Hepatocyte nitric oxide production is induced by Kupffer cells.

To investigate the cellular communication in the liver, nitric oxide (NO) production by sinusoidal cells and hepatocytes by stimulation with cytokines and Kupffer cell-conditioned medium was quantitatively analyzed. NO production by the cells was measured by the Griess reaction, and nitric oxide synthase (iNOS) transcription level by a competitive RT-PCR assay using mutant iNOS mRNA as a standard. NO production and iNOS mRNA transcriptional levels in Kupffer cells were markedly increased by stimulation with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma), and moderately by interleukin-1beta (IL-1beta).

Role of macrophages in regeneration of liver.

In an attempt to clarify the role of macrophages and their mediators during regeneration of the liver, the difference of liver regeneration among C3H/HeN (LPS-responsive strain) and C3H/HeJ (LPS-resistant strain) mice was investigated. After a 67% partial hepatectomy, an increase in the weight of regenerating liver was significantly delayed in the C3H/HeJ mice, as compared with C3H/HeN mice. The number of hepatocytes labeled with antibody against PCNA reached maximum levels 48 hr after partial hepatectomy, but the PCNA labeling index in C3H/HeJ mice was 20% less than that for C3H/HeN mice.

Chemotactic factors released from hepatocytes exposed to acetaminophen.

To clarify the mechanism of neutrophil infiltration in the liver of acetaminophen-induced hepatic injury, chemotactic factor released from hepatocytes exposed to acetaminophen has been investigated. Hepatocytes exposed to acetaminophen release nondialyzable chemotactic factor, although acetaminophen in itself inhibits chemotaxis of neutrophils. Chemotactic activity of the nondialyzable chemotactic factor was reduced after treatment with heat (56 degrees C, 30 min) or trypsin.

Endotoxin induced cellular communication in the liver: murine models for clarification of the role of LPS-responsive macrophages in the pathogenesis of liver diseases.

In several experimental models, lipopolysaccharide (LPS) plays an important role in the pathogenesis of liver diseases. Murine models of C3H/HeN and C3H/HeJ mice have been used to elucidate the role of LPS and its responsive-macrophages in vivo, as C3H/HeN strain mice are known to be LPS-responsive, while C3H/HeJ strain mice are LPS-resistant. Furthermore, release of several kinds of biologically active mediators such as interleukin-1, tumour necrosis factor-alpha, colony stimulating factor and reactive oxygen radical is not enhanced in C3H/HeJ mice even after stimulation with LPS.

Malignant pleural mesothelioma presenting as achalasia.

A 65-year-old man with an occupational history of asbestos exposure developed dysphagia and vomiting. Clinical examinations at onset revealed a dilated esophagus with smooth narrowing at the gastroesophageal junction and no apparent tumor in and around the esophagus. Achalasia was suspected.