Correlation of c-erbB-2 with invasion and metastasis in human gastric cancer.
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Adenocarcinoma↗
Biomedical subjects
T Okuda
Publications and source records attributed to T Okuda.
Correlation between epidermal growth factor receptor concentration and the growth of human gastric cancer xenografts in nude mice.
Seven human gastric cancer xenografts with different concentrations of EGF receptor were established in nude mice. The expression of EGF receptor in the tumors was demonstrated by Western blotting with anti-EGF receptor antibody, binding assay with 125I-EGF and immunohistochemistry with anti-EGF receptor antibody. Western blotting revealed EGF receptor doublet bands at molecular masses of 150 KDa and 170 KDa in all of the samples. The concentration of 125I-EGF binding activity in the tumors ranged from 36.0 to 11,000 fmol/mg protein, with a mean of 345 fmol/mg protein. EGF receptor was also demonstrated immunohistochemically on the apical border of the glands and the cell membrane of the tumor cells. There seemed to be a close correlation between the concentration of 125I-EGF binding activity and the doubling time of these tumors in nude mice (gamma = -0.68). However, no definite correlation was observed between EGF ligand binding and histological features of intestinal type or diffuse type. The expression of EGF receptor appears to facilitate the growth of human gastric cancer xenografts in nude mice.
Animals↗
Anesthesia in Shy-Drager syndrome.
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Journal Article↗
Recurrent coronary artery spasm during a non-cardiac surgical procedure.
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Journal Article↗
Suppressant effects of midazolam on responses of spinal dorsal horn neurones in rabbits.
Recordings of noxious intra-arterial bradykinin (BK)-induced chemonociceptive and spontaneous activity from 30 single spinal lamina V neurones of the dorsal horns in non-anaesthetized and decerebrated rabbits, were performed with tungsten microelectrodes. Intravenous injection of midazolam (0.2 mg/kg; 7 neurones) depressed BK-induced neural discharges by 55.0 +/- 6.2% (P less than 0.05) and 57.9 +/- 8.4% (P less than 0.05) 5 and 25 min after administration, respectively. Treatment with flumazenil (0.2 mg/kg, i.v.; 7 neurones), administered 20 min after midazolam, completely reversed the inhibition by midazolam of the BK-induced spinal lamina V neural responses and spontaneous neuronal activity. In contrast, a large dose of naloxone (1.0 mg/kg, i.v.; 6 neurones), administered 20 min after midazolam, failed to alter the midazolam-induced depressant effects on the nociceptive responses, at the spinal dorsal horn. Treatments with flumazenil (5 neurones) and naloxone (5 neurones) did not influence either the spontaneous or the BK-induced neuronal discharges, recorded in spinal lamina V cells. Midazolam depressed the nociceptive responses probably through its agonistic activity on the binding to the GABA-benzodiazepine-barbiturate system in the spinal dorsal horn.
Animals↗
Suppression of genotoxicity of carcinogens by (-)-epigallocatechin gallate.
Epidemiological evidence shows that green tea may be a factor in lowering cancer risk. We have investigated the possibility that (-)-epigallocatechin gallate (EGCG), a major polyphenol in green tea, might be an antimutagenic substance. In the Ames Salmonella test, EGCG suppressed the direct-acting mutagenicity of 3-hydroxyamino-1-methyl-5H-pyrido-[4,3-b]indole (Trp-P-2(NHOH)) and 2-hydroxyamino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1(NHOH)), the activated forms of food-derived carcinogens 3-amino-1-methyl-5H-pyrido[4,3-b]indole and 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole. EGCG was also effective in reducing the mutagenicity of Trp-P-2(NHOH) in mouse FM3A cells in culture. Furthermore, EGCG demonstrated a suppressive effect in the in vivo Drosophila mutation assays, i.e., the wing spot test, and the DNA repair test, on several carcinogens. EGCG was also effective in inhibiting DNA single-strand breaks in vitro caused by Glu-P-1(NHOH). We conclude that the mechanism of inhibition may not have resulted from direct interaction between EGCG and the mutagens, but rather from indirect interception of mutagen action by EGCG.
Animals↗
Anticarcinogenic effects of (-)-epigallocatechin gallate.
