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Feature Matching via Topology-Aware Graph Interaction Model

IEEE/CAA Journal of Automatica Sinica 2024年第1期11卷 113-130页

作者： Yifan lu Jiayi Ma Xiaoguang mei jun Huang Xiao-Ping Zhang the Electronic Information School Wuhan UniversityWuhan 430072China IEEE Tsinghua Berkeley Shenzhen Institute Shenzhen 518071China the Department of Electrical Computer and Biomedical EngineeringToronto Metropolitan UniversityToronto ON M5B 2K3Canada

Feature matching plays a key role in computer vision. However, due to the limitations of the descriptors, the putative matches are inevitably contaminated by massive outliers.This paper attempts to tackle the outlier filtering problem from two aspects. First, a robust and efficient graph interaction model,is proposed, with the assumption that matches are correlated with each other rather than independently distributed. To this end, we construct a graph based on the local relationships of matches and formulate the outlier filtering task as a binary labeling energy minimization problem, where the pairwise term encodes the interaction between matches. We further show that this formulation can be solved globally by graph cut algorithm. Our new formulation always improves the performance of previous localitybased method without noticeable deterioration in processing time,adding a few milliseconds. Second, to construct a better graph structure, a robust and geometrically meaningful topology-aware relationship is developed to capture the topology relationship between matches. The two components in sum lead to topology interaction matching(TIM), an effective and efficient method for outlier filtering. Extensive experiments on several large and diverse datasets for multiple vision tasks including general feature matching, as well as relative pose estimation, homography and fundamental matrix estimation, loop-closure detection, and multi-modal image matching, demonstrate that our TIM is more competitive than current state-of-the-art methods, in terms of generality, efficiency, and effectiveness. The source code is publicly available at http://***/Yifanlu2000/TIM.

关键词： Feature matching graph cut outlier filtering topology preserving

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Clinical characteristics of delayed generalized erythema associated with cytarabine

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Chronic Diseases and Translational Medicine 2024年第1期10卷 78-80页

作者： He Jiang jun lu mei Wang College of Pharmacy Anhui University of Chinese MedicineHefeiAnhuiChina Department of Pharmacy Children's Hospital of Soochow UniversitySuzhouJiangsuChina

To the Editor,Cytarabine is one of the most used drugs for the treatment of hematological malignancies such as leukemia and non-Hodgkin's lymphoma.In cells,cytarabine is activated into ara-CTP,which can replace deoxycytidine triphosphate(dCTP)and become incorporated into the DNA of proliferating cells.Thus,it can block DNA synthesis,resulting in proliferation arrest and cell death.

关键词： death drugs Clinical

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Ubiquitin-specific protease 21 promotes tumorigenicity and stemness of colorectal cancer by deubiquitinating and stabilizing ZEB1

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World Journal of Gastrointestinal Oncology 2024年第3期16卷 1006-1018页

作者： jun-jun Lin Ye-Cai lu Department of Gastrointestinal Surgery Chaohu Hospital of Anhui Medical UniversityChaohu 238000Anhui ProvinceChina

BACKGROUND Colorectal cancer(CRC)is one very usual tumor together with higher death rate.Ubiquitin-specific protease 21(USP21)has been confirmed to take part into the regulation of CRC progression through serving as a facilitator.Interestingly,the promotive function of USP21 has also discovered in the progression of CRC.ZEB1 has illustrated to be modulated by USP7,USP22 and USP51 in cancers.However,the regulatory functions of USP21 on ZEB1 in CRC progression need more invest-igations.AIM To investigate the relationship between USP21 and ZEB1 in CRC progression.METHODS The mRNA and protein expressions were assessed through RT-qPCR,western blot and IHC assay.The interaction between USP21 and ZEB1 was evaluated through Co-IP and GST pull down assays.The cell proliferation was detected through colony formation assay.The cell migration and invasion abilities were determined through Transwell assay.The stemness was tested through sphere formation assay.The tumor growth was evaluated through in vivo mice assay.RESULTS In this work,USP21 and ZEB1 exhibited higher expression in CRC,and resulted into poor prognosis.Moreover,the interaction between USP21 and ZEB1 was further investigated.It was demonstrated that USP21 contributed to the stability of ZEB1 through modulating ubiquitination level.In addition,USP21 streng-thened cell proliferation,migration and stemness through regulating ZEB1.At last,through in vivo assays,it was illustrated that USP21/ZEB1 axis aggravated tumor growth.CONCluSION For the first time,these above findings manifested that USP21 promoted tumorigenicity and stemness of CRC by deubiquitinating and stabilizing ZEB1.This discovery suggested that USP21/ZEB1 axis may provide novel sights for the treatment of CRC.

