Two parental maps were constructed using a population of 240 clones. Strong correlations were observed between

starch and dry-matter content (r > 0.8, P < 0.0001) in the storage roots, while moderate correlations (r = -0.6, P < 0.0001) were observed for beta-carotene and starch content. In both parental maps, QTL analysis revealed the presence of 13 QTL for storage root dry-matter content, 12 QTL for starch content, and 8 QTL for beta-carotene content. Multiple QTL regression BTSA1 models developed for segregation of alleles in each parent explained 15-24% of the variation in dry-matter content, 17-30% of the starch content, and 17-35% of beta-carotene content. To the best of our knowledge, this research presents the only QTL mapping study published to date for dry-matter, starch, and beta-carotene content in sweetpotato. This work improves our understanding of the inheritance of these important traits in

sweetpotato, and represents a first step toward the long-term goal of developing marker-assisted breeding tools to facilitate sweetpotato breeding efforts.”
“The present study was designed to investigate the protective efficacy MX69 molecular weight of eugenol against skin cancer and probe into the mechanistic aspects. Skin tumors were initiated by applying 160 nmol DMBA and promoted by twice weekly applications of 8.5 nmol

TPA for 28 wk. All mice developed tumors by 13 wk of promotion. However, in mice pretreated with 30 mu L eugenol, no tumors were detected until 8 wk (following anti-initiation protocol) and until 14 wk (following antipromotion protocol) of tumor promotion. PCNA and TUNEL immunohistochemistry of tumors revealed eugenol to ameliorate cell proliferation and elevate apoptosis respectively. The effect of eugenol was assessed on specific stages of carcinogenesis. Initiation with DMBA led to a significant upregulation of p53 expression with a concomitant increase in p21(WAF1) levels in epidermal cells indicating induction of damage to the DNA. However, pretreatment with eugenol led to overexpression of these genes, which probably Pevonedistat helped stimulate apoptosis of the initiated cells. To ascertain the molecular mechanisms implicated in the antitumor promoting activity of eugenol, its effect was investigated on markers of tumor promotion and inflammation: ODC activity and NOS and COX-2 expression, and on levels of proinflammatory cytokines (IL-6, TNF-alpha, and PGE(2)). Eugenol markedly inhibited all. Eugenol also inhibited the upstream signaling molecule: NF-kappa B, which regulates the expression of these genes. TPA-induced depletion of cutaneous GSH and antioxidant enzymes armory was also precluded by eugenol.