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mA reader YTHDF2 governs the onset of atrial fibrillation by modulating Cacna1. translation

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Science China Life Sciences 2024年

作者： Chuansheng Chen Guanghua Wang Qicheng Zou Ke Xiong Zhiwen Chen Beihua Shao Yi Liu Duanyang Xie Yong Ji Key Laboratory of Cardiovascular and Cerebrovascular medicine Nanjing Medical University State Key Laboratory of Cardiovascular Diseases Shanghai East Hospital School of Medicine Tongji University Department of Pathology and Pathophysiology School of Medicine Tongji University Department of Cardiology School of Medicine Tongji University Shanghai Arrhythmia Research Center Shanghai East Hospital School of Medicine Tongji University

Atrial fibrillation（AF） is the most common arrhythmia, which is tightly associated with the abnormal expression and function of ion channels in the atrial cardiomyocytes. N6-methyladenosine（m6A）, a widespread chemical modification in eukaryotic m RNA, is known to play a significant regulatory role in the pathogenesis of heart disease. However, the significance of m6A regulatory proteins in the onset of AF remains unclear. Here, we demonstrate that the m6A reader protein YTHDF2 regulates atrial electrical remodeling and AF onset by modulating the Cav1.2 expression. Firstly, YTHDF2 expression was selectively upregulated in rat atrial cardiomyocytes with AF. Secondly,YTHDF2 knockout reduced AF susceptibility in mice. Thirdly, the knockout of YTHDF2 increased Cav1.2 protein levels in an m6A-independent manner, ultimately prolonging the atrial myocardial refractory period, a critical electrophysiological substrate for the onset of AF. Fourthly, the N-terminal domain of YTHDF2 was identified as critical for Cacna1. m RNA translation regulation. Overall, our findings unveil that YTHDF2 can alter Cav1.2 protein expression in an m6A-independent manner, thereby facilitating the onset of AF. Our study suggests that YTHDF2 may be a potential intervention target for AF.

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CS-FSCL decoding algorithm of polar codes based on critical sets

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Optoelectronics Letters 2024年第7期20卷 418-423页

作者： YUAN Jianguo ZHANG Fengguo HE Jingjie PANG Yu school of Optoelectronic Engineering Chongqing University of Posts and TelecommunicationsChongqing 400065China1

In order to reduce the number of redundant candidate codewords generated by the fast successive cancellation list(FSCL)decoding algorithm for polar codes,a simplified FSCL decoding algorithm based on critical sets(CS-FSCL)of polar codes is *** algorithm utilizes the number of information bits belonging to the CS in the special nodes,such as Rate-1.node,repetition(REP)node and single-parity-check(SPC)node,to constrain the number of the path splitting and avoid the generation of unnecessary candidate codewords,and thus the latency and computational complexity are ***,the algorithm only flips the bits corresponding to the smaller log-likelihood ratio(LLR)values to generate the sub-maximum likelihood(sub-ML)decoding codewords and ensure the decoding *** results show that for polar codes with the code length of 1.24,the code rates of 1.4,1.2 and 3/4,the proposed CS-FSCL algorithm,compared with the conventional FSCL decoding algorithm,can achieve the same decoding performance,but reduce the latency and computational complexity at different list ***,under the list size of L=8,the code rates of R=1.2 and R=1.4,the latency is reduced by 33%and 1.%and the computational complexity is reduced by 55%and 50%,respectively.

关键词： algorithm FSC critical

Heme oxygenase 1.mediated ferroptosis in Kupffer cells initiates liver injury during heat stroke

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Acta Pharmaceutica Sinica B 2024年第9期14卷 3983-4000页

