[A case of IIa + IIb-like advanced gallbladder cancer: usefulness of endoscopic double contrast cholecystography].
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Adenocarcinoma, Papillary↗
Biomedical subjects
Y Fujimoto
Publications and source records attributed to Y Fujimoto.
Induction of a novel gelatinolytic activity in synovial tissue of patients with rheumatoid arthritis.
Gelatinolytic activity induced by longtime incubation at 37 degrees C was found in extracts of rheumatoid synovial tissues. The enzyme activity was assessed by gelatin zymography and 3H-gelatin degradation assay. The observed enzyme had different characteristics from matrix metalloproteinases; it did not require metal ions for activity. However, metallocheltors blocked activation and addition of some metal ions restored the activation. The molecular size of the enzyme was changed time-dependently. The approximate molecular weight of the first enzyme produced by incubation was 65 kDa and it was converted to a broad size molecule with a molecular weight of 50 kDa after further incubation. Substrate specificity was detected for denatured collagen types I, II, III and IV.
Arthritis, Rheumatoid↗
Inactivation of creatine kinase induced by dopa and dopamine in the presence of ferrylmyoglobin.
We investigated the effect of dopa and dopamine on creatine kinase (CK) activity in the presence of ferrylmyoglobin (ferrylMb). CK was sharply inhibited by dopa and dopamine in the presence of ferrylMb. Dopa and dopamine markedly promoted the reduction of ferrylMb to metmyoglobin (metMb). The semiquinone from dopa and dopamine may be involved in CK inactivation. During inactivation of the enzyme, both kinetic parameters Vmax and Km changed. In addition, reduced glutathione restored the activity of CK at an early stage. These results suggest that inactivation of CK is dominantly due to oxidation of sulfhydryl (SH) groups of the enzyme. Other catechols, such as adrenaline and noradrenaline, little inactivated CK activity, whereas they promoted the reduction of ferrylMb to metMb. Other SH enzymes, including alcohol dehydrogenase (ADH) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), were inactivated to a lesser extent by dopa and dopamine in the presence of ferrylMb. Adrenaline and noradrenaline did not significantly prevent the inactivation of ADH and very slightly inhibited GAPDH. These results suggest that dopa and dopamine act as prooxidants to inactivate SH enzymes in the presence of ferrylMb.
Alcohol Dehydrogenase↗
Sphingomyelin inhibits platelet 12-lipoxygenase activity.
The effect of sphingomyelin on the formation of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE), thromboxane B2 and 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT) in washed rabbit platelets was examined. Sphingomyelin had a powerful inhibitory effect on 12-HETE formation, while it produced only a small increase in thromboxane B2 and HHT formation. The sphingomyelin metabolite ceramide did not affect the formation of 12-HETE, thromboxane B2 and HHT. These results suggest that sphingomyelin is a selective inhibitor of platelet 12-lipoxygenase and may have functional effects in platelets.
Animals↗
Inhibition of cholesteryl ester formation in macrophages by azole antimycotics.
Cultured macrophages take up and metabolize cholesterol-containing liposomes, resulting in massive accumulation of cholesteryl esters in the cells. Using this system, the effects of azole antimycotics on cholesteryl ester formation were studied. Incubation of mouse peritoneal macrophages with ketoconazole, miconazole, or econazole (0.1-10 microM) resulted in concentration-dependent inhibition of cholesteryl ester synthesis from endocytosed cholesterol. IC50 values (concentration resulting in 50% inhibition) were 1.4 +/- 0.1 microM, 4.1 +/- 0.2 microM, and 3.6 +/- 0.2 microM for ketoconazole, miconazole, and econazole, respectively. Complete inhibition was observed with 10 microM ketoconazole, and miconazole and econazole, each at 10 microM, caused 70 and 75% inhibition, respectively, of cholesteryl ester synthesis. The mechanism underlying the inhibition by ketoconazole was further studied. Ketoconazole did not appreciably block the uptake of liposomes or formation of triacylglycerol up to 10 microM. Interestingly, ketoconazole suppressed only 30% of 25-hydroxycholesterol-induced endogenous cholesterol esterification under conditions where esterification of endocytosed cholesterol was completely inhibited. Cytochemical studies with filipin-cholesterol staining revealed that ketoconazole induced massive accumulation of endocytosed cholesterol in macrophage phagolysosomes. These results indicate that ketoconazole inhibits cholesteryl ester formation in macrophages by blocking the intracellular transport of endocytosed cholesterol from lysosomes to the endoplasmic reticulum.
