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Biomedical subjects

N Ueda

Publications and source records attributed to N Ueda.

At least 289 records · Page 16Linked to original sources
PubMed1992

Immunoaffinity purification and cDNA cloning of human platelet prostaglandin endoperoxide synthase (cyclooxygenase).

The cDNA for prostaglandin endoperoxide synthase (cyclooxygenase) was cloned from human platelets by the polymerase chain reaction amplification method, and the primary structure of the enzyme was deduced from the nucleotide sequence. The enzyme was composed of 599 amino acids including 23-amino acid signal sequence, and the calculated molecular weight of the mature protein was 65,995. The enzyme was immunoaffinity-purified from human platelets. The N-terminal amino acid sequence determined by Edman degradation was Ala-Asp-Pro-Gly-Ala-Pro-Thr-Pro-, and the result confirmed the primary structure of the enzyme, which was deduced from the cDNA sequence.

Acetylation↗
PubMed1992

Increased 5-lipoxygenase activity in massive hepatic cell necrosis in the rat correlates with neutrophil infiltration.

Rats were treated with heat-killed Propionibacterium acnes and subsequent injection of a small amount of lipopolysaccharide after 7 days. After 24 hr most of the rats died of massive liver cell necrosis. Nonparenchymal liver cells were isolated from this liver injury model and incubated with arachidonic acid. Reverse-phase high-pressure liquid chromatography detected the 5-lipoxygenase metabolites (leukotriene B4 and 5-hydroxy-arachidonic acid), whereas these compounds were produced in negligible amounts when the rats were treated with P. acnes only. Immunohistochemical studies with 5-lipoxygenase antiserum revealed that the injured livers contained a large number of positively stained round cells with segmented nuclei, which were rarely found in the livers treated with P. acnes only. These positively stained cells were histologically identified as neutrophils. The results suggested that the increased 5-lipoxygenase activity in the injured rat liver is attributable to the infiltrating neutrophils rather than to nonparenchymal hepatic cells.

Animals↗
PubMed1992

A case of intraductal papillary adenocarcinoma of the pancreas associated with mass forming chronic pancreatitis.

A case of intraductal papillary adenocarcinoma of the pancreas associated with mass forming chronic pancreatitis without calcifications is described. Pancreatolithiasis, or calcified pancreas, is recognized as a high risk factor for pancreatic cancer. However, epidemiologic studies have found that carcinoma of the pancreas associated with chronic pancreatitis was rare. The question is whether chronic pancreatitis without calcifications is actually a precancerous background lesion or not. This case suggests that hyperplasia of the pancreatic ductal epithelium may be a precancerous lesion for pancreatic cancer in some patients with chronic pancreatitis.

Aged↗
PubMed1992

Intrasplenic pancreatic pseudocyst: a case report.

An intrasplenic pseudocyst associated with the acute relapsing phase of chronic pancreatitis in a 51-year-old woman is reported, with a review of the Japanese literature. The patient was admitted with a complaint of left lateral and back pain. Abdominal US and CT revealed communicating cysts at the pancreatic tail and the subcapsule of the spleen. A repeat US and CT 1 month after admission demonstrated enlargement of the cyst at the pancreatic tail. ERCP revealed a dilated main pancreatic duct without any definite evidence of stenosis, and direct communication with the cyst at the pancreatic tail. Percutaneous cystography revealed that the subcapsular cyst of the spleen, the cyst of the pancreatic tail, and the main pancreatic duct communicated with each other. The cyst contained serous fluid with an amylase content of 57,500 IU/I. Distal pancreatectomy and splenectomy was performed. Histologically, there was a nonepithelial lining on the inner surface of the cysts at the pancreatic tail and the subcapsule of the spleen. Severe chronic inflammatory changes were present in the resected tail of the pancreas. Timely surgical treatment is advocated to reduce the mortality and morbidity associated with complications of intrasplenic pseudocysts.

Alcoholism↗
PubMed1992

Pathogenesis of hepatic atrophy in canine model of hepatolithiasis.

The pathogenesis of the hepatic atrophy that accompanies hepatolithiasis was investigated pathomorphologically using a canine model. Two groups were evaluated: infected and noninfected. In the infected group, inflammation in Glisson's capsule caused by cholangitis involved the portal vein at the region of the large bile duct. At this region, the periportal fibrosis ratio was significantly greater in the infected group than in the noninfected group both at 1 and 3 months. At the regions of the septal and interlobular bile ducts, the caliber ratio of the portal vein in the two experimental groups was less than in the normal liver both at 1 and 3 months. At both regions, the caliber ratio of the portal vein in the infected group was less than in the noninfected group at 3 months. The rate of atrophy was significantly greater in the infected group than in the noninfected group at 3 months. These results suggest that disturbance of the portal venous blood flow attributed to cholangitis of the large bile ducts is one of the most important factors leading to hepatic atrophy in hepatolithiasis.

Animals↗
PubMed1992

Possible induction of fatty acid cyclo-oxygenase in lipopolysaccharide-stimulated rat Kupffer cells.

