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Biomedical subjects

K Sakai

Publications and source records attributed to K Sakai.

At least 649 records · Page 36Linked to original sources
PubMed1994

Transcranial stimulation of the leg area of the motor cortex in humans.

We used transcranial magnetic stimulation on nine normal volunteers to establish an effective way to stimulate the leg area of the motor cortex. Three types of coils: a large figure-eight coil, small figure-eight coil, and a round coil were used. Surface electromyographic activities were recorded from the left tibialis anterior muscle, and the latencies and amplitudes compared with those obtained by anodal electrical stimulation. The most stable responses were obtained when the large figure-eight coil was centered over the vertex and backward current was run through it or when the round coil was centered two to three centimeters anterior to the vertex with left-flowing current in it at the posterior widening. The latencies obtained under these stimulation conditions were the same as those obtained by electrical stimulation. We conclude that direct activation of the pyramidal cells occurs in the leg area of the motor cortex in all forms of magnetic and electrical stimulation.

Electric Stimulation↗
PubMed1994

Bleaching of Hardwood Kraft Pulp with Manganese Peroxidase Secreted from Phanerochaete sordida YK-624.

In vitro bleaching of an unbleached hardwood kraft pulp was performed with manganese peroxidase (MnP) from the fungus Phanerochaete sordida YK-624. When the kraft pulp was treated with partially purified MnP in the presence of MnSO(4), Tween 80, and sodium malonate with continuous addition of H(2)O(2) at 37 degrees C for 24 h, the pulp brightness increased by about 10 points and the kappa number decreased by about 6 points compared with untreated pulp. The pulp brightness was also increased by 43 points to 75.5% by multiple (six) treatments with MnP combined with alkaline extraction. Our results indicate that in vitro degradation of residual lignin in hardwood kraft pulp with MnP is possible.

Journal Article↗
PubMed1994

In vitro bleaching of hardwood kraft pulp by extracellular enzymes excreted from white rot fungi in a cultivation system using a membrane filter.

To clarify the role of excreted extracellular enzymes during long-term incubation in a pulp biobleaching system with white rot fungi, we developed a cultivation system in which a membrane filter is used; this membrane filter can prevent direct contact between hyphae and kraft pulp, but allows extracellular enzymes to attack the kraft pulp. Phanerochaete sordida YK-624 brightened the pulp 21.4 points to 54.0% brightness after a 5-day in vitro treatment; this value was significantly higher than the values obtained with Phanerochaete chrysosporium and Coriolus versicolor after a 7-day treatment. Our results indicate that cell-free, membrane-filtered components from the in vitro bleaching system are capable of delignifying unbleached kraft pulp. Obvious candidates for filterable reagents capable of delignifying and bleaching kraft pulp are peroxidase and phenoloxidase proteins. The level of secreted manganese peroxidase activity in the filterable components was substantial during strain YK-624 in vitro bleaching. A positive correlation between the level of manganese peroxidase and brightening of the pulp was observed.

Journal Article↗
PubMed1994

Purification and characterization of thermostable beta-N-acetylhexosaminidase of Bacillus stearothermophilus CH-4 isolated from chitin-containing compost.

Thermostable exochitinase was purified to homogeneity from the culture fluid of Bacillus stearothermophilus CH-4, which was isolated from agricultural compost containing shrimp and crabs. The enzyme was a single polypeptide with a molecular mass of 74 kDa, and the N-terminal amino acid sequence was WDKVGVTDLI ISLNIPEADAVVVGMTLQLQALHLY. The enzyme specifically hydrolyzed C-4 beta-anomeric bonding of N-acetylchitooligosaccharides, as well as their p-nitrophenyl (pNP) derivatives. The enzyme also hydrolyzed pNP-beta-N-acetyl-D-galactosaminide (26% of the activity of pNP-beta-N-acetyl-D-glucosaminide). These results indicated that the enzyme is a beta-N-acetylhexosaminidase (EC 3.2.1.52). Kms for acetylchitooligosaccharides were 1 x 10(-4) to 6 x 10(-4) M, while those for the pNP derivatives were 4 x 10(-3) to 8 x 10(-3) M. The optimum temperature of the enzyme was 75 degrees C, and it retained 100 and 28% reactivity after heating at 60 and 80 degrees C, respectively. The enzyme exhibited 15 to 20% activity in a reaction mixture containing 80% organic solvents and maintained 91% of its original activity after exposure to 8 M urea. The optimum and stable pH was around 6.5. Fe2+, Zn2+, and Ca2+ activated the enzyme, but Hg2+ was inhibitory. N-Acetyl-D-glucosamine inhibited the enzyme competitively (Ki = 4.3 x 10(-4) M), whereas N-acetyl-D-galactosamine did not; in contrast, D-glucosamine and D-galactosamine activated it.

