Biomedical subjects

A Murakami

Publications and source records attributed to A Murakami.

At least 127 records · Page 7Linked to original sources

PubMed1999

Extracardiac conduit replacement with autologous tissue only, via a left anterior small thoracotomy.

A 13-year-old boy, who had undergone a Rastelli procedure 8 years before, developed severe extracardiac conduit stenosis and infectious endocarditis. Sternal re-entry appeared to be dangerous and to require extensive adhesiolysis. Through a left anterior small thoracotomy, however, good exposure was obtained and the operation was performed safely and much less invasively. The main pulmonary artery was reconstructed with autologous tissues only, i.e. fibrous tissue bed and broadly based pericardial pedicle. There was no residual stenosis. The patient convalesced rapidly.

Adolescent↗

PubMed1999

Immunomodulatory action of citrus auraptene on macrophage functions and cytokine production of lymphocytes in female BALB/c mice.

The modifying effects of auraptene isolated from the peel of citrus fruit (Citrus natsudaidai Hayata) on macrophage and lymphocyte functions were investigated in mice. Female BALB/c mice were gavaged with auraptene at a dose of 100, 200 or 400 mg/kg once a day for 10 consecutive days. Glucose consumption of peritoneal macrophages was significantly higher than that in the control group (P < 0.05-0.001) in auraptene-treated mice at all doses at 24, 48 and 72 h incubation except for mice given 200 mg/kg auraptene at 24 h incubation. Activity of acid phosphatase in peritoneal macrophages was significantly increased in mice treated with auraptene at a dose level of 100 mg/kg (P < 0.001). Activity of beta-glucuronidase in peritoneal macrophages in the auraptene-treated mice at all doses was significantly higher than that in the control group (P < 0.001), but there was no significant difference in lactate dehydrogenase activity of peritoneal macrophages at any dose. Interleukin (IL)-1beta production of peritoneal macrophages in the auraptene-treated mice at all doses was significantly higher than that in the control group (P < 0.05-0.001). Tumor necrosis factor alpha production of peritoneal macrophages in mice gavaged with auraptene at a dose of 200 mg/kg was significantly higher than that in the control group (P < 0.05). Auraptene did not affect proliferation of spontaneous splenic lymphocytes in mice at any dose. Stimulation indices in mice given auraptene at a dose of 200 mg/kg were significantly higher than that in the control group (P < 0.05). When spleenic lymphocytes were cultured without concanavalin A (Con A), IL-2 and interferon (IFN) gamma productions were not detectable in the supernatant. However, IL-2 and IFN production stimulated by Con A were significantly increased in mice gavaged with auraptene at dose levels of 100 and 200 mg/kg (P 0.05-0.001). Auraptene did not enhance spontaneous IL-4 production by splenocytes. There was no significant difference in IL-4 production of splenic lymphocytes stimulated by Con A in all groups. These findings might suggest that oral administration of citrus auraptene effectively enhanced macrophage and lymphocyte functions in mice.

Acid Phosphatase↗

PubMed1999

Study on RNA structure by pyrene-labeled 2'-O-methyloligoribonucleotides.

Properties of 2'-O-methyloligoribonucleotides containing 2'-O-(1-pyrenylmethyl)uridine were investigated as the fluorescent probe to search the single strand regions on RNA secondary and tertiary structure. The pyrene-labeled 2'-O-methyloligoribonucleotide (OMUpy) showed remarkable increase of fluorescence intensity to 333-fold at 375 nm when hybridized with the complementary oligoribonucleotide. When OMUpy, complementary to loop or stem regions, was applied to E. coli 5S-rRNA, the fluorescence intensities were increased in a sequence specific manner. The difference of the fluorescence intensities corresponds to the higher-order structure of 5S-rRNA, suggesting that pyrene-labled 2'-O-methyloligoribonucleotide can be applicable to search single strand regions of RNA.

