How important is the stability of gene products in the process of gene expression? We use a dual-compartment mathematical model to demonstrate the effects that changing the rates of synthesis and degradation of hypothetical mRNAs and proteins would have on the final concentration of protein. The model predicts that the concentration of protein at steady state equals the product of the rate constants for synthesis of mRNA and protein (ks1 and ks2) divided by the product of the rate constants for degradation (kd1 and kd2) and that the rate at which protein concentration changes depends on the rate constants for degradation of both the mRNA and the protein. This permits great flexibility in controlling induction kinetics for particular gene products, since their synthesis, translation, and degradation may be regulated coordinately to permit induction to be stable or transient or to amplify the final yield of protein. We suggest single exons may encode structural features that cause both mRNAs and proteins to be labile, thereby ensuring that modal stabilities of highly regulated macromolecules are similar.

Very long chain fatty alcohols obtained from plant waxes and beeswax have been reported to lower plasma cholesterol in humans. This review discusses nutritional or regulatory effects produced by wax esters or aliphatic acids and alcohols found in unrefined cereal grains, beeswax, and many plant-derived foods. Reports suggest that 5-20 mg per day of mixed C24-C34 alcohols, including octacosanol and triacontanol, lower low-density lipoprotein (LDL) cholesterol by 21%-29% and raise high-density lipoprotein cholesterol by 8%-15%. Wax esters are hydrolyzed by a bile salt-dependent pancreatic carboxyl esterase, releasing long chain alcohols and fatty acids that are absorbed in the gastrointestinal tract. Studies of fatty alcohol metabolism in fibroblasts suggest that very long chain fatty alcohols, fatty aldehydes, and fatty acids are reversibly inter-converted in a fatty alcohol cycle. The metabolism of these compounds is impaired in several inherited human peroxisomal disorders, including adrenoleukodystrophy and Sjögren-Larsson syndrome. Reports on dietary management of these diseases confirm that very long chain fatty acids (VLCFA) are normal constituents of the human diet and are synthesized endogenously. Concentrations of VLCFA in blood plasma increase during fasting and when children are placed on ketogenic diets to suppress seizures. Existing data support the hypothesis that VLCFA exert regulatory roles in cholesterol metabolism in the peroxisome and also alter LDL uptake and metabolism.

We tested whether polyphenolic substances in extracts of commercial culinary herbs and spices would inhibit fructose-mediated protein glycation. Extracts of 24 herbs and spices from a local supermarket were tested for the ability to inhibit glycation of albumin. Dry samples were ground and extracted with 10 volumes of 50% ethanol, and total phenolic content and ferric reducing antioxidant potential (FRAP) were measured. Aliquots were incubated in triplicate at pH 7.4 with 0.25 M fructose and 10 mg/mL fatty acid-free bovine albumin. Fluorescence at 370 nm/440 nm was used as an index of albumin glycation. In general, spice extracts inhibited glycation more than herb extracts, but inhibition was correlated with total phenolic content (R(2) = 0.89). The most potent inhibitors included extracts of cloves, ground Jamaican allspice, and cinnamon. Potent herbs tested included sage, marjoram, tarragon, and rosemary. Total phenolics were highly correlated with FRAP values (R(2) = 0.93). The concentration of phenolics that inhibited glycation by 50% was typically 4-12 microg/mL. Relative to total phenolic concentration, extracts of powdered ginger and bay leaf were less effective than expected, and black pepper was more effective. Prevention of protein glycation is an example of the antidiabetic potential for bioactive compounds in culinary herbs and spices.

Background: This study tested the ability of a characterized extract of Polygonum cuspidatum (PCE) to inhibit mouse ear inflammation in response to topical application of 12-Otetradecanoylphorbol-13-acetate (TPA).

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