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ALKBH5 gene polymorphisms and risk of neuroblastoma in Chinese children from Jiangsu Province

Cancer Innovation 2024年第2期3卷 72-79页

作者： Qian Guan Xinxin Zhang Jiabin Liu Chunlei Zhou Jinhong Zhu haiyan wu Zhenjian Zhuo Jing He Department of Pediatric Surgery Guangzhou Institute of PediatricsGuangdong Provincial Key Laboratory of Research in Structural Birth Defect DiseaseGuangdong Provincial Clinical Research Center for Child HealthGuangzhou Women and Children's Medical CenterGuangzhou Medical UniversityGuangzhouGuangdongChina Department of Pathology Children's Hospital of Nanjing Medical UniversityNanjingJiangsuChina Department of Clinical Laboratory BiobankHarbin Medical University Cancer HospitalHarbinHeilongjiangChina Laboratory Animal Center School of Chemical Biology and BiotechnologyPeking University Shenzhen Graduate SchoolShenzhenGuangdongChina

Background:Neuroblastoma is one of the most common extracranial malignant solid tumors in children.AlkB homolog 5(ALKBH5)is an RNA N6-methyladenosine(m6A)demethylase that plays a critical role in tumorigenesis and development.We assessed the association between single nucleotide polymorphisms(SNPs)in ALKBH5 and the risk of neuroblastoma in a case-control study including 402 patients and 473 non-cancer controls.Methods:Genotyping was determined by the TaqMan method.The association between ALKBH5 polymorphisms(rs1378602 and rs8400)and the risk of neuroblastoma was evaluated using the odds ratio(OR)and 95%confidence interval(CI).Results:We found no strong association of ALKBH5 rs1378602 and rs8400 with neuroblastoma risk.Further stratification analysis by age,sex,primary site,and clinical stage showed that the rs1378602 AG/AA genotype was associated with a lower risk of neuroblastoma in males(adjusted OR=0.58,95%CI=0.35–0.97,p=0.036)and children with retroperitoneal neuroblastoma(adjusted OR=0.58,95%CI=0.34–0.98,p=0.040).Conclusions:ALKBH5 SNPs do not seem to be associated with neuroblastoma risk.More studies are required to confirm this negative result and reveal the relationship between gene polymorphisms of the m6A modifier ALKBH5 and neuroblastoma.

关键词： ALKBH5 neuroblastoma polymorphism susceptibility

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Promoting interactions between cognitive science and large language models

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The Innovation 2024年第2期5卷 9-10页

作者： Youzhi Qu Penghui Du Wenxin Che Chen Wei Chi Zhang Wanli Ouyang Yatao Bian Feiyang Xu Bin Hu Kai Du haiyan wu Jia Liu Quanying Liu Department of Biomedical Engineering Southern University of Science and TechnologyShenzhen 518055China Shanghai AI Laboratory Shanghai 200232China Tencent AI Lab Shenzhen 518057China iFLYTEK AI Research Hefei 230088China School of Medical Technology Beijing Institute of TechnologyBeijing 100081China Institute for Artificial Intelligence Peking UniversityBeijing 100871China Centre for Cognitive and Brain Sciences and Department of Psychology University of MacaoMacao 999078China Department of Psychology Tsinghua UniversityBeijing 100084China

Large language models(LLMs)have made unprecedented progress,demonstrating human-like language proficiency and an extraordinary ability to encode complex knowledge.The emergence of high-level cognitive capabilities in LLMs,such as in-context learning and complex reasoning,suggests a path toward the realization of artificial general intelligence(AGI).However,we lack scientific theories and tools to assess and interpret such an emergence of the advanced intelligence of LLMs.Artificial intelligence(AI)has been extensively applied in various areas of fundamental science to accelerate scientific research.

关键词： cognitive such language

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Level pinning of anti-PT-symmetric circuits for efficient wireless power transfer

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National Science Review 2024年第1期11卷 215-224页

作者： Zhiwei Guo Fengqing Yang haiyan Zhang Xian wu Qiong wu Kejia Zhu Jun Jiang Haitao Jiang Yaping Yang Yunhui Li Hong Chen MOE Key Laboratory of Advanced Micro-Structured Materials School of Physics Sciences and Engineering Tongji University Department of Electrical Engineering Tongji University School of Automotive Studies Tongji University

