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Tongxinluo Activates PI3K/AKT Signaling Pathway to Inhibit Endothelial Mesenchymal Transition and Attenuate Myocardial Fibrosis after Ischemia-Reperfusion in Mice

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Chinese Journal of Integrative Medicine 2024年第7期30卷 608-615页

作者： WEI Ya-ru HOU Yun-long YIN Yu-jie LI Zhen LIU Yi HAN Ning-xin WANG Zi-xuan LIU Lu WANG Xiao-qi hao yuan-jie MA Kun GU Jiao-jiao JIA Zhen-hua Graduate School Hebei University of Chinese Medicine Shijiazhuang Yiling Pharmaceutical New Drug Evaluation Center Hebei Institute of Integrated Traditional and Western Medicine National Key Laboratory for Innovation and Transformation of Luobing Theory Department of Cardiology Hebei Yiling Hospital Graduate School Hebei Medical University

Objective: To investigate the potential role of Tongxinluo(TXL) in attenuating myocardial fibrosis after myocardial ischemia-reperfusion injury(MIRI) in mice. Methods: A MIRI mouse model was established by left anterior descending coronary artery ligation for 45 min. According to a random number table, 66 mice were randomly divided into 6 groups(n=11 per group): the sham group, the model group, the LY-294002 group, the TXL group, the TXL+LY-294002 group and the benazepril(BNPL) group. The day after modeling, TXL and BNPL were administered by gavage. Intraperitoneal injection of LY-294002 was performed twice a week for 4 consecutive weeks. Echocardiography was used to measure cardiac function in mice. Masson staining was used to evaluate the degree of myocardial fibrosis in mice. Qualitative and quantitative analysis of endothelial mesenchymal transition(EndMT) after MIRI was performed by immunohistochemistry, immunofluorescence staining and flow cytometry, respectively. The protein expressions of platelet endothelial cell adhesion molecule-1(CD31), α-smoth muscle actin(α-SMA), phosphatidylinositol-3-kinase(PI3K) and phospho protein kinase B(p-AKT) were assessed using Western blot. Results: TXL improved cardiac function in MIRI mice, reduced the degree of myocardial fibrosis, increased the expression of CD31 and inhibited the expression of α-SMA, thus inhibited the occurrence of EndMT(P0.05). In addition, the use of the PI3K/AKT pathway-specific inhibitor LY-294002 to block this pathway and combination with TXL intervention, eliminated the protective effect of TXL, further supporting the protective effect of TXL. Conclusion: TXL activated the PI3K/AKT signaling pathway to inhibit EndMT and attenuated myocardial fibrosis after MIRI in mice.

关键词： myocardial fibrosis endothelial mesenchymal transition myocardial ischemia-reperfusion injury phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway

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VR技术应用于绘本课程的价值、困境与出路

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陕西学前师范学院学报 2024年第3期40卷 31-38页

作者：袁昊杰李伟东北师范大学教育学部吉林长春130024

VR技术是构建元宇宙世界的核心技术之一,兼具沉浸性、交互性、构想性三大特征。基于VR技术特征构建的绘本课程体系能够弥补传统绘本课程的不足,为幼儿提供全新的绘本课程体验,突出表现为:沉浸性破隔离;交互性变主动;构想性融时空。但VR... 详细信息

VR技术是构建元宇宙世界的核心技术之一,兼具沉浸性、交互性、构想性三大特征。基于VR技术特征构建的绘本课程体系能够弥补传统绘本课程的不足,为幼儿提供全新的绘本课程体验,突出表现为:沉浸性破隔离;交互性变主动;构想性融时空。但VR技术应用于绘本课程也存在诸多现实困境,如:前期投入成本高,普及推广难度大;教师能力需提升,评价机制待商榷;安全风险影响大,家长接受程度低;儿童发展差异大,潜在问题待理清。针对这些困境,应推动产学研深度融合,以科研推动其普及;创新绘本课程教学模式,以创新带动其转型;增强VR技术的实践效能,以实效论证其价值;加强VR技术的安全性,以安全促进其应用。

关键词： VR虚拟现实技术绘本课程数字化

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家庭社会经济地位对家庭内部支持和学前儿童社会能力的影响——基于学前儿童父亲样本的研究

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陕西学前师范学院学报 2024年第1期40卷 9-18页

作者：袁昊杰岳亚平赵一霏雷佳媛东北师范大学教育学部吉林长春130024 河南大学教育学部河南开封475004

家庭是学前儿童最早接触的核心微观环境系统,家庭社会经济地位及家庭中父亲为学前儿童提供的教育、心理、生活、游戏支持深刻影响着学前儿童的社会能力。对河南省629位学前儿童父亲展开问卷调查,研究发现:父亲家庭支持和儿童的社会能力... 详细信息

