Comparison of experimental stresses and deflections with those predicted by a strain energy method for an F8U-3 wing loaded in torsion

The stress level in the milled skin at the root of a tapered, multicell swept wing is predicted by means of a matrix-force method. The solution is achieved by minimizing the internal strain energy, and the results compared with experimental tests. A single loading, consisting of a nose-up couple, is applied to each tip rib. The loading is transferred from the tip rib to an idealized structure by means of simple torsion theory. The idealized structure represents the inboard one-half of each semi-span. Results indicate that an accurate solution of the stress distribution in the actual wing can be achieved provided that the root boundary conditions are preserved. An extension of the analysis is suggested in order to more closely define the maximum accuracy inherent in the particular matrix-force method of solution.http://www.archive.org/details/comparisonofexpe00holgLieutenant Commander, United States NavyCaptain, United States Marine CorpsApproved for public release; distribution is unlimited

Activation of Membrane Androgen Receptors in Colon Cancer Inhibits the Prosurvival Signals Akt/Bad In Vitro and In Vivo and Blocks Migration via Vinculin/Actin Signaling

Recently, we reported that membrane androgen receptors (mARs) are expressed in colon tumors triggering strong apoptotic responses. In the present study, we analyzed mAR-induced downstream effectors controlling cell survival and migration of Caco2 colon cancer cells. We show that long-term activation of mAR downregulated the activity of PI-3K and Akt and induced de-phosphorylation/activation of the proapoptotic Bad (p-Bad). Moreover, treatment of APCMin/+ mice, which spontaneously develop intestinal tumors, with mAR-activating testosterone conjugates reduced the tumor incidence by 80% and significantly decreased the expression of p-Akt and p-Bad levels in tumor tissue. Furthermore, mAR activation strongly inhibited Caco2 cell migration. In accordance with these findings, vinculin, a protein controlling cell adhesion and actin reorganization, was effectively phosphorylated upon mAR activation. Phosphorylation inhibitors genistein and PP2 inhibited actin reorganization and restored motility. Moreover, silencing vinculin by appropriate siRNA’s, or blocking actin reorganization by cytochalasin B, restored the migration potential. From these results we conclude that mAR activation inhibits the prosurvival signals Akt/Bad in vitro and in vivo and blocks migration of colon cancer cells via regulation of vinculin signaling and actin reorganization, supporting the powerful tumoristatic effect of those receptors