ABSTRACT
Textural profile, pasting behavior, gelatinization characteristics, sedimentation volume, and gel consistency of acetylated (Ac) and enzyme (glucoamylase)-modified (EM) potato and sweet potato flours have been investigated to determine their suitability in products such as baked goods, soup, and pudding. Dough hardness of Ac and EM samples was significantly higher than their native samples (P < 0.01). Dough cohesiveness of modified potato did not change, while it decreased in modified sweet potato. With increase in moisture, textural properties of modified samples, in general, showed reduced values. Rapid Visco Analyser showed least pasting viscosities of Ac flours due to restricted swelling of starch granules while EM flours exhibited high viscosities. Acetylated samples showed reduced gelatinization temperature (GT), and enthalpy (DeltaH) compared to native samples, whereas enzyme-treated samples showed no significant changes in GT, indicating their comparable crystallinity values with those of native samples. Modified flour samples had lower sediment volumes and gel consistency, and the gel consistency of EM flour correlated with its cold paste viscosity.
Subject(s)
Flour , Food Handling/methods , Gels/chemistry , Ipomoea batatas/chemistry , Solanum tuberosum/chemistry , Acetylation , Chemical Phenomena , Chemistry, Physical , Drug Stability , Flour/analysis , Flour/standards , Glucan 1,4-alpha-Glucosidase/metabolism , Solanum tuberosum/standards , ViscosityABSTRACT
Atherosclerosis is a leading cause of cardiovascular disease in the westernized world. This review highlights emerging evidence linking atherosclerosis to the CD40-CD40 ligand (CD154) pathway. Recently, atherosclerosis has been associated with chronic inflammation, linking it to the immune system. This novel viewpoint may serve as an additional target for therapeutic intervention. CD40 and CD154 are highly expressed in atherosclerotic human plaques. Recent data from preclinical animal models of atherosclerosis show that disruption of the CD40-CD154 pathway can prevent atherosclerotic progression and may reverse established lesions. Blockade of the CD40-CD154 pathway by biologicals or small molecules may prove valuable in the treatment of atherosclerosis.