Positron Emission Tomography Lung Image Respiratory Motion Correcting with Equivariant Transformer

In addressing the challenge of motion artifacts in Positron Emission Tomography (PET) lung scans, our studyintroduces the Triple Equivariant Motion Transformer (TEMT), an innovative, unsupervised, deep-learningbasedframework for efficient respiratory motion correction in PET imaging. Unlike traditional techniques,which segment PET data into bins throughout a respiratory cycle and often face issues such as inefficiency andoveremphasis on certain artifacts, TEMT employs Convolutional Neural Networks (CNNs) for effective featureextraction and motion decomposition.TEMT’s unique approach involves transforming motion sequences into Liegroup domains to highlight fundamental motion patterns, coupled with employing competitive weighting forprecise target deformation field generation. Our empirical evaluations confirm TEMT’s superior performancein handling diverse PET lung datasets compared to existing image registration networks. Experimental resultsdemonstrate that TEMT achieved Dice indices of 91.40%, 85.41%, 79.78%, and 72.16% on simulated geometricphantom data, lung voxel phantom data, cardiopulmonary voxel phantom data, and clinical data, respectively. Tofacilitate further research and practical application, the TEMT framework, along with its implementation detailsand part of the simulation data, is made publicly accessible at https://github.com/yehaowei/temt.

基于生物信息学分析探索PCDHGB4在肺鳞癌发生中的作用

背景与目的 肺鳞状细胞癌(lung squamous cell carcinoma,LUSC)是非小细胞肺癌(non-small cell lung cancer,NSCLC)的亚型之一。有报道原钙黏蛋白γ家族的成员能通过抑制Wnt信号通路来调节肿瘤细胞的生长,原钙黏蛋白γ B4 (protocadherin-gamma subfamily B4,PCDHGB4)作为家族成员在LUSC中的研究少有报道,本研究旨在通过生物信息学方法探究PCDHGB4在LUSC发生发展中的作用及潜在的预后价值。方法应用癌症基因组图谱(The Cancer Genome Atlas,TCGA)、cBioPortal和UALCAN等数据库,对PCDHGB4在LUSC中的表达与预后、临床病理特征、免疫细胞浸润、免疫调节基因、免疫检查点抑制剂(immune checkpoint inhibitors,ICIs)和甲基转移酶等进行分析。单细胞水平的研究对细胞亚型的聚类结果和PCDHGB4在不同免疫细胞亚群中的表达情况进行了分析。此外,我们还比较了LUSC组织与正常组织中PCDHGB4的启动子甲基化水平,并对其进行了蛋白质-蛋白质相互作用和突变分析。最后基于差异表达基因进行富集分析。结果生信分析结果显示PCDHGB4在LUSC组织的表达水平低于正常组织。生存分析显示,PCDHGB4表达增加与患者较差的预后有关。单细胞分析显示,PCDHGB4主要在T细胞、单核细胞或巨噬细胞以及树突状细胞中表达,进一步发现PCDHGB4在肿瘤免疫中发挥着不可忽视的作用,并证实了PCDHGB4与免疫检查点途径基因、免疫调节基因和甲基转移酶有一定的相关性。此外,通过富集分析发现PCDHGB4参与了癌症相关的多条通路。结论PCDHGB4在LUSC中低表达,PCDHGB4与患者预后不良有关,并且PCDHGB4与肿瘤免疫细胞浸润和通路密切相关。PCDHGB4可能是LUSC潜在的预后标志物和免疫治疗新靶点。

Improving thermal efficiency and stability of laser welding process for magnesium alloy by combining power modulation and subatmospheric pressure environment

The laser welding(LW)process of highly reflective materials presents low thermal efficiency and poor stability.To solve the problem,the effects of subatmospheric environment on LW process,technological parameters in subatmospheric environment on weld formation and welding with sinusoidal modulation of laser power on the stability of LW process in subatmospheric environment were explored.The AZ31magnesium(Mg)alloy was used as the test materials.The test result revealed that the weld penetration in subatmospheric environment can increase by more than ten times compared with that under normal pressure.After the keyhole depth greatly rises,significantly periodic local bulge is observed on the backwall surface of the keyhole and the position of the bulge shifts along the direction of the keyhole depth.Eventually,the hump-shaped surface morphology of the welded seam is formed;moreover,the weld width in local zones in the lower part of the welded seam remarkably grows.During LW in subatmospheric environment,the weld penetration can be further greatly increased through power modulation.Besides,power modulation can inhibit the occurrence of bulges in local zones on the backwall of the keyhole during LW in subatmospheric environment,thus further curbing the significant growth of the weld widths of hump-shaped welding beads and local zones in the lower part of welded seams.Finally,the mechanism of synchronously improving the thermal efficiency and stability of LW process of highly reflective materials through power modulation in subatmospheric environment was illustrated.This was conducted according to theoretical analysis of recoil pressure and observation results of dynamic behaviors of laser induced plasma clouds and keyholes in the molten pool through high speed photography.