In response to stimulation with lipopolysaccharide, isolated rat Kupffer cells released increased amounts of prostaglandin E2, prostaglandin D2, 6-keto-prostaglandin F1 alpha, and thromboxane B2. There was a lag of 2-6 hours before a significant release of these metabolites into the medium was detected. Nonstimulated Kupffer cells converted exogenous arachidonic acid to prostaglandins and thromboxane B2, and a major product was prostaglandin D2. Twenty-four hours after stimulation with lipopolysaccharide, Kupffer cells produced approximately 7 times more prostaglandin E2 and 2 times more prostaglandin D2, 6-keto-prostaglandin F1 alpha; and thromboxane B2 than nonstimulated cells. Western immunoblotting of microsomal proteins prepared from the stimulated rat Kupffer cells showed a 70-kilodalton component that was immunoreactive with a polyclonal anticyclo-oxygenase antibody. The intensity of the band increased with the time of the lipopolysaccharide stimulation. These results suggest that the accelerated arachidonate metabolism in lipopolysaccharide-stimulated rat Kupffer cells might be attributed to an induction of the cyclo-oxygenase enzyme.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Synchronous cancer of the biliary tract and pancreas associated with anomalous arrangement of the pancreaticobiliary ductal system.

A 58-year-old man on abdominal ultrasonography and CT had an irregularly elevated lesion at the neck of the gallbladder and a cyst of approximately 6.5 cm in diameter at the pancreatic tail. Percutaneous transhepatic cholangiography revealed a 2-cm shadow defect at the neck of the gallbladder and an irregular, translucent 30 x 12 mm lesion in the intrapancreatic bile duct. Total pancreatectomy and extended cholecystectomy with regional lymph node dissection was performed. An anomalous arrangement of the pancreaticobiliary ductal system (AAPBD) was demonstrated by postoperative contrast radiography of resected specimen. The lesions of the gallbladder and common bile duct were papillary adenocarcinoma. In addition, papillary adenocarcinoma was limited almost entirely to the mucosal layer of the main pancreatic duct and its branches, from the junction of the common bile duct and pancreatic duct to the pancreatic tail. The three tumors were not continuous. The cyst at the pancreatic tail was a pseudocyst. This case represents synchronous cancer of the gallbladder, common bile duct, and pancreas associated with AAPBD.

Adenocarcinoma, Papillary↗
PubMed1992

Localization of arachidonate 12-lipoxygenase in canine brain tissues.

The cytosol fraction from a thoroughly irrigated canine cerebrum was subjected to immunoaffinity chromatography using a monoclonal antibody against porcine leukocyte 12-lipoxygenase. Arachidonate 12-lipoxygenase eluted from the column with some retardation. The enzyme, with a specific activity of 9 nmol/min/mg of protein, converted arachidonic acid to 12(S)-hydroperoxy-5,8,10,14-eicosatetraenoic acid. The enzyme was active not only with arachidonic acid, but also with linoleic and alpha-linolenic acids. In contrast, 12-lipoxygenase of canine platelets was almost inactive with linoleic and alpha-linolenic acids, and the platelet enzyme was also distinguished from the cerebral enzyme in terms of reactivity with the anti-12-lipoxygenase antibody. 12-Lipoxygenase activity was also detected in the cytosol fractions of other parts of canine brain: basal ganglia, hippocampus, cerebellum, olfactory bulb, and medulla oblongata.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Oncotic pressure regulates gene transcriptions of albumin and apolipoprotein B in cultured rat hepatoma cells.

The mechanism of the accelerated syntheses of albumin and apolipoprotein B (apo B) in response to decreased oncotic pressure was investigated in cultured rat hepatoma H4-II-E cells. Addition of dextran (mol wt 6-9 x 10(4)) to the culture medium decreased the levels of albumin and apo B mRNAs in an oncotic pressure-dependent manner. The reductions of both mRNAs were attenuated with increase in the molecular weight of dextran, which resulted in a decrease in oncotic pressure. Addition of macromolecule increased the viscosity in medium; however, alteration of viscosity appeared not to correlate with albumin and apo B mRNA levels. Transcriptional run-on assays with isolated nuclei from dextran-treated vs. untreated hepatoma cells indicated that the changes in steady-state mRNA levels were mainly controlled at the transcriptional step. Treatment with cycloheximide increased albumin mRNA to the basal level, which was effectively suppressed by dextran, and resulted in superinduction of apo B mRNA. These changes occurred primarily at the transcriptional step. These results suggest that regulations of the expressions of the albumin and apo B genes for adaptive increases in the mRNAs may require the continued synthesis of a labile protein(s) or a limiting transcription factor(s). We conclude that oncotic pressure plays an important role in regulation of expression of the albumin and apo B genes at the transcriptional step.

Animals↗
PubMed1992

Role of intracellular calcium in hydrogen peroxide-induced renal tubular cell injury.