作者： Ru Li Riqing Wei Chenxin Liu Keying Zhang Sixiao He Zhifeng Liu Junhao Huang Youyong Tang Qiyuan An Ligen Lin Lishe Gan Liying Zhao Xiaoming Zou Fudi Wang Yuan Ping Qiang Ma The Seventh Affiliated Hospital Southern Medical UniversityFoshan 528244China Department of Biopharmaceutics School of Laboratory Medicine and BiotechnologySouthern Medical UniversityGuangzhou 510000China Medical Critical Care medicine General Hospital of Southern Theatre Command of PLAGuangzhou 510000China Guangdong Branch Center National Clinical Research Center for Geriatric Diseases(Chinese PLA General Hospital)Guangzhou 510000China State Key Laboratory of Quality Research in Chinese medicine Institute of Chinese Medical SciencesUniversity of MacaoAvenida da UniversidadeTaip1Macao 999078China school of Pharmaceutical Sciences Zhejiang Chinese Medical UniversityHangzhou 311402China Department of General Surgery Nanfang Hospitalthe First School of Clinical MedicineSouthern Medical UniversityGuangzhou 510000China The Fourth Affiliated Hospital the First Affiliated HospitalSchool of Public HealthInstitute of Translational MedicineCancer CenterState Key Laboratory of Experimental HematologyZhejiang University School of MedicineHangzhou 310000China The First Affiliated Hospital the Second Affiliated HospitalBasic Medical SciencesSchool of Public HealthHengyang Medical SchoolUniversity of South ChinaHengyang 421200China College of Pharmaceutical Sciences Zhejiang UniversityHangzhou 310000China Liangzhu Laboratory Zhejiang University Medical CenterHangzhou 310000China Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy School of Laboratory Medicine and BiotechnologySouthern Medical UniversityGuangzhou 510000China

With the escalating prevalence of global heat waves,heat stroke has become a prominent health concern,leading to substantial liver *** other forms of liver injury,heat strokeinduced damage is characterized by heat cytotoxicity and heightened inflammation,directly contributing to elevated mortality *** clinical assessments have identified elevated bilirubin levels as indicative of Kupffer cell dysfunction,their specific correlation with heat stroke liver injury remains *** hypothesis proposes the involvement of Kupffer cell ferroptosis during heat stroke,initiating IL-1.mediated *** single-cell RNA sequencing of murine macrophages,a distinct and highly susceptible Kupffer cell subtype,Clec4Ft/CD206t,emerged,with heme oxygenase 1.HMOX-1.playing a pivotal ***,heat-induced HMOX-1.regulated by early growth response factor 1.mediated ferroptosis in Kupffer cells,specifically in the Clec4F t/CD206 t subtype(KC2),activating phosphatidylinositol 4-kinase beta and promoting PI4P *** cascade triggered NLRP3 inflammasome activation and maturation of *** findings underscore the critical role of targeted therapy against HMOX-1.in ferroptosis within Kupffer cells,particularly in Clec4F t/CD206 t *** an approach has the potential to mitigate inflammation and alleviate acute liver injury in the context of heat stroke,offering a promising avenue for future therapeutic interventions.

关键词： Heat stroke Liver injury Kupffer cells Ferroptosis Heme oxygenase 1 Phosphatidylinositol 4-kinase beta NLRP3 Early growth response factor 1

Endorepellin downregulation promotes angiogenesis after experimental traumatic brain injury

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Neural Regeneration Research 2024年第5期19卷 1092-1097页

作者： Qian Zhang Yao Jing Qiuyuan Gong Lin Cai Ren Wang Dianxu Yang Liping Wang Meijie Qu Hao Chen Yaohui Tang Hengli Tian Jun Ding Zhiming Xu Department of Gerontology Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Department of Neurosurgery Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Department of Neurology Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina school of Biomedical Engineering and Med-X Research Institute Shanghai Jiao Tong UniversityShanghaiChina Department of Neurology Affiliated Hospital of Qingdao UniversityQingdaoShandong ProvinceChina