Base Sequence↗

PubMed1999

Photodynamic antisense regulation using psoralen-conjugated oligo(nucleoside phosphorothioate)s (I). Growth regulation of cervical carcinoma cells.

To increase the antisense regulatory effect of oligo(nucleoside phosphorothioate)s (S-Oligo), a photo-crosslinking reagent, 4, 5', 8-trimethylpsoralen, was used in this study. Psoralen-conjugated oligo(nucleoside phosphorothioate) (Ps-S-Oligo) complementary to the human papillomavirus type 18 (HPV18) mRNA drastically inhibited the cellular proliferation of cervical cancer cells only upon UVA-irradiation. In contrast, Ps-S-Oligos with mismatched sequences and scrambled one showed lesser inhibitory effects than that with matched one. These results suggest that psoralen-conjugated antisense S-Oligo has significant potential to regulate gene expression upon UVA-irradiation.

Cell Division↗

PubMed1999

Identification of zerumbone in Zingiber zerumbet Smith as a potent inhibitor of 12-O-tetradecanoylphorbol-13-acetate-induced Epstein-Barr virus activation.

Zerumbone was isolated from the rhizomes of Zingiber zerumbet Smith as a potent inhibitor of tumor promoter 12-O-tetradecanoylphorbol-13-acetate-induced Epstein-Barr virus activation. The IC50 value of zerumbone (0.14 microM) is noticeably lower than those of the anti-tumor promoters we have hitherto obtained. Interestingly, alpha-humulene lacking the carbonyl group at the 8-position in zerumbone was inactive (IC50 > 100 microM), while 8-hydroxy-alpha-humulune was markedly active (IC50 = 0.95 microM).

Anticarcinogenic Agents↗

PubMed1999

[Kerato-epithelin mutation (R 555 Q) in a case of Reis-Bücklers corneal dystrophy].

BACKGROUND: Mutations in the kerato-epithelin gene on chromosome 5 q 31 are known to cause four distinct autosomal dominant diseases of the human cornea: Reis-Bücklers, granular, lattice, and Avellino corneal dystrophy. Mutation of arginin to glutamine in codon 555 (R 555 Q) in kerato-epithelin was recently reported in four blood-related patients with Reis-Bücklers corneal dystrophy. CASE: A 42 year-old female has had photophobia with decreasing vision since the age of 20 years. Her corrected visual acuity was 0.5 in both eyes. She showed subepithelial opacities in both corneas characteristic of Reis-Bücklers corneal dystrophy. METHOD: The DNA was extracted from leukocytes according to standard protocols. The keratoepithelin gene was examined for a mutation by the polymerase chain reaction (PCR) and direct sequencing. FINDINGS: We identified kerato-epithelin mutation R 555 Q. The patient's two children and 50 controls did not show missense mutation. CONCLUSION: Kerato-epithelin mutation R 555 Q was present in a Japanese patient with Reis-Bücklers corneal dystrophy.

Adult↗

PubMed1999

Oral manifestations of Schimmelpenning syndrome: case report and review of literature.

Schimmelpenning syndrome (SS) is characterised by specific skin manifestations, skeletal defects, and central nervous system abnormalities. Here, the SS is briefly reviewed, and the oral and dental manifestations are described in a patient whose medical findings were previously published and included severe hypophosphatemic rickets. Significant oral and dental features included papillomatous lesions of the gingiva, hemihyperplasia (hemihypertrophy) of the tongue, bone cysts, aplasia of teeth, enlarged pulp chambers, hypoplastic or absent enamel, and an odontodysplasia-like permanent tooth.

Adolescent↗

PubMed1998

Isolation and characterization of the human X-arrestin gene.

