Biomedical subjects
Publications and source records attributed to I Fujii.
Pick's disease is a rare cause of dementia. We studied two clinical cases of Pick's disease in its early stage. A computed tomography (CT) demonstrated lobar atrophy affecting primarily the anterior portions of the frontal lobes and the inferior portions of the temporal lobes. The fact that the characteristic pattern of lobar atrophy is already apparent in the early stage of the disease was demonstrated.
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Clinical and morphological features in 10 cases of "apical hypertrophic cardiomyopathy" (apical type) were analyzed and compared with those in classic hypertrophic cardiomyopathy with asymmetric septal hypertrophy (ASH). The hypertrophic pattern of the interventricular septum (IVS) was evaluated on the two-dimensional echocardiographic (2-D) left ventricular (LV) long-axis view. Thirty-one of 70 patients with ASH were characterized by predominant hypertrophy of the basal IVS (Type I). Seventeen patients had predominant hypertrophy of the apical IVS (Type III). Diffuse IVS hypertrophy was noted in 22 patients (Type II). Electrocardiographic similarity was documented between cases with Type III and apical type; that is, a low incidence of abnormal Q waves, a high incidence of giant negative T waves, and frequent absence of Q waves. In Type I and II, abnormal Q waves were frequently observed, while giant negative T waves were rare. On the 2-D LV short-axis view at the papillary muscle level, three groups with ASH revealed similar distributions of myocardial hypertrophy characterized by extension of hypertrophy to the LV anterior free all and papillary muscles. Most cases with apical type had a similar distribution of hypertrophy, but its degree was significantly less severe than that of ASH. Comparison of diastolic LV configurations on left ventriculograms and/or the 2-D apical two-chamber views indicated the morphologic continuity among the three types with ASH and the apical type. Clinical features in cases of the apical type were obviously less severe than those of three groups with ASH, as indicated by a significantly larger proportion of asymptomatic patients (90%), absence of sudden death and rare documentation of malignant ventricular arrhythmias on 24-hours ambulatory electrocardiography. In conclusion, apical type can be categorized as a part of hypertrophic cardiomyopathy with a wide morphologic spectrum rather than the separate disease entity, and it is characterized by giant negative T waves with minimum clinical manifestations.
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Echocardiographic and electrocardiographic findings in 74 adults with hypertrophic cardiomyopathy (HCM) were analyzed to identify the pattern of myocardial hypertrophy as a possible determinant of abnormal Q waves. The pattern of septal hypertrophy along the left ventricular long axis was divided into 3 types based on the site of maximum septal hypertrophy: basal, diffuse and apical types. Abnormal Q waves defined by the revised Minnesota Codes (either I-I, I-II or I-III) were noted in 31 cases (42%). The total incidence of abnormal Q waves in the basal type (15/26, 58%) and in the diffuse type (12/22, 55%) was significantly higher (p less than 0.001 and p less than 0.01, respectively) than that in the apical type (4/26, 15%). The abnormal Q waves defined by the strict criteria of Code I-I were significantly more prevalent (p less than 0.05) in the basal type than in the diffuse type, although there was no significant difference in the total incidence of abnormal Q waves between these 2 groups. Thirty-six patients with an extension of hypertrophy to the right ventricle (RVH) had a significantly higher incidence of abnormal Q waves than 22 patients without RVH (56% vs 27%, p less than 0.05). Furthermore, close relationships of RVH to the location of abnormal Q waves were documented. In conclusion, the abnormal Q waves in HCM may be related to the pattern of septal hypertrophy along the left ventricular long axis and to RVH.
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Incidence and prognostic significance of repetitive ventricular premature contractions in various cardiac diseases were evaluated retrospectively with 593 consecutive patients referred for the 24-hour continuous electrocardiographic monitoring (Holter monitoring). Primary cardiac diagnoses for 308 patients with structural heart diseases included previous myocardial infarction (MI) in 151 patients, angina pectoris in 34, congestive cardiomyopathy (COCM) in 21, valvular heart disease in 29, hypertensive heart disease (HHD) in 18, conduction disturbance in 28, and other cardiovascular abnormalities in 17 patients. Other 285 patients (48%) had no known structural heart disease. Repetitive ventricular premature contractions (VPCs) was defined as the occurrence of self-terminating two (couplet), three (triplet) or more consecutive VPCs without associated hemodynamic sequelae. Holter monitoring was done with simultaneous two-channel recordings. Repetitive VPCs were seen in 96 patients; 17% of patients with MI, 52% of COCM and 7% of no structural hart disease. Among 308 patients with structural heart disease, 91 had congestive heart failure and 42% of these had repetitive VPCs, whereas only 17% of patients without congestive heart failure had repetitive VPCs. Coronary arteriographic and ventriculographic findings were reviewed in 91 patients with previous MI. Neither the degree of coronary artery involvements nor left ventricular ejection fraction had influence on the occurrence of repetitive VPCs. Four hundreds and sixty-nine patients under the age of 69 years were followed from 6 to 36 months (mean 19 months). Thirteen patients including 5 cases with MI (4% of the cases with MI), 4 with COCM (21% of COCM) and 4 with other structural heart disease (4% of other disease) died suddenly in the follow-up period. In the patients followed, 72 had repetitive VPCs and 9 of them died suddenly. These 9 patients consisted of 4 patients with MI (25% of the cases with MI having repetitive VPCs), 4 with COCM (40% of COCM) and 1 with other structural heart disease (3% of other disease). Thus, patients with MI or COCM had higher incidence of repetitive VPCs and they are at a high risk for sudden cardiac death.
