IF 7.8 1区医学

Aging Cell Pub Date : 2024-09-10 DOI: 10.1111/acel.14330

Sisi Yang, Ziliang Ye, Panpan He, Yuanyuan Zhang, Mengyi Liu, Chun Zhou, Yanjun Zhang, Xiaoqin Gan, Yu Huang, Hao Xiang, Xianhui Qin

{"title":"Plasma proteomics for risk prediction of Alzheimer's disease in the general population","authors":"Sisi Yang, Ziliang Ye, Panpan He, Yuanyuan Zhang, Mengyi Liu, Chun Zhou, Yanjun Zhang, Xiaoqin Gan, Yu Huang, Hao Xiang, Xianhui Qin","doi":"10.1111/acel.14330","DOIUrl":"https://doi.org/10.1111/acel.14330","url":null,"abstract":"We aimed to develop and validate a protein risk score for predicting Alzheimer's disease (AD) and compare its performance with a validated clinical risk model (Cognitive Health and Dementia Risk Index for AD [CogDrisk‐AD]) and apolipoprotein E (APOE) genotypes. The development cohort, consisting of 35,547 participants from England in the UK Biobank, was randomly divided into a 7:3 training–testing ratio. The validation cohort included 4667 participants from Scotland and Wales in the UK Biobank. In the training set, an AD protein risk score was constructed using 31 proteins out of 2911 proteins. In the testing set, the AD protein risk score had a C‐index of 0.867 (95% CI, 0.828, 0.906) for AD prediction, followed by CogDrisk‐AD risk factors (C‐index, 0.856; 95% CI, 0.823, 0.889), and APOE genotypes (C‐index, 0.705; 95% CI, 0.660, 0.750). Adding the AD protein risk score to CogDrisk‐AD risk factors (C‐index increase, 0.050; 95% CI, 0.008, 0.093) significantly improved the predictive performance for AD. However, adding CogDrisk‐AD risk factors (C‐index increase, 0.040; 95% CI, −0.007, 0.086) or APOE genotypes (C‐index increase, 0.000; 95% CI, −0.054, 0.055) to the AD protein risk score did not significantly improve the predictive performance for AD. The top 10 proteins with the highest coefficients in the AD protein risk score contributed most of the predictive power for AD risk. These results were verified in the external validation cohort. EGFR, GFAP, and CHGA were identified as key proteins within the protein network. Our result suggests that the AD protein risk score demonstrated a good predictive performance for AD risk.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":7.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142192214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comparative single‐cell transcriptomic analysis across tissues of aging primates reveals specific autologous activation of ZNF281 to mitigate oxidative stress in cornea 对衰老灵长类动物各组织的单细胞转录组比较分析表明，ZNF281 的特异性自体激活可减轻角膜的氧化应激反应

IF 7.8 1区医学

Aging Cell Pub Date : 2024-09-10 DOI: 10.1111/acel.14319

Yuhua Xiao, Xu Chen, Zheyao Chen, Wangxuan Dai, Xing Hu, Shuyao Zhang, Jiawei Zhong, Jia Chen, Xu Liu, Lingyi Liang, Youjin Hu

