基于PAM-RTM的CFRP平板RTM工艺及孔隙缺陷仿真

树脂传递模塑(RTM)成型过程中不同工艺参数对碳纤维增强树脂基复合材料(CFRP)构件质量和性能有极大影响。为了精准设计RTM成型参数,降低最终构件的孔隙缺陷含量,分析充模过程中两种尺度孔隙率的变化及在构件中的分布规律,基于PAM-RTM软件对CFRP平板模型RTM成型的充模及双尺度孔隙形成进行了仿真模拟。分析了不同树脂黏度、浇注压力对填充时间及宏观和微观孔隙分布、孔隙率的影响规律;在构件中选取了不同位置的横向轴线并对比轴上宏观/微观孔隙的含量及分布特征,分析随着距离浇注口位置变化孔隙率的变化规律。结果表明,在恒压浇注条件下,浇注压力越大,树脂黏度越小,填充时间越短;树脂黏度为0.1Pa·s、浇注压力为1.5MPa时,充模时间最小,为13.11s。宏观孔隙率随浇注压力升高而减小,微观孔隙率则相反。宏观孔隙在开始填充一段时间后形成,孔隙率最终在出胶口达到最大值;微观孔隙则在填充初始阶段开始形成,孔隙率随着填充距离增加逐渐减小。3条横向轴上两种尺度孔隙率的变化趋势相近;浇注压力影响宏观孔隙开始形成的位置及微观孔隙结束形成的位置,并影响填充结束时的最大宏观孔隙率和填充开始时的最大微观孔隙率。

Atherosis-associated lnc_000048 activates PKR to enhance STAT1-mediated polarization of THP-1 macrophages to M1 phenotype

Our previous study has demonstrated that lnc_000048 is upregulated in large-artery atherosclerotic stroke and promotes atherosclerosis in ApoE^(-/-)mice.However,little is known about the role of lnc_000048 in classically activated macrophage(M1)polarization.In this study,we established THP-1-derived testing state macrophages(M0),M1 macrophages,and alternately activated macrophages(M2).Real-time fluorescence quantitative PCR was used to verify the expression of marker genes and the expression of lnc_000048 in macrophages.Flow cytometry was used to detect phenotypic proteins(CD11b,CD38,CD80).We generated cell lines with lentivirus-mediated upregulation or downregulation of lnc_000048.Flow cytometry,western blot,and real-time fluorescence quantitative PCR results showed that down-regulation of lnc_000048 reduced M1 macrophage polarization and the inflammation response,while over-expression of lnc_000048 led to the opposite effect.Western blot results indicated that lnc_000048 enhanced the activation of the STAT1 pathway and mediated the M1 macrophage polarization.Moreover,catRAPID prediction,RNA-pull down,and mass spectrometry were used to identify and screen the protein kinase RNA-activated(PKR),then catRAPID and RPIseq were used to predict the binding ability of lnc_000048 to PKR.Immunofluorescence(IF)-RNA fluorescence in situ hybridization(FISH)double labeling was performed to verify the subcellular colocalization of lnc_000048 and PKR in the cytoplasm of M1 macrophage.We speculate that lnc_000048 may form stem-loop structure-specific binding and activate PKR by inducing its phosphorylation,leading to activation of STAT1 phosphorylation and thereby enhancing STAT1 pathway-mediated polarization of THP-1 macrophages to M1 and inflammatory factor expression.Taken together,these results reveal that the lnc_000048/PKR/STAT1 axis plays a crucial role in the polarization of M1 macrophages and may be a novel therapeutic target for atherosclerosis alleviation in stroke.