Both reactive oxygen metabolites and calcium have been implicated in ischemic and toxic renal tubular cell injury. However, the role of calcium in oxidant injury to renal tubular cells has not been previously examined. In the present study we examined the role of intracellular free Ca2+ ([Ca2+]i) in H2O2-mediated injury to LLC-PK1 cells, a renal tubular epithelial cell line. H2O2 induced a significant rise in [Ca2+]i within 1 min after exposure of cells to 5 mM H2O2, with a sustained rise in [Ca2+]i during the course of experiments, reaching a value of 1.3 microM at 60 min (n = 10). The rise in [Ca2+]i preceded sublethal cell injury as measured by [3H]adenine release or irreversible cell injury as determined by trypan blue exclusion. Buffering [Ca2+]i with quin-2 (50 microM) and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA, 50 microM) was highly protective against the H2O2-induced cell injury. For example, at 120 min after exposure of cells to 5 mM H2O2, irreversible cell injury was reduced from 45 +/- 8 to 9 +/- 1% (n = 3) by quin-2. The acetoxymethyl ester of quin-2 (quin-2/AM) and BAPTA/AM did not interfere with the trypan blue exclusion assay or scavenge H2O2. Preventing mobilization of Ca2+ from intracellular storage sites using 8-(N,N-dimethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8, 10(-4) M) significantly reduced the rise in [Ca2+]i and thus prevented H2O2-mediated cytotoxicity to LLC-PK1 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Buffers↗
PubMed1992

Endonuclease-induced DNA damage and cell death in oxidant injury to renal tubular epithelial cells.

Hydrogen peroxide (H2O2)-induced DNA damage and cell death have been attributed to the direct cytotoxicity of H2O2 and other oxidant species generated from H2O2. We examined the possibility that oxidants activate endonucleases leading to DNA damage and cell death in renal tubular epithelial cells, similar to that described for apoptosis. Within minutes, H2O2 caused DNA strand breaks in a dose-dependent manner, followed by cell death. DNA fragmentation was demonstrated both by the release of [3H]thymidine in 27,000-g supernatant as well as the occurrence of low molecular weight DNA fragments on agarose gel electrophoresis, characteristic of endonuclease cleavage. Endonuclease inhibitors, aurintricarboxylic acid, Evans blue, and zinc ion prevented H2O2-induced DNA strand breaks, fragmentation, and cell death. Inhibitors of protein or mRNA synthesis had only minor protection against H2O2-induced DNA damage in contrast to complete protection reported in apoptotic thymocytes. Micrococcal endonuclease induced similar DNA strand breaks in LLC-PK1 cells, and the endonuclease inhibitors prevented the events confirming the ability of endonucleases to induce DNA damage. The protective effect of aurintricarboxylic acid was not due to the prevention of the rise in intracellular free calcium. We conclude that endonuclease activation occurs as an early event leading to DNA damage and cell death in renal tubular epithelial cells exposed to oxidant stress and, in contrast to apoptotic thymocytes, does not require macromolecular synthesis.

Animals↗
PubMed1992

Mesangial cell growth in genetically hypertensive rats and effect of calcium antagonists upon this growth.

Mesangial cells play an important role in physiological and pathophysiological regulation of glomerular functions. To explore the involvement of deranged mesangial cell functions in the pathogenesis of hypertension, the growth activity of mesangial cells was compared in stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY). Upon exposure to fetal calf serum, the growth rate was significantly higher in mesangial cells cultured from glomeruli of 4-week old SHRSP than in those of age-matched WKY. This abnormally high growth of SHRSP mesangial cells was significantly inhibited by dihydropyridine calcium antagonists. Of the three antagonists tested, manidipine was the most potent inhibitor. Significant growth inhibition occurred at a concentration as low as 10(-12) M; inhibition as high as 65% was found at 10(-6) M. Calcium antagonists, particularly manidipine, may prevent or delay the development of hypertension not only through vasodilation but also through inhibition of mesangial cell growth. By slowing mesangial cell proliferation, calcium antagonists also may slow the progression of hypertension-induced glomerular sclerosis.

Animals↗
PubMed1992

[Clinical significance of posttetanic count (PTC) during onset and spontaneous offset of neuromuscular blockade induced by vecuronium].

To compare the clinical difference of posttetanic count (PTC) during onset and spontaneous offset, the changes of PTC during an intense neuromuscular blockade induced by vecuronium (0.08 mg.kg-1, i.v.) were measured using a neuromuscular transmission analyzer in 64 adult patients anesthetized with nitrous oxide and halothane. Furthermore, intubation score was evaluated when zero PTC was obtained. The obvious movement of diaphragm associated with endotracheal intubation was observed in 9 out of 20 patients (45%) even when it was performed after obtaining zero PTC. The difference of PTC responses between the onset and the offset was found. The difference was that, during the onset, a tetanic response was observed obviously and the height of the posttetanic single twitch was low, and during offset, even when no response was observed, the height of a posttetanic single twitch response was high with the same PTC. These facts indicate that the same PTC has different clinical significance during onset and offset.

Adult↗