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Biomedical subjects

Y Noda

Publications and source records attributed to Y Noda.

At least 217 records · Page 12Linked to original sources
PubMed1997

[Fulminant subacute sclerosing panencephalitis: clinical and neuropathological observations].

We describe a 3-year-old boy with subacute sclerosing panencephalitis (SSPE) who died 4 months after its onset. His initial symptoms were drowsiness and left hemiplegia. He became comatose in 10 days, and developed a decortical posture after 45 days. He suffered from multiple cerebral hemorrhage and infarction 3 months later. Oligodendrocytes were positively stained by immunocytochemical stain with a complement-fixing measles antibody. Light microscopy revealed glial nodules, perivascular cuffing and reactive gliosis. Small arteries showed intimal thickening with resultant occlusion and occasional recanalization. These findings suggested vascular involvement in SSPE. This case illustrates the difference between the fulminant and chronic forms of SSPE.

Brain↗
PubMed1997

[Changes in serum anti-Helicobacter pylori IgG antibody, pepsinogen I, and pepsinogen II after eradication therapy of Helicobacter pylori].

To investigate the changes in serum anti-Helicobacter pylori IgG antibody (HP Ab), pepsinogen I (PG I), pepsinogen II (PG II), and pepsinogen I/II ratio (PG I/II) after eradication therapy of Helicobacter pylori (HP), we studied 78 patients with HP-positive peptic diseases. They received combination therapy (proton pump inhibitor + amoxicillin: n = 17, proton pump inhibitor + amoxicillin + clarithromycin: n = 61). In the 68 patients in whom HP was eradicated, HP Ab, PG I, and PG II decreased and PG I/II increased significantly after eradication. Especially, the decrease in PG II and the increase in PG I/II were rapid and remarkable, found 2 months after the beginning of eradication therapy, and then continued. On the other hand, in the patients in whom HP was not eradicated, HP Ab and PG I/II did not change significantly, while PG I and PG II temporarily increased at the end of administration of proton pump inhibitor. In conclusion, it seems that the measurement of PG II and PG I/II is useful for the early detection of HP eradication.

Amoxicillin↗
PubMed1997

Effect of beclomethasone dipropionate inhalation on eosinophilic bronchitis in patients with silicosis.

The efficacy of beclomethasone dipropionate (CAS 5534-09-8, BDP, beclomethasone) inhalation therapy over the course of 12 months were evaluated in 42 patients with established chronic silicosis. Their pulmonary functions were monitored every 3 months and volume of sputum production was established daily. Subjects were divided randomly into two groups; 21 patients (BDP group) were treated with BDP (400 micrograms/day) by way of a metered-dose inhaler, while the 21 controls did not receive the BDP inhalation therapy. Although FVC (forced vital capacity), FEV1 (forced expiratory volume in 1 s), MMEF (maximal mean expiratory flow) and arterial blood oxygen tension did not improve significantly, sputum production significantly decreased in the BDP group. The patients who responded most dramatically to the treatment presented with sputum eosinophilia and elevated serum IgE levels prior to therapy. Pulmonary tuberculosis or exacerbation of chronic airway infection was not observed in any of the patients. These results suggest that corticosteroid inhalation therapy is helpful in the management of chronic silicosis, especially in patients with sputum eosinophilia. Positive atopic factors may be related to the pathogenesis of eosinophilic bronchitis, a complication of chronic silicosis.

Aged↗
PubMed1996

In vivo functional interaction between phencyclidine binding sites and sigma receptors to produce head-weaving behavior in rats.

To investigate the in vivo functional interaction between phencyclidine (1-(1-phenylcyclohexyl)piperidine; PCP) binding sites and sigma receptors, we examined the effects of sigma receptor ligands on stereotyped head-weaving behavior induced by PCP, a putative PCP/sigma receptor ligand, and (+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclo-hepten-5,10-imin e ((+)-MK-801; dizocilpine), a selective PCP binding site ligand, in rats. PCP (7.5 mg/kg, i.p.)-induced head-weaving behavior was inhibited by both N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)-phenyl]-ethylamine (NE-100; 0.03-1.0 mg/kg, p.o.), a selective sigma1 receptor ligand, and alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperidine butanol (BMY-14802; 3 and 10 mg/kg, p.o.), a prototype sigma receptor ligand, in a dose-dependent manner, whereas NE-100 (0.1-1.0 mg/kg, p.o.) and BMY-14802 (3 and 10 mg/kg, p.o.) did not inhibit dizocilpine (0.25 mg/kg, s.c.)-induced head-weaving behavior. These results suggest that NE-100 and BMY-14802 act via sigma receptors. Dizocilpine-induced head-weaving behavior was potentiated by 1,3-di-o-tolyl-guanidine (DTG; 0.03-0.3 microg/kg, i.v.) and (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-3-PPP; 3 and 6 mg/kg, i.p.), sigma1/sigma2 receptor ligands, as well as by (+)-N-allyl-normetazocine ((+)-SKF-10,047: 8 mg/kg, i.p.), a sigma1 receptor ligand, while DTG (0.3 microg/kg, i.v.), (+)-3-PPP (6 mg/kg, i.p.) and (+)-SKF-10,047 (8 mg/kg, i.p.) did not induce this behavior. Potentiation of dizocilpine-induced head-weaving behavior by DTG (0.3 microg/kg, i.v.), (+)-3-PPP (6 mg/kg, i.p.) and (+)-SKF-10,047 (8 mg/kg, i.p.) was completely blocked by NE-100 (0.1 mg/kg, p.o.) and BMY-14802 (10 mg/kg, p.o.). These results suggest that PCP binding sites and sigma receptors are involved in PCP-induced head weaving behavior, and that sigma1 receptors play an important role in modulation of the head-weaving behavior.

