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Biomedical subjects

M Sanada

Publications and source records attributed to M Sanada.

At least 109 records · Page 6Linked to original sources
PubMed1978

Surface immunoglobulin of human lymphocytes.

Using ferritin as surface marker, the localization of the surface immunoglobulin (Ig) was studied on peripheral lymphocytes from normal human individuals and patients with macroglobulinaemia Waldenström by scanning immunoelectron microscopy. Normal IgG-, IgM-lymphocytes and pathological IgM-lymphocytes were then compared with regard to their topographical differences. In all cells examined, IgG- and IgM-conjugated ferritin particles were detected all over the cell surface, but the distribution of the former on the normal IgG-lymphocytes was slightly more diffuse than that of the latter on the normal and pathological IgM-lymphocytes. Furthermore, in the pathological IgM-lymphocytes, the clustered IgM-conjugated ferritin particles were found in great number on the microvilli. Normal IgG-lymphocytes were almost always characterized by short rod-like microvilli standing densely and vertically on the cell surface. Some of normal IgM-lymphocytes had a similar appearance to those of normal IgG-lymphocytes (type A) but others (type B) had tilted rod-like microvilli or wide plate-like processes on their surface. As for IgM-lymphocytes of macroglobulinaemia, most lymphocytes had tilted rodlike mirovilli and wide plate-like processes similar to type B, whereas a minor population of the pathological lymphocytes carried long, thin rod-like microvilli standing vertically on the surface.

Aged↗
PubMedDate not supplied

Increased lipoprotein X causes hyperlipidemia during intravenous administration of 10% fat emulsion in man.

To clarify the mechanisms of hyperlipidemia during intravenous Intralipid 10%, lipoprotein profiles including lipoprotein X were studied in 13 patients receiving 2.0 g of fat per kilogram per day by Intralipid 10% over a period of 8 weeks. All patients were fed exclusively by total parenteral nutrition providing 1.1 g of amino acid and 30 kcal/kg per day. Intravenous administration of Intralipid 10% caused a marked increase of low-density lipoprotein (LDL), phospholipid, and cholesterol, especially free cholesterol, whereas triglyceride, very-low-density lipoprotein, and high-density lipoprotein remained within the normal range. Lipid composition of LDL approximated that of lipoprotein X progressively with the intravenous Intralipid 10%. Quantification of lipoprotein X revealed that its increase was proportionate with that of LDL and total lipid. From these findings, hyperlipidemia during intravenous Intralipid 10% is induced almost exclusively by the increased lipoprotein X.

Adult↗
PubMedDate not supplied

Intravenous intralipid 10% vs. 20%, hyperlipidemia, and increase in lipoprotein X in humans.

To clarify the mechanisms of hyperlipidemia caused by infusion of Intralipid 10%, we compared lipoprotein metabolism during intravenous Intralipid 10% and Intralipid 20%, which contains only half the amount of egg yolk lecithin for the same content of triglyceride as Intralipid 10%. Ten patients receiving 20 ml.kg-1.day-1 of Intralipid 10% and 10 receiving 10 ml.kg-1.day-1 of Intralipid 20% were fed exclusively by total parenteral nutrition (TPN) providing 1.1 g amino acid and 30 kcal.kg-1.day-1 for 4-6 wk. Intravenous Intralipid 10% caused a marked increase in low-density lipoprotein (LDL), together with increases in phospholipid and cholesterol, especially free cholesterol. The progressive increase in lipoprotein X was in proportion with that of LDL or total lipid, whereas no increase in lipids, LDL, or lipoprotein X was observed during intravenous Intralipid 20%. A significant increase in apolipoproteins CIII and E with Intralipid 10% also caused a rise in lipoprotein X. With Intralipid 20%, however, the alterations in apolipoproteins were not observed. Lecithin:cholesterol acyltransferase (LCAT) activity was significantly elevated with Intralipid 10 but not 20%. Disappearance of lipoprotein X after cessation of Intralipid 10% was relatively rapid, and the half-life was 24-60 h. From these findings, the hyperlipidemia with Intralipid 10% was caused almost exclusively by the increase in lipoprotein X. The excess lecithin may be responsible for the formation of and increase in lipoprotein X. Furthermore, it was revealed that Intralipid 20% could be safely used without inducing hyperlipidemia.

Adult↗