Search PubMed⌕ Search

Biomedical subjects

T Murayama

Publications and source records attributed to T Murayama.

At least 199 records · Page 11Linked to original sources
PubMed1995

Testing and classification methods for the biodegradabilities of organic compounds under anaerobic conditions.

Biodegradability is one of the most important characteristics of an organic compound for predicting its fate and life in the environment and its application in biological wastewater treatment. But there is no general testing method for biodegradability under anaerobic conditions. The biodegradabilities of thirteen principal organic compounds was investigated in a batch test using vials under various conditions, such as the concentration of an organic compound, the cultivation method and the concentration of anaerobic bacteria for seeding. Two test methods in the standard concentration and the low concentration were developed. A new method to classify the biodegradabilities of organic compounds into thirteen ranks was proposed by considering inhibition, complete biodegradation and first step biodegradation.

Bacteria, Anaerobic↗
PubMed1995

A suppressor mutation which suppresses adenylyl cyclase mutations in Neurospora crassa.

A spontaneous suppressor mutant, hah, which suppressed the colonial growth of adenylyl cyclase mutants (cr-1) was isolated. The morphology of cr-1 hah was filamentous, but slightly different from that of wild type on solid medium. The hah strain formed many high aerial hyphae, but did not form any conidia. The expression levels of an adenylyl cyclase gene, nac, in both hah and cr-1 hah were much higher than those in wild type or in cr-1. The level of cAMP in cr-1 was very low but returned to close to the wild-type level in the cr-1 hah suppressed strain, whereas that in the strain carrying hah alone was similar to or a little higher than that in wild type. The hah gene was located 13.3 map units from in1 on the right arm of the linkage group V. The hah mutation was recessive and allele specificity of hah for the suppression of cr-1 mutations was weak.

Adenylyl Cyclases↗
PubMed1995

Production of metallothionein in copper- and cadmium-resistant strains of Saccharomyces cerevisiae.

Certain mutants of the yeast Saccharomyces cerevisiae show copper or cadmium resistance. Both copper- and cadmium-resistant strains produce the same metallothionein with 53 amino acid residues which causes metal detoxification by chelating copper or cadmium. The metal detoxification role is the only known function of the metallothionein in yeast. The MT is encoded by the CUP1 gene on chromosome VIII which is expressed by induction with metals. The CUP1 is amplified to 3-14 copies with 2 kb-tandem-repeat units in the metal-resistant strains, whereas the wild-type strain contains only a single copy of the CUP1. Although transcription of CUP1 is inducible by metals, the ACE1 protein serves a dual function as a sensor for copper and an inducer for CUP1 transcription in the copper-resistant strain. In the cadmium-resistant strain, the heat-shock factor having a point mutation may be the regulator for CUP1 transcription. Therefore, it has been clarified that production of MT in yeast is controlled by two systems, the amplification of CUP1 and its transcriptional regulation.

Amino Acid Sequence↗
PubMed1995

Nickel resistance mechanisms in yeasts and other fungi.

This review describes nickel toxicity and nickel resistance mechanisms in fungi. Nickel toxicity in fungi is influenced by environmental factors such as pH, temperature and the existence of organic matter and other ions. We describe resistance mechanisms in nickel-resistant mutants of yeasts and filamentous fungi which were obtained by exposure to a mutagen or by successive culture in media containing increasing concentrations of nickel ion. Nickel resistance may involve: (1) inactivation of nickel toxicity by the production of extracellular nickel-chelating substances such as glutathione; (2) reduced nickel accumulation, probably by modification of a magnesium transport system; (3) sequestration of nickel into a vacuole associated with free histidine and involving Ni-insensitivity of vacuolar membrane H(+)-ATPase.

Drug Resistance, Microbial↗
PubMed1995

Effects of orally administered Clostridium butyricum MIYAIRI 588 on mucosal immunity in mice.

The activation of local mucosal immunity by Clostridium butyricum MIYAIRI 588 (CBM588) was investigated in germ-free mice. An increase of polyclonal IgA production in the small intestine or secretion into the intestinal lumen was observed in mice mono-associated with CBM588 and fed a diet containing killed vegetative cells of CBM588 (VCBM). However, fecal IgA of anti-CBM588 was rarely formed in mice administered CBM588 during 6 weeks from administration. Cholera toxin was administered orally to SPF mice fed a diet containing CBM588, and IgA secretion of anti-cholera toxin was enhanced in mice fed a VCBM diet. In addition, the production of IgA, IgM and IgG in Peyer's patch cell culture was increased in the presence of VCBM. These results suggest that oral administration of CBM588 stimulates polyclonal mucosal immune activity and shows adjuvant activity for anti-cholera toxin.

