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K Hosoi

Publications and source records attributed to K Hosoi.

132 records · Page 8Linked to original sources
PubMedDate not supplied

Preparation and disposition of asialofetuin-labelled liposome.

A liposome labelled with asialofetuin(AF-liposome) was prepared by the detergent dialysis method. Asialofetuin in the amount of 34-68 micrograms were imposed among the 1 microM of phospholipids constituting the outer surface of liposome. The AF-liposome containing [14C]-cholesterol in the lipid layer and [3H]-sucrose in the aqueous layer was intravenously administered to rats. Both radioactivities were biphasically cleared from systemic circulation at rates faster than that of the fetuin-labelled liposome. These radioactivities were recovered in the liver by about 90 per cent within 60 min, and per gram of tissue, were highest in this organ. In an in vitro experiment using isolated rat hepatocytes, the high affinity of the AF-liposome toward hepatocytes was observed from scanning electron micrographs. Based on these findings, the AF-liposome may possibly be stable in circulation and function as a carrier of encapsulated drugs to hepatocytes.

Animals↗
PubMedDate not supplied

Specific incorporation of asialofetuin-labeled liposomes into hepatocytes through the action of galactose-binding protein.

Asialofetuin-labelled liposomes (AF-liposomes) having mean diameters of 0.13 micron ([S]) and 0.35 micron ([L]) were obtained by the subsequent extrusion method in combination with dialysis. Intravenously administered AF-liposomes [S] were rapidly cleared from the systemic circulation. By pre- and post-treatment of the rats with free asialofetuin (AF), the rate of elimination decreased to that of non-labelled liposomes (N-liposomes) [S]. The liver uptake of AF-liposomes [S] (60 per cent of dose in 30 min) was about twice that of N-liposomes [S]. Forty-seven per cent of the AF-liposomes [S] incorporated into the liver were found in the parenchymal cell fraction as against 20 per cent in the non-parenchymal cell fraction. In contrast, N-liposomes [S] were taken up primarily by non-parenchymal cells as was also the case for AF- or N-liposomes [L]. Both the lipid and aqueous markers of AF-liposomes [S] were detected in subcellular fractions of the liver, but their distribution was noted to change differently with the lapse of time. Intravenously administered AF-liposomes [S] were specifically recognized by galactose-binding protein and underwent disruption in the cell after being taken up by hepatocytes. AF-liposomes [S] may possibly be utilized to deliver drugs into hepatocytes.

Animals↗
PubMedDate not supplied

Effects of pertussis toxin on signal transductions via P2-purinergic receptors in A-431 human epidermoidal carcinoma cells.

In A-431 cells, stimulation of P2-purinergic receptors with extracellular ATP caused production of inositol 1,4,5-trisphosphate (InsP3), followed by mobilization of Ca2+ from intracellular stores; Ca2+ influx from the extracellular fluid and breakdown of phosphatidylcholine (PtdCho) also accompanied this InsP3/Ca2+ signalling. When A-431 cells were pretreated with pertussis toxin (PTX), production of InsP3 and elevation of cytosolic Ca2+ were strongly inhibited. PTX also inhibited the Ca2+ influx, but the effect was much weaker than that for InsP3/Ca2+ elevation. No inhibitory effect was observed in ATP-stimulated PtdCho breakdown. These results suggest that there is a system(s) which mediates the functions of P2-purinergic receptors in addition to PTX-sensitive G-proteins.

Adenosine Triphosphate↗
PubMedDate not supplied

[Detection of right-to-left shunt flow in atrial septal defect using transesophageal color and pulsed Doppler echocardiography].

The clinical significance of right-to-left (R-L) shunt flow dynamics in atrial septal defects (ASD) were investigated using transesophageal color and pulsed Doppler echocardiography in 30 patients with ASD of the ostium secundum type, including 20 with systolic pulmonary artery pressures (sPA) less than 40 mmHg, 4 with sPA of 40 to 60 mmHg, 3 with sPA of 90 mmHg or greater, 2 with pulmonic stenosis and 1 with Ebstein's anomaly. R-L shunting was detected by a shunt flow signal across the defect during a cardiac cycle. The timing of the R-L shunt was compared with various parameters obtained by echocardiography or cardiac catheterization. R-L shunt flow at the onset of ventricular contraction or closing phase of the tricuspid valve was detected in five patients with isolated ASD associated with increased mean right atrial pressure, but no severe pulmonary hypertension. R-L shunt flow during systole was detected in five of 26 patients with isolated ASD and tricuspid regurgitation and in one patient with Ebstein's anomaly. The tricuspid regurgitation signals in three of the five patients were directed toward the defect, while the other two had massive tricuspid regurgitation. R-L shunt flow during mid-diastole was detected in three patients without pulmonary hypertension. Massive left-to-right shunt flows occurred during the phase from end-systole to early diastole. R-L shunt flow during atrial systole was detected in three patients with severe pulmonary hypertension and two with pulmonic stenosis. The severe pulmonary hypertension patients, in particular, showed the aliasing signal as a high speed shunt flow, and in two of these, R-L shunt flow continued from atrial systole to early ventricular systole, and was also observed in early diastole. R-L shunt flow was detected in ASD patients with and without pulmonary hypertension, and was influenced by right atrial pressure at the phase of tricuspid valve closing, volume or direction of tricuspid regurgitation, rebound flow due to massive left-to-right shunt flow, grade of right ventricular distensibility or pulmonary hypertension, and other cardiac complications.

Adolescent↗