家庭是学前儿童最早接触的核心微观环境系统,家庭社会经济地位及家庭中父亲为学前儿童提供的教育、心理、生活、游戏支持深刻影响着学前儿童的社会能力。对河南省629位学前儿童父亲展开问卷调查,研究发现:父亲家庭支持和儿童的社会能力均处于中等水平;家庭社会经济地位、家庭内部支持与学前儿童的社会能力三者之间存在显著的正相关;Bootstrap法检验表明,家庭内部支持在家庭社会经济地位与学前儿童社会能力之间存在显著的中介效应。因此,为提升学前儿童的社会能力,应提升对学前儿童父亲的社会支持,增强父亲的育儿意识与能力;优化父亲对儿童家庭支持的结构,为幼儿提供适宜的家庭支持;构建家、园、社协同育儿共同体,塑造幼儿发展的良好生态圈。

关键词：家庭社会经济地位家庭支持学前儿童社会能力

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Application of non-mydriatic fundus photography-assisted telemedicine in diabetic retinopathy screening

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World Journal of Diabetes 2024年第2期15卷 251-259页

作者： Wan Zhou Xiao-Jing yuan jie Li Wei Wang hao-Qiang Zhang yuan-yuan Hu Shan-Dong Ye Department of Endocrinology The First Affiliated Hospital of University of Science and Technology of ChinaDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230001Anhui ProvinceChina Department of Endocrinology Anhui Provincial HospitalAffiliated to Anhui Medical UniversityHefei 230001Anhui ProvinceChina

BACKGROUND Early screening and accurate staging of diabetic retinopathy(DR)can reduce blindness risk in type 2 diabetes patients.DR’s complex pathogenesis involves many factors,making ophthalmologist screening alone insufficient for prevention and treatment.Often,endocrinologists are the first to see diabetic patients and thus should screen for retinopathy for early intervention.AIM To explore the efficacy of non-mydriatic fundus photography(NMFP)-enhanced telemedicine in assessing DR and its various stages.METHODS This retrospective study incorporated findings from an analysis of 93 diabetic patients,examining both NMFP-assisted telemedicine and fundus fluorescein angiography(FFA).It focused on assessing the concordance in DR detection between these two methodologies.Additionally,receiver operating characteristic(ROC)curves were generated to determine the optimal sensitivity and specificity of NMFP-assisted telemedicine,using FFA outcomes as the standard benchmark.RESULTS In the context of DR diagnosis and staging,the kappa coefficients for NMFPassisted telemedicine and FFA were recorded at 0.775 and 0.689 respectively,indicating substantial intermethod agreement.Moreover,the NMFP-assisted telemedicine’s predictive accuracy for positive FFA outcomes,as denoted by the area under the ROC curve,was remarkably high at 0.955,within a confidence interval of 0.914 to 0.995 and a statistically significant P-value of less than 0.001.This predictive model exhibited a specificity of 100%,a sensitivity of 90.9%,and a Youden index of 0.909.CONCLUSION NMFP-assisted telemedicine represents a pragmatic,objective,and precise modality for fundus examination,particularly applicable in the context of endocrinology inpatient care and primary healthcare settings for diabetic patients.Its implementation in these scenarios is of paramount significance,enhancing the clinical accuracy in the diagnosis and therapeutic management of DR.This methodology not only streamlines patient evaluation but also contributes substantially to the optimi

关键词： Diabetes Diabetic retinopathy Non-mydriatic fundus photography-assisted telemedicine Fundus fluorescein angiography

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Hapln1 promotes dedifferentiation and proliferation of iPSC-derived cardiomyocytes by promoting versican-based GDF11 trapping

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Journal of Pharmaceutical Analysis 2024年第3期14卷 335-347页

作者： Ding-Jun hao Yue Qin Shi-jie Zhou Bu-Huai Dong Jun-Song Yang Peng Zou Li-Ping Wang yuan-Ting Zhao Department of Spine Surgery Honghui HospitalXi'an Jiaotong UniversityXi'an710054China Department of Anesthesiology Honghui HospitalXi'an Jiaotong UniversityXi'an710054China Department of Cardiovascular Medicine Honghui HospitalXi'an Jiaotong UniversityXi'an710054China State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy West China HospitalSichuan UniversityChengdu610041China