METTL3 regulates glucose transporter expression in placenta exposed to hyperglycemia through the mTOR signaling pathway

Background:Alterations in the placental expression of glucose transporters(GLUTs),the crucial maternal-fetal nutrient transporters,have been found in women with hyperglycemia in pregnancy(HIP).However,there is still uncertainty about the underlying effect of the high-glucose environment on placental GLUTs expression in HIP.Methods:We quantitatively evaluated the activity of mammalian target of rapamycin(mTOR)and expression of GLUTs(GLUT1,GLUT3,and GLUT4)in the placenta of women with normal pregnancies(CTRL,n=12)and pregnant women complicated with poorly controlled type 2 diabetes mellitus(T2DM,n=12)by immunohistochemistry.In addition,BeWo cells were treated with different glucose concentrations to verify the regulation of hyperglycemia.Then,changes in the expression of GLUTs following the activation or suppression of the mTOR pathway were also assessed using MHY1485/rapamycin(RAPA)treatment or small interfering RNA(siRNA)-mediated silencing approaches.Moreover,we further explored the alteration and potential upstream regulatory role of methyltransferase-like 3(METTL3)when exposed to hyperglycemia.Results:mTOR,phosphorylated mTOR(p-mTOR),and GLUT1 protein levels were upregulated in the placenta of women with T2DM compared with those CTRL.In BeWo cells,mTOR activity increased with increasing glucose concentration,and the expression of GLUT1,GLUT3,and GLUT4 as well as GLUT1 cell membrane translocation were upregulated by hyperglycemia to varying degrees.Both the drug-mediated and genetic depletion of mTOR signaling in BeWo cells suppressed GLUTs expression,whereas MHY1485-induced mTOR activation upregulated GLUTs expression.Additionally,high glucose levels upregulated METTL3 expression and nuclear translocation,and decreasing METTL3 levels suppressed GLUTs expression and mTOR activity and vice versa.Furthermore,in METTL3 knockdown BeWo cells,the inhibitory effect on GLUTs expression was eliminated by activating the mTOR signaling pathway using MHY1485.Conclusion:High-glucose environment-induced upregulation of METTL3 in trophoblasts regulates the expression of GLUTs through mTOR signaling,contributing to disordered nutrient transport in women with HIP.

circRNAs deregulation in exosomes derived from BEAS-2B cells is associated with vascular stiffness induced by PM_(2.5)

As an environmental pollutant,ambient fine particulate matter (PM_(2.5)) was linked to cardiovascular diseases.The molecular mechanisms underlying PM_(2.5)-induced extrapulmonary disease has not been elucidated clearly.In this study the ambient PM_(2.5)exposure mice model we established was to explore adverse effects of vessel and potential mechanisms.Long-term PM_(2.5)exposure caused reduced lung function and vascular stiffness in mice.And chronic PM_(2.5)induced migration and epithelial-mesenchymal transition (EMT) phenotype in BEAS-2B cells.After PM_(2.5)treatment,the circRNAs and mRNAs levels of exosomes released by BEAS-2B cells were detected by competing endogenous RNA (ceRNA) array,which contained 1664 differentially expressed circRNAs (DE-circRNAs) and 308 differentially expressed m RNAs (DE-mRNAs).By bioinformatics analysis on host genes of DE-circRNAs,vascular diseases and some pathways related to vascular diseases including focal adhesion,tight junction and adherens junction were enriched.Then,ceRNA network was constructed,and DE-mRNAs in ceRNA network were conducted functional enrichment analysis by Ingenuity Pathway Analysis,which indicated that hsa_circ_0012627,hsa_circ_0053261and hsa_circ_0052810 were related to vascular endothelial dysfunction.Furthermore,it was verified experimentally that Exo^(PM2.5)could induce endothelial dysfunction by increased endothelial permeability and decreased relaxation in vitro.In present study,we investigated in-depth knowledge into the molecule events related to PM_(2.5) toxicity and pathogenesis of vascular diseases.

Catalase promotes whitefly adaptation to high temperature by eliminating reactive oxygen species

Thermal stress usually leads to excessive production of reactive oxygen species(ROS)in all aerobic organisms.Catalases(CAT)are the key antioxidant enzymes,which act as the first line of defense against ROS in the antioxidant pathway.The highly invasive and widely distributed whitefly Bemisia tabaci MED damages plants by feeding as well as by transmitting many plant viruses.Previous studies have shown that strong adaptability to high temperature helps explain the spread of MED around the world.However,the mechanism underlying high temperature adaptation of this pest is not well understood.In this study,6 CAT genes were identified from the MED genome and transcriptome dataset,among which BtCAT1,BtCAT2,and BtCAT3 were found to be highly expressed in adults.The expression of BtCAT1,BtCAT2,or BtCAT3 increased with induction temperature and induction time.The MED was exposed with mean high temperature(30℃ or 35℃)and a short-term extremely high temperature(39℃ or 41℃)after the silencing of BtCAT1,BtCAT2,or BtCAT3 to significantly increased ROS levels by at least 0.5 times and significantly decreased survival rate and fecundity of MED adults.The ROS level in the treated specimens gradually returned to a normal level after 24 h at 25℃,but the survival rate still declined significantly.Taken together,our results demonstrate that CAT could help B.tabaci adapt to long-term mean high temperatures and short-term extremely high temperatures by eliminating excessive ROS.