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Biomedical subjects

Y Jinno

Publications and source records attributed to Y Jinno.

124 records · Page 7Linked to original sources
PubMed1985

Novel structure of the 5' end region of the human argininosuccinate synthetase gene.

The structure of the 5' end region of the human argininosuccinate synthetase (AS) gene was analyzed in detail. The 5' flanking region up to 350 nucleotides from the putative transcription initiation site is unusually G+C rich (80%). Three repeats of a CCGCCC sequence and one complementary GGGCGG sequence are present in this region. It contains no CCAAT box-like sequence, but does contain one typical TATA box and a 20 bases-long inverted repeat sequence that could form a stem and loop structure just upstream from the TATA box. An octanucleotide sequence, AGAAGTGA, found in the 5' flanking region of the AS gene is also commonly present in those regions of the two other human genes expressed mainly in the liver. These structural features of the AS gene indicate that it shares common structures with two completely different groups of genes, i.e. tissue-specific genes and housekeeping ones. Moreover, two enhancer core-like sequences, alternating purine-pyrimidines tracts and two independent Alu type highly repetitive sequences are apparent in the first intron of the AS gene.

Argininosuccinate Synthase↗
PubMed1984

Study on established lymphoid cells in maple syrup urine disease. Correlation with clinical heterogeneity.

Branched-chain keto acid dehydrogenase complex (BCKAD) was measured in lymphoid cells established from five patients with maple syrup urine disease (MSUD) and six control subjects. Two other MSUD lymphoid cell lines obtained from The Human Genetic Mutant Cell Repository were used as references. One day after subculture, the cells grew logarithmically up to 4-5 days. With this cell growth, BCKAD activity increased greatly in controls, but not in MSUD cells. The maximum BCKAD activity of MSUD cells was less than 7% and 13%-16% of the control in classic and variant types, respectively. Leucine added to culture medium at the concentration of 10-20 mM significantly inhibited cell growth in MSUD cells alone, and with increasing concentration and impaired enzyme activity in a cell line, the effect became more prominent. The effects of isoleucine and valine were mild and did not differ between control and MSUD cells.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1984

Complementation analysis in lymphoid cells from five patients with different forms of maple syrup urine disease.

The possibility of genetic heterogeneity in maple syrup urine disease was investigated by measuring branched-chain ketoacid dehydrogenase in polyethylene glycol-induced heterokaryons of lymphoid cells. The lymphoid cell lines from five patients with varying forms of the disease were established after incubation with Epstein-Barr virus. The results suggested that there are at least two genetic complementation groups in the disease.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1982

Skin histidase activity and urine formiminoglutamic acid (FIGLU) in patients with histidinemia found by screening newborn infants.

Skin histidase activities and urine formiminoglutamic acid (FIGLU) levels were measured in 20 patients with histidinemia, identified by Guthrie's screening method, and their family members as well as control subjects. There was a significant positive correlation between skin histidase activities and the amounts of urine FIGLU. Although the difference of skin histidase activity and the amount of urinary FIGLU was significant between any two of the three groups (i.e. controls, parents and patients; p less than 0.005), these levels ranged widely and a considerable number of the cases overlapped among groups. When a discriminant function was computed to obtain the minimum probability of misclassification between the groups using the above two parameters, a better segregation was observed. However, even though the number of misclassifications decreased, the overlapping cases were still present, especially between the parent and patient groups. It is concluded that either skin histidase activity, urine FIGLU, or both, can be used as genetic markers of the disease to a large but still limited extent.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

Trisomy 17p due to A t(5;17) (p15;p11) pat translocation.

A 6-month-old Japanese boy with trisomy 17p, resulting from a paternal balanced translocation t(5;17)(p15;p11), is described. Comparison of his clinical features with those of two previously reported patients with trisomy 17p revealed a characteristic combination of clinical features. They included intra- and extra-uterine growth retardation, developmental retardation, microcephaly, internal hydrocephalus, a facies with lateral displacement of the inner canthi, antimongoloid slanting of the palpebral fissures, a broad nasal bridge, and micrognathism, low-set, large and simple ears, a short and webbed neck, and flexion deformities of the fingers. The external genitalia in the two male patients were characterized by a small penis, undescended testes and a hypoplastic scrotum. Congenital cardiac defect was present in two of the three patients.

