Aging and Disease最新文献

{"title":"Effects of Lipid Metabolites and Cross Organ Lipid Metabolism Regulation on Bone Homeostasis.","authors":"Mengyuan Li, Jiaheng Zhang, Jiaqian Tang, Chang Zhou, Guomin Zhang, Huiping Liu, Xiaoming Lei","doi":"10.14336/AD.2025.0575","DOIUrl":"10.14336/AD.2025.0575","url":null,"abstract":"<p><p>Osteoporosis is a metabolic bone disease characterized by the loss and destruction of bone microstructure. Its incidence rate increases with age and is an important public health problem. Recently, the relationship between lipid metabolism and osteoporosis has received widespread attention. Lipid metabolites, such as fatty acids, cholesterol, and adipose tissue-derived hormones, participate in maintaining bone metabolism homeostasis through key molecular networks that regulate bone cell function. In addition, the interaction between lipid metabolism and bone tissue involves cross-organ regulatory mechanisms, including the bone-adipose, bone-pancreas, and bone-gut axes. This study considers the types of lipid metabolites and their effects on bone cell function as a starting point for exploring the interaction between lipid metabolism and bone tissue. Furthermore, this study elucidated the specific mechanism of action of lipid metabolites on osteocytes, analyzed the relationship between lipid metabolism abnormalities and osteoporosis, and provided ideas for further clinical research on lipid metabolism-related osteoporosis.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Insights into the Mechanism and Treatment of Diabetes-Related Brain Complications: Focusing on the Blood-Brain Barrier Impairment.","authors":"Caiyi Long, Yueheng Pu, Shunseng Keng, Jiajing Tao, Boxun Zhang, Rensong Yue","doi":"10.14336/AD.2025.0296","DOIUrl":"10.14336/AD.2025.0296","url":null,"abstract":"<p><p>Diabetes mellitus often leads to secondary brain disorders, thus increasing the risk of mortality. The blood-brain barrier (BBB) is a peripheral-central defense mechanism that significantly impacts diabetes-related brain complications. Under hyperglycemic conditions, the BBB undergoes pathological structural alterations, leading to increased permeability and transport dysfunction. Clinically, BBB damage induces diabetes-related brain complications such as cognitive impairment, stroke, and depression. Notably, BBB damage can occur before the onset of disease symptoms in the brain and may serve as a predictor of disease progression and prognosis. Hyperglycemia is the main cause of BBB damage and can induce oxidative stress, inflammatory response, Advanced glycation end products (AGEs) accumulation, and high-mobility group box 1 (HMGB1) signaling axis activation. These factors lead to endothelial dysfunction, disruption of tight junction proteins, loss of pericytes, activation of astrocytes and microglia, disruption of the actin cytoskeleton, alterations in the basement membrane, and an increase in matrix metalloproteinases (MMPs). Collectively, these processes contribute to brain injury in patients with diabetes. Lifestyle interventions and hypoglycemic, antihypertensive, and lipid-lowering agents play therapeutic roles in BBB damage and diabetes-related brain complications. However, the role of some drugs in this context is controversial and remains known only at the animal and cellular levels. Several studies have investigated the therapeutic potential of targeted nanomedicines and natural compounds; however, it remains challenging to translate their research findings to clinical practice. In conclusion, this review highlights the clinical evidence, pathological mechanisms, and existing treatment options for BBB damage in patients with diabetes-related brain complications. It also demonstrates the potential of targeted nanomedicines and natural compounds, providing a foundation for future research.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise as a Metabolic Regulator: Targeting AMPK/mTOR-Autophagy Crosstalk to Counteract Sarcopenic Obesity.","authors":"Daoqi Zhang, Congfei Lu, Kai Sang","doi":"10.14336/AD.2025.0419","DOIUrl":"10.14336/AD.2025.0419","url":null,"abstract":"<p><p>Sarcopenic obesity (SO), a geriatric syndrome characterized by the coexistence of progressive skeletal muscle atrophy and excessive adipose tissue accumulation, represents a growing public health challenge associated with aging populations. While multifactorial pathogenesis involves chronic inflammation, hormonal changes, and mitochondrial dysfunction, sedentary lifestyles and aging remain primary modifiable and non-modifiable risk factors, respectively. Mechanistically, exercise exerts dual therapeutic