一种面向112 Gb/s PAM4接收机的自适应均衡设计方案

提出了一种适用于超短距离(Very Short Reach,VSR)信道、面向112 Gb/s PAM4(Pulse Amplitude Modulation 4)接收机的自适应均衡设计方案。在该方案中,接收机前端利用3个连续时间线性均衡器(Continuous Time Linear Equalizer,CTLE)对信号分别在高频、中频和低频进行补偿,可变增益放大器(Variable Gain Amplifier,VGA)和饱和放大器(Saturation Amplifier,SatAmp)则用于对信号幅值的缩放。除了3个数据采样器外,引入4个辅助采样器用于进一步改善阈值自适应算法性能。同时,采用符号最小均方算法,利用接收端数据采样器和辅助采样器之间的偏移推动辅助参考电压收敛到信号星座电平,从而确保PAM4接收信号的眼图在垂直方向上3个眼睛具有相等的间隔和恒定的信噪比(Signal-to-Noise Ratio,SNR)。仿真结果表明,所提出的112 Gb/s PAM4接收机能够在损耗为15 dB的信道上实现小于10~(-12)的误码率,并且具有良好的眼图性能,其最差眼高为75 mV,眼宽为0.34 UI(Unit Interval),与传统方案相比具有显著的性能提升。

Neutrophil peptide 1 accelerates the clearance of degenerative axons during Wallerian degeneration by activating macrophages after peripheral nerve crush injury

Macrophages play an important role in peripheral nerve regeneration,but the specific mechanism of regeneration is still unclear.Our preliminary findings indicated that neutrophil peptide 1 is an innate immune peptide closely involved in peripheral nerve regeneration.However,the mechanism by which neutrophil peptide 1 enhances nerve regeneration remains unclear.This study was designed to investigate the relationship between neutrophil peptide 1 and macrophages in vivo and in vitro in peripheral nerve crush injury.The functions of RAW 264.7 cells we re elucidated by Cell Counting Kit-8 assay,flow cytometry,migration assays,phagocytosis assays,immunohistochemistry and enzyme-linked immunosorbent assay.Axonal debris phagocytosis was observed using the CUBIC(Clear,Unobstructed Brain/Body Imaging Cocktails and Computational analysis)optical clearing technique during Wallerian degeneration.Macrophage inflammatory factor expression in different polarization states was detected using a protein chip.The results showed that neutrophil peptide 1 promoted the prolife ration,migration and phagocytosis of macrophages,and CD206 expression on the surfa ce of macrophages,indicating M2 polarization.The axonal debris clearance rate during Wallerian degeneration was enhanced after neutrophil peptide 1 intervention.Neutrophil peptide 1 also downregulated inflammatory factors interleukin-1α,-6,-12,and tumor necrosis factor-αin invo and in vitro.Thus,the results suggest that neutrophil peptide 1 activates macrophages and accelerates Wallerian degeneration,which may be one mechanism by which neutrophil peptide 1 enhances peripheral nerve regeneration.

基于PAM聚类的轨道交通站点画像分析

文章基于多源数据融合方法,从客流水平、居民需求、接驳特性、周边设施4个维度对轨道站点特征进行提取与构建。采用PAM算法对站点进行聚类研究,最终形成6类站点画像的标签。在此基础上探索站点功能定位、客流模式之间的内在关系,梳理不同类型站点在城市化进程中面临的阶段性矛盾,指导客流预测任务、引流策略制定等后续工作。

The heterogeneity of tumor-associated macrophages and strategies to target it

Tumor-associated macrophages(TAMs)are emerging as targets for tumor therapy because of their primary role in promoting tumor progression.Several studies have been conducted to target TAMs by reducing their infiltration,depleting their numbers,and reversing their phenotypes to suppress tumor progression,leading to the development of drugs in preclinical and clinical trials.However,the heterogeneous characteristics of TAMs,including their ontogenetic and functional heterogeneity,limit their targeting.Therefore,in-depth exploration of the heterogeneity of TAMs,combined with immune checkpoint therapy or other therapeutic modalities could improve the efficiency of tumor treatment.This review focuses on the heterogeneous ontogeny and function of TAMs,as well as the current development of tumor therapies targeting TAMs and combination strategies.