{"title":"Comparative single‐cell transcriptomic analysis across tissues of aging primates reveals specific autologous activation of ZNF281 to mitigate oxidative stress in cornea","authors":"Yuhua Xiao, Xu Chen, Zheyao Chen, Wangxuan Dai, Xing Hu, Shuyao Zhang, Jiawei Zhong, Jia Chen, Xu Liu, Lingyi Liang, Youjin Hu","doi":"10.1111/acel.14319","DOIUrl":"https://doi.org/10.1111/acel.14319","url":null,"abstract":"Reactive oxygen species (ROS) and oxidative stress accelerate cellular aging, but their impact on different tissues varies. The cornea, known for its robust antioxidant defense systems, is relatively resistant to age‐related diseases like cancer. However, the precise mechanisms by which the cornea maintains ROS homeostasis during aging remain unclear. Through comparative single‐cell transcriptomic analysis of the cornea and other tissues in young and old nonhuman primates, we identified that a ZNF281 coding transcriptomic program is specifically activated in cornea during aging. Further investigation revealed that ZNF281 forms a positive feedback loop with FOXO3 to sense elevated levels of ROS and mitigate their effects potentially by regulating the mitochondrial respiratory chain and superoxide dismutase (SOD) expression. Importantly, we observed that overexpression of ZNF281 in MSCs prevented cellular senescence. In summary, these findings open up possibilities for understanding tissue‐specific aging and developing new therapies targeting ROS damage.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":7.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142192215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The longevity factor spermidine is part of a highly heritable complex erythrocyte phenotype associated with longevity. 长寿因子亚精胺是与长寿相关的高遗传性复杂红细胞表型的一部分。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-07 DOI: 10.1111/acel.14311

Cameron J Kaminsky, Jericha Mill, Viharkumar Patel, Dylan Pierce, Amelia Haj, Aaron S Hess, Lingjun Li, Thomas Raife

{"title":"The longevity factor spermidine is part of a highly heritable complex erythrocyte phenotype associated with longevity.","authors":"Cameron J Kaminsky, Jericha Mill, Viharkumar Patel, Dylan Pierce, Amelia Haj, Aaron S Hess, Lingjun Li, Thomas Raife","doi":"10.1111/acel.14311","DOIUrl":"https://doi.org/10.1111/acel.14311","url":null,"abstract":"Extreme longevity in humans is known to be a heritable trait. In a well-established twin erythrocyte metabolomics and proteomics database, we identified the longevity factor spermidine and a cluster of correlated molecules with high heritability estimates. Erythrocyte spermidine is 82% heritable and significantly correlated with 59 metabolites and 22 proteins. Thirty-eight metabolites and 19 proteins were >20% heritable, with a mean heritability of 61% for metabolites and 49% for proteins. Correlated metabolites are concentrated in energy metabolism, redox homeostasis, and autophagy pathways. Erythrocyte mean cell volume (MCV), an established heritable trait, was consistently negatively correlated with the top 25 biomolecules most strongly correlated with spermidine, indicating that smaller MCVs are associated with higher concentrations of spermidine and correlated molecules. Previous studies have linked larger MCVs with poorer memory, cognition, and all-cause mortality. Analysis of 432,682 unique patient records showed a linear increase in MCV with age but a significant deviation toward smaller than expected MCVs above age 86, suggesting that smaller MCVs are associated with extreme longevity. Consistent with previous reports, a subset of 78,158 unique patient records showed a significant skewing toward larger MCV values in a deceased cohort compared to an age-matched living cohort. Our study supports the existence of a complex, heritable phenotype in erythrocytes associated with health and longevity.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuropeptides regulate embryonic salivary gland branching through the FGF/FGFR pathway in aging klotho-deficient mice. 神经肽通过 FGF/FGFR 通路调节老化 klotho-deficient 小鼠的胚胎唾液腺分支。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-06 DOI: 10.1111/acel.14329

