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Experimental autoimmune hepatitis was produced by immunizing Wistar rats with syngeneic liver proteins. Mononuclear cells infiltrating the liver tissue were identified by immunohistochemical techniques using monoclonal antibodies specific for subpopulations of rat lymphocytes. The strong infiltration of CD8+ cytotoxic T lymphocytes (CTL) were found in the portal areas. Subpopulations of mononuclear cells infiltrating the liver, spleen cells and peripheral blood lymphocytes were identified by flow cytometry. Flow cytometric analysis revealed the presence of CD5- and CD8+ lymphocytes in the liver tissues. Mononuclear cells infiltrating the liver were isolated from Wistar rats having autoimmune hepatitis to determine whether those exhibit cytotoxicity against syngeneic hepatocytes; they exhibited cytotoxicity against isolated syngeneic hepatocytes, but failed to lyse K562 cells, syngeneic concanavalin A-activated splenocytes and allogeneic hepatocytes. Depletion of CD8+ T cells significantly reduced the cytotoxic ability of mononuclear cells infiltrating into the liver against syngeneic hepatocytes. These findings support the idea that liver cell injury in experimental autoimmune hepatitis may at least in part be mediated by CTL. [ABSTRACT FROM AUTHOR]

We report changes in free radical-metabolizing enzymes and the increased generation of lipid peroxides associated with extreme metal accumulation in the liver of the Long-Evans with cinnamon-like coat color (LEC) rat, a new mutant strain displaying hereditary hepatitis and subsequent hepatocellular carcinoma. The activity of free radical-metabolizing enzymes and lipid peroxides, and the concentration of metal in the liver were determined sequentially after birth. Mn-superoxide dismutase activity significantly increased immediately after the onset of hepatitis in LEC rats, whereas no remarkable change was observed in control rats. Cu, Zn-superoxide dismutase activity in LEC rats was similar to that in control rats. Glutathione reductase activity increased, while glutathione peroxidase activity was lower in LEC rats than in control rats throughout the observation periods. Lipid peroxides, estimated by thiobarbituric acid reaction, also increased 4- to 5-fold immediately after the onset of hepatitis in LEC rats. Copper concentration was 30- to 50-fold higher in the liver of LEC rats than in control rats, and the iron content also increased significantly before and after the onset of hepatitis. These findings suggested that an oxidant injury generated by toxic metals could be one of the factors responsible for hepatocellular damage in this unique hereditary hepatitis. [ABSTRACT FROM AUTHOR]

Fischer rats became resistant to syngeneic hepatocellular carcinoma (FAA-HTC1) cells on repeated sensitization with mitomycin C-treated FAA-HTC1 cells. In contrast, FAA-HTC1 cells injected into the liver killed normal control Fischer rats within 2 months. Histopathological studies revealed massive accumulation of mononuclear cells in the tumor tissues of sensitized rats that rejected syngeneic FAA-HTC1 cells, whereas very few mononuclear cells were found in the tumor tissues of control rats. Cell populations infiltrating the tumor tissues were identified by flow cytometric analysis. Mononuclear cells found within the regressing tumors of the sensitized rats were identified as mostly T cells, and two-thirds of these T cells were CD8-positive. Compared with the activity in control rats, the killer activity of mononuclear cells infiltrating tumors was significantly increased in the sensitized rats 7 days after tumor inoculation. Depletion of CD8(+) T cells significantly reduced the cytotoxicity of mononuclear cells infiltrating tumors obtained from sensitized rats. In contrast, depletion of CD16(+) cells reduced the cytotoxicity of mononuclear cells infiltrating tumors obtained from both control and sensitized rats. Furthermore, the CD16(+) cell-depleted fraction of mononuclear cells infiltrating tumors showed significant cytotoxicity against FAA-HTC1 cells, but failed to show cytotoxicity against other syngeneic tumor cells or allogeneic hepatoma cells. [ABSTRACT FROM AUTHOR]

GeneFields®-Hair is a simple analysis kit that uses nucleic acid chromatography and polymerase chain reaction (PCR) to identify animal species of hair-like food contaminants. In this study, we evaluated GeneFields®-Hair as a simple and rapid method for identifying animal species from hair-like materials collected in forensic science, such as at crime scenes. The use of this kit with other human biological materials (whole blood, head dandruff, nails, saliva, oral mucosa, sebum, and urine) was also investigated. Animal body hair samples were pretreated by grinding in a buffer solution, centrifuged, and the supernatant was used for PCR. Nucleic acid chromatography of the PCR products allowed the identification of the animal species by the presence or absence of coloration on the decision line. For human biological materials, nucleic acid chromatography was performed after the appropriate pretreatment like body hair material. The determination of some animal species was difficult, even if they had a dedicated DNA Strip determination line. Furthermore, animals from the same family but different genera were sometimes detected on the same determination line. All the human biological samples were correctly identified. Smartphone photographs of the coloration of the judgment line were processed using the ImageJ software for quantitative determination., Competing Interests: Declaration of Competing Interest The authors declare that there are no financial or other relations that could lead to a conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

We report here two cases of neuroendocrine carcinoma which occurred in the biliary system. The prognosis of neuroendocrine carcinoma in the biliary system is generally poor. However, based on the preoperative pathological diagnosis of neuroendocrine carcinoma, multidisciplinary treatment consisting of preoperative chemotherapy, chemoradiation therapy, curative resection and adjuvant chemotherapy seemed to be very effective and long-term survival was obtained in our two cases. Therefore it is essential to diagnose preoperatively to improve prognosis.

