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Biomedical subjects

S Shibata

Publications and source records attributed to S Shibata.

At least 541 records · Page 30Linked to original sources
PubMed1990

[Intraperitoneal administration of anti-cancer drug with cisplatinum (CDDP)].

Six patients were administered cisplatinum (CDDP) i.p. There were four cases with peritoneal dissemination of gastric cancer after gastrectomy and the other two, for whom prophylactic intraperitoneal administration of CDDP had been attempted to prevent peritoneal metastasis. The dose of CDDP was 75-140 mg/body (58-90 mg/m2). The results were 1 PR, 2 NC and 1 PD. The PR case was given intraperitoneal CDDP combined with RF thermotherapy. Liver dysfunctions, renal dysfunctions, bone marrow suppressions, and GI tract disturbances were observed as toxic reactions. The degrees of side effects after i.p. administration were less severe than after i.v. administration. However the indication of CDDP i.p. administration should be decided after case conferences. On pharmacokinetics, non-protein bound platinum was detected at 24 hours after i.p. administration, in ascites and plasma. The concentration of platinum in ascites was about three-fold than in plasma. It was considered that CDDP absorption from ascites into plasma depended on the state of peritoneal dissemination of cancer.

Adult↗
PubMed1990

[Ultrastructure of capillary permeability in human brain tumor: primary meningeal malignant melanoma].

The tumor vessels of a primary meningeal malignant melanoma were studied by electron microscopy. There were numerous endothelial fenestrae and basal lamina abnormalities in the intrinsic tumor capillaries. They resembled the tumor vessels found in nonglial tumors, but were distinctly different from those seen in glial tumors with nonfenestrated capillaries. These findings were anticipated because leptomeninges have fenestrated capillaries.

Basement Membrane↗
PubMed1989

Preparation and characterization of antibodies against 6-O-alpha-D-xylopyranosyl-beta-D-glucopyranose (beta-isoprimeverose), the disaccharide unit of xyloglucan in plant cell-walls.

The p-aminophenyl beta-glycoside of 6-O-alpha-D-xylopyranosyl-D-glucopyranose (isoprimeverose), the disaccharide unit of plant xyloglucan, was coupled to bovine serum albumin, and the resulting glycoconjugate was used as an immunogen for the immunization of a rabbit. The immunochemical specificities of the rabbit antiserum raised against the glycoconjugate were characterized by immunodiffusion, quantitative precipitation, and hapten inhibition. After removal of anti-bovine serum albumin antibodies, the antiserum exhibited a specificity for the introduced disaccharide unit of the artificial antigen. The antibody-combining site was also shown to recognize the aglycon portion of the introduced hapten. The antiserum interacted with some xyloglucans, such as those from tamarind seed and the cell wall of pea stem. beta-Isoprimeverose and alpha-D-xylopyranosides were good inhibitors of the xyloglucan-antibody precipitation system, indicating that the antibodies recognize the beta-isoprimeverose unit of the xyloglucan.

Antibodies↗
PubMed1989

Production and characterization of antisera raised to the manninotrionate group [alpha-D-Galp-(1----6)-alpha-D-Galp-(1----6)-D-gluconate].

Manninotrionate [alpha-D-Galp-(1----6)-alpha-D-Galp-(1----6)-D-gluconate] was coupled to bovine serum albumin (BSA), and antisera were raised in rabbits to this carbohydrate-protein conjugate. The antisera were studied by quantitative precipitation and hapten inhibition. Antisera against the manninotrionate-BSA conjugate showed the greatest reactivity with the homologous manninotrionate-BSA antigen, but also cross-reacted extensively with a manninotrionate-ovalbumin conjugate. The antisera gave weak precipitin reactions with beef-lung galactan, guaran, gum arabic, and larch arabinogalactan. Quantitative hapten-inhibition studies with a series of galactosyloligosaccharides indicated that the antisera possess a high degree of specificity toward terminal alpha-D-Galp-(1----6)-alpha-D-Galp units. The antisera did not agglutinate Ehrlich ascites tumor-cells, which have been demonstrated to contain cell-surface glycoproteins having alpha-D-galactosyl end-groups.

