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Biomedical subjects

K Matsuda

Publications and source records attributed to K Matsuda.

At least 451 records · Page 25Linked to original sources
PubMed1993

[Postictal aphasia and its generating mechanism in 3 patients with localization-related epilepsy].

Semiology of postictal aphasia as well as its generating mechanism involving both the epileptogenic zone and language area has not yet been sufficiently elucidated. Therefore, postictal aphasias were studied in 3 patients with localization-related epilepsy. Postictal motor aphasia was observed in a patient (patient 1) with frontal lobe epilepsy whose recovery of language function progressed from loss of language function, to Broca's aphasia, and eventually to poor spontaneous speech. Postictal sensory aphasia was observed in 2 patients (patient 2 and 3) with temporal lobe epilepsy whose recovery of language function progressed from loss of language function, to jargon, and eventually to circumlocutory anomic speech. Both patient 2 and 3 did not show fluent speech. Seizure manifestations, EEG, IMP-SPECT and MRI indicated that epileptogenic zones were in the left frontal lobe including Broca's area in patient 1, the mesial part of the left temporal lobe in patient 2, and the middle and posterior part of the left temporal lobe including Wernicke's area in patient 3. A postictal verbal dichotic listening test showed the reduction of correct responses by right ear in the patient 3. Postictal auditory verbal learning tests showed the impairment of verbal memorization in patient 2 and 3. The impairment of verbal memorization was particularly marked in patient 2. These results suggest that 1) the characteristics of postictal motor and sensory aphasia are clearly elucidated by analyzing the sequence of recovery from postictal language dysfunction, 2) postictal aphasia is generated by the epileptogenic zone involving the language area or the ictal discharges propagating to the language area, and 3) not only the disturbance of language function, but also the impairment of verbal memorization seems to participate in the disturbance of repeating and understanding sentences in the patient with postictal sensory aphasia.

Adult↗
PubMed1993

Toxicity of the novel anti-peptic ulcer agent catena-(S)-[mu-[Na- (3-aminopropionyl)histidinato(2-)-N1,N2,Q:N tau]-zinc in male cynomolgus monkeys.

A preliminary dose-range finding study and a 13-week toxicity study were performed in male cynomolgus monkeys with catena-(S)-[mu-[N a-(3-aminopropionyl) histidinato (2-)-N1,N2,O:N tau]-zinc] (Z-103, CAS 107667-60-7), a novel anti-peptic ulcer agent, as part of a safety evaluation program. In the preliminary ascending dose study emesis was observed in animals treated at 625 mg/kg and transient reductions in food intake with associated body weight loss in a male treated at 625 or 312.5 mg/kg. Plasma zinc levels were also increased in all animals treated at 625 or 312.5 mg/kg. As a result dosages of 0, 20, 63 and 200 mg/kg/day were selected for the 13-week toxicity study. In this study, treatment-related changes were confined to the 200 mg/kg/day dosage and consisted of emesis, piloerection and transient body weight loss in one animal, increased plasma zinc concentrations, and zinc and copper deposition in the liver and kidneys without any associated morphological change. The no observed effect level was estimated to be 63 mg/kg/day in this study.

Animals↗
PubMed1993

[Effect of prostaglandin E2 on the proliferation of cultured guinea pig gastric mucous cells].

To understand the mechanism by which prostaglandins (PGs) preserve gastric mucosal integrity, we established a primary cultured monolayer of guinea pig gastric mucous cells, and by using this culture system, we studied whether endogenously released PGE2 could influence the proliferation of the mucous cells. By the histochemical and morphological analysis at 24h of the culture periods, the cells were recognized to contain PAS-positive mucous granules with only 3% of them being parietal cells. Although the cells which were simultaneously labeled with [3H] arachidonic acid in 0.5% serum-containing medium synthesized and released radiolabeled PGE2, PGI2 and PGA2, the release of PGE2 was more markedly observed and was partially dependent upon arachidonic acid added to the culture medium. By radioimmunoassay of the culture media, the mucous cells were found to release PGE2 in a time-dependent manner in response to 10% serum. Pretreatment of the cells with 10(-4)M indomethacin not only inhibited PGE2 release but also inhibited increase in cell number. However, the addition of PGE2 dose-dependently restored the indomethacin-induced inhibition of cell growth with the maximal increase almost to the control level at 10(-6)M PGE2. These results suggest that PGE2 endogenously released from the cells may exert a proliferative effect on gastric mucous cells.

