A Fully-Integrated Reconfigurable Dual-Band Transceiver for Short Range Wireless Communications in 180 nm CMOS

© 2015 IEEE. Personal use of this material is permitted. Permission from IEEE must be obtained for all other users, including reprinting/ republishing this material for advertising or promotional purposes, creating new collective works for resale or redistribution to servers or lists, or reuse of any copyrighted components of this work in other works.A fully-integrated reconfigurable dual-band (760-960 MHz and 2.4-2.5 GHz) transceiver (TRX) for short range wireless communications is presented. The TRX consists of two individually-optimized RF front-ends for each band and one shared power-scalable analog baseband. The sub-GHz receiver has achieved the maximum 75 dBc 3rd-order harmonic rejection ratio (HRR3) by inserting a Q-enhanced notch filtering RF amplifier (RFA). In 2.4 GHz band, a single-ended-to-differential RFA with gain/phase imbalance compensation is proposed in the receiver. A ΣΔ fractional-N PLL frequency synthesizer with two switchable Class-C VCOs is employed to provide the LOs. Moreover, the integrated multi-mode PAs achieve the output P1dB (OP1dB) of 16.3 dBm and 14.1 dBm with both 25% PAE for sub-GHz and 2.4 GHz bands, respectively. A power-control loop is proposed to detect the input signal PAPR in real-time and flexibly reconfigure the PA's operation modes to enhance the back-off efficiency. With this proposed technique, the PAE of the sub-GHz PA is improved by x3.24 and x1.41 at 9 dB and 3 dB back-off powers, respectively, and the PAE of the 2.4 GHz PA is improved by x2.17 at 6 dB back-off power. The presented transceiver has achieved comparable or even better performance in terms of noise figure, HRR, OP1dB and power efficiency compared with the state-of-the-art.Peer reviewe

Adrenomedullin expression in epithelial ovarian cancers and promotes HO8910 cell migration associated with upregulating integrin α5β1 and phosphorylating FAK and paxillin

<p>Abstract</p> <p>Background</p> <p>Epithelial ovarian cancer (EOC) is one of the leading causes of cancer deaths in women worldwide. Adrenomedullin (AM) is a multifunctional peptide which presents in various kinds of tumors.</p> <p>Methods</p> <p>In this study, we characterized the expression and function of AM in epithelial ovarian cancer using immunohistochemistry staining. Exogenous AM and small interfering RNA (siRNA) specific for AM receptor CRLR were treated to EOC cell line HO8910. Wound healing assay and flow cytometry were used to measure the migration ability and expression of integrin α5 of HO8910 cells after above treatments. Western blot was used to examine the phosphorylation of FAK and paxillin.</p> <p>Results</p> <p>We found that patients with high AM expression showed a higher incidence of metastasis, larger residual size of tumors after cytoreduction and shorter disease-free and overall survival time. Exogenous AM induced ovarian cancer cell migration in time- and dose- dependent manners. AM upregulated the expression of integrin α5 and phosphorylation of FAK, paxillin as well.</p> <p>Conclusions</p> <p>Our results suggested that AM contributed to the progression of EOC and had additional roles in EOC cell migration by activating the integrin α5β1 signaling pathway. Therefore, we presumed that AM could be a potential molecular therapeutic target for ovarian carcinoma.</p

Boosting Few-Shot Text Classification via Distribution Estimation

Distribution estimation has been demonstrated as one of the most effective approaches in dealing with few-shot image classification, as the low-level patterns and underlying representations can be easily transferred across different tasks in computer vision domain. However, directly applying this approach to few-shot text classification is challenging, since leveraging the statistics of known classes with sufficient samples to calibrate the distributions of novel classes may cause negative effects due to serious category difference in text domain. To alleviate this issue, we propose two simple yet effective strategies to estimate the distributions of the novel classes by utilizing unlabeled query samples, thus avoiding the potential negative transfer issue. Specifically, we first assume a class or sample follows the Gaussian distribution, and use the original support set and the nearest few query samples to estimate the corresponding mean and covariance. Then, we augment the labeled samples by sampling from the estimated distribution, which can provide sufficient supervision for training the classification model. Extensive experiments on eight few-shot text classification datasets show that the proposed method outperforms state-of-the-art baselines significantly.Comment: Accepted to AAAI 202

Image dataset of tea chrysanthemums in complex outdoor scenes

There is currently no publicly available tea chrysanthemum dataset to the authors’ knowledge. Consequently, we provide an image dataset for six varieties of tea chrysanthemums in three camera view angles obtained under complex outdoor scenes, and this open-source image dataset can greatly promote the development of tea chrysanthemums detection methodology

Kinases Mst1 and Mst2 positively regulate phagocytic induction of reactive oxygen species and bactericidal activity