Arrestins are signal transduction modulators that quench the activated state of receptors. X-arrestin (ARRX) is specifically expressed in the red-, green-, and blue-sensitive cone photoreceptors, and is most likely a modulator of cone phototransduction. The human gene for X-arrestin at Xcen-Xq22 has been shown to be approximately 20kb in size and to consist of 17 exons and 16 introns. The exons are generally small, including exon 16 of 10bp, and are clustered into three groups, separated by the two largest introns. This gene structure is generally similar to that of S-antigen, the rod photoreceptor arrestin. There is remarkable similarity, however, among the individual exons between the two genes in that 10 of the exons are identical in size. The 5' upstream region of the X-arrestin gene contains TATA and CAAT boxes, typical of genes expressed in a tissue-specific manner, in contrast to the S-antigen gene, which lacks these promoter sequences. The promoter elements, common to both the X-arrestin and S-antigen genes, include the Ret-1/PCE-1 (PCE-1-like in X-arrestin), CRX, and the thyroid hormone/retinoic acid-responsive sequences, the former two being present in a number of photoreceptor-expressed genes. Three CRX-binding elements, 15bp apart, are present in a cluster. The common promoter elements between the cone-expressed genes, X-arrestin and color opsins, include the TATA box, PCE-1, and CRX-binding sequences, the combination of which might be important for directing cone-specific expression.

Amino Acid Sequence↗

PubMed1998

Suppression of tumor promoter-induced oxidative stress and inflammatory responses in mouse skin by a superoxide generation inhibitor 1'-acetoxychavicol acetate.

Double applications of phorbol esters trigger excessive reactive oxygen species (ROS) production in mouse skin. Previously reported data suggest that the two applications induce distinguishable biochemical events, namely, priming and activation. The former is characterized as a recruitment of inflammatory cells, such as neutrophils, by chemotactic factors to inflammatory regions and edema formation. The latter is responsible for ROS generation. Thus, inhibitory effects of 1'-acetoxychavicol acetate (ACA), previously reported to be a superoxide generation inhibitor in vitro, on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative stress and inflammatory responses in mouse skin model were examined using a double application of ACA. We demonstrated that two pretreatments and pretreatment with ACA (810 nmol) in the activation phase suppressed double TPA application-induced H2O2 formation in mouse skin. ACA exhibited no inhibitory effects on edema formation and the enhancement of myeloperoxidase activity during the first TPA treatment, whereas the anti-inflammatory agent genistein administered at the same dose inhibited both biomarkers. No inhibitory potential of ACA for TPA-induced H2O2 formation in the priming phase was confirmed. On the other hand, in the in vitro study, ACA inhibited ROS generation in differentiated HL-60 cells more strongly than did 1'-hydroxychavicol, which showed no inhibition by pretreatment in the activation phase. In addition, allopurinol did not inhibit double TPA application-induced H2O2 formation in mouse skin. These findings suggest that the NADPH oxidase system of neutrophils rather than the epithelial xanthine oxidase system is dominant for the O2--generating potential in double TPA-treated mouse skin. ACA significantly inhibited mouse epidermis thiobarbituric acid-reacting substance formation, known as an overall oxidative damage biomarker. Moreover, histological studies demonstrated that ACA inhibited double TPA treatment-induced morphological changes reflecting inflammatory response, such as edema formation, leukocyte infiltration, hyperplasia, and cell proliferation. Furthermore, pretreatment with ACA but not 1'-hydroxychavicol in the activation phase inhibits double TPA application-induced increases in both number of leukocytes and proliferating cell nuclear antigen index. These results suggested that ROS from leukocytes including O2- plays an important role for continuous and excessive production of chemotactic factors, leading to chronic inflammation and hyperplasia, which are inhibitable by ACA. Thus, we concluded that O2- generation inhibitors are agents that effectively inhibit oxidative stress and inflammatory responses in mouse skin.

Animals↗

PubMed1998

Analysis of deleted variant of hepatocyte growth factor by alanine scanning mutagenesis: identification of residues essential for its biological function and generation of mutants with enhanced mitogenic activity on rat hepatocytes.