Location of infarct lesions (IL) demonstrated by two-dimensional echocardiography (2DE) was correlated with electrocardiographic patterns of myocardial infarction and with the sites of obstructive lesions in the individual coronary arteries. The left ventricular wall was displayed by phased-array 2DE in 47 patients with healed myocardial infarction, 29 of whom underwent coronary arteriography. Segmental analysis of IL was performed on 14 segments, 10 of which were obtained by the parasternal short-axis recordings at the mitral (basal) and papillary muscle (mid) levels (each level containing the anterior septum, anterior wall, lateral wall, posterior wall, and posterior septum). The remaining 4 segments (septum, anterior wall, lateral wall, posterior wall) were obtained by the apical 2-chamber and 4-chamber recordings. IL were defined as akinesis, thinning, increased echo density, or absent systolic thickening of the left ventricular wall. All 22 patients with anterior infarction (Q in V1-V4) had IL in the mid anterior septum which was specific for the lesion of the left anterior descending artery (LAD). The presence or absence of the r wave in V1 could not predict the involvement of this segment. IL in the apical anterior wall and septum were observed in 21 of 22 patients. The presence of Q waves in V5, V6 suggested the additional involvement of the apical posterior wall. Additional Q waves in I, aVL indicated the extension of IL from the mild anterior septum to the basal anterior septum, anterior wall, and mid anterior wall. The basal and mid lateral walls appeared normal in most patients. This pattern of IL distribution was observed in 5 of 6 patients with a stenosis on the proximal LAD. All 14 patients with inferior infarction (Q in II, III, aVF) had IL in the mid posterior wall and posterior septum. In contrast, 5 patients with infero-posterior infarction (Q in II, III, aVF + R in V1) and 6 patients with posterior infarction (R in V1) had IL in the mid lateral as well as the mid posterior wall without an involvement of the posterior septum. Coronary arteriography revealed that all of the 10 patients with inferior infarction had a stenosis in the right coronary artery, whereas 6 patients with infero-posterior or posterior infarction invariably had a stenosis in the left circumflex coronary artery. It was concluded that 2DE provides a reliable method for detecting IL and anatomic location of myocardial infarction reflecting a specific coronary artery disease.
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CD/CRJ rats were subjected to localized X-irradiation of the stomach and given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water. Rats given MNNG alone and non-treated rats were used as controls. Upon sacrifice at 15 months after the initial MNNG administration, intestinal metaplasia was observed; the histology was of complete type and the incidence was 100% in rats treated with X-rays and MNNG, whereas in rats treated with MNNG alone the intestinal metaplasia was of incomplete type and its incidence was 80%. However, the incidence of gastric cancer in rats treated with MNNG alone was 25%.
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A 31-month-old female mongrel dog was orally administered with 50 mg or 100 mg of N-nitrosobutylurea (NBU) in gelatin-capsule 3 times per week for 19 months with interposing periods of complete suspension. Thirty-four foci of signet ring cell carcinoma were found in the antral region of the stomach. The majority of the foci (31 foci) were early cancer, and the remaining foci were invasive cancer. In addition to these lesions, there was "a single gland cancer" in which a row of cancer cells was confined to a single gland. The whole gland was composed of two cell layers; the inner layer facing the lumen was normal gastric cells and the outer layer was atypical or neoplastic cells underlaid by the basement membrane. Mitosis was frequently observed on the bottom of the gland. Atypical or neoplastic cells seemed to mature gradually through a process of upward migration with increase in cytoplasmic Alcian blue-PAS and HID-AB positive mucin. Some of the cells rich in mucin moved into the lamina propria. The other cells remained in the flow of the regular cell renewal system of the normal gastric cells and reached the top of the gland. This observation revealed a mode of incipient gastric cancer growth, which starts and spreads within a single gland, before it invades the surrounding lamina propria.
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Subcutaneous injection of W/Fu rat stomach antigen emulsified with an equal volume of Freund's complete adjuvant at 1 week interval for a total of 2 administrations induced atrophic gastritis in A/HeJ mice. From the second week after the last injection the parietal cell mass decreased. At the same time, Alcian blue-PAS positive cells and Paneth-like cells appeared. Furthermore, the activity of alkaline phosphatase and disaccharidase of the small intestinal mucosa was biochemically demonstrated in the atrophic glandular stomach.