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Biomedical subjects

Y Maeda

Publications and source records attributed to Y Maeda.

At least 505 records · Page 28Linked to original sources

Hardness of denture reline materials polymerized with different techniques.

Two kinds of hard type self-cured denture reline materials were polymerized using three different techniques: (1) on a surface of glass plate, (2) under water, (3) under water with some hardening agent. Hardness of specimens were measured longitudinally during three weeks periods of storage in water at 37 degrees C. Results of our study indicated that the specimen cured with the special hardening agent showed the higher hardness than those cured only in water. Most of the hardness changes took place during first three days of the experiment period.

Acrylic Resins↗

Regulation of mouse UBF gene by multiple growth-related control elements.

Transcription of the mouse Upstream Binding Factor (mUBF) gene, that encodes one of the essential transcription factors for ribosomal DNA transcription, starts from several nucleotides. Neither typical TATA-box nor CCAAT-box is found upstream of the transcription initiation site. In the promoter region, there are eight GC-boxes, eight AP-2 binding consensus sequences, four cAMP response elements, and several serum response element equivalent sequences. These elements appear to play a positive role for the regulation of the mUBF gene as a whole. Among serum response elements, members located between -1182 and -343 are indeed responsive to serum, suggesting their important role in the high expression of mUBF under cell growth conditions.

Animals↗

Hypoxia/reoxygenation-mediated induction of astrocyte interleukin 6: a paracrine mechanism potentially enhancing neuron survival.

To elucidate mechanisms underlying neuroprotective properties of astrocytes in brain ischemia, production of neurotrophic mediators was studied in astrocytes exposed to hypoxia/reoxygenation (H/R). Rat astrocytes subjected to H/R released increased amounts of interleukin (IL) 6 in a time-dependent manner, whereas levels of tumor necrosis factor and IL-1 remained undetectable. IL-6 transcripts were induced in hypoxia and the early phase of reoxygenation, whereas synthesis and release of IL-6 antigen/activity occurred during reoxygenation. Elevated levels of IL-6 mRNA were due, at least in part, to increased transcription, as shown by nuclear runoff analysis. The mechanism stimulating synthesis and release of IL-6 antigen by astrocytes was probably production of reactive oxygen intermediates (ROIs), which occurred within 15-20 minutes after placing hypoxia cultures back into normoxia, as the inhibitor diphenyl iodonium inhibited the burst of ROIs and subsequent IL-6 generation (blockade of nitric oxide formation had no effect on ROI generation or IL-6 production). Enhanced IL-6 generation was also observed in human astrocytoma cultures exposed to H/R. Survival of differentiated PC12 cells exposed to H/R was potentiated by conditioned medium from H/R astrocytes, an effect blocked by neutralizing anti-IL-6 antibody. In a gerbil model of brain ischemia, IL-6 activity was lower in the hippocampus, an area sensitive to ischemia, compared with IL-6 activity in the cortex, an area more resistant to ischemia. IL-6 antigen, demonstrated immunohistochemically, was increased in astrocytes from ischemic regions of gerbil brain. These data suggest that H/R enhances transcription of IL-6, resulting in increased translation and release of IL-6 antigen after the burst of ROI generated early during reoxygenation. Release of IL-6 from astrocytes could exert a paracrine neurotrophic effect in brain ischemia.

Animals↗

High conservation of subunit composition of RNA polymerase I(A) between yeast and mouse and the molecular cloning of mouse RNA polymerase I 40-kDa subunit RPA40.

Mouse RNA polymerase I (or A) was purified from an ascites cell line MH134 to virtual homogeneity using a novel purification procedure and examined for subunit composition. In marked contrast to older purifications that reported 5-8 subunits, polymerase I was found to have 11 subunits with remarkable correspondence to those of yeasts. The cDNA encoding a 40-kDa subunit of this enzyme, designated RPA40, was isolated. It predicts a polypeptide of 355 amino acids (M(r) = 40,065) and is encoded by a single copy gene. Protein sequence analysis reveals that RPA40 is the homolog of yeast RPC40, having homology to alpha subunit of Escherichia coli RNA polymerase, yeast RPB3, and human RPB33 RNA polymerase II subunits. The high conservation of this subunit among distant eukaryotes and different RNA polymerases suggests functional importance of this protein as a core subunit.

