天博《科学》（20230915出版）一周论文导读—新闻—科学网
来源：天博企业
发表时间:
2024-08-19
编译 | 未玖
Science, 15 SEP 2023, VOL 381, ISSUE 6663
《科学》2023年9月15日，第381卷，6663期
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人工智能Artificial Intelligence
Edge learning using a fully integrated neuro-inspired memristor chip
使用全集成类脑忆阻器芯片举行边沿进修
▲ 作者：Wenbin Zhang, Peng Yao, Bin Gao, Qi Liu, Dong Wu, Qingtian Zhang, et al.
▲ 链接：https://www.science.org/doi/full/10.1126/science.ade3483
▲ 择要：
进修对于在边沿智能装备顺应差别的运用场景以及用户很是主要。当前练习神经收集的技能需要于计较以及存储单位之间挪动年夜量数据，这拦阻了于边沿装备上实现进修。
研究组开发了一种全集成忆阻器芯片，提高了进修威力，降低了能耗。STELLAR架构中包孕进修算法、硬件实现以及并行电导调制计谋的方案，是经由过程使用忆阻器交织阵列来促成片上进修的通用要领，而与忆阻器器件类型无关。
于这项研究中履行的使命包孕运动节制、图象分类以及语音辨认。
▲ Abstract：
Learning is highly important for edge intelligence devices to adapt to different application scenes and owners. Current technologies for training neural networks require moving massive amounts of data between computing and memory units, which hinders the implementation of learning on edge devices. We developed a fully integrated memristor chip with the improvement learning ability and low energy cost. The schemes in the STELLAR architecture, including its learning algorithm, hardware realization, and parallel conductance tuning scheme, are general approaches that facilitate on-chip learning by using a memristor crossbar array, regardless of the type of memristor device. Tasks executed in this study included motion control, image classification, and speech recognition.
Powerful, soft combustion actuators for insect-scale robots
用在虫豸级呆板人的强盛、软燃烧致动器
▲ 作者：Cameron A. Aubin, Ronald H. Heisser, Ofek Peretz, Julia Timko, Jacqueline Lo, E. Farrell Helbling, et al.
▲ 链接：https://www.science.org/doi/full/10.1126/science.adg5067
▲ 择要：
虫豸相对于在其较小的身体，拥有惊人的强盛气力以及耐力。虫豸级呆板人只管遵照不异的缩放定律，但与虫豸比拟机能却年夜年夜降落，这是由于当前微致动器技能由低能量密度电源驱动，孕育发生的力以及/或者位移都很小。使用高能量密度化学燃料为小型软致动器提供动力是一种潜于解决方案。
研究组展示了一个325毫克的软燃烧微致动器，可实现140%的位移，事情频次 100赫兹，并孕育发生 9.5牛顿的力。哄骗这些致动器为一个虫豸巨细的四足呆板人提供动力，该呆板人展示了各类步态模式、标的目的节制以及22倍在其体重的有用载荷威力。这些特性使虫豸呆板人可以或许于坎坷地形以及障碍物上挪动。
▲ Abstract：
Insects perform feats of strength and endurance that belie their small stature. Insect-scale robots—although subject to the same scaling laws—demonstrate reduced performance because existing microactuator technologies are driven by low–energy density power sources and produce small forces and/or displacements. The use of high–energy density chemical fuels to power small, soft actuators represents a possible solution. We demonstrate a 325-milligram soft combustion microactuator that can achieve displacements of 140%, operate at frequencies 100 hertz, and generate forces 9.5 newtons. With these actuators, we powered an insect-scale quadrupedal robot, which demonstrated a variety of gait patterns, directional control, and a payload capacity 22 times its body weight. These features enabled locomotion through uneven terrain and over obstacles.
医学Medicine
MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease
于模仿阿尔茨海默病的人类神经元异种移动物中MEG3激活坏逝世性凋亡
▲ 作者：Sriram Balusu, Katrien Horré, Nicola Thrupp, Katleen Craessaerts, An Snellinx, Lutgarde Serneels, et al.