Adjuvants, Immunologic↗
PubMed1995

Two-dimensional domain shape transitions in photosensitive monolayer assemblies.

Bubble-stripe shape transitions of gaseous domains are observed in Langmuir monolayers of porphyrin/arachidic acid and porphyrin/spiropyran mixtures using fluorescence microscopy. Characteristics of the transition such as critical bubble size are found to be controllable by subphase pH or UV/visible irradiation. These features are discussed in terms of a balance between dipolar repulsions and line tension in the monolayer.

Benzopyrans↗
PubMed1995

Optical neural device based on memory-type organic photoconductors.

A variable-sensitivity organic-photoconductive device has been developed by using a memory-type organic photoconductor. The device is composed of an input layer and a memory layer acting as a charge generation and a charge transport layer, respectively. A persistent high-sensitivity state, which corresponds to a modulation of synaptic weights in a neuron model, was obtained by blue light illumination. A photochemical reaction of thiomichler's ketone (TMK) in the memory layer was found to be responsible for the memory formation. As a potential application of this memory-type organic photoconductor to an optical neural device, 2-D pattern storage and calculations were performed successfully.

Animals↗
PubMed1995

Effects of protein kinase C and A activation on ATP-stimulated release of [3H]noradrenaline from PC12 cells.

The influence of activation of protein kinase C (PKC) and cyclic AMP on noradrenaline (NA) release in the neurosecretory rat pheochromocytoma PC12 cell line was investigated. External ATP induced [3H]NA release from prelabeled PC12 cells, in the presence of extracellular CaCl2. The potency order of ATP analogs was adenosine 5'-O-(gamma-thiotriphosphate) > or = ATP > 2-methylthio ATP > 2',3'-O-(4-benzoyl)benzoyl ATP. alpha,beta-Methylene ATP, beta gamma-methylene ATP, and 8-bromo ATP were inactive. Neither ADP, GTP, nor ITP was active. The addition of phorbol 12-myristate 13-acetate (PMA) or agents elevating the cyclic AMP content, such as vasoactive intestinal peptide (VIP) or an adenosine analog, also stimulated [3H]NA release. Not only high K(+)- but also ATP-stimulated [3H]NA release was enhanced by co-addition with PMA or agents elevating the cyclic AMP content. PMA and VIP had no effect on the cytosolic free Ca2+ concentration ([Ca2+]i) or on the ATP-stimulated [Ca2+]i rise, although both stimulatory effects on [3H]NA release were dependent on extracellular CaCl2. The addition of PMA stimulated [3H]NA release dose-dependently, and enhanced 300 microM (maximal dose) ATP-stimulated [3H]NA release without changing the affinity for ATP. The effect of PMA was inhibited by PKC inhibitors such as calphostin C and in PKC-depleted cells, and potentiated by elevation of cyclic AMP. These data suggest that the process of ATP-stimulated NA release, not ATP-stimulated Ca2+ influx, is regulated by the dual, PKC- and cyclic AMP-dependent mechanisms, positively and independently. Treatment with pertussis toxin had no effect on the ATP-stimulated [Ca2+]i rise or [3H]NA release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Establishment of a myeloid leukaemic cell line (SKNO-1) from a patient with t(8;21) who acquired monosomy 17 during disease progression.

