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1. |
State of hepatitis B viral DNA in the liver of patients with hepatocellular carcinoma and chronic liver disease |
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Liver,
Volume 6,
Issue 4,
1986,
Page 189-198
Hajime Hada,
Terukatsu Arima,
Kazumi Togawa,
Yoshio Okada,
Shigeru Morichika,
Hideo Nagashima,
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摘要:
ABSTRACT‐In order to clarify the relationship between the integration of hepatitis B virus (HBV) DNA and human hepatocellular carcinoma (HCC), the states of HBV DNA in liver tissues were examined by the Southern blot hybridization procedure. Integration of HBV DNA was found in 12 of 25 HCC cases and 5 of 12 cirrhotic cases. Of these 17 cases, 11 were positive for serum hepatitis B virus surface antigen (HBsAg) and the remaining six were positive for more than one of the serum HBV‐related antibodies. In all three cases of chronic hepatitis and 18 controls, integration of HBV DNA could not be detected. Free viral DNA was found in 12 of 15 cases with serum HBsAg. One patient without serum HBsAg also had free viral DNA in the liver. Integration of HBV DNA could be observed in HCC cases positive for serum HBsAg at the highest frequency. However, there was one HCC case from an HBsAg carrier in whom integration of HBV DNA might not have a causal effect on malignant transformation, because integrated HBV DNA could be detected only in a non‐tumor region. Since integrated HBV DNA could not be detected in 13 of 25 HCC cases,Other etiologic factors than the integration of HBV DNA must also be taken intoconsideration fo
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01065.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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2. |
Sepsis and cholestasis: thein vitroeffects of bacterial products on14C‐taurocholate uptake by isolated rat hepatocytes |
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Liver,
Volume 6,
Issue 4,
1986,
Page 199-204
G. Y. Minuk,
N. Rascanin,
E. S. Sarjeant,
C. H. Pai,
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摘要:
ABSTRACT‐Bacterial endotoxins are known to be an important cause of cholestasis, yet not all organisms that cause cholestasis produce endotoxins. In order to determine whether bacterial products other than endotoxins may be involved in the cholestatis process,14C‐taurocholate (TC) uptake by isolated rat hepatocytes was measured in the presence of mid‐log, stationary and mid‐death phase bacterial broth supernatants from eight common bacterial pathogens. The results were then correlated with a quantitative assessment of endotoxin production by each organism. Supernatants fromHaemophilus influenzae, Pseudomonas aeruginosaandKlebsiella pneumoniademonstrated a striking inhibitory effect on bile salt uptake (77.2 ± 6.7, 46.9 ± 6.5 and 32.9 ± 7.1% maximum inhibition of14C‐TC uptake, respectively) when compared to sterile broth controls.Streptococcus faecalis(Enterococcus),Escherichia coli, Staphylococcus aureusandBacteroides fragilisproducts, on the other hand, had relatively minor effects (12.3 ± 5.2, 12.0 ± 7.5, 8.4 ± 6.7 and0.05).14C‐TC uptake inhibition did not correlate with the amount of endotoxin produced by each organism (r = 0.251). The results of this study indicate that bacteria produce a factor other than endotoxin that significantly inhibits bile salt uptake by isolated rat hepatocytes. It is conceivable that this factor not only contributes to the cholestasis caused by endotoxin‐producing organisms but could also play an important role in the cholestasis caused by infection with non‐e
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01066.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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3. |
Immunohistochemical study on bile ductular proliferation in various hepatobiliary diseases |
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Liver,
Volume 6,
Issue 4,
1986,
Page 205-211
Yasuni Nakanuma,
Goroku Ohta,
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摘要:
