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Biomedical subjects

K Shimamoto

Publications and source records attributed to K Shimamoto.

At least 289 records · Page 16Linked to original sources
PubMed1991

Anaerobic induction and tissue-specific expression of maize Adh1 promoter in transgenic rice plants and their progeny.

In order to analyze expression of the maize alcohol dehydrogenase 1 gene (Adh1), its promoter was fused with the gusA reporter gene and introduced into rice by protoplast transformation. Histochemical analysis of transgenic plants and their progeny showed that the maize Adh1 promoter is constitutively expressed in root caps, anthers, anther filaments, pollen, scutellum, endosperm and shoot and root meristem of the embryo. Induction of expression by the Adh1 promoter was examined using seedlings derived from selfed progeny of the transgenic plants. The results showed that expression of the Adh1 promoter was strongly induced (up to 81-fold) in roots of seedlings after 24 h of anaerobic treatment, concomitant with an increase in the level of gusA mRNA. 2,4-D also induced Adh1 promoter-directed expression of gusA to a similar extent. In contrast, little induction by anaerobic treatment was detected in transformed calli, leaves or roots of primary transformants or shoots of seedlings. A detailed examination of seedling roots during anaerobic treatment revealed that the induction started first at the meristem and after 3 h there was strong induction in the elongation zone which is located 1-2 mm above the meristem; the induction then progressed upward from this region. Our results suggest that transgenic rice plants carrying the gusA reporter gene fused with promoters are useful for the study of anaerobic regulation of genes derived from graminaceous species.

Alcohol Dehydrogenase↗
PubMed1991

Does myocardial stunning contribute to infarct size limitation by ischemic preconditioning?

BACKGROUND: The mechanism through which ischemic preconditioning causes cardioprotection is unknown. The present study investigated the role of stunning in preconditioning. METHODS AND RESULTS: We studied three different protocols of preconditioning: two cycles of 2-minute ischemia separated by 5-minute reperfusion (2'PC), one cycle of 5-minute ischemia by 5-minute reperfusion (5'PC1), and two cycles of 5-minute ischemia separated by 5-minute reperfusion (5'PC2). In the first series of experiments, the stunning associated with 2'PC, 5'PC1, or 5'PC2 was assessed using an epicardial Doppler transducer in anesthetized open-chest rabbits. The thickening fraction (percent baseline) of the preconditioned region was 76.8 +/- 7.2% (mean +/- SEM) after 2'PC but 31.4 +/- 9.2% and 34.3 +/- 9.7% after 5'PC1 and 5'PC2, respectively, which were significantly lower, thus indicating more severe stunning than that after 2'PC. In the second series of experiments, a branch of the left circumflex artery was occluded for 30 minutes and then reperfused for 72 hours in four groups of rabbits. One group was not preconditioned and three groups were preconditioned with 2'PC, 5'PC1, or 5'PC2 protocols before the 30-minute ischemia. In contrast to the differences observed in the stunning in the first series of experiments, histological infarct size was similar in the three preconditioned groups (21.1 +/- 3.0% of area at risk after 2'PC, 20.1 +/- 3.4% after 5'PC1, 16.4 +/- 4.2% after 5'PC2), all of which were significantly smaller than that in the unpreconditioned group (43.9 +/- 5.0%). The third series of experiments examined the degree of stunning by 2'PC, 5'PC1, or 5'PC2 and the size of infarct (tetrazolium staining) in the same animal after 30-minute ischemia/3-hour reperfusion; again, the results showed no significant correlation between degree of stunning and infarct size. CONCLUSIONS: The myocardial infarct size-limiting effect of preconditioning did not correlate with the degree of myocardial stunning accompanying preconditioning. Thus, it is unlikely that myocardial stunning contributes to the cardioprotective effect of ischemic preconditioning.

Animals↗
PubMed1991

Inhibition of thromboxane A2 synthetase failed to limit myocardial infarct size in a rabbit ischemia-reperfusion model.

