115 results about "Syndrome c" patented technology

A method of determining the presence of soybean sudden death syndrome resistance in the soybean plant in a greenhouse setting, the method comprising the steps of: (a) inoculating soil with a low density inoculum of Fusarium solani; (b) planting a soybean plant in said inoculated soil; (c) growing said plant in said soil in a greenhouse; (d) isolating Fusarium solani-infected tissue from said plant; (e) culturing said infected tissue for a period of time sufficient to allow for fungal colony forming unit growth; (f) scoring at least one of disease severity and infection severity in said plant using the number of said fungal colony forming units; and (g) correlating at least one of said disease severity and said infection severity to at least one of disease severity and infection severity data from genetic markers associated with soybean sudden death syndrome resistance to identify a correlation, wherein a statistically significant correlation indicates presence of soybean sudden death syndrome resistance in said soybean plant. Also provided is a method of characterizing resistance to soybean sudden death syndrome in a soybean plant, the method comprising the steps of: (a) isolating roots from a soybean plant infected by Fusariurn solani; (b) culturing the root on a culture plate including a restrictive growth medium that provides for slow fungal growth and restricted bacterial growth; (c) determining root infection severity by statistically evaluating the number of Fusarium solani colony forming units on said culture plate; and (d) characterizing resistance to soybean sudden death syndrome in said soybean plant based on said determined root infection severity.

Annatto extract composition (AEC), including cis and trans geranyl geraniols (GG) and tocopherol-free C-5 unsubstituted tocotrienols (T3), increases the de novo synthesis of intermediate isoprenoid and distal protein products, including endogenous coenzyme Q10 (CoQ10), dolichols (DL) and all subsequent GG-prenylated and DL-glycosylated proteins, including GG-porphyrinated hemes. This intermediate and distal product replenishment by AEC reverses maladies of myotoxicity (of both drug and non-drug origins), including maladies that affect the muscle, kidney, eye, GI tract and skin, nerve, blood, and CoQ10-related syndromes of energetics and LDL protection. AEC anabolically increases the endogenous de novo CoQ10 synthesis via GG elongation / prenylation of side-chain and conversely CoQ10 catabolically increases the endogenous de novo GG synthesis via beta-oxidation of CoQ10. Also, such AEC decreases de novo synthesis and increases disposal of triglycerides (TG) in humans via PPAR activation and SREBP deactivation. Such drop in TG by AEC reverses maladies of insulin resistance (IR) and metabolic syndrome (MS), prediabetes, diabetes and diabetes-related cardiovascular diseases (CVD). GG activates PPAR and down regulates SREBP transcription factors. This AEC, containing GG, inhibits cancer growth whether or not GG involvement in protein prenylation is required.