基于稀疏重建的信号DOA估计

从稀疏信号重建角度提出了一种改进的波达方向(DOA)估计方法。由于最小冗余线阵(MRLA)能以较少的阵元数获得较大的阵列孔径,将MRLA与l1-SVD方法相结合估计信号的DOA。仿真结果表明,经多次实验验证,所提方法是有效的,相比l1-SVD方法可以估计出更多信源的DOA,并且可以用较少的阵元数估计更多的信源DOA,具有信源过载能力。     

一种针对图像模糊的无参考质量评价指标

在成像模型的基础上,分析了图像模糊的原因,提出了一种为图像构造参考图像的方法,进而将结构相似度(SSIM)评价方法引入到无参考图像质量评价中,提出一种无参考结构清晰度(NRSS)的新的无参考图像质量评价方法,将其用于对模糊图像的质量评价。该方法通过低通滤波器来构造参考图像,通过计算原始图像与参考图像的结构相似度值来评价原始图像质量,很好地结合了成像系统的数学模型和结构相似度评价方法的优势,实验结果表明无参考结构清晰度评价指标能够给出和主观评价方法以及其余有参考评价方法一致的结果。     

Reduced VDAC1, Maintained Mitochondrial Dynamics and Enhanced Mitochondrial Biogenesis in a Transgenic Tau Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most common forms of neurodegeneration, defined by reduced cognitive function, which is caused by the gradual death of neurons in the brain. Recent studies have shown an age-dependent rise in the levels of voltage-dependent anion channel 1 (VDAC1) in AD. In addition, we discovered an aberrant interaction between VDAC1 and P-TAU in the brains of AD patients, which led to abnormalities in the structural and functional integrity of the mitochondria. The purpose of our study is to understand the protective effects of reduced VDAC1 against impaired mitochondrial dynamics and defective mitochondrial biogenesis in transgenic TAU mice. Recently, we crossed heterozygote VDAC1 knockout (VDAC1^+/−) mice with transgenic TAU mice to obtain double-mutant VDAC1^+/−/TAU mice. Our goal was to evaluate whether a partial decrease in VDAC1 lessens the amount of mitochondrial toxicity in transgenic Tau (P301L) mice. We found that mitochondrial fission proteins were significantly reduced, and mitochondrial fusion and biogenesis proteins were increased in double-mutant mice compared to TAU mice. On the basis of these discoveries, the current work may have significance for the development of reduced-VDAC1-based treatments for individuals suffering from AD as well as other tauopathies.     

GmIAA27 Encodes an AUX/IAA Protein Involved in Dwarfing and Multi-Branching in Soybean

Soybean plant height and branching affect plant architecture and yield potential in soybean. In this study, the mutant dmbn was obtained by treating the cultivar Zhongpin 661 with ethylmethane sulfonate. The dmbn mutant plants were shorter and more branched than the wild type. The genetic analysis showed that the mutant trait was controlled by a semi-dominant gene. The candidate gene was fine-mapped to a 91 kb interval on Chromosome 9 by combining BSA-seq and linkage analysis. Sequence analysis revealed that Glyma.09g193000 encoding an Aux/IAA protein (GmIAA27) was mutated from C to T in the second exon of the coding region, resulting to amino acid substitution of proline to leucine. Overexpression of the mutant type of this gene in Arabidopsis thaliana inhibited apical dominance and promoted lateral branch development. Expression analysis of GmIAA27 and auxin response genes revealed that some GH3 genes were induced. GmIAA27 relies on auxin to interact with TIR1, whereas Gmiaa27 cannot interact with TIR1 owing to the mutation in the degron motif. Identification of this unique gene that controls soybean plant height and branch development provides a basis for investigating the mechanisms regulating soybean plant architecture development.     

Neuronal ApoE Regulates the Cell-to-Cell Transmission of α-Synuclein

The presence of protein inclusions, called Lewy bodies (LBs) and Lewy neurites (LNs), in the brain is the main feature of Parkinson’s disease (PD). Recent evidence that the prion-like propagation of α-synuclein (α-syn), as a major component of LBs and LNs, plays an important role in the progression of PD has gained much attention, although the molecular mechanism remains unclear. In this study, we evaluated whether neuronal ApoE regulates the cell-to-cell transmission of α-syn and explored its molecular mechanism using in vitro and in vivo model systems. We demonstrate that neuronal ApoE deficiency attenuates both α-syn uptake and release by downregulating LRP-1 and LDLR expression and enhancing chaperone-mediated autophagy activity, respectively, thereby contributing to α-syn propagation. In addition, we observed that α-syn propagation was attenuated in ApoE knockout mice injected with pre-formed mouse α-syn fibrils. This study will help our understanding of the molecular mechanisms underlying α-syn propagation.     

Reg-1α, a New Substrate of Calpain-2 Depending on Its Glycosylation Status

Reg-1α/lithostathine, a protein mainly associated with the digestive system, was previously shown to be overexpressed in the pre-clinical stages of Alzheimer’s disease. In vitro, the glycosylated protein was reported to form fibrils at physiological pH following the proteolytic action of trypsin. However, the nature of the protease able to act in the central nervous system is unknown. In the present study, we showed that Reg-1α can be cleaved in vitro by calpain-2, the calcium activated neutral protease, overexpressed in neurodegenerative diseases. Using chemical crosslinking experiments, we found that the two proteins can interact with each other. Identification of the cleavage site using mass spectrometry, between Gln⁴ and Thr⁵, was found in agreement with the in silico prediction of the calpain cleavage site, in a position different from the one reported for trypsin, i.e., Arg¹¹-Ile¹² peptide bond. We showed that the cleavage was impeded by the presence of the neighboring glycosylation of Thr⁵. Moreover, in vitro studies using electron microscopy showed that calpain-cleaved protein does not form fibrils as observed after trypsin cleavage. Collectively, our results show that calpain-2 cleaves Reg-1α in vitro, and that this action is not associated with fibril formation.