Abnormalities, Multiple↗
PubMed1981

Ring chromosome 11 [46,XX,r(11) (p15q25)] associated with clinical features of the 11q- syndrome.

A 2-year-old girl with a ring of chromosome 11[46,XX,r(11)(p15q25)] was reported. Her clinical features included growth and psychomotor retardation, microbrachycephaly, hypertelorism, strabismus externus, short nose, low nasal bridge, low-set ears, microretrognathism, short neck, small opening of vagina with large clitoris, deformity of nails, café-au-lait spot of the skin, general hirsutism, congenital heart disease, generalized convulsions, and pancytopenia. Most of these features are those characteristic of the 11q- syndrome. The fact that the patients with the deletion distal from q22 (reported cases) to q25 (our case) had a common phenotype suggests that the loss of the q25 leads to qter segment is mainly responsible for the characteristic clinical features of the 11q- syndrome.

Child, Preschool↗
PubMedDate not supplied

Are cerebrovascular factors involved in Alzheimer's disease?

Recent epidemiological studies have shown that vascular risk factors may be involved in Alzheimer's disease (AD) as well as dementia in general. To investigate the relation between a vascular disorder and AD pathology, current criteria are defective because most depend on exclusion of a cerebrovascular disorder. Epidemiological studies have indicated the possibilities that arteriosclerosis, abnormal blood pressure, diabetes mellitus and smoking may be related to the pathogenesis of AD. As for the mechanism that vascular disorders influence AD, it is presumed that amyloid deposition may be caused by a vascular disorder. Alternatively, a vascular event may cause progression of subclinical AD to a clinical stage. Insulin resistance and apolipoprotein E may also be involved in these mechanisms. Our studies show that ischemia-induced the Alzheimer-associated gene presenilin 1 (PS1) and endoplasmic reticulum-stress, generated from a vascular disorder, may unmask clinical AD symptoms caused by presenilin mutation, suggesting that a vascular factor might be involved in the onset of familial AD.

Alzheimer Disease↗
PubMedDate not supplied

Tolerance to the increase in coronary blood flow induced by KRN2391.

We examined whether KRN2391, isosorbide dinitrate and nitroglycerin induced tolerance in coronary arteries. Intracoronary arterial administration of KRN2391 (1 microgram), isosorbide dinitrate (30 micrograms) or nitroglycerin (3 micrograms) produced equipotent coronary vasodilatation. Development of tolerance was determined by whether the increase in coronary blood flow, caused by intracoronary arterial administration of these drugs, was attenuated by intravenous infusion of KRN2391, isosorbide dinitrate or nitroglycerin. The increase in coronary blood flow, caused by intracoronary arterial administration of KRN2391 was not affected by intravenous infusion of KRN2391 (0.3 or 1 micrograms/kg/min), isosorbide dinitrate (30 or 100 micrograms/kg/min) or nitroglycerin (1 or 3 micrograms/kg/min). The increase in coronary blood flow, caused by intracoronary arterial administration of isosorbide dinitrate or nitroglycerin, was significantly diminished by intravenous infusion of isosorbide dinitrate and nitroglycerin, but was unaffected by intravenous infusion of KRN2391. The present results suggest that KRN2391 does not induce acute tolerance by itself or cross-tolerance between KRN2391 and other nitrates.

Animals↗
PubMedDate not supplied

Comparative cardiovascular effects of KRN2391 and other coronary vasodilators in anesthetized open-chest dogs.

