerebral ischemia with a blood flow reduction of approximately 30%. This was considered to be due to reduced blood pressure plus transient autonomic dysfunction, or dysautoregulation, during the ventricular tachycardia. Mild and transient reactive hyperemia occurred immediately after termination of the dysrhythmia, but continuous reductions of cerebral blood flow were observed thereafter for 3 h. This delayed hypoperfusion is attributable to either vasoconstriction of the large resistance vessels or changes in the hemorheological properties of the blood caused by cerebral ischemia. Ventricular tachycardia of the type reported has significant and long-lasting effects on the cerebral microcirculation.

Animals↗
PubMed1992

Estimation of plasma glucose fluctuation with a combination test of hemoglobin A1c and 1,5-anhydroglucitol.

We investigated the effect of plasma glucose fluctuation on hemoglobin A1c (HbA1c) and plasma 1,5-anhydroglucitol (AG) levels, especially in insulin-dependent diabetes mellitus (IDDM). Plasma AG is a new marker that provides sensitive and analytical information on glycemic control. The basic mechanisms underlying both the reduction and recovery of the plasma AG level, ie, the excretion into urine with glucosuria and the amount supplied to the body, were presumed to be similar in IDDM and non-insulin-dependent diabetes mellitus (NIDDM) patients. The correlation coefficient for mean plasma glucose and AG was -.591, and it was .578 for mean plasma glucose and HbA1c in IDDM patients. In NIDDM, the correlation between mean plasma glucose and AG was -.869, and between mean plasma glucose and HbA1c, .875. The plasma AG levels in the IDDM group showed a lower range than in the NIDDM group, even with similar HbA1c levels. All the cases showing lower plasma AG levels among those with similar HbA1c levels manifested greater fluctuation of plasma glucose and a larger amount of urinary glucose. The lower AG level in IDDM patients was reversible to the level in NIDDM patients when the greater fluctuation of plasma glucose was corrected. Thus, it was suggested that because urinary glucose excretion is intermittently high in IDDM patients, plasma AG is frequently low, even though the mean plasma glucose and HbA1c levels suggest good control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Enhancement of S-antigen and its mRNA in the irides of uveitic patients.

S-antigen (S-Ag) and its mRNA were analysed by immunohistochemistry and in situ hybridization in 32 iridectomy specimens from 29 uveitic patients and 10 non-uveitic patients. S-Ag was detected in one iris and its mRNA was detected in 12 uveitic patients. Neither S-Ag nor its mRNA was found in the controls (P < 0.003). Ten of the 12 patients who had detectable S-Ag mRNA, while only four of the 17 patients who did not, had received corticosteroids for more than 3 years (P = 0.006). We also demonstrated S-Ag and its mRNA in bovine iris by immunoprecipitation and polymerase chain reaction. These results indicate that S-Ag and its mRNA accumulate in the irides of some uveitic patients. This accumulation may be the result of local immunoregulatory factors and an effect of corticosteroid treatment, and may modulate ocular inflammation.

Adrenal Cortex Hormones↗
PubMed1992

Origin and disposal of 1,5-anhydroglucitol, a major polyol in the human body.

The origin and disposal of 1,5-anhydro-D-glucitol (AG), one of the main polyols found in the human body, was studied in normal subjects and diabetic patients. AG was detected in various kinds of foods. The mean AG supplement through foods was estimated to be approximately 4.38 mg/day, which was compatible with that calculated in a food analysis (average 0.22 mg AG/100 kcal in Japanese foods) on eight healthy subjects. The mean AG excretion in urine was approximately 4.76 mg/day in these subjects. Excretion into stools was negligible. From observations on the patients without oral supplement of AG, 0.4 mg of daily de novo synthesis of AG was strongly suggested. It was also implied that urinary AG excretion occurred soon after food ingestion and that its amount was closely correlated with daily supplement through foods. Thus the fundamental kinetics of AG were recognized as follows: 1) AG in the body originates mainly from foods and is well absorbed in the intestine, 2) AG is little degraded and metabolized in the body, and 3) an equilibrium exists between oral supplement plus a small but steady amount of de novo synthesis and excretion in urine.

Adult↗
PubMed1992

Animal species differences in erythrocyte aggregability.