Endorepellin plays a key role in the regulation of angiogenesis,but its effects on angiogenesis after traumatic brain injury are *** study explored the effects of endorepellin on angiogenesis and neurobehavioral outcomes after traumatic brain injury in *** were randomly divided into four groups:sham,controlled cortical impact only,adeno-associated virus(AAV)-green fluorescent protein,and AAV-shEndorepellin-green fluorescent protein *** the controlled cortical impact model,the transduction of AAV-shEndorepellin-green fluorescent protein downregulated endorepellin while increasing the number of CD31./Ki-67+proliferating endothelial cells and the functional microvessel density in mouse *** changes resulted in improved neurological function compared with controlled cortical impact *** blotting revealed increased expression of vascular endothelial growth factor and angiopoietin-1.in mice treated with AAV-shEndorepellin-green fluorescent *** radiation angiography showed that endorepellin downregulation promoted angiogenesis and increased cortical neovascularization,which may further improve neurobehavioral ***,an in vitro study showed that downregulation of endorepellin increased tube formation by human umbilical vein endothelial cells compared with a *** analysis found that endorepellin downregulation may mediate angiogenesis by activating vascular endothelial growth factor-and angiopoietin-1.related signaling pathways.

关键词： angiogenesis controlled cortical impact endorepellin neurological function traumatic brain injury

E-MobileNeXt: face expression recognition model based on improved MobileNeXt

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Optoelectronics Letters 2024年第2期20卷 122-128页

作者： ZHANG Xiang YAN Chunman school of Physics and Electronic Engineering Northwest Normal UniversityLanzhou 730070China1

In response to the high complexity and low accuracy of current facial expression recognition networks, this paper proposes an E-Mobile Ne Xt network for facial expression recognition. E-Mobile Ne Xt is built based on our proposed E-Sand Glass block. In addition, we also improve the overall performance of the network through Rep Conv and SGE attention mechanisms. The experimental results show that the network model improves the expression recognition accuracy by 6.5% and 7.1.% in RAF-DB and CK+ datasets, respectively, while the parameter and floating-point operations decreased by 0.79 M and 4.2 M compared with Mobile Ne Xt.

关键词： facial mechanisms. network

Autophagy plays a pro-apoptotic role in arsenic trioxide-induced cell death of liver cancer

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Journal of Integrative medicine 2024年第3期22卷 295-302页

作者： Zhengting Deng Shufang Liang Guokai Huang Yuqian Wang Xiaoyu Tu Yani Zhang Shu Li Tao Liu Binbin Cheng Taizhou Hospital of Traditional Chinese medicine Nanjing University of Chinese MedicineTaizhou 225300Jiangsu ProvinceChina Oncology Department of Traditional Chinese medicine The First Affiliated Hospital of Naval Medical UniversityShanghai 200433China school of Traditional Chinese {1. Nanjing University of Chinese MedicineNanjing 210023Jiangsu ProvinceChina Department of Gastroenterology Baoshan Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghai 201900China

Objective: The effects of arsenic trioxide(As2O3) on hepatocellular carcinoma have been documented widely. Autophagy plays dual roles in the survival and death of cancer cells. Therefore, we investigated the exact role of autophagy in As2O3-induced apoptosis in liver cancer ***: The viability of hepatoma cells was determined using the MTT assay with or without fetal bovine serum. The rate of apoptosis in liver cancer cells treated with As2O3was evaluated using flow cytometry, Hoechst 33258 staining, and TUNEL assays. The rate of autophagy among liver cancer cells treated with As2O3was detected using immunofluorescence, Western blot assay and transmission electron ***: Upon treatment with As2O3, the viability of HepG2 and SMMC-7721.cells was decreased in a time-and dose-dependent manner. The apoptosis rates of both liver cancer cell lines increased with the concentration of As2O3, as shown by flow cytometry. Apoptosis in liver cancer cells treated with As2O3was also shown by the activation of the caspase cascade and the regulation of Bcl-2/Bax ***, As2O3treatment induced autophagy in liver cancer cells;this finding was supported by Western blot, immunofluorescence of LC3-II and beclin 1. and transmission electron microscopy. In liver cancer cells, As2O3inhibited the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/AKT/mTOR) signal pathway that plays a vital role in both apoptosis and autophagy. The PI3K activator SC-79 partially reversed As2O3-induced autophagy and apoptosis. Furthermore, inhibiting autophagy with 3-methyladenine partially reversed the negative effects of As2O3on cell *** starvation increased autophagy and amplified the effect of As2O3on cell ***: As2O3induces apoptosis and autophagy in liver cancer cells. Autophagy induced by As2O3may have a proapoptotic effect that helps to reduce the viability of liver cancer cells. This study provides novel insights