Amino Acid Sequence↗
PubMed1994

Naming difficulties in alexia with agraphia for kanji after a left posterior inferior temporal lesion.

The case is described of a patient with alexia and agraphia for kanji, and severe anomia after a subcortical haemorrhage in the left posterior inferior temporal area. Magnetic resonance imaging at four months after onset showed a lesion in the inferior temporal and fusiform gyri, extending from the temporo-occipital junction toward the anterior third of the temporal lobe. Comparison with other reported cases of alexia with agraphia and anomia made it clear that when accompanied by severe anomia, the lesions extended either forward to the anterior part of the middle temporal gyrus or medially to the parahippocampal gyrus. It is suggested that the disconnection of association fibres between the parahippocampal, fusiform, middle, and inferior temporal gyri, especially between the parahippocampal gyrus and the other temporal gyri, or the cortical damage to the posterior part of these gyri is essential for the production of anomia.

Aged↗
PubMed1994

Venous distensibility during pregnancy. Comparisons between normal pregnancy and preeclampsia.

Preeclampsia is associated with increased peripheral resistance. This study was performed to determine whether an increase of venous distensibility occurs as well in preeclampsia. We obtained venous distensibility by measuring the venous pressure-volume relation in the forearm with a water-filled plethysmograph. Twenty-one women with normal pregnancy, 12 women with severe preeclampsia, and 8 women with mild preeclampsia were studied during the third trimester and/or 6 weeks after the delivery. Ten nonpregnant normotensive women were also studied. Venous distensibility was greater (P < .01) in normal pregnant women and smaller (P < .01) in women with preeclampsia during pregnancy than postpartum. The magnitude of the decrease of venous distensibility correlated with the severity of preeclampsia. Venous distensibility was similar between normotensive nonpregnant women, women with normal pregnancy during the postpartum period, and women with preeclampsia during the postpartum period. Thus, venous distensibility increased during normal pregnancy. In preeclampsia, the decrease of venous distensibility occurred during pregnancy but was reversed postpartum. These results may suggest that a decrease of venous distensibility occurs during preeclampsia. These venous abnormalities may contribute to impaired control of hemodynamics in preeclampsia during pregnancy.

Adult↗
PubMed1994

Modulating the phase transition temperature and thermosensitivity in N-isopropylacrylamide copolymer gels.

Temperature-responsive copolymer (or ternary copolymer) gels of N-isopropylacrylamide (IPAAm) were synthesized with hydrophobic alkyl methacrylate (RMA), hydrophilic acrylamide (AAm), N,N'-dimethylacrylamide (DMAAm), and N-acryloylpyrrolidine (APy) as comonomers. The effects of these comonomers on the phase transition temperature (LCST) and the thermosensitivity have been discussed. The LCST of poly(IPAAm) gel in phosphate buffered saline (PBS) was lowered by the introduction of hydrophobic RMA, and the change in equilibrium swelling ratio with temperature change became smaller with an increase in RMA content. However, a stable skin layer to achieve complete 'on-off' regulation of drug release was formed at a higher temperature by RMA due to hydrophobic interaction of alkyl chains. The LCST of poly(IPAAm-co-AAm) gel increased with an increase in AAm content. However, the thermosensitivity of the gel became smaller. It was suggested that hydrophilic AAm prevented the formation of a dense skin layer at a higher temperature. It was difficult to obtain a complete 'off' state due to an insufficiently dense skin layer in order to stop the drug release. The LCST was raised and great thermosensitivity was possible by the introduction of DMAAm or APy. Poly(IPAAm-co-DMAAm) enabled 'on-off' drug release in response to smaller temperature changes around the body temperature. The molecular design to control transition temperature and thermosensitivity of gel was established.

