Colon carcinogenesis on the identical litters of WF-Osaka rat strain bred in two different animal rooms.
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Adenocarcinoma↗
Biomedical subjects
K Saeki
Publications and source records attributed to K Saeki.
Induced adenocarcinoma of the ascending colon of ACI rats by intraperitoneal injection of the serum from WF-Osaka cancer carrying rats.
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Adenocarcinoma↗
Involvement of Mu receptors in the opioid-induced increase in the turnover of mouse brain histamine.
The effects of i.c.v. injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5] enkephalin (0.5 microgram i.c.v.) was antagonized by naloxone (0.3 microgram i.c.v.) but not by ICI 174,864 (5 micrograms i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 microgram i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 microgram i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 microgram i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10(-7) and 10(-6) M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10(-6) M) was blocked completely by naloxone (10(-6) M) but not by tetrodotoxin (10(-6) M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.
Animals↗
[Prevention of immunodeficiency induced by cancer chemotherapy with BCG].
MFC (MMC, 5-FU and cytosine-arabinoside) therapy applied with the liver organism Bacillus Calmette-Guérin (BCG) for the treatment of postoperative patients with cancer of the digestive organs presenting at stage II and III. Immunological parameters included skin reaction by purified protein derivative (PPD), lymphatic blastogenesis test using phytohemagglutinin (PHA) and lymphatic subsets. The frequency of MFC therapy was significantly higher in the MFC plus BCG group than in the MFC group (p less than 0.001). At the completion of MFC therapy, both of PHA blastogenesis rate, OKT4/OKT8 and OKT3 were all within the normal limits. The PPD skin reaction was positive (18.2 +/- 4.0mm) as before the start of MFC therapy. These results suggest that BCG immunotherapy may potentiate the effect of chemotherapy.
Aged↗
Hydrolysis of phosphatidate by human placental alkaline phosphatase.
Highly purified alkaline phosphatase of human placenta catalyzed the hydrolysis of phosphatidate with quantitative formation of almost stoichiometric amounts of diglyceride and inorganic phosphate. In the presence of sodium deoxycholate, the activity was maximal at pH 8.8. The activity was strongly inhibited by L-phenylalanine but scarcely affected by NaF. These results show that alkaline phosphatase hydrolyzes phosphatidate under different conditions from those for activity of phosphatidate phosphohydrolase.
Alkaline Phosphatase↗
Position of the amino terminus of myosin light chain 1 and light chain 2 determined by electron microscopy with monoclonal antibody.
The position of the N terminus of myosin light chain 1 (LC1) and myosin light chain 2 (LC2) of rabbit skeletal muscle was mapped on the myosin head with a monoclonal antibody (SI304), which recognized the amino acid sequence N-trimethylalanyl-prolyl-lysyl-lysyl at the N terminus of LC1 and LC2. The complex of the antibody and myosin was observed by electron microscopy. By selective cleavage of the N terminus of LC1 or LC2 with papain or chymotrypsin, the position of the N terminus of LC1 and LC2 was determined separately. The N terminus of LC2 is located at the head-rod junction. The N terminus of LC1 is 11 nm (+/- 3 nm, standard deviation) from the head-rod junction. This position is near the actin-binding site of the myosin head.
Amino Acid Sequence↗
A novel alkaline phosphatase isozyme in human adipose tissue.
A novel alkaline phosphatase (AP) isozyme was found in human adipose tissue. Adipose tissue alkaline phosphatase differed in enzymatic properties from liver, placental and intestinal alkaline phosphatases. On electrophoresis it showed the same mobility as intestinal alkaline phosphatase, but after treatment with neuraminidase its mobility was decreased to the same as or slightly less than that of neuraminidase-treated liver alkaline phosphatase. Its inhibition by amino acids, inactivation by urea and activation by Mg2+ were almost the same to those of liver alkaline phosphatase. However, at 56 and 65 degrees C it was more stable than liver alkaline phosphatase. Alkaline phosphatase activity was demonstrated histochemically in adipose tissue with naphthol AS-MX phosphate as substrate. It was localized in the wall of blood capillaries, but not present in adipocytes.
