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At least 721 records · Page 40Linked to original sources
PubMed1988

Observations on dopamine receptor antagonists and gastric ulceration associated with experimental anorexia cachexia.

Gastric ulceration is frequently reported to occur in tumour-bearing animals and man, even when such tumours are not associated with organs of digestion. That central and peripheral dopamine (DA) containing neurones may be relevant to this phenomenon, is supported by the fact that the DA receptor antagonists domperidone (0.1 and 0.05 mg/kg) and pimozide (0.1 mg/kg) were observed to prevent gastric ulceration commonly reported in rats bearing the Walker 256 carcinosarcoma. Daily administration of these drugs prevented the formation of ulcers similar to those observed in vehicle-treated animals. These results demonstrate that DA neurone function is important in the formation of gastric ulcers in tumour-bearing animals and suggest that such compounds may be useful in cancer management.

Animals↗
PubMed1985

Cancer cachexia: a manifestation of hypersensitivity?

More than thirty years ago, as a corollary of the experimental analysis of the systemic hypersensitivity reaction, it was postulated that the general symptoms of tuberculous patients may be due to the action of the specific antigen upon the sensitized host. The same hypothesis can be extrapolated in order to interpret some hitherto unexplained findings that are observed in cancer hosts, as well as organ transplant recipients.

Animals↗
PubMed2005

Activation of UCPs gene expression in skeletal muscle can be independent on both circulating fatty acids and food intake. Involvement of ROS in a model of mouse cancer cachexia.

Implantation of a fast growing tumour to mice (Lewis lung carcinoma) resulted in a clear cachectic state characterized by a profound muscle wasting. This was accompanied by a significant increase in both UCP2 and UCP3 gene expression in skeletal muscle and heart. Interestingly, this increase in gene expression was not linked to a rise in circulating fatty acids or in a decrease in food intake, as previously reported in other pathophysiological states. These results question the concept that hyperlipaemia is the only factor controlling UCP gene expression in different pathophysiological conditions. In addition, the present work suggests that UCPs might participate in a counter-regulatory mechanism to lower the production of ROS.

Animals↗