Global trends in publications regarding macrophages-related diabetic foot ulcers in the last two decades

BACKGROUND Diabetic foot ulcers(DFUs)are one of the most severe and popular complications of diabetes.The persistent non-healing of DFUs is the leading cause of amputation,which causes significant mental and financial stress to patients and their families.Macrophages are critical cells in wound healing and perform essential roles in all phases of wound healing.However,no studies have been carried out to systematically illustrate this area from a scientometric point of view.Although there have been some bibliometric studies on diabetes,reports focusing on the investigation of macrophages in DFUs are lacking.AIM To perform a bibliometric analysis to systematically assess the current state of research on macrophage-related DFUs.METHODS The publications of macrophage-related DFUs from January 1,2004,to December 31,2023,were retrieved from the Web of Science Core Collection on January 9,2024.Four different analytical tools:VOSviewer(v1.6.19),CiteSpace(v6.2.R4),HistCite(v12.03.07),and Excel 2021 were used for the scientometric research.RESULTS A total of 330 articles on macrophage-related DFUs were retrieved.The most published countries,institutions,journals,and authors in this field were China,Shanghai Jiao Tong University of China,Wound Repair and Regeneration,and Aristidis Veves.Through the analysis of keyword co-occurrence networks,historical direct citation networks,thematic maps,and trend topics maps,we synthesized the prevailing research hotspots and emerging trends in this field.CONCLUSION Our bibliometric analysis provides a comprehensive overview of macrophage-related DFUs research and insights into promising upcoming research.

SWIR FluorescenceImaging In Vivo Monitoring and Evaluating Implanted M2 Macrophages in Skeletal Muscle Regeneration

Skeletal muscle has a robust regeneration ability that is impaired by severe injury,disease,and aging.resulting in a decline in skeletal muscle function.Therefore,improving skeletal muscle regeneration is a key challenge in treating skeletal muscle-related disorders.Owing to their significant role in tissue regeneration,implantation of M2 macrophages(M2MФ)has great potential for improving skeletal muscle regeneration.Here,we present a short-wave infrared(SWIR)fluorescence imaging technique to obtain more in vivo information for an in-depth evaluation of the skeletal muscle regeneration effect after M2MФtransplantation.SWIR fluorescence imaging was employed to track implanted M2MФin the injured skeletal muscle of mouse models.It is found that the implanted M2MФaccumulated at the injury site for two weeks.Then,SWIR fluorescence imaging of blood vessels showed that M2MФimplantation could improve the relative perfusion ratio on day 5(1.09±0.09 vs 0.85±0.05;p=0.01)and day 9(1.38±0.16 vs 0.95±0.03;p=0.01)post-injury,as well as augment the degree of skeletal muscle regencration on day 13 post-injury.Finally,multiple linear regression analyses determined that post-injury time and relative perfusion ratio could be used as predictive indicators to evaluate skeletal muscle regeneration.These results provide more in vivo details about M2MФin skeletal muscle regeneration and confirm that M2MФcould promote angiogenesis and improve the degree of skeletal muscle repair,which will guide the research and development of M2MФimplantation to improve skeletal muscle regeneration.

Sulfated Cyclocarya paliurus polysaccharides exert immunomodulatory potential on macrophages via Toll-like receptor 4 mediated MAPK/NF-κB signaling pathways

The biological activity of plant polysaccharides can be enhanced by sulfated modification.In this study,the immunomodulatory effect of sulfated Cyclocarya paliurus polysaccharides(SCP3)on macrophages RAW264.7 and its potential molecular mechanism were investigated.Results showed that SCP3 at 25-100μg/m L increased viability and improved phagocytosis of RAW264.7 cells.Meanwhile,SCP3 could activate mitogen-activated protein kinase(MAPK)and nuclear factor kappa B(NF-κB)signaling pathways,which increased the phosphorylation of Erk1/2,JNK,p38 and NF-κB p65,promoting secretion of cytokines tumor necrosis factorα(TNF-α),interleukin 6(IL-6)and nitric oxide(NO)as well as the production of reactive oxygen species(ROS).In addition,Toll-like receptor 4(TLR4)receptor inhibitors were able to block the production of NO and TNF-αby SCP3-stimulated macrophages.Based on Western blot analysis and validation using specific inhibitors against MAPK and NF-κB signaling pathways,the results demonstrated that SCP3 induced macrophages activation and enhanced TNF-αand NO production via TLR4-mediated MAPK and NF-κB pathways.In summary,SCP3 has significant immunomodulatory potential.The underlying molecular mechanism was that SCP3 activates macrophages via TLR4 receptors to promote ROS production,which in turn activates the downstream MAPK/NF-κB signaling pathway and then increases the secretion levels of cytokines and NO.