Adipose Tissue↗
Effects of pentagastrin and carbachol on the gastric histamine level in alpha-fluoromethylhistidine-treated mice and rats.
The gastric mucosal histamine level in mice increased by about 80% and 100% after fasting for 24 and 48 h, respectively. In non-fasted mice, alpha-fluoromethylhistidine (alpha-FMH), a specific histidine decarboxylase inhibitor, significantly decreased the histamine level, the reduction amounting to 35% and 49%, 2 h and 4 h after treatment, respectively. In mice fasted for 24 h, a significant decrease of 42% was observed 4 h after treatment. However, in mice fasted for 48 h, no significant decrease was seen even 4 h after alpha-FMH treatment. Therefore, the histamine-releasing effect of re-feeding and drugs on the gastric mucosa was examined in vivo, using animals fasted for 48 h and subsequently treated with alpha-FMH. Food given simultaneously with alpha-FMH to 48-h fasted mice significantly decreased the histamine level 4 h later. Pentagastrin and carbachol administered alone (0.25-2.0 mg/kg, i.p.) had no significant effect on the histamine level. However, the combined treatment with these drugs significantly decreased the histamine level. In rats fasted for 48 h and treated with alpha-FMH, pentagastrin (0.25 and 0.5 mg/kg, i.p.) but not carbachol (0.125-0.5 mg/kg, i.p.) caused a significant decrease in the mucosal histamine level. In contrast to mice, the effect of the combined treatment with pentagastrin and carbachol was not synergistic in rats. These findings suggest that gastrin acts synergistically with acetylcholine in the histamine release from the gastric mucosa in mice, whereas such synergism may not occur in rats.
Animals↗
Effects of halothane, enflurane and pentobarbital on brain histamine dynamics in mice.
The effects of halothane, enflurane, ketamine and pentobarbital on brain histamine dynamics were examined in mice. Brain histamine and tele-methylhistamine, a predominant metabolite of brain histamine, were simultaneously measured by high-performance liquid chromatography with fluorescence detection. Anaesthesia with the four agents had no effect on brain histamine content. The tele-methylhistamine content significantly increased during 1 h and 2 h anaesthesia with halothane (0.051 mmol/l or 0.76 mol/l) and 2 h anaesthesia with enflurane (0.11 mol/l or 0.16 mol/l). Enflurane and pentobarbital significantly inhibited the histamine depletion induced by alpha-fluoromethylhistidine (50 mg/kg, intraperitoneally), a specific inhibitor of histidine decarboxylase, suggesting that these agents decrease the histamine turnover. However, halothane and ketamine were ineffective in this respect. These results emphasize that various anaesthetics have different influences on brain histamine dynamics. Since there have been findings suggesting that brain histaminergic systems are involved in physiological functions such as regulation of blood pressure, body temperature and hormone secretion, changes in the brain histamine turnover should be given due attention with regard to physiological changes during anaesthesia.
Anesthetics↗
Involvement of opioid receptors in phencyclidine-induced enhancement of brain histamine turnover in mice.
When the histamine (HA) turnover in the brain of mice was estimated on the basis of the pargyline-induced accumulation of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, the enhancing effect of phencyclidine (PCP) on the HA turnover was antagonized by a large dose of naloxone. However, a dopamine receptor antagonist haloperidol, which is also a potent sigma receptor antagonist, did not inhibit the effect of PCP on the HA turnover. [D-Ala2,D-Leu5]enkephalin, a prototypic delta opioid agonist, markedly enhanced the HA turnover. The effect of this peptide was demonstrated not only when the HA turnover was determined by the pargyline-induced t-MH accumulation but when it was estimated by the HA depletion induced by alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. A sigma agonist, SKF-10047, and a kappa agonist, ethylketazocine, had no PCP-like enhancing effect on the HA turnover. These results suggest that PCP enhances the brain HA turnover in mice by stimulating, probably indirectly, endogenous opioid systems.
Analgesics, Opioid↗
Feeding-related circadian variation in tele-methylhistamine levels of mouse and rat brains.
