This study was designed to determine if trauma causes the release of adult-derived blastomere-like stem cells (BLSCs) from skeletal muscle into the circulating blood of adult pigs. Experimental procedures followed the guidelines of Fort Valley State University's Institutional Animal Care and Utilization Committee. Pigs were traumatized by splenectomy followed by pancreatectomy. Blood samples and skeletal muscle biopsies were taken before and after trauma. Adult-derived BLSCs were isolated from skeletal muscle and blood samples following established procedures. Nontraumatized skeletal muscle contained approximately 277 million BLSCs per gram of muscle. After trauma, skeletal muscle contained approximately 2 million BLSCs per gram of muscle. Blood taken before trauma contained approximately 22 million BLSCs per milliliter, whereas approximately 512 million BLSCs per milliliter were present within the blood after trauma. Blood values were statistically significant with a P < 0.05. This report is the first demonstration that trauma causes the release of adult-derived BLSCs from skeletal muscle into blood. Further studies are required to elucidate the roles that adult-derived BLSCs play in the response to injury and in the healing process. Surgeons must take a role in this evolving field.

Suboptimal intake of various nutritional factors, especially the vitamins, has been considered by many investigators as setting the stage for and contributing to the development of different types of malignant disease. With reference to oral cancer, Orr' in 1933 published a paper dealing with the epidemiologic distribution of oral cancer in India and other geographically adjacent areas. In this report Orr mentions the possible relationship of endemic malnutrition (especially vitamin A deficiency) to the observed high incidence of oral tumors.In 1942 in this country, Abels, Rekers, Martin and Rhoads2 reported on the relationship between dietary deficiency and the occurrence of lingual papillary atrophy and leukoplakia-the latter considered to be a precancerous oral lesion. In this study of human subjects, these authors found that administration of large amounts of brewer's yeast as a source of vitamin B-complex resulted in marked improvement of both lesions in many cases. They therefore suggested that vitamin B-complex deficiency resulted in certain epithelial disorders, including the precancerous lesion, leukoplakia. The observation on rats maintained on a diet low in vitamin B-complex that there was decreased oxidation in epidermal and dermal tissues would give indirect support to this contention, although this effect has been specifically related to riboflavin deficiency by Adams.3With reference to experimentally induced tumors, conflicting results have been reported concerning modification in cancer development by alterations in dietary B vitamins. For example, Morris and Lippincott4 in 1941 reported retardation of growth of spontaneous mammary adenocarcinomas in mice when these animals were maintained on a pantothenic acid deficiency. In 1943, Morris and Robertson5 reported somewhat the same findings on mice held on an extreme riboflavin deficiency.Choline deficiency, on the other hand when studied by Engel, Copeland, and Salmon,6 resulted in neoplasms in rats but no neoplastic change in rats maintained on the same diet supplemented with 0.2 per cent choline chloride.Kreshover7 in 1952 reported on the effect of vitamin B-complex deficiency in mice exposed to daily application of whole cigarette smoke to ears and lips. Although there were no demonstrable lesions on the lips of these animals, he does describe an increased severity of ulceration with epithelial dyskeratosis in the ears of these animals subjected

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