Agglutination Tests↗
PubMed1989

Effects of melatonin on neuronal activity in the rat suprachiasmatic nucleus in vitro.

The pineal hormone melatonin is believed to act directly on the hypothalamic suprachiasmatic nuclei (SCN), which are principal circadian pacemakers in rodents, although direct demonstration of this is lacking. To determine whether the SCN are sensitive to melatonin electrophysiologically, we investigated the effect of melatonin on rat SCN single-unit activity in an in vitro hypothalamic slice preparation. SCN single-unit activity was inhibited by melatonin superfusion during the late subjective day in a dose-dependent manner but not at other times of day, supporting the view that melatonin acts directly on SCN neurons.

Action Potentials↗
PubMed1989

Cachectin/TNF kills or inhibits the differentiation of 3T3-L1 cells according to developmental stage.

The effects of cachectin/tumor necrosis factor (TNF) on growth and differentiation of 3T3-L1 cells were examined. This fibroblastic cell line can be induced to differentiate into a mature cell type having the biochemical and morphological characteristics of normal adipocytes. At various stages of growth and differentiation, 3T3-L1 cells were exposed to 2.5 x 10(-16) to 2.5 x 10(-8) M (4.2 fg/ml to 420 ng/ml = ca. 1.2 x 10(-14) to 1.2 x 10(-16) U/ml) recombinant human cachectin/TNF for 24 hr, after which cytotoxicity or differentiation was evaluated. During log-phase cell growth, cachectin/TNF had no significant effect on cell viability, and the preadipocytic cells were also resistant to the cytotoxic effect of cachectin/TNF at the contact-inhibited confluent stage. However, when cachectin/TNF was added to the cells during induced differentiation, only 20% of the cells survived. After differentiation into adipocytes, cells regained their resistance to cachectin/TNF-induced cytotoxicity. Cachectin/TNF also markedly affected the differentiation of 3T3-L1 cells into adipocytes. When cells in the confluent phase of growth were exposed to cachectin/TNF for 24 hr, their subsequent hormone-induced differentiation to adipocytes was inhibited. Like cachectin/TNF, IL-1 also induces suppression of lipoprotein lipase and enhances lipolysis in differentiated 3T3-L1 adipocytes; however, in contrast to cachectin/TNF, IL-1 had no effect on the viability or differentiation of pre-adipocyte 3T3-L1 cells. These results indicate that the cytotoxic action of cachectin/TNF varies in the same cell type depending on the stage of growth or differentiation. The results also imply that cachectin/TNF may play a normal role in controlling the differentiation of certain types of cells in vivo including adipocyte lineages.

Animals↗
PubMed1989

Effects of benzodiazepine and GABA antagonists on anticonflict effects of antianxiety drugs injected into the rat amygdala in a water-lick suppression test.

In order to elucidate the role of the amygdala in rat conflict behavior in a water lick suppression test, we examined the effect of lesions of various nuclei of the amygdaloid complex on this behavior. An anticonflict effect was produced by a lesion of the anterior part of central and basolateral amygdala, and lesion to the posterior part of the central amygdala, but not by posterior of the basolateral amygdala or medial amygdala lesions. These results suggest that the amygdala, especially the anterior part of the central and basolateral nuclei, plays an important role in conflicting behavior of rats in the water lick test. In a second experiment, the effects of benzodiazepine- and GABA-antagonists on the anticonflict action of diazepam, zopiclone, and phenobarbital injected into the anterior part of central and basolateral amygdala were examined, also using a water lick suppression test. A dose-dependent anticonflict action was produced by systemic administration as well as by intra-amygdala injection of diazepam, zopiclone, lormetazepam, flurazepam and phenobarbital. The order of potency was lormetazepam greater than zopiclone greater than or equal to diazepam greater than flurazepam greater than or equal to phenobarbital for both routes of injection. The anticonflict effects of diazepam and zopiclone injected into the amygdala were completely reversed by Ro15-1788 and beta-CCM but not by bicuculline, while the anticonflict effect of phenobarbital was reversed by beta-CCM but not by Ro15-1788 or bicuculline. The present results strongly suggest that the anterior nuclei of central and basolateral amygdala are important sites of action of antianxiety drugs, and that an anticonflict action produced by intra-amygdala injection of benzodiazepines or barbiturate is mediated through the different receptor mechanisms.

