Group-SMA Algorithm Based Joint Estimation of Train Parameter and State

The braking rate and train arresting operation is important in the train braking performance. It is difficult to obtain the states of the train on time because of the measurement noise and a long calculation time. A type of Group Stochastic M-algorithm (GSMA) based on Rao-Blackwellization Particle Filter (RBPF) algorithm and Stochastic M-algorithm (SMA) is proposed in this paper. Compared with RBPF, GSMA based estimation precisions for the train braking rate and the control accelerations were improved by 78% and 62%, respectively. The calculation time of the GSMA was decreased by 70% compared with SMA

MicroRNA-7 inhibits epithelial-to-mesenchymal transition and metastasis of breast cancer cells via targeting FAK expression

10.1371/journal.pone.0041523PLoS ONE78

Targeting codon 158 p53-mutant cancers via the induction of p53 acetylation

Abstract: Gain of function (GOF) DNA binding domain (DBD) mutations of TP53 upregulate chromatin regulatory genes that promote genome-wide histone methylation and acetylation. Here, we therapeutically exploit the oncogenic GOF mechanisms of p53 codon 158 (Arg158) mutation, a DBD mutant found to be prevalent in lung carcinomas. Using high throughput compound screening and combination analyses, we uncover that acetylating mutp53R158G could render cancers susceptible to cisplatin-induced DNA stress. Acetylation of mutp53R158G alters DNA binding motifs and upregulates TRAIP, a RING domain-containing E3 ubiquitin ligase which dephosphorylates IĸB and impedes nuclear translocation of RelA (p65), thus repressing oncogenic nuclear factor kappa-B (NF-ĸB) signaling and inducing apoptosis. Given that this mechanism of cytotoxic vulnerability appears inapt in p53 wild-type (WT) or other hotspot GOF mutp53 cells, our work provides a therapeutic opportunity specific to Arg158-mutp53 tumors utilizing a regimen consisting of DNA-damaging agents and mutp53 acetylators, which is currently being pursued clinically

A common MET polymorphism harnesses HER2 signaling to drive aggressive squamous cell carcinoma.

c-MET receptors are activated in cancers through genomic events like tyrosine kinase domain mutations, juxtamembrane splicing mutation and amplified copy numbers, which can be inhibited by c-MET small molecule inhibitors. Here, we discover that the most common polymorphism known to affect MET gene (N375S), involving the semaphorin domain, confers exquisite binding affinity for HER2 and enables METN375S to interact with HER2 in a ligand-independent fashion. The resultant METN375S/HER2 dimer transduces potent proliferative, pro-invasive and pro-metastatic cues through the HER2 signaling axis to drive aggressive squamous cell carcinomas of the head and neck (HNSCC) and lung (LUSC), and is associated with poor prognosis. Accordingly, HER2 blockers, but not c-MET inhibitors, are paradoxically effective at restraining in vivo and in vitro models expressing METN375S. These results establish METN375S as a biologically distinct and clinically actionable molecular subset of SCCs that are uniquely amenable to HER2 blocking therapies

Mechanically Robust Hybrid Coatings for Antifogging, Antireflection, and Self‐Cleaning Applications

Abstract In this work, a novel multifunctional film with durable antifogging performance and remarkable optical property is designed. By doping and hybridization to build an organic–inorganic siloxane network, the surface achieves long‐lasting wettability and superhydrophilicity with a water contact angle of 0°, which is maintained within 10° for over 130 days. The low refractive index endows the hybrid film with excellent optical property, which the average transmittance (380–1100 nm) of the film is 97.60% with the peak transmittance of 99.48%. By this design, the film performs well in the felt abrasion test, water impact test, X‐cut tape test, tape‐peeling test, chemical stability test, and anti‐dust test. Due to the abundant hydroxyl radicals on the surface, the film also exhibits excellent performance, achieving 92.73% degradation of methylene blue solution (10 ppm) and 39.53% degradation of rhodamine B (10 ppm) with good reproducibility in cyclic measurements