Wireless power transfer(WPT) technology based on magnetic resonance(a basic physical phenomenon)can directly transfer energy from the source to the load without wires and other physical contacts, and has been successfully applied to implantable medical devices, electric vehicles, robotic arms and other fields.However, due to the frequency splitting of near-field coupling, the resonant WPT system has some unique limitations, such as poor transmission stability and low efficiency. Here, we propose anti-resonance with level pinning for high-performance WPT. By introducing the anti-resonance mode into the basic WPT platform, we uncover the competition between dissipative coupling and coherent coupling to achieve novel level pinning, and construct an effective anti-parity-time(anti-PT)-symmetric non-Hermitian system that is superior to previous PT-symmetric WPT schemes. On the one hand, the eigenvalue of the anti-PT-symmetric system at resonance frequency is always pure real in both strong and weak coupling regions, and can be used to overcome the transmission efficiency decrease caused by weak coupling, as brought about by, for example, a large size ratio of the transmitter to receiver, or a long transmission distance.On the other hand, due to the level pinning effect of the two kinds of coupling mechanisms, the working frequency of the system is guaranteed to be locked, so frequency tracking is not required when the position and size of the receiver change. Even if the system deviates from the matching condition, an efficient WPT can be realized, thereby demonstrating the robustness of the level pinning. The experimental results show that when the size ratio of the transmitter coil to the receiver coil is 4.29(which is in the weak coupling region), the transfer efficiency of the anti-PT-symmetric system is nearly 4.3(3.2) times higher than that of the PT-symmetric system when the matching conditions are satisfied(deviated). With the miniaturization and integration of devices in mind, a synthetic anti-PT-symmetric sy

关键词： non-Hermitian system wireless power transfer anti-PT-symmetric circuits synthetic dimension metamaterials

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Mechanism of Wendan decoction in preventing obesity by regulating multiple signal pathway networks based on gene promoter methylation

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Journal of Traditional Chinese Medical Sciences 2024年第1期11卷 93-100页

作者： haiyan Yang Meiling Ren Ziting wu Jinchao Li Ping Wang School of Traditional Chinese Medicine Jiangxi University of Chinese MedicineNanchang 330004China Graduate School Jiangxi University of Chinese MedicineNanchang 330004China

Objective:To investigate the potential mechanism of Wendan decoction in obesity by screening target genes with promoter region methylation changes and constructing a multiple signaling pathways network based on promoter methylation.Methods:The methylation degree of Itgad,Col8a1,Adra2b,Jund,Rab2a,Wnt8b,Fzd9,B4galt7,Pik3cd,Creb1,Stard8,and Mmp1 in the abdominal adipose tissue of obese rats was determined using the Agena MassARRAY system.Western blot was performed to assess protein expression levels.Target genes were identified based on the methylation degree in the promoter region and protein expression.Enrichment analysis of signaling pathways was conducted to identify relevant target genes and obtain a multiple signaling pathway network associated with obesity.Core and terminal effector molecules in the pathway networks were selected as research targets for reverse transcription-polymerase chain reaction(RT-PCR)analysis.Results:Four genes(Adra2b,Creb1,Itgad,and Pik3cd)showed a degree of promoter methylation consistent with their respective protein expression levels.Among them,Adra2b,Creb1,and Pik3cd expression increased,while that of Itgad decreased.Enrichment analysis revealed that Creb1 and Pik3cd were involved in 6 signaling pathways related to obesity:tumor necrosis factor(TNF)signaling pathway,growth hormone synthesis/secretion and action,adenosine 5'-monophosphate-activated protein kinase(AMPK)signaling pathway,relaxin signaling pathway,cyclic nucleotide(cAMP)signaling pathway,and phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway.Subsequently,a multiple signaling pathways network was constructed based on promoter methylation.Key molecules including protein kinase B(AKT),mechanistic target of rapamycin complex 1(mTORC1),and unc-51 like autophagy activating kinase 1(ULK1),as well as terminal effector molecules interleukin-1β(IL-1β),interleukin-6(IL-6),and chemokine(C-X-C motif)ligand 2(CXCL2)were selected as research targets.Wendan decoction decreased the expressions of AKT,mTORC1,IL-1

关键词： Wendan decoction Obesity Signal pathway Methylation

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Thylakoid engineered M2 macrophage for sonodynamic effect promoted cell therapy of early atherosclerosis

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Nano Research 2024年第4期17卷 2919-2928页

作者： Guanghao wu Changwen Mu Qianru Zhao Yao Lei Ran Cheng Weidong Nie Jiamin Qu Yuping Dong Ruili Yang haiyan Xie State Key Laboratory of Natural and Biomimetic Drugs School of Pharmaceutical SciencesChemical Biology CenterPeking UniversityBeijing 100191China School of Materials Science and Engineering Beijing Institute of TechnologyBeijing 100081China School of Life Science Beijing Institute of TechnologyBeijing 100081China School of Stomatology Peking UniversityBeijing 100081China

Atherosclerosis is the most common cause of cardiovascular diseases that contribute to the major morbidity worldwide,but still lacking of effective treatment strategy.Here,a hybrid cell is constructed for the sonodynamic effect promoted cell therapy of early atherosclerosis by fusing M2 macrophages with thylakoid(TK)membranes.After systemic administration,the obtained TK-M2 actively accumulates in the early atherosclerotic plaques,wherein M2 macrophages relieve the cholesterol accumulation and the inflammation in the foam cells.Meanwhile,the TK membranes decorated on the M2 macrophages exhibit both type I and type II sonodynamic effects under ultrasound(US)activation,inducing the direct apoptosis of foam cells.The cooperation of M2 and TK leads to significant outcome in eliminating atherosclerotic plaques without obvious side-effects,providing a new avenue for atherosclerosis treatment.