Animals↗
Activation of PPARgamma inhibits cell growth and induces apoptosis in human gastric cancer cells.
We investigated the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and the role of PPARgamma in cell growth in human gastric cancer cells. Reverse transcription-polymerase chain reaction, Northern blot and Western blot analyses showed that a human gastric cancer cell line, MKN45, expressed PPARgamma mRNA and protein. Luciferase assay in MKN45 cells showed that troglitazone, a selective ligand for PPARgamma, transactivated the transcription of a peroxisome proliferator response element-driven promoter. Troglitazone or pioglitazone, selective ligands for PPARgamma, inhibited the growth of MKN45 cells in a dose-dependent manner. Co-incubation of MKN45 cells with troglitazone induced DNA ladder formation. These results suggest that human gastric cancer cells express PPARgamma and that activation of PPARgamma inhibits cell growth and induces apoptosis in gastric cancer cells.
Acyl-CoA Oxidase↗
Spontaneous epidural hematoma following a shunt in an infant with congenital factor X deficiency. Case report and literature review.
The authors describe a case of an infant with congenital factor X deficiency. The patient presented with a central nervous system hemorrhage followed by hydrocephalus. He underwent a ventriculoperitoneal shunt and, during the postoperative period, developed a spontaneous epidural hematoma, which was evacuated. The clinical and pathophysiological aspects of this case are discussed based on a literature review.
Adult↗
Existence of acyl-CoA hydrolase-mediated pathway supplying arachidonic acid for prostaglandin synthesis in microsomes from rabbit kidney medulla.
We have previously shown that acyl-coenzyme A (CoA) hydrolase that hydrolyzes arachidonoyl-CoA (AA-CoA) to arachidonic acid (AA) and CoA is present in the cytosol of rabbit kidney medulla and that this enzyme can supply AA for prostaglandin (PG) synthesis in this region. In the present study, the existence of the acyl-CoA hydrolase-mediated pathway that supplies AA available for PG synthesis in microsomes from the kidney medulla was examined. AA-CoA (20 microM) was preincubated with the 105,000 g pellet (microsomes, 0.5 mg of protein) from the medulla for 5 min at 37 degrees C followed by incubation with the medulla microsomes (0.5 mg of protein) (the source of PG synthesizing enzymes) in the presence of hydroquinone and reduced glutathione for 5 min at 37 degrees C. The PGs formed were measured by high-pressure liquid chromatography using 9-anthryldiazomethane for derivatization. The addition of the microsomal fraction from the medulla in the preincubation mixture increased total PG formation from 3.86 to 8.70 nmol, and this stimulatory effect was somewhat weaker than that of the cytosolic fraction. On the other hand, the microsomal fraction in the kidney cortex has an extremely lower capacity to supply AA for PG synthesis than do medulla microsomes. These results suggest that, in kidney medulla, the microsomes as well as the cytosol have the potential route that supplies AA from AA-CoA for PG synthesis and that this pathway is mediated by acyl-CoA hydrolase.
Acyl Coenzyme A↗
Biosynthesis of 20-hydroxyecdysone in Ajuga hairy roots: fate of 6alpha- and 6beta-hydrogens of lathosterol.
The fate of 6alpha- and 6beta-hydrogens of lathosterol during the transformation into 20-hydroxyecdysone was chased by feeding [3alpha,6beta-2H2]- and [3alpha,6alpha-2H2]-lathosterols to hairy roots of Ajuga reptans var. atropurpurea. The behavior of 6beta-hydrogen, which mostly migrated to the C-5 position of 20-hydroxyecdysone, was in agreement with that of C-6 hydrogen of cholesterol. The results strongly supported the view that cholesterol and lathosterol are first metabolized into 7-dehydrocholesterol, which is then converted into 20-hydroxyecdysone via 7-dehydrocholesterol 5alpha,6alpha-epoxide in the hairy roots.