Fasudil-modified macrophages reduce inflammation and regulate the immune response in experimental autoimmune encephalomyelitis

Multiple sclerosis is characterized by demyelination and neuronal loss caused by inflammatory cell activation and infiltration into the central nervous system.Macrophage polarization plays an important role in the pathogenesis of experimental autoimmune encephalomyelitis,a traditional experimental model of multiple sclerosis.This study investigated the effect of Fasudil on macrophages and examined the therapeutic potential of Fasudil-modified macrophages in experimental autoimmune encephalomyelitis.We found that Fasudil induced the conversion of macrophages from the pro-inflammatory M1 type to the anti-inflammatory M2 type,as shown by reduced expression of inducible nitric oxide synthase/nitric oxide,interleukin-12,and CD16/32 and increased expression of arginase-1,interleukin-10,CD14,and CD206,which was linked to inhibition of Rho kinase activity,decreased expression of toll-like receptors,nuclear factor-κB,and components of the mitogen-activated protein kinase signaling pathway,and generation of the pro-inflammatory cytokines tumor necrosis factor-α,interleukin-1β,and interleukin-6.Crucially,Fasudil-modified macrophages effectively decreased the impact of experimental autoimmune encephalomyelitis,resulting in later onset of disease,lower symptom scores,less weight loss,and reduced demyelination compared with unmodified macrophages.In addition,Fasudil-modified macrophages decreased interleukin-17 expression on CD4^(+)T cells and CD16/32,inducible nitric oxide synthase,and interleukin-12 expression on F4/80^(+)macrophages,as well as increasing interleukin-10 expression on CD4^(+)T cells and arginase-1,CD206,and interleukin-10 expression on F4/80^(+)macrophages,which improved immune regulation and reduced inflammation.These findings suggest that Fasudil-modified macrophages may help treat experimental autoimmune encephalomyelitis by inducing M2 macrophage polarization and inhibiting the inflammatory response,thereby providing new insight into cell immunotherapy for multiple sclerosis.

Effect of tubastatin A on NLRP3 inflammasome activation in macrophages under hypoxia/ reoxygenation conditions

BACKGROUND:There are currently no effective drugs to mitigate the ischemia/reperfusion injury caused by fluid resuscitation after hemorrhagic shock(HS).The aim of this study was to explore the potential of the histone deacetylase 6(HDAC6)-specific inhibitor tubastatin A(TubA)to suppress nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome activation in macrophages under hypoxia/reoxygenation(H/R)conditions.METHODS:The viability of RAW264.7 cells subjected to H/R after treatment with different concentrations of TubA was assessed using a cell-counting kit-8(CCK8)assay.Briefly,2.5μmol/L TubA was used with RAW264.7 cells under H/R condition.RAW264.7 cells were divided into three groups,namely the control,H/R,and TubA groups.The levels of reactive oxygen species(ROS)in the cells were detected using fluorescence microscopy.The protein expression of HDAC6,heat shock protein 90(Hsp90),inducible nitric oxide synthase(iNOS),NLRP3,gasdermin-D(GSDMD),Caspase-1,GSDMD-N,and Caspase-1 p20 was detected by western blotting.The levels of interleukin-1β(IL-1β)and IL-18 in the supernatants were detected using enzyme-linked immunosorbent assay(ELISA).RESULTS:HDAC6,Hsp90,and iNOS expression levels were significantly higher(P<0.01)in the H/R group than in the control group,but lower in the TubA group than in the H/R group(P<0.05).When comparing the H/R group to the control group,ROS levels were significantly higher(P<0.01),but significantly reduced in the TubA group(P<0.05).The H/R group had higher NLRP3,GSDMD,Caspase-1,GSDMD-N,and Caspase-1 p20 expression levels than the control group(P<0.05),however,the TubA group had significantly lower expression levels than the H/R group(P<0.05).IL-1βand IL-18 levels in the supernatants were significantly higher in the H/R group compared to the control group(P<0.01),but significantly lower in the TubA group compared to the H/R group(P<0.01).CONCLUSION:TubA inhibited the expression of HDAC6,Hsp90,and iNOS in macrophages subjected to H/R.This inhibition led to a decrease in the content of ROS in cells,which subsequently inhibited the activation of the NLRP3 inflammasome and the secretion of IL-1βand IL-18.