Amygdala↗
PubMed1989

Ultrastructure of capillary walls in human brain tumors.

Changes in capillary walls between human glial, non-glial and metastatic brain tumors were studied with conventional ultrathin section and freeze-fracture replica techniques. The following results were obtained. (1) In glial tumors, ultrathin section studies showed cell junctions of the capillaries were either short or elongate. Moreover, endothelial hyperplasia, surface infolding of endothelial cells, irregularity of the basal lamina and a large extravascular space were observed. Freeze-fracture replicas of capillary endothelium showed tight junctions as two to seven strands. In addition, pinocytotic vesicles had increased markedly and were an average of 25 per microns 2. Both ultrathin and freeze fracture studies showed that, in contrast to malignant gliomas, there were only slight changes in benign astrocytomas. (2) In non-glial tumors, ultrathin sections showed surface infoldings, increased vesicles, many fenestrations of endothelial cells, irregularity of basal lamina and enlarged perivascular space. Freeze-fracture replicas of vascular endothelium, showed that the average number of pinocytotic vesicles and fenestrations were 25 and 22 per microns 2, respectively. Moreover, the tight junction was composed of one or two strands which appeared to be a discontinuous array of particles. (3) In metastatic brain tumors, ultrathin studies showed capillary endothelia were proliferated, had marked infolding, and showed an increased number of pinocytotic vesicles and many fenestrations. Moreover, short and elongate intercellular junctions were presented but no open junction was detected. Finally the basal lamina lost its three-layered appearance and was irregular in width. Freeze-fracture replicas showed pinocytotic vesicles had increased and were 24 per microns 2 on average in four cases, but fenestrations and tight junctions could not be detected. The most fundamental feature of vessels in these three different kinds of tumors was whether they were fenestrated or not. Glial tumors were non-fenestrated, whereas non-glial and metastatic tumors were fenestrated.

Brain Neoplasms↗
PubMed1989

Osteonectin inhibiting de novo formation of apatite in the presence of collagen.

The effect of bone matrix protein of osteonectin on de novo formation of apatite was studied in a wide range of calcium phosphate solutions in the presence of collagen. In every solution, from which amorphous calcium phosphate, octacalcium phosphate, or apatite precipitated as a possible initial phase, osteonectin at concentrations less than 1 microM retarded the precipitation, subsequent transformation to apatite, and ripening crystal growth of apatite. Collagen present as either reconstituted or denatured form had no effect on the osteonectin-associated reactions as well as osteonectin-free reactions, and no structural correlation was observed between collagen fibrils and any of the calcium phosphates that appeared in our system. Direct measurement of free calcium levels in the solutions suggested that the reduction in calcium activity due to complexing with osteonectin hardly explained the inhibitory activity of osteonectin in retarding the formation of apatite. Instead, our transmission electron microscopic (TEM) observation strongly suggested that the primary mechanism for osteonectin to inhibit the formation of apatite is to block growth sites of calcium phosphates nucleated. The apatite thus formed in the presence of osteonectin showed less resolved X-ray diffraction patterns, partly because of smaller crystallites as suggested by TEM.

Animals↗
PubMed1989

Bay K 8644-induced potentiation of the contractile response of rabbit iliac artery to caffeine in a Ca2+-free medium.

