Search PubMed⌕ Search

Biomedical subjects

Takashi Ueda

Publications and source records attributed to Takashi Ueda.

82 records · Page 5Linked to original sources
PubMed2002

Hematin is one of the cytotoxic factors in pancreatitis-associated ascitic fluid that causes hepatocellular injury.

BACKGROUND: We recently demonstrated that pancreatitis-associated ascitic fluid (PAAF) contains cytotoxic factor(s), inducing apoptosis in hepatocytes, and that PAAF induces hepatic adenosine triphosphate depletion, hepatocellular acidosis, and accumulation of hepatic intracellular sodium. Because ascitic fluid and serum from patients with hemorrhagic pancreatitis contain a lot of hematin, we aimed to test the hypothesis that hematin can induce hepatocellular injury, and then we compared its cytotoxicity with that of PAAF. METHODS: In vivo effects of intraperitoneal injection of hematin into the liver of healthy rats were evaluated with in situ nick-end labeling, blood biochemical analysis, and nuclear magnetic resonance spectroscopy. In vitro cytotoxic and apoptosis-inducing activities of hematin on rat primary culture hepatocytes were investigated with a cellular proliferation assay kit and DNA fragmentation enzyme-linked immunosorbent assay, respectively. Furthermore, PAAF was fractionated with Sephacryl S-300 gel column chromatography, and cytotoxic activities of its fractions on a human hepatoma cell line (HuH-7) were compared with those of hematin. RESULTS: Intraperitoneal injection of hematin into healthy rats caused apoptosis in the hepatocytes and elevated serum glutamate oxaloacetic transaminase and lactate dehydrogenase levels. Intraperitoneal injection of hematin also caused a significant decrease in the hepatic beta-adenosine triphosphate/inorganic phosphate ratio, severe hepatic intracellular acidosis, and a significant increase of hepatic intracellular sodium (Na(+)) concentration, similar to the effects of PAAF. In vitro, hematin decreased hepatocyte viability and increased the DNA fragmentation of hepatocytes, similar to the effects of 10% PAAF. Albumin reversed the cytotoxic effects of hematin and PAAF on HuH-7 cells nearly completely and partially, respectively. Fractionation of PAAF and hematin by gel column chromatography revealed that the first peak of cytotoxic activity of PAAF corresponded to that of hematin and that the cytotoxic activity was reversed by albumin nearly completely. CONCLUSIONS: These results suggest that hematin is one of the cytotoxic factors in PAAF that causes hepatocellular injury and that cellular injuries caused by hematin may be involved in the development of multiple organ failure associated with severe acute pancreatitis.

Albumins↗
PubMed2002

Splenic atrophy in experimental severe acute pancreatitis.

INTRODUCTION: In severe acute pancreatitis, immunologic impairment is supposed to be linked to the development of subsequent infectious complications. AIM: To examine alterations of spleen in rat experimental severe acute pancreatitis. METHODOLOGY: Severe necrotizing pancreatitis was induced by retrograde injection of 3% sodium deoxycholate into the biliopancreatic ducts of male Wistar rats. RESULTS: In the rats with pancreatitis 12 and 24 hours after the induction, splenic weights were significantly lower than those of sham-operated rats. Numbers of splenocytes were also significantly reduced simultaneously. By in situ nick-end labeling, DNA fragmentation enzyme linked immunosorbent assay (ELISA), and DNA electrophoresis, no apoptosis was detected on the splenocytes from the rats with pancreatitis 6, 12, and 24 hours after the onset. Peripheral lymphocytes in the rats with pancreatitis were significantly decreased 6, 12, and 24 hours after the onset compared with those in sham-operated rats. With antecedent splenectomy, peripheral lymphocyte counts 12 hours after the onset were significantly lower than those in rats who had not undergone splenectomy. Moreover, nuclear fragmentation was noted, and DNA fragments were significantly increased in peripheral lymphocytes at 6 hours in sodium deoxycholate pancreatitis. CONCLUSION: These results indicate that splenic atrophy resulting from splenocyte reduction occurs in rat experimental severe acute pancreatitis. It is suggested that splenocytes are recruited into systemic circulation in response to peripheral lymphocyte reduction as a result of apoptosis.

Acute Disease↗
PubMed2002

Involvement of the vacuoles of the endodermis in the early process of shoot gravitropism in Arabidopsis.

The endodermal cells of the shoot are thought to be the gravity-sensing cells in Arabidopsis. The amyloplasts in the endodermis that sediment in the direction of gravity may act as statoliths. Endodermis-specific expression of SGR2 and ZIG using the SCR promoter could complement the abnormal shoot gravitropism of the sgr2 and zig mutants, respectively. The abnormalities in amyloplast sedimentation observed in both mutants recovered simultaneously. These results indicate that both genes in the endodermal cell layer are crucial for shoot gravitropism. ZIG encodes AtVTI11, which is a SNARE involved in vesicle transport to the vacuole. The fusion protein of SGR2 and green fluorescent protein localized to the vacuole and small organelles. These observations indicate that ZIG and SGR2 are involved in the formation and function of the vacuole, a notion supported by the results of subcellular analysis of the sgr2 and zig mutants with electron microscopy. These results strongly suggest that the vacuole participates in the early events of gravitropism and that SGR2 and ZIG functions are involved.

