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Biomedical subjects

S Daikoku

Publications and source records attributed to S Daikoku.

At least 37 records · Page 2Linked to original sources
PubMed1999

Influence of calcium antagonists on long-term survival of patients treated with coronary angioplasty.

A meta-analysis reported that nifedipine increased mortality dose-dependently in patients with coronary artery disease. However, there have been few studies (specifically in Asians) on the long-term prognosis of patients treated with calcium antagonists after successful coronary angioplasty (PTCA). The subjects consisted of 583 consecutive patients (461 males, aged 59 +/- 10), who underwent successful elective PTCA between 1985 and 1990. First, they were divided into two groups; the calcium antagonist (+) group (n = 560) and the calcium antagonist (-) group (n = 23), and were evaluated in terms of total survival and cardiac events. Second, the calcium antagonist (+) group was further divided into 4 groups according to calcium antagonist type, i.e., short-acting nifedipine group (n = 156), long-acting nifedipine group (n = 203), diltiazem group (n = 184) and the other group (n = 17), and these groups were evaluated in the same way. The primary end-point was set as death from any cause. Secondary end-points were any cardiac events, including non-fatal acute myocardial infarction, coronary artery bypass surgery and repeat PTCA. The mean follow-up period was 4.5 +/- 1.8 years. A multivariate analysis was performed with the Cox proportional-hazard model. The Kaplan-Meier analysis showed that the calcium antagonist (-) group had significantly worse prognoses than the calcium antagonist (+) group (p < 0.05), and that there was no significant difference among the prognoses of the four calcium antagonists groups. The multivariate analysis revealed that the use of a calcium antagonist was one of the independent factors positively contributing to the prognosis. The use of any type of calcium antagonist did not increase mortality in patients who underwent successful elective PTCA, rather, it contributed to a favorable outcome.

Aged↗
PubMed1999

The olfactory origin of luteinizing hormone-releasing hormone (LHRH) neurons. A new era in reproduction physiology.

This paper reviews those studies which conceived the concept that the brain LHRH-synthesizing neurons originate in the nasal placode. LHRH isolated from mammalian hypothalamus in 1971 was first shown immunohistochemically two years later in the hypothalamic neurons which project processes to the median eminence, to release it into the portal capillaries in the guinea pig. At an early stage of development, the LHRH cells were found in the nasal placode but not in the hypothalamus as shown in in vivo and in vitro developmental studies. The cells arising in the brain were delayed. This discrepancy was solved in 1989-1990 by findings that the cells derived in the placode at an early stage left the site and migrated to the forebrain vesicles along the placode-derived terminal and vomeronasal nerve fibers, both of which were found to express immunoreactive cell adhesion molecules. The neurons, after reaching the surface of the forebrain vesicles, entered into the brain by the guidance of the cell adhesion molecule-positive fibers, and came to be distributed not only in the hypothalamus but also in the telencephalon cortex, midbrain, limbic brain, and main and accessory olfactory bulbs. The attention to these heterogeneties led to discussion of the possible neurobiological significance of this peculiar peripheral neurogenesis from an evolutionary viewpoint.

Animals↗
PubMed1998

Spatiotemporal appearance of developing LHRH neurons in the rat brain.

To obtain insight into the development of the heterogeneous intracerebral populations of luteinizing hormone-releasing hormone (LHRH) neurons, their spatiotemporal appearance was examined at different stages in normal rat embryos, in nasal epithelial explants in vitro, and in intrauterine nasal-operated embryos. Following the appearance of nerve cell adhesion molecule in the nasal placode at embryonic day (E) 12.5, LHRH neurons, generated in the nasal placode at E13.5, penetrated the forebrain vesicle (FV) by E14.5-15.5. After E16.5, as the FV elongated to form the olfactory bulb, the migrating neurons traversed posteriorly through the interhemispheric space to penetrate the septopreoptic (S-P) area. By E18.5, LHRH neurons were detected in the preoptic-diagonal band (P-D) area as well as in the S-P region, along with some scattered extrahypothalamic LHRH neurons. To determine the source of these neurons, we separately cultured dissected parts of E12.5 nasal pit epithelium. Neuronal generation was predominantly from the medial wall epithelium (NAP), but some LHRH neurons originated in the roof epithelium. Cocultures of the NAP (E12.5) with the FV, median eminence-arcuate complex, Rathke's pouch, mesencephalon, or medulla oblongata from E14.5 embryos revealed the ability of LHRH cells to penetrate all of these tissues. Uni- or bilateral nasal destruction was conducted at E16.5 or E15.5, respectively, and examined at E18.5 and E21.5. In the operated embryos, most LHRH neurons were present in the P-D system and some in the S-P area. This finding suggests that the neurons generated before E15.5 are primarily predisposed to form the P-D system, whereas those derived afterward form the S-P system.