Animals↗
PubMed1996

Acute phencyclidine induces aversion, but repeated phencyclidine induces preference in the place conditioning test in rats.

Phencyclidine (PCP) is a drug that has been widely abused in the past two decades. PCP produces place aversion, but not preference, in the place conditioning test. The present study examined PCP-induced place conditioning behavior in rats treated with PCP repeatedly. In naive rats, PCP (2-8 mg/kg i.p.) dose dependently produced place aversion, but did not produce any effect in rats treated with PCP (10 mg/kg i.p.) for 14 days. indicating that tolerance developed to PCP-induced place aversion on repeated PCP treatment. In rats treated with PCP (10 mg/kg i.p.) for 28 days, PCP (2-8 mg/kg i.p.) dose dependently produced place preference. These findings suggest that some changes in neuronal function induced by the repeated PCP treatment may play an important role in the addiction to this drug.

Animals↗
PubMed1996

Functional changes in neuronal systems induced by phencyclidine administration.

To analyze the mechanisms of PCP abuse, we investigated the changes in PCP-induced motivational properties and neuronal functions in animals. First, we determined that PCP-induced withdrawal syndrome may, in part, be produced by 5-HTergic neuronal systems. Second, using rats treated with subacute PCP, we established that subacute PCP may produce behavioral changes (stereotyped behaviors and hyperlocomotion), mediated by both dopaminergic, 5-HTergic neuronal, and NO systems. Third, using the place conditioning paradigm, we confirmed that (1) both dopamine-D1 and 5-HT2A receptors, but not sigma receptors, may be involved in PCP-induced place aversion, and (2) subacute PCP produces place preference. Finally, we demonstrated that subacute PCP may produce neurochemical changes (the number of 5-HT2A receptors, dopamine turnover, NO synthesis, and immediate early gene expression). These results suggested that several neuronal changes may be related to behavioral changes induced by subacute PCP. Furthermore, it is hypothesized that the alternations of several neuronal systems may establish PCP abuse via the changes of the immediate early gene expression and NO activity induced by subacute PCP treatment. Further studies using receptor selective ligands and sensitive probes that could associate with the pharmacological actions of PCP may elucidate the mechanisms of PCP abuse.

Animals↗
PubMed1996

Comparison of dose-dependent enhancing effects of gamma-ray irradiation on urethan-induced lung tumorigenesis in athymic nude (nu/nu) mice ac (nu/+) littermates.

The role of immunological surveillance in carcinogenesis is still controversial. In our previous experiments, urethan-induced lung tumorigenesis in athymic (nu/nu) mice and euthymic (nu/+) littermates was examined, and it was concluded that immunosurveillance mediated by T cells could not be demonstrated. However, the reported enhancement of development of various tumors following ionizing radiation might be achieved through modulating the host immunological conditions. In the present experiment, nu/nu and littermate nu/+ mice were treated with 1-4 Gy gamma-rays alone at 6 weeks of age or treated with urethan at 0.5 mg/g body weight when aged 14 days followed by 1-4 GY gamma-rays 4 weeks later. Lung tumors were assessed at 6.5 months of age. Ionizing radiation itself caused a very low incidence of these lesions. On the other hand, multiplicities and incidences of lung tumors after urethan treatment at 0.5 mg/g body weight were similar between the two phenotypically different groups of mice (1.66 and 1.84 tumors/mouse, 73% and 80% incidences, for nu/nu and nu/+ cases respectively). This urethan-induced lung tumorigenesis was significantly enhanced by gamma-rays in both nu/nu and nu/+ mice, and the magnitude of tumor enhancement was somewhat higher in nu/+ mice than in nu/nu mice, especially with a 2-Gy dose. In conclusion, it may be said that lung tumorigenicity of gamma-ray irradiation itself and the enhancing effect of radiation on urethan-induced tumorigenesis are scarcely influenced by immunosurveillance mechanisms mediated by T cells.

