A hybrid multiagent approach for global trajectory optimization

In this paper we consider a global optimization method for space trajectory design problems. The method, which actually aims at finding not only the global minimizer but a whole set of low-lying local minimizers(corresponding to a set of different design options), is based on a domain decomposition technique where each subdomain is evaluated through a procedure based on the evolution of a population of agents. The method is applied to two space trajectory design problems and compared with existing deterministic and stochastic global optimization methods

A compilation of observations from moored current meters and thermographs. Vol. 5. Oregon continental shelf 31 July-21 September 1969

Observations from an instrument array moored over the continental shelf off Oregon from 31 July to 21 September 1969 are presented. Temperature, current and wind observations were obtained every 20 minutes. First order statistics, histograms, progressive vector diagrams and time series plots are presented. Supplementary wind observations at Newport are also described. It is recommended that wind observations be part of a future coastal current observational program and that thermographs be placed in positions with a large temperature gradient

Developing a reliable strategy to infer the effective soil hydraulic properties from field evaporation experiments for agro-hydrological models

The Richards equation has been widely used for simulating soil water movement. However, the take-up of agro-hydrological models using the basic theory of soil water flow for optimizing irrigation, fertilizer and pesticide practices is still low. This is partly due to the difficulties in obtaining accurate values for soil hydraulic properties at a field scale. Here, we use an inverse technique to deduce the effective soil hydraulic properties, based on measuring the changes in the distribution of soil water with depth in a fallow field over a long period, subject to natural rainfall and evaporation using a robust micro Genetic Algorithm. A new optimized function was constructed from the soil water contents at different depths, and the soil water at field capacity. The deduced soil water retention curve was approximately parallel but higher than that derived from published pedo-tranfer functions for a given soil pressure head. The water contents calculated from the deduced soil hydraulic properties were in good agreement with the measured values. The reliability of the deduced soil hydraulic properties was tested in reproducing data measured from an independent experiment on the same soil cropped with leek. The calculation of root water uptake took account for both soil water potential and root density distribution. Results show that the predictions of soil water contents at various depths agree fairly well with the measurements, indicating that the inverse analysis is an effective and reliable approach to estimate soil hydraulic properties, and thus permits the simulation of soil water dynamics in both cropped and fallow soils in the field accurately

Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2

Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-α expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the β-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17β-estradiol (E2) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E2 was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E2 suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E2 inhibition. E2 increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E2 was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GH/JAK/STAT pathway, in which SOCS-2 plays a central mechanistic role

Enhancing quantum efficiency of thin-film silicon solar cells by Pareto optimality

We present a composite design methodology for the simulation and optimization of the solar cell performance. Our method is based on the synergy of different computational techniques and it is especially designed for the thin-film cell technology. In particular, we aim to efficiently simulate light trapping and plasmonic effects to enhance the light harvesting of the cell. The methodology is based on the sequential application of a hierarchy of approaches: (a) full Maxwell simulations are applied to derive the photon’s scattering probability in systems presenting textured interfaces; (b) calibrated Photonic Monte Carlo is used in junction with the scattering matrices method to evaluate coherent and scattered photon absorption in the full cell architectures; (c) the results of these advanced optical simulations are used as the pair generation terms in model implemented in an effective Technology Computer Aided Design tool for the derivation of the cell performance; (d) the models are investigated by qualitative and quantitative sensitivity analysis algorithms, to evaluate the importance of the design parameters considered on the models output and to get a first order descriptions of the objective space; (e) sensitivity analysis results are used to guide and simplify the optimization of the model achieved through both Single Objective Optimization (in order to fully maximize devices efficiency) and Multi Objective Optimization (in order to balance efficiency and cost); (f) Local, Global and “Glocal” robustness of optimal solutions found by the optimization algorithms are statistically evaluated; (g) data-based Identifiability Analysis is used to study the relationship between parameters. The results obtained show a noteworthy improvement with respect to the quantum efficiency of the reference cell demonstrating that the methodology presented is suitable for effective optimization of solar cell devices

Aberrant substrate engagement of the ER translocon triggers degradation by the Hrd1 ubiquitin ligase

Little is known about quality control of proteins that aberrantly or persistently engage the endoplasmic reticulum (ER)-localized translocon en route to membrane localization or the secretory pathway. Hrd1 and Doa10, the primary ubiquitin ligases that function in ER-associated degradation (ERAD) in yeast, target distinct subsets of misfolded or otherwise abnormal proteins based primarily on degradation signal (degron) location. We report the surprising observation that fusing Deg1, a cytoplasmic degron normally recognized by Doa10, to the Sec62 membrane protein rendered the protein a Hrd1 substrate. Hrd1-dependent degradation occurred when Deg1-Sec62 aberrantly engaged the Sec61 translocon channel and underwent topological rearrangement. Mutations that prevent translocon engagement caused a reversion to Doa10-dependent degradation. Similarly, a variant of apolipoprotein B, a protein known to be cotranslocationally targeted for proteasomal degradation, was also a Hrd1 substrate. Hrd1 therefore likely plays a general role in targeting proteins that persistently associate with and potentially obstruct the translocon

Regulation of Signaling at Regions of Cell-Cell Contact by Endoplasmic Reticulum-Bound Protein-Tyrosine Phosphatase 1B

Protein-tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed PTP that is anchored to the endoplasmic reticulum (ER). PTP1B dephosphorylates activated receptor tyrosine kinases after endocytosis, as they transit past the ER. However, PTP1B also can access some plasma membrane (PM)-bound substrates at points of cell-cell contact. To explore how PTP1B interacts with such substrates, we utilized quantitative cellular imaging approaches and mathematical modeling of protein mobility. We find that the ER network comes in close proximity to the PM at apparently specialized regions of cell-cell contact, enabling PTP1B to engage substrate(s) at these sites. Studies using PTP1B mutants show that the ER anchor plays an important role in restricting its interactions with PM substrates mainly to regions of cell-cell contact. In addition, treatment with PTP1B inhibitor leads to increased tyrosine phosphorylation of EphA2, a PTP1B substrate, specifically at regions of cell-cell contact. Collectively, our results identify PM-proximal sub-regions of the ER as important sites of cellular signaling regulation by PTP1B