PoWRKY71 is involved in Paeonia ostii resistance to drought stress by directly regulating light-harvesting chlorophyll a/b-binding 151 gene

Although the functions of WRKY transcription factors in drought resistance are well known,their regulatory mechanisms in response to drought by stabilising photosynthesis remain unclear.Here,a differentially expressed PoWRKY71 gene that was highly expressed in drought-treated Paeonia ostii leaves was identified through transcriptome analysis.PoWRKY71 positively responded to drought stress with significantly enhanced expression patterns and overexpressing PoWRKY71 in tobacco greatly improved plant tolerance to drought stress,whereas silencing PoWRKY71 in P.ostii resulted in a drought-intolerant phenotype.Furthermore,lower chlorophyll contents,photosynthesis,and inhibited expression of photosynthesis-related light-harvesting chlorophyll a/b-binding 151(CAB151)gene were found in PoWRKY71-silenced P.ostii.Meanwhile,a homologous system indicated that drought treatment increased PoCAB151 promoter activity.Interactive assays revealed that PoWRKY71 directly bound on the W-box element of PoCAB151 promoter and activated its transcription.In addition,PoCAB151 overexpressing plants demonstrated increased drought tolerance,together with significantly higher chlorophyll contents and photosynthesis,whereas these indices were dramatically lower in PoCAB151-silenced P.ostii.The above results indicated that PoWRKY71 activated the expression of PoCAB151,thus stabilising photosynthesis via regulating chloroplast homeostasis and chlorophyll content in P.ostii under drought stress.This study reveals a novel drought-resistancemechanism in plants and provides a feasible strategy for improving plant drought resistance via stabilising photosynthesis.

155例鎖骨骨折的手術治療

目的分析本院10年來收治155例鎖骨骨折的手術治療情況。方法本院從1993年2月-2002年12月十年期間收治鎖骨骨折363例,其中155例採用手術治療;分析其療效。結果男:女=126:29;年齡9~78歲-19-40歲佔97例。左:右:雙側=63:89:3。其發病原因以直接碰傷爲主(108例)。其中交通傷(49例)爲主要損傷原因。新鮮骨折151例,陳舊骨折祗有4例。粉碎性骨折較多,有114例,單純骨折41例:骨折部位分成内:中:外(三段)爲0:145:9(次)。手術治療以克氏針内固定爲主(153例),其中118例加鋼絲結紮粉碎骨片。改進入釘方向,使保留在皮下的釘尾,留在鎖骨的胸骨端皮下,避免病人在側臥時碰撞留在鎖骨的肩胛骨端釘尾產生不舒服感覺。術後除一例感染外,其餘無感染,153例先後回院複查,均能骨性癒合,拆除内固定材料。未發現有不連接者。結論鎖骨骨折是一種常見的創傷性疾病,其發生的主要原因爲直接碰傷-以交通意外爲主。骨折好發在中1/3段。克氏針加鋼絲結紮粉碎骨片是首選的手術治療方法。

进入纠错量子时代

In the past few decades,control and engineering technologies have experienced rapid development in various quantum computation platforms,from the realization of single-qubit gates to the implementation of high-quality two-qubit gates,and from the fabrication of a few physical qubits to the integration,calibration,and control of exceeding 50 physical qubits on a single chip.We have arrived at the noisy intermediate-scale quantum(NISQ)era[1],in which quantum systems with 50–100 noisy physical qubits can show superiority over classical systems in some applications,although the performance is limited by operation errors.In addition to finding valuable applications,another parallel and critical task is to scale up the system dimension and optimize the parameters to realize quantum error correction(QEC)to suppress errors.Recent experiments[2–5]on QEC reveal that we are entering the error-corrected quantum(ECQ)era.In this paper,we are going to introduce these advancements and summarize the challenges in this era as shown in Fig.1.

Potentiating CD8^(+) T cell antitumor activity by inhibiting PCSK9 to promote LDLR-mediated TCR recycling and signaling

Metabolic regulation has been proven to play a critical role in T cell antitumor immunity.However,cholesterol metabolism as a key component of this regulation remains largely unexplored.Herein,we found that the low-density lipoprotein receptor(LDLR),which has been previously identified as a transporter for cholesterol,plays a pivotal role in regulating CD8+T cell antitumor activity.Besides the involvement of cholesterol uptake which is mediated by LDLR in T cell priming and clonal expansion,we also found a non-canonical function of LDLR in CD8+T cells:LDLR interacts with the T-cell receptor(TCR)complex and regulates TCR recycling and signaling,thus facilitating the effector function of cytotoxic T-lymphocytes(CTLs).Furthermore,we found that the tumor microenvironment(TME)downregulates CD8+T cell LDLR level and TCR signaling via tumor cell-derived proprotein convertase subtilisin/kexin type 9(PCSK9)which binds to LDLR and prevents the recycling of LDLR and TCR to the plasma membrane thus inhibits the effector function of CTLs.Moreover,genetic deletion or pharmacological inhibition of PCSK9 in tumor cells can enhance the antitumor activity of CD8+T cells by alleviating the suppressive effect on CD8+T cells and consequently inhibit tumor progression.While previously established as a hypercholesterolemia target,this study highlights PCSK9/LDLR as a potential target for cancer immunotherapy as well.

具有增强计算效率和收敛性的多分辨率非线性拓扑优化

高昂的计算成本和算法收敛困难是非线性拓扑优化的两大核心难题.为此,基于多分辨率设计策略和附加超弹性技术,提出了一种考虑几何非线性和材料非线性的多分辨率非线性拓扑优化方法.在固体各向同性材料惩罚方法框架中建立多分辨率非线性拓扑优化策略,并采用Neo-Hookean超弹性材料本构模型表征材料非线性.利用粗糙的分析网格用于有限元计算,而精细的材料网格用于描述材料构型.为了解决算法非线性收敛问题和降低灵敏度计算复杂度,联合ANSYS软件与附加超弹性技术进行非线性有限元计算.在灵敏度分析过程中,提出了一种应变能重分配策略,将Neo-Hooken和二阶Yeoh超弹性分析单元的应变能转换为对应的材料单元应变能.数值算例表明了所提出方法的三个显著优点:(1)可显著提高计算效率;(2)进一步弥补了基于附加超弹性技术的非线性拓扑优化方法在解决非线性拓扑优化问题时所遇到的收敛困难,该效果在三维问题中更为显著;(3)可在个人计算机上成功处理高分辨率三维复杂非线性拓扑优化问题.

Correction to:Potentiating CD8^(+)T cell antitumor activity by inhibiting PCSK9 to promote LDLR-mediated TCR recycling and signaling

Figure 1.LDLR deficiency hinders the antitumor activity of CD8^(+)T cells.(A)Transcriptional level of genes involved in cholesterol transport in naïve CD8^(+)T cells,CTLs and CD8^(+)TILs(isolated at Day3 or Day7 post CTLs adoptive transfer),(n=4).(B)LDLR expression level on CTLs and CD8^(+)TILs(isolated at Day3 post CTLs adoptive transfer),(n=4).