1. In a Ca2+-free medium caffeine (10 mM) was still able to cause a phasic contraction in rabbit iliac arteries. 2. Bay K 8644 at 10(-6) but not at 10(-7) M potentiated the residual response to caffeine in a Ca2+-free medium. In a Ca2+-free medium with or without KCl (40 mM), Bay K 8644, however, caused no contraction. 3. Nifedipine (10(-6) M) did not affect the residual caffeine-response or the potentiating effect of Bay K 8644. Verapamil (10(-6) M), however, inhibited both the caffeine response and the potentiation. 4. Bay K 8644 (10(-6) M) potentiated the contractile response to Ca2+ (0.01-2.4 mM) in a Ca2+-free medium containing KCl. The potentiation was equally inhibited by nifedipine or verapamil. 5. La#+ (1 mM), EGTA (0.1 mM), or vanadate (10(-4) M) completely inhibited the Bay K 8644-induced potentiation without affecting the residual caffeine response. 6. These results suggest that the potentiating action of Bay K 8644 on the residual caffeine response in a Ca2+-deficient medium may not be related to voltage-dependent Ca2+ channels. In addition, the activity of Ca2+-ATPase in sarcolemmal membranes may be important in this potentiation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Potentiating effect of Bay K 8644 on the noradrenaline-induced contraction in rabbit renal and femoral arteries.

1. In rabbit renal and femoral arteries, Bay K 8644 produced a contraction and nifedipine inhibited it. 2. Bay K 8644 potentiated the responses to noradrenaline (NA) and potassium (K+). In the presence of nifedipine, Bay K 8644 potentiated NA. 3. In a Ca2+-free medium with EGTA, NA produced a transient contraction which was not affected by Bay K 8644 or nifedipine. Bay K 8644 enhanced the Ca2+-induced contraction in a Ca2+-free medium containing EGTA, nifedipine and NA. 4. The combined treatment with nimodipine and nifedipine further inhibited the Bay K 8644 induced potentiation of Ca2+ responses in the presence of NA as compared to nifedipine alone. 5. In the presence of but not absence of Bay K 8644, Ca2+ caused contractions in a Ca2+-free medium containing EGTA, nifedipine and KCl. 6. Vanadate further enhanced the Bay K 8644 induced potentiation of the Ca2+ responses in the presence of K+ but not NA. 7. These results suggest that, in rabbit renal and femoral arteries, Bay K 8644 does not affect the intracellular translocation of Ca2+ but increases Ca2+-influx activated by K+ or NA. Bay K 8644-induced potentiation of NA responses is likely due to an increase in Ca2+-influx through voltage operated channels (VOC) activated by NA. Also, K+ activated VOC may be coupled to Ca2+-extrusion pumps more than NA activated VOC.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Vasorelaxing action of melatonin in rabbit basilar artery.

1. In rabbit basilar arteries, melatonin (10(-5)-10(-3) M) and nifedipine (10(-10)-10(-8) M) inhibited the responses to KCl and 5-hydroxytryptamine. 2. Melatonin or nifedipine inhibited the Ca2+-responses in a Ca2+-free medium containing KCl (40 mM) or 5-HT (10(-5) M). 3. A combined treatment with nifedipine and melatonin caused no further inhibition of the Ca2+ response in the presence of K+ as compared to a single treatment with melatonin. 4. However, the combined treatment caused a greater inhibition of the Ca2+-response in the presence of 5-HT than the single treatment with either agent. 5. These results suggest that melatonin and nifedipine inhibit the same Ca2+ channels activated by KCl. Further, 5-HT-activated Ca2+ channels which are inhibited by melatonin may be different from nifedipine-sensitive Ca2+ channels activated by 5-HT.

Animals↗
PubMed1989

Inhibitory effects of TYB 3823, a new antiarrhythmic agent, on mechanical responses in the vascular smooth muscles.

