United States Department of the Army

About: United States Department of the Army is a government organization based out in Arlington, Virginia, United States. It is known for research contribution in the topics: Poison control & Population. The organization has 32668 authors who have published 42453 publications receiving 947075 citations. The organization is also known as: DA & U.S. Department of the Army.

Dispersive properties of finite, one-dimensional photonic band gap structures : applications to nonlinear quadratic interactions

Abstract: We discuss the linear dispersive properties of finite one-dimensional photonic band-gap structures. We introduce the concept of a complex effective index for structures of finite length, derived from a generalized dispersion equation that identically satisfies the Kramers-Kronig relations. We then address the conditions necessary for optimal, phase-matched, resonant second harmonic generation. The combination of enhanced density of modes, field localization, and exact phase matching near the band edge conspire to yield conversion efficiencies orders of magnitude higher than quasi-phase-matched structures of similar lengths. We also discuss an unusual and interesting effect: counterpropagating waves can simultaneously travel with different phase velocities, pointing to the existence of two dispersion relations for structures of finite length.

The Tarsal-tunnel Syndrome

Abstract: A case report illustrating the essential features of the tarsal-tunnel syndrome in a twenty-year-old white male army recruit is described. It is assumed that this syndrome is commonly misdiagnosed and that it occurs more frequently than the literature would lead one to believe.

Organic luminescent materials

Abstract: An organic luminescent material including a compound of the following formula: wherein: R 1 , R 2 , R 3 , R 4 , R 5 , R 6 , R 7 , R 8 , R 9 , R 10 , R 11 and R 12 are individual groups, and at least one group is not hydrogen among the R 1 , R 3 , R 7 , and R 9 groups. Group 1: hydrogen, or alkyl of from 1 to 48 carbon atoms, and each R 1 , R 2 , R 3 , R 4 , R 5 , R 6 , R 7 , R 8 , R 9 , R 10 , R 11 and R 12 can connect with their neighboring group to form 5 or 6 member cyclic or aromatic ring system, and Group 2: aryl or substituted aryl of from 5 to 48 carbon atoms, or 4 to 48 carbon atoms necessary to complete a fused aromatic ring of naphthenyl, anthracenyl, pyrenyl, or perylenyl; and Group 3: heteroaryl or substituted heteroaryl of from 5 to 24 carbon atoms, or 4 to 48 carbon atoms necessary to complete a fused heteroaromatic ring of furyl, thienyl, pyridyl, quinolinyl and other heterocyclic systems; and Group 4: alkoxyl, amino, alkyl amino, aryl amino dialkyl amino, or diaryl amino of from 1 to 24 carbon atoms; and Group 5: a group consist of F, Cl, Br, I, CN, NCS, NCO, B(OH) 2 , B(OCH 2 CH 2 O), B[OC(CH 3 ) 2 C(CH 3 ) 2 O], SO 2 R 13 , SO 3 R 14 , SO 2 NR 2 , SiR 3 , SiHR 2 , SiR 2 OH, where R, R 13 and R 14 is hydrogen, chlorine, bromine, alkyl group containing 1-12 carbon atoms, and aryl; and Group 6: a group of formula -LY n R 15 where n is 0 to 18, Y is a alkyl group contains 1 to 24 carbon atoms, R 15 is a hydrogen, hydroxy, amino, alkylamino, arylamino, alkyl arylamino, diarylamino, dialkylamino, or —COR 16 where R 16 is a hydrogen, chlorine, COCl, alkyl group containing 1-12 carbon atoms, —NR 2 , —NHR and aryl, or —COOR 17 where R 17 is a hydrogen, alkyl group containing 1-12 carbon atoms, aryl, COR, 2,4-dinitrophenyl, N-imido or —NR 2 ; and L is a direct bond or C═O.

Pathogenesis of Ebola Hemorrhagic Fever in Primate Models: Evidence that Hemorrhage Is Not a Direct Effect of Virus-Induced Cytolysis of Endothelial Cells

Abstract: Ebola virus (EBOV) infection causes a severe and often fatal hemorrhagic disease in humans and nonhuman primates. Whether infection of endothelial cells is central to the pathogenesis of EBOV hemorrhagic fever (HF) remains unknown. To clarify the role of endothelial cells in EBOV HF, we examined tissues of 21 EBOV-infected cynomolgus monkeys throughout time, and also evaluated EBOV infection of primary human umbilical vein endothelial cells and primary human lung-derived microvascular endothelial cells in vitro. Results showed that endothelial cells were not early cellular targets of EBOV in vivo, as viral replication was not consistently observed until day 5 after infection, a full day after the onset of disseminated intravascular coagulation. Moreover, the endothelium remained relatively intact even at terminal stages of disease. Although human umbilical vein endothelial cells and human lung-derived microvascular endothelial cells were highly permissive to EBOV replication, significant cytopathic effects were not observed. Analysis of host cell gene response at 24 to 144 hours after infection showed some evidence of endothelial cell activation, but changes were unremarkable considering the extent of viral replication. Together, these data suggest that coagulation abnormalities associated with EBOV HF are not the direct result of EBOV-induced cytolysis of endothelial cells, and are likely triggered by immune-mediated mechanisms.