关键词： atherosclerosis thylakoid ultrasound M2 macrophage

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Transfer of disulfide bond formation modules via yeast artificial chromosomes promotes the expression of heterologous proteins inKluyveromyces marxianus

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mLife 2024年第1期3卷 129-142页

作者： Pingping wu Wenjuan Mo Tian Tian Kunfeng Song Yilin Lyu haiyan Ren Jungang Zhou Yao Yu Hong Lu State Key Laboratory of Genetic Engineering School of Life SciencesFudan UniversityShanghaiChina Shanghai Engineering Research Center of Industrial Microorganisms ShanghaiChina

Kluyveromyces marxianus is a food-safe yeast with great potential for producing heterologous proteins.Improving the yield in K.marxianus remains a challenge and incorporating large-scale functional modules poses a technical obstacle in engineering.To address these issues,linear and circular yeast artificial chromosomes of K.marxianus(KmYACs)were constructed and loaded with disulfide bond formation modules from Pichia pastoris or K.marxianus.These modules contained up to seven genes with a maximum size of 15 kb.KmYACs carried telomeres either from K.marxianus or Tetrahymena.KmYACs were transferred successfully into K.marxianus and stably propagated without affecting the normal growth of the host,regardless of the type of telomeres and configurations of KmYACs.KmYACs increased the overall expression levels of disulfide bond formation genes and significantly enhanced the yield of various heterologous proteins.In high-density fermentation,the use of KmYACs resulted in a glucoamylase yield of 16.8 g/l,the highest reported level to date in K.marxianus.Transcriptomic and metabolomic analysis of cells containing KmYACs suggested increased flavin adenine dinucleotide biosynthesis,enhanced flux entering the tricarboxylic acid cycle,and a preferred demand for lysine and arginine as features of cells overexpressing heterologous proteins.Consistently,supplementing lysine or arginine further improved the yield.Therefore,KmYAC provides a powerful platform for manipulating large modules with enormous potential for industrial applications and fundamental research.Transferring the disulfide bond formation module via YACs proves to be an efficient strategy for improving the yield of heterologous proteins,and this strategy may be applied to optimize other microbial cell factories.

关键词： disulfide bond formation expression of heterologous proteins Kluyveromyces marxianus telomere yeast artificial chromosome

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Prognostic value of calcium and phosphorus status in elderly heart disease patients with tricuspid regurgitation

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Chinese Medical Journal 2024年第5期137卷 613-615页

作者： Qingrong Liu Kai Cao Ziang Li Yunqing Ye Qian Zhang Hongliang Zhang haiyan Xu Zhe Li Yongjian wu CHINA-DVD Collaborators Department of Cardiology Beijing Aerospace General HospitalBeijing 100076China Department of Cardiology Fuwai HospitalNational Center for Cardiovascular DiseaseChinese Academy of Medical Science and Peking Union Medical CollegeBeijing 100037China Department of Beijing Institute of Ophthalmology Beijing Tongren HospitalCapital Medical UniversityBeijing 100000China 不详

To the Editor:Tricuspid regurgitation(TR)associated with valve disease is a general medical issue with growing prevalence and socioeconomic burden.TR,especially moderate or severe TR,has been reported to be associated with an increased risk of heart failure and mortality.^([1])Studies have shown that blood calcium levels and blood phosphorus levels have a great influence on the human body,especially on the cardiovascular system.Elevated serum calcium levels were reported to be a risk factor for cardiovascular disease.^([2])A meta-analysis reported that moderate dietary calcium intake protects against cardiovascular and all-cause mortality and that calcium supplementation reduces mortality in women.^([3])

关键词： mortality regurgitation cardiovascular

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CYP3A5 unexpectedly regulates glucose metabolism through the AKT-TXNIP-GLUT1 axis in pancreatic cancer

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Genes & Diseases 2024年第4期11卷 381-399页

作者： Ming Shao Qingfei Pan haiyan Tan Jing wu Ha Won Lee Andrew D.Huber William C.Wright Ji-Hoon Cho Jiyang Yu Junmin Peng Taosheng Chen Department of Chemical Biology and Therapeutics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Computational Biology St.Jude Children's Research HospitalMemphisTN 38105USA Center for Proteomics and Metabolomics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Structural Biology St.Jude Children's Research HospitalMemphisTN 38105USA Department of Developmental Neurobiology St.Jude Children's Research HospitalMemphisTN 38105USA

