Biomedical subjects

I Ogata

Publications and source records attributed to I Ogata.

At least 19 recordsLinked to original sources

PubMed1996

Small hepatocellular carcinoma in patients with chronic liver damage: prospective comparison of detection with dynamic MR imaging and helical CT of the whole liver.

PURPOSE: To compare contrast material-enhanced dynamic magnetic resonance (MR) imaging with helical computed tomography (CT) for the detection of small hepatocellular carcinoma (HCC) in patients with chronic liver damage. MATERIALS AND METHODS: Fifty patients with chronic hepatitis or liver cirrhosis underwent dynamic contrast-enhanced fast low-angle shot MR imaging and multiple-phase helical CT. Arterial, portal-venous, and delayed-phase images were compared. Diagnostic ability with both techniques was evaluated by means of receiver operating characteristic (ROC) analysis; images in patients with (n = 27) and those without (n = 15) HCC in whom the same anatomic levels were available for both examinations were assessed. Seventy-two lesions were evaluated, and tumor diameter ranged from 0.5 to 3.0 cm (mean, 1.9 cm). RESULTS: ROC analysis showed that the arterial-phase images obtained with both techniques allowed better detection of HCC. Diagnostic ability was significantly better with arterial-phase MR imaging (mean area under the ROC curve [Az] = 0.96) than arterial-phase CT (Az = 0.87) or with images from any other phase (P < .05). For the delayed phase, diagnostic capability was significantly better with CT (Az = 0.84) than with MR imaging (Az = 0.77) (P < .05). CONCLUSION: Arterial-phase dynamic MR imaging is superior to helical CT for the detection of HCC in patients with chronic liver damage.

Aged↗

PubMed1996

Gadolinium-enhanced breath-hold three-dimensional MR angiography of the portal vein: value of the magnetization-prepared rapid acquisition gradient-echo sequence.

The authors evaluated magnetic resonance (MR) angiography of the portal vein performed with a breath-hold, gadolinium-enhanced, magnetization-prepared rapid acquisition gradient-echo sequence in five volunteers and 24 patients. The main portal vein and its branches and the liver were depicted clearly in all images. The hepatic vein was clearly depicted in 21 of the 24 patients. MR angiography performed with this sequence allowed high-quality imaging of the portal and hepatic veins.

Adult↗

PubMed1996

Multiple-phase helical CT of the liver for detecting small hepatomas in patients with liver cirrhosis: contrast-injection protocol and optimal timing.

OBJECTIVE: Helical CT scanners allow multiple-phase sequential scans of the entire liver to be obtained during a single bolus injection of contrast material. The purpose of this study was to compare two injection protocols and to establish timing that would optimize detection of hepatomas less than 3 cm in diameter. SUBJECTS AND METHODS: Triple-phase helical CT of the liver was evaluated in 217 patients who had liver cirrhosis and were referred for known or suspected hepatomas. Proof of individual neoplasms was based on biopsy results, surgical findings, or findings of other imaging studies. Sixty percent nonionic contrast material, infused at 2 or 4 ml/sec, was followed by sequential arterial-phase, portal-venous phase, and equilibrium-phase helical scans of the liver. Aortic and hepatic enhancement curves were constructed by measuring CT attenuation. The CT attenuation values of individual tumor lesions were also measured. We compared the degree of enhancement of normal structures and tumors obtained with four scan protocols (injection at 2 ml/sec with a 30-sec scan delay [n = 54], injection at 2 ml/sec with a 35-sec scan delay [n = 47], injection at 4 ml/sec with a 20-sec scan delay [n = 56], and injection at 4 ml/sec with a 25-sec scan delay [n = 60] and determined the optimal injection protocol and timing for CT acquisition. RESULTS: Peak aortic and hepatic enhancement was obtained earlier with the 4-ml/sec protocol (at 24 sec and 61 sec versus 36 sec and 90 sec for the 2-ml/sec protocol). The peak attenuation value of the aorta was higher with the 4-ml/sec protocol (330 H versus 186 H for the 2-ml/sec protocol). However, peak hepatic attenuation was similar for both protocols (98 H for the 4-ml/sec protocol versus 92 H for the 2-ml/sec protocol). Liver-tumor contrast was highest in the arterial phase with both protocols. The next highest contrast was obtained during the equilibrium phase. Liver-tumor contrast in the portal-venous phase was significantly lower than that in the other two phases. Tumor enhancement was significantly higher in scans obtained using the 4-ml/sec protocol with a delay time of 25 sec than those obtained with a delay time of 20 sec. In 109 hepatomas, 35 tumors were only seen or were most conspicuous during the arterial phase, four tumors were most conspicuous during the equilibrium phase, and one tumor was most conspicuous during the portal-venous phase. CONCLUSION: Arterial-phase helical CT of the liver after 4-ml/sec injection of contrast material significantly improves detection of hepatomas less than 3 cm in diameter when performed in addition to delayed scanning. Portal-venous phase helical CT is of limited value in detecting small hepatomas.