Amino Acid Sequence↗

Presence of cholesterol 7 alpha-hydroxylase enzyme protein in COS-cells leads to increased HMG CoA reductase activity.

Transfection of COS-cells with a cDNA coding for human cholesterol 7 alpha-hydroxylase resulted in significant production of cholesterol 7 alpha-hydroxylase enzyme and intracellular accumulation of the product, 7 alpha-hydroxycholesterol. Presence of this enzyme activity was always associated with increased HMG CoA reductase activity. In five different independent transfection experiments resulting in a cholesterol 7 alpha-hydroxylase activity of 0.26 +/- 0.05 pmol/min/mg in the transfected cells, the HMG CoA reductase activity increased to 158 +/- 14% of that of the control cells (p < 0.01). This change was not associated with significant changes in the cholesterol content or LDL-receptor expression of the COS-cells. It is evident that the two key enzymes in cholesterol synthesis and degradation interact with each other also in extra-hepatic cells that are unable to degrade cholesterol into bile acids. Possible mechanisms for the finding is discussed.

Animals↗

Inhibition of growth of human small cell lung cancer by bromocriptine.

Bromocriptine, a dopaminergic agonist, inhibited the growth of human small cell lung cancer (SCLC) implanted as tumor xenografts in athymic nude mice; the effect was dose dependent. In mice bearing a SCLC with ectopic vasopressin production, plasma levels of human vasopressin-associated neurophysin decreased concomitantly. Electron microscopy of tumor tissues revealed marked degenerative changes, including pyknosis, densely aggregated chromatin masses, and vacuolization of cytoplasm after bromocriptine treatment. When a SCLC cell line, NCI-H69, was grown in semisolid medium, bromocriptine inhibited its clonal growth in a dose-related manner. Coincubation with dopamine D2 receptor antagonist, metoclopramide, or domperidone, completely blocked the inhibitory effect of bromocriptine. Receptor studies with a dopamine D2 receptor ligand, [125I]iodosulpride, showed high affinity binding sites on the membranes of SCLC cells. These results indicate that SCLC cells are enriched with dopamine D2 receptors, which may mediate the growth-inhibitory effect of bromocriptine on SCLC. Dopaminergic agonists may be useful in the medical treatment of SCLC.

Animals↗

Studies on neurokinin antagonists. 4. Synthesis and structure-activity relationships of novel dipeptide substance P antagonists: N2-[(4R)-4-hydroxy-1-[(1-methyl-1H-indol-3-yl)carbonyl]-L-prolyl]-N- methyl-N-(phenylmethyl)-3-(2-naphthyl)-L-alaninamide and its related compounds.

As an extension of our studies on discovering a novel substance P (SP) antagonist, we modified the previously reported dipeptide, N2-[N2-(1H-indol-3-ylcarbonyl)-L-lysyl]-N-methyl-N-(phenyl-methyl) -L- phenylalaninamide (2b). The lysine part in 2b was first optimized to a (2S,4R)-hydroxyproline derivative (3h), which is 2-fold more potent than 2b in [3H]SP binding assay using guinea pig lung membranes. Next we modified the 1H-indol-3-ylcarbonyl part in 3h. Introduction of a methyl group at the indole nitrogen enhanced the oral activity, while retaining the binding activity. Finally, we modified the phenylalanine part to culminate in the most potent compound 7k (FK888), which is a potent SP antagonist with NK1 selectivity as well as oral activity.

Animals↗

Precise expression of the cAMP receptor gene, CAR1, during transition from growth to differentiation in Dictyostelium discoideum.

The gene expressions associated with the switch-over from cell proliferation of Dictyostelium discoideum to differentiation have been analyzed using temperature shift and differential plaque hybridization methods. Quit1 was cloned as a specifically expressed gene when cells were starved just before the PS point (putative shift point from growth to differentiation). The coding region of the Quit1 gene is identical to that of the cAMP receptor 1 (CAR1) gene, which is essential for development. Quit1 mRNA was specifically expressed just after starvation of cells at around the PS point, thus indicating the importance of CAR1 for cellular differentiation as well as the actual existence of the PS point.

Alternative Splicing↗

Molecular genetics for clinical management of colorectal carcinoma. 17p, 18q, and 22q loss of heterozygosity and decreased DCC expression are correlated with the metastatic potential.

