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Biomedical subjects

J Murakami

Publications and source records attributed to J Murakami.

At least 127 records · Page 7Linked to original sources

Base line tenting: a sign of duodenal ulcer disease.

Indirect signs such as clover-leaf deformity, pseudodiverticulum formation, eccentric location of pyloric channel, and flattening of the fornix are of considerable value in the radiologic detection of an ulcer crater. We have found another indirect sign, base line tenting (BLT) to be very useful in the detection and diagnosis of duodenal ulcer disease. This is characterized by interruption of the base line of the bulb, with 2 associated perpendicular lines extending from the base and converging to a point in the duodenal bulb. After we observed this sign in various patients with peptic ulcer disease, a prospective investigation was performed involving 62 patients with duodenal ulcer disease over a period of 2 years. We found the BLT sign in 52 (83.8%). To date, no false-positive incidence has been identified. We concluded that BLT is a most valuable sign in the radiologic identification of duodenal ulcer disease.

Duodenal Ulcer↗

Mitochondrial genomes in intraspecies mammalian cell hybrids display codominant or dominant/recessive behavior.

A unique type of nonstochastic mitochondrial DNA (mtDNA) segregation was found in mammalian cells. In human cell hybrids isolated from the fusion of HeLa cells with 23, GM639, A549, or 293 cells, HeLa mtDNA was always lost from the hybrids, whereas both parental mtDNAs were maintained in hybrids of HeLa X 143BTK-. Similar phenomena were observed in mouse cell hybrids isolated by the fusion of cells with different mtDNA types. Types 1, 2, and 3, can be distinguished from each other by restriction fragment-length polymorphisms. The mouse cell hybrids between cells with type 1 and type 2 mtDNA always lost type 2 mtDNA, whereas the hybrids between cells with type 2 and type 3 mtDNA retained both types stably. These observations suggest that either a codominant or a dominant/recessive relationship may be present in intraspecies mitochondrial genomes of human and mouse cells. When the mitochondrial genomes in cell hybrids are codominant, stochastic segregation occurs while nonstochastic segregation occurs when they are in the dominant/recessive relationship. These concepts may help elucidate organelle heredity in animals.

Animals↗

A novel method for measuring the erythrocyte deformability, under oscillatory shear stress.

A novel apparatus for detecting a subtle decrease in erythrocyte deformability was developed. The oscillatory shape change of erythrocytes was monitored under an oscillatory shear stress (modulating the oscillation frequency in the range of 9-90 dyn/cm2). The ellipsoidal deformation of intact erythrocytes perfectly followed the oscillatory force of up to about 2 Hz, but the diamide-treated cells showed a phase difference of the oscillatory deformation at 1.7 Hz.

Erythrocyte Deformability↗

[Changes of erythrocyte deformability induced by calcium accumulation and calmodulin inhibitors].

The deformability of human erythrocytes was investigated with a rheoscope to study the role of intracellular calcium in the dynamic cytoskeletal structure. Calcium was loaded to or depleted from erythrocytes with a calcium ionophore (A 23187) in a Na- or a K-HEPES buffer. (1) After calcium loading in the Na-HEPES buffer, the cell volume of erythrocytes was greatly reduced due to dehydration. On the contrary, upon calcium-loading or -depletion in the K-HEPES buffer, the intracellular calcium content could be varied in the range of 1/4 to 3 times as much as that of control cells without the reduction of mean cell volume. Further incubation without A 23187 and calcium in the K-HEPES buffer enabled the calcium-loaded erythrocytes to restore the cell shape and the ATP concentration. (2) When intracellular calcium content was increased to above 1.5 times of the normal value, the deformability was distinctly decreased. On the other hand, the deformability was unchanged when the intracellular calcium content was reduced below the normal level. (3) The deformability, once decreased due to the calcium accumulation, was recovered by the treatment with a calmodulin inhibitor, W-7 or trifluoperazine, while these drugs were not effective on the deformability of control or calcium-depleted erythrocytes. We conclude that the membrane stiffness which influence the deformability of erythrocytes, is modulated by the intracellular calcium content through the interaction between the calcium-calmodulin complex and the cytoskeletal proteins.

Calcium↗

A contribution of calmodulin to cellular deformability of calcium-loaded human erythrocytes.