Cholesterol↗
C(13)-Norisoprenoid glucoconjugates from lulo (Solanum quitoense L.) leaves.
With the aid of multilayer coil countercurrent chromatography, subsequent acetylation, and liquid chromatographic purification of a glycosidic mixture obtained from lulo (Solanum quitoense L.) leaves, three C(13)-norisoprenoid glucoconjugates were isolated in pure form. Their structures were elucidated by NMR, MS, and CD analyses to be the novel (6R,9R)-13-hydroxy-3-oxo-alpha-ionol 9-O-beta-D-glucopyranoside (4a), the uncommon (3S,5R,8R)-3, 5-dihydroxy-6,7-megastigmadien-9-one 5-O-beta-D-glucopyranoside (citroside A) (5a), and the known (6S,9R)-vomifoliol 9-O-beta-D-glucopyranoside (6a). Enzymatic treatment of compound 5a showed the formation of 3-hydroxy-7,8-didehydro-beta-ionone (7), an important lulo peeling volatile, which in its turn after chemical reduction and heated acid catalyzed rearrangement generates beta-damascenone (9) and 3-hydroxy-beta-damascone (10).
Fruit↗
Proline-rich antimicrobial peptide, PR-39 gene transduction altered invasive activity and actin structure in human hepatocellular carcinoma cells.
PR-39 is an endogenous proline-rich antimicrobial peptide which induces the synthesis of syndecan-1, a transmembrane heparan sulphate proteoglycan involved in cell-to-matrix interactions and wound healing. Previously, we revealed that the expression of syndecan-1 was reduced in human hepatocellular carcinomas with high metastatic potential and speculated that syndecan-1 played an important role in inhibition of invasion and metastasis. It is assumed that a modification of this process with PR-39 and syndecan-1 may result in a new strategy by which it can inhibit the invasion and metastasis. Therefore, we transduced a gene of PR-39 into human hepatocellular carcinoma cell line HLF, which shows a low expression of syndecan-1 and a high in vitro invasive activity, and examined whether this procedure could reduce the invasive activity of tumour cells. In two transfectants with PR-39 gene, the syndecan-1 expression was induced and the invasive activity in type I collagen-coated chamber was inhibited. Moreover, these transfectants showed the suppression of motile activity assayed by phagokinetic tracks in addition to the disorganization of actin filaments observed by a confocal imaging system. In contrast, five transfectants with syndecan-1 gene in the HLF cells revealed suppression of invasive activity but did not alter the motile activity and actin structures of the cell. These results suggest that PR-39 has functions involved in the suppression of motile activity and alteration of actin structure on human hepatocellular carcinoma cells in addition to the suppression of invasive activity which might result from the induction of syndecan-1 expression.
Actin Cytoskeleton↗
Improvement of exercise capacity of rats with chronic heart failure by long-term treatment with trandolapril.
1. The effects of long-term treatment with trandolapril, an angiotensin I-converting enzyme inhibitor, on exercise capacity of rats with chronic heart failure (CHF) following coronary artery ligation were examined. CHF was developed by 8 weeks after the coronary artery ligation. 2. The running time of rats with CHF in the treadmill test was shortened to approximately 65% of that of sham-operated rats (16.3+/-1.2 vs. 25.1+/-1.6 min, n = 7; P<0.05). ATP, creatine phosphate (CP), and lactate contents of the gracilis muscle of rats with CHF were similar to those of sham-operated rats before running. After running, ATP and CP were decreased and lactate was increased in both rats with CHF and sham-operated rats. There were no significant differences in the levels of energy metabolites between rats with CHF and sham-operated rats. The rates of decrease in ATP and CP and rate of increase in lactate in the gracilis muscle of rats with CHF during exercise were greater than those of sham operated rats (2.5, 2.0 and 1.5 fold high, respectively), suggesting wastage of energy during exercise in the animals with CHF. 3. Myofibrillar Ca2+ -stimulated ATPase (Ca-ATPase) activity of skeletal muscle of rats with CHF was increased over that of the sham-operated control (62.03+/-1.88 vs. 52.34+/-1.19 micromol Pi mg(-1) protein h(-1) n = 7; P<0.05). The compositions of myosin heavy chain (MHC) isoforms of gracilis muscle were altered by CHF; decreases in MHC types I and IIb and an increase in MHC type IIa were found (P<0.05). 4. Rats with CHF were treated with 1 mg kg(-1) day(-1) trandolapril from the 2nd to 8th week after surgery. Treatment with trandolapril prolonged the running time, reversed the rates of decrease in ATP and CP and the rate of increase in lactate, and restored the Ca-ATPase activity (51.11+/-0.56 micromol Pi mg(-1) protein h(-1), n = 7; P<0.05) and composition ratio of MHC isoforms in the gracilis muscle. 5. The results suggest that long-term trandolapril treatment of rats with CHF may restore their ability to utilize energy without wastage and thus improve exercise capacity.