Interactions between myoblasts and macrophages under high glucose milieus result in inflammatory response and impaired insulin sensitivity

BACKGROUND Skeletal muscle handles about 80% of insulin-stimulated glucose uptake and become the major organ occurring insulin resistance(IR).Many studies have confirmed the interactions between macrophages and skeletal muscle regulated the inflammation and regeneration of skeletal muscle.However,despite of the decades of research,whether macrophages infiltration and polarization in skeletal muscle under high glucose(HG)milieus results in the development of IR is yet to be elucidated.C2C12 myoblasts are well-established and excellent model to study myogenic regulation and its responses to stimulation.Further exploration of macrophages'role in myoblasts IR and the dynamics of their infiltration and polarization is warranted.AIM To evaluate interactions between myoblasts and macrophages under HG,and its effects on inflammation and IR in skeletal muscle.METHODS We detected the polarization status of macrophages infiltrated to skeletal muscles of IR mice by hematoxylin and eosin and immunohistochemical staining.Then,we developed an in vitro co-culture system to study the interactions between myoblasts and macrophages under HG milieus.The effects of myoblasts on macrophages were explored through morphological observation,CCK-8 assay,Flow Cytometry,and enzyme-linked immunosorbent assay.The mediation of macrophages to myogenesis and insulin sensitivity were detected by morphological observation,CCK-8 assay,Immunofluorescence,and 2-NBDG assay.RESULTS The F4/80 and co-localization of F4/80 and CD86 increased,and the myofiber size decreased in IR group(P<0.01,g=6.26).Compared to Mc group,F4/80+CD86+CD206-cells,tumor necrosis factor-α(TNFα),inerleukin-1β(IL-1β)and IL-6 decreased,and IL-10 increased in McM group(P<0.01,g>0.8).In McM+HG group,F4/80+CD86+CD206-cells,monocyte chemoattractant protein 1,TNFα,IL-1βand IL-6 were increased,and F4/80+CD206+CD86-cells and IL-10 were decreased compared with Mc+HG group and McM group(P<0.01,g>0.8).Compered to M group,myotube area,myotube number and E-MHC were increased in MMc group(P<0.01,g>0.8).In MMc+HG group,myotube area,myotube number,E-MHC,GLUT4 and glucose uptake were decreased compared with M+HG group and MMc group(P<0.01,g>0.8).CONCLUSION Interactions between myoblasts and macrophages under HG milieus results in inflammation and IR,which support that the macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR.

Interplay between mesenchymal stem cells and macrophages:Promoting bone tissue repair

The repair of bone tissue damage is a complex process that is well-orchestrated in time and space,a focus and difficulty in orthopedic treatment.In recent years,the success of mesenchymal stem cells(MSCs)-mediated bone repair in clinical trials of large-area bone defects and bone necrosis has made it a candidate in bone tissue repair engineering and regenerative medicine.MSCs are closely related to macrophages.On one hand,MSCs regulate the immune regulatory function by influencing macrophages proliferation,infiltration,and phenotype polarization,while also affecting the osteoclasts differentiation of macrophages.On the other hand,macrophages activate MSCs and mediate the multilineage differentiation of MSCs by regulating the immune microenvironment.The cross-talk between MSCs and macrophages plays a crucial role in regulating the immune system and in promoting tissue regeneration.Making full use of the relationship between MSCs and macrophages will enhance the efficacy of MSCs therapy in bone tissue repair,and will also provide a reference for further application of MSCs in other diseases.