Arabidopsis↗
PubMed2002

Olprinone: a phosphodiesterase III inhibitor with positive inotropic and vasodilator effects.

Olprinone is a newly developed phosphodiesterase III inhibitor characterized by several properties. First, olprinone has positive inotropic and vasodilator actions and improves myocardial mechanical efficiency. Second, olprinone augments cerebral blood flow by a direct vasodilatory effect on cerebral arteries. The cerebrovascular reactivity to olprinone is marked in patients with impaired cerebral circulation. Third, olprinone selectively improves carotid artery distensibility, which may be attributable to differences in the arterial structural components or the reactivity of smooth muscle cells to olprinone. Fourth, olprinone improves inadequate redistribution of brain perfusion and may prevent cerebral metabolic abnormalities in heart failure.

Carotid Arteries↗
PubMed2002

Amiloride-blockable acid-sensing ion channels are leading acid sensors expressed in human nociceptors.

Many painful inflammatory and ischemic conditions such as rheumatoid arthritis, cardiac ischemia, and exhausted skeletal muscles are accompanied by local tissue acidosis. In such acidotic states, extracellular protons provoke the pain by opening cation channels in nociceptors. It is generally believed that a vanilloid receptor subtype-1 (VR1) and an acid-sensing ion channel (ASIC) mediate the greater part of acid-induced nociception in mammals. Here we provide evidence for the involvement of both channels in acid-evoked pain in humans and show their relative contributions to the nociception. In our psychophysical experiments, direct infusion of acidic solutions (pH > or = 6.0) into human skin caused localized pain, which was blocked by amiloride, an inhibitor of ASICs, but not by capsazepine, an inhibitor of VR1. Under more severe acidification (pH 5.0) amiloride was less effective in reducing acid-evoked pain. In addition, capsazepine had a partial blocking effect under these conditions. Amiloride itself neither blocked capsaicin-evoked localized pain in human skin nor inhibited proton-induced currents in VR1-expressing Xenopus oocytes. Our results suggest that ASICs are leading acid sensors in human nociceptors and that VR1 participates in the nociception mainly under extremely acidic conditions.

Acid Sensing Ion Channels↗
PubMed2002

[A case of spontaneous rupture of the urinary bladder followed by pneumomediastinum].

A 67-year-old male admitted to our hospital with a complaint of gross hematuria and lower abdominal pain. He was being followed up at our hospital for prostate cancer with multiple bone metastases. He was diagnosed with spontaneous rupture of the urinary bladder by abdominal computed tomography. Chest X-ray and chest computed tomography also showed pneumomediastinum. An urgent operation revealed a rupture of the urinary bladder 3 cm in length. We briefly reviewed 122 cases of spontaneous rupture of the urinary bladder reported in the Japanese literature.

Aged↗
PubMedDate not supplied

Contrast transesophageal echocardiography in diagnosing congenital enlargement of the right atrium--a case report.

Congenital malformation of the right atrium or the coronary sinus is rare, and cases are classified into 1 of the following 4 categories: (1) congenital enlargement of right atrium, (2) single diverticulum, (3) multiple diverticula of the right atrium, and (4) diverticulum of the coronary sinus. This report presents a 63-year-old man with cardiomegaly and no chest symptoms. A chest radiograph revealed an enlarged cardiac silhouette with a prominent right heart border. Although a transesophageal echocardiography revealed marked enlargement of the right atrium, neither further anomaly nor massive regurgitation was observed. The systolic pulmonary artery pressure derived from the peak velocity of mild tricuspid regurgitation was 38 mm Hg. Secondary enlargement of the right atrium due to atrial septal defect or pulmonary venous connection anomaly was deemed negligible by use of transesophageal contrast echocardiography, and primary enlargement of the right atrium was confirmed. Transesophageal echocardiography using ultrasound contrast was determined to be feasible for diagnosing congenital malformation of the right atrium.

Cardiomegaly↗
PubMedDate not supplied

Left atrial thrombosis in achalasia--a case report.

An 81-year-old woman came to the clinic with aphasia and gait disturbance. A transthoracic echocardiogram showed left atrial (LA) thrombus at the posterobasal site, which was compressed by a large mass with high echo intensity. A chest computed tomography scan revealed dilatation of the esophagus, compressing the LA from the posterior side. An endoscopy showed a bolus and much foulness in the distended esophagus, which were immediately eliminated by an endoscopic procedure. The LA thrombus, as shown by transesophageal echocardiography, spontaneously resolved without any neurologic signs. The authors assumed that the dilatated esophagus compressed the LA, and this may have produced the abnormal flow dynamics in the LA. The injury of endocardial surface produced by the distension or turbulent flow, in addition to dehydration, may have augmented a coagulability in the LA.

Aged↗