Animals↗
PubMed1992

Expression of only one of two types of mRNA transcribed from the serine dehydratase gene is repressed in hepatoma cells.

The expressions of mRNA for serine dehydratase in H4IIE, HTC, and HepG2 hepatoma cells were investigated. Of the two types of mRNA transcribed from the single copy of the rat serine dehydratase gene, expression of only that encoding 35 kDa serine dehydratase is repressed in these cells. The other type coding the 8.9 kDa truncated translation product is expressed at a similar level to that in hepatocytes in primary culture and is not under hormonal control.

Alternative Splicing↗
PubMed1992

Expression of two types of neurofibromatosis type 1 gene transcripts in gastric cancers and comparison of GAP activities.

To understand the molecular mechanism of gastric tumorigenesis, the status of neurofibromatosis type 1 (NF1) gene was analyzed in human gastric cancer cell lines. Although the sequencing of the GTPase activating protein (GAP)-related region of NF1 (NF1-GRD) revealed no apparent mutation, the NF1-GRD transcript (type I) and that containing an additional 63 bp insert in the center of NF1-GRD (type II) were equally expressed in most gastric cancer cells. By contrast, type II was predominantly expressed in normal stomach mucosa. When these two types of NF1-GRD were bacterially expressed and their GAP activities were tested, both types of NF1-GRD similarly stimulated ras GTPase activity. However, arachidonic acid inhibited GAP activities of two types of NF1-GRD to different extents. These results suggest that the increased expression of type I NF1 protein may modulate ras-related signal transduction and it may be related to the control of the gastric cellular proliferation.

Arachidonic Acid↗
PubMed1992

p53 gene mutations in human gastric cancer: wild-type p53 but not mutant p53 suppresses growth of human gastric cancer cells.

To further investigate the role of p53 gene inactivation in gastric tumorigenesis, the mutational status of the p53 gene in primary human gastric cancer samples was examined. Reverse transcriptase polymerase chain reaction and subsequent direct sequencing of the p53 gene from gastric cancer samples revealed frequent point mutations of the p53 gene: some of these coincided with those previously identified in gastric cancer cell lines. In addition, both allelic deletion analysis using pYNZ 22 and polymerase chain reaction-restriction fragment length polymorphism analysis demonstrated an allelic deletion of the p53 gene in cancer tissue which contained a point mutation of the p53 gene in the remaining allele. Transfection of the wild-type or mutant p53 genes into gastric cancer cells showed that the wild-type but none of the mutated p53 genes suppressed the colony formation of gastric cancer cells. Furthermore, the incorporation of thymidine into DNA was reduced in cancer cells expressing the wild-type p53 gene. The glutathione S-transferase-wild type p53 fusion protein bound to simian virus 40 large T antigen in COS-1 cell lysate. None of the p53 fusion proteins containing mutations at codons 143, 175, 248, or 273 bound to simian virus 40 large T antigen. By contrast, two different mutant p53 fusion proteins containing mutations specifically observed in gastric cancer bound to simian virus 40 large T antigen. These results indicate that inactivation of the p53 gene through mutations and the allelic deletion may play an important role in gastric tumorigenesis. These mutations may cause a conformational change in the p53 protein resulting in the loss of the suppression by p53 of the growth of gastric cells, partly through disruption of the association of p53 protein with a cellular component.

Antigens, Viral, Tumor↗
PubMed1992

Missense mutations and a deletion of the p53 gene in human gastric cancer.