Circadian changes in the brain histamine (HA) and tele-methylhistamine (t-MH) levels were studied in mice and rats after adaptation to an alternating 12-h light/dark cycle (lights on at 0600). Although there was no significant circadian fluctuation of the brain HA levels, the levels of t-MH, a major metabolite of brain HA, showed a marked circadian variation. In mice, the t-MH levels were about 80 ng/g from 1200 to 1800 but about two times higher values were obtained from 2400 to 0600 of the next morning. In rats, the t-MH levels ranged from 24 to 28 ng/g at 0600 and 1200, slightly increased at 1800, and reached at 2400 a peak twice as high as the levels seen during the light period. The t-MH levels again rapidly decreased during the subsequent 3 h. In mice fasted from 1200, the t-MH levels did not increase during the period of darkness. When mice were fed at 1200 after a 24-h fast, a significant increase in the t-MH levels was observed at 1800. There was no significant circadian variation of the HA and t-MH levels in the plasma of mice and rats. These results suggest that circadian variation in brain t-MH levels is related to feeding and possible subsequent changes in elimination of t-MH from the brain and/or turnover of HA in the brain. This phenomenon should be given due attention when HA dynamics in the brain are being assessed.
Animals↗
Differentiation between eclampsia and cerebrovascular disorders by brain CT scan in pregnant patients with convulsive seizures.
Six pregnant women with convulsions between 25 to 40 weeks of gestation were experienced. Among them, 4 patients were diagnosed as having intracranial hemorrhage and two as simple eclampsia. With the aid of brain CT scan, one case of arteriovenous malformation was detected and treated surgically with good prognosis for both the mother and the fetus. Two patients were diagnosed to have cerebral hemorrhage with subsequent penetration into the lateral ventricles and were treated conservatively. Their fetuses were delivered alive by cesarean section, but the mothers expired. The other patient with cerebral hemorrhage was treated surgically, and both the mother and the fetus survived. One of the simple eclampsia patients was noted to have a growth retarded fetus at 32 weeks of pregnancy with subsequent intra-uterine death, but the mother recovered after conservative treatment. Another patient at 40 weeks of pregnancy was also treated conservatively and both the fetus and the mother survived. Brain CT scan findings differed between these two eclampsia patients; local brain edema for the second patient and generalized brain edema for the first patient. Thus more active application of brain CT scan is recommended in managing pregnant patients with convulsions.
Adult↗
Mechanism of the central hyperglycemic action of histamine in mice.
The effect of i.c.v. administration of histamine (HA) on the plasma glucose level was examined in mice. HA (0.09-180 nmol) increased dose-dependently the plasma glucose level, 30 min after the injection. Even a low dose of 0.45 nmol produced a significant effect. The pretreatment with metoprine, an inhibitor of HA-N-methyltransferase, heightened the peak of the hyperglycemic response markedly and prolonged the duration. Systemic administration of the H1-receptor antagonists mepyramine (0.5-2 mg/kg), chlorpheniramine (1-4 mg/kg) and promethazine (1-4 mg/kg), inhibited dose-dependently the HA-induced hyperglycemia, whereas an H2-receptor antagonist, cimetidine (80 nmol i.c.v.), was without effect. The hyperglycemic response to HA disappeared in bilaterally adrenalectomized mice. Although the treatment of mice with metyrapone reduced the plasma corticosterone level to less than 15% of the control value, the hyperglycemic response to HA was still observed. After the administration of HA, there was a significant elevation of plasma norepinephrine levels. Increase in the plasma epinephrine was more marked than the norepinephrine response. Pretreatment with phentolamine (5 mg/kg i.p.) but not propranolol (15 mg/kg i.p.) inhibited the HA-induced hyperglycemia by about 50% and the combination of same doses of phentolamine and propranolol blocked the response completely. These results suggest that the central hyperglycemic effect of HA is produced mainly by an increase in the sympathetic outflow, followed by an increase in catecholamine secretion from the adrenal medulla. It is likely that the stimulation of H1, but not H2, receptors in the brain is involved in this response.
Adrenalectomy↗
Involvement of opioid and non-opioid mechanisms in footshock-induced enhancement of brain histamine turnover in mice.
