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Biomedical subjects

S Kitagawa

Publications and source records attributed to S Kitagawa.

At least 289 records · Page 16Linked to original sources
PubMed1987

[Superselective transarterial embolisation of the hypogastric artery and it's branches in the management of unresectable intrapelvic malignant tumors with minor surgical procedures].

Three patients with recurrent uterine cancer, unresectable rectal cancer, and recurrent rectal cancer in the pelvis were treated by percutaneous superselective transarterial embolisation (TAE) of the hypogastric artery and it's branches with ethanol or gelatin sponge particles. TAE was performed for the control of life-threatening hemorrhage, severe pain and the diminishing tumor's bulk. In addition to conservative cares, this TAE needed minor surgical procedures such as urinary diversion, colostomy and drainage of abdominal abscess just when urinary bladder's necrosis, rectosigmoidal necrosis and peritonitis would be expected before and after the TAE. One local hematoma in the site inserted catheter and right ischiadic nerve paralysis occurred by TAE. Two patients died on 6 days and 2 months after TAE, respectively, however one patient is still alive one year after the TAE without the growth of tumours. As a result, this TAE with minor surgical procedures is expected as a suitable treatment for the improvement of the survival and quality of life in the patients with unresectable intrapelvic tumors.

Adult↗
PubMed1986

Characterization of a membrane-associated 3,3',5-triiodo-L-thyronine binding protein by use of monoclonal antibodies.

Four mouse hybridoma cell lines have been isolated which secrete antibodies to the membrane-associated thyroid hormone binding protein (Mr 55,000) from human epidermoid carcinoma A431 cells. J6 is rat specific; J2 is human and monkey specific; J8 and J9 have a wider specificity and react with similar thyroid hormone binding proteins (p55) from human, monkey, rat, and hamster. None of these antibodies reacts with mouse cells. J2, J6, and J9 are of the IgG1k class, and J8 is an IgAk antibody. p55 was characterized by using these monoclonal antibodies. It is not posttranslationally processed by glycosylation, phosphorylation, or sulfation. It has a cellular degradation rate t1/2 approximately equal to 3.2 h. Using immunofluorescence and electron microscopic immunocytochemistry, p55 was found to be associated with the lumenal face of the endoplasmic reticulum and nuclear envelope. When cell homogenates were prepared, significant amounts of p55 were released into the 110000g supernatant, indicating that p55 is loosely associated with the endoplasmic reticulum and nuclear envelope.

Animals↗
PubMed1986

Deactivation of the respiratory burst in activated macrophages: evidence for alteration of signal transduction.

Enhanced function of the respiratory burst, measured as stimulated release of superoxide anion (O2-) or hydrogen peroxide, characterizes activated macrophages. Activated macrophages undergo a decline in their capacity to release O2- (a deactivation) when placed in culture for 3 days. To better understand the molecular basis for the enhanced respiratory burst of activated macrophages, we explored the mechanisms underlying deactivation of activated mouse peritoneal macrophages. Deactivation was observed when the assay was performed in a physiologic Na+ buffer, and by day 3 of culture, release of O2- from activated macrophages stimulated with phorbol myristate acetate (PMA) was almost identical to that in resident (nonactivated) macrophages. In contrast, when the assay was performed in a buffer in which Na+ was replaced by K+, release of O2- from activated macrophages on day 3 was equal to or greater than that on day 0, suggesting that the enzyme responsible for the respiratory burst was not altered during culture. The number and affinity of PMA receptors were not changed during culture and were not affected by high external K+. Continuous assay of O2- release by coverslip-adherent macrophages in a cuvette indicated that the lag time between addition of stimulus and release of O2- was reduced, and the initial rate of O2- release was enhanced in K+ buffer. The potency of monovalent cations to support O2- release was K+ greater than Rb+ greater than choline+ greater than Cs+ = Na+ greater than Li+, suggesting that characteristics such as ionic radius or molecular size influence this effect, and the effect is not due simply to absence of Na+. Extracellular Ca2+ or Mg2+ was required for the maximal effect of high external K+, and enhancement by high K+ and divalent cations increased progressively during culture. These findings suggest that deactivation is caused primarily by changes in signal transduction from PMA receptors to the respiratory burst enzyme, rather than by changes in these receptors or the enzyme itself, and that signal transduction can differ in different macrophage populations.

