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Biomedical subjects

Y Yajima

Publications and source records attributed to Y Yajima.

At least 127 records · Page 7Linked to original sources
PubMed1989

[The role of the cytoskeletal components in cell culture in collagen gel as a model system of vitreous contraction].

We previously reported a cell culture system in artificial collagen gel as a model system of vitreous contraction. In this report, the epithelium cultured in the collagen gel elongated and induced gel contraction. The motile cytoskeletal components were thought to be important for morphological changes of the cells and the gel contraction. In order to examine the relationship between the cytoskeletal components and morphological changes of the cells and gel contraction, colchicine and cytochalasin B, known to be inhibitors for microtubules and microfilaments respectively, were added to the gels and the culture media. Bovine lens epithelia were cultured in the gels and the media containing 0-1000 nM colchicine or 0-10 microM cytochalasin B. Both inhibitors arrested the elongation of the cells and the contraction of the gels. These results suggested that the cell movement caused by the functions of microtubules and microfilaments were related to the vitreous contraction.

Animals↗
PubMed1989

[Change of blood lentinan level in patients with advanced cancers].

A conventional limulus test can detect not only endotoxin but also beta(1----3) glucan. Therefore, with a quantitative limulus test, the limulus colorimetric test, we studied the pharmacokinetics of lentinan, an antitumor beta(1----3) glucan preparation, in the blood of 10 healthy volunteers and 20 patients with advanced cancers. The calibration curve of lentinan in the human plasma was linear in the range of 0 to 100 ng/ml. Two mg of lentinan was administered once a week and blood samplings for the measurement were done immediately before the next lentinan administration to document trough-levels serially at a week interval. Trough-levels tended to rise gradually and showed a rapid elevation between 4 and 8 weeks after beginning of administration. This phenomenon may correlate closely with the antitumor effect of lentinan and, therefore, deserves further investigations.

Antineoplastic Agents↗
PubMed1988

Role of calcium in suppression of glucagon release from isolated diabetic rat pancreata.

To investigate the role of extracellular Ca2+ (Ca2+) in suppression of glucagon release in diabetic animals, pancreata were isolated from streptozotocin-diabetic rats and perfused with a 15 mM glucose solution containing one of the following: (1) Ca2+ 2.1 mM and insulin 22 microU/ml, (2) Ca2+ 2.1 mM and insulin 110 microU/ml, (3) Ca2+ 2.1 mM and insulin (-) or (4) Ca2+ 0.2 mM and insulin 110 microU/ml. Although perfusion with 22 microU/ml of insulin did not alter glucagon release, perfusion with 110 microU/ml of insulin in the presence of Ca2+ and glucose significantly reduced the release of glucagon from 1.9 +/- 0.3 ng/min to 1.2 +/- 0.3 ng/min for the first 3 min. The absence of insulin enhanced glucagon release from the baseline level of 1.0 +/- 0.1 ng/min to 1.6 +/- 0.3 ng/min at 11 min and to 1.4 +/- 0.2 ng/min at 21 min. Deprivation of Ca2+ in the perfusate also enhanced glucagon release from the baseline level of 0.8 +/- 0.1 ng/min to 1.2 +/- 0.3 ng/min for the first 4 min. It is concluded that insulin suppresses glucagon release and Ca2+ is needed for the suppression of glucagon release in the presence of both insulin and glucose in streptozotocin-diabetic rat pancreata.

Animals↗
PubMed1988

Effects of cholera toxin on the coupling of thyrotropin-releasing hormone to a guanine nucleotide-binding protein in cultured GH3 cells.

The effects of cholera toxin on the coupling of the thyrotropin-releasing hormone (TRH) receptor to a guanine nucleotide-binding (G) protein were examined in a GH3 clonal strain of rat pituitary tumor cells. Incubation of the cells with cholera toxin (50 ng/ml) for 16 hr caused a decrease in [3H]methyl-TRH binding to 59% of the control level and in TRH-stimulated low Km GTPase activity from 143 to 107% of the control level in the membrane-containing fraction. The effects of cholera toxin were time dependent; TRH-stimulated GTPase activity was reduced after a 3-hr incubation, whereas cholera toxin decreased [3H]methyl-TRH binding in the membrane-containing fraction after a 5-hr incubation. These results suggest that the inhibition of TRH-stimulated GTPase activity by cholera toxin treatment is not due to the decrease of receptor binding caused by this toxin. On the other hand, incubation of GH3 cell membranes with preactivated cholera toxin and NAD+ did not substantially alter the binding of [3H]methyl-TRH. In contrast, the cholera toxin-treated membranes demonstrated a partial reduction in the activity of TRH-induced low Km GTPase activity and a 10-fold increase in the concentration of guanine nucleotide required for a half-maximal effect in regulating the TRH receptor affinity for [3H]methyl-TRH. These data suggest that cholera toxin may act directly on a G protein that is associated with TRH-receptors.

Animals↗
PubMed1987

A case of liver cirrhosis complicated with endotoxemia and disseminated intravascular coagulation: a case report.

A 59-year-old female was admitted to our hospital because of massive ascites and increasing jaundice, suggesting a severe decompensated state of liver cirrhosis. On the third hospital day, she was diagnosed as disseminated intravascular coagulation (DIC) from a coagulofibrinolytic study and developed renal failure. Continuous drip infusion of gabexate mesilate, a synthetic inhibitor of serine-protease, was found to be successful in managing DIC, followed by the restoration of renal function. During the clinical course, blood endotoxin, assayed by the chromogenic method, was initially 11 pg/ml and increased, in accordance with the elevation of serum FDP, to a level of 110 pg/ml when renal failure occurred. A proportional relationship was observed between changes in blood endotoxin and serum FDP throughout the course. This finding may be an important clue in studying the mechanism of DIC and non-septic endotoxemia both developing in liver cirrhosis.

