The role of the surgeon as intensivist: an international perspective.

Purpose Of Review: Critical care is a young specialty. It emerged less than 50 years ago in response to new technologies that could prolong the survival of patients who previously would have died. The diseases that posed this threat to life were varied and the original practitioners of critical care came from a variety of medical backgrounds, and created a multidisciplinary specialty.

Intraperitoneal administration of pMP6/liposome complexes inhibits the growth of co-localized colon-26 adenocarcinoma cells by inducing a tumor-specific immune response.

Background: In our previous study, we found complexes of the non-coding pMP6 plasmid and cationic liposomes which exerted antitumor activity in the C26 model. We now sought to unravel the underlying protective effector mechanism(s).

Materials And Methods: C26 recipients (i.

Interleukin 10 regulates cell surface and soluble LIR-2 (CD85d) expression on dendritic cells resulting in T cell hyporesponsiveness in vitro.

Dendritic cells (DC) are unique in their ability to stimulate naive T cells to proliferate and to differentiate into effector T cells. DC, however, can also inhibit T cell activation and play a role in central and peripheral tolerance. IL-10 has been shown to render DC tolerogenic by unknown mechanisms.

In vivo gene transfer of murine interleukin-4 inhibits colon-26-mediated cancer cachexia in mice.

Cancer cachexia has been suggested to be mediated by various cytokines derived either from tumor or host tissue. In the murine colon-26 (C-26) adenocarcinoma model IL-1, secreted by tumor-infiltrating mononuclear phagocytes, has an important role in induction of cancer cachexia. In order to suppress production of IL-1 in peritoneal macrophages we have used liposome-mediated gene transfer of the anti-inflammatory cytokine mIL-4, known as a potent inhibitor of IL-1 production.

Interleukin-10-deficient mice and inflammatory bowel disease associated cancer development.

Interleukin-10-deficient mice develop colitis and colorectal cancer similar to the inflammatory bowel disease associated cancer in humans. The aim of this study was to identify possible mutations of oncogenes and tumour suppressor genes involved in tumorigenesis in Interleukin-10 (IL-10)-deficient mice. Twenty colon carcinomas from IL-10-deficient mice were screened for mutations in the K-ras and p53 genes by 'cold' single-strand-conformation polymorphism.