Geodetic research studies Final technical report

Geopotential surface measurement of ocean using altimeter dat

Multitasking by the OC lineage during bone infection: Bone resorption, immune modulation, and microbial niche

Bone infections, also known as infectious osteomyelitis, are accompanied by significant inflammation, osteolysis, and necrosis. Osteoclasts (OCs) are the bone-resorbing cells that work in concert with osteoblasts and osteocytes to properly maintain skeletal health and are well known to respond to inflammation by increasing their resorptive activity. OCs have typically been viewed merely as effectors of pathologic bone resorption, but recent evidence suggests they may play an active role in the progression of infections through direct effects on pathogens and via the immune system. This review discusses the host- and pathogen-derived factors involved in the in generation of OCs during infection, the crosstalk between OCs and immune cells, and the role of OC lineage cells in the growth and survival of pathogens, and highlights unanswered questions in the field

A Quantum-Quantum Metropolis Algorithm

Recently, the idea of classical Metropolis sampling through Markov chains has been generalized for quantum Hamiltonians. However, the underlying Markov chain of this algorithm is still classical in nature. Due to Szegedy's method, the Markov chains of classical Hamiltonians can achieve a quadratic quantum speedup in the eigenvalue gap of the corresponding transition matrix. A natural question to ask is whether Szegedy's quantum speedup is merely a consequence of employing classical Hamiltonians, where the eigenstates simply coincide with the computational basis, making cloning of the classical information possible. We solve this problem by introducing a quantum version of the method of Markov-chain quantization combined with the quantum simulated annealing (QSA) procedure, and describe explicitly a novel quantum Metropolis algorithm, which exhibits a quadratic quantum speedup in the eigenvalue gap of the corresponding Metropolis Markov chain for any quantum Hamiltonian. This result provides a complete generalization of the classical Metropolis method to the quantum domain.Comment: 7 page

National Geodetic Satellite Program, Part II: Smithsonian Astrophysical Observatory

A sequence of advances in the determination of geodetic parameters presented by the Smithsonian Astrophysical Observatory are described. A Baker-Nunn photographic system was used in addition to a ruby-laser ranging system to obtain data for refinement of geodetic parameters. A summary of the data employed to: (1) derive coordinates for the locations of various tracking stations; and (2) determine the gravitational potential of the earth, is presented

TNF receptor-activated factor 2 mediates cardiac protection through noncanonical NF-κB signaling

To elucidate the mechanisms responsible for cytoprotective effects of TNF receptor-activated factor 2 (TRAF2) in the heart, we employed genetic gain- and loss-of-function studies ex vivo and in vivo in mice with cardiac-restricted overexpression of TRAF2 (Myh6-TRAF2LC). Crossing Myh6-TRAF2LC mice with mice lacking canonical signaling (Myh6-TRAF2LC/Myh6-IκBαΔN) abrogated the cytoprotective effects of TRAF2 ex vivo. In contrast, inhibiting the JAK/STAT pathway did not abrogate the cytoprotective effects of TRAF2. Transcriptional profiling of WT, Myh6-TRAF2LC, and Myh6-TRAF2LC/Myh6-IκBαΔN mouse hearts suggested that the noncanonical NF-κB signaling pathway was upregulated in the Myh6-TRAF2LC mouse hearts. Western blotting and ELISA for the NF-κB family proteins p50, p65, p52, and RelB on nuclear and cytoplasmic extracts from naive 12-week-old WT, Myh6-TRAF2LC, and Myh6-TRAF2LC/Myh6-IκBαΔN mouse hearts showed increased expression levels and increased DNA binding of p52 and RelB, whereas there was no increase in expression or DNA binding of the p50 and p65 subunits. Crossing Myh6-TRAF2LC mice with RelB-/+ mice (Myh6-TRAF2LC/RelB-/+) attenuated the cytoprotective effects of TRAF2 ex vivo and in vivo. Viewed together, these results suggest that crosstalk between the canonical and noncanonical NF-κB signaling pathways is required for mediating the cytoprotective effects of TRAF2