Loop algorithms for quantum simulations of fermion models on lattices.
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Journal Article↗
Biomedical subjects
N Kawashima
Publications and source records attributed to N Kawashima.
Reduction in ATP-sensitive potassium channel-mediated antinociception in diabetic mice.
To test our hypothesis that the abnormally low efficacy of mu-opioid agonists in diabetic mice may be due to functional changes in ATP-sensitive potassium channels, we evaluated the effects of cromakalim on the tail-flick latencies in diabetic and non-diabetic mice. Anti nociceptive effects of morphine (10 micrograms, ICV) in diabetic mice were significantly less than that in non-diabetic mice. Morphine-induced antinociception in non-diabetic mice was antagonized by pretreatment with glibenclamide (30 micrograms, ICV), an ATP-sensitive potassium channel blocker. Cromakalim (0.3 and 1 micrograms, ICV) produced significant, dose-dependent antinociception in non-diabetic mice, which was significantly reduced by pretreatment with glibenclamide. However, cromakalim did not markedly affect the tail-flick latencies in diabetic mice, even at higher doses (3 micrograms, ICV). On the other hand, [D-Pen2,5]enkephaline (DPDPE, 5 micrograms, ICV), a selective delta-opioid receptor agonist, produced significant antinociception in both diabetic and non-diabetic mice. Since pretreatment with glibenclamide significantly reduced the antinociceptive effect of DPDPE in non-diabetic mice but not in diabetic mice, delta-opioid receptor-mediated antinociception in diabetic mice may be independent of potassium channels. These results suggest that dysfunction of ATP-sensitive potassium channels may contribute to the demonstrated poor antinociceptive response of diabetic mice to mu-opioid agonists.
Adenosine Triphosphate↗
Effects of an apovincaminic acid derivative VA-045 on neuronal activity in rat brain stem reticular formation.
Extracellular single unit and spontaneous cortical electroencephalographic (ECoG) recordings were made in the brain stem reticular formation (RF) and the frontal cortex, respectively, of urethane-anesthetized rats. VA-045, an apovincaminic acid derivative had no significant effects on the spontaneous firing rate of the RF neurons and ECoG. Closed head injury (CHI) was induced by dropping a 400 g weight through a tube from 70 cm on a steel helmet placed on the vertex. CHI led to a reduction in the firing rate of RF neurons and ECoG synchronization. VA-045 dose-dependently reversed the CHI-induced decrease in the firing rate of RF and led to ECoG desyncronization. Clonidine, an alpha 2 adrenoceptor agonist, and scopolamine, a muscarinic receptor antagonist, also reduced the firing rate of RF neurons and led to ECoG synchronization. VA-045 dose-dependently antagonized the effects of clonidine, but not the effects of scopolamine on RF neuronal activity and ECoG. Thus, VA-045 has an ameliorating effect on the CHI-induced depression of neuronal activity in the RF. A central alpha 2 adrenoceptor antagonistic action may be involved.
Animals↗
Distribution of Ia antigen-expressing nonlymphoid cells in various stages of induced periapical lesions in rat molars.
Periapical lesions were experimentally produced in rat lower first molars by exposing the pulp to the oral environment for 1 to 56 days. Temporal changes in the number and distribution of la antigen-expressing nonlymphoid cells in the periapical tissue were examined immunohistochemically on decalcified cryostat sections using OX6, a monoclonal antibody against rat la antigen. Influx of la-positive exudative cells into the periapical tissue was observed from 1 day postoperatively. Between 14 and 28 days when expansion of the periapical lesion was most evident, numerous la-positive macrophage-like and dendritic cell-like cells of diverse morphologies were found in the periapical tissue. The number of these cells showed further increase at 56 days postoperatively, when the lesion expansion had ceased. These results suggest the involvement of la antigen-expressing nonlymphoid cells in the development and perpetuation of periapical pathosis. They may act primarily as antigen-presenting cells, which are essential for the initiation of antigen-specific immune defense.