CYP3A5 is a cytochrome P450(CYP)enzyme that metabolizes drugs and contributes to drug resistance in cancer.However,it remains unclear whether CYP3A5 directly influences cancer progression.In this report,we demonstrate that CYP3A5 regulates glucose metabolism in pancreatic ductal adenocarcinoma.Multi-omics analysis showed that CYP3A5 knockdown re-sults in a decrease in various glucose-related metabolites through its effect on glucose trans-port.A mechanistic study revealed that CYP3A5 enriches the glucose transporter GLUT1 at the plasma membrane by restricting the translation of TXNIP,a negative regulator of GLUT1.Notably,CYP3A5-generated reactive oxygen species were proved to be responsible for atten-uating the AKT-4EBP1-TXNIP signaling pathway.CYP3A5 contributes to cell migration by maintaining high glucose uptake in pancreatic cancer.Taken together,our results,for the first time,reveal a role of CYP3A5 in glucose metabolism in pancreatic ductal adenocarcinoma and identify a novel mechanism that is a potential therapeutic target.

关键词： Cell migration CYP3A5 Glucose metabolism GLUT1 Pancreatic cancer TXNIP

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Physical activity and exercise in liver cancer

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Liver Research 2024年第1期8卷 22-33页

作者： haiyan Chen Huimin Zhou Bo wu Hanxiao Lu Jie Zhang Yan Zhang Yuanlong Gu Guangwen Zhou Jie Xiang Jun Yang Department of General Surgery Affiliated Hospital of Jiangnan UniversityJiangsuChina School of Medicine Jiangnan University WuxiJiangsuChina Department of General Surgery Shanghai Sixth People's HospitalShanghaiChina Department of Endocrinology Wuxi Mingci Cardiovascular HospitalWuxiJiangsuChina

Sarcopenia and physical deconditioning are common complications in patients with liver cancer,which are frequently caused by insufficient physical activity and poor nutritional status,resulting in physical frailty and a significant impact on the patient's physical fitness.Notably,sarcopenia,frailty,and poor cardiopulmonary endurance have all been linked to higher mortality rates among patients with liver cancer.Exercise intervention significantly improves various health parameters in liver cancer patients,including metabolic syndrome,muscle wasting,cardiorespiratory endurance,health-related quality of life,and reduction in hepatic venous pressure gradient.However,the link between physical exercise and liver cancer is commonly overlooked.In this article,we will examine the impact of exercise on liver cancer and present the most recent evidence on the best types of exercise for various stages of liver cancer.This article also summarizes and discusses the molecular mechanisms that control metabolism and systemic immune function in tumors.In brief,physical exercise should be considered an important intervention in the prevention and treatment of liver cancer and its complications.

关键词： Physical activity(PA) Exercise Liver cancer Sarcopenia Frailty Rehabilitation

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GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling

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Oncology Research 2024年第2期32卷 361-371页

作者： TINGTING LI WEI ZHONG LIU YANG ZHIYU ZHAO LI WANG CONG LIU WANYUN LI haiyan LV SHENGYU WANG JIANGHUA YAN TING wu GANG SONG FANGHONG LUO Cancer Research Center School of MedicineXiamen UniversityXiamen361000China Department of Pharmacy Xiamen Mental Health CenterXiamen Xianyue HospitalXiamen361000China

The high mortality rate associated with gastric cancer(GC)has resulted in an urgent need to identify novel therapeutic targets for GC.This study aimed to investigate whether GAIP interacting protein,C terminus 1(GIPC1)represents a therapeutic target and its regulating mechanism in GC.GIPC1 expression was elevated in GC tissues,liver metastasis tissues,and lymph node metastases.GIPC1 knockdown or GIPC1 blocking peptide blocked the platelet-derived growth factor receptor(PDGFR)/PI3K/AKT signaling pathway,and inhibited the proliferation and migration of GC cells.Conversely,GIPC1 overexpression markedly activated the PDGFR/PI3K/AKT signaling pathway,and promoted GC cell proliferation and migration.Furthermore,platelet-derived growth factor subunit BB(PDGF-BB)cytokines and the AKT inhibitor attenuated the effect of differential GIPC1 expression.Moreover,GIPC1 silencing decreased tumor growth and migration in BALB/c nude mice,while GIPC1 overexpression had contrasting effects.Taken together,our findings suggest that GIPC1 functions as an oncogene in GC and plays a central role in regulating cell proliferation and migration via the PDGFR/PI3K/AKT signaling pathway.

关键词： GIPC1 PDGFR Gastric cancer Proliferation Migration

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