Endotoxin has been identified as a principal mediator of sepsis, often with resulting multiple organ failure. Although interferon ␥ (IFN-␥) has a central role in controlling bacterial infection through the activation of macrophages and T lymphocytes, it can also enhance the harmful effects of the inflammatory response. To examine the role of IFN-␥ in lipopolysaccharide (LPS)-induced injury, we administered LPS (20 or 800 g/mouse) alone or as low-dose LPS (20 g/mouse) 7 days after heat-killed Propionibacterium acnes (P. acnes) injection into wild-type C57BL/6 (B6) mice or IFN-␥-deficient (GKO) mice (B6 background). Although low-dose (20 g) LPS alone had no effect on survival, the administration of 800 g LPS alone resulted in 100% mortality in both B6 and GKO mice without significant hepatic mononuclear cellular infiltration or differences in elevated plasma tumor necrosis factor ␣ (TNF-␣), interleukin 6 (IL-6), and IL-12 levels. In contrast, mortality after low-dose (20 g) LPS challenge in P. acnes-primed B6 mice was 100%, but 0% in GKO mice. In vivo plasma cytokine (IFN-␥, TNF-␣, IL-6, and IL-12) levels and in vitro cytokine production by hepatic mononuclear cells were significantly higher in B6 mice compared with GKO mice. Associated hepatic mononuclear cellular infiltration, multifocal liver necrosis, hepatomegaly, and splenomegaly were found in B6 mice, but not in GKO mice. Finally, the anti-inflammatory NK1.1؉CD4؉ cell proportion of hepatic infiltrating mononuclear cell numbers 7 days after P. acnes administration was significantly reduced in B6 compared with GKO mice, whereas the proportion of inflammatory NK1.1؉CD4؊ cells was increased. In conclusion, these data suggest that IFN-␥ mediates P. acnes-primed low-dose LPS injury through the hepatic infiltration of mononuclear cells and the subsequent elevation of inflammatory cytokines after LPS challenge, whereas the lethal effects of high-dose LPS alone does not depend on the presence of IFN-␥. (HEPATOLOGY 2002;35: 805-814.)
Several studies have revealed the diagnostic value of fluorodeoxyglucose-positron emission tomography for breast carcinomas. However, breast carcinomas display considerable variation in 18F-labeled 2-fluoro-2-deoxy-D-glucose uptake, and few papers have reported the clinical utility of the standardized uptake values (SUV). The purpose of this study is to investigate the relationship between SUV assessed by positron emission tomography (PET) and the clinicopathological characteristics of breast carcinoma. We reviewed 52 breast carcinomas of 45 patients presented at our department between January 2004 and July 2005. We compared the histopathological findings of the breast carcinomas with the preoperative SUV. Of the 52 breast carcinomas, 49 (94%) were detected by preoperative PET. A positive correlation was found between the SUV and tumor size ( P < 0.01), histological grade ( P < 0.01), the expression of the estrogen receptor ( P < 0.001), progesterone receptor ( P < 0.01), and p53 ( P < 0.01). The number of metastatic axillary lymph nodes (r = 0.73; P < 0.0001) and the MIB-1 labeling rates (r = 0.5; P < 0.01) correlated with the SUV of the breast carcinomas. No relationship existed between the SUV and the following: histological tumor types ( P = 0.07), human epidermal growth factor receptor-2 status ( P = 0.10), and the presence of metastatic lymph nodes ( P = 0.10). The SUV of the breast carcinomas correlate with several histopathological and immunohistochemical prognostic factors. We can obtain information on the degree of malignancy of the carcinoma and prognostic factors by preoperative PET examination.
Using direct chimpanzee inoculation as an assay method, we tested the abilities of the following chemical or physical treatments to inactivate hepatitis B virus in human plasma: 1% aqueous glutaraldehyde at 24 degrees C for 5 min, 0.1% aqueous glutaraldehyde at 24 degrees C for 5 min, 80% ethyl alcohol at 11 degrees C for 2 min, and heat at 98 degrees C for 2 min. All treatments were shown to be effective, indicating that the resistance level of the hepatitis B virus is not extreme.
The hemolytic activity of the thermostable direct hemolysin produced by Vibrio parahaemolyticus was inhibited by a ganglioside mixture. The ganglioside component which inhibited the hemolysin was not GM1 ganglioside.
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