Animals↗
PubMed1998

Previous angina reduces in-hospital death in patients with acute myocardial infarction.

There is little information on how previous angina influences in-hospital deaths secondary to acute myocardial infarction (MI). This study evaluated the causes of in-hospital deaths in MI patients with and without previous angina. A total of 2,264 consecutive patients were admitted to our hospital due to acute MI. These patients were divided into 2 groups according to the presence or absence of prior MI. Both groups were further divided according to the presence or absence of previous angina. The causes of in-hospital deaths were classified into 4 categories: (1) cardiogenic shock or congestive heart failure, (2) cardiac rupture, (3) arrhythmia, and (4) other causes. In patients with a first MI, the in-hospital mortality rate was lower in patients with previous angina than those without (6.9% vs 11.4%, p <0.01). There was no significant difference between these patients with and without previous angina in in-hospital deaths due to cardiogenic shock or congestive heart failure, arrhythmia, or other causes. Death due to cardiac rupture was less frequent in patients with previous angina (1.4% vs 5.0%, p <0.01). In patients with prior MI, the in-hospital mortality rate was lower in patients with than without previous angina (17.7% vs 25.3%, p <0.05). In contrast to patients with their first MI, there was a trend toward a lower incidence of in-hospital death due to cardiogenic shock or congestive heart failure in patients with previous angina (12.8% vs 19.0%, p = 0.05). There were no significant differences in in-hospital deaths due to cardiac rupture, arrhythmia, and other causes between the 2 subgroups. In multivariate analysis, previous angina was an independent predictor of in-hospital death. Thus, in-hospital deaths after acute MI in patients with previous angina were less because of less cardiac rupture in patients with a first MI and less cardiogenic shock or congestive heart failure in patients with prior MI.

Aged↗
PubMed1998

Correlation of residual stenosis immediately after coronary angioplasty with long-term prognosis.

This study evaluated the correlation of residual stenosis after percutaneous transluminal coronary angioplasty with the long-term prognosis. Among consecutive 1,230 patients who underwent coronary angioplasty in the National Cardiovascular Center in Osaka, Japan, 894 patients had de novo lesions. Of these, the 70 patients with acute myocardial infarctions and 105 with unstable angina who had emergency coronary angioplasties were excluded from the study. Among the remaining 719 patients, successful dilatation of the main target vessel was achieved in 592 patients, who then comprised the study group. They were divided into three groups according to their residual stenosis (RS) immediately after coronary angioplasty: group A, RS < 15% (n=208); group B, 15% < or = RS < or = 35% (n=286), and group C, 35% < RS < 50% (n=98). The duration of follow-up was 1,668, 1,660, and 1,680 days in group A, B, and C, respectively. The groups A, B, and C were not significantly different in terms of age, history of myocardial infarction, left ventricular ejection fraction, number of diseased vessels and target vessels, and risk factors such as hypertension, hyperlipidemia, and diabetes mellitus. Primary end point of follow-up was defined as death from any cause and the second end point was occurrence of cardiac events. Kaplan-Meier survival analysis showed significant differences among the three groups. Moreover, survival curves seem to be dependent on the degree of post-procedural residual stenosis. Multivariate analysis using a Cox proportional hazard regression model showed that age, ejection fraction, and residual stenosis were independent determinants of event-free, cardiac, and total survival. Residual stenosis immediately after coronary angioplasty is an independent contributor to long-term clinical prognosis in patients treated with successful balloon coronary angioplasty.

Analysis of Variance↗
PubMed1998

Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction.