Species differences in erythrocyte aggregability were investigated employing our whole blood erythrocyte aggregometer. Blood was sampled from seven species, including humans and anesthetized (30 mg/kg pentobarbital) animals. The erythrocyte aggregation rates were the following (in s-1): cats, 0.213 +/- 0.027 (means +/- SD); dogs, 0.164 +/- 0.027; men, 0.112 +/- 0.025; rats, 0.111 +/- 0.005; domestic rabbits, 0.049 +/- 0.021; and mongolian gerbils, 0.034 +/- 0.015. Domestic fowls did not exhibit erythrocyte aggregograms like those seen in the other species. Statistical analysis revealed significant differences among the erythrocyte aggregation rates of the different species (multiple-comparisons with an overall significance level of 0.05) except between men and rats and between rabbits and gerbils. No single factor which is known to accelerate the erythrocyte aggregation rate (hematocrit, fibrinogen, etc.) was correlated with the erythrocyte aggregation rate except the globulin concentration in the blood. The failure to detect erythrocyte aggregation in domestic fowls was probably attributable to their erythrocyte shape. These results suggest that each species has its own proper tendency for erythrocyte aggregation. This factor must be taken into consideration when the blood circulation is discussed among different animal species.

Animals↗
PubMed1992

Expression of the angiotensinogen gene and localization of its protein in the human heart.

BACKGROUND: There have been no reports on the presence of the tissue renin-angiotensin system in the human heart, although the presence of angiotensinogen has been described in the animal heart. METHODS AND RESULTS: To determine whether angiotensinogen is synthesized in the human heart, we examined angiotensinogen messenger RNA (mRNA) synthesis in autopsy hearts by using ribonuclease protection assay. As a result, angiotensinogen mRNA was detected in the atrial muscle, muscles of the conduction system, and the left ventricular wall. In the left ventricular wall, mRNA expression was more prominent in the subendocardial muscles than in the midcardial or epicardial muscles. Using a monoclonal antibody to human angiotensinogen in immunoblotting experiments, we detected two closely spaced bands at approximately 70 kd in the heart, which was quite consistent with the human angiotensinogen molecule. Immunohistochemical studies with this monoclonal antibody demonstrated intense immunoreactivity in the atrial muscles, the muscles of the conduction system, and those of the subendocardial layers. CONCLUSIONS: We conclude that angiotensinogen was synthesized in the human heart. It was evident that the localization of angiotensinogen was not ubiquitous in the cardiac muscles, showing its predilection for the atrial muscles, muscles of the conduction system, and subendocardial layer of the left ventricle.

Angiotensin II↗
PubMed1992

Developmental expression of S-antigen in fetal human and rat eye.

Development expression of S-antigen and its mRNA in human and rat fetal retina was studied by immunocytochemical and in situ hybridization techniques. Immunocytochemistry indicated that S-antigen was present after 4 months gestation in the fetal human retina. In the rat, S-antigen was detected in the retina only after birth. In situ hybridization studies indicated that the S-antigen mRNA was present at 13 weeks gestational age in the human and at 15 days in the rat embryo. S-antigen mRNA was expressed not only in the retina but also in ocular tissues of neural crest origin in the fetus.

Adult↗
PubMed1992

N-RAS activation in the terminal stage of undifferentiated chronic myeloproliferative disease.

The relationship between activation of the N-RAS gene and the leukemic progression of undifferentiated chronic myeloproliferative disease (UCMPD) was investigated in a 71-year-old male. Hematologically, it was difficult to differentiate the UCMPD from chronic myelogenous leukemia. Chromosomal analysis revealed no Philadelphia chromosome (Ph1-), and DNA analysis revealed no BCR rearrangement (BCR-) either at the beginning or in the terminal stages of the disease. We performed a tumorigenicity assay, using NIH3T3 cells, and molecular analysis, using the polymerase chain reaction (PCR) and direct sequencing. The DNA of leukemic cells at the beginning of the leukemic progression did not show any abnormalities, but at the terminal stage of the disease the DNA showed a point mutation in codon 12 (GGT----GCT) of the N-RAS gene. Interestingly, a codon 13 mutation (GGT----GTT) was also detected by tumorigenicity assay. These observations suggest that the activated N-RAS gene contributes to the hematologic progression of UCMPD.

Aged↗
PubMed1992

[Two cases of paranasal sinusitis with choanal polyp in children].

Patients with choanal polyp often suffer from maxillary sinusitis of the same side. Hence, Caldwell-Luc operation in addition to polypectomy has been recommended for the treatment of choanal polyp. Choanal polyp occurs more frequently in children with nasal polyp(s) than in adults with nasal polyp(s). For this reason, it is preferable to perform surgery so as to preserve the maxillary sinus as much as possible. The authors surgically treated two children with choanal polyp. A 12-year-old girl had a choanal polyp arising from the posterior portion of the middle turbinate and received an osteoplastic maxillary operation and functional endoscopic sinus surgery (FESS). The other, a 13-year-old girl, with an antro-choanal polyp underwent FESS only. One year after surgery, both patients showed no recurrence of polyp and had recovered an aerated maxillary sinus cavity covered with normal mucous membrane. Based on the experiences of these two cases, FESS appears to be very helpful in treating children with choanal polyp and paranasal sinusitis.

Adolescent↗
PubMed1992

Effect of acetaldehyde on ethanol absorption in the canine jejunum.