Animals↗
[Case of secondary carnitine deficiency (in a patient undergoing hemodialysis), developing rhabdomyolysis due to dehydration and the action of a hypolipemic agent].
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Adult↗
The effects of cyclosporine on morphine-induced antinociception in diabetic mice.
The effects of cyclosporine on the antinociceptive effect of morphine were examined in diabetic mice. Sensitivities to the antinociceptive effect of morphine (5 mg/kg s.c.) in diabetic mice which had been pretreated with cyclosporine (30 mg/kg per day s.c.) for 14 days returned to those in vehicle-treated nondiabetic mice. Naive mice which had been injected with the supernatant of spleen cell homogenate (SSCH) from vehicle-treated diabetic mice were less sensitive to morphine-induced antinociception. However, adoptive transfer of SSCH from cyclosporine-treated diabetic mice to naive mice had no effect on the recipients' antinociceptive sensitivities to morphine. These results suggest that the abnormal antinociceptive effect of morphine and the immune responses of diabetic mice may somehow be related.
Analgesics↗
Effect of diabetes on the antinociceptive effect of beta-endorphin.
We examined whether streptozotocin-induced diabetes can modulate beta-endorphin-induced antinociception in mice. While beta-endorphin administered i.c.v. produced a dose-dependent inhibition of the tail-flick response in both diabetic and non-diabetic mice, the antinociceptive response was greater in diabetic mice than in non-diabetic mice. The ED50 value of beta-endorphin administered i.c.v. in diabetic mice was significantly lower than that in non-diabetic mice. The antinociceptive effects of beta-endorphin administered i.c.v. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of naltrindole, a selective delta-opioid receptor antagonist. beta-Endorphin administered i.t. also produced a dose-dependent antinociception in both diabetic and non-diabetic mice. However, the ED50 value of kappa-opioid receptor antagonist. On the other hand, the antinociceptive potency of DPDPE, a selective delta-opioid agonist, administered i.t. is significantly increased in diabetic mice, as compared with non-diabetic mice, whereas, the antinociceptive potency of U-50,488H, a kappa-opioid receptor agonist, administered i.t. is significantly less than in non-diabetic mice. These results suggest that diabetes may modulate beta-endorphin-induced antinociception differently at the spinal and supraspinal levels.
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
Antinociceptive effects of intrathecally administered endothelin-1 in mice.
Intrathecal administration of endothelin-1 (ET-1) produced dose-dependent antinociceptive effects in the tail-flick test. The antinociceptive effects of ET-1 were attenuated significantly by pretreatment with naloxone and the delta receptor-selective antagonist naltrindole. The antinociceptive effects of ET-1 were also significantly attenuated by pretreatment with verapamil, an L-type Ca(2+)-channel blocker. These results suggest that the mechanism underlying the antinociceptive effects of ET-1 involves mediation, at least in part, by Ca(2+)-induced release of endogenous opioids, which act on delta-opioid receptors.
Animals↗
Possible involvement of mu 2-mediated mechanisms in mu-mediated antitussive activity in the mouse.
The effect of pretreatment with naloxonazine on mu-opioid agonist-mediated antitussive effects was studied in mice. The antitussive effects of [D-Ala2, MePhe4, Gly-ol5]enkephalin (DAMGO) and morphine were significantly antagonized by naloxone pretreatment, 1 mg/kg given i.p. 5 min earlier, but not by naloxonazine pretreatment, 35 mg/kg given s.c. 24 h earlier. In contrast, the antinociceptive effects of these mu agonists, as determined by the tail-flick method, were significantly reduced by pretreatment with both naloxone and naloxonazine. These results suggest that mu 2 rather than mu 1 mechanisms are involved in mu-mediated antitussive effects.
Analgesics↗
Long-term follow-up of patients with Duchenne muscular dystrophy receiving ventilatory support.