▲ 链接：https://www.science.org/doi/full/10.1126/science.abp9556
▲ 择要：
神经元遗失是阿尔茨海默病（AD）的一个决议性特性，但其潜于机制尚不清晰。
研究组将人类或者小鼠神经元异种移植到AD小鼠模子的年夜脑中。成果只要人类神经元显示缠结、Gallyas银染色、颗粒空泡变性（GVD）、磷酸化tau血液生物标记物以及相称年夜的神经元遗失。长非编码RNA MEG3于人类神经元中被强烈上调。这类神经元特同性长非编码RNA于AD患者中也被上调。
MEG3零丁表达足以于体外引诱人神经元坏逝世性凋亡。经由过程受体彼此作用卵白激酶1（RIPK1）、RIPK3或者混淆谱系激酶布局域样卵白（MLKL）的药理学或者基因学操作来下调MEG3以及按捺坏逝世性凋亡，可拯救异种移植人类神经元中的神经元遗失。该模子提供了潜于的AD医治要领，并展现了人类对于AD的特定易感性。
▲ Abstract：
Neuronal cell loss is a defining feature of Alzheimer’s disease (AD), but the underlying mechanisms remain unclear. We xenografted human or mouse neurons into the brain of a mouse model of AD. Only human neurons displayed tangles, Gallyas silver staining, granulovacuolar neurodegeneration (GVD), phosphorylated tau blood biomarkers, and considerable neuronal cell loss. The long noncoding RNA MEG3 was strongly up-regulated in human neurons. This neuron-specific long noncoding RNA is also up-regulated in AD patients. MEG3 expression alone was sufficient to induce necroptosis in human neurons in vitro. Down-regulation of MEG3 and inhibition of necroptosis using pharmacological or genetic manipulation of receptor-interacting protein kinase 1 (RIPK1), RIPK3, or mixed lineage kinase domain-like protein (MLKL) rescued neuronal cell loss in xenografted human neurons. This model suggests potential therapeutic approaches for AD and reveals a human-specific vulnerability to AD.
Conserved γδ T cell selection by BTNL proteins limits progression of human infla妹妹atory bowel disease
BTNL卵白守旧的γδ T细胞选择限定了人类炎症性肠病的进展
▲ 作者：Robin J. Dart, Iva Zlatareva, Pierre Vantourout, Efstathios Theodoridis, Ariella Amar, Shichina Kannambath, et al.
▲ 链接：https://www.science.org/doi/full/10.1126/science.adh0301
▲ 择要：
小鼠上皮内γδ T细胞包孕差别的构造掩护细胞，由上皮嗜丁酸卵白样（BTNL）异构体选择。
为了确定这类生物学是否于人类中守旧，研究组对于人结肠γδ T细胞区室举行了表征，确定了一个包孕共表达T细胞受体Vγ4以及上皮联合整合素CD103的表型差别亚群的多样性库。该亚群于炎症性肠病中不可比例地削减以及掉调，而医治中CD103+γδ T细胞恢复与炎症性肠病的连续减缓相干。
此外，具备种系BTNL3/BTNL8亚型的人也体现出CD103+Vγ4+细胞掉和谐缺掉，研究组确定这是穿透性克罗恩病（CD）的一个伤害要素。是以，BTNL依靠性的选择以及/或者维持差别的构造内涵γδ T细胞好像是一个进化上守旧的轴，限定了全世界病发率不停上升的繁杂、多要素、构造毁伤疾病的进展。
▲ Abstract：
Murine intraepithelial γδ T cells include distinct tissue-protective cells selected by epithelial butyrophilin-like (BTNL) heteromers. To determine whether this biology is conserved in humans, we characterized the colonic γδ T cell compartment, identifying a diverse repertoire that includes a phenotypically distinct subset coexpressing T cell receptor Vγ4 and the epithelium-binding integrin CD103. This subset was disproportionately diminished and dysregulated in infla妹妹atory bowel disease, whereas on-treatment CD103+γδ T cell restoration was associated with sustained infla妹妹atory bowel disease remission. Moreover, CD103+Vγ4+cell dysregulation and loss were also displayed by humans with germline BTNL3/BTNL8 hypomorphism, which we identified as a risk factor for penetrating Crohn’s disease (CD). Thus, BTNL-dependent selection and/or maintenance of distinct tissue-intrinsic γδ T cells appears to be an evolutionarily conserved axis limiting the progression of a complex, multifactorial, tissue-damaging disease of increasing global incidence.