A novel cell line SKNO-1 was established from the bone marrow cells of a 22-year-old male suffering from acute myeloblastic leukaemia (AML) M2 with t(8;21) whose disease became resistant to chemotherapy after acquisition of 17 monosomy. SKNO-1 has been maintained for more than 36 months as a granulocyte-macrophage colony-stimulating factor (GM-CSF) dependent line. Morphologically, SKNO-1 cells were myeloblasts somewhat matured. The cells grow in suspension with a doubling time of 48-72 h. The survival and growth of SKNO-1 cells was absolutely dependent on granulocyte-macrophage colony stimulating factor (GM-CSF). SKNO-1 cells possessed t(8;21) and monosomy 17 which were observed in original leukaemic cells. We confirmed that the AML1 gene, located on chromosome 21, was rearranged and the AML1-MTG8 fusion transcript was expressed in SKNO-1 cells. Over-expression and mutation of the p53 gene were also detected in SKNO-1. It is likely that alterations of AML1 or MTG8 gene and p53 gene contribute to a disease progression in this case. Since t(8;21) translocation is a common chromosome abnormality in AML, and inactivation of the p53 gene may play a crucial role in disease progression in AML, SKNO-1 would be a useful tool for analysing the molecular mechanisms in myeloid leukaemogenesis.

Adult↗
PubMed1995

Enhancement of natural killer cell activity in human immunodeficiency virus-infected subjects by in vitro treatment with biologic response modifier OK-432.

A decrease in natural killer (NK) cell function has been related to the progression of human immunodeficiency virus (HIV) infection. In the present study, we assessed the ability of a streptococcus-derived biologic response modifier, OK-432, to augment NK lysis of uninfected K562 and U937 cells and HIV-infected U937 cells by peripheral blood mononuclear cells (PBMC) from HIV-seropositive homosexual men. Optimal two- to fourfold increases in lysis of the three targets were observed after pretreatment of PBMC from HIV-negative subjects for 4 h with 2 micrograms of OK-432 per ml. This effect was related primarily to gamma interferon (IFN-gamma) production induced by OK-432 and was not linked to production of tumor necrosis factors alpha and beta or to monocytes in the cultures. The enhancing effect of OK-432 on NK cell function was diminished but still evident in PBMC from subjects with relatively early-phase (< 3-year) HIV infection and high CD4+ cell counts and was lower in subjects with longer-term HIV infection (> 3 years), in association with reduced production of IFN-gamma. Augmentation of NK cell activity in HIV-infected men by OK-432 was comparable to that induced by treatment of cells with 1,000 U of IFN-alpha or interleukin 2 per ml. The data suggest that the NK cell-enhancing effects of OK-432 are at least in part mediated by IFN-gamma and that OK-432 may be effective in treatment of patients with early-phase HIV infection.

Adult↗
PubMed1995

Aspergillus culture filtrates and sputum sols from patients with pulmonary aspergillosis cause damage to human respiratory ciliated epithelium in vitro.

Aspergillus species frequently colonize lower respiratory tracts and lungs with localized underlying conditions (healed tuberculous cavity, cystic fibrosis, bronchiectasis, etc.) even in subjects without systemic predisposing factors. We investigated the in vitro effects of culture filtrates of Aspergillus species and sputum sols from patients with pulmonary aspergillosis on ciliary beat frequency (CBF) and epithelial integrity of human respiratory ciliated epithelium. Culture filtrates of 25 clinically isolated fungi (16 Aspergillus fumigatus, three Aspergillus niger, one Aspergillus flavus, three Candida albicans, and two Cryptococcus neoformans) were obtained by culturing the fungi in Medium-199 at 37 degrees C for 7 days, and five sputum sols were obtained from patients with pulmonary aspergillosis infected by A. fumigatus. During 6 h experiments using a photometric technique, 14 out of 16 A. fumigatus culture filtrates caused progressive and significant reduction in CBF associated with marked epithelial disruption, whilst the culture filtrates of A. niger and A. flavus caused minor epithelial damage without slowing of CBF, and Medium-199 alone (Control) showed neither epithelial damage nor slowing of CBF. All of the sputum sols also caused significant slowing of CBF as well as epithelial disruption. Culture filtrates of C. albicans and Cr. neoformans had no effects on human respiratory epithelium. We conclude that Aspergillus species, especially A. fumigatus release a factor (or factors) which causes damage to respiratory epithelium and slows CBF, and that these factors may contribute to the colonization of the lower respiratory tracts by the Aspergillus species and may possibly contribute to the further proliferation and spread of the lesions in pulmonary aspergillosis.

Adult↗
PubMed1995

[Ryanodine receptors in the central nervous system].