To understand the structure-function relationship of hepatocyte growth factor (HGF) in more detail, we analyzed one of the other forms of HGF, deleted variant of HGF (dHGF), by alanine scanning mutagenesis. We show here that there are at least four sites important for dHGF to stimulate DNA synthesis in cultured adult rat hepatocytes, and that the residues of HGF essential for exerting its biological activity are not identical to those of dHGF. In addition, two mutants showed a decrease (approximately three-fold) in EC50 compared with wild-type dHGF in an assay of mitogenic activity on rat hepatocytes.

Alanine↗

PubMed1998

Structure of the mouse osteoclastogenesis inhibitory factor (OCIF) gene and its expression in embryogenesis.

Osteoclastogenesis inhibitory factor (OCIF) is a novel soluble-form member of the tumor necrosis factor receptor family and is involved in the regulation of bone mass. Here we isolated genomic and cDNA clones for mouse OCIF and determined their structures. Mouse OCIF gene spans 29 kb and contains five exons of 270, 367, 192, 225 and 1765 bp long. Four cysteine-rich domains and two death domain homologous regions characterized in human OCIF are rigidly conserved in mouse OCIF. The onset of OCIF gene expression in mouse embryogenesis is at day 8.5. In a pregnant female mouse, OCIF gene is expressed in decidua, a maternal tissue surrounding each embryo, immediately after implantation. The isolation of mouse OCIF gene should facilitate studies on OCIF knock-out mice for a better understanding of the role of OCIF in vivo.

Amino Acid Sequence↗

PubMed1998

Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor/osteoprotegerin.

Osteoclasts are multinucleated cells that resorb bone. Osteoclastogenesis inhibitory factor (OCIF), also called osteoprotegerin (OPG), acts as a naturally occurring decoy receptor for osteoclast differentiation factor, which mediates an essential signal to osteoclast progenitors for their differentiation into osteoclasts. Here we show that the OCIF/OPG knockout mice exhibited severe osteoporosis due to enhanced osteoclastogenesis when they grew to be adults. These mice were viable and fertile. They exhibited marked bone loss accompanied by destruction of growth plate and lack of trabecular bone in their femurs. The strength of their bones dramatically decreased. These results demonstrate that OCIF/OPG is a key factor acting as a negative regulator against osteoclastogenesis. The OCIF/OPG knockout mice provide the first animal model for osteoporosis without other obvious abnormalities.

Animals↗

PubMed1998

Citrus auraptene exerts dose-dependent chemopreventive activity in rat large bowel tumorigenesis: the inhibition correlates with suppression of cell proliferation and lipid peroxidation and with induction of phase II drug-metabolizing enzymes.

In our previous short-term experiment, Citrus auraptene inhibited the development of azoxymethane (AOM)-induced aberrant crypt foci, which are precursor lesions for colorectal carcinoma. In the present study, the possible inhibitory effect of dietary administration of auraptene was investigated using an animal colon carcinogenesis model with a colon carcinogen AOM. Male F344 rats were given s.c. injections of AOM (15 mg/kg body weight) once a week for 3 weeks to induce colon neoplasms. They also received diets containing 100 or 500 ppm auraptene for 4 weeks in groups of "initiation" feeding, starting 1 week before the first dosing of AOM. The diets containing auraptene were also given to rats for 38 weeks in groups of "postinitiation" feeding. At the termination of the study (38 weeks), dietary administration of auraptene caused dose-dependent inhibition in AOM-induced large bowel carcinogenesis. Auraptene feeding during the initiation phase reduced the incidence of colon adenocarcinoma by 49% at 100 ppm (P = 0.099) and 65% at 500 ppm (P = 0.0075). Auraptene administration during the postinitiation phase inhibited the incidence of colon adenocarcinoma by 58% at 100 ppm (P = 0.021) and 65% at 500 ppm (P = 0.0075). Also, the multiplicity of colon carcinoma was significantly reduced by initiation feeding at a dose level of 500 ppm (P < 0.01) and postinitiation feeding at a level of 100 and 500 ppm (P < 0.05 and P < 0.01, respectively). Feeding of auraptene suppressed the expression of cell proliferation biomarkers (ornithine decarboxylase activity and polyamine content) in the colonic mucosa and reduced the production of aldehydic lipid peroxidation [malondialdehyde and 4-hydroxy-2(E)-nonenal]. In addition, auraptene increased the activities of Phase II drug-metabolizing enzymes (glutathione S-transferase and quinone reductase) in the liver and colon. These findings suggest that the inhibitory effects of auraptene on AOM-induced colon tumorigenesis at the initiation level might be associated, in part, with increased activity of Phase II enzymes, and those at the postinitiation stage might be related to suppression of cell proliferation and lipid peroxidation in the colonic mucosa.