Angiotensin-Converting Enzyme Inhibitors↗
Simultaneous measurement of prostaglandin and arachidonoyl CoA formed from arachidonic acid in rabbit kidney medulla microsomes: the roles of Zn2+ and Cu2+ as modulators of formation of the two products.
Under physiological conditions, small amounts of free arachidonic acid (AA) is released from membrane phospholipids, and cyclooxygenase (COX) and acyl-CoA synthetase (ACS) act competitively on this fatty acid to form prostaglandins (PGs) and arachidonoyl-CoA (AA-CoA). To date, there is no information about the factors deciding the metabolic fate of free AA into these two pathways. In this study, we tried to establish a method for the simultaneous measurement of PG and AA-CoA synthesis from exogenous AA in microsomes from rabbit kidney medulla. The kidney medulla microsomes were incubated with [14C]-AA in 0.1 M-Tris/HCI buffer (pH 8.0) containing cofactors of COX (reduced glutathione and hydroquinone) and cofactors of ACS (ATP, MgCl2 and CoA). After incubation, PG (as total PGs), AA-CoA and residual AA were separated by selective extraction using petroleum ether and ethyl acetate. When 60 microM AA was used as the substrate, indomethacin (an inhibitor of COX) and triacsin C (an inhibitor of ACS) reduced only PG and AA-CoA formation, respectively. On the other hand, when 5 microM AA was used as the substrate, indomethacin and triacsin C came to increase significantly the AA-CoA and PG formation, respectively. Thus, the experiments utilizing indomethacin and triacsin C revealed that the incubation using 60 microM AA can simultaneously detect the changes in the activities of COX and ACS caused by drugs, while the incubation using 5 microM AA can detect the changes in the product formation elicited by the resulting shunt of AA. Further, using these incubation conditions, the effects of Zn2+ and Cu2+ on the PG and AA-CoA formation were examined. Zn2+ inhibited the AA-CoA synthesis from 60 microM AA without affecting the PG synthesis. In contrast, when 5 microM AA was used as the substrate, a significant increase in the PG formation was observed in the presence of this ion, indicating that drug actions on the PG formation from AA by the kidney medulla microsomes may change depending on the substrate concentration. On the other hand, Cu2+ increased PG synthesis and inhibited AA-CoA synthesis from both 60 and 5 microM AA. These results suggest that the simultaneous measurements of PG and AA-CoA formation by the kidney medulla microsomes under high (60 microM) and low (5 microM) substrate concentrations can investigate the direct and indirect actions of drugs on the COX and ACS activities, and are useful for clarifying the haemostatic control of the metabolic fate of AA into the two enzymatic pathways. Furthermore, this study showed that Zn2+ and Cu2+ can modulate PG and AA-CoA formation by affecting COX activity, ACS activity, and/or the AA flow into the two enzymatic pathways.
Acyl Coenzyme A↗
Triterpenoid saponins from Vaccaria segetalis.
A new triterpenoid saponin, named segetoside C (1), and two known saponins, vaccaroid A (vaccaroside A) (2) and dianoside G (3), have been isolated from the seeds of Vaccaria segetalis. On the basis of chemical reaction and spectral data, the structure of segetoside C (1) has been established as: gypsogenic acid-28-O-[beta-D-glucopyranosyl-(1-->3)]-[6-O-acetyl-beta-D-glucopyra-nosyl-(1-->2)-beta-D-glucopyranosyl-(1-->6)]-beta-D-glucopyranoside.
