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Biomedical subjects

K Suda

Publications and source records attributed to K Suda.

At least 253 records · Page 14Linked to original sources

Electrofocusing pattern of fucosyltransferase activity in human leukemic cells.

Fucosyltransferase (FT) activity of normal lymphocytes, normal granulocytes, and various types of human leukemic cells and electrofocusing pattern of FT activity in human leukemic cells and normal lymphocytes were examined using asialofetuin as an acceptor. Levels of FT activity in normal lymphocytes were higher than those of normal granulocytes in which FT activity was almost undetectable. The FT activity was higher in blast cells of acute myeloblastic leukemia and chronic myelogenous leukemia in blast crisis than in blast cells of acute lymphoblastic leukemia and the chronic phase of chronic myelogenous leukemia. The level of FT activity was lower in cells of chronic lymphocytic leukemia than that of normal lymphocytes, but it was higher than that of normal granulocytes. Three main isoelectric forms of FT in leukemic blast cells were identified by isoelectrofocusing, and they each had a characteristic focusing point: around pH 4.5 (peak 1); pH 4.9 (peak 2); and pH 5.2 (peak 3). In blast cells of myeloid leukemia, the activity of peak 3 was markedly higher than those of peaks 1 and 2. In blast cells of lymphoid leukemia, the activity of peak 3 was also the highest, but the activity of peak 2 was higher than that in myeloid blast cells. In normal lymphocytes, the major isoelectric form of FT was focused at around pH 4.9 and peak 3 was undetectable. These results indicated apparent differences not only in FT activity but also in isoelectric forms of FT between myeloid leukemic cells and lymphoid leukemic cells.

Blast Crisis↗

A yeast mutant lacking mitochondrial porin is respiratory-deficient, but can recover respiration with simultaneous accumulation of an 86-kd extramitochondrial protein.

A yeast mutant lacking the only known pore-forming protein of the mitochondrial outer membrane was constructed by gene disruption. The mutant retained all other major proteins of the mitochondrial outer membrane, but was severely deficient in mitochondrial cytochromes and initially did not grow on the non-fermentable carbon source, glycerol. However, it could slowly adapt to glycerol; adaptation was accompanied by the partial restoration of cytochrome levels and massive accumulation of an 86-kd polypeptide in extramitochondrial cell fractions.

Bacterial Outer Membrane Proteins↗

Clinicopathologic and experimental studies on cases of abnormal pancreatico-choledocho-ductal junction.

An abnormal pancreatico-choledocho-ductal junction, in which free communication between the pancreatic duct and the common bile duct was present, was observed in 17 out of 120 cases (14.2%) of biliary tract carcinoma and in all of four cases of congenital biliary dilatation, but in noe of about 200 control patients without biliary tract disease. Outstanding findings in the pancreas, such as degeneration of the ductal epithelium and interlobular fibrosis, were found in 6 of 21 cases of abnormal junction. In an experimental study using 63 puppies given choledocho-pancreatic end-to-side ductal anastomosis, dilatation of the bile duct of varying degree occurred and mucosal hyperplasia of the biliary tract was observed in 12 of 25 anastomosed dogs for a duration of more than one month. Cell kinetics in biliary tract mucosa observed by the use of monoclonal antibody against bromodeoxyuridine (BrdU) was obviously elevated in dogs subject to long-term follow-up. As for pancreatic lesions, the incidence and histologic findings were similar to those of human studies, as follows: chronic pancreatitis in only a few animals, mild periductal parenchymatous change in 15 puppies and no significant change in 44 puppies. Therefore, an abnormal pancreatico-choledocho-ductal junction may be one of the significant factors producing biliary dilatation, biliary tract carcinoma and pancreatitis.

Animals↗

The islets of Langerhans in uremic patients receiving chronic hemodialysis.

Ten autopsied cases of uremia (none with diabetes mellitus) who had been treated with hemodialysis were studied histopathologically. Hyaline replacement of islets of Langerhans was found in 6 out of 10 cases, while such a change was observed in only 1 of 15 control non hemodialzyed controls. These 6 cases had received hemodialysis therapy for a duration of more than 2 years and 10 months. The hyaline material in the islets of Langerhans was confirmed as the presence of amyloid by electron microscopy. Clinically, urinary glucose was present in 1 out of 3 patients and the blood glucose level was moderately elevated in 2 other cases. Therefore, it should be emphasized that care should be taken about glucose tolerance in uremic patients receiving chronic hemodialysis.

Adult↗

Effects of monensin on the Na+ pump activity and the release of amylase and sialic acid in dog submandibular glands.

The effects of monensin on the Na+,K+-ATPase activity and the release of amylase and sialic acid were investigated in dog submandibular gland pieces. Monensin stimulated the Na+,K+-ATPase activity and amylase release in a dose-dependent manner. Moreover, this agent increased the Na+,K+-ATPase activity and the release of amylase and sialic acid induced by pilocarpine. These results suggest that monensin increases the release of amylase and sialic acid in dog submandibular glands, in part, through the Na+ pump activated due to the Na+ influx.

Amylases↗

Effects of Ca2+ and calmodulin antagonists on the Na+ pump activity induced by pilocarpine in dog submandibular gland.