Animals↗
PubMed1996

Reduction in the number of NADPH-diaphorase-positive cells in the cerebral cortex and striatum in aged rats.

Nitric oxide (NO) plays an important role as a diffusible messenger in learning and memory. To determine whether changes in NO production in the brain may be involved in aging-associated brain dysfunction, we measured the performance of aged rats in a radial arm maze task, and carried out histochemical examination of the changes in NADPH diaphorase (NADPH-d)-containing neurons in the brains of aged rats. The performance of aged rats (30 months old) in a radial arm maze task was significantly impaired compared to the performance of young rats (3 months old). The number of neurons containing NADPH-d reactivity in the cerebral cortex and striatum of aged rats was significantly reduced, by approximately 50 and 30 percent, respectively, compared to that in young rats. NO synthase activity in discrete brain regions of aged rats, i.e., in the cerebral cortex, striatum and hippocampus was not different from that in young rats, although the activity in the cerebellum of aged rats was significantly lower than that in young rats. These results suggest that the reduction in the number of NADPH-d-positive cells in the brains of aged rats may be involved in aging-associated learning impairment in rats.

Aging↗
PubMed1996

Role of nitric oxide and cyclic GMP in the dizocilpine-induced impairment of spontaneous alternation behavior in mice.

The activation of N-methyl-D-aspartate receptors induces the synthesis of nitric oxide, which activates soluble guanylate cyclase and leads to the formation of cyclic GMP in the brain. The inhibition of nitric oxide production, as well as the blockade of N-methyl-D-aspartate receptors, has been reported to prevent the induction of hippocampal long-term potentiation and learning and memory formation in vivo, although the effects of inhibitors of nitric oxide synthase are still controversial. We investigated the putative role of nitric oxide and cyclic GMP in dizocilpine-induced memory impairment in mice. The nitric oxide synthase inhibitors, NG-nitro-L-arginine methyl ester and 7-nitro indazole, as well as dizocilpine, a non-competitive N-methyl-D-aspartate receptor antagonist, dose-dependently impaired spatial working memory in mice, assessed by their spontaneous alternation behavior in a Y-maze. The inhibitory effects of both NG-nitro-L-arginine methyl ester and dizocilpine on their behavior were completely reversed by 8-bromo-cyclic GMP. Cyclic GMP levels in the cerebellum were reduced by treatment with dizocilpine. NG-Nitro-L-arginine methyl ester and 7-nitro indazole reduced cyclic GMP levels in the cerebral cortex/hippocampus and cerebellum, and the suppressive effect of NG-nitro-L-arginine methyl ester on cyclic GMP levels in the cerebral cortex/hippocampus was reversed by co-treatment with L-arginine. Cyclic AMP levels in the brain were not affected by treatment with either dizocilpine, NG-nitro-L-arginine methyl ester, or 7-nitro indazole. Neither NG-nitro-L-arginine methyl ester nor L-arginine had any effect on monoamine and acetylcholine metabolism in the brain. These results suggest that the reduction in nitric oxide/cyclic GMP production in the brain may be responsible for dizocilpine-induced impairment of spontaneous alternation behavior in a Y-maze.

Animals↗
PubMed1996

Guanidino compounds generate reactive oxygen species.

Methylguanidine, guanidinoacetic acid and guanidinosuccinic acid are endogenous substances in body tissues. Extremely high levels of these substances are known to be related to the pathogenesis of epilepsy and renal failure such as uremia. In this study it was demonstrated that methylguanidine, guanidinoacetic acid and guanidinosuccinic acid, and arginine generate hydroxyl radicals in aqueous solution. These findings suggest that a high level of guanidino compounds accumulating near or within cells such as neurons (in an epileptogenic focus) or nephrons (in uremic patients) may cause free radical damage leading to these clinical disorders. Arginine may have a similar role in the pathogenesis of hyperarginemia.

Electron Spin Resonance Spectroscopy↗
PubMed1996

Reconstruction of two-dimensional current distribution from tangential MCG measurement.

We describe a two-dimensional reconstruction method for tangential magnetocardiograms (MCGs). This method is based on two-dimensional Fourier analysis, and we used a new type of window function for tangential MCG to solve the problem of the small number of measurement points. By using this method, cardiac activity can be estimated as a two-dimensional current distribution. To determine the effectiveness of this method, we measured tangential MCGs of normal subjects, and compared the estimated current distribution with the actual cardiac muscle activity. Using this method, we were able to clearly show cardiac activity.

Adult↗
PubMed1996

Age of onset of posterior vitreous detachment.