Effects of interleukin-10 treated macrophages on bone marrow mesenchymal stem cells via signal transducer and activator of transcription 3 pathway

BACKGROUND Alveolar bone defects caused by inflammation are an urgent issue in oral implant surgery that must be solved.Regulating the various phenotypes of macrophages to enhance the inflammatory environment can significantly affect the progression of diseases and tissue engineering repair process.AIM To assess the influence of interleukin-10(IL-10)on the osteogenic differentiation of bone marrow mesenchymal stem cells(BMSCs)following their interaction with macrophages in an inflammatory environment.METHODS IL-10 modulates the differentiation of peritoneal macrophages in Wistar rats in an inflammatory environment.In this study,we investigated its impact on the proliferation,migration,and osteogenesis of BMSCs.The expression levels of signal transducer and activator of transcription 3(STAT3)and its activated form,phos-phorylated-STAT3,were examined in IL-10-stimulated macrophages.Subsequently,a specific STAT3 signaling inhibitor was used to impede STAT3 signal activation to further investigate the role of STAT3 signaling.RESULTS IL-10-stimulated macrophages underwent polarization to the M2 type through substitution,and these M2 macrophages actively facilitated the osteogenic differentiation of BMSCs.Mechanistically,STAT3 signaling plays a crucial role in the process by which IL-10 influences macrophages.Specifically,IL-10 stimulated the activation of the STAT3 signaling pathway and reduced the macrophage inflammatory response,as evidenced by its diminished impact on the osteogenic differentiation of BMSCs.CONCLUSION Stimulating macrophages with IL-10 proved effective in improving the inflammatory environment and promoting the osteogenic differentiation of BMSCs.The IL-10/STAT3 signaling pathway has emerged as a key regulator in the macrophage-mediated control of BMSCs’osteogenic differentiation.

80 Gbit/s PAM4光接收机低噪声模拟前端电路设计

采用UMC 28 nm CMOS工艺,设计了一款应用于光接收机、工作在80 Gbit/s PAM4的低噪声模拟前端电路(AFE)。对噪声和带宽进行折中设计,采用了跨阻放大器(TIA)级联连续时间线性均衡器(CTLE)技术和输入电感峰化技术。为了更好地控制低频增益,进一步拓展带宽,采用了跨导跨阻(g_(m)-TIA)结构的VGA。在输入电容100 fF和供电电压1.2 V下,实现的跨阻增益为48.5 dBΩ,带宽为36.1 GHz,平均等效输入噪声电流为22.6pA/√Hz,功耗为14.5 mW。

基于45 nm SOI CMOS的56 Gbit/s PAM-4光接收机前端设计

在光接收电路设计中,光电二极管的寄生电容以及大的输入电阻会导致接收机带宽下降,造成严重的符号间干扰(Inter-Symbol Interference,ISI)。噪声性能是高速跨阻放大器(Transimpedance Amplifier,TIA)最重要的指标之一,跨阻值决定系统的噪声性能,同时也限制了数据速率。针对100G/400G互补金属氧化物半导体(Complementary Metal Oxide Semiconductor,CMOS)光接收机应用,基于45 nm绝缘衬底上的硅(Silicon-On-Insulator,SOI)工艺设计了一种采用四电平脉冲幅度调制(4-level Pulse Amplitude Modulation,PAM-4)、工作速率为56 Gbit/s(28 Gbaud/s)的低噪声光接收机前端放大器。小带宽TIA和用于带宽拓展的跨导/跨导(g_(m)/g_(m))放大器组成两级接收前端,在改善噪声性能的同时有效提高了带宽。采用反相器结构来增大先进CMOS工艺下的跨导和改善线性度。可变增益放大器(Variable Gain Amplifier,VGA)采用折叠Gilbert结构设计,采用并联峰化电感来提高带宽。整体电路的增益动态范围为51.6~70.6 dB,-3 dB带宽达到20.1 GHz;等效输入噪声电流密度为17.3 pA=Hz^(12);电路采用GF 45 nm SOI CMOS工艺实现,在1.1 V和1.3 V电源电压下功耗为65 mW;版图核心面积为600μm*240μm。

