Camellia sinensis CsMYB4a participates in regulation of stamen growth by interaction with auxin signaling transduction repressor CsAUX/IAA4

Subgroup 4(Sg4)members of the R2R3-MYB are generally known as negative regulators of the phenylpropanoid pathway in plants.Our previous research showed that a R2R3-MYB Sg4 member from Camellia sinensis(CsMYB4a)inhibits expression of some genes in the phenylpropanoid pathway,but its physiological function in the tea plant remained unknown.Here,CsMYB4a was found to be highly expressed in anther and filaments,and participated in regulating filament growth.Transcriptome analysis and exogenous auxin treatment showed that the target of CsMYB4a might be the auxin signal pathway.Auxin/indole-3-acetic acid 4(AUX/IAA4),a repressor in auxin signal transduction,was detected from a yeast two-hybrid screen using CsMYB4a as bait.Gene silencing assays showed that both CsIAA4 and CsMYB4a regulate filament growth.Tobacco plants overexpressing CsIAA4 were insensitive to exogenous a-NAA,consistent with overexpression of CsMYB4a.Protein-protein interaction experiments revealed that CsMYB4a interacts with N-terminal of CsIAA4 to prevent CsIAA4 degradation.Knock out of the endogenous NtIAA4 gene,a CsIAA4 homolog,in tobacco alleviated filament growth inhibition and a-NAA insensitivity in plants overexpressing CsMYB4a.All results strongly suggest that CsMYB4a works synergistically with CsIAA4 and participates in regulation of the auxin pathway in stamen.

Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates inflammatory response ulcerative colitis through TLR4/NF-κB signaling pathway

BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achieving complete remission in patients with intermittent periods of activity followed by dormancy is challenging.Moreover,no study has explored the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.AIM To explore the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.METHODS This prospective clinical study included patients who met the exclusion criteria in 2020 and 2021.The patients with UC were divided into two groups(control and experimental).The peripheral blood of the experimental and control groups were collected under aseptic conditions.The expression of TLR4 protein,NF-κB,IL-6,and IL-17 was detected in the peripheral blood of patients in the experimental group and control group before and 1 month after taking the drug.Linear co rrelation analysis was used to analyze the relationship between the expression level of TLR4 protein and the expression levels of downstream signal NF-κB and inflammatory factors IL-6 and IL-17,and P<0.05 was considered statistically significant.RESULTS There were no significant differences in the patient characteristics between the control and experimental groups.The results showed that the expression levels of TLR4 and NF-κB in the experimental group were significantly lower than those in the control group(P<0.05).The levels of IL-6 and IL-17 in the experimental group were significantly lower than those in the control group(P<0.05).The TLR4 protein expression in the experimental group was positively correlated with the expression level of downstream signal NF-κB and was positively correlated with the levels of downstream inflammatory cytokines IL-6 and IL-17(r=0.823,P<0.05).CONCLUSION Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates the inflammatory response of UC through the TLR4/NF-κB signaling pathway.

Induced neural stem cells regulate microglial activation through Akt-mediated upregulation of CXCR4 and Crry in a mouse model of closed head injury

Microglial activation that occurs rapidly after closed head injury may play important and complex roles in neuroinflammation-associated neuronal damage and repair.We previously reported that induced neural stem cells can modulate the behavior of activated microglia via CXCL12/CXCR4 signaling,influencing their activation such that they can promote neurological recovery.However,the mechanism of CXCR4 upregulation in induced neural stem cells remains unclear.In this study,we found that nuclear factor-κB activation induced by closed head injury mouse serum in microglia promoted CXCL12 and tumor necrosis factor-αexpression but suppressed insulin-like growth factor-1 expression.However,recombinant complement receptor 2-conjugated Crry(CR2-Crry)reduced the effects of closed head injury mouse serum-induced nuclear factor-κB activation in microglia and the levels of activated microglia,CXCL12,and tumor necrosis factor-α.Additionally,we observed that,in response to stimulation(including stimulation by CXCL12 secreted by activated microglia),CXCR4 and Crry levels can be upregulated in induced neural stem cells via the interplay among CXCL12/CXCR4,Crry,and Akt signaling to modulate microglial activation.In agreement with these in vitro experimental results,we found that Akt activation enhanced the immunoregulatory effects of induced neural stem cell grafts on microglial activation,leading to the promotion of neurological recovery via insulin-like growth factor-1 secretion and the neuroprotective effects of induced neural stem cell grafts through CXCR4 and Crry upregulation in the injured cortices of closed head injury mice.Notably,these beneficial effects of Akt activation in induced neural stem cells were positively correlated with the therapeutic effects of induced neural stem cells on neuronal injury,cerebral edema,and neurological disorders post–closed head injury.In conclusion,our findings reveal that Akt activation may enhance the immunoregulatory effects of induced neural stem cells on microglial activation via upregulation of CXCR4 and Crry,thereby promoting induced neural stem cell–mediated improvement of neuronal injury,cerebral edema,and neurological disorders following closed head injury.

