In the non-cirrhotic stage of nonalcoholic steatohepatitis, angioarchitecture of portal veins and lobular architecture are maintained.

The morphogenesis of lobular restructuring to liver cirrhosis in nonalcoholic steatohepatitis (NASH) is yet to be clearly understood. Therefore, we observed tissue samples from three biopsies and one autopsy with NASH in the non-cirrhotic stage three-dimensionally to elucidate the evolution of fibrosis and the changes of angioarchitecture. Histologic reconstructions revealed that pericellular fibrosis developed around the central vein in the early stage and gradually progressed to arch-shaped band-like fibrosis connecting the central veins in the neighboring lobules.

Prediction of clinically insignificant prostate cancer by detection of allelic imbalance at 6q, 8p and 13q.

The criterion tumor volume (TV) for clinically insignificant prostate cancer has been reported, but it differs from study to study: some have reported TV < 200 mm(3); others, < 500 mm(3). The aim of the present study was to distinguish clinically insignificant cancers from significant ones using molecular biological methods. A total of 184 microscopic cancers (MC) defined as limited within a 3 mm circle and 82 main tumor (MT) nodules were selected.

Lecithin: retinol acyltransferase protein is distributed in both hepatic stellate cells and endothelial cells of normal rodent and human liver.

Background: To determine the extent to which hepatic stellate cell (HSC) activation contributes to liver fibrosis, it was found necessary to develop an alternative structural and functional stellate cell marker for in situ studies. Although several HSC markers have been reported, none of those are associated with particular HSC functions.

Aim: The present study was undertaken to examine whether lecithin:retinol acyltransferase (LRAT), the physiological retinol esterification enzyme of the liver, is a potential and relevant tissue marker for HSC.

Identification of minimal regions of deletion at 8p23.1-22 associated with metastasis of hepatocellular carcinoma.

Aims/background: Loss of heterozygosity (LOH) at 8p is the most frequent chromosomal alteration in tumorigenesis of human cancers. However, the genetic change in metastasis of hepatocellular carcinoma (HCC) still has to be investigated.

Methods: We used 16 microsatellite markers informative in Japanese patients, selected from among 61 published microsatellite markers at 8p23.

Frequent loss of heterozygosity in two distinct regions, 8p23.1 and 8p22, in hepatocellular carcinoma.

Aim: To identify the precise location of putative tumor suppressor genes (TSGs) on the short arm of chromosome 8 in patients with hepatocellular carcinoma (HCC).

Methods: We used 16 microsatellite markers informative in Japanese patients, which were selected from 61 published markers, on 8p, to analyze the frequency of loss of heterozygosity (LOH) in each region in 33 cases (56 lesions) of HCC.

Results: The frequency of LOH at 8p23.

An autopsy case showing massive fibrinoid necrosis of the portal tracts of the liver with cholangiographic findings similar to those of primary sclerosing cholangitis.

An 81-year-old Japanese man with jaundice was strongly suspected clinically of having primary sclerosing cholangitis based on clinical examinations and later died of hepatic failure. The entire course of the disease lasted about 10 mo. The autopsy revealed extensive fibrinoid necrosis in the liver, kidney, spleen, pancreas, lung, lymph nodes, and pleura.