Ryanodine receptor (RyR) is a calcium release channel protein on the intracellular Ca(2+)-store. While inositol 1,4,5-trisphosphate receptor (IP3R), another intracellular calcium release channel protein, is mainly found in non-muscle cells, such as neurons and hepatocytes, and smooth muscles, RyR is the Ca(2+)-release channel protein in skeletal and cardiac muscles. At least three genetically distinct isoforms of RyR are identified: isoform proteins Ryr1, Ryr2, and Ryr3 expressed by ryr1, ryr2 and ryr3, respectively. In the central nervous system where IP3R is much more abundant than RyR, the main isoform of RyR is Ryr2, which is specific to the cardiac ventricular muscle. Recently, ryr3 was detected in specific regions of the brain. In this paper, the heterogeneous distribution and localization of RyR isoforms in the brain are summarized. The discussion extends into their putative functions, especially potential involvement in neuronal plasticity.

Animals↗
PubMed1995

ATP receptor-mediated increase of Ca ionophore-stimulated arachidonic acid release from PC12 pheochromocytoma cells.

Phospholipase A2 has recently been proposed as the effector enzyme involved in the receptor-mediated release of arachidonic acid (AA). Released AA and its metabolites have been demonstrated to play an important role in the regulation of cell functions. [3H]AA release from prelabeled PC12 cells was stimulated by a Ca ionophore such as ionomycin or A23187. Although ATP and its effective analog, adenosine 5'-O-(3-thiotrisphosphate) (ATP gamma S), 2-methylthio ATP and 3'-O-(4-benzoyl)benzoyl ATP, did not stimulate [3H]AA release on their own, they did enhance Ca ionophore-stimulated [3H]AA release. The effect of ATP analogs was dose-dependent. ADP, UTP, GTP, ITP, alpha beta-methylene ATP, beta gamma-methylene ATP and 8-bromo ATP showed no effect or very limited effect. The effect of ATP gamma S was antagonized by suramin, a putative P2Y receptor antagonist. The effective ATP analogs also increased [Ca2+]i (cytosolic free Ca2+ concentration) via Ca2+ influx. However, the addition of 50 mM KCl or 10 microM bradykinin, which are well-known to increase [Ca2+]i by different pathways, did not stimulate [3H]AA release, either with or without the Ca ionophore. The addition of phorbol 12-myristate 13-acetate, an activator of protein kinase C, showed no effect on [3H]AA release, either with or without the Ca ionophore. These data suggest that 1) ATP increased Ca ionophore-stimulated AA release via a P2Y-like ATP receptor, and that 2) the elevation of [Ca2+]i by ATP does not quantitatively explain the ATP-stimulated AA release in PC12 cells.

Adenosine Triphosphate↗
PubMed1995

Assessment of left ventricular myocardial perfusion and diastolic function during acetylcholine-induced diffuse coronary vasoconstriction by Doppler echocardiography and thallium-201 scintigraphy.

BACKGROUND: We investigated whether diffuse coronary vasoconstriction induced by acetylcholine caused myocardial ischemia. METHODS: We studied 30 patients (40 coronary arteries) with spontaneous chest pain or equivocal studies on treadmill exercise testing and no significant coronary stenosis or previous myocardial infarction. During the acetylcholine provocation test, Doppler echocardiography was performed, and thallium-201 was injected intravenously for scintigraphy. We used Doppler echocardiography to measure the ratio of early-to-late peak mitral flow (E:A ratio). RESULTS: When acetylcholine was injected, the coronary arteries showed three different responses. Diffuse coronary vasoconstriction without chest pain or ischemic changes on the ECG was induced in 18 (45%) arteries and the E:A ratio decreased from 0.83 +/- 0.13 to 0.77 +/- 0.13 (P = 0.031). In 17 vessels (control arteries), the E:A ratio did not change significantly (from 0.88 +/- 0.15 to 0.88 +/- 0.18; P = 0.95). In five arteries, focal spasm was induced and the E:A ratio decreased from 0.83 +/- 0.18 to 0.66 +/- 0.13 (P = 0.043). Transient defects on thallium-201 scintigraphy were observed in the territory of eight (80%) arteries with diffuse vasoconstriction and in one (20%) control artery (P = 0.047). CONCLUSIONS: Diffuse coronary vasoconstriction induced by intracoronary acetylcholine can decrease the regional myocardial blood flow (as shown by thallium-201 scintigraphy) and can cause global left ventricular diastolic dysfunction (as shown by the results of Doppler echocardiography).

Acetylcholine↗