Naloxone (1-10 mg/kg, i.p.) dose-dependently inhibited the footshock-induced elevation in levels of tele-methylhistamine (t-MH), a predominant metabolite of brain histamine (HA), although this compound had no effect on the HA dynamics in the non-shocked control mice. Footshock significantly enhanced the HA depletion induced by alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. However, in mice treated with naloxone (5 mg/kg, i.p.) footshock did not significantly facilitate the alpha-fluoromethylhistidine-induced HA depletion. In mice which had been rendered morphine-tolerant following an s.c. implantation of a pellet containing 50 mg of morphine base 3 days before, footshock produced no significant elevation of the t-MH level. The treatment with alpha-methyl-p-tyrosine, p-chlorophenylalanine or atropine had no significant influence on the footshock-induced t-MH elevation. The t-MH elevation was the most marked in the midbrain. In the hypothalamus and pons-medulla oblongata, no significant change in the t-MH level was produced by footshock. These results suggest that footshock increases the HAergic activity in the mouse brain partly through activation of opioid-related mechanisms and that alterations in HA dynamics differ with region of the brain.
Animals↗
Preliminary crystallographic study of a ribulose-1,5-bisphosphate carboxylase-oxygenase from Chromatium vinosum.
Crystals of a ribulose-1,5-bisphosphate carboxylase-oxygenase from Chromatium vinosum were obtained with the hanging-drop vapor diffusion technique, using polyethylene glycol 4000 as precipitant. The crystal belongs to the cubic system, space group I432, with unit cell dimension a = 245.9 A. An asymmetric unit includes one-quarter (L2S2, L: large subunit, S: small subunit) of a hexadecameric molecule (L8S8, 544,000 Mr), which is located on the crystallographic point symmetry 222 or 4. The crystal diffracts to at least 3.0 A resolution.
Chromatium↗
Diazepam-induced decrease in histamine turnover in mouse brain.
The effect of diazepam on brain histamine turnover was examined in mice. The steady state levels of histamine and tele-methylhistamine remained unchanged following the i.p. administration of 0.2-20 mg/kg of diazepam. However, diazepam in doses over 5 mg/kg significantly decreased histamine turnover, as estimated from the accumulation of tele-methylhistamine after pargyline treatment. Other benzodiazepines such as chlordiazepoxide, nitrazepam and estazolam in high doses also decreased histamine turnover. The inhibitory effect of diazepam on histamine turnover was antagonized by the pretreatment with a benzodiazepine antagonist Ro 15-1788. The histamine turnover was significantly inhibited by 2 mg/kg of muscimol. Diazepam (0.2-1 mg/kg) markedly and dose-dependently potentiated the inhibitory effect of 1 mg/kg of muscimol from non-significant to highly significant levels. The potentiation by diazepam was also antagonized by Ro 15-1788. Therefore, diazepam probably decreases histamine turnover in the brain via the benzodiazepine-GABA receptor complex.
Animals↗
Brain histamine turnover enhanced by footshock.
When footshock was given to mice at 15-s intervals for 30-120 min, there was a significant increase in the brain level of tele-methyl-histamine (t-MH), a predominant metabolite of brain histamine (HA). This footshock-induced elevation of the t-MH level also occurred in mice pretreated with pargyline but not in mice pretreated with metoprine. The footshock facilitated the HA depletion induced by a-fluoromethylhistidine. These results suggest that footshock increases the brain HA turnover.
Animals↗
Comparison of effects of phencyclidine and methamphetamine on body temperature in mice: a possible role for histamine neurons in thermoregulation.
We compared the effects of phencyclidine (PCP) and methamphetamine on body temperature and brain histamine turnover in mice. Methamphetamine at 5 and 10 mg/kg produced dose-related increases in rectal temperature, whereas PCP given in the same doses had no significant effect. In mice pretreated with alpha-fluoromethylhistidine, an inhibitor of histidine decarboxylase, PCP produced a marked hyperthermia. PCP markedly accelerated brain histamine turnover, as measured by the accumulation of tele-methylhistamine, a predominant metabolite of brain histamine, following administration of pargyline. Methamphetamine had no significant effect on the histamine dynamics. These results suggest involvement of brain histaminergic neurons in the action of PCP but not methamphetamine, and the presence of a histaminergic thermoregulatory mechanism.
Animals↗