Nguyen Khanh Toan, Soo-A Kim, Sang-Gun Ahn

{"title":"Neuropeptides regulate embryonic salivary gland branching through the FGF/FGFR pathway in aging klotho-deficient mice.","authors":"Nguyen Khanh Toan, Soo-A Kim, Sang-Gun Ahn","doi":"10.1111/acel.14329","DOIUrl":"https://doi.org/10.1111/acel.14329","url":null,"abstract":"Salivary gland branching morphogenesis is regulated by the functional integration of neuronal signaling, but the underlying mechanisms are not fully understood in aging accelerated klotho-deficient (Kl-/-) mice. Here, we investigated whether the neuropeptides substance P (SP) and neuropeptide Y (NPY) affect the branching morphogenesis of embryonic salivary glands in aging Kl-/- mice. In the salivary glands of embryonic Kl-/- mice, morphological analysis and immunostaining revealed that epithelial bud formation, neuronal cell proliferation/differentiation, and the expression of the salivary gland functional marker ZO-1 were decreased in embryonic ductal cells. Incubation with SP/NPY at E12-E13d promoted branching morphogenesis, parasympathetic innervation, and epithelial proliferation in salivary glands of embryonic Kl-/- mice. The ERK inhibitor U0126 specifically inhibited neuronal substance-induced epithelial bud formation in the embryonic salivary gland. RNA-seq profiling analysis revealed that the expression of fibroblast growth factors/fibroblast growth factors (FGFs/FGFRs) and their receptors was significantly regulated by SP/NPY treatment in the embryonic salivary gland (E15). The FGFR inhibitor BGJ389 inhibited new branching formation induced by SP and NPY treatment and ERK1/2 expression. These results showed that aging may affect virtually the development of salivary gland by neuronal dysfunction. The neuropeptides SP/NPY induced embryonic salivary gland development through FGF/FGFR/ERK1/2-mediated signaling.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blockade of dopamine D3 receptors improves hippocampal synaptic function and rescues age-related cognitive phenotype. 阻断多巴胺 D3 受体可改善海马突触功能，并挽救与年龄相关的认知表型。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-05 DOI: 10.1111/acel.14291

Maria Rosaria Tropea, Marcello Melone, Domenica Donatella Li Puma, Valeria Vacanti, Giuseppe Aceto, Bruno Bandiera, Roberta Carmela Trovato, Sebastiano Alfio Torrisi, Gian Marco Leggio, Agostino Palmeri, Marcello D'Ascenzo, Fiorenzo Conti, Claudio Grassi, Daniela Puzzo

{"title":"Blockade of dopamine D3 receptors improves hippocampal synaptic function and rescues age-related cognitive phenotype.","authors":"Maria Rosaria Tropea, Marcello Melone, Domenica Donatella Li Puma, Valeria Vacanti, Giuseppe Aceto, Bruno Bandiera, Roberta Carmela Trovato, Sebastiano Alfio Torrisi, Gian Marco Leggio, Agostino Palmeri, Marcello D'Ascenzo, Fiorenzo Conti, Claudio Grassi, Daniela Puzzo","doi":"10.1111/acel.14291","DOIUrl":"https://doi.org/10.1111/acel.14291","url":null,"abstract":"Dopamine D3 receptors (D3Rs) modulate neuronal activity in several brain regions including the hippocampus. Although previous studies reported that blocking D3Rs exerts pro-cognitive effects, their involvement in hippocampal synaptic function and memory in the healthy and aged brain has not been thoroughly investigated. We demonstrated that in adult wild type (WT) mice, D3R pharmacological blockade or genetic deletion as in D3 knock out (KO) mice, converted the weak form of long-term potentiation (LTP1) into the stronger long-lasting LTP (LTP2) via the cAMP/PKA pathway, and allowed the formation of long-term memory. D3R effects were mainly mediated by post-synaptic mechanisms as their blockade enhanced basal synaptic transmission (BST), AMPAR-mediated currents, mEPSC amplitude, and the expression of the post-synaptic proteins PSD-95, phospho(p)GluA1 and p-CREB. Consistently, electron microscopy revealed a prevalent expression of D3Rs in post-synaptic dendrites. Interestingly, with age, D3Rs decreased in axon terminals while maintaining their levels in post-synaptic dendrites. Indeed, in aged WT mice, blocking D3Rs reversed the impairment of LTP, BST, memory, post-synaptic protein expression, and PSD length. Notably, aged D3-KO mice did not exhibit synaptic and memory deficits. In conclusion, we demonstrated the fundamental role of D3Rs in hippocampal synaptic function and memory, and their potential as a therapeutic target to counteract the age-related hippocampal cognitive decline.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rejuvenation of the reconstitution potential and reversal of myeloid bias of aged HSCs upon pH treatment. pH 处理可恢复老化造血干细胞的重组潜能并逆转其骨髓偏向。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-05 DOI: 10.1111/acel.14324