Carcinoma, Hepatocellular↗

PubMed1995

Blood coagulation equilibrium in rat liver microcirculation as evaluated by endothelial cell thrombomodulin and macrophage tissue factor.

The regulatory mechanisms of microcirculation might differ in the liver from other organs, because macrophages are resident in the hepatic sinusoids and sinusoidal endothelial cells are unique in shape and function. Thrombomodulin expression in endothelial cells and tissue factor activity in isolated macrophages were studied in the liver and lung of rats. In normal rats, the thrombomodulin expression was minimal in hepatic sinusoids, but prominent in pulmonary capillaries, while the tissue factor activity in the presence of endotoxin was higher in pulmonary macrophages than in Kupffer cells, although the levels in the absence of endotoxin were comparable in both cells. The tissue factor activity in hepatic macrophages was increased after priming of the cells with Corynebacterium parvum or after induction of liver necrosis or cirrhosis with carbon tetrachloride. In the necrotic or cirrhotic liver, increased thrombomodulin expression was seen along capillaries extending in necrotic areas and regenerating nodules, but this increase was minimal in the Corynebacterium parvum-treated rat liver. Blood coagulation equilibrium in microcirculation regulated by endothelial cells and macrophages may differ between the liver and lung. Such equilibrium in the liver may vary depending on pathological status.

Animals↗

PubMed1994

Evidence that impaired intracellular collagen synthesis reduces proliferation in cultured rat hepatocytes.

Contribution of collagen to cell proliferation was studied in cultured hepatocytes. When alpha,alpha'-dipyridyl, an iron chelator which blocks hydroxylation of prolyl and lysyl residues of procollagen and expression of procollagen mRNA, was added to the medium of rat hepatocytes in primary culture, DNA synthesis of the cells was reduced in a dose-related manner without changes in protein synthesis. The reduction of collagen synthesis was parallel with the changes of DNA synthesis. The addition of P-1894B or minoxidil, which inhibits specifically prolyl hydroxylase or lysyl hydroxylase, respectively, also produced similar results. However, the DNA synthesis was not affected by beta-aminopropionitrile fumarate, which inhibits cross linking in extracellular collagen maturation, nor by purified bacterial collagenase. Intracellular processing of collagen synthesis may be required for proliferation in cultured rat hepatocytes.

2,2'-Dipyridyl↗

PubMed1994

Oxidative stress in hepatocytes and stimulatory state of Kupffer cells after reperfusion differ between warm and cold ischemia in rats.

Rat liver was kept at 4 degrees C or 37 degrees C in MEM, and reperfused through a closed circulation from the hepatic vein to the portal vein at 37 degrees C with the same solution. Although purine nucleoside phosphorylase and ALT activities were increased in the perfusate, depending on the duration of ischemia at both 4 degrees C and 37 degrees C, the ratio of the latter to the former was significantly higher after 37 degrees C-ischemia than after 4 degrees C-ischemia. The stimulation stage of Kupffer cells evaluated in situ by formazan deposition after liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was elevated after 4 degrees C-ischemia longer than 1 h, but not after 37 degrees C-ischemia. In contrast, the degree of oxidative stress in hepatocytes assessed by formazan deposition after liver perfusion with nitro blue tetrazolium alone was greater after 37 degrees C-ischemia than after 4 degrees C-ischemia. These results suggest that oxidative stress in hepatocytes and the stimulatory state of Kupffer cells after ischemia-reperfusion may differ between 4 degrees C-ischemia and 37 degrees C-ischemia, probably leading to different development of liver damage.

Alanine Transaminase↗

PubMed1993

Rat liver fat-storing cell lines express sarcomeric myosin heavy chain mRNA and protein.