The role of thromboxane A2 (TXA2) in myocardial necrosis during coronary occlusion and reperfusion was investigated by using a new long-acting TXA2 synthetase inhibitor, DP1904. A rabbit coronary branch was occluded for 30 min and then reperfused for 72h. Infarct size and area at risk were determined histologically and by fluorescent particles, respectively, for 4 groups; a saline receiving control group (C group), a DP1904 treated group (DP group), a heparin treated group (H group), and a DP1904 plus heparin treated group (DP-H group). The H group and DP-H group were included to examine the influence of heparinization on the effect of DP1904. In the DP and DP-H groups, 10 mg/kg of DP1904 was injected i.v. 2h before coronary occlusion, as well as 24 and 48h after reperfusion. This dose of DP1904 (10 mg/kg i.v.) was able to inhibit serum thromboxane B2 formation ex vivo to 1.1% of the control level 2h after its administration, and to 39.5% at 24h, in the rabbit (n = 5). The H and DP-H groups received 1000 units of heparin i.v. 3 min prior to coronary occlusion. The size of the area at risk, heart rate, blood pressure, and rate-pressure products were comparable between the 4 groups. Mortality was not significantly different in any group. Myocardial infarct size as the percentage of area at risk was 43.6 +/- 3.9% in C group (n = 10), 41.1 +/- 4.4% in DP group (n = 9), 47.8 +/- 3.0% in H group (n = 13), and 44.7 +/- 4.0% in DP-H group (n = 10), which were not significantly different. These findings suggest that TXA2 does not contribute directly to myocardial necrosis during coronary occlusion and reperfusion in the rabbit.

Animals↗
PubMed1991

A case of congenital left ventricular diverticulum with pulmonary stenosis and its scintigraphic characteristics.

We encountered a 31-year-old female patient with mild valvular pulmonary stenosis who had no abnormality in the electrocardiogram but pulmonary dilatation in the chest radiograph. Two-dimensional echocardiography and magnetic resonance imaging demonstrated two small protrusions at the interventricular septum indicating diverticula. Large perfusion defects were observed at the anterior wall in the thallium-201 myocardial tomograms. Short axial and vertical long axial images by ECG-gated blood pool tomography revealed an out-pouching best seen during diastole and a good contraction during systole in the corresponding areas. These findings suggested the presence of thin but normal myocardium in the anterior wall, i.e. a muscular type of left ventricular diverticulum. The presence of the muscular type of left ventricular diverticulum at the anterior and septal walls was confirmed by contrast left ventriculography. A congenital diverticulum at the anterior and septal walls with pulmonary stenosis is very rare. Furthermore, its scintigraphic images were quite characteristic and useful for its diagnosis.

Adult↗
PubMed1991

Site-related difference in the prevalence of mitral valve prolapse. Relation to the prevalence and severity of mitral regurgitation.

In this study, 431 consecutive patients with mitral valve prolapse (MVP) diagnosed by two-dimensional echocardiography were employed to further investigate the site-related difference in the prevalence of MVP. Following echocardiographic determination of the site and severity of MVP, a pulsed-Doppler technique was further performed to assess the existence and severity of mitral regurgitation (MR) in all patients. These patients were then classified by age in 10-year groups with patients older than 60 years being enrolled in one group. The younger groups accounted for a large number of the patients with MVP in our study, with the number of patients being reduced with age. In addition, female patients tended to predominate up until the 50s, but not in the 50 and older groups. The prevalence of MVP at the centro-medial site of the anterior mitral leaflet (AML) predominated in all age groups, gradually decreasing with age, except for a peak in the 40s, before continuing to decline in the 50 and older groups. On the other hand, the prevalence of MVP at the lateral site of the AML and at the posterior mitral leaflet (PML) increased with age. In the 50 and older age groups, the prevalence of MVP at these sites increased steeply with age. However, the prevalence of MVP at both the lateral site of the AML and PML did not significantly increase with age. The trend shown above was not significantly different for gender. The number of patients with MR increased with age independent of the site of MVP. However, the prevalence and severity of MR associated with MVP at the lateral site of the AML and/or at the PML were significantly greater than at the other sites up until the 50s (p less than 0.05). When patients were older than 50 years, this significant site-related difference in the prevalence of MR was not observed because of the higher prevalence of MR in the older patients in this study. Forty-one patients could be followed for 2 to almost 5 years. Three of the 41 patients were observed to have MVP at the centro-medial site of the AML in the initial examination, but the site of MVP had extended to the lateral side of the AML in the final examination. Two patients with MVP at all 3 sites of the AML demonstrated an increase in the severity of MVP. However, there were no newly documented cases of MR among those patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1991

Myocardial accumulation of monoclonal antimyosin Fab in hypertrophic cardiomyopathy and postpartum cardiomyopathy.

Indium-111-antimyosin Fab scan was performed in patients with hypertrophic and postpartum cardiomyopathies to assess whether or not myocardial damage can be delineated. In two patients with hypertrophic cardiomyopathy, intense and diffuse antimyosin uptake was observed, although there was no evidence of acute myocardial damage or wall motion abnormality. A patient with postpartum cardiomyopathy showed a dense and relatively localized accumulation in the left ventricular anterior wall in association with thallium perfusion and wall motion abnormalities. Thus, antimyosin scanning can delineate not only manifested but also subclinical myocardial damage in hypertrophic and postpartum cardiomyopathies which may not be detectable by other techniques.

