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Biomedical subjects

Y Yawata

Publications and source records attributed to Y Yawata.

At least 127 records · Page 7Linked to original sources
PubMed1985

A marked increase of calcium uptake in the ATP-depleted red cells of patients with iron deficiency.

Calcium (Ca) uptake was markedly increased in ATP-depleted red cells of patients with iron deficiency anemia (IDA) compared to ATP-depleted normal red cells. The extent of increased Ca uptake was related to the severity of iron deficiency as judged by decreased mean cell volume. Moreover, the increased Ca uptake returned to normal levels after oral iron supplementation therapy. The net calcium content of fresh red cells from iron-deficient individuals was the same as in red cells from normal subjects. Sodium influx and ferric ion uptake appeared to be virtually unaffected in the iron deficient red cells.

Adenosine Triphosphate↗
PubMed1985

An increased calcium accumulation in ATP-depleted red cells of the patients with paroxysmal nocturnal hemoglobinuria.

A marked increase in calcium (Ca) uptake (85.5 +/- 39.0 nmoles/ml RBC/2 hr) was observed in ATP-depleted red cells of patients with paroxysmal nocturnal hemoglobinuria (PNH) as compared to ATP-depleted normal red cells (8.0 +/- 2.0). The extent of increased Ca uptake in the PNH red cells was related to the extent of increased sensitivity to complement, as judged by the sugar water test (p less than 0.001) and the acidified serum test (p less than 0.001), and inversely correlated to the decreased activity of red cell acetylcholinesterase (p less than 0.01). The results may indicate that increased calcium uptake in PNH red cells is a possible intrinsic defect of the red cell membranes in the disorder.

Adenosine Triphosphate↗
PubMed1985

Heinz body formation in red cell membrane disorders: its acceleration in membrane lipid abnormalities.

Abnormal Heinz body formation in the presence of acetylphenyl hydrazine was observed in some patients with red cell membrane abnormalities, such as hereditary red cell membrane high phosphatidyl choline haemolytic anaemia, congenital haemolytic anaemias of unknown origin, acquired hyperlipidaemia and paroxysmal nocturnal haemoglobinuria. No abnormality of haemoglobin composition or of oxidation-reduction activities was noted in 66 patients studied. No abnormal Heinz body formation was seen in hereditary spherocytosis, hereditary elliptocytosis or hereditary stomatocytosis with normal membrane lipids, but increased Heinz body formation was observed in some patients with red cell membrane lipid abnormalities. The extent of abnormal Heinz body formation inversely correlated with a decreased molar ratio of free cholesterol to phosphatidyl choline in these red cells. Heinz body formation, therefore, may be abnormal in some red cell membrane disorders, especially when membrane lipid abnormalities exist.

Anemia, Hemolytic↗
PubMed1985

Hyperglycaemic effect of glucagon administered intracerebroventricularly in the rat.

The intracerebroventricular (icv) administration of 100 ng glucagon resulted in more prolonged and pronounced elevations of plasma glucose levels than the intravenous injection of 100 ng glucagon. Insignificant changes in plasma IRI and IRG levels after icv glucagon administration contrasted to marked increases in both IRI and IRG levels after the iv injection. Icv glucagon-induced hyperglycaemia was completely prevented by the prior administration of atropine, phentolamine or hexamethonium, and partially inhibited by bilateral adrenalectomy, but not by propranolol pretreatment. These findings suggested that the hyperglycaemic effect is brought about through cholinergic and alpha-adrenergic neural pathways and partly via the adrenal medulla.

Adrenalectomy↗
PubMed1984

Increased calcium uptake in the red cells of unsplenectomized patients with hereditary spherocytosis: significant contribution of reticulocytosis.

The presence of abnormal calcium (Ca) metabolism in the red cells of hereditary spherocytosis (HS) patients has long been in dispute. Thus, to clarify the discrepancies of experimental results published previously, Ca metabolism in the red cells was investigated in 12 unsplenectomized and 6 splenectomized HS patients. A marked increase of Ca uptake was observed in the ATP-depleted red cells of the unsplenectomized HS patients. The increased red cell Ca uptake was normalized after splenectomy in the same HS patients. The extent of increased Ca uptake was well correlated to the degree of reticulocytosis (p less than 0.001). The observation was confirmed by the fractionation studies of the HS red cells. Ca uptake was not increased in the spherocyte-rich bottom fraction, if reticulocytosis was not present. No significant difference was observed in red cell calcium content between normal and HS patients, neither unsplenectomized nor splenectomized.

Adenosine Triphosphate↗
PubMed1984

Observations on plasma and red cell lipids in hereditary spherocytosis.

Plasma lipids and red cell lipids were determined in hereditary spherocytosis (HS), 15 unsplenectomized and eight splenectomized patients. Plasma lipids (cholesterol: total, free and high density lipoproteins, free fatty acids, and phospholipids) were markedly decreased in HS, especially in the unsplenectomized patients. Concomitantly, red cell membrane lipids (free cholesterol and phospholipids: total, phosphatidyl ethanolamine, sphingomyelin, phosphatidyl choline, and lysophosphatidyl choline) were also diminished. The plasma lipids stay low even after splenectomy although partially restored. Thus, decreased membrane surface, a hallmark of HS, could be partly attributed to the diminished membrane lipids induced by plasma lipid abnormalities in the patients.

Cholesterol↗
PubMed1984

Self-adaptive modification of red-cell membrane lipids in lecithin: cholesterol acyltransferase deficiency. Lipid analysis and spin labeling.