To investigate the molecular pathogenesis of human gastric cancers the p53 gene, a suppressor oncogene, was analyzed in 12 human gastric cell lines. Southern blot and Northern blot analysis revealed a total deletion of p53 gene in KATO-III cells but no major abnormality of p53 gene in other cell lines. By the use of the reverse-transcriptase polymerase chain reaction and direct sequencing 7 cell lines showed point mutations of p53 gene resulting in amino-acid substitutions. Most of them were rare mutations which had not been observed in other types of cancers. One of these mutations was also detected through the use of PCR and oligomer-specific hybridization. Six out of 7 cell lines with mutations of p53 gene also lost one allele of chromosome 17p. Immunoblotting of cell lysates with an antibody specific to p53 demonstrated the absence of p53 protein in KATO-III cell. By contrast, the high levels of the p53 protein were observed in 5 cell lines all of which contained mutations of p53 gene. These results further suggest that the inactivation of p53 gene may play an important role in the transformation of gastric cells to the malignant phenotype. KATO-III cells might be a good model for studying the significance of the loss of p53 gene in cellular transformation.

Alleles↗
PubMed1992

Effects of antiulcer drugs on phosphatidylcholine synthesis in isolated guinea pig gastric glands.

To better understand phosphatidylcholine synthesis in the stomach, we isolated guinea pig gastric glands and examined their [3H]choline incorporation into phosphatidylcholine in response to either antiulcer drugs such as geranylgeranylacetone (GGA) and H2-receptor antagonists or agents that cause phosphatidylcholine synthesis in other tissues. [3H]Choline incorporation was stimulated by GGA, palmitate, and 12-O-tetradecanoylphorbol-13-acetate (TPA). Dibutyryl cyclic-AMP had no effect. By contrast with GGA, famotidine, ranitidine, and cimetidine equipotently inhibited [3H]choline incorporation into phosphatidylcholine. GGA, palmitate, and TPA increased phosphatidyl-[3H]choline and decreased phosphoryl-[3H]choline as compared with control in tissues that had been pulsed with [3H]choline. On the other hand, no more decrease in [3H]choline incorporation at chase periods was observed in pulse-labeled glands in response to each H2-receptor antagonist. The particulate fraction of glands that had been incubated with GGA or palmitate had more CTP-phosphocholine cytidylyltransferase activity than that of glands incubated without agents. A decrease in choline kinase activity was not observed in the cytosolic fraction of glands that had been incubated with cimetidine. These results suggest that GGA and palmitate stimulate phosphatidylcholine synthesis by activating cytidylyltransferase, and H2-receptor antagonists may affect phosphatidylcholine synthesis by inhibiting choline uptake in the gastric glands.

Analysis of Variance↗
PubMed1992

M3 muscarinic receptors mediate pepsinogen secretion via polyphosphoinositide hydrolysis in guinea pig gastric chief cells.

The muscarinic receptor system involved in pepsinogen secretion from isolated guinea pig gastric chief cells was investigated by evaluating the effect of muscarinic receptor antagonists on carbamylcholine (CCh)-stimulated chief cell responses. CCh stimulated the hydrolysis of polyphosphoinositide in chief cells at the same concentrations as it stimulated pepsinogen secretion. Each of five different muscarinic receptor antagonists, atropine, pirenzepine, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), AF-DX116 and scopolamine, inhibited both pepsinogen secretion and inositol phosphate accumulation stimulated by graded concentrations of CCh. The pA2 values of the antagonists calculated from data on inositol phosphate accumulation and pepsinogen secretion (atropine = scopolamine = 4-DAMP greater than pirenzepine greater than AF-DX116) suggest that the muscarinic acetylcholine receptor in gastric chief cells is the M3 subtype. On the other hand, CCh did not affect the adenylate cyclase/cAMP signaling pathway in gastric chief cells. All pA2 values of the antagonists were also in agreement with the Ki values determined by [3H]NMS binding to chief cells. Furthermore, GTP gamma S reduced [3H]acetylcholine binding to chief cell membranes in a concentration-dependent manner. The present study, therefore, suggests that muscarinic M3 receptors, which may be coupled to a G protein, mediate pepsinogen secretion, probably by activation of the polyphosphoinositide second messenger system in guinea pig gastric chief cells.

Animals↗
PubMed1992

Evaluation of a bilayer artificial skin capable of sustained release of an antibiotic.