Adult↗
PubMed1990

A potent metabotropic glutamate receptor agonist: electrophysiological actions of a conformationally restricted glutamate analogue in the rat spinal cord and Xenopus oocytes.

The (2S,3S,4S) isomer of alpha-(carboxycyclopropyl)glycine (L-CCG-I), a conformationally restricted glutamate analogue, caused a marked depolarization of motoneurons in the isolated rat spinal cord, which was almost insensitive to CPP and CNQX. Depolarizing responses to L-CCG-I were markedly decreased by reducing the temperature of the bathing fluid. Similar results were obtained in the case of trans-ACPD, which is a metabotropic glutamate receptor agonist, but the depolarizing action of L-CCG-I was more potent than that of trans-ACPD. In Xenopus oocytes injected with poly(A)+ mRNA extracted from the rat brain, L-CCG-I induced significant oscillatory chloride currents, suggesting that L-CCG-I is a potent agonist for metabotropic-type glutamate receptors.

Amino Acids, Dicarboxylic↗
PubMed1990

Enhancement of foreign gene expression by a dicot intron in rice but not in tobacco is correlated with an increased level of mRNA and an efficient splicing of the intron.

The first intron of castor bean catalase gene, cat-1 was placed in the N-terminal region of the coding sequence of the beta-glucuronidase gene (gusA) and the intron-containing gusA was used with the cauliflower mosaic virus (CaMV) 35S promoter. Using this plasmid, pIG221, the effect of the intron on expression of beta-glucuronidase (GUS) activity was examined in transgenic rice calli and plants (a monocotyledon), and transgenic tobacco plants (a dicotyledon). The intron-containing plasmid increased the level of GUS enzyme activity 10 to 40-fold and 80 to 90-fold compared with the intronless plasmid, pBI221, in transgenic rice protoplasts and transgenic rice tissues, respectively. In contrast, the presence of the intron hardly influenced the expression of the GUS activity in transgenic tobacco plants. Northern blot analysis showed that the catalase intron was efficiently spliced in rice cells while transgenic tobacco plants contained both spliced and unspliced gusA transcripts in equal amounts. Furthermore, the level of the mature gusA transcript in transformed rice calli was greatly increased in the presence of the intron. The catalase intron was removed at the same splice junctions in transgenic rice and tobacco plants. These findings indicate that the stimulating effect of the intron on GUS expression is correlated with an efficient splicing of pre-mRNA and an increased level of mature mRNA.

Base Sequence↗
PubMed1990

Molecular changes in protoplast-derived rice plants.

To determine whether regeneration of rice plants from protoplast culture induces DNA polymorphisms, progeny plants from direct regenerants of such cultures were examined for restriction fragment length polymorphisms (RFLP analysis). Significantly increased levels of DNA polymorphism were found compared with those in non-tissue culture control plants. Analysis with gene sequences representative of different functional domains, revealed that such polymorphisms are apparently widespread and not associated with any particular region. Analysis by comparative digestion with both methylation-sensitive and insensitive restriction enzymes revealed that methylation changes cannot be regarded as a major factor in the induction of these DNA polymorphisms.

DNA↗
PubMed1990

The transient increase of urinary digitalis-like substance excreted during excess sodium intake in reduced renal mass rats.

Urinary immunoreactive endogenous digitalis-like substance (EDLS) excretion was studied in gradually reduced renal mass rats (RRM). Urinary EDLS increased immediately after the start of 1% NaCl ingestion, then it returned to the basal level 2 weeks later. Both urinary sodium excretion and urinary EDLS were significantly higher in 3/6 and 4/6 RRM than in control until 2 weeks after starting 1% NaCl. However, there was no difference in blood pressure between the groups. Transient EDLS increase may play an important role in maintaining sodium and water homeostasis, but its transient increase apparently does not contribute to blood pressure elevation.

Animals↗
PubMed1990

Suppressed dopaminergic activity and water-sodium handling in the kidneys at the prehypertensive stage of essential hypertension.

1. In this study, the question of whether the suppression of the renal dopaminergic system is primary or not was investigated. 2. Renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension (FH(-] and those with a family history of hypertension (FH(+]. 3. A significant decrease in urinary free dopamine excretion was noted, and the responses of urine volume, urinary sodium excretion, and fractional excretion of sodium to infused dopamine were significantly augmented in FH(+). In addition, a normal level of l-dopa delivery at the renal proximal tubules and a significant reduction in the conversion of l-dopa to dopamine in the kidney were found in FH(+). 4. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and that the reduction in the conversion of l-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+).

Adult↗
PubMed1990

Re-evaluation of the plasma renin-angiotensin system in anephric patients.

