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Biomedical subjects

T Morisaki

Publications and source records attributed to T Morisaki.

At least 145 records · Page 8Linked to original sources
PubMed1986

Characterization of purine nucleoside phosphorylase in leukemia.

Purine nucleoside phosphorylase (PNP) activity was determined in mononuclear cells from 49 patients with various types of leukemia. A low level of PNP activity was found in mononuclear cells from patients with acute myeloid and lymphoblastic leukemia and with chronic lymphocytic leukemia. Enzymatic and immunological studies on PNP from leukemic cells of these patients revealed no differences in Michaelis constant for inosine, thermostability, electrophoretic mobility, immunological reactivity, or specific activity between the PNP of leukemic cells and that of normal mononuclear cells. These results suggest that the decrease in PNP activity of leukemic cells is due to a decreased rate of enzyme synthesis. Thus, the abnormality of PNP activity might be due to an alteration in the regulatory mechanism of enzyme synthesis in the purine metabolism in the leukemic clone.

Humans↗
PubMed1985

Adenosine deaminase (ADA) in leukemia: clinical value of plasma ADA activity and characterization of leukemic cell ADA.

Adenosine deaminase (ADA) activity was measured in plasma, erythrocytes, and mononuclear cells from 18 patients with acute and chronic leukemia. High levels of ADA activities were found in plasma, erythrocytes, and mononuclear cells from patients with acute leukemia, especially acute lymphoblastic leukemia, and blastic crisis of chronic myeloid leukemia. Serial determination of plasma ADA activities was done in 9 patients with acute leukemia. All patients untreated or in relapse had an elevation of plasma ADA activity, which decreased to normal or subnormal levels during complete remission. On starch gel electrophoresis, plasma ADA in leukemic patients separated into two bands. The major band showed a mobility identical to that of normal red cells and mononuclear cells, and the minor band corresponded to that of normal plasma ADA. Enzymatic and immunological studies were performed on ADA from leukemic cells of acute myeloid and lymphoblastic leukemia. There were no differences in Michaelis constant for adenosine, thermostability, electrophoretic mobility, immunological reactivity, and specific activity between ADA of leukemic cells and normal mononuclear cells. These results strongly suggest that the increased ADA activity in leukemic cells is caused by an increased synthesis of a structurally normal enzyme and that increased plasma ADA activity in leukemic patients reflects an increment of leukemic cells in bone marrow. Therefore, serial determination of plasma ADA activities seems to provide a good indicator of the total mass of leukemic cells in bone marrow.

Acute Disease↗
PubMed1984

Gd(-) Gifu and Gd(-) Fukuoka. Two new variants of glucose-6-phosphate dehydrogenase found in Japan.

Two new glucose-6-phosphate dehydrogenase (G6PD) variants were discovered in Japan. The first, found in a 9-year-old male, was associated with chronic hemolysis and hemolytic crises after upper respiratory infections. The enzyme activity of the variant was 2.9% of normal. The patient's G6PD showed an increased utilization of substrate analogue, deamino-NADP, and thermal instability. The second variant occurred in a 7-year-old male with drug-induced hemolysis. The main enzymatic characteristics were reduced enzyme activity, being 6.4% of normal, faster-than-normal anodal electrophoretic mobility, slightly high Michaelis constant for glucose-6-phosphate, thermal instability, and biphasic pH optima. Enzymatic properties of these variants allowed each to be distinguished from previously reported variants. The first variant was designated Gd(-)Gifu and the other, Gd(-)Fukuoka.

Child↗
PubMed1984

A unique electrophoretic slow-moving glucose 6-phosphate dehydrogenase variant (G6PD Asahikawa) with a markedly acidic pH optimum.

A new glucose 6-phosphate dehydrogenase (G6PD) variant associated with chronic nonspherocytic hemolytic anemia was discovered in Japan. The patient showed hemolytic crises after upper respiratory infections. The enzyme activity was about 3.8% of the normal. The partially purified enzyme revealed slow anodal electrophoretic mobility, high Km NADP, marked thermal-instability, and increased affinity for a substrate analogue (deamino-NADP). A particular characteristic of this enzyme was a biphasic pH curve with a greatly increased activity at low pH values. From these results, this variant was clearly different from hitherto observed G6PD variants, and was designated G6PD Asahikawa.

Anemia, Hemolytic↗
PubMed1983

G6PD Sendagi: a new glucose-6-phosphate dehydrogenase variant associated with congenital hemolytic anemia.

A new glucose-6-phosphate dehydrogenase (G6PD) variant associated with chronic nonspherocytic hemolytic anemia was discovered. It was found in a 2-year-old male who had a hemolytic crisis after an upper respiratory tract infection. The enzyme activity of the variant was 8.4% of that of the normal enzyme. The enzymatic characteristics were slower than normal anodal electrophoretic mobility, low Km G6P, normal Km NADP, increased utilization of substrate analogues, high Ki NADPH, decreased heat stability, and an alkaline pH optimum. From these results, this was considered to be a new variant and was designated G6PD Sendagi.

Anemia, Hemolytic, Congenital↗
PubMed1983

[Two-dimensional echocardiographic observation of a rapidly growing floating left atrial ball thrombus: report of a case with mitral stenosis].

