Multi-model recursive identification for nonlinear systems with non-uniformly sampling

A recursive least squares based on Multi-model is proposed for non-uniformly sampled-data nonlinear (NUSDN) systems. The corresponding state space model of an NUSDN system is derived using lifting technique. Taking advantage of the Fuzzy c-Mean Clustering algorithm, NUSDN is divided into several local models. The basic idea is that the NUSDN system is viewed as a model switching system under a given rule. Once the local models are identified, the global model is determined. A pH neutralization process validate the performance of the proposed algorithm.     

Photocurrent Enhancement in Si-Ge Photodetectors by Utilizing Surface Plasmons

A circular slit-groove surface plasmon polaritons (SPPs) launcher surrounding a photodetector is employed theoretically to enhance the photocurrent of atypical Si-Ge photodetectors. The slit and grooves are designed such that the SPPs are focused at the center of the absorption layer of the photodetector to result in additional electric current. Fabry–Perot resonance condition accurately calculates the period of the groove, slit-groove distance, photodetector radius, and slit-photodetector distance. The manipulation leads to constructive interference between the incident light impinging from the top and the SPPs propagating toward the photodetector. Simulation result shows that photocurrent increases by approximately 13-fold when the SPPs are introduced.     

FlhF regulates the number and configuration of periplasmic flagella in Borrelia burgdorferi

The Lyme disease bacterium Borrelia burgdorferi has 7–11 periplasmic flagella (PF) that arise from the cell poles and extend toward the midcell as a flat-ribbon, which is distinct from other bacteria. FlhF, a signal recognition particle (SRP)-like GTPase, has been found to regulate the flagellar number and polarity; however, its role in B. burgdorferi remains unknown. B. burgdorferi has an FlhF homolog (BB0270). Structural and biochemical analyses show that BB0270 has a similar structure and enzymatic activity as its counterparts from other bacteria. Genetics and cryo-electron tomography studies reveal that deletion of BB0270 leads to mutant cells that have less PF (4 ± 2 PF per cell tip) and fail to form a flat-ribbon, indicative of a role of BB0270 in the control of PF number and configuration. Mechanistically, we demonstrate that BB0270 localizes at the cell poles and controls the number and position of PF via regulating the flagellar protein stability and the polar localization of the MS-ring protein FliF. Our study not only provides the detailed characterizations of BB0270 and its profound impacts on flagellar assembly, morphology and motility in B. burgdorferi, but also unveils mechanistic insights into how spirochetes control their unique flagellar patterns.     

Foliar Spray with 24-Epibrassinolide Enhanced Strawberry Fruit Quality,Phytochemical Content,and Postharvest Life

Journal of Plant Growth Regulation - Activation of complex metabolic pathways and antioxidant activities is necessary for enhancing quality and health promoting capacity of food crops. Plant growth...     

Biomimetic Approaches to Functional Surfaces, Surface Wetting and Fluids Drag Reduction

In the natural world,plants and animals haveevolved over time to best adapt to the environment.Theyinteract very effectively with the surrounding environmentby exchanging energies and mass flow across theircuticles of specific micro structures and functions toachieve perfect energy balance.Such different functionsmay include the limitation of uncontrolled loss of water,protection from solar radiation,micro effect of inducedturbulence on flow drag reduction,defence againstpathogens,changing surface wettability and hydropho-     

Residue Histidine 50 Plays a Key Role in Protecting α-Synuclein from Aggregation at Physiological pH

α-Synuclein (αSyn) aggregation is involved in the pathogenesis of Parkinson disease (PD). Recently, substitution of histidine 50 in αSyn with a glutamine, H50Q, was identified as a new familial PD mutant. Here, nuclear magnetic resonance (NMR) studies revealed that the H50Q substitution causes an increase of the flexibility of the C-terminal region. This finding provides direct evidence that this PD-causing mutant can mediate long range effects on the sampling of αSyn conformations. In vitro aggregation assays showed that substitution of His-50 with Gln, Asp, or Ala promotes αSyn aggregation, whereas substitution with the positively charged Arg suppresses αSyn aggregation. Histidine carries a partial positive charge at neutral pH, and so our result suggests that positively charged His-50 plays a role in protecting αSyn from aggregation under physiological conditions.     

Cucurbitacin I Induces Protective Autophagy in Glioblastoma in Vitro and in Vivo

There is an urgent need for new therapeutic avenues to improve the outcome of patients with glioblastoma multiforme (GBM). Current studies have suggested that cucurbitacin I, a natural selective inhibitor of JAK2/STAT3, has a potent anticancer effect on a variety of cancer cell types. This study showed that autophagy and apoptosis were induced by cucurbitacin I. Exposure of GBM cells to cucurbitacin I resulted in pronounced apoptotic cell death through activating bcl-2 family proteins. Cells treatment with cucurbitacin I up-regulated Beclin 1 and triggered autophagosome formation and accumulation as well as conversion of LC3I to LC3II. Activation of the AMP-activated protein kinase/mammalian target of rapamycin/p70S6K pathway, but not the PI3K/AKT pathway, occurred in autophagy induced by cucurbitacin I, which was accompanied by decreased hypoxia-inducible factor 1α. Stable overexpression of hypoxia-inducible factor 1α induced by FG-4497 prevented cucurbitacin I-induced autophagy and down-regulation of bcl-2. Knockdown of beclin 1 or treatment with the autophagy inhibitor 3-methyladenine also inhibited autophagy induced by cucurbitacin I. A coimmunoprecipitation assay showed that the interaction of Bcl-2 and Beclin 1/hVps34 decreased markedly in cells treated with cucurbitacin I. Furthermore, knockdown of beclin 1 or treatment with the lysosome inhibitor chloroquine sensitized cancer cells to cucurbitacin I-induced apoptosis. Finally, a xenograft model provided additional evidence for the occurrence of cucurbitacin I-induced apoptosis and autophagy in vitro. Our findings provide new insights into the molecular mechanisms underlying cucurbitacin I-mediated GBM cell death and may provide an efficacious therapy for patients harboring GBM.