Hyaluronan and proteoglycan link protein 1(Hapln1)supports active cardiomyogenesis in zebrafish hearts,but its regulation in mammal cardiomyocytes is unclear.This study aimed to explore the potential regulation of Hapln1 in the dedifferentiation and proliferation of cardiomyocytes and its therapeutic value in myocardial infarction with human induced pluripotent stem cell(hiPSC)-derived cardiomyocytes(CMs)and an adult mouse model of myocardial infarction.HiPSC-CMs and adult mice with myocardial infarction were used as in vitro and in vivo models,respectively.Previous single-cell RNA sequencing data were retrieved for bioinformatic exploration.The results showed that recombinant human Hapln1(rhHapln1)promotes the proliferation of hiPSC-CMs in a dose-dependent manner.As a physical binding protein of Hapln1,versican interacted with Nodal growth differentiation factor(NODAL)and growth differentiation factor 11(GDF11).GDF11,but not NODAL,was expressed by hiPSC-CMs.GDF11 expression was unaffected by rhHapln1 treatment.However,this molecule was required for rhHapln1-mediated activation of the transforming growth factor(TGF)-β/Drosophila mothers against decapentaplegic protein(SMAD)2/3 signaling in hiPSC-CMs,which stimulates cell dedifferentiation and proliferation.Recombinant mouse Hapln1(rmHapln1)could induce cardiac regeneration in the adult mouse model of myocardial infarction.In addition,rmHapln1 induced hiPSC-CM proliferation.In conclusion,Hapln1 can stimulate the dedifferentiation and proliferation of iPSC-derived cardiomyocytes by promoting versican-based GDF11 trapping and subsequent activation of the TGF-β/SMAD2/3 signaling pathway.Hapln1 might be an effective hiPSC-CM dedifferentiation and proliferation agent and a potential reagent for repairing damaged hearts.

关键词： Hapln1 Versican GDF11 iPSC-CMs Cardiomyocyte proliferation

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Diagnosis and therapy of tacrolimus toxicity in a liver transplant recipient during COVID-19 treatment

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Hepatobiliary & Pancreatic Diseases International 2024年第3期23卷 326-330页

作者： Feng Zhu Yi-Ming Wang Ming Ni yuan Liang jie-Hui Huang Xue-hao Wang Feng Cheng Ling Lu Hepatobiliary Center The First Affiliated Hospital of Nanjing Medical UniversityKey Laboratory of Liver TransplantationChinese Academy of Medical SciencesNHC Key Laboratory of Liver TransplantationResearch Unit of Liver Transplantation and Transplant ImmunologyChinese Academy of Medical SciencesNanjing 210000China Department of Respiratory and Critical Care Medicine Wuxi Fifth People’s HospitalWuxi 214000China Jiangsu Key Laboratory of Cancer Biomarkers Prevention and TreatmentCollaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjing 210000China

To the Editor:SARS-CoV-2,the pathogen responsible for the pandemic of coronavirus disease 2019(COVID-19),has had profound impacts on human health,and its antagonist Paxlovid is a commonly used treatment option[1].However,treatment selection for immunosuppressed patients,such as liver recipients,remains uncertain due to potential drug interactions and the risk of immunosuppressant dosage adjustment,which can cause liver injury[2].

关键词： dosage treatment antagonist

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NLRP3 activation in macrophages promotes acute intestinal injury in neonatal necrotizing enterocolitis

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World Journal of Pediatrics 2024年第2期20卷 153-164页

作者： Bo Shi Cheng-jie Lyu Zhen-Kai Le hao-Sen Ji Yi Xiao yuan-yuan Zhang Shou-Jiang Huang Lin-Jun Yu Qiang Shu Jin-Fa Tou Deng-Ming Lai Department of Neonatal Surgery Children’s HospitalZhejiang University School of MedicineNational Clinical Research Center for Child HealthHangzhou 310052China Department of Pulmonology Children’s HospitalZhejiang University School of MedicineNational Clinical Research Center for Child HealthHangzhou 310052China Department of Thoracic and Cardiovascular Surgery Children’s HospitalZhejiang University School of MedicineNational Clinical Research Center for Child HealthHangzhou 310052China