关键词： Ubiquitin-specific protease 21 ZEB1 Stemness Colorectal cancer

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Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage

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Neural Regeneration Research 2024年第1期19卷 161-170页

作者： Guoqiang Zhang Jianan lu Jingwei Zheng Shuhao mei Huaming Li Xiaotao Zhang An Ping Shiqi Gao Yuanjian Fang jun Yu Department of Neurosurgery The Second Affiliated Hospital of Zhejiang University School of MedicineHangzhouZhejiang ProvinceChina Department of Neurosurgery Huashan Hospital of Fudan University School of MedicineShanghaiChina Clinical Research Center for Neurological Diseases of Zhejiang Province HangzhouZhejiang ProvinceChina Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases HangzhouZhejiang ProvinceChina

Preclinical and clinical studies have shown that microglia and macrophages participate in a multiphasic brain damage repair process following intracerebral hemorrhage.The E26 transformation-specific sequence-related transcription factor Spi1 regulates microglial/macrophage commitment and maturation.However,the effect of Spi1 on intracerebral hemorrhage remains unclear.In this study,we found that Spi1 may regulate recovery from the neuroinflammation and neurofunctional damage caused by intracerebral hemorrhage by modulating the microglial/macrophage transcriptome.We showed that high Spi1expression in microglia/macrophages after intracerebral hemorrhage is associated with the activation of many pathways that promote phagocytosis,glycolysis,and autophagy,as well as debris clearance and sustained remyelination.Notably,microglia with higher levels of Soil expression were chara cterized by activation of pathways associated with a variety of hemorrhage-related cellular processes,such as complement activation,angiogenesis,and coagulation.In conclusion,our results suggest that Spi1 plays a vital role in the microglial/macrophage inflammatory response following intracerebral hemorrhage.This new insight into the regulation of Spi1 and its target genes may advance our understanding of neuroinflammation in intracerebral hemorrhage and provide therapeutic targets for patients with intracerebral hemorrhage.

关键词： intracerebral hemorrhage macrophage microglia neuroinflammation phagocytosis PI3K/AKT/mTOR signaling pathway Spi1 transcriptomics

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Protein Kinase C Controls the Excitability of Cortical Pyramidal Neurons by Regulating Kv2.2 Channel Activity

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Neuroscience Bulletin 2022年第2期38卷 135-148页

作者： Zhaoyang Li Wenhao Dong Xinyuan Zhang jun-mei lu Yan-Ai mei Changlong Hu State Key Laboratory of Medical Neurobiology Institutes of Brain Science and School of Life SciencesFudan UniversityShanghai 200438China

The family of voltage-gated potassium Kv2 channels consists of the Kv2.1 and Kv2.2 subtypes.Kv2.1 is constitutively highly phosphorylated in neurons and its function relies on its phosphorylation state.Whether the function of Kv2.2 is also dependent on its phosphorylation state remains unknown.Here,we investigated whether Kv2.2 channels can be phosphorylated by protein kinase C(PKC)and examined the effects of PKC-induced phosphorylation on their activity and function.Activation of PKC inhibited Kv2.2 currents and altered their steadystate activation in HEK293 cells.Point mutations and specific antibodies against phosphorylated S481 or S488 demonstrated the importance of these residues for the PKC-dependent modulation of Kv2.2.In layer Ⅱ pyramidal neurons in cortical slices,activation of PKC similarly regulated native Kv2.2 channels and simultaneously reduced the frequency of action potentials.In conclusion,this study provides the first evidence to our knowledge that PKC-induced phosphorylation of the Kv2.2 channel controls the excitability of cortical pyramidal neurons.

关键词： Kv2.2 PKC Phosphorylation Pyramidal neurons Excitability

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Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/m TOR Signaling Pathway

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Chinese Journal of Integrative Medicine 2024年第3期30卷 251-259页

作者： YAO jun-peng FENG Xiu-mei WANG lu LI Yan-qiu ZHU Zi-yue YAN Xiang-yun YANG Yu-qing LI Ying ZHANG Wei Acupuncture and Tuina School Chengdu University of Traditional Chinese MedicineChengdu611137China Department of Rehabilitation Medicine Guanghan People’s HospitalGuanghanSichuan Province618399China Academic Affairs Office Chengdu University of Traditional Chinese MedicineChengdu611137China