BACKGROUND: The molecular genetic changes associated with colorectal carcinoma are among the best understood of any common human cancer. The genetic changes during the late stages of colorectal carcinomas may be useful in clinical management for determining the metastatic potential of the carcinoma. METHODS: Tumor tissues were evaluated by restriction fragment length polymorphism (RFLP) analysis of chromosomes 5q, 17p, 18q, and 22q (n = 98), by reverse transcription-polymerase chain reaction (RT-PCR) analysis of messenger RNA expression of the DCC gene (deleted in colorectal carcinoma) (n = 27) and by immunohistochemical analysis of p53 protein expression (n = 44). RESULTS: Loss of heterozygosity (LOH) on chromosomes 17p, 18q, and 22q, but not on 5q, was much more frequently detected in advanced carcinomas than in intramucosal carcinomas (P < 0.01). 17p LOH was significantly correlated with vascular invasion (P < 0.001), whereas 18q LOH was correlated with lymphatic invasion and hepatic metastasis (P < 0.01), and 22q LOH was correlated with lymph node metastasis (P < 0.05). LOH on 5q did not show a significant correlation with any factors of tumor invasion or metastasis. DCC expression was not observed in any of five hepatic metastasis or in five of seven advanced carcinomas that were accompanied by hepatic metastasis (10 of 12). However, a similar lack of expression was observed in only 5 of 15 carcinomas without hepatic metastasis (P < 0.05). p53 Expression was found to vary in both primary and metastatic carcinomas by immunohistochemistry. CONCLUSIONS: The clinical application of molecular genetics (i.e., RFLP analysis of chromosome 17p, 18q, and 22q and RT-PCR analysis of DCC expression into messenger RNA) can be used to determine the metastatic potential of colorectal carcinomas.

Adult↗

Alteration of asparagine-linked glycosylation in serum transferrin of patients with hepatocellular carcinoma.

The asparagine-linked sugar chains in serum transferrin purified from patients with hepatocellular carcinoma (n = 13), healthy individuals (n = 5) and patients with liver cirrhosis (n = 6) were compared. Sugar chains released with N-glycanase from desialylated and pepsin-digested transferrin were derivatized by reductive pyridylamination. Analysis of the sugar chains by high performance liquid chromatography in combination with exoglycosidase digestion revealed an increase of a biantennary complex-type sugar chain with a fucosylated trimannosyl core; Gal beta 1-4GlcNAc beta 1-2Man alpha 1-6(Gal beta 1-4GlcNAc beta 1-2Man alpha 1-3) Man beta 1-4GlcNAc beta 1-4(Fuc alpha 1-6)GlcNAc in 7 of 13 cancer patients and an increase of a sugar chain with a fucosylated trimannosyl core and bisecting N-acetylglucosamine; Gal beta 1-4GlcNAc beta 1-2Man alpha 1-6(GlcNAc beta 1-4) (Gal beta 1-4GlcNAc beta 1-2Man alpha 1-3)Man beta 1-4GlcNAc beta 1-4(Fuc alpha 1-6)GlcNAc in one of the 13 cancer patients. Further, the fucosylated alteration of the sugar chain was detected also in alpha 1-antitrypsin, hemopexin, alpha 1-acid glycoprotein and alpha 2-HS glycoprotein from one of the patients with increased fucosylated transferrin.

Asparagine↗

Interleukin-6 in transcatheter arterial embolization for patients with hepatocellular carcinoma. Effects of serine protease inhibitor.

BACKGROUND: Modulation of serum levels of circulating cytokines and inflammatory responses with a serine protease inhibitor was studied in 34 patients with hepatocellular carcinoma (HCC) after transcatheter arterial embolization (TAE). METHODS: The 34 patients were randomly divided into two groups: 17 patients received 500 mg gabexate mesilate, a serine protease inhibitor, intravenously twice a day for 5 days after TAE, and the remaining 17 patients did not receive the drug. RESULTS: In the patients not given the drug, circulating interleukin-6 (IL-6) markedly increased 1 day after TAE, reached a peak (approximately 8 times the pretreatment value) after 4 days, and remained elevated 7 days after TAE. In comparison, in the patients given the drug, circulating IL-6 was at a significantly lower level at 4 and 7 days after TAE (P < 0.05, respectively). Both groups did not show significant change in circulating interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) during the week after TAE. The drug also showed a tendency to keep patient temperature below 38 degrees C, and the elevation of serum C-reactive protein (CRP) concentration to less than 1 mg/dl after TAE (P < 0.05, respectively). CONCLUSIONS: The serum level of circulating IL-6 can be modulated by serine protease inhibitor, and this may contribute to suppressing inflammatory responses, such as fever and acute-phase protein synthesis, in the liver after TAE.

