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A conference paper on whether a rat colon carcinoma cell line CC531s could induce apoptosis in liver sinusoidal endothelial cells (SLECs). Apoptosis was visualized by markers such as Hoechst and Propidium iodide and cells were recorded by time lapse video microscopy with and without an antagonistic antibody for FasL. The paper concludes that CC531s cells can induce apoptosis in LSECs and antagonistic antibody against FasL.

A conference paper about professor, anatomist, and physiologist Karl Wilhelm Kupffer and his contributions to modern hepatology is presented. It discusses Kupffer's professional career. It also highlights Kupffer's scientific contributions to the state-of-the-art views of the sinusoidal cells in the liver.

A conference paper about results of in situ and vital studies on liver development, metamorphosis and formation of adult vascular elements in medaka. These studies were facilitated by use of the see-through medaka, a vertebrate model with a transparent body throughout life. Pigment interference is not a problem in this model. Medaka are being utilized to examine endocrine disruptors, liver carcinogenesis and the efficiency of waste water treatment and reuse systems.

A conference paper that analyzes proteoglycans involved in sporozoite targeting to the liver and the route of the parasites into the liver parenchyma is presented. It examines the interaction between Plasmodium sporozoites and sinusoidal cells from rat liver. It proposes that sporozoite infection of the liver involves three steps, namely, arrest in the sinusoid, gliding to and passage through Kupffer cells, and invasion of hepatocytes.

A conference paper on an in vivo method for determining endosomal distribution of both ligand and asialoglycoprotein receptor (ASGPR) in rat liver is presented. Results suggest that the isolation of two distinct endosome populations, as well as the characterization of both the ligand and receptor content of the isolated endosomes is possible. Findings also reveal that isolation of the endosomes into fractions enriched in either early or late endosomes was accomplished.

A conference paper on whether or not the pores on sinusoidal endothelial cells (SECs) under three-dimensional perfusion co-culture treatment with Swinholide-A behave like those in primary culture cells is presented. Results reveal that the number of pores on M1 cells in co-culture was increased by the effect of actin inhibitor. Both share stress and cell-to-cell interaction are vital factors of reappearance of fenestrae in immortalized endothelial cells.

A conference paper about the sinusoidal endothelium and space of Disse in ageing Papio hamadrayas is presented. It examines the livers of young and old baboons to confirm that pseudocapillarization is a generalized aging change across species. Results reveal that significant age-related changes occur in the perisinusoidal region of the baboon liver.

The article reports on the effects of ischemic pre- and postconditioning on hypoxia inducible factor 1a (HIF-1a), vascular endothelial growth factor A (VEGF-A) and transforming growth factor b (TGFb) in liver tissue by testing on rat liver. It states that 28 rats were characterized from preconditioning to postconditoning ischemic. Results suggested that ischemic conditioning prevent HIF-1a mRNA entrance in the rat liver.

Background: Kupffer cells are well known macrophages of the liver, however, the developmental characteristics of Kupffer cells in mice are not well understood. To clarify this matter, the characteristics of Kupffer macrophages in normal developing mouse liver were studied using light microscopy and immunocytochemistry. Methods: Sections of liver tissue from early postnatal mice were prepared using immunocytochemical techniques. The Kupffer cells were identified by their immunoreactivity to the F4/80 antibody, whereas endothelial cells were labelled with the CD-34 antibody. In addition, Kupffer cells and endothelial cells were labelled by systemically injected fluorescently labelled latex microspheres. Tissue slices were examined by fluorescence microscopy. Results: Intravenous or intraperitonal injections of microspheres yielded similar patterns of liver cell labelling. The F4/80 positive Kupffer cells were labelled with both large (0.2 μm) and small (0.02 μm) diameter microspheres, while endothelial cells were labelled only with the smaller diameter microspheres. Microsphere labelling of Kupffer cells appeared stable for at least 6 weeks. Cells immunoreactive for F4/80 were identified as early as postnatal day 0, and these cells also displayed uptake of microspheres. Numbers of F4/80 Kupffer cells, relative to numbers of albumin positive hepatocytes, did not show a significant trend over the first 2 postnatal weeks. Conclusions: Kupffer cells of the developing mouse liver appear quite similar to those of other mammalian species, confirming that the mouse presents a useful animal model for studies of liver macrophage developmental structure and function. [ABSTRACT FROM AUTHOR]