Objective:To explore the mechanism of electroacupuncture(EA) in promoting recovery of the facial function with the involvement of autophagy,glial cell line-derived neurotrophic factor(GDNF),and phosphatidylinositol-3-kinase(PI3K)/mammalian target of rapamycin(mTOR) signaling pathway.Methods:Seventy-two male Sprague-Dawley rats were randomly allocated into the control,sham-operated,facial nerve injury(FNI),EA,EA+3-methyladenine(3-MA),and EA+GDNF antagonist groups using a random number table,with 12 rats in each group.An FNI rat model was established with facial nerve crushing method.EA intervention was conducted at Dicang(ST 4),Jiache(ST 6),Yifeng(SJ 17),and Hegu(LI 4) acupoints for 2 weeks.The Simone’s 10-Point Scale was utilized to monitor the recovery of facial function.The histopathological evaluation of facial nerves was performed using hematoxylin-eosin(HE) staining.The levels of Beclin-1,light chain 3(LC3),and P62 were detected by immunohistochemistry(IHC),immunofluorescence,and reverse transcriptionpolymerase chain reaction,respectively.Additionally,IHC was also used to detect the levels of GDNF,Rai,PI3K,and mTOR.Results:The facial functional scores were significantly increased in the EA group than the FNI group(Plusions:EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI.EA may exert this neuroreparative effect through mediating the release of GDNF,activating the PI3

关键词： electroacupuncture facial nerve injury autophagy glial cell line-derived neurotrophic factor phosphatidylinositol-3-kinase/mammalian target of rapamycin Chinese medicine

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Photocatalytic reduction of CO_(2) with H_(2)O into C_(2)H_(6) mediated by dual metalation strategy

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Science China Chemistry 2024年第5期67卷 1381-1383页

作者： mei Wang Tong-Bu lu School of Materials Science and Engineering Institute for New Energy Materials&Low Carbon TechnologiesTianjin University of TechnologyTianjin 300384China

Artificial solar-energy-driven CO_(2) reduction into value-added fuels under mild conditions provides a promising strategy to mitigate energy crisis and alleviate environmental issues around the world. Among diverse products of CO_(2) reduction reaction, C_(2+) compounds are more desirable in terms of their high energy density and commercial value [1].Thus far, various photocatalysts have been constructed for CO_(2) reduction.

关键词： reduction desirable value

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Effect of short neuropeptide F signaling on larval feeding in Mythimna separata

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Insect Science 2024年第2期31卷 417-434页

作者： mei-mei Li Qi Yang Li-Hui Chen Yan-Ying Li jun-Xiang Wu Xiang-Li Xu State Key Laboratory of Crop Stress Biology in Arid Areas College of Plant ProtectionNorthwest A&F UniversityYanglingShaanxi ProvinceChinaand School of Agricultural Sciences Jiangxi Agricultural UniversityNanchangChina

Mythimna separata is a notorious phytophagous pest which poses serious threats to cereal crops owing to the gluttony of the larvae.Because short neuropeptide F(sNPF)and its receptor sNPFR are involved in a diversity of physiological functions,especially in functions related to feeding in insects,it is a molecular target for pest control.Herein,an sNPF and 2 sNPFRs were identified and cloned from M.separata.Bioinformatics analysis revealed that the sNPF and its receptors had a highly conserved RLRFamide C-terminus and 7 transmembrane domains,respectively.The sNPF and its receptor genes were distributed across larval periods and tissues,but 2 receptors had distinct expression patterns.The starvation-induced assay elucidated that sNPF and sNPFR expression levels were downregulated under food deprivation and recovered with subsequent re-feeding.RNA interference knockdown of sNPF,sNPFR1,and sNPFR2 by injection of double-stranded RNA into larvae not only suppressed food consumption and increased body size and weight,but also led to decrease of glycogen and total lipid contents,and increase of trehalose compared with double-stranded green fluorescent protein injection.Furthermore,molecular docking was performed on the interaction mode between sNPFR protein and its ligand sNPF based on the 3-dimensional models constructed by AlphaFold;the results indicated that both receptors were presumably activated by the mature peptide sNPF-2.These results revealed that sNPF signaling played a considerably vital role in the feeding regulation of M.separata and represents a potential control target for this pest.