We, retrospectively, examined the clinical course, decline in pulmonary function, and requirements for ventilatory assistance in 54 patients with Duchenne-type muscular dystrophy (DMD) who were followed in the muscle disease ward of the National Hospital in Kagoshima, Japan, over the past 20 years. The percentage of the predicted vital capacity (%VC) declined in relation to age and stage of disease. Most patients required assisted ventilation when the %VC fell below 10%. Twenty patients were treated with a negative pressure chest respirator. Six of these died at the mean age of 23.2 years after being on the respirator for a mean period of 18 months. Fourteen patients are surviving at a mean age of 23.5 years after being on the respirator for a mean period of 39 months.
Adolescent↗
Activation of central ATP-sensitive potassium channels produces the antinociception and spinal noradrenaline turnover-enhancing effect in mice.
ICV cromakalim, a K+ channel opener, produced antinociception. This effect was completely antagonized by ICV glibenclamide, a selective adenosine triphosphate-sensitive K+ channel (KATP channel) blocker. Furthermore, direct opening of central KATP channels by ICV cromakalim increased the spinal noradrenaline (NA) turnover. On the other hand, the antinociception induced by ICV morphine (mu opioid agonist), but not ICV U-50,488H (kappa opioid agonist) was markedly potentiated by cromakalim. These findings suggest that the opening of central KATP channels may elicit the antinociceptive effect and activate the descending NAergic pathway, and central KATP channels play an important role as a modulator of the antinociception induced by mu agonists but not kappa agonists.
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
The effect of chronic treatment with naltrindole, a selective delta-opioid antagonist, on mu-opioid receptor-mediated antinociception in diabetic mice.
The effects of chronic treatment with naltrindole (NTI), a selective delta-opioid receptor antagonist, on the antinociceptive effects of mu-opioid agonists, such as morphine and [D-Ala2, N-MePhe4, Gly-ol(5)]enkephalin (DAMGO) were examined in diabetic mice. Antinociception induced by morphine (10 micrograms, ICV) and DAMGO (0.5 microgram, ICV) was significantly lower in diabetic mice than in non-diabetic mice. The low sensitivities to the antinociceptive potencies of ICV morphine (10 micrograms) and DAMGO (0.5 micrograms) in diabetic mice were reversed compared with those in saline-treated non-diabetic mice when diabetic mice had been pretreated with NTI (2 mg/kg per day, SC) for 14 days. Naive mice which had been injected with spleen mononuclear cells from saline-treated diabetic mice were less sensitive to DAMGO-induced antinociception. However, adoptive transfer of spleen mononuclear cells from NTI-treated diabetic mice to naive mice had no effect on the recipients' antinociceptive sensitivity to DAMGO. These results suggest that the effect of NTI on the sensitivity to mu-opioid agonists in diabetic mice may be due to the immunosuppressive effects of NTI.
Analgesics↗
Immunohistochemical detection of prostaglandin I2 synthase in various calcified tissue-forming cells in rat.
Localization of prostaglandin (PG) I2 synthase immunoreactivity was examined in demineralized sections of rat pulpal, periodontal and skeletal tissues using isn-1, a monoclonal antibody raised against the enzyme. Various calcified tissue-forming cells, i.e. odontoblasts, osteoblasts, osteocytes, cementoblasts, cementocytes and chondrocytes, were similarly immunoreactive for PGI2 synthase, suggesting that they are capable of producing PGI2. In odontoblasts and chondrocytes, the reactivity increased gradually with maturation. Weak immunoreactivity was also observed in endothelial cells and fibroblast-like cells in pulpal and periodontal tissues. However, no reactivity was seen in ameloblasts. These results suggest the possible involvement of PGI2 in the regulation of the metabolism of various calcified tissues. Monoclonal antibodies such as isn-1 may become useful markers of the maturation of calcified tissue-forming cells of mesenchymal origin.
Animals↗
Serum glucose level-dependent and independent modulation of mu-opioid agonist-mediated analgesia in diabetic mice.