关键词： Apoptosis Arsenic trioxide Autophagy Primary liver cancer

A pregnant patient with type II osteogenesis imperfecta pregnancy

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World Journal of Emergency medicine 2024年第1期15卷 75-76页

作者： Chenyu Jiang Chenyi Bao Shujuan Shu Department of Obstetrics Women’s HospitalSchool of MedicineZhejiang UniversityHangzhou 310006China

Osteogenesis imperfecta(OI)is a primary bone fragility disorder with an estimated prevalence of 1.1.,000 births and is a hereditary syndrome characterized by one or more of the following:fractures,blue sclerae,impaired hearing,defective dentition,and hyperlaxibility throughout life.[1.2]We report a pregnant woman with type II OI and review her prenatal counseling,diagnosis,and pregnancy management to assist obstetricians in understanding the disease and managing it in emergency situations.

关键词： pregnancy impaired diagnosis

Pancreatic panniculitis as the first presentation of pancreatic ductaladenocarcinoma

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Hepatobiliary & Pancreatic Diseases International 2024年第1期23卷 106-108页

作者： Wei-Fang Zhu Shan Fang Jian-Jun Qiao Department of Dermatology the First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China

To the Editor:Pancreatic panniculitis,also known as pancreatic fat necrosis or enzymatic panniculitis,is a rare type of panniculitis that occurs in 0.3%−3%of patients with pancreatic disease such as acute or chronic pancreatitis and pancreatic carcinoma,especially acinar cell carcinoma[1.2].The clinical manifestations are nonspecific erythema tender nodules.

关键词： Pancreatic acute adenocarcinoma

GPCR-Gs mediates the protective effects of ginsenoside Rb1.against oxygen-glucose deprivation/re-oxygenation-induced astrocyte injury

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Journal of Traditional Chinese Medical Sciences 2024年第1期11卷 33-43页

作者： Xi Wang Ying Liu Juan Li Jiayu Xie Yi Dai Minke Tang school of Chinese Materia Medica Beijing University of Chinese MedicineBeijing 102488China Taihe Hospital Hubei University of MedicineShiyan 442000China school of {1. Hyogo Medical UniversityNishinomiya 663-8501Japan

Objectives:To investigate whether the protective actions of ginsenoside Rb1.Rb1.on astrocytes are mediated through the G_(s)-type G-protein-coupled receptor(GPCR-G_(s)).Methods:Primary astrocyte cultures derived from neonatal mouse brain were *** injury was induced via oxygen-glucose deprivation/re-oxygenation(OGD/R).Cell morphology,viability,lactate dehydrogenase(LDH)leakage,apoptosis,glutamate uptake,and brain-derived neurotrophic factor(BDNF)secretion were assessed to gauge cell survival and *** blot was used to investigate the cyclic adenosine monophosphate(cAMP)and protein kinase B(Akt)signaling ***-G_(s)-specific inhibitors and molecular docking were used to identify target ***:Rb1.at concentrations ranging from 0.8 to 5μM did not significantly affect the viability,glutamate uptake,or BDNF secretion in normal ***/R reduced astrocyte viability,increasing their LDH leakage and apoptosis *** also decreased glutamate uptake and BDNF secretion by these ***1.had protective effects of astrocytes challenged by OGD/R,by improving viability,reducing apoptosis,and enhancing glutamate uptake and BDNF ***,Rb1.activated the cAMP and Akt pathways in these *** the GPCR-G_(s) inhibitor NF449 was introduced,the protective effects of Rb1.completely disappeared,and its activation of cAMP and Akt signaling pathways was significantly ***:Rb1.protects against astrocytes from OGD/R-induced injury through GPCR-G_(s) mediation.

关键词： Ginseng Ginsenoside Rb1 Receptor GPCR Astrocytes Neuroprotective effects