BACKGROUND: Our research objective is to develop nontoxic cancer chemopreventive agents and to apply these agents in treating humans. We are identifying agents that inhibit the process of tumor promotion in two-stage carcinogenesis experiments on mouse skin. METHODS: We review (a) the inhibitory effect of penta-O-galloyl-beta-D-glucose (5GG) on tumor promotion by teleocidin, one of the 12-O-tetradecanoylphorbol-13-acetate (TPA)-type tumor promoters (5GG is structurally similar to (-)-epigallocatechin gallate (EGCG) and is isolated from hydrolyzed tannic acid); (b) the inhibitory effects of EGCG, the main constituent of Japanese green tea, on tumor promotion with two tumor promoters, teleocidin and okadaic acid, a non-TPA-type tumor promoter; (c) the mechanisms of action of EGCG, a single application of which reduced the specific binding of [3H]TPA and [3H]okadaic acid to a particulate fraction of mouse skin; and (d) the anticarcinogenic effects of EGCG on duodenal carcinogenesis induced by N-ethyl-N'-nitro-N-nitrosoguanidine in male C57BL/6 mice. EGCG is a nontoxic compound. CONCLUSION: We believe that the main constituent of Japanese green tea, EGCG, is a practical cancer chemopreventive agent available in everyday life.
Animals↗
Inhibition of human immunodeficiency viral replication by tannins and related compounds.
Among 87 chemically defined tannins and related compounds, several hydrolyzable tannins, but not condensed tannins or other lower molecular weight polyphenols, significantly inhibited both the cytopathic effect of human immunodeficiency virus (HIV) and the expression of HIV antigen in human lymphotropic virus type I (HTLV-1)-positive MT-4 cells. The 50% effective concentrations (2.0-4.8 micrograms/ml) of the active compounds were 13- to 15-fold lower than their 50% cytotoxic concentrations. Their anti-HIV activity was demonstrated to be mediated, at least in part, by inhibition of HIV adsorption to the cells.
Adsorption↗
Secretion and function of the third component of complement (C3) by murine leukocytes.
Our new finding of de novo synthesis and secretion of C3 by both murine peritoneal macrophages and polymorphonuclear leukocytes (PMN) was confirmed by the incorporation of [35S]methionine into C3 molecules and their complete inhibition by cycloheximide. The methods of secretion of C3 from these two types of cells were compared by examining the C3 contents in their culture supernatants. Completely different modes of secretion were observed, i.e. although macrophages synthesize and secrete C3 constitutively, PMN has a mechanism to store the already synthesized C3 in the cell and secrete it in response to stimuli. Protein kinase C (PKC) activators, e.g. 12-O-tetradecanoyl-phorbol 13-acetate, dioctanoyl glycerol, and mezerein, as well as calcium ionophore A23187 stimulate the secretion of C3 from PMN. These results suggest the involvement of PKC and the calmodulin pathway. A very sensitive method for measuring C3 activity was developed which enabled us to show for the first time that C3 secreted by PMN had opsonizing activity and that particles cultured with PMN were phagocytosed effectively.
Animals↗
[Kinetics of the complement subcomponent C1q production of peritoneal macrophages in NZB/W F1 female mice].
To clarify the role of local production (exohepatic) of complement on primary host defense mechanisms against microbial infections in the host who decreased the amount of complement in serum, the kinetics of the complement production by the complement-producing cells in exohepatic tissue was examined by measuring the amount of C1q, subcomponent of the first complement component, in cultured supernatant of the monolayer of peritoneal macrophages (PM phi) collected from 5, 15, 35, and 48 weeks-old female mice of NZB/W F1 (B/W F1). The C1q production of PM phi in B/W F1 mice showed remarkable decrease at 15 weeks-old. After that, however, the C1q producibility of PM phi recovered gradually and, at mice 48 weeks old, the complement produced finally exceeded the amount observed in mice 5 weeks-old, contrariwise the C1q values in serum were significantly lowering in the same aged mice. The increased production of C1q of PM phi was observed in both 35 and 48 weeks-old mice, of which the value corresponded with increase of anti-nuclear antibody titer in serum and of the amount of protein in urine. On female mice of ddY (control), the amount of C1q production of PM phi in 5 weeks-old mice was two-fold higher than that of 5 weeks-old B/WF1 mice. But at 15 weeks, the production showed a 1/2 decrease in that of mice 5 weeks-old and the decreased values were kept to 35 weeks-old.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Stability of meropenem and effect of 1 beta-methyl substitution on its stability in the presence of renal dehydropeptidase I.