A bilayer artificial skin, composed of an upper silicone sheet and a lower collagen sponge, has been developed by modifying a technique proposed by Yannas and Burke. We have applied it clinically with success, but infection sometimes occurred in the area where the artificial skin was placed. To use it safely in an infected wound, we developed a new type of artificial skin capable of sustained release of antibiotic. Microspheres of poly-L-lactic acid containing an antibiotic, were installed in the upper silicone sheet. The usefulness of the new type of artificial skin was suggested by in vitro studies.

Biocompatible Materials↗
PubMed1992

Resistance to a new catecholic cephem, BO-1341, in Pseudomonas aeruginosa PAO.

Two distinct types of mutant resistant to the catecholic cephem BO-1341 were isolated spontaneously from Pseudomonas aeruginosa PAO2146: (i) a mutant (CCB5-type) which produced beta-lactamase constitutively, and which appeared to result from a mutation in the regulatory gene (blaI at 41 min) controlling the structural gene (blaP at 25 min); (ii) a mutant (CCB7-type) with specific resistance to BO-1341. Induction of beta-lactamase production in strain CCB7 by BO-1341 was diminished markedly when compared with that in the parent strain. This was not the case for ceftazidime or cefoxitin, suggesting impaired uptake of BO-1341 as an explanation for the resistance. Electrophoretic analysis demonstrated increased production of a 55 kDa protein in the periplasmic space and a 84 kDa outer membrane protein. These data suggested that specific resistance to BO-1341 might involve quantitative alterations in the composition of the outer membrane and periplasmic proteins.

Cefoxitin↗
PubMed1992

Purification and localization of a calcium-binding protein in human spermatozoa.

The purpose of this study was to purify a calcium-binding protein (CalBP) from human spermatozoa of 226 men and to determine the localization of this protein in spermatozoa. The sperm cells were extracted with 0.6 M KCl, and the KCl extract was then subjected to gel filtration and high performance liquid chromatography. Two CalBPs of Mr = 38 kDa and 52 kDa were found by 45Ca(2+)-binding on blotted proteins. Only a 52 kDa CalBP (CalBP-52) was purified to a final yield of 0.007%. The isoelectric point of this protein was 5.1. The human CalBP-52 reacted with rabbit antiserum directed against rat 52 kDa CalBP. An immunocytochemical study showed that this protein was localized on the sperm head. It is postulated that this protein may have important functions related to Ca(2+)-transport into sperm cells.

Animals↗
PubMed1992

Conditions for omitting invasive long-term monitoring before surgical resection in patients with temporal lobe epilepsy.

The omission of invasive long-term monitoring before surgical resection in patients with epilepsy should be permitted only for those in whom the epileptogenic focus is presumed to localize unilaterally in the mesial aspect of the temporal lobe. The localization may well be confirmed through noninvasive measures. Retrospective analyses of data obtained from noninvasive investigations (scalp-recorded and sphenoidal EEGs, neuroimages, and electroclinical seizure manifestations) were carried out in 58 patients. The localization of their epileptogenic focus was subsequently confirmed by the implantation of both intracerebral and subdural electrodes; the focus had an amygdalohippocampal origin in 41 patients and a lateral temporal origin in 17 patients. From the comparison of noninvasive findings between these two groups, we propose the following indispensable conditions for omitting an invasive evaluation: 1. Appearance of focal epileptic discharges unilaterally in the sphenoidal lead observed during the simple phase of partial seizures, or unilateral discharges with predominancy in the sphenoidal lead during the early phase of complex partial seizures. 2. Interictal spikes on scalp-recorded EEGs localizing unilaterally in the anterior region of the temporal lobe, and if bilaterally independent, presenting with unilateral predominancy in a ratio of greater than 4:1. 3. Presence of autonomic signs in the initial phase of signal symptoms. 4. Neuroimaging findings in the mesial temporal region: elongated T2 on MRI and hippocampal atrophy, or a tumorous lesion. The lateralization conforms to interictal and ictal paroxysmal EEG findings. There were 8 patients with seizure of amygdalohippocampal origin who satisfied all the indispensable condition, but not a single patient with seizures of lateral temporal origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