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Biomedical subjects

Y Hirota

Publications and source records attributed to Y Hirota.

At least 469 records · Page 26Linked to original sources
PubMed1982

Physical map of the nrdA-nrdB-ftsB-glpT region of the chromosomal DNA of Escherichia coli.

Seven pLC plasmids (pLC 3-46, 8-12, 8-24, 8-29, 14-12, 19-24 and 42-17) which complemented nrdA, nrdB, ftsB and/or glpT mutations of Escherichia coli were analyzed. A restriction map of each plasmid was constructed and restriction fragments were subcloned into pBR322. A physical map of approx. a 15 X 10(6) Mr segment of the chromosomal DNA was deduced from the overlapping region of the pLC plasmids. The pLC plasmids and newly constructed plasmids were examined for the ability to rescue the mutations. The complementation tests defined the location of the genes in the 15 X 10(6) Mr segment in the following order: nrdA-nrdB-ftsB-glpT. Functional nrdAB and ftsB genes were located in the 3.1 X 10(6) Mr EcoRI-PstI fragment.

Base Sequence↗
PubMed1982

Hfr-mediated conjugative transfer of pBR322 vector carrying the chromosomal DNA of Escherichia coli.

Hybrid plasmids consisting of a non-mobilized plasmid, pBR322, and a segment of chromosomal DNA of Escherichia coli could be transferred from an Hfr donor to recipient cells by a bacterial mating. When the chromosomal DNA in the plasmid corresponded to the early transfer region of the Hfr, the frequency of the transfer was high. The recA function of both donor and recipient cells was required in the transfer. The physical association of the hybrid plasmid with the transferring Hfr chromosome through the homologous sequences may mediate the transfer of the non-mobilized plasmid. This phenomenon is useful for the determination of the chromosomal location of an unidentified fragment cloned in a non-mobilized plasmid.

Chromosome Mapping↗
PubMed1982

A clinical study of left ventricular diastolic properties.

Left ventricular (LV) diastolic properties were evaluated in 150 patient with various heart diseases, including 22 normal subjects, using high fidelity pressure tracing and good quality LV cineangiogram. Impaired LV relaxation was demonstrated in hypertrophic cardiomyopathy (HCM), congestive cardiomyopathy (CCM), hypertensive heart disease (HHD), coronary artery disease (CAD) with and without LV asynergy, mitral stenosis (MS), and mitral regurgitation (MR) with significantly prolonged time constant of the LV pressure fall (time constant T). LV preload, defined as the stress to the ventricle at the end-diastole, was elevated in MR and in patients with CCM and congestive heart failure (CHF). Although LV end-diastolic pressure was high in HCM, preload was in the normal range. Diastolic elastic stiffness constant (K) was elevated in HCM, and slightly (0.05 less than p less than 0.1) high in HHD, and end-diastolic elastic stiffness was elevated in MR, and in patients with CCM and CHF. These observations indicate that the relaxation abnormality is present in the majority of patients with heart diseases. The elevation of preload might be a fundamental cause of LV dilatation in MR by stretching the myocardium, and the elevation of it in CCM coincides with the appearance of CHF. The chamber stiffness is increased in association with an increasing muscle mass without chamber enlargement.

Adult↗
PubMed1982

A clinical study on the role of the renin-angiotensin-aldosterone system and catecholamines in chronic congestive heart failure.

In order to evaluate the roles of the renin-angiotensin-aldosterone system and of catecholamines in 117 normotensive patients with chronic congestive heart failure (CHF), a study was made of the relationships between plasma concentrations, hepatic extraction of these humoral factors and hemodynamic parameters. In 6 patients with moderate to severe CHF, the acute effect of oral; administration of angiotensin I converting enzyme inhibitor, SQ 14225 (captopril), on mean arterial pressure (MAP), peripheral venous pressure (VP) and these humoral factors was investigated. In patients with CHF of Class III-IV (according to NYHA classification), the urinary norepinephrine (U-NE) excretion increased. Plasma norepinephrine (P-NE) levels increased in proportion to the severity of CHF (p less than 0.001) and had a positive correlation with systemic vascular resistance (SVR) (p less than 0.01), VP (p less than 0.05), pulmonary artery wedge pressure (PWP) (p less than 0.01) and plasma renin activity (PRA) (p less than 0.01). P-NE correlated negatively with the cardiac index (p less than 0.02). Hepatic extraction of norepinephrine (EX-NE) was reduced in patients with elevated right atrial pressure (RAP) (p less than 0.05) and negatively correlated with VP (p less than 0.05). In patients with elevated P-NE, U-NE increased significantly (p less than 0.01), despite their decreased renal clearance of norepinephrine (CNE) (p less than 0.02). There was no significant difference in EX-NE between these patients and patients with normal P-NE. PRA was higher in Class III-IV patients than in Class I-II patients in the prediuretic period (p less than 0.01). PA showed a significant positive correlation with PRA (p less than 0.001). Hepatic extraction of aldosterone (EX-A) was reduced in patients with elevated RAP (p less than 0.05) and was negatively correlated with VP (p less than 0.05). Following captopril administration, PRA increased consistently and PA decreased. MAP fell, especially in 2 patients with mitral stenosis. The heart rate tended to decrease. VP also fell with symptomatic improvement. The decline in VP was correlated with the decrease in P-NE (p less than 0.01). These findings suggest that the sympathetic nervous system contributes to the elevation of SVR and PWP even before frank heart failure develops. The rise of P-NE seems to be due to increased norepinephrine release from sympathetic nerve beds, whereas a decrease in hepatic extraction and renal clearance probably has only a minor effect. The renin-angiotensin system also seems to contribute to elevation of SVR, to maintain effective arterial pressure by enhanced sympathetic activity, and the renin-angiotensin system seems to be a main determinant of PA in CHF.