effects: (1) hypertrophy of type II muscle fibers through IGF-1/Akt/mTORC1 signaling activation, and (2) enhanced lipid β-oxidation via AMPK/PGC1α axis stimulation, thereby mitigating both sarcopenia and adiposity. The autophagy-lysosome system, a conserved cellular quality-control mechanism, orchestrates organelle turnover and nutrient recycling through three distinct pathways: macroautophagic, chaperone-mediated autophagy, and mitophagy. In SO, impaired proteolytic and lipolytic processes converge to induce autophagic flux blockade, manifested by accumulated p62/SQSTM1 and reduced LC3-II/LC3-I ratio. Targeting the AMPK/mTOR signaling nexus, which senses cellular energy status, emerges as a strategic intervention. Exercise-mediated ATP depletion activates AMPK while suppressing mTORC1, thereby synchronously inducing autophagy initiation (ULK1 phosphorylation) and lysosomal biogenesis (TFEB nuclear translocation). This metabolic reprogramming ultimately restores proteostasis and lipid homeostasis in myocytes and adipocytes.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-dependent Transcriptional and Circuit Alterations in the brain Underlie Post-Anesthesia Neurobehavioral Dysfunction.","authors":"Yun Li, Cosar Uzun, Syed Taufiqul Islam, Balaji Krishnamachary, Hangnoh Lee, Zihui Wang, Hui Li, Shaolin Liu, Junfang Wu","doi":"10.14336/AD.2025.0596","DOIUrl":"10.14336/AD.2025.0596","url":null,"abstract":"<p><p>With rising life expectancy, more elderly individuals are undergoing surgery, highlighting the need to understand postoperative neurological complications. Studies have linked general anesthesia (GA) to olfactory dysfunction (OD) and cognitive decline following operation (OP), though mechanisms remain unclear. Using aged C57BL/6 mice subjected to laparotomy and 2-hour isoflurane exposure, we assessed behavioral and molecular outcomes through functional tests and bulk RNA sequencing (RNAseq). We observed persistent OD in the weeks following GA/OP, along with reduced limb strength and motor coordination, indicative of increased frailty. While no immediate cognitive deficits were apparent, aged mice exhibited delayed cognitive impairments, including diminished learning and memory in Y-maze and novel object recognition tasks, as well as increased apathy in nest-building behavior. RNAseq of the olfactory bulb (OB) at 1-day post-GA/OP revealed upregulation of ubiquitin-dependent proteins and catabolic processes in the aged mice compared to sham group. In contrast, transcriptomic analysis of the hippocampus (HI) at 5 weeks after GA/OP showed more extensive molecular pathway changes, correlating with the delayed impairment of cognitive functions. Compared to young adult mice, aged GA/OP mice demonstrated upregulated expression of genes associated with innate immunity and reduced neurogenesis in the OB, along with increased gliogenesis and reduced RNA splicing activity in the HI. Additionally, in vivo electrophysiology recordings from the OB mitral cell layer revealed alterations in neuronal excitability and circuit disruptions after GA/OP. Taken together, our findings provided functional, molecular, and circuit-level insights into the age-dependent persistent olfactory impairment and delayed cognitive dysfunctions following general anesthesia and surgery.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microcirculation Dysfunction in Subacute Stroke: The Role of Delayed Capillary Pericyte Loss.","authors":"Yiya Xu, Chao Chen, Jilin Weng, Ting Chen, Yingchao He, Zhiwei Song, Yinzhou Wang","doi":"10.14336/AD.2025.0197","DOIUrl":"10.14336/AD.2025.0197","url":null,"abstract":"<p><p>Post-recanalization microcirculation dysfunction is common and significantly contributes to poor outcomes in ischemic stroke. Pericytes have been shown to mediate the \"no-reflow\" phenomenon by constricting capillaries in experimental stroke models, implicating their critical role in early microcirculation dysfunction. However, little is known about the long-term fate of pericytes and their contribution to sustained microcirculation dysfunction in prolonged period of time. We conducted repeated longitudinal observations of pericyte fate and function, as well as blood flow dynamics across multiple vascular segments, using two-photon imaging in PDGFRβ-tdTomato mice subjected to transient middle cerebral artery occlusion (tMCAO) over a 14-day period. Multivariate analysis was performed to identify imaging features independently associated with capillary perfusion on day 14. Types of pericyte death were assessed using immunohistochemistry and Western blot analysis. Fasudil and the RIPK1 inhibitor necrostatin-1 