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Biomedical subjects

M Murakami

Publications and source records attributed to M Murakami.

At least 649 records · Page 36Linked to original sources
PubMed1995

Changes of P300 latency with age in childhood epilepsy.

Auditory event-related potentials (P300 latency; odd-ball paradigm) were examined in 129 patients with childhood epilepsies and 53 controls. The P300 latency in the patients with epilepsies (373 +/- 39.4 ms) was significantly longer than in controls (356 +/- 38.4), and the prolongation was greatest in the patients with symptomatic partial epilepsies (390 +/- 40.5), mild in those with idiopathic generalized epilepsies (370 +/- 24.3), and minimum in those with idiopathic partial epilepsies (363 +/- 28.9). Abnormal P300 latency occurred at all ages during childhood in patients with symptomatic partial epilepsies, and at older ages in patients with idiopathic generalized epilepsies. The shortening of latency with age was relatively small in patients with epilepsies compared with controls. These results suggest that the prolongation of P300 latency (i.e., existence of cognitive disturbance) displays characteristic changes with age in each epileptic syndrome.

Adolescent↗
PubMed1995

Hyperventilation activation on EEG recording in children with epilepsy.

In 20 patients with epilepsy, electroencephalography (EEG) slowing was quantitatively characterized during standardized hyperventilation activation (respiratory rate: 30/min, threefold elevation of total expiratory volume, duration: 4 min) and changes in cerebral blood flow and velocity in the right common carotid artery were monitored with the Doppler ultrasonic method. Thirteen age-matched normal children served as controls. The results were as follows: (1) EEG slowing in the epilepsy group was greater compared with controls. (2) There was a significant decrease in mean frequency (decrease in alpha power and increase in delta power) during hyperventilation in the epilepsy group, but no significant change in the controls. (3) The decrease in cerebral blood flow (CBF) was greater in the epilepsy group at the beginning of hyperventilation, possibly related to the greater EEG slowing. (4) The percentage of CBF at the end of hyperventilation was similar in the epilepsy and control groups. The difference in EEG response to hyperventilation between the 2 groups may be due to differences in the decrease in CBF volume and the sensitivity of the change in CBF.

Blood Flow Velocity↗
PubMed1995

Biological effects of active oxygen on an X-ray-sensitive mutant mouse cell line (SL3-147).

The biological effects of active oxygen species were examined in a mutant mouse cell line (SL3-147) that is deficient in the repair of DNA double-strand breaks. This mutant cell line shows different sensitivities to X-rays, hydrogen peroxide, paraquat and menadione when compared to the wild-type cell line (LTA). SL3-147 was more sensitive to X-rays, hydrogen peroxide and paraquat, but was less sensitive to menadione in side by side comparisons to LTA cells. The greater number of DNA double-strand breaks in SL3-147 appears to account for the line's greater sensitivity to X-rays and paraquat. DNA damage other than double-strand breaks or injury to non-DNA targets, however, is responsible for the differences between LTA and SL3-147 in their sensitivities to hydrogen peroxide and menadione.

Animals↗
PubMed1995

Granulomatous lesions caused by Pseudomonas aeruginosa in the ostrich (Struthio camelus).

Granulomatous lesions were observed in imported ostriches aged 3 months. Clinically, the birds showed lassitude, incoordination, and inappetence. At necropsy, yellowish white nodules often accompanied by a pseudodiphtheritic membrane were found in the oral, pharyngeal, tracheal and air sac mucosae, the lungs, oesophageal serosa, and abdominal peritoneum. Histopathological examination revealed purulent granulomatous lesions containing central bacterial colonies with an outer shell and club formation. The bacteria were small Gram-negative bacilli, which showed positive immunohistochemical staining for Pseudomonas aeruginosa. The bacterial colonies were positive for chicken IgM. Clubs around the colonies were negative for P. aeruginosa and chicken IgM. Such findings have not previously been reported in the ostrich.

Animals↗
PubMed1995

Photic stimulation study of changing the arterial partial pressure level of carbon dioxide.