关键词： feeding regulation Mythimna separata pest control target RNA interference short neuropeptide F sNPF receptors

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Recent progress of in-situ characterization of LiNi_(1−x−y)Co_(x)Mn_(y)O_(2) cathodes for lithium metal batteries: A mini review

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Nano Research 2024年第3期17卷 1384-1401页

作者： Huanzhu Lv Xiaoqi Zhu jun mei Yuanhua Xia Bin Wang Institute of Fundamental and Frontier Science University of Electronic Science and Technology of ChinaChengdu 611731China Chengdu Development Center of Science and Technology China Academy of Engineering PhysicsChengdu 610200China Key Laboratory of Neutron Physics and Institute of Nuclear Physics and Chemistry China Academy of Engineering Physics(CAEP)Mianyang 621999China

In the context of the gradual popularity of electric vehicles(EVs),the development of lithium battery systems with high energy density and power density is regarded as the foremost way to improve the range of EVs.LiNi_(1-x-y)Co_(x)Mn_(y)O_(2)(NCM)cathodes have been the focus of researchers due to their high energy density,excellent power performance,and low-temperature resistance.However,the elaboration of the decay mechanism of NCM cathode based on lithium metal batteries(LMBs)is still being restricted to the primary level.In the past decades,the development and application of advanced in-situ characterization tools have facilitated researchers'understanding of the internal operation mechanism of batteries during charging and discharging.In this minireview,the latest progress of in-situ observation of the NCM cathode by X-ray diffraction(XRD),fourier transform infrared(FT-IR)spectroscopy,Raman spectroscopy,atomic force microscopy(AFM),transmission electron microscope(TEM),optical microscope,and other characterization tools is summarized.The mechanisms of structural degradation,cathode-electrolyte interfaces(CEIs)composition,and dynamic changes of NCM,electrolyte breakdown,and gas production are elaborated.Finally,based on the existing research progress,the opportunities and challenges for future in-situ characterization technology in the study of the mechanism of LMBs are discussed in depth.Therefore,the purpose of this minireview is to summarize recent work that focuses on the outstanding application of in-situ characterization techniques in the mechanistic study of LMBs,and pointing the way to the future development of high energy density and power density LMBs systems.

关键词： lithium metal batteries(LMBs) In-situ characterization LiNi_(1-x-y)Co_(x)Mn_(y)O_(2)(NCM)

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KAT7/HMGN1 signaling epigenetically induces tyrosine phosphorylation-regulated kinase 1A expression to ameliorate insulin resistance in Alzheimer’s disease

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World Journal of Psychiatry 2024年第3期14卷 445-455页

作者： Qun-Shan lu Lin Ma Wen-Jing Jiang Xing-Bang Wang mei lu Department of Geriatric Medicine Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina Key Laboratory of Cardiovascular Proteomics of Shandong Province Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina

BACKGROUND Epidemiological studies have revealed a correlation between Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2D).Insulin resistance in the brain is a common feature in patients with T2D and AD.KAT7 is a histone acetyltransferase that participates in the modulation of various genes.AIM To determine the effects of KAT7 on insulin patients with AD.METHODS APPswe/PS1-dE9 double-transgenic and db/db mice were used to mimic AD and diabetes,respectively.An in vitro model of AD was established by Aβstimulation.Insulin resistance was induced by chronic stimulation with high insulin levels.The expression of microtubule-associated protein 2(MAP2)was assessed using immunofluorescence.The protein levels of MAP2,Aβ,dual-specificity tyrosine phosphorylation-regulated kinase-1A(DYRK1A),IRS-1,p-AKT,total AKT,p-GSK3β,total GSK3β,DYRK1A,and KAT7 were measured via western blotting.Accumulation of reactive oxygen species(ROS),malondialdehyde(MDA),and SOD activity was measured to determine cellular oxidative stress.Flow cytometry and CCK-8 assay were performed to evaluate neuronal cell death and proliferation,respectively.Relative RNA levels of KAT7 and DYRK1A were examined using quantitative PCR.A chromatin immunoprecipitation assay was conducted to detect H3K14ac in DYRK1A.RESULTS KAT7 expression was suppressed in the AD mice.Overexpression of KAT7 decreased Aβaccumulation and MAP2 expression in AD brains.KAT7 overexpression decreased ROS and MDA levels,elevated SOD activity in brain tissues and neurons,and simultaneously suppressed neuronal apoptosis.KAT7 upregulated levels of p-AKT and p-GSK3βto alleviate insulin resistance,along with elevated expression of DYRK1A.KAT7 depletion suppressed DYRK1A expression and impaired H3K14ac of DYRK1A.HMGN1 overexpression recovered DYRK1A levels and reversed insulin resistance caused by KAT7 depletion.CONCluSION We determined that KAT7 overexpression recovered insulin sensitivity in AD by recruiting HMGN1 to enhance DYRK1A acetylation.Our findings suggest that KAT7 is a novel and

关键词： Alzheimer's disease Diabetes Insulin resistance KAT7 Dual-specificity tyrosine phosphorylation-regulated kinase-1A HMGN1

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