PAM对不同雨强下黑土区土质堤防侵蚀的影响

[目的]探究不同浓度PAM的防侵蚀效果,进而为东北黑土区土质堤防治理提供理论依据。[方法]采用人工模拟降雨试验,共设置2个降雨强度(60,90 mm/h),5个PAM浓度(0,2,3,4,5 g/m^(2)),观察不同雨强下PAM对坡面产流产沙、坡面侵蚀特征的影响,分析了各侵蚀形态下的水力学参数。[结果](1)在同一PAM浓度下,坡面平均产流率、平均产沙率随雨强的增大而增大。(2)在两个雨强下,平均产流率存在拐点,3 g/m^(2)的平均产流率最小;平均产沙率随着PAM浓度的增长而降低,5 g/m^(2)平均产沙率最小。(3)降雨强度60 mm/h,坡面的侵蚀形态主要表现为溅蚀和面蚀;降雨强度90 mm/h,坡面侵蚀特征表现为面蚀,部分伴有细沟侵蚀。(4)雷诺数(Re)小于500,均为层流,弗罗德数(Fr)小于1,属于缓流。降雨强度对水流剪切力、水流功率和单位水流功率的影响均大于PAM浓度。[结论]东北黑土区坡面施加PAM,可有效改良土壤结构,土壤水分入渗能力增强,减少了坡面侵蚀产沙,对于土质堤防侵蚀防治起到了一定的效果。

200 Gbit/s PAM4光发射组件封装技术研究

针对200 Gbit/s PAM4光收发模块的设计需求,提出了一种基于四阶脉冲幅度调制(PAM4)、数据传输速率达200 Gbit/s的光发射组件封装方案。该封装内部集成了4路PAM4电/光转换通道,单通道数据传输速率为50 Gbit/s。介绍了该200 Gbit/s PAM4光发射组件的组成和技术难点,然后对其中的50 Gbit/s数据传输通道进行了建模、仿真和优化,最后完成了样品的测试。测试结果表明:样品的单通道PAM4数据速率可达50 Gbit/s,整体PAM4数据速率可达200 Gbit/s,满足光收发模块的设计需求。

基于PAM-SSD-LSTM的短期风速预测

为提高短期风速预测的准确性,提出一种基于PAM聚类、奇异谱分解(SSD)和LSTM神经网络的组合预测模型来预测短期风速,以解决上述问题。首先,为提高神经网络的学习效率,采用PAM算法对原始风速数据进行相似日聚类;其次,SSD具有抑制模态混叠和虚假分量产生的优点,使用SSD分解风速序列,提取多尺度规律;最后,由于LSTM神经网络捕捉长时间依赖的序列的波动规律的能力较强,使用LSTM神经网络对分解后的风速分量进行预测,将各分量预测值叠加得到最终预测结果。实验结果表明,基于PAM-SSD-LSTM的组合预测模型可有效提高风速短期预测的准确率。

不同盐碱胁迫条件下PAM施用深度对藜麦生长及产量的影响

以‘陇藜4号’为试验材料,采用根管土柱栽培的方式,研究了不同程度盐碱胁迫(S1:轻度盐碱胁迫;S2:中度盐碱胁迫;S3:重度盐碱胁迫)条件下土壤调理剂PAM施用深度(PAM_(0-10):距地表0~10 cm;PAM_(10-20):距地表10~20 cm;PAM_(20-30):距地表20~30 cm;PAM_(0-30):距地表0~30 cm)对藜麦根系生长、叶片渗透调节物质含量、植株生物量及产量的影响。结果表明:在PAM施用深度为0~10 cm时,轻度盐胁迫处理藜麦的根长、生物量及产量指标较对照组(S0:不加入盐碱和PAM)分别高出35.71%、15.48%和4.60%,表明藜麦具有较强的耐盐能力。当盐碱胁迫增加到一定程度(S2和S3处理)时,藜麦的形态指标有显著下降趋势,与对照组处理相比重度盐胁迫藜麦的根长、生物量下降幅度最大,平均分别下降了53.72%和62.99%,但在同等重度盐碱胁迫程度时,PAM_(0-10)处理能够缓解盐碱对藜麦生长产生的胁迫作用,与对照组相比藜麦的根长和生物量分别降低了39.31%和45.42%。综合各项指标,盐碱胁迫条件下不同PAM施用方式对藜麦各生长指标的影响均表现为表层集中施用(PAM_(0-10))处理的效果最佳(P<0.05)。隶属函数分析显示,不同处理对藜麦生长的缓解程度表现为:S1>S2>S3,PAM_(0-10)>PAM_(0-30)>PAM_(10-20)>PAM_(20-30),说明在实际栽培过程中采用表层(0~10 cm)集中施用PAM的方式对盐碱胁迫下藜麦生长的缓解效果最为明显。