ABSTRACT‐Proliferation of the two types of bile ductules, typical and atypical, in the portal and periportal areas was examined in various liver diseases other than cirrhosis to determine any difference in their immunohistochemical properties and presumed histogenesis. While the typical ductules with a well‐formed lumen were frequently seen in a large spectrum of diseases, atypical ductules with a poorly defined lumen were encountered much more frequently in prolonged biliary diseases, including primary biliary cirrhosis and primary sclerosing cholangitis, than in nonbiliary hepatic diseases. Immunocytochemically, cytoplasmic keratin was intensively positive in typical ductules, and the degree of its intensity and extent was variable in atypical ductules. Simultaneously, some of the periportal hepatocytes revealed weak staining for keratin. Luminal borders of typical ductules usually revealed an expression of both carcinoembryonic antigen and epithelial membrane antigen, while atypical ductules and periportal hepatocytes lacked epithelial membrane antigen. The atypical ductules, together with the adjoining hepatocytes, appeared on occasion to form anastomosing cords in prolonged biliary diseases. Thus, atypical ductules seem likely to originate from ductular transformation of the periportal hepatocytes and the typical ductules might result from the proliferation of preexisting interlobular bile ducts and ductu
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01067.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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4. |
Natural killer (NK) cell activity and itsin vitroresponse to interferon‐α(Le) in chronic liver diseases and hepatocellular carcinoma |
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Liver,
Volume 6,
Issue 4,
1986,
Page 212-220
Nobuyuki Hirai,
Yasuhiro Kato,
Kenichi Kobayashi,
Nobu Hattori,
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摘要:
ABSTRACT‐The natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) in patients with various chronic liver diseases, and itsin vitroresponse to human interferon‐α(Le) were investigated using a 16‐h 51‐Cr releasing cytotoxicity assay against YAC‐1 or RSa target cells. The NK cell activity was found to be higher in chronic active hepatitis (CAH) and liver cirrhosis (LC) patients without HCC, whereas it was slightly lower in LC patients with hepatocellular carcinoma (HCC), than in normal controls. By the addition of IFN‐α(Le)in vitro, the NK cell activity was clearly and dose‐dependently augmented, even in chronic liver diseases, as well as in normal controls. The magnitude of this augmentation by 10000 IU/ml of IFN‐α(Le) in the various chronic liver diseases was not significantly different from that in normal controls. The results suggested that the response of NK cells to IFN‐α(Le) is not impaired even in chronic liver disease conditions, while the level of NK cell activity may vary according to the type of chronic liver disease and may decrease
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01068.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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5. |
Portal hypertension: a permissive factor only in the development of ascites and variceal bleeding |
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Liver,
Volume 6,
Issue 4,
1986,
Page 221-226
William G. Rector,
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摘要:
ABSTRACT‐It is controversial whether the occurrence of ascites and gastrointestinal bleeding in cirrhosis is related to the severity of portal hypertension. Portal pressure was examined in 124 unselected patients with portal hypertension due to chronic liver disease to evaluate this issue. Portal pressure was less in patients without complications of chronic liver disease (11.7 ± 3.0 mmHg, n = 16) as compared to patients who had bled from varices or erosive gastritis (16.6 ± 3.4 mmHg, p<0.001, n = 49), who had ascites (16.2 ± 3.0 mmHg, p<0.001, n = 78) or both (16.5 ± 3.0 mmHg, p<0.001, n = 19). Portal pressure was similar in patients bleeding from varices and erosive gastritis (16.7 ± 3.4 mmHg, n = 43; vs 16.2 ± 4.0 mmHg, n = 6, respectively) and in patients with refractory and nonrefractory ascites (16.2 ± 3.5, n = 21; vs 16.2 ± 3.5 mmHg, n = 57). The lowest portal pressure recorded in a patient with variceal bleeding was 9.0 mmHg. The lowest portal pressure recorded in a patient with ascites was 8.0 mmHg. Esophageal varices (graded 0–4 at endoscopy) were larger in patients with a history of bleeding from esophageal varices as compared to patients without such a history (3.2 ± 0.7 vs 2.0 ± 0.9, p<0.001). Serum albumin concentration was greater in patients without ascites as compared to patients with ascites (33 ± 5 vs 26 ± 5 g/1 p<0.001) but was similar in patients with refractory and nonrefractory ascites (25 ± 7 vs 26 ± 5 g/1, respectively). These data suggest that portal hypertension is a permissive factor only in the development of ascites and gastrointestinal bleeding in patients with chro