The stability of meropenem in the presence of renal dehydropeptidase I (DHP-I) varied extremely with the animal source of the enzyme. Meropenem, compared with imipenem, was rather easily hydrolyzed by DHP-Is from mice, rabbits, and monkeys, while it showed a higher resistance to guinea pig and beagle dog DHP-Is. In addition, meropenem was four times more resistant than imipenem to human DHP-I. The 1 beta-methyl substituent on carbapenems, i.e., meropenem and 1 beta-methyl imipenem, made them considerably more resistant to mouse and swine DHP-Is than the 1-unsubstituted derivatives are.
Animals↗
Insulin secretion from ob/ob mouse pancreatic islets: effects of neurotransmitters.
Effects of glucose, acetylcholine, and norepinephrine on insulin secretion from pancreatic islets of 8- to 9-wk-old female genetically obese (ob/ob) and lean mice were determined. The ob/ob islets were 60% larger in diameter than lean mouse islets, secreted fourfold more insulin in response to glucose, and secreted insulin at lower glucose concentrations than lean islets. In the presence of 15 mM glucose, ob/ob islets showed an 8-fold greater absolute increase in insulin secretion in response to acetylcholine and a 12-fold greater absolute decrease in insulin secretion in response to norepinephrine inhibition compared with lean islets. In the presence of 5 mM glucose, acetylcholine increased insulin secretion by threefold from ob/ob islets with no effect on lean islets. When both ob/ob and lean islets were stimulated by glucose to equivalent levels of insulin secretion, acetylcholine potentiated glucose-induced insulin secretion equally in ob/ob and lean islets. Enhanced glucose-induced responsiveness of ob/ob islets thus can explain the greater acetylcholine potentiation of insulin secretion and probably the greater norepinephrine inhibition of insulin secretion in ob/ob islets compared with lean islets. These data are consistent with the hypotheses that the major alteration in ob/ob mouse islets is in glucose sensitivity and responsiveness, which subsequently increases ob/ob islet susceptibility to neural regulation of insulin secretion.
Acetylcholine↗
Beta-lactamase stability and inhibitory activity of meropenem combined with a potent antibacterial activity.
The affinity of meropenem for various known types of beta-lactamases and its stability to them were tested in comparison with other beta-lactams, including imipenem. Meropenem exhibited a marked stability to all beta-lactamases tested and was only hydrolyzed by Xanthomonas maltophilia beta-lactamase, as were other beta-lactams. This was responsible for the potent antibacterial activities of meropenem against beta-lactamase-producing strains. Meropenem and imipenem had almost the same, relatively high affinity for beta-lactamases; however, they had a lower affinity than clavulanic acid for penicillin beta-lactamases and cefoxitin for cephalosporin beta-lactamases. Meropenem also had higher beta-lactamase inhibitory activity than imipenem. Meropenem inhibited type III (TEM-1), Ia Citrobacter freundii and Ic Proteus vulgaris beta-lactamases in a progressive manner. Meropenem was thought to be a potent inhibitor of various beta-lactamase because of its ability to form stable enzyme-meropenem acyl-complexes. Meropenem generally exhibited a lower induction potential than imipenem against five clinical isolates of C. freundii, Enterobacter cloacae and Pseudomonas aeruginosa, but its induction potential was higher than that of ceftazidime. Meropenem induced beta-lactamases at concentrations above the MIC.
Bacteria↗
Metabolic response to treatment with cold, paraquat, or 3-amino-1,2,4-triazole in leaves of winter wheat.
