Current treatments for bone loss injuries involve autologous and allogenic bone grafts, metal alloys and ceramics. Although these therapies have proved useful, they suffer from inherent challenges, and hence, an adequate bone replacement therapy has not yet been found. We hypothesize that graphene may be a useful nanoscaffold for mesenchymal stem cells and will promote proliferation and differentiation into bone progenitor cells. In this study, we evaluate graphene, a biocompatible inert nanomaterial, for its effect on in vitro growth and differentiation of goat adult mesenchymal stem cells. Cell proliferation and differentiation are compared between polystyrene-coated tissue culture plates and graphene-coated plates. Graphitic materials are cytocompatible and support cell adhesion and proliferation. Importantly, cells seeded on to oxidized graphene films undergo osteogenic differentiation in fetal bovine serum-containing medium without the addition of any glucocorticoid or specific growth factors. These findings support graphene's potential to act as an osteoinducer and a vehicle to deliver mesenchymal stem cells, and suggest that the combination of graphene and goat mesenchymal stem cells provides a promising construct for bone tissue engineering.

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Cyclooxygenase-2 (Cox-2) is commonly upregulated during human colorectal tumorigenesis, and its contribution to this process has been clearly demonstrated in genetic mouse models. The only other species that naturally develops intestinal cancer with any frequency is the domestic dog. Intestinal carcinogenesis in humans has been strongly linked to environmental factors such as diet, which may be shared by household pets. We have previously reported that beta-catenin is overexpressed in the neoplastic epithelium of canine colorectal polyps, as it is in humans and rodents. We now show that Cox-2 is also upregulated in the majority of these lesions. Thirteen out of 20 colorectal adenomas (65%) contained immunohistochemically detectable Cox-2 protein restricted to the nonneoplastic tumor stroma, including myofibroblasts and a-smooth muscle actin-negative mesenchymal cells morphologically consistent with macrophages and/or fibroblasts. In contrast to benign polyps, seven of 15 adenocarcinomas (47%) also expressed Cox-2 in the neoplastic epithelium. These changes duplicate molecular changes in human intestinal tumorigenesis and substantiate a fundamental role for both beta-catenin and Cox-2 in intestinal neoplasia.

The results of this study confirm that donor-to-donor variation in equine BMMSCs exists and this variation can be documented using in vitro assays. Subjective assessment suggests that the rate of proliferation tends to correlate with differentiation potential.

Hormone ablation therapy typically causes regression of prostate cancer and represents an important means of treating this disease, particularly after metastasis. However, hormone therapy inevitably loses its effectiveness as tumors become androgen-independent, and this conversion often leads to death because of subsequent poor responses to other forms of treatment. Because environmental factors , such as diet , have been strongly linked to prostate cancer , we examined the affects of dietary polyunsaturated fatty acids (PUFAs; at 1.5 wt%) on growth of androgen-dependent (CWR22) and androgen-independent (CWR22R) human prostatic cancer xenografts, the acute response of CWR22 tumors to ablation therapy, and their progression to androgen independence. Significant diet-induced changes in tumor n-3 or n-6 PUFA content had no affect on CWR22 or CWR22R tumors growing with or without androgen support, respectively. However, dietary changes that increased tumor eicosapentaenoic acid and linoleic acid content enhanced responses to ablation therapy, measured by cancer cell apoptosis and mitosis. In addition, relapse to androgen-independent growth (measured by renewed increases in tumor volume and serum prostate-specific antigen after ablation) positively correlated with tumor arachidonic acid content. There was no correlation between expression of 15-lipoxygenase isozymes or their products and tumor growth or responses to ablation. In conclusion, dietary n-3 PUFA may enhance the response of prostate cancer to ablation therapy and retard progression to androgen-independent growth by altering tumor PUFA content.