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01069.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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6. |
Steroids in chronic B‐hepatitis. A randomized, double‐blind, multinational trial on the effect of low‐dose, long‐term treatment on survival |
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Liver,
Volume 6,
Issue 4,
1986,
Page 227-232
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摘要:
ABSTRACT‐The effect of long‐term, low‐dose prednisolone treatment on the survival of patients with chronic B‐hepatitis was studied in a randomized, double‐blind multicentre trial. Twenty‐two centres from 11 European countries included 99 patients in the trial. Survival analysis showed 2.9 (95% confidence limit 0.9‐9) times greater mortality in the prednisolone than in the placebo group (P = 0.07). In a Cox regression analysis, correcting for the influence of other prognostic factors, the detrimental effect of prednisolone treatment was unchanged. Mortality increased significantly with age, and patients without piece‐meal necrosis had 7 times higher mortality than those with this change on entry to the trial. It is concluded that long‐term, low‐dose prednisolone treatment is very unlikely to be beneficial, and should be considered harmful in chronic B‐hepatitis, particularly in the most seve
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01070.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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7. |
The blood hepatocytic barrier: a light microscopical, transmission‐ and scanning electron microscopic study |
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Liver,
Volume 6,
Issue 4,
1986,
Page 233-245
Thomas Horn,
Hans Lyon,
Per Christoffersen,
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摘要:
ABSTRACT‐The normal blood hepatocytic barrier (BHB), comprised by the endothelial lining cells and the perisinusoidal space, was investigated, and it was concluded that the BHB is a complex structure in which each individual part serves several functions. Immunohistochemical staining for factor VIII showed endothelial lining cells to be positive. By TEM and SEM the endothelial cells were seen to be fenestrated without a basal lamina. They possess numerous endocytotic vesicles. The perisinusoidal space contains the lipocytes and a matrix composed of fibrils, and a microfilamentous to granular material. The nature of these matrix components was poorly analyzable by conventional methods. Lipocytes were visualized by LM in: 1) sections stained with oil red 0 after fixation in Baker's formol‐calcium and following post‐fixation in dichromate, and 2) toluidine‐blue‐stained Epon‐embedded sections. TEM revealed numerous cytoplasmic processes rich in microfilaments encircling th
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01071.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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8. |
Effect of acetaldehyde on collagen synthesis by fat‐storing cells isolated from rats treated with carbon tetrachloride |
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Liver,
Volume 6,
Issue 4,
1986,
Page 246-251
Yasushi Shiratori,
Takafumi Ichida,
Tateo Kawase,
Eddie Wisse,
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摘要:
ABSTRACT‐In an attempt to elucidate the role of fat‐storing cells (FSCs) in alcoholic liver fibrosis, we examined the effects of ethanol and acetaldehyde on collagen synthesis by FSCs isolated from CCl4‐treated or normal rats. Isolated FSCs from normal rats showed characteristic lipid droplets in the cytoplasm. FSCs from CCl4‐treated rats showed an abundant rough endoplasmic reticulum and a small number of lipid droplets. Collagen synthesis by the cells from CCl4‐treated rats was 4–5‐fold enhanced as compared with untreated rats. Though ethanol had an inhibitory effect on collagen synthesis by FSCs, acetaldehyde stimulated collagen production by the cells from CCl4‐induced hepatic fibrosis, whereas collagen synthesis by the cells from normal rats was not influenced by acetaldehyde. From these results, FSCs are morphologically and functionally changed in liver fibrosis, and the transitional state of FSCs might be important in the pathogenesis of alcoholic
ISSN:0106-9543
DOI:10.1111/j.1600-0676.1986.tb01072.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
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