Acrylamides↗
PubMed1994

A non-glycosylated form of pulmonary surfactant protein A appears in rat amniotic fluid.

Surfactant protein A (SP-A) is a family of glycoproteins that have a triplet with 26, 32 and 36 kDa under reducing conditions in rat lung. We wanted to evaluate the SP-A forms in amniotic fluid of pregnant rats compared to those found in rat lungs. By Western blot analysis, glycosylated SP-A, was not found in the amniotic fluid in contrast to the pulmonary surfactant triplet SP-A, which comprises a 26 kDa protein and its glycosylated 32 and 36 kDa forms. The SP-A concentration in amniotic fluid was barely detectable at 18 days of gestation (20 +/- 12 ng.ml-1), and then increased and reached 700 +/- 333 ng.ml-1 at the final gestational day 21, as determined by an enzyme-linked immunoabsorbent assay. Immunohistochemically, SP-A was found in some epithelial cells of larger respiratory bronchi, but not, or to a lesser degree, in smaller respiratory bronchi at gestational day 18. At 21 days of gestation, SP-A was detected in bronchial and bronchiolar nonciliated epithelial Clara cells, alveolar epithelial type II cells and some alveolar macrophages. The ratio of the 26, 32 and 36 kDa SP-A forms in bronchoalveolar, bronchobronchiolar and tracheal lavage fluids prepared from adult rats was 6:29:65, 84:5:11 and 100:0:0, respectively. These findings show the presence of a non-glycosylated SP-A in rat amniotic fluid. This may reflect the increased ratio of non-glycosylated SP-A to bronchoalveolar, bronchobronchiolar and tracheal lavage fluids, respectively.

Amniotic Fluid↗
PubMed1994

Sendai virus infection changes the subcellular localization of tryptase Clara in rat bronchiolar epithelial cells.

Tryptase Clara activates the infectivity of Sendai and influenza viruses proteolytically. In this study, we investigated changes in the subcellular localization of tryptase Clara in rat bronchioles with progression of Sendai virus infection. Tryptase Clara and Sendai virus F2 antigen were localized by light and electron immunohistochemical studies. In the uninfected rat lung, tryptase Clara was specifically localized in the secretory granules of respiratory bronchiolar epithelial nonciliated cells, but not in bronchiolar ciliated, or alveolar cells. In the initial stage of Sendai virus infection with slight pathological changes, however, anti-tryptase Clara was highly reactive in luminal peripheral membranes of both nonciliated and ciliated epithelial cells of the bronchioles together with some Sendai virus envelope glycoprotein, F2 antigen. In the progressed stage, tryptase Clara was hard to detect, with heavy accumulation of F2 antigen in the epithelial cells. These immunohistochemical results support our previous findings that in the bronchial lavage fluid tryptase Clara is significantly increased both in amount and activity after viral infection. These results suggest that Sendai virus stimulates the secretion of tryptase Clara from nonciliated bronchiolar epithelial cells to the airway lumen. Accumulation of tryptase Clara on the luminal surface of the bronchiolar epithelial cells and/or in the airway lumen may produce favourable conditions for proteolytic viral activation and multiplication.

Animals↗
PubMed1994

Mitochondrial encephalomyopathy: elevated visual cortex lactate unresponsive to photic stimulation--a localized 1H-MRS study.