Aldosterone↗
PubMed1982

[Midsystolic closure of the aortic valve in hypertrophic nonobstructive cardiomyopathy].

Midsystolic cessation of left ventricular contraction was documented in a patient with hypertrophic nonobstructive cardiomyopathy (HCM) associated with Cushing's syndrome (adrenal adenoma) without history of hypertension. The carotid pulse tracing showed a rapid upstroke with a prominent percussion wave which was rapidly decayed at midsystole followed by a tiny tidal wave. The decay of this percussion wave coincided in timing with midsystolic closure of the aortic valve in the echocardiogram. The left ventricle (LV) was symmetrically hypertrophied (wall thickness = 1.8 cm). The motion of the interventricular septum and LV posterior wall appeared trapezoid, and the contraction of these walls was normal in early-systole followed by the sudden cessation at midsystole till end-systole. Systolic anterior motion of the mitral valve was not observed. Cardiac catheterization revealed no pressure gradient in the LV even after the various provocative maneuvers. The left ventriculogram simultaneously recorded with LV pressure showed that LV ejection was completed at midsystole, when LV pressure fell from 98 to 83 mmHg. Mitral regurgitation was not observed. Midsystolic cessation of left ventricular contraction in this case is thought to be the cause of sudden interruption of forward aortic flow, resulting in a bifid carotid pulse and midsystolic closure of the aortic valve in the echocardiogram.

Adult↗
PubMed1981

Nucleotide sequence of the asnA gene coding for asparagine synthetase of E. coli K-12.

We have subcloned the asnA gene of E. coli K-12, a gene coding for asparagine synthetase, from a previously cloned 6 mega-dalton segment of E. coli chromosome containing the DNA replication origin, ori, and asnA. The complete nucleotide sequence of the asnA gene was determined: the region of the structural gene extends 990 base-pairs at nucleotide positions 1434-2423 (see Fig. 3), which codes for a polypeptide of 330 amino-acid residues with a molecular weight of 36,688 daltons. The nucleotide sequences of the promoter and the ribosome-binding site of the gene are also assigned. We discuss the properties of its polypeptide.

Amino Acid Sequence↗
PubMed1981

Mutations in the gene coding for Escherichia coli DNA topoisomerase I affect transcription and transposition.

Mutations in top, the structural gene for Escherichia coli DNA topoisomerase I, have been identified and mapped at 28 min on the chromosome, near cysB. Strains carrying deletions of the top gene are viable. The top mutations, however, do exert pleiotropic effects on transcription and transposition. Mutants lacking DNA topoisomerase I have a more rapid rate of induction and a higher level of catabolite-sensitive enzymes including tryptophanase and beta-galactosidase. This general activation of transcription by top mutations can be attributed to an increase in the negative superhelicity of the DNA in vivo when the topoisomerase activity is abolished. The frequency of transposition of Tn5, a transposon carrying kanamycin resistance, is decreased by a factor of 40 or more in top mutants. A direct or indirect role of the topoisomerase in transposition is discussed. The transposition frequency of Tn3, however, is not dependent on top. Based on the studies of the E. coli top mutants, it appears that the supX gene, which was originally studied in Salmonella typhimurium [Dubnau, E. & Margolin, P. (1972) Mol. Gen. Genet. 117, 91-112] is likely to be the structural gene for DNA topoisomerase I.

Chromosomes, Bacterial↗
PubMed1981

Enhancing effect of surgical bursectomy on antibody response.

Effect of surgical bursectomy on antibody response was studied in chicks injected intrabursally with sheep red blood cells (SRBC) and Brucella abortus on day 2 of life and challenged intravenously with the same antigens on day 9. Bursectomy performed 2 days after the priming resulted in a significantly decreased anti-SRBC plaque-forming cell (PFC) response, whereas bursectomy performed 4 or 5 days after the priming clearly enhanced the PFC response. The enhancing effect of bursectomy on the PFC response was also observed if the priming was made intravenously. In antibody titers against SRBC the enhancing effect was observed only if a secondary and tertiary challenge was performed at the age of 28 and 36 days, respectively. Titers of Brucella antibodies were either reduced by the bursectomy (performed 2 or 4 days after the intrabursal priming) or left unaffected (bursectomy performed 5 days after the priming). These findings are discussed in relation to bursa-derived suppressor cells.

Animals↗
PubMed1981

T cell dependent B cell differentiation in the chicken.

Transplantation of bursa cells into surgically thymectomized (STx), cyclophosphamide(CY)-treated and X-irradiated (X) newly hatched chicks resulted in a morphological and functional reconstitution of the bursa-dependent immune system only when the transplanted bursa cells were supplemented with thymus cells. Without supplementation with thymus cells, morphological restoration of the bursa, antibody formation to sheep red blood cells and Brucella abortus, and germinal center formation remained deeply deficient. Bursa cells alone induced a full reconstitution of the bursa-dependent immunity in non-thymectomized. CY-treated and X-irradiated cell recipients. The incomplete restoration of STx-CY-X chickens after transplantation of bursa cells was not due only to lack of T helper cells, as indicated by the incomplete restoration of the bursal morphology and of antibody formation against Brucella abortus, a thymus-independent antigen. It is concluded that T cells are necessary for the B cell differentiation in the bursa of Fabricius. The mechanism behind this phenomenon remains unclear but our results indicate that a complete T cell function is not a prerequisite for this, since STx-CY-X birds reconstituted with bursa and thymus cells together did not have their mitogen (PHA, Con A) responses normalized.

Animals↗