Optimising models for prediction of tropospheric scintillation on satellite links

A phenomenon that also causes impairment in the received signal strength of the RF signal in satellite links operating at frequencies above 10 GHz, especially in those systems that operate at higher frequencies with small fade margins, is the tropospheric scintillation that occurs in the lower layer of the troposphere. In order to estimate the intensity, i.e. the variance between the scintillation amplitude fluctuations, there are several models in the literature, whose accuracy depends on the locality in which the models are implemented. In this Letter, new models are developed for the prediction of tropospheric scintillation that adjusts to localities in Spain, specifically Madrid city, based on measurements of the aforementioned phenomenon reported from Spain and the bios-inspired technique Cuckoo Search (CS). The results obtained, evaluated in terms of the root mean square error, were totally satisfactory, being the most outstanding cases the improved versions of the Ortgies-T, Statistical Temperature and Humidity 2 and Statistical Temperature and Refractivity 2 models

Lateral adhesion drives reintegration of misplaced cells into epithelial monolayers.

Cells in simple epithelia orient their mitotic spindles in the plane of the epithelium so that both daughter cells are born within the epithelial sheet. This is assumed to be important to maintain epithelial integrity and prevent hyperplasia, because misaligned divisions give rise to cells outside the epithelium. Here we test this assumption in three types of Drosophila epithelium; the cuboidal follicle epithelium, the columnar early embryonic ectoderm, and the pseudostratified neuroepithelium. Ectopic expression of Inscuteable in these tissues reorients mitotic spindles, resulting in one daughter cell being born outside the epithelial layer. Live imaging reveals that these misplaced cells reintegrate into the tissue. Reducing the levels of the lateral homophilic adhesion molecules Neuroglian or Fasciclin 2 disrupts reintegration, giving rise to extra-epithelial cells, whereas disruption of adherens junctions has no effect. Thus, the reinsertion of misplaced cells seems to be driven by lateral adhesion, which pulls cells born outside the epithelial layer back into it. Our findings reveal a robust mechanism that protects epithelia against the consequences of misoriented divisions.The authors are grateful to R. Nieuwburg, the St Johnston group, and other Gurdon Institute members for suggestions. We thank the Bloomington Stock Center, J. Knoblich, and the TRiP at Harvard Medical School (NIH/NIGMS R01-GM084947) for fly stocks. We thank N. Lowe for technical assistance. This work was supported by a Wellcome Trust Principal Fellowship to D.St.J. (080007), and by core support from the Wellcome Trust (092096) and Cancer Research UK (A14492). D.T.B. was supported by a Marie Curie Fellowship and the Wellcome Trust. H.E.L. was supported by a Herchel Smith Studentship.This is the author accepted manuscript. The final version is available from NPG via http://dx.doi.org/10.1038/ncb324

Accumulation of Endogenous LITAF in Aggresomes

LITAF is a 161 amino acid cellular protein which includes a proline rich N-terminus and a conserved C-terminal domain known as the simple-like domain. Mutations in LITAF have been identified in Charcot-Marie tooth disease, a disease characterized by protein aggregates. Cells transfected with cellular LITAF reveal that LITAF is localized to late endosomes/lysosomes. Here we investigated the intracellular localization of endogenous LITAF. We demonstrated that endogenous LITAF accumulates at a discrete cytoplasmic site in BGMK cells that we identify as the aggresome. To determine the domain within LITAF that is responsible for the localization of LITAF to aggresomes, we created a construct that contained the C-terminal simple-like domain of LITAF and found that this construct also localizes to aggresomes. These data suggest the simple-like domain is responsible for targeting endogenous LITAF to the aggresome

Modeling organic transformations by microorganisms of soils in six contrasting ecosystems: Validation of the MOMOS model

CDCHTULA (project C-765-95-01-B) and FONACIT (F-2002000424). We would like to thank Zulay Mendez for her technical assistance in the laboratory and Yann Martineau (SETEC International, F-13127 Vitrolles, France) and Klaas Metselaar (Soil Physics, Wageningen University, Netherlands) for the orientation in the modeling process. Amer geophysical union WashingtonInternational audienceThe Modeling Organic Transformations by Microorganisms of Soils (MOMOS) model simulates the growth, respiration, and mortality of soil microorganisms as main drivers of the mineralization and humification processes of organic substrates. Originally built and calibrated using data from two high-altitude sites, the model is now validated with data from a (14)C experiment carried out in six contrasting tropical ecosystems covering a large gradient of temperature, rainfall, vegetation, and soil types from 65 to 3968 m asl. MOMOS enabled prediction of a greater number of variables using a lower number of parameter values than for predictions previously published on this experiment. The measured (14)C mineralization and transfer into microbial biomass (MB) and humified compartments were accurately modeled using (1) temperature and moisture response functions to daily adjust the model responses to weather conditions and (2) optimization of only one parameter, the respiration rate k(resp) of soil microorganisms at optimal temperature and moisture. This validates the parameterization and hypotheses of the previous calibration experiment. Climate and microbial respiratory activity, related to soil properties, appear as the main factors that regulate the C cycle. The k(resp) rate was found to be negatively related to the fine textural fraction of soil and positively related to soil pH, allowing the proposition of two transfer functions that can be helpful to generalize MOMOS application at regional or global scale

Statistical analysis of nanoparticle dosing in a dynamic cellular system

The delivery of nanoparticles into cells is important in therapeutic applications1, 2, 3 and in nanotoxicology4. Nanoparticles are generally targeted to receptors on the surfaces of cells and internalized into endosomes by endocytosis5, 6, 7, 8, 9, but the kinetics of the process and the way in which cell division redistributes the particles remain unclear. Here we show that the chance of success or failure of nanoparticle uptake and inheritance is random. Statistical analysis of nanoparticle-loaded endosomes indicates that particle capture is described by an over-dispersed Poisson probability distribution that is consistent with heterogeneous adsorption and internalization. Partitioning of nanoparticles in cell division is random and asymmetric, following a binomial distribution with mean probability of 0.52–0.72. These results show that cellular targeting of nanoparticles is inherently imprecise due to the randomness of nature at the molecular scale, and the statistical framework offers a way to predict nanoparticle dosage for therapy and for the study of nanotoxins