To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiated HCCs. Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24-25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13-14 (37%), 4q13-22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well-differentiated HCCs (PF.05), whereas a loss of 13q13-14 and amplification of 11q13 were linked to moderately and poorly differentiated HCCs (PF.01). These observations suggest that a gain of 8q24 is an early event and that a loss of 13q13-14 and amplification of 11q13 are a late event in the course of liver carcinogenesis. A gain of 10q (7/41) was detected exclusively in cases with HCV infection. In contrast, an amplification of 11q13 was preferentially found in HBV-positive HCCs. These findings raise the hypothesis that, although many genetic alterations are basically common to both HCV-positive and HBV-positive tumors, the process of carcinogenesis may be to some extent different between these two types of tumors. (HEPATOLOGY 1999;29:1858-1862.) Hepatocellular carcinoma (HCC) is one of the most common human malignant tumors in the world. 1 It is widely accepted that hepatitis B (HBV) or C virus (HCV) infection, subsequent chronic inflammation and hepatocyte regeneration play important roles in the development of HCC. 2,3,4 However, the effects of viral infection on hepatocellular transformation remain to be determined. Accordingly, it remains unknown whether carcinogenetic process is different in HBV-positive and HCV-positive livers. HCC, like many other tumors, is considered to develop and progress as a consequence of an accumulation of genetic alterations. 5 Many investigators have made varying attempts to find genes implicated in hepatocarcinogenesis to construct a genetic pathway in the progression of HCC. 6,7,8,9 Although frequent allelic losses at loci of chromosomes 1p, 4q, 5p, 5q, 8p, 10p, 11q, 13q, 16q, and 17p have been reported in HCCs, 10,11 most of these studies failed to provide consistent information concerning genetic changes leading to the evolution of HCC. Comprehensive analysis is necessary to thoroughly understand the complicated genetic alterations in malignant tumors. Determination of these comprehensive genetic changes in solid tumors is practically difficult, because the examination of many individual genes by conventional methods is laborious and cumbersome. Screening for chromosomal regions with frequent gains and losses is one of t...

The fruit body of Grifola frondosa (maitake), Basidiomycetes was confirmed to contain substances with anti-diabetic activity. When 1 g/d of powdered fruit body of maitake was given orally to a genetically diabetic mouse (KK-Ay), blood glucose reduction was observed, in contrast to the control group in which the blood glucose increased with ageing. Moreover, levels of insulin and triglyceride in plasma demonstrated a change similar to blood glucose with feeding of maitake. Ether-ethanol-soluble (ES) and hot water-soluble (WS) fractions were prepared from the fruit body and their hypoglycemic activity was examined. Blood glucose-lowering activity was found when ES-fraction or WS-50% ethanol float (X) fraction was administered orally, but other WS-fractions were inactive. These results suggest that the anti-diabetic activity was present not only in the ES-fraction consisting of lipid but also in the X-fraction of peptidoglycan (sugar:protein = 65:35).

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Carbon monoxide (CO) adsorption at 90 K on Cu(100), (110), and (111) covered with submonolayer Fe at room temperature has been investigated using infrared reflection absorption spectroscopy (IRRAS). Saturated adsorption of CO on the 0.3-monolayer (ML)-thick Fe/Cu(111) bimetallic surface yields two C-O stretch bands at 2075 and 2015 cm -1 due to adsorption on the uncovered Cu and on deposited Fe, respectively. The former band agrees in frequency with the C-O stretch band on the clean Cu(111) surface, indicating that the deposited Fe does not affect the Cu surface. In contrast, on the 0.3-ML Fe/Cu(100) surface, an additional C-O stretch band emerges at 2104 cm -1 on the high-frequency side of the band (2090 cm -1 ) due to CO adsorbed on the uncovered Cu surface. This band arises from CO bound to Cu atoms formed by intermixing of the deposited Fe and substrate Cu atoms. Even more intense Fe-Cu intermixing occurs on the 0.3-ML Fe/Cu(110) surface; for saturated adsorption, the corresponding band is observed at 2108 cm -1 , and its relative intensity to the C-O band on the uncovered Cu surface is much stronger than on the 0.3-ML Fe/Cu(100) surface. This severe intermixing at the Cu(110) substrate surface is explained in terms of a high surface energy and the specific surface lattice structure.