1. TYB 3823 (3 x 10(-5) M to 10(-3) M) but not lidocaine (10(-4) M) inhibited the contractile response to norepinephrine in rabbit aorta in a competitive manner. On the other hand, TYB 3823 had no effect on contractile responses to histamine, 5-hydroxytryptamine, high KCl and Ca2+. 2. In rabbit aorta, TYB 3823 (10(-5) M and 10(-4) M) but not lidocaine (10(-4) M) also antagonized the ouabain-induced contraction and this action was less potent than that of phentolamine (10(-6) M). 3. In rabbit coronary arteries precontracted with KCl (40 mM), either TYB 3823 or lidocaine inhibited the isoproterenol-induced relaxation to the same levels. Propranolol at 10(-8) M shifted the relaxation curve for isoproterenol to the right and at 10(-6) M it almost completely prevented the relaxation. Further, the effect of a combined treatment with propranolol (10(-8) M) and TYB 3823 (3 x 10(-5) M) was not different from that of a single treatment with propranolol (10(-8) M). 4. In rabbit iliac arteries, TYB 3823 (3 x 10(-5) M and 10(-4) M) but not lidocaine (10(-4) M) suppressed the contractile response to caffeine in a Ca2+-free medium with EGTA and nifedipine. Nitroglycerin (10(-4) M) also inhibited the response but this action was less potent than that of TYB 3823. The combined treatment of the tissue with TYB 3823 and nitroglycerin (both 10(-4) M) further inhibited the responses to caffeine as compared to a single treatment with each drug. 5. These results suggested that TYB 3823 may interfere with the responses due to the mobilization of intracellular Ca2+ activated by caffeine and also has both alpha- and beta-adrenoceptor blocking actions on the vascular smooth muscles.

Animals↗
PubMed1989

Effects of Chinese drugs "xiebai" and "dasuan" on human platelet aggregation (Allium bakeri, A. sativum).

Adenosine (1), guanosine (2), and tryptophan (3), as well as beta-sitosterol beta-D-glucoside (4) were isolated from the n-butanol-soluble fraction of Xiebai, the tuber of Allium bakeri Reg., which was recognized to have an anti-platelet aggregation effect. Moreover, 1 and 2 were also isolated from the n-butanol-soluble fraction of Dasuan, the tuber of A. sativum L. Compound 1 showed a significant inhibitory activity against both the primary and secondary wave aggregation of human platelet induced by 2 microM ADP, whereas compounds 2-4 showed no or very low inhibitory effects. The structure-activity relationships on human platelet aggregation with regard to 1, 2 and their derivatives, adenosine 2'-monophosphate (5), adenosine 5'-monophosphate (6), adenosine triphosphate (7), guanosine 3'-monophosphate (8), and guanosine 5'-monophosphate (9), and guanylyl(3'----5')adenosine (10) are discussed. Compounds 5-7 and 10 also inhibited the primary and secondary wave aggregation with a dose-dependent response.

Adenosine↗
PubMed1989

Electrophysiological effects of FK664, a new cardiotonic agent, on preparations from guinea pig ventricle and from rabbit sino-atrial node.

Effects of the cardiotonic agent FK664, 6-(3, 4-dimethoxy-phenyl)-1-ethyl-4-mesitylimino-3-methyl-3,4-dihydro-2 (1H)-pyrimidone, on isolated guinea pig ventricular muscles and rabbit sinus node pacemaker cells were studied using micro-electrode techniques. In ventricular muscles driven at 0.5-1.0 Hz, FK664 above 3 mumol.litre-1 caused an increase in contractile force and a shortening of time to peak tension. This positive inotropic effect of FK664 was accompanied by a slight elevation of the early plateau phase of the action potential, while other action potential variables were unaffected. The change in contractile force induced by FK664 was abolished in a low Ca2+ medium (0.12 mmol.litre-1) or by treatment with ryanodine (2 mumol.litre-1), whereas it was relatively well preserved in the preparations pretreated with nefedipine (1 mumol.litre-1). The slow action potentials induced by isoprenaline (0.3 mumol.litre-1) in high K+ medium (30 mmol.litre-1) and the slow inward current measured by single sucrose gap voltage clamp at a holding potential of -40 mV were unaffected by FK664. In sinus node pacemaker cells, FK664 (1-10 mumol.litre-1) caused a dose dependent acceleration of phase 4 depolarisation and a shortening of spontaneous firing cycle length. This positive chronotropic effect of FK664 was markedly inhibited in a low Ca2+ medium (0.3 mmol.litre-1). These findings suggest that FK664 has positive inotropic and chronotropic effects on the heart, due to an enhancement of transsarcolemmal calcium influx through the low threshold, dihydropyridine insensitive Ca2+ channel population.

Action Potentials↗