Background: DT diaphorase (DTD; NAD(P)H:quinone oxidoreductase; EC 1.6.99.2) catalyses the two electron reduction of quinones, thus preventing redox cycling and consequently quinone dependent production of reactive oxygen species. In rat and mouse, a wide range of chemicals including polyaromatic hydrocarbons, azo dyes and quinones induces DTD. Bifunctional compounds, such as β-naphthoflavone (β-NF) and benzo(a)pyrene (B(a)P), induce DTD together with CYP1A and phase II enzymes by a mechanism involving the aryl hydrocarbon receptor (AHR). Monofunctional induction of DTD is mediated through the antioxidant response element and does not lead to the induction of AHR dependent enzymes, such as CYP1A. The aim of this study was to investigate the effects of prooxidants (both bifunctional and monofunctional) on the activity of hepatic DTD in rainbow trout (Oncorhynchus mykiss) in order to evaluate DTD suitability as a biomarker. We also investigated the effect of β-NF on hepatic DTD activity in perch (Perca fluviatilis), shorthorn sculpin (Myoxocephalus scorpius), eelpout (Zoarces viviparus), brown trout (Salmo trutta) and carp (Cyprinus carpio). In addition, the effect of short term exposure to prooxidants on catalase activity was investigated. Results: In rainbow trout, hepatic DTD activity is induced by the bifunctional AHR agonists β-NF and B(a)P and the monofunctional inducers naphthazarin, menadione and paraquat. Although exposure to both B(a)P and β-NF led to a strong 7-ethoxyresorufin-O-deethylase (EROD) induction, none of the monofunctional compounds affected the rainbow trout EROD activity. DTD was not induced by β-NF in any of the other fish species. Much higher DTD activities were observed in rainbow trout compared to the other fish species. Catalase activity was less responsive to short term exposure to prooxidants compared to DTD. Conclusion: Since rainbow trout hepatic DTD activity is inducible by both monofunctional and bifunctional inducers, it is suggested that rainbow trout DTD may be regulated by the same mechanisms, as in mammals. The fact that DTD is inducible in rainbow trout suggests that the enzyme may be suitable as a part of a biomarker battery when rainbow trout is used in environmental studies. It appears as if DTD activity in rainbow trout is higher and inducible compared to the other fish species studied. [ABSTRACT FROM AUTHOR]

Background: During the early stages of systemic inflammation, the liver integrity is compromised by microcirculatory disturbances and subsequent hepatocellular injury. Little is known about the relationship between the hemoglobin oxygen saturation (HbsO2) in sinusoids and the hepatocellular mitochondrial redox state, in early systemic inflammation. In a murine model of early systemic inflammation, we have explored the association between the sinusoidal HbsO2 detected with a remission spectroscopy system and 1.) the NAD(P)H autofluorescence (an indicator of the intracellular mitochondrial redox state) and 2.) the markers of hepatocellular injury. Results: Animals submitted to 1 hour bilateral hindlimb ischemia (I) and 3 hours of reperfusion (R) (3.0 h I/R) exhibited lower HbsO2 values when compared with sham. Six hours I/R (1 hour bilateral hindlimb ischemia and 6 hours of reperfusion) and the continuous infusion of endothelin-1 (ET-1) further aggravated the hypoxia in HbsO2. The detected NAD(P)H autofluorescence correlated with the detected HbsO2 values and showed the same developing. Three hours I/R resulted in elevated NAD(P)H autofluorescence compared with sham animals. Animals after 6.0 h I/R and continuous infusion of ET-1 revealed higher NAD(P)H autofluorescence compared with 3.0 h I/R animals. Overall the analysed HbsO2 values correlated with all markers of hepatocellular injury. Conclusion: During the early stages of systemic inflammation, there is a significant decrease in hepatic sinusoidal HbsO2. In parallel, we detected an increasing NAD(P)H autofluorescence representing an intracellular inadequate oxygen supply. Both changes are accompanied by increasing markers of liver cell injury. Therefore, remission spectroscopy in combination with NAD(P)H autofluorescence provides information on the oxygen distribution, the metabolic state and the mitochondrial redox potential, within the mouse liver. [ABSTRACT FROM AUTHOR]

A preface for the January 2004 issue of the periodical "Comparative Hepatology" is presented.

The article offers information on the journal "Comparative Hepatology," published by BioMed Central. It reports that the "Comparative Hepatology" is an Open Access, peer-reviewed online journal for liver-oriented research, publishing basic and applied studies in biology, veterinary and human medicine. It reports that the journal's articles are all Open Access.