To investigate the effect of the level of baseline cerebral blood flow (CBF) on local CBF augmentation by activation, we have used positron emission tomography to measure regional CBF (rCBF) in 12 normal volunteers with and without photic stimulation during hypocapnia, normocapnia, and hypercapnia. The increase in rCBF in the primary visual cortex by photic stimulation was 10.8 +/- 3.1, 18.6 +/- 9.3, and 19.5 +/- 6.1 ml 100 ml-1 min-1 in hypo-, normo-, and hypercapnia, respectively. The increase was significantly smaller in hypocapnia than in normocapnia (p < 0.005). The fractional CBF increase caused by the photic stimulation was the same in all breathing conditions. This result indicates that the magnitude of the CBF increase induced by neuronal activity correlates proportionally with the level of baseline CBF.

Adult↗
PubMed1995

A novel analog of TRH, YM14673, causes a decrease in brain TRH receptors in vitro.

Biochemical mechanisms by which analogs of thyrotropin-releasing hormone (TRH) produce their potent neuropharmacological actions on the brain remain ill-defined. We tested effects of YM14673, a novel analog of TRH, on TRH receptors in rat brains in vitro. No significant binding of [3H]YM14673 to brain plasma membranes occurred. In contrast, preincubation of membranes with YM14673 caused dose-dependent decreases in TRH binding. This was not due to competition for TRH binding sites or existence of metabolites of YM14673. Preincubation with DN1417 (an another TRH analog), cyclo(His-Pro) or methionine-enkephalin did not affect the binding. Affections of YM14673 on TRH binding were observed when cerebral cortical membranes were studied; those were not seen in membranes prepared from hypothalamus, striatum, midbrain, hippocampus, or pons-medulla. The present data indicate that YM14673 exerts its characteristic neuro-pharmacological functions through interacting with TRH binding sites in the brain.

Animals↗
PubMed1995

A reference of the GOLD classification of monoclonal antibodies against carcinoembryonic antigen to the domain structure of the carcinoembryonic antigen molecule.

The epitopes of 42 well-characterized monoclonal antibodies (MAbs) against carcinoembryonic antigen (CEA) from 10 different research groups were mapped in terms of domain structure (domains N, A1-B1, A2-B2, and A3-B3) of the CEA molecule on the basis of the reactivities with recombinant CEA proteins expressed in Chinese hamster ovary cells. Thirty-six of the 42 MAbs tested have previously been classified into 5 essentially nonoverlapping epitope groups (GOLD 1-5) by cross-competition assays among MAbs for CEA binding (Hammarström S, et al.: Cancer Res. 1989; 49:4852-4858). The epitopes recognized by GOLD 2 MAbs were all present on domain A2-B2, those for GOLD 5 MAbs were all on domain N, and those for GOLD 4 were mapped around domains A1-B1 and A2-B2. On the other hand, the epitopes for GOLD 1 MAbs were distributed into domains N, A2-B2, and A3-B3, and those for GOLD 3 MAbs were separated into domains N and A3-B3. Although the exact reasons for the dispersed patterns of GOLD 1 and 3 MAbs on the domain structure of the CEA molecule are unclear at present, several factors, such as a spatial relation or a close proximity of epitopes, conformation dependency, and repetitivity of epitopes, may be considered as possible explanations. The epitope mapping reported here helps form the basis for understanding the relation between the chemical structure and antigenic activities of the CEA molecule and may be useful to study the functions of the CEA molecule, especially those of the respective domains.

Animals↗
PubMed1995

Prevention of autoimmune symptoms in autoimmune-prone mice by elimination of B-1 cells.