To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive ventricular remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (deltaEDVI), ESVI (deltaESVI), and EF (deltaEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with deltaEDVI (r = 0.48 and 0.54; both p < 0.01), whereas plasma BNP on day 7 more closely correlated with deltaEDVI (r = 0.77; p < 0.001). When study patients were divided into two groups according to plasma BNP on day 7, the group with BNP higher than 100 pg/ml showed greater increases in left ventricular volume and less improvement in EF compared with the other group with BNP lower than 100 pg/ml (deltaEDVI = 10.4 +/- 8 vs -3.4 +/- 9 ml/m2, deltaESVI = 6.2 +/- 7 vs -4.9 +/- 5 ml/m2, and deltaEF = 1.0% +/- 4% vs 4.9% +/- 5%; p < 0.05, respectively). Multiple regression analysis revealed that only plasma BNP on day 7, but not ANP, peak creatine phosphokinase level, left ventricular end-diastolic pressure, or acute-phase EF, correlated independently with deltaEDVI (p < 0.01). These results suggest that plasma BNP may be a simple and useful biochemical marker for the prediction of progressive ventricular remodeling within the first 30 days of acute myocardial infarction.

Adult↗
PubMed1998

Increased plasma adrenomedullin levels in patients with acute myocardial infarction in proportion to the clinical severity.

OBJECTIVES: To investigate the pathophysiological role of adrenomedullin in myocardial infarction. PATIENTS AND DESIGN: Plasma concentrations of adrenomedullin, atrial natriuretic factor, and brain natriuretic peptide were measured by radioimmunoassay in 31 patients with acute myocardial infarction over four weeks, and in 44 normal subjects. RESULTS: In patients with acute myocardial infarction, plasma adrenomedullin reached a peak of (mean (SD) 14.0 (9.0) pmol/l at 24 hours after the onset of symptoms and remained increased at all sampling points except the four week point compared with the value in normal subjects (5.0 (2.0) pmol/l). Adrenomedullin concentrations on admission were higher in patients from Killip class II, III, and IV than class I, and correlated positively with peak plasma creatine kinase and left ventricular end diastolic volume index, and negatively with left ventricular ejection fraction. The values from 12 to 48 hours were negatively correlated with systemic vascular resistance index. During the time course studied, adrenomedullin concentrations were positively correlated with atrial natriuretic factor (r = 0.40, p < 0.001) and brain natriuretic peptide (r = 0.53, p < 0.001). CONCLUSIONS: Plasma adrenomedullin concentrations increased in the acute phase of myocardial infarction in proportion with clinical severity suggesting that adrenomedullin may play an important role in the pathophysiology of myocardial infarction.

Adrenomedullin↗
PubMed1998

Cardioprotective effect of intravenous nicorandil in patients with successful reperfusion for acute myocardial infarction.

This study was designed to assess the cardioprotective effect of intravenous nicorandil, a potassium channel opener, in preventing reperfusion injury in acute myocardial infarction. Seventy patients were treated with placebo or nicorandil concomitant with reperfusion therapy in a prospective, randomized, double-blind fashion within 6 h after the onset of acute myocardial infarction. Nicorandil was administered before reperfusion as a 2-mg bolus iv injection followed by continuous infusion of 2-6 mg/h for the next 3 h. Thirty-six patients (17 in the placebo group, 19 in the nicorandil group) who demonstrated both complete occlusion of an infarct-related vessel before treatment and successful reperfusion were included in the final analysis. No significant changes in left ventricular ejection fraction were observed between the immediate and chronic phases in each group. In the analysis of regional ventricular function, the placebo group did not show any significant change in regional chord shortening (26.8+/-8.2 vs 24.3+/-7.3%, NS) or hypocontractile perimeter (36.4+/-28.2% vs 28.3+/-24.8%, NS) between immediate and chronic phase left ventriculograms. In contrast, in the nicorandil group, a significant increase in regional chord shortening (21.5+/-11.0% vs 25.8+/-11.3%, p<0.05) and a significant decrease in hypocontractile perimeter (33.3+/-19.6% vs 25.6+/-24.3%, p<0.05) were observed in the chronic phase left ventriculogram. Thus, nicorandil may be a useful adjunctive therapy for preserving myocardial contractile function in patients with acute myocardial infarction undergoing reperfusion therapy.

