Radar Signal Intra-Pulse Modulation Recognition Based on Deep Residual Network

In view of low recognition rate of complex radar intra-pulse modulation signal type by traditional methods under low signal-to-noise ratio(SNR),the paper proposes an automatic recog-nition method of complex radar intra-pulse modulation signal type based on deep residual network.The basic principle of the recognition method is to obtain the transformation relationship between the time and frequency of complex radar intra-pulse modulation signal through short-time Fourier transform(STFT),and then design an appropriate deep residual network to extract the features of the time-frequency map and complete a variety of complex intra-pulse modulation signal type recognition.In addition,in order to improve the generalization ability of the proposed method,label smoothing and L2 regularization are introduced.The simulation results show that the proposed method has a recognition accuracy of more than 95%for complex radar intra-pulse modulation sig-nal types under low SNR(2 dB).

Pravastatin alleviates lipopolysaccharide-induced placental TLR4 over-activation and promotes uterine arteriole remodeling without impairing rat fetal development

Preeclampsia is associated with over-activation of the innate immune system in the placenta,in which toll-like receptor 4（TLR4） plays an essential part.With their potent anti-inflammatory effects,statins have been suggested as potential prevention or treatment of preeclampsia,although evidence remains inadequate.Herewith,we investigated whether pravastatin could ameliorate preeclampsia-like phenotypes in a previously established lipopolysaccharide（LPS）-induced rat preeclampsia model,through targeting the TLR4/NF-κB pathway.The results showed that pravastatin reduced the blood pressure [maximum decline on gestational day（GD） 12,（101.33±2.49） mmHg vs.（118.3±1.37） mmHg,P〈0.05] and urine protein level [maximum decline on GD9,（3,726.23± 1,572.86） μg vs.（1,991.03 ±609.37）μg,P〈 0.05],which were elevated following LPS administration.Pravastatin also significantly reduced the rate of fetal growth restriction in LPS-treated rats（34.10% vs.8.99%,P〈0.05）.Further pathological analyses suggested a restoration of normal spiral artery remodeling in preeclampsia rats by pravastatin treatment.These effects of pravastatin were associated with decreased TLR4/NF-κB protein levels in the placenta and IL-6/MCP-1 levels in serum.Additionally,no obvious abnormalities in fetal liver,brain,and kidney were found after administration of pravastatin.These results provide supportive evidence for use of pravastatin in preventing preeclampsia.

Upregulation of CD81 in trophoblasts induces an imbalance of Treg/Th17 cells by promoting IL-6 expression in preeclampsia

The disturbance of maternal immune tolerance to a semiallogeneic fetus is recognized as one of the key pathologies of preeclampsia(PE),in which an imbalance between the inflammation-limiting regulatory T cells(Tregs)and the inflammationmediating Th17 cells plays an essential role.Previously,we reported that the abnormal upregulation of tetraspannin CD81 in trophoblast cells(fetal component)participated in the pathogenesis of PE.However,as one of the potential immune regulatory molecules,whether CD81 induces PE by interfering with the balance of the maternal immune system has not yet been clarified.Thus,we investigated the relationship between the upregulation of CD81 in trophoblast cells and the imbalance of Treg and Th17 cells in mothers.Here,we demonstrated that upregulation of CD81 in trophoblast cells was accompanied by a decrease in Treg cells and an increase in Th17 cells in both the basal plate(placental maternal side)and peripheral blood of patients with PE.In vitro culture of naïve T cells with medium from the CD81-overexpressing trophoblast cell line HTR-8 resulted in enhanced differentiation of T cells into Th17 cells and decreased the formation of Tregs,which was dependent on the paracrine signaling of IL-6 in trophocytes,induced by CD81.In a CD81-induced PE rat model,we found a significant shift of T cell differentiation towards Th17 cells,and administration of IL-6 antibody mitigated the PE phenotype and the imbalance of the Treg/Th17 cells.These results define a vital regulatory cascade involving trophocyte-derived CD81,IL-6,and maternal Treg/Th17 cells in the pathogenesis of PE and suggests new therapeutic approaches based on CD81 and IL-6 downregulation to prevent human PE.

Placenta-derived IL-32β activates neutrophils to promote preeclampsia development

Immune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia(PE).Neutrophils(PMNs)are activated in PE patients,but the mechanism and consequences of PMN activation need to be further explored.Here,we demonstrated that interleukin-32(IL-32)expression was significantly upregulated in syncytiotrophoblasts(STBs)and that IL-32β was the major isoform with increased expression in the placenta of severe PE(sPE)patients.Furthermore,the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients,indicating that IL-32 in the serum is derived mainly from the placenta.Then,in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells(HUVECs)and enhance the expression of vascular cell adhesion molecule-1(VCAM-1)and intercellular cell adhesion molecule-1(ICAM-1)in HUVECs,which could be reversed by preincubation with the NADPH oxidase inhibitor VAS 2870.In addition,we showed that IL-32β mainly activated PMNs by binding to proteinase 3.Finally,IL-32β administration induced a PE-like phenotype in a pregnant mouse model.This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.