π/4-DQPSK调制的快速位同步捕获和位同步跟踪

低速率数字移动突发通信中，存在着较大的多普勒频移．本文根据π／４ＤＱＰＳＫ本身的特点，提出了一种与信号能量检测、频移初捕并行处理的位定时捕获算法，与先信号能量检测，再估计多普勒频移，然后进行位定时捕获的串行处理相比，有较明显的优越性，同时本文还给出了一种很简捷的位定时跟踪算法，并对此作了计算机仿真．

π/4-DQPSK快速位同步捕获和跟踪算法

为了在π/4-DQPSK解调中能快速实现位同步捕获和跟踪,提出将中频差分检测和同步头捕获跟踪相结合的并行处理方法,根据π/4-DQPSK本身的特点,按照π/4-DQPSK解调中的快速同步捕获和位同步跟踪改进算法,结合信号能量检测、频移初捕并行处理的位定时算法,采用FPGA(fied program grid array)技术实现π/4-DQPSK解调中的快速同步捕获和位同步跟踪。实验结果表明最快可以在8个符号位时稳定恢复时钟同步信号,具有捕获周期短,位定时准确,抗干扰能力强,不受频差影响,适合于高传输码率的跳频通信接收系统应用。

高速突发模式下π/4-DQPSK的相位捕获与跟踪

高速突发通信系统要求同步时间尽可能短,通过对一种数据辅助式快速相位捕获算法的分析,提出一种π/4-DQPSK调制信号的载波同步方案。仿真表明,当信噪比不小于8 dB时,该相位捕获算法仅需10个左右码元符号就能快速捕获载波相位。通过-π/4相位旋转运算,将π/4-DQPSK变换成DQPSK信号解调判决,能带来4 dB左右的解调增益,并可以将常用的QPSK载波跟踪环应用于π/4-DQPSK通信系统,硬件实现简单,便于系统的数字化。

π/4-DQPSK和π/4-QPSK在移动信道中的性能仿真分析

利用计算机 Monte-Carlo 仿真实验,通过与 BPSK 比较,分析了在理想高斯白噪声(AWGN)信道中,π/4-DQPSK 和相干π/4-QPSK 的抗噪声性能;同时分析了两者在多径衰落信道中的抗衰落和抗多径性能。仿真结果表明.在 AWGN 信道中,π/4-QPSK 的抗噪声性能与 BPSK 相同,但优于π/4-DQPSK 3dB;在多径衰落信道中,π/4-DQPSK 和π/4-QPSK 的抗多径衰落性能均优于 BPSK。

π/4-DQPSK调制快速位定时捕获算法的DSP实现

阐述利用一种新的π／4－DQPSK调制快速位定时捕获算法进行低速率数字移动突发通信，并利用TMSC54xDSP芯片实现该算法的关键技术。实验表明，较之常规算法，该算法能够更加有效地克服多普勒频移并快速实现位定时捕获。

π/4-DQPSK调制与解调在System View中的仿真实现

以System View为软件设计平台,在计算机辅助设计思想下,利用其与Matlab的接口功能,方便快捷地实现差分正交相移键控信号———π/4-DQPSK的调制解调,对其频谱特性、动态、静态性能和在高斯噪声信道条件下系统的抗噪声性能做了详细分析.并在相同信道条件下分析比较π/4-DQPSK和QPSK的频谱及抗噪声性能.仿真结果表明,π/4-DQPSK的频谱扩展现象优于QPSK.

用Duffing振子阵列解调微弱π/4-DQPSK信号

首次提出了微弱π/4-DQPSK信号Dumng振子阵列的解调算法,并用计算机对此算法进行了相应的仿真验证,同时还创造性地提出了星座图重叠划分,功率谱熵计算阵列和Dumng振子码元分界点搜寻器。先将π/4-DQPSK星座图的8个点划分成相重叠的四个区域,然后用功率谱熵来判定不同区域内Dumng振子的不同响应,最后依据当前时刻Duffing振子阵列的不同响应来断定所传送的数字信息。计算机仿真结果表明,本算法切实可行,在高斯信道中解调信噪比最低可达-15.6 dB。