Animals↗
PubMed1986

Latero-lateral end anastomosis for right hemicolectomy using staplers.

In seven patients undergoing right hemicolectomy for benign or malignant diseases, latero-lateral end anastomoses were made using stapling devices, LS (linear stapler) and GIA (gastrointestinal anastomosis). As no complications directly related to the anastomosis occurred, we conclude that anastomosis using stapling devices for right hemicolectomy is a safe and rapid procedure.

Adult↗
PubMed1986

[A new anticancer preparation, 5-fluorouracil-poly-L-lactic acid microcapsule, and its therapeutic evaluation].

An attempt was made to develop the new anticancer drug inducing enhanced tumor response to arterial chemoembolization therapy. 5-Fluorouracil (5-FU) was microencapsulated with poly L-lactic acid by the organic phase separation technique. This granular preparation containing 5-FU (FU-PLA-mc) was about 200 micron in diameter and was about 40% in 5-FU content. The release of 5-FU in vitro from FU-PLA-mc gradually increased, extending over 50 hours to reach maximum level. When 75 mg of FU-PLA-mc (5-FU content, 30 mg) was infused into normal rabbits through femoral arteries, maximum level of 5-FU in blood was 1.03 +/- 0.16 microgram/g after 15 minutes. Meanwhile, arterial infusion of the same dosage of FU-PLA-mc into VX2 tumor bearing rabbits resulted in the production of high level of 5-FU (2.1 +/- 0.5 micrograms/g) in tumors even after 72 hours. In vivo anticancer effect of FU-PLA-mc was significantly demonstrated; when 75 mg of FU-PLA-mc was administrated to VX2 tumor bearing rabbits through arterial infusion, T/C ratio of mean tumor weight was 0.01% on the 14th day after infusion. After hepatic arterial embolization with FU-PLA-mc in normal rabbits, elevation of serum transaminases was observed, but it was transient. Hepatic arterial chemoembolization with FU-PLA-mc was carried out for 8 patients with hepatic malignancies. Of these 8 patients, partial response was obtained in 3 patients and no severe complication was observed.

Adult↗
PubMed1985

Solubilization and characterization of a membrane 3, 3', 5-triiodo-L-thyronine binding protein from rat pituitary tumor GH3 cells.

To understand the mechanism by which T3 enters cells and carries out its biological functions membrane binding sites for 3, 3', 5-triiodo-L-thyronine were solubilized from rat pituitary tumor GH3 cells by detergents. Among three detergents tested, CHAPS is the best in preserving hormonal binding affinity and specificity. Least square analysis of the binding data show one class of binding site with a Kd of (6.35 +/- 1.27) nM and Bmax of (0.84 +/- 0.056) pmoles/50 micrograms protein. Hormone binding activity is lost by heating, pronase digestion and in the absence of NaCl. The pH optimum for binding is 7.0 and the binding activity is enhanced by dithiothreitol. The solubilization of membrane-associated thyroid hormone binding proteins will facilitate further characterization and exploration of their biological functions.

Animals↗
PubMed1985

Effects of long-chain cis-unsaturated fatty acids and their alcohol analogs on aggregation of bovine platelets and their relation with membrane fluidity change.

The effects of long-chain cis-unsaturated fatty acids with different alkyl chain lengths and different numbers of double bonds on aggregation of bovine platelets and membrane fluidity were investigated. All the cis-unsaturated fatty acids tested inhibited aggregation and at the same time increased membrane fluidity in accordance with their inhibitory effects. The saturated fatty acids and trans-unsaturated fatty acid tested for comparison had much lower or no effects on aggregation and membrane fluidity. The inhibitory effects of mono cis-unsaturated fatty acids increased with increase of their alkyl chain length. cis-Unsaturated fatty acids with two or more double bonds had more inhibitory effects than mono-unsaturated fatty acids. The position of the double bonds had less influence than the number of double bonds. We also examined the effects of cis-unsaturated fatty acids on membrane fluidity with diphenylhexatriene and anthroyloxy derivatives of fatty acids as probes and observed increased fluidity to be considerable in the membrane. The alcohol analogs of cis-unsaturated fatty acids also inhibited aggregation and increased membrane perturbation. These results suggest that the inhibition of platelet aggregation by cis-unsaturated compounds is due to perturbation of the lipid layer.