The effects of Ca2+ and calmodulin antagonists on the Na+,K+-ATPase activity were investigated in dog submandibular gland pieces. The Na+,K+-ATPase activity of the gland pieces which were incubated in the presence of 5 microM A23187, a Ca2+ ionophore, was about 2-fold of that seen in the control medium. Verapamil, diltiazem and La3+ (Ca2+ antagonists) and chlorpromazine, trifluoperazine and W-7 (calmodulin antagonists) had no significant effect on the Na+,K+-ATPase activity in the control medium, but significantly inhibited that induced by pilocarpine. These results suggest that the Na+ pump activity is modified by the Ca2+ influx from the extracellular spaces and the intracellular Ca2+-calmodulin complex.

Animals↗

Does calmodulin participate as an intermediate in the process of glycogenolysis in rat submandibular gland?

A role of calmodulin in the process of the glycogenolysis induced by adrenaline was investigated in rat submandibular gland. When the slice was incubated in the Ca2+-free medium, the adrenaline-induced glycogenolysis was significantly inhibited. Moreover, the inhibition of glycogenolysis induced in the Ca2+-free medium was further enhanced by addition of 2 mM EGTA. Chlorpromazine, trifluoperazine and W-7, calmodulin antagonists, had no effect on the glycogenolysis induced by adrenaline. These results suggest that the adrenaline-induced glycogenolysis is dependent on the presence of Ca2+ and that calmodulin does not participate in the process of glycogenolysis in rat submandibular gland.

Animals↗

[Hypertrophic non-obstructive cardiomyopathy assessed by dipyridamole thallium single photon emission computed tomography: comparisons with hypertrophic cardiomyopathy with a dilated heart].

Thallium-201 (Tl) single photon emission computed tomography (SPECT) after dipyridamole infusion (0.56 mg/kg) was performed in 23 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) and in seven patients with HCM simulating dilated cardiomyopathy (HCM-DCM) to clarify the mechanism and clinical significance of decreased coronary vasodilatory reserve. The coronary vasodilatory reserve in the hypertrophied area assessed by SPECT was compared with the findings of echocardiography, left ventriculography and endomyocardial biopsy. 1. Eleven patients with HNCM had no perfusion defects in the hypertrophied area (group I), but the other 12 patients (52.2%) had such defects (group II). All seven patients with HCM-DCM had perfusion defects in the anterior or septal walls (group III). Redistribution was observed in 11 of the 12 patients in group II and in three of the seven patients in group III. 2. The regional washout rate was relatively low in the upper septum in group II and in the anterior wall and upper septum in group III. Thus, coronary vasodilatory reserve in the hypertrophied area was decreased in groups II and III. 3. Echocardiographically, the degree of hypertrophy did not differ between groups I and II, but the latter had significantly greater left ventricular diastolic dimension (42.3 mm vs 49.5 mm: p less than 0.05) and lower percent fractional shortening (%FS) (43.7% vs 35.6%: p less than 0.05). However, group III showed thinner left ventricular wall, much greater diastolic dimension (60.9 mm vs 49.5 mm: p less than 0.05), and lower %FS (24.0% vs 35.6%: p less than 0.05) than did those of group II. 4. On left ventriculography, those in group II showed larger left ventricular end-diastolic volume index (93.9 ml/m2 vs 79.7 ml/m2: p less than 0.05) than that of group I. Left ventricular ejection fraction showed the same tendency, but this was not statistically significant. 5. On endomyocardial biopsy, the specimens of the patients in group II had significantly higher percent fibrosis than did those of group I (11.4% vs 6.8%: p less than 0.05). These findings suggest that the mechanism of decreased coronary vasodilatory reserve in the hypertrophied area may be related to myocardial fibrosis, and this decrease may induce left ventricular dysfunction and compensatory dilatation.

Adult↗

Morphological and immunological change in the predominant type of leukaemic cells in a patient with T-cell chronic lymphocytic leukaemia.

A case of T-cell chronic lymphocytic leukaemia is described. Intracerebellar tumour was demonstrated by the characteristic feature of contrast-enhanced computerized tomography and was evidenced by surgical procedure. Histological examination revealed lymphocyte infiltration in the cerebellum. Initially, the majority of leukaemic cells were mature, medium-sized lymphocytes with surface marker phenotype of E+, OKT3+, OKT4+, OKT6-, OKT8-. In the terminal stage, large atypical lymphocytes which were morphologically distinct from the original lymphocytes and had different surface marker phenotype of E+, OKT3+, OKT4-, OKT6-, OKT8+, Leu7+ became increasingly prominent. The remaining medium-sized lymphocytes were morphologically and immunologically unchanged. Subsequently, the disease developed to a more aggressive pattern and the patient died in spite of chemotherapy.

Adult↗

Augmentation of catecholamine-stimulated [3H]GDP release in adipocyte membranes from exercise-trained rats.

The effects of exercise training on the catecholamine-stimulated [3H]GDP release in rat adipocyte membranes prelabeled with [3H]GTP and the adenylate cyclase activity were investigated. Exercise training significantly increased the release of [3H]GDP in response to (-)isoproterenol. The adenylate cyclase activity induced by a nonhydrolyzable guanine nucleotide analogue, Gpp(NH)p, was significantly greater in exercise-trained rats.

Adenylyl Cyclases↗