π/4-DQPSK信号的多普勒频移快捕和跟踪

提出了一种适用于数字卫星移动突发通信系统的多普勒频移快捕和跟踪方法。该方法根据突发通信时帧结构的特点，利用独特码的调制输出进行多普勒频移的快捕，并根据π/4-DQPSK信号的特点，采用判决反馈PLL环跟踪多普勒频移的变化。仿真结果表明，采用该方法的解调器误比特率．Pb与成形滤波器的滚降系数n无关。多普勒频移在-Rs／2～Rs／2范围内变化时，对解调器的误比特率Pb没有影响。

π/4-DQPSK调制快速位定时捕获算法及其DSP实现

阐述利用一种新的π 4 -DQPSK调制快速位定时捕获算法进行低速率数字移动突发通信 ,并利用TMSC5 4xDSP芯片实现该算法的关键技术。实验表明 。

π/4-DQPSK调制技术的仿真及实现

介绍了π/4-DQPSK调制解调的基本原理,在MATLAB7.0.4中对其进行了仿真,画出了误比特率曲线;并完成了π/4-DQPSK调制器的FPGA实现,在Quartus8.0中验证了实现的正确性。

π/4-DQPSK调制解调系统的关键技术

针对π/4-DQPSK调制解调系统中成形滤波、量化误差和数字下变频中的低通滤波器等关键技术进行研究.在此基础上,对于接收端有频偏的相干解调系统采用改进的具有2个Timing Er-ror信号的Gardner位同步算法,并用simulink实现整个调制解调系统.从仿真结果可以看出,改进的Gardner同步算法能帮助系统有效地补偿频偏,并且使系统具有非常好的误码性能.

基于DDS的π/4-DQPSK调制器设计

π/4-DQPSK调制方式广泛应用于无线通信领域,而全数字合成技术应用于卫星通信和移动通信领域。简要介绍了DDS原理和π/4-DQPSK调制原理。提出了一种新颖的全数字中频π4-DQPSK调制器,该调制器采用DDS技术和先进的FPGA技术。给出了该调制器的硬件实现,并从原理上进行了必要的分析。实验结果表明:提出的设计方案能很好地实现π/4-DQPSK调制,与一般的调制器相比,具有可重新配置、灵活性好、工作更加稳定等优点。

基于MATLAB的π/4-DQPSK设计与仿真

针对移动通信信道的功率受限和频谱受限问题,π/4-DQPSK调制解调技术应运而生。该文首先分析了π/4-DQPSK信号的基本原理与实现方法;其次,设计了基于MATLAB的理想π/4-DQPSK信号的仿真程序;最后,仿真了π/4-DQPSK的调制解调过程。结果表明:该仿真方法正确可行,可供其它程序方便调用,为硬件的设计与研制提供一定的参考作用。

一种基于CPLD的π/4-DQPSK调制器的设计与实现

根据π/4-DQPSK信号的特点,对它的调制实现方法进行了研究.在研究的基础上,提出了一种用VHDL语言设计实现π/4-DQPSK调制器的设计方案.详细叙述了其工作原理及设计思想,用复杂可编程逻辑器件CPLD实现了映射编码和逻辑选相,在D/A转换器等配合下实现了π/4-DQPSK调制并给出了用复杂可编程逻辑器件CPLD实现部分的仿真波形.

π/4-DQPSK信号的判决反馈差分检测

π/4-DQPSK是一种比较适合在移动通信中使用的调制方式,传统的差分检测方法误码率比QPSK相干解调恶化大约2.3dB,利用判决反馈的信号估计出参考信号,对π/4DQPSK信号进行多码元差分检测。该方法与传统的检测方法相比,不需要增加乘法运算,易于工程实现。计算机仿真结果表明在高斯信道中,相对于传统的差分检测方法,无频率偏移时,判决反馈多码元差分检测方法在误码率为10-4时,性能改善大约1.6dB;剩余频率偏移值为符号速率的0.5%时,性能改善约1dB。

全数字π/4-DQPSK调制的FPGA设计

本文根据软件无线电思想,介绍全数字π/4-DQPSK调制原理,并基于XILINX公司的ISE开发平台,采用Spar-tan-Ⅱ系列芯片详细给出编程实现π/4-DQPSK调制的全过程,实现时输入码率200Kbps,中频455KHz。基于可动态配置的FPGA的实现只需通过软件对其参数进行简单设置,就可完成对不同数据传输率、不同载波频率的π/4-DQPSK调制。

实现π/4-DQPSK调制的一种快速算法

针对π/4-DQPSK调制数字化实现的运算量大、高速调制难的问题,提出了一种适合于数字调制的快速算法。该算法基于TMS320C54xDSP处理器,应用查找表的方法完成π/4-DQPSK的差分编码与符号映射,应用波形存储的方法完成I、Q通道的成形滤波,用选通直读的方法实现载波调制,整个调制过程中不需要乘法运算,节约了调制时间。仿真结果验证了该方法的有效性。