An automated system for spacecraft proximity operations

With the advent of multiple-vehicle operations in support of the space station, on-orbit refurbishment, and several other missions, there is a need to intelligently plan proximity operations trajectories that will conserve limited available fuel while avoiding collisions. Upon reaching the objective, the capture process entails several unique considerations, such as coordinating motion with a tumbling target, the capture itself, and adapting to control of the new configuration resulting from the capture operation. This paper outlines a systematic process of technical development over several years at the Draper laboratory, culminating in a capability to perform manual augmented or fully autonomous rendezvous, capture, and control of the resulting configuration

Mechanical characterization of disordered and anisotropic cellular monolayers

We consider a cellular monolayer, described using a vertex-based model, for which cells form a spatially disordered array of convex polygons that tile the plane. Equilibrium cell configurations are assumed to minimize a global energy defined in terms of cell areas and perimeters; energy is dissipated via dynamic area and length changes, as well as cell neighbour exchanges. The model captures our observations of an epithelium from a Xenopus embryo showing that uniaxial stretching induces spatial ordering, with cells under net tension (compression) tending to align with (against) the direction of stretch, but with the stress remaining heterogeneous at the single-cell level. We use the vertex model to derive the linearized relation between tissue-level stress, strain and strain-rate about a deformed base state, which can be used to characterize the tissue's anisotropic mechanical properties; expressions for viscoelastic tissue moduli are given as direct sums over cells. When the base state is isotropic, the model predicts that tissue properties can be tuned to a regime with high elastic shear resistance but low resistance to area changes, or vice versa.Comment: 9 figure

Population synthesis of HII galaxies

We study the stellar population of galaxies with active star formation, determining ages of the stellar components by means of spectral population synthesis of their absorption spectra. The data consist of optical spectra of 185 nearby ($z \leq 0.075$) emission line galaxies. They are mostly HII galaxies, but we also include some Starbursts and Seyfert 2s, for comparison purposes. They were grouped into 19 high signal-to-noise ratio template spectra, according to their continuum distribution, absorption and emission line characteristics. The templates were then synthesized with a star cluster spectral base. The synthesis results indicate that HII galaxies are typically age-composite stellar systems, presenting important contribution from generations up to as old as 500 Myr. We detect a significant contribution of populations with ages older than 1 Gyr in two groups of HII galaxies. The age distributions of stellar populations among Starbursts can vary considerably despite similarities in the emission line spectra. In the case of Seyfert 2 groups we obtain important contributions of old population, consistent with a bulge. From the diversity of star formation histories, we conclude that typical HII galaxies in the local universe are not systems presently forming their first stellar generation.Comment: 12 pages, 4 figures, MNRAS in pres

Fibroblast growth factor receptor 4 single nucleotide polymorphism Gly388Arg in head and neck carcinomas

BACKGROUND Head and neck squamous cell carcinoma (HNSCC) is considered to be a progressive disease resulting from alterations in multiple genes regulating cell proliferation and differentiation like receptor tyrosine kinases (RTKs) and members of the fibroblast growth factor receptors (FGFR)-family. Single-nucleotide polymorphism (SNP) Arg388 of the FGFR4 is associated with a reduced overall survival in patients with cancers of various types. We speculate that FGFR4 expression and SNP is associated with worse survival in patients with HSNCC. AIM To investigate the potential clinical significance of FGFR4 Arg388 in the context of tumors arising in HNSCC, a comprehensive analysis of FGFR4 receptor expression and genotype in tumor tissues and correlated results with patients' clinical data in a large cohort of patients with HNSCC was conducted. METHODS Surgical specimens from 284 patients with HNSCC were retrieved from the Institute of Pathology at the Ludwig-Maximilian-University in Germany. Specimens were analyzed using immunohistochemistry and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The expression of FGFR4 was analyzed in 284 surgical specimens of HNSCC using immunohistochemstry. FGFR4 polymorphism was detected by PCR-RFLP. Patients' clinical data with a minimum follow-up of 5 syears were statistically evaluated with a special emphasis on survival analysis employing Kaplan-Meier estimator and Cox regression analysis. RESULTS Concerning the invasive tumor areas the intensity of the FGFR4 expression was evaluated in a four-grade system: no expression, low expression, intermediate and high expression. FGFR4 expression was scored as "high" (+++) in 74 (26%), "intermediate" (++) in 103 (36.3%), and "low" (+) in 107 (36.7%) cases. Analyzing the FGFR4 mutation it was found in 96 tumors (33.8%), 84 of them (29.6%) having a heterozygous and 12 (4.2%) homozygous mutated Arg388 allele. The overall frequency concerning the mutant alleles demonstrated 65% vs 34% mutated alleles in general. FGFR4 Arg388 was significantly associated with advanced tumor stage (P < 0.004), local metastasis (P < 0.0001) and reduced disease-free survival (P < 0.01). Furthermore, increased expression of FGFR4 correlated significantly with worse overall survival (P < 0.003). CONCLUSION In conclusion, the FGFR4 Arg388 genotype and protein expression of FGFR4 impacts tumor progression in patients with HNSCC and may present a useful target within a multimodal therapeutic intervention

Preliminary input to the space shuttle reaction control subsystem failure detection and identification software requirements (uncontrolled)

The current baseline method and software implementation of the space shuttle reaction control subsystem failure detection and identification (RCS FDI) system is presented. This algorithm is recommended for conclusion in the redundancy management (RM) module of the space shuttle guidance, navigation, and control system. Supporting software is presented, and recommended for inclusion in the system management (SM) and display and control (D&C) systems. RCS FDI uses data from sensors in the jets, in the manifold isolation valves, and in the RCS fuel and oxidizer storage tanks. A list of jet failures and fuel imbalance warnings is generated for use by the jet selection algorithm of the on-orbit and entry flight control systems, and to inform the crew and ground controllers of RCS failure status. Manifold isolation valve close commands are generated in the event of failed on or leaking jets to prevent loss of large quantities of RCS fuel

Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease

Apoptosis is a carefully orchestrated and tightly controlled form of cell death, conserved across metazoans. As the executioners of apoptotic cell death, cysteine-dependent aspartate-directed proteases (caspases) are critical drivers of this cellular disassembly. Early studies of genetically programmed cell death demonstrated that the selective activation of caspases induces apoptosis and the precise elimination of excess cells, thereby sculpting structures and refining tissues. However, over the past decade there has been a fundamental shift in our understanding of the roles of caspases during cell death-a shift precipitated by the revelation that apoptotic cells actively engage with their surrounding environment throughout the death process, and caspases can trigger a myriad of signals, some of which drive concurrent cell proliferation regenerating damaged structures and building up lost tissues. This caspase-driven compensatory proliferation is referred to as apoptosis-induced proliferation (AiP). Diverse mechanisms of AiP have been found across species, ranging from planaria to mammals. In this review, we summarize the current knowledge of AiP and we highlight recent advances in the field including the involvement of reactive oxygen species and macrophage-like immune cells in one form of AiP, novel regulatory mechanisms affecting caspases during AiP, and emerging clinical data demonstrating the critical importance of AiP in cancer