Fat-storing cells (FSC, lipocytes, or Ito cells) of liver store vitamin A and are the main producers of extracellular matrix in normal and cirrhotic liver. During liver injury, FSC undergo an activation process characterized by a decrease in vitamin A storage and an increase in cell proliferation and extracellular matrix deposition. This activation process also occurs upon culturing FSC from normal liver. In contrast to most cells of nonmuscle origin, activated FSC express two cytoskeletal proteins normally found in muscle, desmin, and smooth muscle alpha-actin. Based on their strategic perisinusoidal location, it has been hypothesized that FSC play a role in regulating blood flow. However, the nature of the contractile elements involved in this process remains to be determined. In this communication we demonstrate the presence of a sarcomeric myosin in proteins solubilized from liver biomatrix. In addition we demonstrate the expression of sarcomeric myosin heavy chain (MHC) mRNA and protein in two FSC clones derived from a CCl4-cirrhotic rat liver (CFSC). Through cloning the cDNA corresponding to the MHC gene expressed in these cells we demonstrate that it encodes fast IId skeletal MHC and thus represents a marker normally seen in adult muscle. The unexpected expression of an adult stage skeletal muscle molecular motor in FSC from cirrhotic liver is consistent with the proposed specialized contractile capacity of these cells.

Adipocytes↗

PubMed1993

Sinusoidal endothelial cell damage by activated macrophages in rat liver necrosis.

BACKGROUND: Massive hepatic necrosis caused by fibrin deposition in the hepatic sinusoids develops with hepatic macrophage activation in rats given endotoxin after administration of heat-killed Corynebacterium parvum. Targeted cells of such macrophages were investigated. METHODS: In C. parvum-treated rats, the pathological appearance of liver cells was serially measured in serum following endotoxin administration and compared with the appearance in the perfusate during closed liver perfusion with endotoxin. RESULTS: Serum activities of tumor necrosis factor, purine nucleoside phosphorylase present in both hepatocytes and sinusoidal endothelial cells, and levels of alanine aminotransferase were higher after 30 minutes, 1 hour, and 3 hours, respectively. Pretreatment of rats with gadolinium chloride, an inhibitor of macrophage function, reduced this liver injury. Although alanine aminotransferase activity remained almost unchanged in the liver perfusate, purine nucleoside phosphorylase activity increased. This increase was reduced when rats were pretreated with gadolinium chloride. There was sinusoidal endothelial cell damage around hepatic macrophages in the liver perfused with endotoxin. CONCLUSIONS: Activated hepatic macrophages may cause sinusoidal endothelial cell damage leading to hepatocyte necrosis in rats given C. parvum and endotoxin.

Alanine Transaminase↗

PubMed1993

Hyperechoic renal tumors: anechoic rim and intratumoral cysts in US differentiation of renal cell carcinoma from angiomyolipoma.

To determine whether angiomyolipomas (AMLs) and renal cell carcinomas (RCCs) can be differentiated at ultrasonography (US), the authors retrospectively evaluated the sonographic appearances of 31 AMLs and 38 RCCs. Sonograms were evaluated by three radiologists without knowledge of histologic findings, with respect to the echogenicity of the tumor, predominant echotexture, and whether an anechoic rim was present. All patients had also undergone computed tomography (CT) to check for tumoral fat. Intratumoral fat was evident at CT in 28 of the 31 AMLs. RCCs had no fat at CT or histologic evaluation. An anechoic rim was evident in 32 of 38 (84%) RCCs, and 10 RCCs had small anechoic areas with back echo enhancement, which corresponded to intratumoral cysts or cystic necrosis at histologic evaluation. The anechoic rim and areas indicative of cysts were not found in AMLs. Demonstration of an anechoic rim and/or intratumoral cysts in a hyperechoic mass at US suggests that the tumor is an RCC.

Adult↗

PubMed1993

[An autopsy case of the sinus of Valsalva aneurysm involved with tuberculous inflammation, leading to complete heart block].

A case is presented of unruptured aneurysm of the non coronary sinus of Valsalva, causing involvement of A-V node and right coronary artery compression. The patient was a 68 year-old woman with a complaint of general fatigue. Electrocardiogram showed complete A-V block. Computed tomography showed an aneurysm of the non coronary sinus of Valsalva. A temporary pacemaker was implanted, but the patient developed respiratory failure and heart failure and died. At autopsy, macroscopically disseminated tuberculosis was noted in both lungs and kidneys. Microscopically a tuberculous inflammatory lesion extending into the A-V node was found. We report this rare case with some consideration of the literature.

