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To nondestructively detect the mold growth process on silk, a coaxial concave reflection conical fiber optic sensor was developed using conical quartz fibers, fiber connectors, fiber couplers, and a plastic fixator. We established a theoretical model of this sensor and studied the influence of its structural parameters on its sensitivity, characterized the morphology of Aspergillus niger, and detected its growth process on a silk surface. A linear relationship between the sensor’s output signal and the mold height was found. The sensor sensitivity, maximum detection error, and low limit of detection were 2.4 E-5 AU/µm, 7.83%, and 10 µm, respectively.

Polypropylene is considered to be the material of choice for environmentally friendly high voltage direct current cable insulation. The high power transmission of electrical energy exposes insulating materials to high temperatures and electric fields, resulting in the degradation of material properties. This paper reports that organic molecular semiconductors with strong electron affinity can effectively modulate electrical properties of polypropylene. The charge injection and transport process are analyzed by considering a combination of relations describing various conduction models in dielectrics, including the Richardson–Schottky (RS) emission and the hopping conduction. Based on the performed experiments, a modified Wiesmann–Zeller (WZ) model is proposed to simulate the electrical treeing process of polypropylene. The electrical treeing results are well verified with the simulation results, which offer a valuable tool for further analysis of the effect of intrinsic barrier height, hopping distance, and activation energy on the electrical degradation in the material. This work provides an insightful analysis of multiple charge transport mechanisms affecting the electrical degradation of the polymer, which is crucially essential for the rational design of high-performance insulation materials.

The flux weakening control method of permanent magnet synchronous motor makes it run in a wide speed range. In this paper, one way to configure parameter of flux weakening current PI regulator is proposed for the flux weakening control. It is based on the mathematical model of the system. To avoid the fault that occurs when torque current is smaller than flux weakening current, some correction for flux weakening current has been done. In the end, a measure to optimize the flux weakening control process was proposed.

To find novel isoform of PIK3IP1 and analyze their effects on cell viability, subcellular localization, and expression profile in cell lines.RT-PCR was used to clone PIK3IP1 and its novel splicing isoform PIK3IP1-v1 from multi-tissue cDNA pool. By cell-based assays, we studied how PIK3IP1 and PIK3IP1-v1 affected the activity of Renila luciferase and morphological change in the HEK 293T cells. Furthermore, flow cytometry experiment was used to validate that overexpression of both splicing isoforms could induce cell apoptosis. Bioinformatics analysis was used to identify structural characteristics of these two splicing isoforms. By fluorescence microscopy assay, we identified their subcellular localization. RT-PCR was used to detect the expression of PIK3IP1 in the cell lines.PIK3IP1 and its novel splicing isoform PIK3IP1-v1 were cloned and constructed into the pcDNA-and pEGFP-expression plasmids. They both had signal peptide and transmembrane domain. Nevertheless, PIK3IP1-v1 was in absence of an extracellular Kringle domain. They could inhibit the activity of Renila luciferase and induce cell apoptosis. Simultaneously, both splicing isoforms are validated with subcellular localization on cell membrane and lowly expressed in many cell lines.PIK3IP1-v1 is a novel splicing isoform of PIK3IP1. Both of them are located on cell membrane and can induce cell apoptosis.

Objectives To search for mutations in the Frizzled-4 gene ( FZD4 ) in Chinese patients with familial exudative vitreoretinopathy (FEVR) and to delineate the mutation-associated clinical features. Methods Forty-eight Chinese patients with FEVR and 100 unrelated control subjects were recruited and had complete ophthalmic examinations performed. The coding regions of FZD4 were screened for mutations by polymerase chain reaction and direct sequencing. Multiple sequence alignment was conducted to evaluate the conservation of residues among different FZD4 homologs and the human Frizzled family. Genotype-phenotype correlations were also analyzed. Results Twelve putative disease-causing mutations were identified in total, 9 of which were novel: 1 deletion (P14fsX57), 1 nonsense mutation (S491X), and 7 missense mutations (G22E, E180K, T237R, R253C, F328S, A339T, and D470N). Three reported FZD4 mutations were also detected: H69Y, M105V, and W496X. Remarkably, 2 patients who harbored compound heterozygous mutations (H69Y with E180K or W496X) had a more severe ocular phenotype than carriers of a single H69Y mutation. Conclusions FZD4 mutations were responsible for FEVR in 15 of 48 Chinese patients (31.3%) in this study, similar to other ethnic groups. This study supports the highly polymorphic nature of FZD4 with a differential mutation profile in the Chinese population. Clinical Relevance The profile of the mutations obtained in FZD4 further illustrates the complexity of FEVR and provides a better understanding of the genotype-phenotype correlations.