Recently published literature on the onset of posterior vitreous detachment is reviewed here. Aging causes posterior vitreous detachment, and its prevalence increases proportionally with age. The onset of posterior vitreous detachment is associated with refractive error. Investigation of the prevalence and onset age of posterior vitreous detachment indicates that the higher the degree of myopia, the earlier the onset age. There are some reports on the onset age of posterior vitreous detachment in men compared with women. One indicates that posterior vitreous detachment occurs earlier in women, and another reports no difference. No difference has been found between blacks and whites or between whites and Japanese.

Age Factors↗
PubMed1996

Role of nitric oxide in the development of tolerance and sensitization to behavioural effects of phencyclidine in mice.

1. To determine whether nitric oxide (NO) was involved in tolerance and sensitization to the effects of phencyclidine (PCP), we examined NO synthase activity and the number of NADPH-diaphorase (NADPH-d)-positive cells in discrete brain regions of saline-, acute PCP- and repeated PCP-treated mice. We also investigated the effects of a NO synthase inhibitor, NG-nitro-L- arginine methyl ester (L-NAME), on the behavioural changes induced by repeated PCP treatment in mice. 2. Acute PCP (1, 3, and 10 mg kg-1, s.c.) treatment induced dose-dependent hyperlocomotion, motor incoordination and stereotyped behaviours, consisting of sniffing, head movement and ataxia in mice. 3. In mice treated repeatedly with PCP (1, 3, and 10 mg kg-1 day-1), s.c., once a day for 14 days), the sniffing, head movement, ataxia and motor incoordination induced by PCP were attenuated (indicating the development of tolerance to these behaviours), whereas the hyperlocomotion induced by PCP was potentiated (indicating the development of sensitization to hyperlocomotion). The development of tolerance and sensitization to PCP-induced behaviours in the repeated PCP-treated mice was more marked at the dose of 10 mg kg-1 day-1) than at other doses. 4. NO synthase activity in the cerebral cortex and cerebellum, but not in the striatum and hippocampus, was significantly decreased by acute PCP (10 mg kg-1) treatment in comparison with saline treatment, and such changes in activity in the cerebral cortex and cerebellum were reversed by repeated PCP treatment (10 mg kg-1 day-1). 5. The number of neurones containing NADPH-d reactivity in the cerebral cortex, nucleus accumbens, and striatum of acute and repeated PCP-treated mice showed no change in comparison with saline-treated mice. 6. Tolerance to PCP (10 mg kg-1 day-1)-induced ataxia and motor incoordination was significantly attenuated by combined treatment with L-NAME (50 mg kg-1 day-1 i.p.). 7. Sensitization to PCP-induced hyperlocomotion was further enhanced by combined treatment with L-NAME (50 mg kg-1 day-1). However, NG-nitro-D-arginine methyl ester (D-NAME, 50 mg kg-1 day-1, i.p.), a less active enantiomer of L-NAME, had no effect, suggesting a stereospecific mechanism. 8. The PCP-induced behaviours in animals that had exhibited tolerance and sensitization to PCP (10 mg kg-1 day-1) were not influenced by acute L-NAME (5 and 50 mg kg-1, i.p.) or D-NAME (50 mg kg-1, i.p.) treatment. 9. These results suggest that NO may play an important role in the development, but not in the maintenance, of tolerance and sensitization to the effect of PCP in mice.

Animals↗
PubMed1996

Encapsulation of VIP into liposomes restores vasorelaxation in hypertension in situ.

The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) elicits vasodilation in the in situ peripheral microcirculation of hamsters with spontaneous hypertension and whether encapsulation of VIP into liposomes modulates this response. Using intravital microscopy, we found that suffusion of VIP (0.05 and 0.1 nmol) alone over cheek pouch resistance arterioles of normotensive hamsters elicited significant vasodilation that was potentiated and prolonged by encapsulation of the peptide into liposomes (P < 0.05). By contrast, VIP (0.5 and 0.1 nmol) had no significant effects on arteriolar diameter in hamsters with spontaneous hypertension. However, encapsulation of VIP into liposomes restored its vasorelaxant effects in hypertensive animals, although the duration of vasodilation was significantly shorter in comparison with controls (P < 0.05). Empty liposomes had no significant effects on arteriolar diameter in either group. These data indicate that VIP-induced vasodilation in the peripheral microcirculation in situ is impaired in essential hypertension and that encapsulation of VIP into liposomes restores, in part, this response.

Acetylcholine↗
PubMed1996

Rhabdomyolysis following status asthmaticus.

A case of rhabdomyolysis following an asthmatic attack is reported. A 71-year-old man was admitted because of wheezing and hypoxemia. Brown urine was present on admission. Although these symptoms completely disappeared with the treatment with aminophylline, salbutamol and corticosteroid, transiently elevated serum creatine phosphokinase and myoglobinuria were present. Rhabdomyolysis has rarely been reported in cases of bronchial asthma. This case represents an extremely rare case of rhabdomyolysis following status asthmaticus.

Aged↗