Background Macrophages are involved in various immune inflammatory disease conditions.This study aimed to investigate the role and mechanism of macrophages in regulating acute intestinal injury in neonatal necrotizing enterocolitis(NEC).Methods CD68,nucleotide-binding oligomerization domain,leucine-rich repeat,and pyrin domain-containing 3(NLRP3),cysteine aspartate-specific protease-1(caspase-1),and interleukin-1β(IL-1β)in paraffin sections of intestinal tissues from NEC and control patients were detected with immunohistochemistry,immunofluorescence,and western blot.Hypertonic pet milk,hypoxia and cold stimulation were used to establish a mouse(wild type and Nlrp3^(-/-))model of NEC.The mouse macrophage(RAW 264.7)and rat intestinal epithelial cell-6 lines were also cultured followed by various treatments.Macrophages,intestinal epithelial cell injuries,and IL-1β release were determined.Results Compared to the gut“healthy”patients,the intestinal lamina propria of NEC patients had high macrophage infiltration and high NLRP3,caspase-1,and IL-1β levels.Furthermore,in vivo,the survival rate of Nlrp3^(-/-)NEC mice was dramatically improved,the proportion of intestinal macrophages was reduced,and intestinal injury was decreased compared to those of wild-type NEC mice.NLRP3,caspase-1,and IL-1β derived from macrophages or supernatant from cocultures of macrophages and intestinal epithelial cells also caused intestinal epithelial cell injuries.Conclusions Macrophage activation may be essential for NEC development.NLRP3/caspase-1/IL-1β cellular signals derived from macrophages may be the underlying mechanism of NEC development,and all these may be therapeutic targets for developing treatments for NEC.

关键词： Caspase-1 Interleukin-1β Macrophage Necrotizing enterocolitis NLRP3

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Targeted knockdown of PGAM5 in synovial macrophages efficiently alleviates osteoarthritis

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Bone Research 2024年第1期12卷 215-226页

作者： Yuhang Liu Ruihan hao Jia Lv jie yuan Xuelei Wang Churong Xu Ding Ma Zhouyi Duan Bingjun Zhang Liming Dai Yiyun Cheng Wei Lu Xiaoling Zhang Department of Orthopedic Surgery Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine(SJTUSM)Shanghai 200092China National Facility for Translational Medicine Shanghai 200240China Shanghai Frontiers Science Center of Genome Editing and Cell Therapy Shanghai Key Laboratory of Regulatory BiologySchool of Life SciencesEast China Normal UniversityShanghai 200241China Department of Orthopaedic Surgery The Second Hospital of Shanxi Medical UniversityTaiyuan 030001China CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthChinese Academy of SciencesShanghai 200031China School of Medicine Shanghai UniversityShanghai 200444China

Osteoarthritis(OA)is a common degenerative disease worldwide and new therapeutics that target inflammation and the crosstalk between immunocytes and chondrocytes are being developed to prevent and treat OA.These attempts involve repolarizing pro-inflammatory M1 macrophages into the anti-inflammatory M2 phenotype in synovium.In this study,we found that phosphoglycerate mutase 5(PGAM5)significantly increased in macrophages in OA synovium compared to controls based on histology of human samples and single-cell RNA sequencing results of mice models.To address the role of PGAM5 in macrophages in OA,we found conditional knockout of PGAM5 in macrophages greatly alleviated OA symptoms and promoted anabolic metabolism of chondrocytes in vitro and in vivo.Mechanistically,we found that PGAM5 enhanced M1 polarization via AKT-mTOR/p38/ERK pathways,whereas inhibited M2 polarization via STAT6-PPARγpathway in murine bone marrow-derived macrophages.Furthermore,we found that PGAM5 directly dephosphorylated Dishevelled Segment Polarity Protein 2(DVL2)which resulted in the inhibition ofβ-catenin and repolarization of M2 macrophages into M1 macrophages.Conditional knockout of both PGAM5 andβ-catenin in macrophages significantly exacerbated osteoarthritis compared to PGAM5-deficient mice.Motivated by these findings,we successfully designed mannose modified fluoropolymers combined with siPGAM5 to inhibit PGAM5 specifically in synovial macrophages via intra-articular injection,which possessed desired targeting abilities of synovial macrophages and greatly attenuated murine osteoarthritis.Collectively,these findings defined a key role for PGAM5 in orchestrating macrophage polarization and provides insights into novel macrophage-targeted strategy for treating OA.

关键词： osteoarthritis metabolism inhibited

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A compact multi-pixel superconducting nanowire single-photon detector array supporting gigabit space-to-ground communications

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Light(Science & Applications) 2024年第2期13卷 254-266页

作者： hao hao Qing-yuan Zhao Yang-Hui Huang jie Deng Fan Yang Sai-Ying Ru Zhen Liu Chao Wan hao Liu Zhi-Jian Li Hua-Bing Wang Xue-Cou Tu La-Bao Zhang Xiao-Qing Jia Xing-Long Wu Jian Chen Lin Kang Pei-Heng Wu Research Institute of Superconductor Electronics(RISE) School of Electronic Science and EngineeringNanjing UniversityNanjingJiangsu 210023China Purple Mountain Laboratories NanjingJiangsu 211111China Hefei National Laboratory HefeiAnhui 230088China National Laboratory of Solid State Microstructures and Department of Physics Nanjing UniversityNanjing 210023China