Aldehydes↗

PubMed1998

Identification of heparin-binding stretches of a naturally occurring deleted variant of hepatocyte growth factor (dHGF).

A deleted variant of hepatocyte growth factor (dHGF) is a naturally occurring major variant of HGF, which lacks five consecutive amino acid residues in the first kringle domain. While both HGF and dHGF bind to heparin, the residues involved in the binding to heparin have not been identified in either protein. To identify the residues involved in the binding, we made a series of dHGF mutants in which basic residues in the N-terminal and the first kringle domains were replaced with alanine residue. The analysis of heparin-binding ability revealed that three stretches, 42RCTRNK in the hairpin loop structure, and 2RKRR and 27KIKTKK in the N-terminal basic region, are involved in the binding. Alanine substitution of each basic residue except 3K and 27K in the stretches reduced the heparin-binding ability of dHGF, and the decrease was additive. Conversely, lysine substitution of 37D, 38Q or 64Q in the N-terminal domain increased heparin-binding ability. These results suggest that stretches distant from each other in the primary structure come into close proximity when the polypeptide folds into protein, and form a heparin-binding site with clusters of basic residues.

Amino Acid Sequence↗

PubMed1998

Acquisition of a new type of fructose-1,6-bisphosphatase with resistance to hydrogen peroxide in cyanobacteria: molecular characterization of the enzyme from Synechocystis PCC 6803.

We have previously described that Synechococcus PCC 7942 cells contain two fructose-1,6-bisphosphatase isozymes, designated F-I and F-II the former belongs to a new type of fructose-1,6-bisphosphatase, while the latter is a typical enzyme similar to the cytosolic and chloroplastic forms from eukaryotic cells [Tamoi et al., Arch. Biochem. Biophys., 334, 1996, 27-36]. The genes of F-I and F-II were found in three species of cyanobacteria, Synechocystis PCC 6803, Anabaena 7120, and Plectonema boryanum according to the results of Southern hybridization with a probe from the S. 7942 F-I and F-II genes. In Western blotting, antibody raised against the S. 7942 F-I cross-reacted with a protein band corresponding to the F-I in each crude extract from cyanobacterial cells, whereas the antibody against F-II failed to cross-react with any protein band corresponding to the F-II. In cyanobacterial cells, only one form of F-I has been resolved by ion-exchange chromatography at same concentration of NaCl as shown in the F-I of S. 7942. The F-I from Synechocystis 6803 has been purified to electrophoretic homogeneity. The enzyme hydrolyzed both fructose 1,6-bisphosphate and sedoheptulose 1,7-bisphosphate. The apparent K(m) values of the enzyme for fructose 1,6-bisphosphate and sedoheptulose 1,7-bisphosphate were 57 +/- 2.4 and 180 +/- 6.3 microM, respectively. The enzyme activity was inhibited by AMP with a Ki value of 0.57 +/- 0.03 mM for fructose 1,6-bisphosphate and 0.35 +/- 0.02 mM for sedoheptulose 1,7-bisphosphate. The enzyme showed a molecular mass of 168 kDa which was composed of four identical subunits. The activities of FBPase and SBPase from the F-I were resistant to hydrogen peroxide up to 1 mM. The nucleotide sequence of the S. 6803 F-I gene showed an open reading frame of 1164 bp that encoded a protein of 388 amino acid residues (approx. molecular mass of 41.6 kDa). The deduced amino acid sequences had homologous sequences with the S. 7942 F-I.

