Effects of Growth Regulators on Fruit Set and Growth of the Acerola (Malpighia glabra L.)

The low natural fruit set of acerola in Hawaii, attributed to absence of pollen transferring agents, indicated the feasibility of growth regulator application to induce fruit set. Among the several growth regulators tried initially, 4-chlorophenoxyacetic acid (PCA) and indolebutyric acid ( IBA) were found to be effective in promoting fruit set, the f rmer being more efficient over a wider range of concentration. PCA exhibited some phytotoxic effects in the nature of leaf curling, yellowing, and even death of young vegetative tips. Phytotoxic effects were reduced in severity with decrease in concentration. lBA at 100 ppm effected approximately 60 percent fruit set without any apparent phytotoxic effects. Under field conditions the satisfactory fruit set and lack of phytotoxic effects with IBA at 100 ppm make this a highly desirable compound, but the wide use of it may be prohibited by its high cost. On the other hand, PCA at 50 ppm can induce as much fruit set as lBA at 100 ppm, and phytotoxic effects are mild with early recovery. Furthermore, the very low cost of this material makes its use economically feasible

The Role of Cellular Senescence in Werner Syndrome: Toward Therapeutic Intervention in Human Premature Aging

Werner syndrome (WS) is a premature aging disorder used as a model of normal human aging. WS individuals have several characteristics of normal aging, such as cataracts, hair graying, and skin aging, but manifest these at an early age. Additionally, WS individuals have high levels of inflammatory diseases, such as atherosclerosis and type 2 diabetes. The in vivo aging in WS is associated with accelerated aging of fibroblasts in culture. The cause of the accelerated senescence is not understood, but may be due to the genomic instability that is a hallmark of WS. Genome instability results in activation of stress kinases, such as p38, and the p38-specific inhibitor SB203580, prevents the accelerated senescence seen in WS fibroblasts. However, oxidative damage plays a role, as low oxygen conditions and antioxidant treatment revert some of the accelerated senescence phenotype. The effects of oxidative stress appear to be suppressible by SB203580; however, it does not appear to be transduced by p38. As SB203580 is known to inhibit other kinases in addition to p38, this suggests that more than one kinase pathway is involved. The recent development of p38 inhibitors with different binding properties, specificities, and oral bioavailability, and of new potent and selective inhibitors of JNK and MK2, will make it possible to dissect the roles of various kinase pathways in the accelerated senescence of WS cells. If this accelerated senescence is reflective of WS aging in vivo, these kinase inhibitors may well form the basis of antiaging therapies for individuals with WS