该研究成果揭示了吞噬性细胞内Hippo信号通路关键激酶Mst1和Mst2通过活化Rac家族蛋白来调节线粒体向吞噬小泡募集并释放ROS来清除病原体，这个生物学过程在天然免疫和宿主防御中发挥着重要作用。该成果解析了人的Mst1基因缺失或Rac2基因突变引发免疫缺陷综合症的致病机理，为研究人类感染性疾病提供了全新的视角。 该论文的主要工作由2012级博士生耿晶、2013级博士生孙秀峰以及王平、张世浩和王晓珍等学生共同承担，并与厦门市第一医院、台湾长庚大学、中国科学技术大学等单位合作完成，通讯作者为周大旺教授和陈兰芬教授。该研究工作获得了“青年千人计划”、国家自然科学基金委和科技部的资助。Mitochondria need to be juxtaposed to phagosomes for the synergistic production of ample reactive oxygen species (ROS) in phagocytes to kill pathogens. However, how phagosomes transmit signals to recruit mitochondria has remained unclear. Here we found that the kinases Mst1 and Mst2 functioned to control ROS production by regulating mitochondrial trafficking and mitochondrion-phagosome juxtaposition. Mst1 and Mst2 activated the GTPase Rac to promote Toll-like receptor (TLR)-triggered assembly of the TRAF6-ECSIT complex that is required for the recruitment of mitochondria to phagosomes. Inactive forms of Rac, including the human Rac2D57N mutant, disrupted the TRAF6-ECSIT complex by sequestering TRAF6 and substantially diminished ROS production and enhanced susceptibility to bacterial infection. Our findings demonstrate that the TLR-Mst1-Mst2-Rac signaling axis is critical for effective phagosome-mitochondrion function and bactericidal activity.Supported by the National Basic Research Program (973) of China (2015CB910502 to L.C.), China's 1000 Young Talents Program (D.Z. and L.C.), the 111 Projects (B12001 and B06016), the Fundamental Research Funds for the Central Universities of China-Xiamen University (CXB2014004 to J.Z.; 20720140551 to L.C.; and 2013121034 and 20720140537 to D.Z.), the National Natural Science Foundation of China (31270918, 81222030 and J1310027 to D.Z.; 81372617, 81422018 and U1405225 to L.C.; 81472229 to L.H.; and 81302529 to X.L.), the Natural Science Foundation of Fujian (2013J06011 to D.Z. and 2014D007 to X.L.), the US National Institutes of Health (RO1 CA136567 for J.A.) and institutional funds from Massachusetts General Hospital (for J.A.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

BIOMECHANICAL REGULATION OF CELL PROLIFERATION, EPITHELIAL-MESENCHYMAL TRANSITION AND INVASION

Cells in epithelial tissues adhere to an underlying extracellular matrix (ECM) and respond to changes in its physical properties by altering gene expression and behavior. The mechanical properties of the ECM, including the matrix stiffness, are therefore central to developmental, physiological, and pathological processes. In the context of cancer, increased tissue stiffness and interstitial fluid pressure are inherent features of tumorigenesis, which promote malignant transformation of surrounding cells and correlate with poor survival. These processes depend on the synergistic effects of mechanical signals such as ECM stiffness and chemical signals such as Wnt, TGFβ and proteases in the cellular microenvironment. This dissertation explores how mechanical and biochemical signals are integrated to control cell behaviors including proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and invasion. We used engineered substrata to recapitulate the mechanical stiffnesses of the normal mammary gland as well as that of breast tumors. We found that exposure to Wnt3a increased proliferation of mammary epithelial cells cultured on stiff substrata, with compliances characteristic of breast tumors, but not of cells on soft substrata, with compliances comparable to that of normal mammary tissue. Depleting integrin-linked kinase (ILK), which functions as a signaling hub for cellular mechanotransduction, rendered cells unresponsive to Wnt3a on both substrata. Ectopic expression of ILK permitted Wnt3a to induce proliferation of cells on both microenvironments. We further showed that ILK regulates expression of the Wnt receptor frizzled-1 (Fzd1), suggesting the existence of a positive feedback loop between Wnt3a, ILK and Fzd1. Following these findings, we examined the role of ILK and tissue stiffness in regulating cell fate in response to TGFβ1. We found that ILK controls the switch between apoptosis and EMT downstream of TGFβ1 through modulating the fine balance between cell-cell and cell-matrix adhesions. Specifically, depletion of ILK leads to increased E-cadherin-based cell-cell adhesion and cortical actin and decreased focal adhesions and stress fibers in mammary epithelial cells. These changes favor apoptosis and suppress EMT downstream of TGFβ1, regardless of matrix stiffness. Similarly, soft matrix also favors apoptosis downstream of TGFβ1 while stiff matrix promotes EMT, suggesting that depletion of ILK disrupts the ability of a cell to sense a mechanically stiff microenvironment. Taken together, these findings suggest that tissue mechanics regulates the cellular response to Wnt and TGFβ under physiological and pathological microenvironmental conditions. We also highlighted the role of ILK in mediating the responses to matrix stiffness and tuning the proliferative and potential tumorigenic behaviors of mammary epithelial cells to Wnt3a and TGFβ1. These results provide insight into the molecular mechanisms underlying the effects of a pathological microenvironment on neoplastic progression

Influence of Ethnic Group-Membership and Gaze Direction on the Perception of Emotions. A Cross-Cultural Study between Germany and China

Emotional facial expressions provide important nonverbal cues in human interactions. The perception of emotions is not only influenced by a person's ethnic background but also depends on whether a person is engaged with the emotion-encoder. Although these factors are known to affect emotion perception, their impact has only been studied in isolation before. The aim of the present study was to investigate their combined influence. Thus, in order to study the influence of engagement on emotion perception between persons from different ethnicities, we compared participants from China and Germany. Asian-looking and European-looking virtual agents expressed anger and happiness while gazing at the participant or at another person. Participants had to assess the perceived valence of the emotional expressions. Results indicate that indeed two factors that are known to have a considerable influence on emotion perception interacted in their combined influence: We found that the perceived intensity of an emotion expressed by ethnic in-group members was in most cases independent of gaze direction, whereas gaze direction had an influence on the emotion perception of ethnic out-group members. Additionally, participants from the ethnic out-group tended to perceive emotions as more pronounced than participants from the ethnic in-group when they were directly gazed at. These findings suggest that gaze direction has a differential influence on ethnic in-group and ethnic out-group dynamics during emotion perception