In a patient with lecithin: cholesterol acyltransferase deficiency, free cholesterol was markedly increased, and esterified cholesterol was diminished. In the patient's plasma, an increase in phosphatidylcholine (PC) and a decrease in sphingomyelin were observed. Concomitantly, an increase in a shorter acyl chain 16:0 was noted in PC, sphingomyelin and phosphatidylethanolamine (PE). In contrast to these results, longer chains such as 22:0 and 24:0 were decreased, especially in sphingomyelin. Unsaturated double bonds such as 18:1 was also increased in PC and PE. In the red-cell membrane lipids, the increase in free cholesterol was counteracted by an increase in PC and by a decrease in sphingomyelin and PE, reflecting changes in the patient's plasma lipids. Increased 16:0 (in PC) and decreased 18:0 and 24:0 were observed. The increased plasma free cholesterol due to metabolic defect (lecithin: cholesterol acyltransferase deficiency) led to decreased red-cell membrane fluidity. This effect appeared to be counteracted by changing phospholipid composition (increased PC and decreased sphingomyelin and PE), by increasing shorter chains (16:0), by decreasing longer chains (18:0 and 24:0) and by increasing unsaturated double bonds (18:2). These results can be interpreted as a self-adaptive modification of lecithin: cholesterol acyltransferase deficiency-induced red-cell membrane abnormalities, to maintain normal membrane fluidity. This speculation was supported by the ESR spin-label studies on the patient's membrane lipids. The normal order parameters in intact red cells and in total lipid liposomes were decreased if cholesterol-depleted membrane liposomes were prepared. Thus, the hardening effect of cholesterol appeared to be counteracted by the softening effects described above. Overall membrane fluidity in intact red cells of the lecithin: cholesterol acyltransferase-deficient patient was maintained normally, judged by order parameters in ESR spin-label studies.

Cholesterol↗
PubMed1984

Decreased sodium influx and abnormal red cell membrane lipids in a patient with familial plasma lecithin: cholesterol acyltransferase deficiency.

Red cell membrane metabolism in familial lecithin:cholesterol acyltransferase (LCAT) deficiency was investigated. The family presented here is the third case discovered in Japan. An increase of free cholesterol was observed in the red cell membranes, concomitant with increased phosphatidyl choline. Osmotic fragility of the patient's red cells was diminished rather than increased. Red cell survival (51Cr T1/2) was shortened (15 days). Sodium influx was markedly decreased, although sodium efflux, both ouabain-sensitive and ouabain-insensitive, was normal. The activity of acetyl-cholinesterase as a marker of the outer leaflet of the red cell membranes was decreased, while the activity of glyceraldehyde-3-phosphate dehydrogenase as a marker of the inner leaflet was normal. No abnormalities of adenosine triphosphatases in red cell membranes were observed. These results suggest that the alteration of cholesterol metabolism in the plasma of LCAT deficiency increases the red cell membrane cholesterol and affects the functions of the red cell membranes, especially of the outer leaflet, which may result in decreased sodium influx.

Blood Transfusion↗
PubMed1984

Disappearance of microspherocytes in peripheral circulation and normalization of decreased lipids in plasma and in red cells of patients with hereditary spherocytosis after splenectomy.

A possible mechanism of the formation of microspherocytosis in unsplenectomized patients with hereditary spherocytosis (HS) was investigated in relation to lipid metabolism in plasma and in red cells of these patients. Plasma lipids (total cholesterol, free cholesterol, high density lipoprotein cholesterol, free fatty acids, and phospholipids) were markedly reduced in unsplenectomized HS patients with microspherocytosis. Red cell membrane lipids (free cholesterol and phospholipids such as phosphatidyl ethanolamine, sphingomyelin, phosphatidyl choline, and lysophosphatidyl choline) were also decreased in these unsplenectomized HS patients. After splenectomy, microspherocytosis disappeared concomitant to substantial normalization of plasma and red cell membrane lipids. These observations suggest that plasma lipid decrement in the unsplenectomized HS patients is at least one of the causative factors in pathogenesis of the formation of microspherocytosis. So-called "splenic conditioning" may not imply a physical "loss" of membrane by fragmentation or pitting of the once-formed HS red cells in the peripheral circulation. Instead, the decreased plasma lipids in the presence of the spleen may affect the de novo synthesis of red cell membrane lipids, resulting in the formation of microspherocytosis.

Adolescent↗
PubMed1984

Hyperglycemic effect of neurotensin.

Mechanisms of hyperglycemic action of neurotensin were investigated in anesthetized dogs. The intravenous administration of neurotensin 1.0 microgram/kg for 5 min induced an immediate decrease in arterial blood pressure and increases in levels of blood glucose, glucagon and insulin. Although blood levels of glucagon and insulin were greatly reduced and not elevated by neurotensin in the presence of somatostatin, the response of blood glucose to neurotensin was similar to that in the absence of somatostatin. The rise in blood glucose produced by intraportal injection of neurotensin was not greater than that produced by injection of the same dose of neurotensin into the femoral vein. The increments of glucagon and insulin secretion caused by the intraportal injection were also the same as those produced by the peripheral injection. Participation of antihypotensive mechanisms in the neurotensin-induced hyperglycemia was investigated by use of alpha-adrenoceptor blockade and baroceptor denervation. Only the combination of somatostatin and alpha-adrenoceptor blockade or the denervation of baroceptors could suppress the hyperglycemic response to neurotensin. Stimulation of the secretion of anterior pituitary hormones by neurotensin infusion could not be recognized in the present experiments. These results suggested the following: 1) both glucagon and catecholamines may contribute to neurotensin-induced hyperglycemia, 2) neurotensin does not directly act on the liver, 3) catecholamine response could be mediated by baroceptor stimulation through hypotension, and 4) the hyperglycemic effect of anterior pituitary hormones does not participate in neurotensin-induced hyperglycemia.

Adrenocorticotropic Hormone↗