Amino Acid Sequence↗

PubMed1998

Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL.

Osteoclasts, the multinucleated cells that resorb bone, develop from hematopoietic cells of monocyte/macrophage lineage. Osteoclast-like cells (OCLs) are formed by coculturing spleen cells with osteoblasts or bone marrow stromal cells in the presence of bone-resorbing factors. The cell-to-cell interaction between osteoblasts/stromal cells and osteoclast progenitors is essential for OCL formation. Recently, we purified and molecularly cloned osteoclastogenesis-inhibitory factor (OCIF), which was identical to osteoprotegerin (OPG). OPG/OCIF is a secreted member of the tumor necrosis factor receptor family and inhibits osteoclastogenesis by interrupting the cell-to-cell interaction. Here we report the expression cloning of a ligand for OPG/OCIF from a complementary DNA library of mouse stromal cells. The protein was found to be a member of the membrane-associated tumor necrosis factor ligand family and induced OCL formation from osteoclast progenitors. A genetically engineered soluble form containing the extracellular domain of the protein induced OCL formation from spleen cells in the absence of osteoblasts/stromal cells. OPG/OCIF abolished the OCL formation induced by the protein. Expression of its gene in osteoblasts/stromal cells was up-regulated by bone-resorbing factors. We conclude that the membrane-bound protein is osteoclast differentiation factor (ODF), a long-sought ligand mediating an essential signal to osteoclast progenitors for their differentiation into osteoclasts. ODF was found to be identical to TRANCE/RANKL, which enhances T-cell growth and dendritic-cell function. ODF seems to be an important regulator in not only osteoclastogenesis but also immune system.

Animals↗

PubMed1998

Screening of edible Japanese plants for nitric oxide generation inhibitory activities in RAW 264.7 cells.

A total of 48 (60 test samples) species of plants commonly eaten in Japan were randomly collected and their methanol extracts were tested for in vitro nitric oxide (NO) generation inhibitory activities in a murine macrophage cell line, RAW 264.7, stimulated with both lipopolysaccharide (LPS, 100 ng/ml) and interferon-gamma (IFN-gamma, 100 U/ml). Seventeen (28.3%) of the 48 extracts strongly inhibited NO generation at a concentration of 200 microg/ml by 70% or more with significant cell viability (>50%). The extracts from avocado, taro, red turnip, sereves, komatsuna, basil, mitsuba and Chinese mustard markedly inhibited iNOS activity. These results suggest that a wide variety of edible plants in Japan contain the secondary metabolites carrying cancer preventive activity through reduction of excess amounts of NO.

Animals↗

PubMed1998

A Dumon stent inserted for bronchial stenosis causing a left bronchopericardial fistula: report of a case.

We present herein the case of a 59-year-old man in whom a Dumon stent, inserted as treatment for stenosis of the left main bronchus, caused a left bronchopericardial fistula. The patient initially presented with severe dyspnea caused by main bronchial stenosis of unknown origin for which a Dumon stent was inserted at a local hospital. The Dumon stent migrated to the endobronchus through the stenosis of the left main bronchus a few days later, and his dyspnea remained unresolved. He was subsequently referred to our department 6 months later, where a left pneumonectomy under supportive cardiopulmonary bypass through the femoral artery and vein was performed, and a postoperative pathological diagnosis of bronchial leiomyosarcoma was made. For this rare group of malignant tumors, early diagnosis permits complete surgical resection of the mass and offers the best prognosis. Excision of the tumor should be performed under cardiopulmonary bypass through the femoral vessels when a risk of sudden rupture of the pulmonary artery or vein exists for any reason.

Bronchi↗