In view of recent observations that a number of extrarenal tissues have the potential to produce angiotensin II and release it in a regulated fashion, we made measurements of immunoreactive angiotensin I (irAng I) and angiotensin II (irAng II), along with active and inactive renin, and angiotensinogen in plasma of seven anephric patients and of 16 normal healthy volunteers to gain insight into possible sources of plasma Ang II. High performance liquid chromatography clearly demonstrated that the predominant component of irAng II in anephric plasma is the biologically active octapeptide Ang II. Plasma renin activity (PRA), and active and inactive renin all were detected in all of the anephrics but their levels were decreased to 33% for PRA, 12% for active renin, and 18% for inactive renin when compared with those in healthy subjects. While plasma angiotensinogen was significantly but only slightly increased in anephric patients (+28% over the mean value for normal subjects), irAng I and irAng II both were present in quantities almost comparable with those in normals. These results suggest that local angiotensin production contributes, in part at least, to the circulating plasma Ang II. Vascular tissue seems to be the best candidate responsible for such a mechanism, on the basis of recent demonstrations of unequivocal, regulated release of Ang II from diverse vascular beds.

Adult↗
PubMed1990

Angiotensin-converting enzyme inhibitors and the kallikrein-kinin system.

The role of plasma kinin in the hypotensive mechanism of angiotensin-converting enzyme (ACE) inhibitors in essential hypertensive patients and in a dog myocardiac ischemic model is discussed. Both an increase in plasma kinin and a decrease in plasma angiotensin II might contribute to the hypotensive effects of ACE inhibitors in a normal-renin group. In a low-renin group, the hypotensive mechanism of this drug may be mainly the increase in plasma kinin levels. The augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of ACE inhibitors, and this mechanism might be explained by the renal blood flow increase and augmented activity in the renal kallikrein-kinin system. In a dog myocardial ischemia model, when an apparent myocardial ischemia occurred in the constricted group, plasma kinin levels in coronary sinus blood increased significantly. Following infusion of kinin into the left main coronary artery, 0.1 ng/kg/min of kinin for 5 min did not cause any change in plasma kinin levels in the artery or coronary sinus. A dose of 10 ng/kg/min of kinin for 5 min produced a significant elevation in plasma kinin in the coronary sinus from 12.8 to 142 pg/ml without any change in plasma kinin in the artery. However, such a level of kinin had no significant effect on coronary circulation, myocardial metabolism, or ECG ST segment in either group. Thus, the role of increased kinin in this dog model still remains unclear. Further studies including the administration of ACE inhibitors or bradykinin antagonist will be necessary to reach conclusions about the role of kinin in the heart.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Dopaminergic activity and water-sodium handling in the kidneys of essential hypertensive subjects: is renal dopaminergic activity suppressed at the prehypertensive stage?

To investigate whether the suppression of the renal dopaminergic system in hypertension is primary or secondary, renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension [FH(-)] and those with a family history of hypertension [FH(+)]. A significant decrease in urinary dopamine excretion was recognized, and the responses of urine volume, urinary sodium excretion, fractional excretion of sodium, and urinary kallikrein and kinin activity to infused dopamine were significantly augmented in FH(+) subjects. In addition, a normal level of L-dopa delivery into the kidney and at the renal proximal tubules and a significant reduction of the conversion from L-dopa to dopamine in the kidney were found in FH(+) subjects. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and a reduction in the conversion from L-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+) subjects.

Adult↗
PubMed1990

In vivo concentrations of kinins and angiotensins.

In the investigation of hypotensive mechanisms for the converting enzyme (ACE) inhibitor, precise methods for plasma kinin and angiotensin II measurement are essential. We describe here determination methods of plasma kinin and angiotensin II, and their applications to converting enzyme inhibitor administration. In our kinin RIA system, a high titered antiserum (final dilution 1:640,000) was used. Sensitivity was 0.25 pg/tube. Regarding plasma kinin measurement, an inhibitor mixture including aprotinin, hexadimethrine, SBTI, phenanthroline and EDTA, was used to collect the plasma sample. The determined plasma kinin levels in normal subjects were below 10 pg/ml. A very sensitive and simplified direct RIA system for plasma angiotensin II was also developed in our laboratory using the very high titered antiserum (final dilution 1:1,500,000). The sensitivity was 0.1 pg/tube, and cross-reactivity of angiotensin I was less than 0.1%. These data suggest that plasma angiotensin II level can be determined directly in very small plasma samples, such as 0.1 ml by this RIA system even in the ACE inhibitor administration. The plasma angiotensin II levels in normal subjects were 12.0 pg/ml. Both of these RIAs which were applied to the clinical experiments of ACE inhibitor administration.

Angiotensin II↗