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Summary Background Colorectal depressed tumours have a tendency to invade deeper mucosal layers and metastasize in the lymph nodes, despite their small size. Aim To investigate the clinical and endoscopic characteristics of depressed early colorectal cancers (intramucosal and submucosal adenocarcinoma) compared with non-depressed early cancers. Methods Five hundred and seventy consecutive early colorectal cancers obtained through endoscopic resection or surgical operation were studied. Early cancers were endoscopically classified as either the depressed or non-depressed type. The age and gender of the patients as well as the size and distribution of the cancers were compared between types. The tumour locations were classified into three groups: caecum to transverse colon (right colon), descending to sigmoid colon (left colon) and rectum. Results Patients were similar with respect to age and gender. The mean size of the depressed type was smaller than that of the non-depressed type (mean 8.4 mm vs. 13.3 mm; P

Background: Previously, we reported that most gastrointestinal tumors could be distinguished with the Light-Induced Fluorescence Endoscopy for GastroIntestine system (LIFE-GI system) using a fiberscope. However, the quality of the fiberscopic images was inferior compared with videoscopic images. Therefore, we developed a new Auto-Fluorescence Imaging (AFI) videoscope system (manufactured by Olympus Corp.). Methods: We evaluated the clinical usefulness of the AFI videoscope system for the detection of colonic neoplasms. Using this system, we observed 168 colonic polyps. Results: Images obtained by AFI provided better brightness than autofluorescence fiberscopic images and lesion margins were clearly evident. It demonstrated excellent recognition capability to a small lesion that was difficult to be detected by conventional observation. Sensitivity was 89% and specificity 81%, with specificity higher than that of the autofluorescence fiberscopic images. Conclusions: This newly developed AFI videoscope system will be useful for the detection of colonic neoplasms.

Administration of phalloidin in vivo to rats causes marked changes in the distribution of actin and myosin in hepatocytes, which accompanies reduced bile flow. We have found that in hepatocytes treated with phalloidin for 3 and 7 days, cellular myosin content increased about 1.5-fold and 4.7-fold, respectively. In addition, total cell protein content and several marker enzyme activities were also elevated by 30-120% depending on the duration of phalloidin treatment. These observations allow us to speculate that phalloidin somehow elicits inhibition of cellular protein degradation, which results in the increase of these protein levels. To examine this possibility further, we analyzed leupeptin-induced density shift of phagolysosomes. In normal liver, the injection of leupeptin/E64c caused an increase in the density of both heterolysosomes and autolysosomes, due to retarded digestion of sequestered proteins as a result of the inhibition of lysosomal cathepsins. Accumulation, in these denser autolysosomes, of lactic dehydrogenase, pyruvate kinase, aldolase, and myosin was demonstrated by enzyme assays and immunoblot analysis. In the phalloidin-treated liver, the increase in the density of autolysosomes and the accumulation of above cytoplasmic enzymes were markedly inhibited. However, phalloidin did not affect the shift in the density of heterolysosomes. From these data, we concluded that autolysosome formation was specifically hindered in phalloidin-treated rat hepatocytes, which results in the reduction of autophagic protein degradation and eventual increase in intracellular protein levels.

Mitochondrial inner membrane proteins extracted from beef heart tissue were examined for reactivity to antimitochondrial antibody (AMA) present in sera of patients with primary biliary cirrhosis (PBC) by an immunoblotting technique. Four proteins, which reacted with AMA, had molecular masses of 70 kDa, 50 kDa, 47 kDa and 40 kDa, as defined by their relative mobility (Rf) in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. All sera of 114 PBC patients were positive with at least one and as many as four of the mitochondrial proteins. The major antigenic proteins of mitochondrial inner membrane to which AMA reacts were the 70 kDa and 47 kDa proteins. All PBC sera containing antibodies to the 50 kDa and/or 40 kDa proteins reacted with 70 kDa as well. The isolation of antigen reacting with AMA of PBC is important to warrant further study of AMA and the cause of the disease. The isolation of responsible antigens had been difficult because the four antigens were insoluble. However, the antigen newly found by us, the 36 kDa fragment, obtained by partial trypsin digestion, is soluble. Using several procedures, the antigenic protein target of AMA was purified from mitochondria for the first time. We determined the N-terminal sequence of the soluble 36 kDa fragment, 25 residues in length. Until now the N-terminal sequence of the 36 kDa protein has not shown significant homology with any known protein. The present results of antigen purification would contribute to the elucidation of the epitopes of AMA antigen.