Disseminated Intravascular Coagulation↗
PubMed1987

The significance of activation of reticuloendothelial function on hepatectomy.

The prognosis of patients after massive hepatectomy is poor in certain cases whose hepatic reserve, including reticuloendothelial function, is deteriorated. We administered OK-432 before 70% hepatectomy on rats to activate the reticuloendothelial function and studied its effect on postoperative course. The elevations in plasma endotoxin, GOT and GTP were attenuated, and the deterioration of the complement activity after hepatectomy was greatly improved by OK-432 treatment. The RNA content in the liver was significantly increased by OK-432 administration. These findings suggest that activation of the reticuloendothelial function at the time of massive hepatectomy enhances endotoxin clearance from blood and thereby contributes in lessening the magnitude of hepatic injury, maintaining the serum complement, and improving liver protein synthesis.

Animals↗
PubMed1987

Activation of reticuloendothelial function for prevention of endotoxemia after hepatectomy in cirrhotic patients.

In order to prevent endotoxemia after hepatectomy in cirrhotic patients, we administered OK-432 before and after hepatectomy to activate the reticuloendothelial function and studied its effect on postoperative endotoxemia. In the cirrhotic group without OK-432 administration (7 patients), the value of endotoxin increased significantly after hepatectomy, compared to the cirrhotic group which received OK-432 administration (5 patients) and the non-cirrhotic group (12 patients), and the endotoxin level was still higher than the preoperative value even on the 14th day. On the other hand, the cirrhotic group with OK-432 administration and the non-cirrhotic group showed minimal increases of endotoxin levels at the first day, which returned to the preoperative values at the third day. Base on these findings, it is suggested that activation of the reticuloendothelial function bears substantial significance as one of the therapeutic modalities for prevention of endotoxemia after hepatectomy in cirrhotic patients.

Biological Products↗
PubMed1986

Pertussis toxin blocks the inhibitory effects of somatostatin on cAMP-dependent vasoactive intestinal peptide and cAMP-independent thyrotropin releasing hormone-stimulated prolactin secretion of GH3 cells.

It was shown that somatostatin (SRIF) inhibited cAMP-dependent vasoactive intestinal peptide (VIP)-stimulated prolactin (PRL) release by a GH3 clonal strain of rat pituitary tumor cells and decreased basal PRL secretion and inhibited PRL release in response to thyrotropin releasing hormone (TRH) whose action was independent of prior synthesis of cAMP. Pretreatment of these cells with pertussis toxin prevented SRIF's inhibitory effects on basal and TRH-stimulated hormone secretion as well as its VIP-stimulated responses. The blockade of SRIF's inhibitory effect on the actions of TRH or VIP was dependent on both the duration of preincubation and concentration of the toxin and was correlated with the ability of the toxin to catalyze the ADP-ribosylation of the 39,000-Da membrane protein. It is likely that this pertussis toxin substrate is involved in signal transduction of SRIF on cAMP-dependent actions of VIP and cAMP-independent action of TRH. However, the mechanism of SRIF's action on TRH is not clear, since SRIF did not affect the intracellular responses by TRH, neither intracellular Ca2+ mobilization nor the increase of 1,2-diacylglycerol formation following the breakdown of polyphosphoinositides.

Animals↗
PubMed1986

Endotoxemia after abdominal surgery.

The blood level of endotoxin after operations in patients with digestive diseases, mainly liver cirrhosis and obstructive jaundice, and the complications most likely related to the presence of endotoxemia were investigated. Twenty-seven patients without either liver cirrhosis or obstructive jaundice showed a minimal elevation of the endotoxin level in blood, as shown by 6.1 +/- 3.9 (mean +/- S.E.) pg/ml at the first postoperative day and there was only one anastomotic leakage. On the other hand, 18 patients with liver cirrhosis showed a notable and persistent endotoxemia after surgery. The cirrhotic patients who especially underwent splenectomy and hepatectomy showed marked elevations of endotoxin level at the first postoperative day, with values of 151.0 +/- 46.1 pg/ml and 101.3 +/- 36.2 pg/ml, respectively, and one of these patients died of hepatic failure. Thirteen patients with obstructive jaundice developed endotoxemia evidenced by the value of 21.6 +/- 4.8 pg/ml at the first day after surgery. Among these patients, two had gastrointestinal bleeding and one developed disseminated intravascular coagulation (DIC). The markedly high and persistent levels of endotoxin in patients with liver cirrhosis or obstructive jaundice may be possibly related with the development of multiple organ failure (MOF).

Cholestasis↗
PubMed1986

Stability of endotoxin detected in human plasma against endotoxin-inactivating factor (EIF): quantitative analysis of EIF using chromogenic endotoxin assay.

Using a quantitative blood endotoxin assay utilizing chromogenic substrate coupled with perchloric acid pretreatment (PCA-LCT), we showed the presence of endotoxin-inactivating factor (EIF) in human plasma in vitro. EIF activity inactivated added endotoxin to about 10(-4) of the initial level within 20 min, followed by a stable phase where the residual endotoxin became resistant to EIF and was not further inactivated. The residual endotoxin may represent the endotoxin in patient plasma which is also EIF resistant. We postulate that endotoxin, upon entering the blood, is rapidly inactivated by chemical modification of its active site, lipid A, through EIF. Subsequently, inactivated endotoxin, mainly consisting of polysaccharide, is gradually removed from circulation by endocytosis in the reticuloendothelial system.

Chromogenic Compounds↗