Aged↗

PubMed1992

In situ detection of oxidative stress in rat hepatocytes.

In rat hepatocytes in primary culture incubated with nitro blue tetrazolium, formazan content was increased by addition of t-butyl hydroperoxide, a potent oxidant, in a dose-related manner, but not by addition of valinomycin, which kills hepatocytes through mitochondrial damage. This increment after t-butyl hydroperoxide addition was not seen in hepatocytes preincubated with deferoxamine mesylate, a ferric iron chelator which inhibits radical formation. Liver perfusion with nitro blue tetrazolium and t-butyl hydroperoxide in rats produced formazan deposition faintly on the surface of hepatocytes throughout the liver and prominently in the cytoplasm of some hepatocytes, which was attenuated when performed following deferoxamine mesylate perfusion. When liver perfusion with nitro blue tetrazolium was performed in carbon tetrachloride-intoxicated rats, formazan deposition appeared diffusely in hepatocytes in the centrilobular areas. Similar deposition was also observed on the surface and in the cytoplasm of hepatocytes in the periportal and mid-zonal areas in rats undergoing post-ischaemic reperfusion. Liver perfusion with nitro blue tetrazolium can detect in situ oxidative stress in hepatocytes and may be a useful tool for studying the role of lipid peroxidation in rat liver injury.

Animals↗

PubMed1992

Hepatocyte membrane stabilization by prostaglandins E1 and E2: favorable effects on rat liver injury.

When prostaglandin (PG) E1 was continuously administered to rats from 24 hours before giving a dose of carbon tetrachloride, deranged serum glutamic pyruvic transaminase levels and prothrombin time were significantly reduced 12 hours after intoxication compared with controls. A similar effect of PGE1 was seen at 24 hours in D-galactosamine-intoxicated rats. Liver histology showed a comparable attenuation of injury in these rats. These results were consistent with reported effects of PGE2, suggesting that both prostaglandins may share a common pathway in protection against liver injury. When PGE1 or 16,16'-dimethyl PGE2 was added to the medium of primary cultured rat hepatocytes, lipid peroxidation-dependent killing of the cells by tert-butyl hydroperoxide was significantly attenuated without affecting the extent of malondialdehyde accumulation compared with controls. Both prostaglandins significantly reduced the extent of increased plasma membrane microviscosity of these cells assessed by 1-[4-(trimethyl-ammonio)phenyl]-6-phenyl-1,3,5-hexatriene. PGE1 and PGE2 may possess cytoprotective effects on liver parenchymal cells through stabilization of membrane microviscosity, which may contribute to protection against liver injury.

16,16-Dimethylprostaglandin E2↗

PubMed1992

Gut-derived substances in activation of hepatic macrophages after partial hepatectomy in rats.

When liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was performed in rats 24 h after two-thirds liver resection, there were marked deposits of formazan converted from nitro blue tetrazolium in hepatic macrophages throughout the liver, indicating macrophage activity. The extent of the deposits was significantly reduced when perfusion was performed following oral administration of polymyxin B sulfate, a non-absorbable bacteriocidal agent against gram-negative bacilli which can also bind endotoxin lipopolysaccharides. Polymyxin B sulfate administration also attenuated the derangements of SGPT and the histological liver injury provoked by endotoxin administration after partial hepatectomy. These results suggests that gut-derived substances sensitive to polymyxin B sulfate may contribute to activation of hepatic macrophages after partial hepatectomy in rats.

Animals↗

PubMed1991

Stimulation of putrescine production by epidermal growth factor in rat liver after partial hepatectomy.

When epidermal growth factor was given to rats after partial hepatectomy, hepatic putrescine content was significantly increased at 4, 6 and 10 hr compared with control rats. Ornithine decarboxylase activity was also increased. Hepatic ornithine decarboxylase messenger RNA content was significantly greater than control levels at 2 hr after epidermal growth factor treatment, but not at 10 hr, when the amount of ornithine decarboxylase messenger RNA in control animals was four times that at 2 hr. When actinomycin D was administered 6 hr after partial hepatectomy, hepatic ornithine decarboxylase activity at 10 hr was reduced to half the control levels. This reduction was attenuated by epidermal growth factor treatment at 6 and 8 hr. Hepatic immunoreactive ornithine decarboxylase protein content showed a highly positive correlation with hepatic ornithine decarboxylase activity at 4, 6 and 10 hr, irrespective of epidermal growth factor treatment. Hepatic spermidine N1-acetyltransferase activity was significantly increased at 6 hr compared with control rats. These results suggest that, after partial hepatectomy in rats, exogenous epidermal growth factor may stimulate hepatic putrescine production by increasing ornithine decarboxylase messenger RNA content and altering posttranscriptional ornithine decarboxylase regulation, as well as enhancing spermidine N1-acetyltransferase activity.