植物学Zoology
Songbird species that display more-complex vocal learning are better problem-solvers and have larger brains
鸣禽发声进修威力越强，越能更好地解决问题，年夜脑也越年夜
▲ 作者：Jean-Nicolas Audet, Mélanie Couture Erich D. Jarvis
▲ 链接：https://www.science.org/doi/full/10.1126/science.adh3428
▲ 择要：
繁杂发声进修是人类白话的一个主要构成部门，始终被以为与更高级的认知威力有关。于统一物种内的个别之间对于该假定的测试尚无定论，也还没有于整个物种间举行过测试。
于这项事情中，研究组评估了23种鸟类中214只个别的一系列认知技术（即解决问题、遐想以及反向进修和自我节制），此中包孕19种野生捕捉的鸣禽、两种驯养鸣禽以及两种野生捕捉的无发声进修鸟类。
成果发明，一个物种的发声进修威力越强，其解决问题的威力就越好，年夜脑也相对于越年夜。当节制非认知变量以及体系发育时，该结论仍建立。研究成果撑持了一种假定，即鸣禽于发声进修、解决问题以及更年夜的年夜脑之间存于着配合的遗传以及认知机制。
▲ Abstract：
Complex vocal learning, a critical component of human spoken language, has been assumed to be associated with more-advanced cognitive abilities. Tests of this hypothesis between individuals within a species have been inconclusive and have not been done across species. In this work, we measured an array of cognitive skills—namely, problem-solving, associative and reversal learning, and self-control—across 214 individuals of 23 bird species, including 19 wild-caught songbird species, two domesticated songbird species, and two wild-caught vocal nonlearning species. We found�첩 that the greater the vocal learning abilities of a species, the better their problem-solving skills and the relatively larger their brains. These conclusions held when controlling for noncognitive variables and phylogeny. Our results support a hypothesis of shared genetic and cognitive mechanisms between vocal learning, problem-solving, and bigger brains in songbirds.
神经科学Neuroscience
Presynaptic Ube3a E3 ligase promotes synapse elimination through down-regulation of BMP signaling
突触前Ube3a E3毗连酶经由过程下调BMP旌旗灯号促成突触消弭
▲ 作者：Kotaro Furusawa, Kenichi Ishii, Masato Tsuji, Nagomi Tokumitsu, Eri Hasegawa Kazuo Emoto
▲ 链接：https://www.science.org/doi/full/10.1126/science.ade8978
▲ 择要：
泛素毗连酶Ube3a掉活致使发育障碍Angelman综合征，而Ube3a剂量增长与自闭症谱系障碍有关。只管Ube3a于包孕突触前的轴突结尾有富厚定位，但人们对于Ube3a的突触前功效及其突触前定位的机制知之甚少。
研究组发明发育性突触消弭需要果蝇神经元的突触前Ube3a活性，并进一步确定了Ube3a与驱动卵白马达彼此作用所必须的布局域。
Angelman综合征相干的彼此作用域错义突变削弱了Ube3a的突触前靶向并制止突触消弭。相反，突触前Ube3a活性的增长会致使早熟突触消弭并侵害突触通报。该研究成果展现了Ube3a的心理作用，并提出了与Ube3a掉调相干的潜于致病机制。
▲ Abstract：
Inactivation of the ubiquitin ligase Ube3a causes the developmental disorder Angelman syndrome, whereas increased Ube3a dosage is associated with autism spectrum disorders. Despite the enriched localization of Ube3a in the axon terminals including presynapses, little is known about the presynaptic function of Ube3a and mechanisms underlying its presynaptic localization. We show that developmental synapse elimination requires presynaptic Ube3a activity in Drosophila neurons. We further identified the domain of Ube3a that is required for its interaction with the kinesin motor. Angelman syndrome–associated missense mutations in the interaction domain attenuate presynaptic targeting of Ube3a and prevent synapse elimination. Conversely, increased Ube3a activity in presynapses leads to precocious synapse elimination and impairs synaptic transmission. Our findings reveal the physiological role of Ube3a and suggest potential pathogenic mechanisms associated with Ube3a dysregulation.
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