Acute Disease↗
PubMed1998

Survival using percutaneous cardiopulmonary support after acute myocardial infarction due to occlusion of the left main coronary artery--a report of two cases.

Two cases of acute myocardial infarction due to an occlusion of the left main coronary artery (LMCA) are presented. Their cardiogenic shock was successfully treated with percutaneous cardiopulmonary support (PCPS), in addition to reperfusion therapy and an intraaortic balloon pump. The 2 patients were able to be weaned from PCPS and discharged from hospital. It is suggested that the early use of PCPS may be life-saving in patients with myocardial infarction due to the occlusion of the LMCA who have progressed to cardiogenic shock.

Acute Disease↗
PubMed1998

High-dose immunoglobulin G therapy for fulminant myocarditis.

The cardiac function of an adult patient with fulminant myocarditis requiring a mechanical circulatory support was improved, along with the suppressed release of inflammatory mediators, after intravenous infusion with high-dose immunoglobulin. This therapy may have immunomodulatory effects and serve as a potential adjunctive therapy for patients with fulminant myocarditis.

Adjuvants, Immunologic↗
PubMed1997

Coronary artery aneurysms detected with ultrafast computed tomography.

A 25-year-old Japanese woman was admitted due to acute inferior myocardial infarction. Coronary angiography showed complete occlusion of the proximal right coronary artery and vague calcification distal to the complete occlusion. Using ultrafast computed tomography, two coronary artery aneurysms in the right coronary artery that could not be detected by coronary angiography were visualized.

Adult↗
PubMed1997

Developmental expression of a novel Kexin family protease, PACE4E, in the rat olfactory system.

PACE4 is a mammalian Kexin family protease that is involved in the maturation of precursor proteins. Four PACE4 isoforms have been identified. We identified a novel PACE4 isoform, PACE4E, from a human cerebellum cDNA library, which possesses a hydrophobic cluster in its C-terminus participating in membrane association. The size of PACE4E mRNA from adult rat brain was estimated by Northern blotting to be 4.4 kb. In situ hybridization histochemistry revealed that the highest level of PACE4E mRNA was expressed in the mitral cells of the adult rat olfactory bulb (OB). The OB is a unique sensory organ in that it has a lifelong regenerating capacity and it affects brain development. We further analyzed the expression of PACE4E mRNA in the developing olfactory system. On day 13.5 of gestation, PACE4E mRNA was expressed at high levels in the neuroepithelium of the forebrain vesicle (FV), olfactory epithelium, and cells in the fiber bundles projecting to the FV. As development proceeded, PACE4E mRNA was expressed in developing mitral cells but decreased in the olfactory epithelium. In the newborn, its expression was confined to the mitral cells in both the main and accessory OB and in some periglomerular cells, as shown in adult rats. The spatio-temporal expression of PACE4E suggests that it plays a role in the establishment and maintenance of the olfactory receptor system.

Animals↗
PubMed1997

Destruction of olfactory inputs affects the morphogenesis of the telencephalon in rats.

We unilaterally destroyed the nasal radix of rat embryos on day 15.5 of gestation (E15.5) in utero so as to block the olfactory inputs to the ipsilateral forebrain vesicle. The embryonic brains were examined after 6 days' survival (E21.5). In the deafferented half of the brain, LHRH neurons were significantly reduced in number, indicating the successful blocking of the olfactory input. On the deafferented side, the olfactory bulb failed to develop, and the telencephalic hemisphere, small in size, accompanied various histogenetic retardations in the primary olfactory cortex, in the cortical plate, and in the hippocampal formation. The striatum revealed remarkable structural differences between the ipsilateral and contralateral sides: on the ipsilateral side, the striatum was small in size and displayed numerical reductions of immunoreactive tyrosine hydroxylase (TH) fibers and substance P (SP) neurons in comparison with those in the contralateral one; in the substantia nigra, TH neurons and SP fibers were less numerous on the deafferented side. There were no remarkable differences in the distribution of TH neurons in the hypothalamus. In view of these sequential histogenetic alterations, it can be assumed that the olfactory inputs play a key role in the telencephalic morphogenesis.

Amygdala↗