We used localized H-magnetic resonance spectroscopy (MRS) to study the metabolic changes in the visual cortex of patients with mitochondrial encephalomyopathy. Measurement of metabolite levels in the occipital visual cortex obtained in the dark with seven normal subjects and with four patients (all four of whom had Kearns-Sayre syndrome [KSS]) showed high lactate levels in the patients. Photic stimulation (PS) in four normal volunteers showed that lactate increased immediately after the start of PS and that it decreased to the baseline level with continued PS. Lactate in the resting state was higher in the KSS patients than in the controls, and, unlike the controls, the KSS patients showed no significant elevation of lactate with PS.

Humans↗
PubMed1994

Enhancing effect of zinc acetate on the binding of 1-nitropyrene to polydeoxyguanylic-polydeoxycytidylic acid in the hypoxanthine-xanthine oxidase system.

The main aim of this research was to investigate whether conformational alteration of polydeoxyguanylic-polydeoxycytidylic acid (poly[dG-dC].poly[dG-dC]) by zinc acetate would have an effect on the binding of 1-nitropyrene(1-NP) to poly[dG-dC].poly[dG-dC]. The binding of 1-NP to poly[dG-dC].poly[dG-dC] in the hypoxanthine-xanthine oxidase system in vitro was increased by zinc acetate. This increase was abolished when EDTA was added to the preincubated mixture of poly[dG-dC].poly[dG-dC] and zinc ions. Neither the production of 1-aminopyrene and its expected intermediates, N-hydroxy-1-aminopyrene and 1-nitrosopyrene, nor the 1-NP remaining in the reaction mixture was altered by the addition of zinc acetate without poly[dG-dC].poly[dG-dC]. From these findings, it seems that the hypoxanthine-xanthine oxidase system is not activated by zinc acetate. On the other hand, under the same reaction conditions but the hypoxanthine-xanthine oxidase system and 1-NP, it has been reported that zinc ions or complexes transform the B-form of poly[dG-dC].poly[dG-dC] to the Z-form. Therefore, these findings indicate that the formation of the Z-form or intermediates from the B-form by zinc ions may promote the binding of 1-NP to poly[dG-dC].poly[dG-dC].

Acetates↗
PubMed1994

[Studies on Fugu (globefish) tetrodotoxin over one century].

One century has passed since fugu toxin was first named tetrodotoxin by Tahara. Chemical problems such as crystallization of tetrodotoxin, followed by structure determination by the research groups headed by Tsuda, Hirata, Woodward, and Mosher, and its subsequent synthesis by Kishi have been solved. In the last 10 years, research on the distribution of tetrodotoxin in nature has shown that tetrodotoxin is not produced by fugu fish, but rather is formed by sea bacteria such as Vibrio, Alteromonas, Photobacterium, and Aeomonas. However, it remains unclear why tetrodotoxin accumulates at a high concentration only in fugu.

Animals↗
PubMed1994

Acute effects of deflazacort and its metabolite 21-desacetyl-deflazacort on allergic reactions.

The acute effects of deflazacort (MDL 458, CAS 14484-47-0) and its metabolite, 21-desacetyl-deflazacort, on allergic reactions in animal models were investigated and compared with those of prednisolone. Deflazacort, 21-desacetyl-deflazacort and prednisolone all inhibited 48-h homologous passive cutaneous anaphylaxis in rats, but had no significant effects on active systemic anaphylaxis in mice, on the Schultz-Dale reaction in the isolated guinea-pig trachea or on compound 48/80-induced histamine release in rat peritoneal mast cells. All three agents inhibited reversed cutaneous anaphylaxis in rats and the Arthus reaction in mice. The inhibitory effects of deflazacort on the passive cutaneous anaphylaxis, the reversed cutaneous anaphylaxis and the Arthus reaction were similar to those of 21-desacetyl-deflazacort and were stronger than those of prednisolone. Delayed type hypersensitivity in mice was also inhibited by deflazacort and 21-desacetyl-deflazacort, but prednisolone, at the doses used in the present study, had little effect on this immune response. These findings indicate that while deflazacort and 21-desacetyl-deflazacort have stronger anti-allergic effects than prednisolone, they seem to have little acute effect on mast cell degranulation or on chemical mediators at the receptor site.

Anaphylaxis↗