We examined the effect of insulin on the analgesic potency of DAMGO, a selective agonist of mu-opioid receptors, in mice which had been rendered diabetic by an injection of streptozotocin (STZ; 200 mg/kg, i.v.) 1 and 2 weeks previously. The analgesic potency of DAMGO, based on the tail-flick test, was significantly decreased in both the 1 and 2-week diabetic mice as compared to its effect in age-matched controls. Sensitivity to the analgesic potency of DAMGO returned to normal when insulin was administered to STZ-induced 1-week diabetic mice. However, pretreatment with insulin had no significant effect on the sensitivity to the analgesic potency of DAMGO in 2-week diabetic mice. These results suggest that the serum glucose levels may possibly be responsible for the altered potency of mu-opioid agonists only during the incipient stages of diabetes.
Analgesics↗
Primary Sjögren's syndrome with subcortical dementia.
A 48-year-old man with primary Sjögren's syndrome (P-SS) developed subcortical dementia, characterized by forgetfulness, poor attention and concentration, slowness of thought process, difficulty to manipulate acquired knowledge, introversive and hostile personality change and inactivity. These were improved by corticosteroid treatment. Magnetic resonance imaging (MRI) revealed small lesions in the subcortical and periventricular white matter. An electroencephalogram (EEG) revealed short runs of theta activities in bilateral parietal areas. Latency of P300 shortened in accordance with clinical improvement. These findings suggest that the cognitive and neuropsychiatric manifestations in P-SS are included in a spectrum of organic brain dysfunction and are treatable.
Brain↗
[Studies on the generation mechanism of non-biological response in distortion product OTO-acoustic emission].
We investigated the effect of non-biological artifacts on the measurement of distortion product oto-acoustic emission (DPOAE) using guinea pigs, and the generation mechanism of this phenomenon is discussed in the present paper. When a sound pressure of a stimulating tone was too large, an overtone was produced within the acoustic probe. When the difference in sound pressure between f1 and f2 was too large, artifacts appeared at frequencies of 2f1-f2 or 2f2-f1. Similar responses were generated when f1 and f2 were identical in sound pressure but exceeded a certain critical level. These non-biological responses could be easily differentiated from biological responses by subjecting the animal to anoxia. The input-output curve of DPOAE was biphasic and clearly showed this critical level in each animal. The results obtained in the present study suggest that the levels of f1 and f2 should be almost equal and should not exceed the observed critical level when measuring DPOAE.
Acoustic Stimulation↗
Effects of diabetes on the antinociceptive effects of intrathecally administered endothelin-1.
Intrathecal administration of endothelin-1 (ET-1) produced a dose-dependent increase in tail-pinch latency, i.e., antinociception, in both diabetic and non-diabetic mice. The dose ranges which produced a significant antinociception in diabetic mice (0.0001 to 0.0003 nmol) were lower than those in non-diabetic mice (0.001 to 0.003 nmol). Furthermore, the antinociceptive effect of ET-1 in diabetic mice was decreased when the doses of ET-1 were increased. Indeed, when ET-1 in a dose of 0.003 nmol, which produced significant antinociception in non-diabetic mice, it had no antinociceptive effect in diabetic mice. These results suggest that the mechanism which underlies the antinociceptive effects of ET-1 is up-regulated in diabetic mice, as compared with that in non-diabetic mice.
Animals↗
Involvement of haloperidol-sensitive sigma-sites in antitussive effects.
The effects of selective sigma-ligands on the capsaicin-induced cough reflex in rats were studied. Intraperitoneal injection of (+)-N-allylnormetazocine ((+)-SKF-10,047) and N,N'-di(ortho-tolyl)guanidine (DTG) in doses that ranged from 0.3 to 3.0 mg/kg decreased the number of coughs dose dependently. The antitussive effects of these sigma-ligands were significantly attenuated by pretreatment with haloperidol. Pretreatment with haloperidol also markedly reduced the antitussive effects of (+/-)-pentazocine and dextromethorphan. These results suggest that haloperidol-sensitive sigma-sites may be involved in the regulation of coughs.
Animals↗