The effect of intracellular calcium on the deformability of human erythrocytes was studied with a rheoscope, especially in relation to the dynamic structure of membrane cytoskeleton. The appropriate calcium-loading and calcium-depletion were performed to intact erythrocytes with A23187 in potassium buffer. The total calcium content was varied in the range of 0.25 to 3 times as much as normal content, without complete ATP depletion and shape change (the reduction of mean cell volume and the condensation of hemoglobin due to dehydration were avoided). Increasing the intracellular calcium content by about 1.5 times of normal, the deformability was distinctly decreased, while calcium depletion did not affect the deformability. Reduced deformability of the calcium-loaded erythrocytes was restored by the treatment with calmodulin inhibitors, W-7 or trifluoperazine. However, such an effect by calmodulin inhibitors was not detected on normal or calcium-depleted erythrocytes. In conclusion, the interaction between calcium-calmodulin complex and cytoskeletal proteins may affect the membrane stiffness which is regulated through the change of the cytoskeletal structure, and contributes to the deformability of erythrocytes.

Calcium↗

Relapsing process in FAB subtypes of adult acute leukemia and its relationship to treatment regimens.

The relapsing process in the bone marrow was studied in those 77 patients with adult acute leukemia, diagnosed according to the FAB classification who achieved complete remission (CR) and then received intermittent multi-drug intensification treatment. Relapse occurred in most of the patients who exhibited Auer rods or Ph1 chromosomes in the bone marrow, or in whom blasts increased to 8% or more, but some patients remained in CR by subsequent treatment, that is, relapsing process was reversible. With our conventional treatment, the relapse or relapsing process occurred in most of the patients with L1, L2 and M1 subtypes within 6 months and was irreversible. It occurred mainly between 5 and 13 months in those with M2, M3 and M5 and was reversible in some cases. Patients with M4 subtype received intensified treatment due to the difficulty of achieving remission; relapse was seen in only 3 of 7 cases. To prevent relapse and attain a potential cure, the treatment should be intensive before the relapsing process with adequate supporting care. In view of the above-mentioned observations, our new treatment protocols for acute leukemia were designed to be more intensive than those conventionally employed, and to be discontinued within approximately 10 months in lymphoblastic leukemia and approximately 8 months in myeloid leukemia.

Adult↗

Slow-growing lung cancer in a fixed population sample. Radiologic assessments.

Radiographs generated during 20 years of biennial chest radiography of 107 patients with histologically proven lung cancers were reviewed for radiological evidence of slow-growing lesions. Twenty-nine of 37 solitary circumscribed peripheral masses which doubled in volume in five or more months prior to any therapy were considered slow growing. By these criteria, 7 (17%) of 41 squamous cell carcinomas were slow growing; whereas 22 (42%) of 52 adenocarcinomas grew slowly. There were no slow-growing tumors among the 14 anaplastic carcinomas or cancers of other histological type. The mean doubling time for the seven squamous cell carcinomas was 5.7 months; that for the 22 adenocarcinomas was 13.1 months. The cancers of females tended to grow more slowly than did those of males. There was no appreciable difference between the mean age of the 29 patients with slow-growing lesions and that of the remaining 78. Not only was the majority of cancer in the present study readily detectable by radiographic screening of the chest; patient survival correlated very well with the growth rates of the lesions, including those of seven resected tumors. The survivals of the seven patients with adenocarcinomas whose lesions were resected were no better than those of the remaining adenocarcinoma patients who had no surgical treatment. The results of this study proved that an appreciable percentage of lung cancers do develop slowly, especially adenocarcinomas.

Adenocarcinoma↗

Screening for lung cancer in a fixed population by biennial chest radiography.

All screening radiographs of the chest and other medical records of 107 patients with histologically proved lung cancer in a fixed population were reviewed to assess the efficacy of biennial chest radiography in detecting lung cancer. Radiographic abnormalities caused by tumors were initially detected in 58 patients (54%); the other 49 (46%) were detected radiographically in subsequent examinations. Thirty-six of the 40 solitary tumors were less than or equal to 4.0 cm in diameter when detected. There were no symptoms in 76% of cases, possibly associated with the predominance of peripheral adenocarcinomas. Routine 36 X 43-cm radiographs, postero-anterior stereoscopic and lateral projections, and comparison with previous radiographs facilitated detection of relatively small tumors in asymptomatic patients. The corrected 5-year survival rate from the time of detection was 20%.

Adenocarcinoma↗