Background: Eating behavior change (EBC) is essential to remedy metabolic syndrome (MetS). We carried out our clinic-based health and nutrition intervention informed by the transtheoretical model (TTM) to promote EBC. In particular, we aimed to foster EBC among individuals who were in the cognitive stage (C-level stage) of their health behavior, in contrast to the model positing that those in C-level stage are less likely to adopt EBC than those in the behavioral stage (B-level stage). The degree of each one's risk for MetS was also examined., Subjects: The study population comprised 108 adults (38 males aged 58 +/- 10.8 SD and 70 females aged 60 +/- 6.6)., Methods: SUBJECTS were given instruction and support for over a 3-month period. MetS diagnostic criteria values, dietary intake and TTM were measured before and/or after the intervention. On the basis of their MetS and TTM scores, subjects were classified into two groups according to risk (high or low) and stage (C or B). Multiple linear regression analysis was performed., Results: In both risk groups, EBC stage scores advanced in many subjects, progressing from C to B-level stage. Reduction in abdominal circumference and improvement of the MetS criteria values were also observed particularly in the high-risk group and those in the B-level stage. Stage-specific improvements in physical characteristics, the MetS criteria values and energy intake were likewise seen in both risk groups. Abdominal circumference reduction was negatively and positively correlated with EBC stage scores and fat energy ratio, respectively., Conclusion: From the results, it was proved that improvements of MetS criteria values concomitantly occurred with reduction of eating energy intake, especially fat energy, as well as advance of EBC from C to B-level stage. In addition, we found it effective to let the participants recognize their degrees of risk for MetS.

We studied about the discrepancies of stage diagnosis between laparoscopic and histological findings in the clinical course of chronic viral hepatitis. We noticed discrepancies in 26% of chronic hepatitis B and 18% of chronic hepatitis C. Many cases were judged more advanced by laparoscopic staging than by histological staging. The group with different stage diagnosis showed high frequency of reddish markings and patchy markings indicating severe necro-inflammatory reaction and regenerative reaction in laparoscopic findings. This suggests that existence of active inflammation might be a cause of discrepancies in stage diagnosis. The cumulative incidence of hepatocellular carcinoma was significantly higher in the cases judged more advanced by laparoscopy even in the same histological stage. This indicates that laparoscopic staging should be more reliable for predicting prognosis in each patient.

Mass screening for liver cancer based mainly on abdominal ultrasound was begun in major cities of Hokkaido, Japan, in November 1981, to enable early detection and treatment of hepatocellular carcinoma (HCC). Serum alpha-fetoprotein levels were also measured to minimize false negative studies. Examinees included those who sought liver disease screening as well as high risk individuals: hepatitis B surface antigen carriers and those with a past or current liver disease, history of blood transfusion, family history of liver cancer, and more recently those with positive anti-hepatitis C antibodies. The examination was carried out on each Saturday and Sunday as one round, and by February 1992 48 rounds had been performed. A total of 8090 individuals were investigated, and HCC was detected in 91 with a detection rate of 1.12%. This rate was 1.6% among 5684 individuals who were selected for high risk. Cumulative rates of survival among these patients were 79.0% at 1 year, 43.8% at 3 years, 19.3% at 5 years and 15.4% at 7 years. These survival rates were comparable with those for the patients with HCC diagnosed during follow-up of chronic liver disease and treated at our hospital. The cost for detecting one HCC patient in this programme was 2,660,000 yen (approximately US$25,000), which was less than those for some other types of cancer in a similar setting. Considering the high detection rate in this programme, we feel that similar programmes should be encouraged and supported.

Many studies have suggested that examination of a patient's serum for viral RNA by reverse transcriptase-polymerase chain reaction (RT-PCR) is the most sensitive and specific serological means of determining chronic HCV infection. Moreover, technique to quantify HCV RNA in serum using PCR technology has been developed, and diagnosis of HCV genotype by PCR with mixed primers has been used for diagnosis of type C hepatitis. Herein, we discuss the laboratory technique and significance of various PCR methods. HCV RNA can be detected by amplification technique of RT-PCR. Primers in the 5'-noncoding region are frequently used to detect HCV RNA, because the RNA sequence in this region is the most conserved. We usually perform 30 cycles of amplification with outer primers and another 30 cycles with inner primers (nested RT-PCR). Using this technique, HCV RNA was detected in 96% of anti-HCV-positive chronic hepatitis patients. This PCR technique gives us important information for the diagnosis of type C chronic hepatitis indicating HCV infection. The competitive PCR technique is usually used to quantify HCV RNA. This method is based on complification of the target RNA with known amounts of synthetic mutant RNA. The mutant RNA should be amplified by the same primers for amplifying target RNA, and should be distinguished from target RNA by the size of the amplified DNA product by making a deletion or restriction site artificially. Quantifying HCV RNA before interferon therapy is useful to predict the effectiveness of the therapy; patients with a large amount of HCV RNA tend to have a poor outcome.(ABSTRACT TRUNCATED AT 250 WORDS)