The effects of acetaldehyde on ethanol absorption from the intestinal tract were studied using canine jejunal segment. A thirty-centimeter jejunal segment with intact vascular supply was isolated, and jejunal absorption studies were performed by administering a 17% ethanol solution (0.4 g/kg) into the lumen of the jejunal segment. In the control group, blood ethanol concentrations in the portal vein increased rapidly, with a peak level of 9.8 +/- 1.9 mM 30 min after administration. In the cyanamide-pretreated group, dogs were injected intravenously with cyanamide (100 mg/kg), an inhibitor of acetaldehyde dehydrogenase, 150 min before ethanol dosing. The blood ethanol concentration in the portal vein of this group, accompanied by a high acetaldehyde concentration, increased gradually, reaching a peak of 10.7 +/- 1.84 mM 120 min after ethanol administration. Each concentration gradient corresponded to the systemic circulatory order from the portal vein for ethanol concentration, and from the hepatic vein for acetaldehyde concentration. The absorbed amount of ethanol in the control and cyanamide-pretreated groups was 94.9 +/- 4.1% and 69.3 +/- 4.8%, respectively. Pharmacokinetic analysis indicated that a presence of high acetaldehyde concentration in the blood resulted in less ethanol reaching the systemic circulation (control: 7.34 +/- 2.95 h-1, cyanamide-pretreated: 1.08 +/- 0.75 h-1). The results also suggest that the absorption of ethanol from the intestine decreases when there is a high acetaldehyde concentration in the blood.

Acetaldehyde↗
PubMed1992

S-antigen localization in developing rds mouse retina.

The morphology of the photoreceptor cell and localization of the cytoplasmic soluble protein, S-antigen, in the retina of the developing retinal degeneration slow (rds) mutant mouse (2-505 postnatal days) were studied by improved immunocytochemical and freeze-substitution methods. Anti-S-antigen antibody labeling was observed first in the postnatal 10-day retina under light microscope. Labeling signals increased progressively to a maximum level in 20 days, and then decreased gradually to an undetectable level by 505 postnatal days. By electron microscopic immunocytochemical methods, S-antigen was detected first in the photoreceptor cells at 3 postnatal days, and increased with development. It was located in the entire cytoplasm of the photoreceptor cell including the rudimentary outer segment, but degenerated and disappeared by 505 postnatal days. S-antigen was also present in the membranous vesicles budding off from the photoreceptor membrane to the subretinal space. The rds photoreceptor cell seems to lose other soluble proteins together with these vesicles. From these results and other published data, we speculate that the degeneration of the photoreceptor cells may be the secondary effects of the loss of a large amount of soluble and membrane proteins following the malfunction of membrane. Recent reports show the rds mouse must have a gene defect in the membrane component such as peripherin or the 39 kDa protein.

Animals↗
PubMed1992

Y-27152, a long-acting K+ channel opener with less tachycardia: antihypertensive effects in hypertensive rats and dogs in conscious state.

(+)-(3S,4R)-4-(N-Acetyl-N-benzyloxyamino)-6-cyano-3,4-dihydro-2,2- dimethyl- 2H-1-benzopyran-3-ol (Y-27152) is a new K+ channel opener with a long duration of action and less tachycardia. In this study, Y-27152 was compared with a K+ channel opener lemakalim and a Ca++ channel blocker nifedipine for antihypertensive activity in conscious spontaneously hypertensive rats (SHR) and two-kidney, one-clip renal hypertensive dogs (RHD). In conscious SHR, Y-27152 (0.1-1 mg/kg, p.o.) produced long-lasting dose-related decreases in systolic blood pressure. At 1 mg/kg, the maximum response occurred 5 to 7 hr after dosing, and 24 hr later, the pressure was still significantly reduced. Heart rate was not changed by these doses of Y-27152, whereas equihypotensive doses of lemakalim or nifedipine were strongly tachycardic. The cardiovascular effects of Y-27152 were antagonized by glibenclamide (20 mg/kg, i.v.). In conscious unrestrained RHD, Y-27152 at doses of 0.01, 0.03 and 0.1 mg/kg lowered blood pressure with a slow onset and long duration of action and had only a minimal effect on heart rate, whereas both lemakalim and nifedipine reduced blood pressure and markedly increased heart rate. No tolerance to the antihypertensive effect of Y-27152 (0.1 mg/kg) occurred during an 8-week repeated daily dosing to RHD and plasma renin activity, and aldosterone levels were not elevated during this period. In rat aortic rings contracted with 20 mM KCl, Y-27152 did not modify the tension; however, its desbenzyl form (Y-26763) produced vasorelaxation, and this effect was antagonized competitively by glibenclamide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

[Complex chromosome aberrations between no. 17 and no. 21 in acute myelo-megakaryocytic leukemia: a case report].