Sachin Kumar, Jeffrey D Vassallo, Kalpana J Nattamai, Aishlin Hassan, Angelika Vollmer, Rebekah Karns, Mehmet Sacma, Travis Nemkov, Angelo D'Alessandro, Hartmut Geiger

引用次数: 0

Targeting TGF-β signaling, oxidative stress, and cellular senescence rescues osteoporosis in gerodermia osteodysplastica. 以 TGF-β 信号、氧化应激和细胞衰老为靶点可拯救老年性骨质疏松症患者的骨质疏松症。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-05 DOI: 10.1111/acel.14322

W L Chan, C H Bucher, J Goldes, A C Ma, M Steiner, B M Willie, S Mundlos, U Kornak

{"title":"Targeting TGF-β signaling, oxidative stress, and cellular senescence rescues osteoporosis in gerodermia osteodysplastica.","authors":"W L Chan, C H Bucher, J Goldes, A C Ma, M Steiner, B M Willie, S Mundlos, U Kornak","doi":"10.1111/acel.14322","DOIUrl":"https://doi.org/10.1111/acel.14322","url":null,"abstract":"GORAB is a key regulator of Golgi vesicle transport and protein glycanation. Loss of GORAB function in gerodermia osteodysplastica (GO) causes shortening of glycosaminoglycan chains, leading to extracellular matrix disorganization that results in wrinkled skin, osteoporosis and elevated TGF-β signaling. In this study, we investigated the role of TGF-β-signaling, oxidative stress, and resulting cellular senescence in the osteoporosis phenotype of GO. Treatment of GorabPrx1 conditional knockouts with the TGF-β neutralizing antibody 1D11 rescued the trabecular bone loss, indicating that TGF-β overactivation causes osteoporosis in GO. Using an inducible knockout system, we demonstrated that TGF-β dysregulation was not a cell-intrinsic effect of GORAB inactivation, but a consequence of a disorganized extracellular matrix. Enhanced TGF-β signaling caused elevated Nox4 expression in GorabPrx1 mutants and in GO patients' fibroblasts, resulting in overproduction of mitochondrial superoxide. The resulting oxidative stress was detected in GORAB null cells and also in wildtype bystander cells. The same effect was observed in zebrafish after TALEN-mediated gorab inactivation, indicating that the pathway is evolutionarily conserved. Treating GorabPrx1 mutants with the antioxidant N-acetylcysteine ameliorated the osteoporosis phenotype. TGF-β induced oxidative stress coincided with accumulation of DNA damage and elevated expression of senescence markers. Inactivation of Cdkn2a in the GorabPrx1 rescued the osteoporosis phenotype. Reduced colony formation and altered subpopulations of bone marrow stromal cells were normalized upon inactivation of Cdkn2a, thus further demonstrating the relevance of cellular senescence in the pathogenesis. Our results shed light on the causative role of a TGF-β-Nox4-senescence axis and therapeutic strategies for GO.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Age and duration of obesity modulate the inflammatory response and expression of neuroprotective factors in mammalian female brain. 肥胖的年龄和持续时间会调节哺乳动物雌性大脑的炎症反应和神经保护因子的表达。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-04 DOI: 10.1111/acel.14313