Carbohydrate Sequence↗
Effect of 13-hydroperoxyoctadecadienoic acid on the supply of arachidonic acid for prostaglandin synthesis from arachidonoyl-CoA mediated by the cytosolic or microsomal acyl-CoA hydrolase in rabbit kidney medulla.
The effects of 13-hydroperoxyoctadecadienoic acid (13-HPODE) on the cytosolic or microsomal acyl-CoA hydrolase (ACH) activity in rabbit kidney medulla and on the ACH-mediated prostaglandin (PG) formation from arachidonoyl-CoA (AA-CoA) were examined. 13-HPODE (10, 20, and 50 microM) had no effect on the cytosolic ACH activity but significantly inhibited the activity of the microsomal enzyme (43-57% inhibition). PG formation was measured as follows: AA-CoA (20 nmol) was preincubated with the cytosolic or microsomal fraction (as the source of ACH) in the presence or absence of 13-HPODE for 5 min at 37 degrees C, followed by incubation with the microsomal fraction (as the source of PG-synthesizing enzymes), hydroquinone and reduced glutathione for 5 min at 37 degrees C, and the PGs formed were measured by HPLC, with use of 9-anthryldiazomethane for derivatization. 13-HPODE reduced the PG formation when the microsomal fraction, but not the cytosolic fraction, was used as the source of ACH (10, 20, and 50 microM; 28-55% inhibition). These results suggest that 13-HPODE may modulate PG levels in rabbit kidney medulla by inhibiting the microsomal ACH activity.
Acyl Coenzyme A↗
Two subunits of the insect 26/29-kDa proteinase are probably derived from a common precursor protein.
We previously identified the 26/29-kDa proteinase in the hemocytes of Sarcophaga peregrina (flesh fly) that appears to participate in elimination of foreign proteins in this insect [Eur. J. Biochem. 209, 939-944 (1992)]. Here, we report the cDNA cloning of this proteinase. The cDNA encodes a protein which includes both the 26- and 29-kDa subunit, strongly suggesting that the both subunits are derived from a single precursor protein. The 26- and 29-kDa subunit located at the amino-terminal and carboxyl-terminal of the precursor protein. The 29-kDa subunit itself appeared to be a proteinase, for this subunit had 52% sequence identity with Sarcophaga cathepsin L, while 26-kDa subunit had no significant similarity. We also showed that 26/29-kDa proteinase was insensitive to specific inhibitors of cathepsin L. These results indicate that this proteinase is a novel member of the papain family. We isolated similar cDNAs from Drosophila melanogaster and Periplaneta americana (cockroach), suggesting that this proteinase is conserved in a wide variety of insects and participates in their defense mechanisms.
Amino Acid Sequence↗
Increase of serum des-gamma-carboxy prothrombin in alcoholic liver disease without hepatocellular carcinoma.
The purpose of this study is to determine serum des-gamma-carboxy prothrombin (DCP) levels in benign liver diseases by a new sensitive method, and to demonstrate the elevation of serum DCP in alcoholic liver disease (ALD) without hepatocellular carcinoma (HCC). Median values of serum DCP were 16.2 mAU/ml (range: 3.2 to 1570 mAU/ml) in ALD and 16.7 mAU/ml (1.2 to 75.4 mAU/ml) in viral liver disease (VLD). Using the cut-off value of 40 mAU/ml as a tumor marker for HCC, 21% (11/52) was positive in ALD and 2% (1/57) was positive in VLD (p = 0.0014, Fisher's exact probability test), and 27% (9/33) was positive in alcoholic liver cirrhosis and 3% (1/39) was positive in viral liver cirrhosis (p = 0.0042, Fisher's exact probability test). The positive rate of DCP was significantly (p < 0.001, Spearman's rank correlation test) correlated with the severity of liver disease in ALD. Serum vitamin K level was not decreased in cases with ALD. In a demonstrable case, serum DCP was decreased after abstinence and was increased again after the beginning of ethanol intake, suggesting the involvement of ethanol to the elevation of serum DCP in ALD. In conclusion, serum DCP was significantly elevated in ALD, compared with VLD, although the mechanism of the elevation of DCP was not clarified. Ethanol intake may act, in part, on the increase of serum DCP in ALD.
Aged↗
Ventricular tachycardia in a patient with cardiac lipoma.
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Administration, Oral↗