This report dealt with a rapidly growing ball thrombus floating in the left atrium in a case with mitral stenosis detected by serial two-dimensional echocardiography and confirmed at operation. A 45-year-old female was admitted to our hospital on January 7, 1982 because of dyspnea, orthopnea and fever. On admission she had typical auscultatory signs of mitral stenosis, and her chest roentgenogram revealed slight pulmonary venous congestion and marked left atrial enlargement. Laboratory findings including complete blood counts, coagulation studies and blood chemistry were normal except a positive CRP test. Two-dimensional echocardiography performed on January 8 revealed a tight mitral stenosis with the mitral orifice area of about 0.9 cm2, and a floating ball thrombus in the left atrium, which was 2.5 X 3 cm in size. Fuzzy echoes flowing slowly around the thrombus were also observed. Intravenous administration of heparin was started immediately. In the next morning (January 9), the two-dimensional echocardiography was reexamined, which revealed a markedly growing thrombus which became 4 X 4 cm in size. Several hours after the reexamination mitral valve replacement was performed. The removed thrombus was 5.5 X 7 cm in size and consisted of three laminated structures. This finding was consistent with the echocardiographic observations. Coagulation studies made just before operation showed increased coagulability. Increased stagnation of blood in the left atrium due to heart failure and a transient increase of blood cell aggregation and coagulability induced by preceding infection might be responsible for the genesis of such a thrombus.

Echocardiography↗
PubMedDate not supplied

Construction of a transplantable tissue-engineered artificial peritoneum.

BACKGROUND: Peritoneal defects lead to serious postoperative problems. Thus the development of physiological material to cover peritoneal defects is very desirable. AIM: The aim of this study was to develop a transplantable artificial peritoneum. METHOD: The artificial peritoneum consisted of collagen gel, fibroblasts, and mesothelial cells, and histological features were analyzed. The artificial peritoneum at the site of a peritoneal defect in the rat was transplanted to the abdominal wall. RESULTS: Histological examination revealed that the artificial peritoneum consisted of a flat mesothelial monolayer upon a stromal matrix. All transplanted artificial peritoneums adapted well to the host and prevented severe adhesion. CONCLUSION: Our artificial peritoneum may be a useful transplantable bioengineered material for repair of surgical peritoneal defects.

Abdominal Wall↗
PubMedDate not supplied

Elevation of serum hepatocyte growth factor concentration in patients with gastric cancer is mediated by production from tumor tissue.

Hepatocyte growth factor (HGF) is a stromal cell-derived cytokine that can stimulate invasion and metastasis of carcinoma cells. Recent studies have shown that the serum HGF concentration is elevated in patients with gastric cancer and may be a useful disease marker. However, the origin of the elevated serum HGF remains undetermined. We investigated the site of HGF production by analyzing the relationships between the HGF expression in tumor tissues, the serum HGF concentrations and inflammation in patients with gastric cancer. The serum and tissue HGF concentrations were measured by an enzyme-linked immunosorbent assay. The serum HGF concentration was higher than the normal cut-off level (0.57 ng/ml) in 44% of the patients. Surgical removal of the tumor significantly reduced the serum HGF concentration, suggesting that the tumor tissue was responsible for the increase. Western blotting analysis showed that the HGF protein was expressed in 20 out of 22 tumor tissues. The concentration of HGF in the tumor tissue was significantly higher than that in normal gastric mucosa. Significant correlation was found between tissue HGF concentrations and serum HGF concentrations. No significant correlation was found between the serum HGF concentration and white blood cell count or C-reactive protein concentration, indicating that the increase in serum HGF is not due to inflammation related to the tumor. These results suggest that the elevated serum HGF concentration in patients with gastric cancer is mediated by production from the tumor tissue.

Adult↗
PubMedDate not supplied

Long-term and short-term survivors after pancreatectomy for pancreatic cancer.

Out of 63 Japanese patients with pancreatic carcinoma who underwent surgical resection, 8 short-term survivors who died within 3 months after resection and 6 long-term survivors who were alive for more than 3 years after resection were compared regarding 26 clinicopathological parameters. The 8 short-term survivors were significantly older than the 6 long-term survivors (63.7 versus 47.8 years, P = 0.0099). The mean peripheral lymphocyte count was significantly smaller in the short-term survivors than in the long-term survivors (1,212 versus 2,115 /microl, P = 0.0459). Operative blood loss was significantly larger in the short-term survivors than in the long-term survivors (2,393 versus 1,043 g, P = 0.0157). The surgical margin was affected by malignant cells in 7 of the 8 short-term survivors, but in only 2 of the 6 long-term survivors (P = 0.0362). Of the 8 short-term survivors, 5 were in comprehensive stage IV and 3 in stage III, while 3 of the 6 long-term survivors were in stage III, two in stage II, and one in stage I (P = 0.0487). All the 8 short-term survivors were of the comprehensive curability C, while 3 of the 6 long-term survivors were of A, one B and the other two C (P = 0.0239). Multiple regression analysis of these 6 profound factors showed that the peripheral lymphocyte count was an independent significant parameter to differentiate the short-term and long-term survivors. These findings suggest that, although the aggressive nature of pancreatic cancer has been accepted, the clinical course after pancreatectomy would also depend upon the immunological state of the patient.

Age Factors↗