Binnur Eroglu, Carlos Isales, Ali Eroglu

{"title":"Age and duration of obesity modulate the inflammatory response and expression of neuroprotective factors in mammalian female brain.","authors":"Binnur Eroglu, Carlos Isales, Ali Eroglu","doi":"10.1111/acel.14313","DOIUrl":"https://doi.org/10.1111/acel.14313","url":null,"abstract":"Obesity has become a global epidemic and is associated with comorbidities, including diabetes, cardiovascular, and neurodegenerative diseases, among others. While appreciable insight has been gained into the mechanisms of obesity-associated comorbidities, effects of age, and duration of obesity on the female brain remain obscure. To address this gap, adolescent and mature adult female mice were subjected to a high-fat diet (HFD) for 13 or 26 weeks, whereas age-matched controls were fed a standard diet. Subsequently, the expression of inflammatory cytokines, neurotrophic/neuroprotective factors, and markers of microgliosis and astrogliosis were analyzed in the hypothalamus, hippocampus, and cerebral cortex, along with inflammation in visceral adipose tissue. HFD led to a typical obese phenotype in all groups independent of age and duration of HFD. However, the intermediate duration of obesity induced a limited inflammatory response in adolescent females' hypothalamus while the hippocampus, cerebral cortex, and visceral adipose tissue remained unaffected. In contrast, the prolonged duration of obesity resulted in inflammation in all three brain regions and visceral adipose tissue along with upregulation of microgliosis/astrogliosis and suppression of neurotrophic/neuroprotective factors in all brain regions, denoting the duration of obesity as a critical risk factor for neurodegenerative diseases. Importantly, when female mice were older (i.e., mature adult), even the intermediate duration of obesity induced similar adverse effects in all brain regions. Taken together, our findings suggest that (1) both age and duration of obesity have a significant impact on obesity-associated comorbidities and (2) early interventions to end obesity are critical to preserving brain health.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rapamycin's lifespan effect is modulated by mito-nuclear epistasis in Drosophila. 雷帕霉素对果蝇寿命的影响受有丝分裂-核上位作用的调节

IF 8 1区医学

Aging Cell Pub Date : 2024-09-03 DOI: 10.1111/acel.14328

Rita Ibrahim, Maria Bahilo Martinez, Adam J Dobson

引用次数: 0

Analysis of the senescence-associated cell surfaceome reveals potential senotherapeutic targets. 衰老相关细胞表面组分析揭示了潜在的衰老治疗靶点。

IF 8 1区医学

Aging Cell Pub Date : 2024-09-03 DOI: 10.1111/acel.14312

Yushuang Deng, Ting Liu, Enzo Scifo, Tao Li, Kan Xie, Bernd Taschler, Sarah Morsy, Kristina Schaaf, Armin Ehninger, Daniele Bano, Dan Ehninger

{"title":"Analysis of the senescence-associated cell surfaceome reveals potential senotherapeutic targets.","authors":"Yushuang Deng, Ting Liu, Enzo Scifo, Tao Li, Kan Xie, Bernd Taschler, Sarah Morsy, Kristina Schaaf, Armin Ehninger, Daniele Bano, Dan Ehninger","doi":"10.1111/acel.14312","DOIUrl":"https://doi.org/10.1111/acel.14312","url":null,"abstract":"The accumulation of senescent cells is thought to play a crucial role in aging-associated physiological decline and the pathogenesis of various age-related pathologies. Targeting senescence-associated cell surface molecules through immunotherapy emerges as a promising avenue for the selective removal of these cells. Despite its potential, a thorough characterization of senescence-specific surface proteins remains to be achieved. Our study addresses this gap by conducting an extensive analysis of the cell surface proteome, or \"surfaceome\", in senescent cells, spanning various senescence induction regimes and encompassing both murine and human cell types. Utilizing quantitative mass spectrometry, we investigated enriched cell surface proteins across eight distinct models of senescence. Our results uncover significant changes in surfaceome expression profiles during senescence, highlighting extensive modifications in cell mechanics and extracellular matrix remodeling. Our research also reveals substantive heterogeneity of senescence, predominantly influenced by cell type and senescence inducer. A key discovery of our study is the identification of four unique cell surface proteins with extracellular epitopes. These proteins are expressed in senescent cells, absent or present at low levels in their proliferating counterparts, and notably upregulated in tissues from aged mice and an Alzheimer's disease mouse model. These proteins stand out as promising candidates for senotherapeutic targeting, offering potential pathways for the detection and strategic targeting of senescent cell populations in aging and age-related diseases.","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":null,"pages":null},"PeriodicalIF":8.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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