Adenosine Diphosphate↗
PubMed1985

Effects of monovalent cations and anions on ADP-induced aggregation of bovine platelets, and mechanisms thereof.

The effects of monovalent cations-inorganic alkali metal cations and organic quaternary ammonium cations-and monovalent inorganic anions on ADP-induced aggregation of bovine platelets were investigated. In the presence of K+, Rb+, Cs+, choline or tetramethylammonium, aggregation proceeded. However, aggregation was markedly restricted in media containing Li+, Na+, tetrabutylammonium or dimethyldibenzylammonium. With anions, aggregation proceeded in the order Cl- greater than Br- greater than I- greater than ClO4- greater than SCN-. The effects of cations significantly depended on Ca2+ concentration, whereas those of the anions depended little on Ca2+. Anions such as SCN- and ClO4- markedly decreased the fluorescence of the surface charge probe 2-p-toluidinyl-naphthalene-6-sulfonate, whereas cations had less pronounced effects. The relative effects of the anions on the fluorescence were consistent with their relative inhibitory effects on aggregation. These results suggest that inhibition of platelet aggregation by the anions is due to a change in the surface change of the platelet plasma membrane. On the other hand, kinetic analysis suggests that the effects of monovalent cations on platelet aggregation are due to their competition with Ca2+ during the process of aggregation.

Adenosine Diphosphate↗
PubMed1985

Relationship between membrane potential changes and superoxide-releasing capacity in resident and activated mouse peritoneal macrophages.

In an attempt to understand better the molecular basis for the enhanced respiratory burst of activated macrophages (M phi), we investigated the relationship between stimulus-induced changes in membrane potential and release of superoxide anion (O2-) in mouse peritoneal M phi. Resident M phi and M phi elicited by injection of lipopolysaccharide (LPS-M phi) or obtained from animals infected with bacille Calmette-Guérin (BCG-M phi) were used. LPS-M phi and BCG-M phi showed more pronounced changes in membrane potential (depolarization) and greater release of O2- on contact with phorbol myristate acetate (PMA) than did resident macrophages. The lag time between addition of stimulus and onset of release of O2- was reduced in activated compared with resident cells. Membrane potential changes began 60 to 90 sec before release of O2- could be detected in each cell type. The dose-response curves for triggering of membrane potential changes and O2- release by PMA were identical. The magnitude of membrane potential changes and of O2- release in LPS-M phi and BCG-M phi declined progressively during in vitro culture, and values on day 3 approached those in resident macrophages ("deactivation"). Extracellular glucose was required for effective stimulated change in membrane potential and O2- release. These findings indicate that membrane potential changes are closely associated with O2- -releasing capacity in macrophages, and that the systems that mediate membrane potential changes and production of O2- develop or decline concomitantly during activation or deactivation of the cells. Although the plasma membrane was highly depolarized by high extracellular K+ or by the sodium ionophore gramicidin, O2- release was not induced by these maneuvers, indicating that changes in membrane potential by themselves are not sufficient to trigger the respiratory burst in macrophages. Release of O2- was not impaired in buffers in which Na+ was completely replaced with equimolar concentrations of K+ or choline+; thus, induction or maintenance of the respiratory burst in M phi does not require an influx of Na+.

Animals↗
PubMed1985

Molecular basis for the enhanced respiratory burst of activated macrophages.

Macrophages elicited by injection of agents that produce inflammation or obtained from animals infected with intracellular parasites are primed so that they respond to phagocytosis or exposure to phorbol myristate acetate with a marked increase in the respiratory burst. This capacity to respond to stimulation with increased release of reactive oxygen metabolites appears to play an essential role in the increased microbicidal capability of activated macrophages. Macrophages can be primed for this capacity by incubation in vitro with bacterial products, proteases, or gamma interferon. The molecular basis for this priming is presently under investigation. An increase in the number or affinity of plasma membrane receptors does not appear to explain priming. Changes in one or more of the transduction events responsible for stimulus-response coupling might lead to more efficient stimulation or function of the enzyme responsible for the respiratory burst; these events are just beginning to be studied in macrophages. Priming can be explained at least in part by a modification of the respiratory burst enzyme such that it binds its substrate NADPH, the source of electrons for reduction of oxygen to superoxide anion, more efficiently. Understanding the molecular basis for priming of the respiratory burst might permit its eventual therapeutic manipulation.

Animals↗