Our recent studies on an autoantibody-transgenic mouse line demonstrated that peritoneal B-1 cells are responsible for autoimmune symptoms. However, whether B-1 cells in the peritoneum are generally involved in the pathogenesis of autoimmune disease remains controversial. To test the possible involvement of peritoneal B-1 cells in autoimmune symptoms of autoimmune-prone NZB mice, we eliminated the peritoneal cells by hypotonic shock with repeated i.p. injection of distilled water every 7 days into neonatal or 8-week-old NZB mice. By this treatment, B-1 cells, which self-renew within the peritoneal cavity, are expected to be preferentially eliminated, while other peritoneal cells can be easily supplied from bone marrows after this treatment. Indeed, in distilled water-treated old NZB mice, the number of B-1 cells decreased in spleen as well as in lamina propria of the gut but the numbers of conventional B cells and T cells did not change. Moreover, the production of autoantibodies against erythrocytes significantly decreased and the occurrence of autoimmune hemolytic anemia was reduced in 12-month-old treated NZB mice. Similarly, the elimination of peritoneal cells of NZB/NZW (NZB/W) F1 mice by water injection decreased anti-DNA IgG antibodies in the sera and reduced the pathological changes of the kidney. These results suggest that peritoneal B-1 cells may be a source of autoantibody-producing cells in autoimmune diseases of NZB and NZB/W F1 mice.

Anemia, Hemolytic, Autoimmune↗
PubMed1995

Exogenous type-II phospholipase A2 stimulates prostaglandin synthesis in rat liver-derived BRL-3A cells in the presence of tumor necrosis factor alpha.

The effect of extracellular type-II phospholipase A2 (PLA2) on prostaglandin (PG) synthesis has been studied using rat liver-derived BRL-3A cells. The addition of type-II PLA2 to the medium of BRL-3A cells resulted in a marked decrease in the enzymatic activity in the medium. An immunochemical study involving an anti-(type-II PLA2) antibody revealed that a significant amount of PLA2 was attached to the surface of type-II PLA2-treated BRL-3A cells. Heparin inhibited the binding of PLA2 almost completely. Only modest release of PGE2 over the control value was observed when cells were treated with PLA2 alone or tumor necrosis factor alpha (TNF alpha) alone, whereas PGE2 production as well as arachidonic acid release from phospholipids was augmented more than additively in the presence of both type-II PLA2 and TNF alpha. Furthermore, pretreatment of cells with type-II PLA2 followed by subsequent stimulation by TNF alpha caused an appreciable increase in PGE2 production. Thus, type-II PLA2 bound to cell-surface heparin-like molecules may exert its activity and participate in eicosanoid generation only in the presence of TNF alpha.

Animals↗
PubMed1995

Therapeutic effects of lansoprazole on peptic ulcers in elderly patients.

We studied the effects of lansoprazole on ulcer healing and Helicobacter pylori infection in elderly patients with peptic ulcers. In a group of 24 patients with gastric ulcers, the H. pylori infection rate was 100%. In the course of gastric ulcer healing with famotidine or lansoprazole alone, the H. pylori infection showed no signs of decline. The ulcer healing rates after 8 weeks were similar between the H2-receptor antagonist famotidine (73%), and the proton pump inhibitor lansoprazole (82%). When eradication of H. pylori infection was attempted by concomitant administration of lansoprazole and amoxicillin 500 mg b.i.d. for 2 weeks, the eradication rate was 33% in the group given lansoprazole 30 mg q.d. plus ampicillin 500 mg b.i.d., whereas it was 77% in the group given lansoprazole 30 mg b.i.d. plus ampicillin 500 mg b.i.d. Lansoprazole is considered to be a useful agent for the treatment of patients with peptic ulcers and H. pylori infection and its effectiveness in H. pylori eradication is improved by b.i.d. administration along with ampicillin.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Central nervous system mediates an antihypertensive property in glucocorticoid hypertension in dogs.