A 10 month-old boy presented with fever. He was diagnosed as having acute myelo-megakaryocytic leukemia by electron microscopic cytochemical examination. In spite of aggressive chemotherapy, complete remission could not be achieved and he died seventeen months after the diagnosis was made. G-band karyotypes of the bone marrow cells revealed 45, XY, -17, -21, + dir tan dup (17;21) (17pter----cen----17q25::17q21----17q25;21q11 ----21qter). Furthermore, the same chromosomal aberrations were detected in the cells which were tetraploid and octaploid. Although, neoplastic changes in the progenitor cells immediately before differentiating to CFU-Meg and CFU-GM, are suggested there is a possibility of clonal evolution.

Chromosome Aberrations↗
PubMed1992

[Studies on ethanol absorption from the intestine--blood ethanol and acetaldehyde concentrations in the various vessels].

We describe the concentration gradient of ethanol at different blood sampling sites of dogs dosed via the jejunal segment or intravenously, and the subsequent recovery of intestinal fluid from the jejunal segment. After laparotomy a 30 cm length of jejunal segment with intact vascular supply was isolated. Blood samples were collected from the portal vein, hepatic vein, aorta and inferior vena cava. A 17% ethanol solution was used for a small dose group (0.4 g/kg) and a 33% solution for a large dose group (0.8 g/kg). In the small dose and large dose groups administered the solution via the jejunal segment, ethanol concentration in the blood of the portal vein increased rapidly and the highest ethanol concentration was detected in the portal vein, followed, in descending order by the hepatic vein, aorta and inferior vena cava. The highest acetaldehyde concentration in blood was detected in the hepatic vein, followed by that in the aorta while the lowest was in the portal vein and inferior vena cava in both groups. Each concentration gradient corresponded in order to systemic circulatory order from the intestine (ethanol absorption site) for ethanol concentration, or from the liver (acetaldehyde formation area) for acetaldehyde concentration. There was no difference in ethanol concentration among the four sampling sites in the case of intravenous ethanol injection, but a gradation of acetaldehyde concentration similar to that in the jejunal segment dosed cases was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1992

Molecular mimicry: uveitis induced in Macaca fascicularis by microbial protein having sequence homology with retinal S-antigen.

S-antigen (S-Ag), a well characterized 45-kDa protein in the photoreceptor cells, induces predominantly T-cell-mediated autoimmune uveitis when injected into experimental animals. Recently, we have shown that native histone H3 protein derived from yeast (Saccharomyces cerevisiae), or a synthetic peptide that is homologous with S-Ag peptide M in having six consecutive amino acids, induces experimental autoimmune uveitis (EAU) similar to that induced by native S-Ag in the Lewis rat. In this study, monkeys (Macaca fascicularis) immunized with histone H3 peptide developed a strong cellular immune response to this peptide as well as to peptide M. However, no significant inflammation or hypervascularization was observed in the retina or the iris during the experimental period, when they were examined clinically with an inverted ophthalmoscope. Histopathological examination showed that all monkeys injected with histone H3 peptide or with native histone H3 lost a large number of photoreceptor rod cells and developed neovascularization in the outer nuclear cell layer of the retina. These histopathological findings in the monkey retina closely resemble those seen in human patients with some types of uveitis. The possible involvement of microbial proteins having sequence homology with normal retinal proteins in the pathogenicity of human uveitis is discussed.

Amino Acid Sequence↗
PubMed1991

The mouse S-antigen gene. Comparison with human and Drosophila.

We have characterized a gene for mouse S-antigen and compared its sequence with that of corresponding human and two recently published Drosophila S-antigen genes. The mouse S-antigen gene was approximately 50 kbp in length and consisted of 16 exons and 15 introns. The length of most exons was less than 100 bp and the smallest one was only 10 bp. In contrast, the length of most introns was larger than 2 kbp and the gene consisted of 97% intron and 3% exon. Both splice sites for donor and accepter were in good agreement with the GT/AG rule. S-antigen genes in human and mouse were highly conserved. In contrast, genes for the Drosophila 49-kDa arrestin homolog and arrestin consist of three introns and four exons and two introns and three exons, respectively. The 5'-flanking region of the mouse S-antigen gene, approximately 1.0 kbp long, had no regulatory elements for transcription such as the TATA, CAAT and GC boxes, while a Drosophila arrestin gene has TATA and CAAT boxes. Interestingly, the 5'-flanking region of the mouse gene had promoter activity in an in vitro transcription assay using a nuclear extract of rat brain. A major transcription start site was found at 387 bp upstream from the translation start codon ATG in mouse. From our results, and those of others, we suggest that the S-antigen gene has evolved from a common ancestor gene by either insertion or deletion of introns. Such an alteration of gene structure may have played a role in the evolution of the S-antigen.

Amino Acid Sequence↗