We treated leaves of winter wheat (Triticum aestivum L.) with cold, paraquat, or 3-amino-1,2,4-triazole and compared the responses. We assayed the activities of glucose-6-phosphate dehydrogenase, catalase, dehydroascorbate reductase and ascorbate free radical reductase and levels of hydrogen peroxide, glucose-6-phosphate, fructose-6-phosphate, ascorbate, dehydroascorbate, reduced and oxidized glutathione. With any of the three treatments, contents of cellular peroxides and hexose phosphates were raised. The content of ascorbate was lowered markedly by paraquat treatment, which produces active oxygen species, whereas such a decrease did not occur in other two treatments. When the plants were treated with 3-amino-1,2,4-triazole, which is a specific inhibitor of catalase, the content of oxidized glutathione increased severalfold. The glucose-6-phosphate dehydrogenase activity increased with all three treatments, but it decreased after glyphosate treatment, which does not stimulate the formation of peroxides. The activities of catalase and dehydroascorbate reductase were increased by the treatment of cold and paraquat, while 3-amino-1,2,4-triazole did not affect the dehydroascorbate reductase activity. The activity of ascorbate free radical reductase increased after treatment by paraquat only.
Amitrole↗
The role of complement receptors in tumor cell destruction.
Murine peritoneal macrophages exuding early after stimulation with the activators of the alternative complement pathway are able to destroy some of the tumor cells. This destruction is inhibited by anti-Mac-1 and anti-C3. The tumor cell killing needs longer incubation time (> 15 hr), and anti-Mac-1 affects the reaction even if it were put into the reaction mixture at later time of incubation. The results suggest that complement produced by macrophage is deposited onto target cells, and the complement binding targets interact with macrophages through the complement receptor type 3 (CR3), which leads to the cell destruction. It is known that fully activated macrophages kill the tumor cells with the aid of antibody (ADCC) or lectin, but we show here another route of tumor cell destruction, that is, some sort of incompletely activated macrophages can kill some type of tumor cells in cooperation with endogenous complement and complement receptors (CR3) without participation of antibody.
Animals↗
[Clinical significance of recombinant human granulocyte colony-stimulating factor (rG-CSF) in the chemotherapy of patients with malignant lymphoma].
We examined the effects of recombinant human granulocyte colony-stimulating factor (rG-CSF) on neutropenia induced by chemotherapy in 10 patients with non-Hodgkin's lymphoma (NHL). The numbers of peripheral blood hematopoietic progenitors were also evaluated before and after administration of rG-CSF. Six patients received an administration of 2 micrograms/kg/body weight of rG-CSF subcutaneously for 14 days after 2nd chemotherapy. Four patients received intravenous infusion of rG-CSF (300 micrograms/body/day) for 4 days from nadir state after chemotherapy. Administration of rG-CSF from the termination of chemotherapy, markedly shortend the period of bone marrow hypoplasia induced by chemotherapy. On the other hand, administration of rhG-CSF from nadir state after chemotherapy have accelerated the recovery of neutrophil counts. In addition, this type of therapy induced 26 to 60 folds increase of peripheral blood hematopoietic progenitors. These results demonstrate the validity of administration of rhG-CSF not only in the chemotherapy of NHL, but also in peripheral blood stem cell transplantation (PBSCT).
Adult↗
[Sharp decline in plasma CEA and reduction of liver metastasis after UFT administration in a patient with recurrent gastric cancer].
Carcinoembryonic antigen (CEA) in plasma is useful for the detection of recurrent colonic or gastric cancer and the monitoring of plasma in patients with recurrent cancer displaying therapeutic effect. We report a sharp decline of CEA in a patient with recurrent gastric cancer by 6 months oral administration of UFT. The patient was an 81-year-old male who had undergone gastrectomy for advanced gastric cancer. Eight months post-operatively, the plasma CEA began to rise logarithmically, and recurrent tumor in the remnant stomach and liver metastasis were detected by fibergastroscope (FGS) and abdominal CT. After administration of UFT at a dose of 300 mg per day, CEA abruptly declined logarithmically and normalized in 6 months. Presently marked reduction of recurrent foci and metastases were found by FGS and abdominal CT. Therefore sequential changes in plasma CEA in this patient can be considered to reflect the effect of therapy for recurrent gastric cancer by UFT.
Adenocarcinoma↗
[Translation of Tabulae Anatomicae in the 19th century and international competition].
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Anatomy↗