Publications by authors named "Xiang Teng"

Utilizing the residual droplet produced from liquid bridge breakup for microdroplet deposition serves as an important supplementary method to conventional printing techniques. However, this approach typically relies on mechanical motion to form and break the liquid bridge between the liquid donor and acceptor surfaces, resulting in a relatively complex process and low printing efficiency (typically limited to several Hertz). Here, we propose a novel contact printing method based on the meniscus vibration (MVCP).

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The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development and homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders. quiescent NSCs extend an actin-rich primary protrusion toward the neuropil.

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The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development and homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders. quiescent NSCs extend an actin-rich primary protrusion toward the neuropil.

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A new study shows that cell size, in conjunction with specific signaling pathways, controls apoptosis within developing tissues. Cells with smaller sizes and relatively smaller sizes compared to their neighbors exhibit an increased likelihood of undergoing apoptosis. These processes are regulated by the Hippo/YAP and Notch pathways, respectively.

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The ability of stem cells to switch between quiescent and proliferative states is crucial for maintaining tissue homeostasis and regeneration. In Drosophila, quiescent neural stem cells (qNSCs) extend a primary protrusion, a hallmark of qNSCs. Here, we have found that qNSC protrusions can be regenerated upon injury.

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The ability of stem cells to switch between quiescent and proliferative states is crucial for maintaining tissue homeostasis and regeneration. Drosophila quiescent neural stem cells (qNSCs) extend a primary protrusion that is enriched in acentrosomal microtubules and can be regenerated upon injury. Arf1 promotes microtubule growth, reactivation (exit from quiescence), and regeneration of qNSC protrusions upon injury.

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The number of cells in tissues is controlled by cell division and cell death, and its misregulation could lead to pathological conditions such as cancer. To maintain the cell numbers, a cell-elimination process called apoptosis also stimulates the proliferation of neighboring cells. This mechanism, apoptosis-induced compensatory proliferation, was originally described more than 40 years ago.

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We report a novel model of lupus-associated cardiovascular pathology accelerated by the TLR7 agonist R848 in lupus-prone B6. (TC) mice. R848-treated TC mice but not non-autoimmune C57BL/6 (B6) controls developed microvascular inflammation and myocytolysis with intracellular vacuolization.

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Accurate segregation of chromosomes during anaphase relies on the central spindle and its regulators. A newly raised concept of the central spindle, the bridging fiber, shows that sliding of antiparallel microtubules (MTs) within the bridging fiber promotes chromosome segregation. However, the regulators of the bridging fiber and its regulatory mechanism on MTs sliding remain largely unknown.

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Recent research achievements in learning from demonstration (LfD) illustrate that the reinforcement learning is effective for the robots to improve their movement skills. The current challenge mainly remains in how to generate new robot motions automatically to perform new tasks, which have a similar preassigned performance indicator but are different from the demonstration tasks. To deal with the abovementioned issue, this article proposes a framework to represent the policy and conduct imitation learning and optimization for robot intelligent trajectory planning, based on the improved locally weighted regression (iLWR) and policy improvement with path integral by dual perturbation (PI-DP).

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Actomyosin networks provide the major contractile machinery for regulating cell and tissue morphogenesis during development. These networks undergo dynamic rearrangements, enabling cells to have a broad range of mechanical actions. How cells integrate different mechanical stimuli to accomplish complicated tasks in vivo remains unclear.

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Adaptive algorithm based on multi-channel linear prediction (MCLP) is an effective dereverberation method. However, the abrupt change of the target speech source position makes it difficult to guarantee both the fast convergence speed and the optimal steady-state behavior. In this letter, the recursive-least-squares (RLS)-based and Kalman-filter-based adaptive MCLP method for speech dereverberation are investigated.

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Cell polarity is facilitated by a rearrangement of the actin cytoskeleton at the cell cortex. The program triggering the asymmetric remodeling of contractile actomyosin networks remains poorly understood. Here, we show that polarization of Caenorhabditis elegans zygotes is established through sequential downregulation of cortical actomyosin networks by the mitotic kinase, Aurora-A.

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Apoptosis is a mechanism of eliminating damaged or unnecessary cells during development and tissue homeostasis. During apoptosis within a tissue, the adhesions between dying and neighboring non-dying cells need to be remodeled so that the apoptotic cell is expelled. In parallel, contraction of actomyosin cables formed in apoptotic and neighboring cells drives cell extrusion.

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Apoptosis, or programmed cell death, is an essential process for the elimination of unnecessary cells during embryonic development, tissue homeostasis, and certain pathological conditions. Recently, an active mechanical function of apoptosis called apoptotic force has been demonstrated during a tissue fusion process of Drosophila embryogenesis. The mechanical force produced during apoptosis is used not only to force dying cells out from tissues in order to keep tissue integrity, but also to change the morphology of neighboring cells to fill the space originally occupied by the dying cell.

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