Acetyltransferases↗

PubMed1991

Insulin and glucagon therapy of acute hepatic failure.

When insulin and glucagon are administered to rats with severe liver injury, survival is enhanced with an attenuation of the liver injury compared to that of untreated controls. In rats with acute liver injury both hormones produce a rapid normalization of hepatic protein content following initiation of DNA synthesis. When rats receive both hormones after partial hepatectomy, the first burst of DNA synthesis reaches a maximum earlier than that seen in controls. Both hormones enhance the increment of hepatic putrescine essential for DNA synthesis through activation of ornithine decaroxylase and/or spermidine-N1-acetyltransferase. The enhancement of putrescine content by each hormone is additive. Putrescine supplementation promotes hepatic DNA synthesis after hepatectomy. Based on these data, we conclude that a combination of insulin and glucagon is effective in the therapy of acute hepatic failure in rats. The restoration of liver function as well as the stimulation of liver cell proliferation via putrescine production may contribute to this effect.

Acetyltransferases↗

PubMed1991

Ornithine decarboxylase induction in partially hepatectomized rat liver and modes of its stimulation by glucagon and insulin.

Hepatic ornithine decarboxylase (ODC) activity increases after partial hepatectomy and this activity is further stimulated by pharmacologic doses of glucagon and insulin. We now present data suggesting that glucagon and insulin stimulate ODC activity by distinct mechanisms. ODC activity increased progressively after partial hepatectomy and reached an initial peak at 4 h. Activity decreased to 50% of its peak value at 6 and 8 h and then rose progressively to a maximum at 12 h. Enzymatic activity was well correlated with the amount of hepatic immunoreactive ODC protein, thus suggesting that increased enzyme activity was due to increased amount of enzyme protein. Hepatic ODC mRNA increased gradually and continuously, reaching the maximal value by 12 h. In rats receiving glucagon after partial hepatectomy, ODC mRNA increased significantly by 2 h and enzyme immunoreactive protein and activity by 2 to 4 h as compared to controls. In contrast, insulin administration only induced a significant increase in enzyme immunoreactive protein and activity 10 to 12 h after partial hepatectomy. No significant changes in ODC mRNA level were observed. Our data suggest that the regulation mechanism of ODC induction following partial hepatectomy differs depending on the time after operation. Our data also suggest that while glucagon appears to regulate ODC activity by a transcriptional mechanism, insulin appears to operate at a post-transcriptional level.

Animals↗

PubMed1991

Evidence for enhanced secretory function of hepatic macrophages after long-term ethanol feeding in rats.

Rats were pair-fed nutritionally adequate liquid diets, containing ethanol as 36% of energy or an isocaloric amount of carbohydrate for 4-6 weeks. Ruffle formation of hepatic macrophages in the periportal area observed with a transmission electron microscope (which reflects their extent in activation) was more remarkable in ethanol-fed rats than in control rats. The ability of hepatic macrophages to produce superoxide anions assessed in situ by formazan deposition after liver perfusion with nitro-blue tetrazolium and phorbol myristate acetate was enhanced after such ethanol feeding. A similar result was seen 24 h after withdrawal of ethanol feeding. These findings suggest that long-term ethanol consumption may activate hepatic macrophages in secretory function.

Animals↗

PubMed1991

Method for in situ evaluation of superoxide production by pulmonary macrophages in the rat.

In order to investigate superoxide production by pulmonary macrophages in the rat, a route was created by ligating both the inferior and superior venae cavae and resecting the aorta after cannulation through the inferior vena cava into the right atrium of the heart. Lung perfusion was performed via this route with nitro blue tetrazolium. Although there was no formazan deposition throughout the lung, it became detectable in both alveolar and interstitial macrophages when phorbol myristate acetate was added to the perfusate. This deposition was markedly enhanced by previous injection of Corynebacterium parvum. The deposition disappeared after further addition of Cu(Lys)2, a scavenger of superoxide anions. This procedure may be useful for estimating in situ the ability of pulmonary macrophages to produce superoxide in the rat.

Animals↗