Experimental Investigation of Roll and Heave Motion Coupling of TriSWACH Ships

Trimaran Small Waterplane Area Centre Hull (TriSWACH) is a concept hybrid hull form between SWATH ships (centre hull) and Trimarans (side hulls). The resistance and seakeeping characteristics of this hull form are currently investigated by the Atlantic Centre for Innovative Design and Control of Small Ships (ACCeSS) consortium, supported by the U.S. Office of Naval Research. The main design advantages of this novel hull are (1) small wave resistance at high speeds; (2) large usable deck area; and (3) superior seakeeping characteristics, compared to monohull ships. Roll damping and response, as key design features for the safety and operational efficiency of the vessel, are currently under investigation. The ultimate goal is to propose an improved method for prediction of roll motions and also investigate how it affects the heaving response of the TriSWACH. This paper presents the findings from roll and heave decay tests, conducted at the U.S. Naval Academy (Annapolis, MD), focusing on the roll damping and the effect of side hull geometry on roll and heave motion coupling. Roll and heave decay tests were conducted for two scale models with different side hull shapes (conventional with haunches and prismatic with no haunches). Significant coupling between roll and heave was observed for the model with conventional side hulls. A quasi-linear method is used to obtain the roll damping coefficients using the experimental data and ITTC recommended semi-empirical method was used to approximate the roll damping coefficients. Both methods have shown good correlation with experimental data

Immune complex-induced, nitric oxide-mediated vascular endothelial cell death by phagocytes is prevented with decoy FcgReceptors

The interaction of Fc gamma receptors (FcγRs) expressed on inflammatory cells and immune-complexes (ICs) results in blood vessel damage during autoimmune vasculitis. Thus we tested if uncoupling these interactions of FcγRs and ICs prevented endothelium damage. Herein, we demonstrate that dimeric FcγR-Igs prevented apoptosis of antibody-coated human umbilical vein endothelial cells (HUVECs) mediated by nitric oxide (NO) released from murine macrophages. FcγR-Igs inhibited the IC-induced upregulation of inducible nitric oxide synthase and NO release by macrophages there by prevented the expression of pro-apoptotic genes in HUVECs. FcgR-Igs did not affect exogenous NO-induced upregulation of pro-apoptotic genes in HUVECs. The co-localization of FcγR-Igs and ICs in the vascular regions of various organs revealed that FcγRs-Igs bind to ICs and prevent vascular endothelial cell death in vivo. In conclusion, these data suggest that IC-induced NO is a major factor promoting blood vessel inflammation and endothelial cell death during IC-mediated vasculitis which can be effectively blocked by dimeric decoy FcγRs