OBJECTIVE: To determine whether the central nervous system has a pressor or a depressor role in glucocorticoid-induced hypertension. METHODS: Intracerebroventricular dexamethasone or its receptor antagonist, RU 38486, was administered in 20 trained conscious dogs. In addition, intracerebroventricular RU 38486 was administered in dogs treated with oral dexamethasone. RESULTS: Intracerebroventricular dexamethasone induced a dose-related reduction in blood pressure accompanied by decreased heart rate and cardiac output. In contrast, intracerebroventricular RU 38486 caused a slight but not significant elevation in blood pressure. Total peripheral resistance showed no significant change throughout the treatment with dexamethasone or RU 38486. In contrast, oral dexamethasone caused significant elevation of blood pressure associated with increased total peripheral resistance and reduced heart rate. In hypertensive dogs treated with oral dexamethasone, intracerebroventricular RU 38486 elicited a more severe form of hypertension accompanied by an attenuation of the heart rate and a reduction in cardiac output. Intracerebroventricular dexamethasone induced a significant reduction in plasma levels of adrenocorticotrophic hormone, cortisol, arginine vasopressin and noradrenaline. In addition, simultaneous central administration of RU 38486 with intracerebroventricular dexamethasone blocked the reduction in blood pressure and heart rate completely. CONCLUSION: The present data strongly suggest that endogenous glucocorticoid in the central nervous system may not have a role in the regulation of systemic haemodynamics and hormones under resting conditions, but does play an important part during the glucocorticoid excess state, for example glucocorticoid hypertension caused by oral treatment with dexamethasone. The glucocorticoid in the central nervous system opposed the elevation of blood pressure in glucocorticoid-induced hypertension by attenuating the reduction in heart rate and cardiac output via direct stimulation of glucocorticoid receptors in the brain.

Animals↗
PubMed1995

Improvement of transdermal delivery of tetragastrin by lipophilic modification with fatty acids.

The in-vitro permeability of chemically modified tetragastrin with fatty acids through the rat skin was studied. The permeability of these compounds through intact skin and stripped skin of rat was determined with a Franz-type diffusion cell. The permeation of tetragastrin across the intact skin was improved by chemical modification with acetic acid and butyric acid. However, tetragastrin and caproyl-tetragastrin did not permeate across the intact skin up to the end of experiment. The permeation of tetragastrin across the stripped skin was improved by chemical modification, the skin flux of these acyl derivatives being in the order:acetyl > butyroyl > caproyl. The stability of tetragastrin in skin homogenate was also significantly improved by chemical modification with fatty acids. These results suggest that chemical modifications of tetragastrin with fatty acids increases its lipophilicity, which makes it permeable across the stratum corneum. Moreover, the chemical modification reduced the degradation of tetragastrin in the viable skin, resulting an increase in permeation of tetragastrin across the skin.

Administration, Cutaneous↗
PubMed1995

A novel integron-like element carrying the metallo-beta-lactamase gene blaIMP.

A plasmid-mediated metallo-beta-lactamase gene was cloned from a carbapenem-resistant Serratia marcescens strain, AK9373. The metallo-beta-lactamase gene was identical to the blaIMP, and it was located in the space between an integrase-like gene and an aac(6')-Ib-like gene. The deduced amino acid sequence for the putative integrase gene showed considerable identity (60.9%) to that of the Escherichia coli integrase reported. Sequences similar to the GTTRRRY and an atypical 59-base element containing a 67-bp inverted repeat sequence, which were peculiar to the integrase-dependent recombination, were also conserved in the flanking regions of the blaIMP gene. These findings imply that the metallo-beta-lactamase gene in S. marcescens AK9373 is carried by a novel integron-like element that is mediated by a transferable large plasmid.

Amino Acid Sequence↗
PubMed1995

Withdrawal of antiepileptic drug treatment in childhood epilepsy: factors related to age.

The clinical and electroencephalographic changes with age were evaluated in 304 patients with childhood epilepsies, whose antiepileptic treatment had been discontinued after a seizure free period of more than three years. The withdrawal rate differed significantly between epileptic syndromes, being higher in idiopathic epilepsy and lower in symptomatic epilepsy. The age at withdrawal was characteristic for each epileptic syndrome, and generally showed two peaks: at preadolescence and early school age. Forty one (13.5%) of the 304 patients experienced relapses. The relapse rate differed between epileptic syndromes. Relapses occurred at a unique age in each epileptic syndrome, and were frequent in preadolescence and early adulthood. Electroencephalography that still showed paroxysmal discharges at withdrawal did not necessarily predict the occurrence of a relapse, but the changes in background activity with age, which may indicate maturation of the CNS, were significantly different between the patients with and those without relapses. The results suggest that age related to each epileptic syndrome should be considered when deciding on withdrawal of antiepileptic drugs.

Adolescent↗