Aged↗

Cell-cycle-dependent sorting in the development of Dictyostelium cells.

The sorting behavior of Dictyostelium discoideum Ax-2 cells and its relation to the cell-cycle phase at the onset of starvation were analyzed with reference to pattern formation, using beta-galactosidase as a cell marker and the temperature-shift method for cell synchronization. Cells transformed with the vector pAct15-Gal showed different sorting behavior during development when they were starved at different cell-cycle phases. Cells (T7) starved at the mid-late G2 phase (just before the PS-point from which cells enter the differentiation phase when starved) aggregated most rapidly and possibly functioned as aggregation centers, but were eventually sorted out to the posterior zone of migrating slugs. In contrast, T1 cells starved at the late G2 phase (just after the PS-point) exhibited slower aggregation compared with T7 cells. During further culture, T1 cells then sorted out to the apical tips of tipped aggregates and were located predominantly in the anterior zone of migrating slugs. Thus, T1 and T7 cells apparently interchange their positions in the cell masses during tip formation. The possible significance of cell-cycle-related sorting presented here is discussed, with special emphasis on pattern formation and cell differentiation.

Animals↗

Inhibitory effects of salmon calcitonin on the tail-biting and scratching behavior induced by substance P and three excitatory amino acids.

We have examined the effects of salmon calcitonin (SCT), injected into the cerebral ventricle (i.c.v.), on the tail-biting and scratching behavior induced by the intrathecal injection of different types of nociceptive agents, i.e., substance P, N-methyl-D-aspartate (NMDA), kainate (KA), and quisqualate (Quis). Tail-biting and scratching behavior induced by the 4 substances was significantly inhibited by SCT (i.c.v.) in the same manner: the dose-response curves were U-shaped, and the most effective dose was 0.1 IU/mouse in all cases. SCT did not, however, completely inhibit tail-biting and scratching behavior. At its most effective dose, the percent inhibition of substance P-, NMDA-, KA- and Quis-induced behavior were 77.9%, 40.2%, 49.4%, and 52.9%, respectively. These results suggest that SCT has the inhibitory effects of substance P- and glutamate receptor agonists-induced nociceptive response in vivo.

Afferent Pathways↗

Seroepidemiology of hepatitis C virus infection in hemodialysis patients and the general population in Fukuoka and Okinawa, Japan.

In 1992, a seroepidemiologic study was carried out among hemodialysis patients and the general population in Fukuoka and Okinawa, Japan to determine the presence of hepatitis C virus (HCV) infection and HCV viremia. The markers used were antibody to HCV, determined by second-generation assay (anti-HCV), and HCV RNA, determined by the polymerase chain reaction. The prevalence of anti-HCV in Fukuoka was 3.3%, 73 per 2237 persons, significantly (P < 0.001) higher than the 0.4%, 5 per 1295, in Okinawa. The prevalence of anti-HCV in hemodialysis patients in Fukuoka was 51.9% (161 of 310 patients), significantly (P < 0.001) higher than the 9.1% (13 of 143 patients) in Okinawa. The ratio of HCV RNA-positive to anti-HCV-positive persons was significantly higher in hemodialysis patients (147/174, 84.5%) than in the general population (49/78, 62.8%) (P < 0.001). Elimination of HCV among hemodialysis patients appears to be difficult, as such patients have lower immune responses than the general population. In Fukuoka, but not in Okinawa, blood used for transfusion was supplied by paid donors at commercial blood banks from 1953 to 1969. This may explain why HCV infection is endemic in Fukuoka and not in Okinawa. Differences between the prevalence of anti-HCV in the hemodialysis patients in Fukuoka and Okinawa reflect differences in the prevalence in the general population in these two areas of Japan.

Adolescent↗