Classical and quantum space-to-ground communications necessitate highly sensitive receivers capable of extracting information from modulated photons to extend the communication distance from near-earth orbits to deep space explorations.To achieve gigabit data rates while mitigating strong background noise photons and beam drift in a highly attenuated free-space channel,a comprehensive design of a multi-functional detector is indispensable.In this study,we present an innovative compact multi-pixel superconducting nanowire single-photon detector array that integrates near-unity detection efficiency(91.6%),high photon counting rate(1.61 Gcps),large dynamic range for resolving different photon numbers(1-24),and four-quadrant position sensing function all within one device.Furthermore,we have constructed a communication testbed to validate the advantages offered by such an architecture.Through 8-PPM(pulse position modulation)format communication experiments,we have achieved an impressive maximum data rate of 1.5 Gbps,demonstrating sensitivities surpassing previous benchmarks at respective speeds.By incorporating photon number information into error correction codes,the receiver can tolerate maximum background noise levels equivalent to 0.8 photons/slot at a data rate of 120 Mbps—showcasing a great potential for daylight operation scenarios.Additionally,preliminary beam tracking tests were conducted through open-loop scanning techniques,which revealed clear quantitative dependence indicating sensitivity variations based on beam location.Based on the device characterizations and communication results,we anticipate that this device architecture,along with its corresponding signal processing and coding techniques,will be applicable in future space-to-ground communication tasks.

关键词： photon supporting correction

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METTL14 downregulation drives S100A4^(+)monocyte-derived macrophages via MyD88/NF-κB pathway to promote MAFLD progression

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Signal Transduction and Targeted Therapy 2024年第5期9卷 2176-2192页

作者： Yue-fan Wang Wen-li Zhang Zhi-xuan Li Yue Liu Jian Tan hao-zan Yin Zhi-chao Zhang Xian-jie Piao Min-hao Ruan Zhi-hui Dai Si-jie Wang Chen-yang Mu Ji-hang yuan Shu-han Sun Hui Liu Fu Yang The Third Department of Hepatic Surgery Eastern Hepatobiliary Surgery Hospital Affiliated to Naval Medical University200438 ShanghaiChina The Department of Medical Genetics Naval Medical University200433 ShanghaiChina Translational Medicine Research Center Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital100048 BeijingChina The Department of Pharmaceutical Analysis School of PharmacyNaval Medical University200433 ShanghaiChina Key Laboratory of Biosafety Defense Ministry of Education200433 ShanghaiChina Shanghai Key Laboratory of Medical Biodefense 200433 ShanghaiChina

Without intervention,a considerable proportion of patients with metabolism‐associated fatty liver disease(MAFLD)will progress from simple steatosis to metabolism‐associated steatohepatitis(MASH),liver fibrosis,and even hepatocellular carcinoma.However,the molecular mechanisms that control progressive MAFLD have yet to be fully determined.Here,we unraveled that the expression of the N6-methyladenosine(m6A)methyltransferase METTL14 is remarkably downregulated in the livers of both patients and several murine models of MAFLD,whereas hepatocyte-specific depletion of this methyltransferase aggravated lipid accumulation,liver injury,and fibrosis.Conversely,hepatic Mettl14 overexpression alleviated the above pathophysiological changes in mice fed on a high-fat diet(HFD).Notably,in vivo and in vitro mechanistic studies indicated that METTL14 downregulation decreased the level of GLS2 by affecting the translation efficiency mediated by YTHDF1 in an m6A-depedent manner,which might help to form an oxidative stress microenvironment and accordingly recruit Cx3cr1^(+)Ccr2^(+)monocyte-derived macrophages(Mo-macs).In detail,Cx3cr1^(+)Ccr2^(+)Mo-macs can be categorized into M1-like macrophages and S100A4-positive macrophages and then further activate hepatic stellate cells(HSCs)to promote liver fibrosis.Further experiments revealed that CX3CR1 can activate the transcription of S100A4 via CX3CR1/MyD88/NF-κB signaling pathway in Cx3cr1^(+)Ccr2^(+)Mo-macs.Restoration of METTL14 or GLS2,or interfering with this signal transduction pathway such as inhibiting MyD88 could ameliorate liver injuries and fibrosis.Taken together,these findings indicate potential therapies for the treatment of MAFLD progression.

关键词： S100A4 MyD88 metabolism

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