Assessing the Decision-Making Process in Human-Robot Collaboration Using a Lego-like EEG Headset

Human-robot collaboration (HRC) has become an emerging field, where the use of a robotic agent has been shifted from a supportive machine to a decision-making collaborator. A variety of factors can influence the effectiveness of decision-making processes during HRC, including the system-related (e.g., robot capability) and human-related (e.g., individual knowledgeability) factors. As a variety of contextual factors can significantly impact the human-robot decision-making process in collaborative contexts, the present study adopts a Lego-like EEG headset to collect and examine human brain activities and utilizes multiple questionnaires to evaluate participants’ cognitive perceptions toward the robot. A user study was conducted where two levels of robot capabilities (high vs. low) were manipulated to provide system recommendations. The participants were also identified into two groups based on their computational thinking (CT) ability. The EEG results revealed that different levels of CT abilities trigger different brainwaves, and the participants’ trust calibration of the robot also varies the resultant brain activities

PDZ-RhoGEF ubiquitination by Cullin3–KLHL20 controls neurotrophin-induced neurite outgrowth

Ubiquitin-dependent degradation of PDZ-RhoGEF restricts RhoA activity to facilitate neurite outgrowth

Inhibition of FAK Signaling Elicits Lamin A/C-Associated Nuclear Deformity and Cellular Senescence

Focal adhesion kinase (FAK) is a non-receptor kinase that facilitates tumor aggressiveness. The effects of FAK inhibition include arresting proliferation, limiting metastasis, and inhibiting angiogenesis. PF-573228 is an ATP-competitive inhibitor of FAK. Treating lung cancer cells with PF-573228 resulted in FAK inactivation and changes in the expressions of lamin A/C and nuclear deformity. Since lamin A/C downregulation or deficiency was associated with cellular senescence, the senescence-associated β-galactosidase (SA-β-gal) assay was used to investigate whether PF-573228 treatment drove cellular senescence, which showed more SA-β-gal-positive cells in culture. p53 is known to play a pivotal role in mediating the progression of cellular senescence, and the PF-573228-treated lung cancer cells resulted in a higher p53 expression level. Subsequently, the FAK depletion in lung cancer cells was employed to confirm the role of FAK inhibition on cellular senescence. FAK depletion and pharmacological inhibition of lung cancer cells elicited similar patterns of cellular senescence, lamin A/C downregulation, and p53 upregulation, implying that FAK signaling is associated with the expression of p53 and the maintenance of lamin A/C levels to shape regular nuclear morphology and manage anti-senescence. Conversely, FAK inactivation led to p53 upregulation, disorganization of the nuclear matrix, and consequently cellular senescence. Our data suggest a new FAK signaling pathway, in that abolishing FAK signaling can activate the senescence program in cells. Triggering cellular senescence could be a new therapeutic approach to limit tumor growth

Women with endometriosis have higher comorbidities: Analysis of domestic data in Taiwan

AbstractEndometriosis, defined by the presence of viable extrauterine endometrial glands and stroma, can grow or bleed cyclically, and possesses characteristics including a destructive, invasive, and metastatic nature. Since endometriosis may result in pelvic inflammation, adhesion, chronic pain, and infertility, and can progress to biologically malignant tumors, it is a long-term major health issue in women of reproductive age. In this review, we analyze the Taiwan domestic research addressing associations between endometriosis and other diseases. Concerning malignant tumors, we identified four studies on the links between endometriosis and ovarian cancer, one on breast cancer, two on endometrial cancer, one on colorectal cancer, and one on other malignancies, as well as one on associations between endometriosis and irritable bowel syndrome, one on links with migraine headache, three on links with pelvic inflammatory diseases, four on links with infertility, four on links with obesity, four on links with chronic liver disease, four on links with rheumatoid arthritis, four on links with chronic renal disease, five on links with diabetes mellitus, and five on links with cardiovascular diseases (hypertension, hyperlipidemia, etc.). The data available to date support that women with endometriosis might be at risk of some chronic illnesses and certain malignancies, although we consider the evidence for some comorbidities to be of low quality, for example, the association between colon cancer and adenomyosis/endometriosis. We still believe that the risk of comorbidity might be higher in women with endometriosis than that we supposed before. More research is needed to determine whether women with endometriosis are really at risk of these comorbidities

Modeling and Design for Electromagnetic Compatibility Issues of Slot-Crossing Signal Lines