The effect of KRN2391 [N-cyano-N'-(2-nitroxyethyl)-3-pyridinecarboximidamide monomethanesulfonate] on the cardiovascular system and on myocardial oxygen consumption was compared with that of nicorandil and nifedipine in anesthetized dogs. Intravenous administration of KRN2391 (3-30 micrograms/kg) and nifedipine (1 and 3 micrograms/kg) decreased mean aortic blood pressure and total peripheral vascular resistance, and increased coronary blood flow, cardiac output and stroke volume. Heart rate was not significantly affected by KRN2391, but slightly increased by 1 microgram/kg of nifedipine. Nicorandil (100 and 300 micrograms/kg, intravenously) decreased mean aortic blood pressure, cardiac output, stroke volume and total peripheral vascular resistance, but did not affect heart rate. Nicorandil also showed a tendency to decrease coronary blood flow after an initial increase. All drugs tested decreased the difference in oxygen concentration between arterial and coronary sinus blood, indicating that these drugs increased the oxygen supply to the heart. Myocardial oxygen consumption was significantly decreased by more than 10 micrograms/kg of KRN2391, but was not affected by nifedipine. Nicorandil showed a tendency to decrease the myocardial oxygen consumption, though not significantly. Thus, KRN2391 may be useful to treat ischemic heart disease, because it increases the coronary blood flow and the oxygen supply to the heart, and decreases the afterload and the myocardial oxygen consumption.

Anesthesia↗
PubMedDate not supplied

Effect of KRN2391, a novel vasodilator, on endothelin-1-induced contraction of porcine coronary artery: comparison with cromakalim, nitroglycerin and nifedipine.

The relaxant effects of KRN2391 (K channel opener and nitrate-like), cromakalim (K channel opener), nitroglycerin (nitrate-like) and nifedipine (Ca channel blocker) were investigated in porcine isolated coronary arteries contracted by endothelin-1 and KCl. KRN2391, nitroglycerin and cromakalim concentration-dependently inhibited the 10(-8) M endothelin-1-induced contraction, but less potently inhibited the 40 mM KCl-induced contraction. Nifedipine concentration-dependently inhibited the 40 mM KCl-induced contraction more strongly than the 10(-8) M endothelin-1-induced contraction. KRN2391 and nitroglycerin produced a complete relaxation of arteries contracted by endothelin-1 at its maximum effect. Cromakalim and nifedipine, both at 3 x 10(-5) M, produced 83.9% and 73.3% of the complete relaxation of the endothelin-1-induced contraction, respectively. In the 40 mM KCl-induced contraction, nifedipine produced a complete relaxation, but KRN2391, cromakalim and nitroglycerin, all at 3 x 10(-5) M, produced a relaxation of 62.7%, 27.1% and 79.4%, respectively. The combination of cromakalim and nitroglycerin relaxed the 10(-8) M endothelin-1- and 40 mM KCl-induced contractions in a concentration-dependent manner. The relaxant effect of this combination was greater against the endothelin-1-induced contraction than against the 40 mM KCl-induced contraction. The maximum relaxation of the combination of cromakalim (3 x 10(-5) M) and nitroglycerin (3 x 10(-6) M) was complete for the endothelin-1-induced contraction but a relaxation of 77.8% was obtained for the 40 mM KCl-induced contraction, i.e. the relaxant effects using this combination were greater than those by cromakalim (3 x 10(-5) M) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Comparison of the anti-vasoconstrictor effects of a novel vasodilator KRN2391, nicorandil and nifedipine on isolated porcine large coronary artery.

The anti-vasoconstrictor profile of KRN2391, a novel vasodilator, was compared with that of nicorandil and nifedipine in isolated porcine large coronary arteries contracted by KCl, noradrenaline, serotonin, acetylcholine, endothelin-1 and U46619, a thromboxane A2 analogue. KRN2391 (10(-8) - 3 x 10(-5) M), nicorandil (10(-7) - 3 x 10(-4) M) and nifedipine (10(-10) - 10(-5) M) inhibited these contractile responses in a concentration-dependent manner. KRN2391 and nicorandil completely abolished these contractile responses at their maximum effects. However, nifedipine caused less inhibition than KRN2391 and nicorandil and did not completely abolish the contractile responses. The relaxant activity of KRN2391 was more potent than that of nicorandil. This study shows that the anti-vasoconstrictor profiles of KRN2391, nicorandil and nifedipine involve different relaxant mechanisms.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