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Transparent ferroelectric crystals with ultrahigh piezoelectricity 期刊论文
NATURE, 2020, 577 (7790) : 350-+
作者:  Qiu, Chaorui;  Wang, Bo;  Zhang, Nan;  Zhang, Shujun;  Liu, Jinfeng;  Walker, David;  Wang, Yu;  Tian, Hao;  Shrout, Thomas R.;  Xu, Zhuo;  Chen, Long-Qing;  Li, Fei
收藏  |  浏览/下载:16/0  |  提交时间:2020/07/03

Transparent piezoelectrics are highly desirable for numerous hybrid ultrasound-optical devices ranging from photoacoustic imaging transducers to transparent actuators for haptic applications(1-7). However, it is challenging to achieve high piezoelectricity and perfect transparency simultaneously because most high-performance piezoelectrics are ferroelectrics that contain high-density light-scattering domain walls. Here, through a combination of phase-field simulations and experiments, we demonstrate a relatively simple method of using an alternating-current electric field to engineer the domain structures of originally opaque rhombohedral Pb(Mg1/3Nb2/3)O-3-PbTiO3 (PMN-PT) crystals to simultaneously generate near-perfect transparency, an ultrahigh piezoelectric coefficient d(33) (greater than 2,100 picocoulombs per newton), an excellent electromechanical coupling factor k(33) (about 94 per cent) and a large electro-optical coefficient gamma(33) (approximately 220 picometres per volt), which is far beyond the performance of the commonly used transparent ferroelectric crystal LiNbO3. We find that increasing the domain size leads to a higher d(33) value for the [001]-oriented rhombohedral PMN-PT crystals, challenging the conventional wisdom that decreasing the domain size always results in higher piezoelectricity(8-10). This work presents a paradigm for achieving high transparency and piezoelectricity by ferroelectric domain engineering, and we expect the transparent ferroelectric crystals reported here to provide a route to a wide range of hybrid device applications, such as medical imaging, self-energy-harvesting touch screens and invisible robotic devices.


  
Injured adult neurons regress to an embryonic transcriptional growth state 期刊论文
NATURE, 2020, 581 (7806) : 77-+
作者:  Wang, Ruicong;  Li, Hongda;  Wu, Jianfeng;  Cai, Zhi-Yu;  Li, Baizhou;  Ni, Hengxiao;  Qiu, Xingfeng;  Chen, Hui;  Liu, Wei;  Yang, Zhang-Hua;  Liu, Min;  Hu, Jin;  Liang, Yaoji;  Lan, Ping;  Han, Jiahuai;  Mo, Wei
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/03

Grafts of spinal-cord-derived neural progenitor cells (NPCs) enable the robust regeneration of corticospinal axons and restore forelimb function after spinal cord injury(1)  however, the molecular mechanisms that underlie this regeneration are unknown. Here we perform translational profiling specifically of corticospinal tract (CST) motor neurons in mice, to identify their '  regenerative transcriptome'  after spinal cord injury and NPC grafting. Notably, both injury alone and injury combined with NPC grafts elicit virtually identical early transcriptomic responses in host CST neurons. However, in mice with injury alone this regenerative transcriptome is downregulated after two weeks, whereas in NPC-grafted mice this transcriptome is sustained. The regenerative transcriptome represents a reversion to an embryonic transcriptional state of the CST neuron. The huntingtin gene (Htt) is a central hub in the regeneration transcriptome  deletion of Htt significantly attenuates regeneration, which shows that Htt has a key role in neural plasticity after injury.


In mouse models of central nervous system injury, Htt is shown to be a key component of the regulatory program associated with reversion of the neuronal transcriptome to a less-mature state.


  
The gut-brain axis mediates sugar preference 期刊论文
NATURE, 2020, 580 (7804) : 511-+
作者:  Wang, Ruicong;  Li, Hongda;  Wu, Jianfeng;  Cai, Zhi-Yu;  Li, Baizhou;  Ni, Hengxiao;  Qiu, Xingfeng;  Chen, Hui;  Liu, Wei;  Yang, Zhang-Hua;  Liu, Min;  Hu, Jin;  Liang, Yaoji;  Lan, Ping;  Han, Jiahuai;  Mo, Wei
收藏  |  浏览/下载:17/0  |  提交时间:2020/07/03

The taste of sugar is one of the most basic sensory percepts for humans and other animals. Animals can develop a strong preference for sugar even if they lack sweet taste receptors, indicating a mechanism independent of taste(1-3). Here we examined the neural basis for sugar preference and demonstrate that a population of neurons in the vagal ganglia and brainstem are activated via the gut-brain axis to create preference for sugar. These neurons are stimulated in response to sugar but not artificial sweeteners, and are activated by direct delivery of sugar to the gut. Using functional imaging we monitored activity of the gut-brain axis, and identified the vagal neurons activated by intestinal delivery of glucose. Next, we engineered mice in which synaptic activity in this gut-to-brain circuit was genetically silenced, and prevented the development of behavioural preference for sugar. Moreover, we show that co-opting this circuit by chemogenetic activation can create preferences to otherwise less-preferred stimuli. Together, these findings reveal a gut-to-brain post-ingestive sugar-sensing pathway critical for the development of sugar preference. In addition, they explain the neural basis for differences in the behavioural effects of sweeteners versus sugar, and uncover an essential circuit underlying the highly appetitive effects of sugar.


Experiments in mice show that a population of neurons in the vagal ganglia respond to the presence of glucose in the gut and connect to neurons in the brainstem, revealing the circuit that underlies the neural basis for the behavioural preference for sugar.


  
PIK3CA variants selectively initiate brain hyperactivity during gliomagenesis 期刊论文
NATURE, 2020, 578 (7793) : 166-+
作者:  Qiu, Chaorui;  Wang, Bo;  Zhang, Nan;  Zhang, Shujun;  Liu, Jinfeng;  Walker, David;  Wang, Yu;  Tian, Hao;  Shrout, Thomas R.;  Xu, Zhuo;  Chen, Long-Qing;  Li, Fei
收藏  |  浏览/下载:8/0  |  提交时间:2020/07/03

Glioblastoma is a universally lethal form of brain cancer that exhibits an array of pathophysiological phenotypes, many of which are mediated by interactions with the neuronal microenvironment(1,2). Recent studies have shown that increases in neuronal activity have an important role in the proliferation and progression of glioblastoma(3,4). Whether there is reciprocal crosstalk between glioblastoma and neurons remains poorly defined, as the mechanisms that underlie how these tumours remodel the neuronal milieu towards increased activity are unknown. Here, using a native mouse model of glioblastoma, we develop a high-throughput in vivo screening platform and discover several driver variants of PIK3CA. We show that tumours driven by these variants have divergent molecular properties that manifest in selective initiation of brain hyperexcitability and remodelling of the synaptic constituency. Furthermore, secreted members of the glypican (GPC) family are selectively expressed in these tumours, and GPC3 drives gliomagenesis and hyperexcitability. Together, our studies illustrate the importance of functionally interrogating diverse tumour phenotypes driven by individual, yet related, variants and reveal how glioblastoma alters the neuronal microenvironment.


Glioblastoma tumours expressing oncogenic PIK3CA variants secrete the glycan GPC3, which promotes the formation of neural synapses, brain synaptic hyperexcitability and gliomagenesis.