本文針對跨槽信號線引發的電磁相容問題，提出相關的解決方案及模型化方法。本文中提出的等效電路，將物理結構以傳輸線模型作為基礎，與其電氣特性建立良好的連結。基於所提出的模型架構，本文提出三種低成本的解決方案分別解決當高速信號線跨越蝕刻溝槽的參考平面時，所誘發之串音、共模輻射及材料損耗所造成的信號失真等問題。 本文首先探討信號線間透過槽線的耦合，所誘發之串音問題。針對此問題，本文提出了一低成本解決方案，透過開路之微帶線與槽線之並聯銜接，可有效地降低因符際干擾所造成之串音。透過模擬及實驗的結果，本文驗證了針對低及高頻率之傳輸速度的設計方法。 其次，針對高速共模雜訊，因激發開槽線所產生之共模輻射議題，本文提出一種接地式共振腔技術，用以降低高頻的共模幅射及模態轉換。透過巧妙的將開路式的微帶線與槽線以並聯形式相連，所形成之接地式共振腔可有效的控制共模傳輸特性，以避免激發類似天線般的槽線。在一實驗實例中，以此低成本結構在2.29到3.48 GHz頻率範圍內，有效降低遠場輻射的電場大小。同時，此電場抑制的頻寬如同所提出結構的共模傳輸頻寬。 最後，本文提出一新穎架構，除具備差模信號等化器的功能外，亦擁有寬頻的共模雜訊抑制。就目前的文獻探討，可知此架構為首次在學術界中被提出，同時具備上述的兩種功能。透過妥善設計耦合槽線及末端之電阻值，將其與差模信號線在接收端附近以並聯方式銜接，此電阻不但可提供差模信號的等化功能，亦可吸收部分的共模雜訊。差模信號的傳輸品質經一實驗實例的量測驗證，在信號傳輸速度為8 Gbps時，相較於未設計等化器結構的情況，可明顯改善接收之眼圖。The dissertation provides solutions and modeling methods for electromagnetic compatibility problems caused by slot-crossing signal traces. Based on the transmission line models, equivalent circuit models for the signal traces were created, which transformed physical configurations into electrical behavior. With the help of the constructed models, low-cost solutions have been proposed to solve the unwanted crosstalk, common-mode radiation and lossy material problems when high-speed signals cross slotted reference plane. In the beginning, the crosstalk between signal traces crossing the same slot is first investigated. By connecting an open-circuited microstrip line in parallel with the slotline between the crossing signal lines, a branched reflector technique is proposed to suppress the crosstalk due to the inter-symbol interference. The design methods both for low- and high-frequency transmission have been proposed and validated by the simulation and experimental results. Second, a grounded resonator technique is designed to reduce common-mode radiation and mode conversion, which are resulted from common-mode noise striding across the slotted plane. By properly linking the open-circuited transmission lines with the slotline, the common-mode transmission can be controlled to prevent excitation of antenna-like slotline. This low-cost solution makes the radiated electric field to be effectively decreased from 2.29 to 3.48 GHz, which is consistent to the designed passband. Finally, a differential-mode equalizer with broadband common-mode suppression is proposed. To the best knowledge of the author, these dual functions are the first time to be integrated in a single structure. Through suitably connecting the coupled slotlines with the differential line structure, the terminated resistors at the end of coupled slotlines provide the equalization and absorption for differential-mode transmission and common-mode noise, respectively. With the experimental validation, the eye-diagram of differential-mode transmission at 8 Gbps has been greatly improved comparing that without the designed configuration

Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy

Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) specifically binds and isomerizes the phosphorylated serine/threonine-proline (pSer/Thr-Pro) motif, which leads to changes in protein conformation and function. Pin1 is widely overexpressed in cancers and plays an important role in tumorigenesis. Mounting evidence has revealed that targeting Pin1 is a potential therapeutic approach for various cancers by inhibiting cell proliferation, reducing metastasis, and maintaining genome stability. In this review, we summarize the underlying mechanisms of Pin1-mediated upregulation of oncogenes and downregulation of tumor suppressors in cancer development. Furthermore, we also discuss the multiple roles of Pin1 in cancer hallmarks and examine Pin1 as a desirable pharmaceutical target for cancer therapy. We also summarize the recent progress of Pin1-targeted small-molecule compounds for anticancer activity

FAK in Cancer: From Mechanisms to Therapeutic Strategies

Focal adhesion kinase (FAK), a non-receptor tyrosine kinase, is overexpressed and activated in many cancer types. FAK regulates diverse cellular processes, including growth factor signaling, cell cycle progression, cell survival, cell motility, angiogenesis, and the establishment of immunosuppressive tumor microenvironments through kinase-dependent and kinase-independent scaffolding functions in the cytoplasm and nucleus. Mounting evidence has indicated that targeting FAK, either alone or in combination with other agents, may represent a promising therapeutic strategy for various cancers. In this review, we summarize the mechanisms underlying FAK-mediated signaling networks during tumor development. We also summarize the recent progress of FAK-targeted small-molecule compounds for anticancer activity from preclinical and clinical evidence