were administered to modulate pericyte dysfunction and survival during the acute and subacute phases of stroke. Outcomes were evaluated by total capillary perfusion, infarct volume, blood brain barrier (BBB) integrity, and neurological function over 14 days. Pericyte loss observed on day 7 post-stroke was independently associated with impaired microcirculation perfusion, as indicated by a reduction in total capillary volume. While fasudil treatment alone improved microcirculation perfusion on day 3, it did not alter pericyte fate or improve outcomes by day 14. Necroptosis was found to contribute to delayed pericyte loss in the ischemic penumbra. Combined therapy with fasudil and necrostatin-1 effectively prevented delayed pericytes loss and improved both microcirculation perfusion and neurological outcomes on day 14. Delayed pericyte loss contributes to irreversible microcirculation dysfunction in the subacute phase of stroke. Targeting pericyte dysfunction and necroptosis following recanalization represents a promising therapeutic strategy for enhance stroke recovery.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blue Zones, an Analysis of Existing Evidence through a Scoping Review.","authors":"Cristina Candal-Pedreira, Julia Rey-Brandariz, Lucía Martín-Gisbert, Ana Teijeiro, Guadalupe García, Alberto Ruano-Ravina, Mónica Pérez-Ríos","doi":"10.14336/AD.2025.0461","DOIUrl":"https://doi.org/10.14336/AD.2025.0461","url":null,"abstract":"<p><p>\"Blue Zones\" refer to geographical regions with a high proportion of centenarians. This review aims to identify and synthesize scientific evidence regarding Blue Zones and their characteristics. A scoping review was conducted following PRISMA-ScR guidelines. Systematic bibliographic searches were performed across major scientific databases up to February 2025. Studies were included if they investigated regions which the authors identified as Blue Zones. Non-naturally occurring Blue Zones were excluded. A narrative synthesis of the evidence was carried out. Sixty-five records were included, identifying ten regions: Ogliastra (Sardinia, Italy), Ikaria (Greece), Cilento (Italy), one municipality in The Netherlands, Menorca (Spain), Okinawa (Japan), Rugao (China), Nicoya (Costa Rica), Martinique/Guadeloupe (French overseas regions in the Caribbean) and Loma Linda (California, United States). Longevity indicators revealed that Ogliastra, Okinawa and Nicoya exhibit higher longevity compared to national averages. Ikaria and Cilento show high life expectancy, the municipality in The Netherlands show a higher proportion of exceptional longevous population than other municipalities, whereas Guadeloupe/Martinique present a higher prevalence of supercentenarian deaths than metropolitan France. Data from Menorca remain inconclusive, and Rugao has fewer centenarians. No studies have been conducted in Loma Linda. Factors associated with longevity include diet, physical activity, climate, genetic factors and geographical isolation. The literature indicates that certain geographical areas demonstrated a higher percentage of centenarians than adjacent areas. While regions such as Okinawa, Ogliastra and Nicoya are well-characterized as Blue Zones, others remain under investigation, and some currently lack sufficient scientific evidence.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced Age Worsens Phenotypes of Ocular Hypertension in Mice.","authors":"Priyamvada M Pitale, Solomon E Gibson, Caroline C Keehn, Arman T Yazdian, Guofu Shen, Benjamin J Frankfort","doi":"10.14336/AD.2025.0349","DOIUrl":"https://doi.org/10.14336/AD.2025.0349","url":null,"abstract":"<p><p>Glaucoma is a neurodegenerative disorder of the optic nerve and retinal ganglion cells (RGCs) and a major cause of blindness. The two most important risk factors for glaucoma are ocular hypertension (OHT) and advanced age. In this study, we explored the combined impact of aging and OHT on retinal neuronal and microvasculature health. We induced OHT using the bead-injection model in 12 week old (young) and 1.5 year old (old) mice and monitored intraocular pressure (IOP) for 2 weeks. We then explored vascular phenotypes, blood retinal barrier components, RGC counts, and electroretinogram (ERG) changes. Aged mice displayed reduced retinal microvasculature complexity, retinal vascular phenotypes in all three retinal capillary plexi (RCPs), and abnormal ERGs. Aging also impacted basement membrane (BM) and tight junction (TJ) morphology. The impact of OHT was much more evident in old mice; RGC loss was exacerbated, retinal vascular phenotypes were magnified across all three RCPs, and BM and TJ phenotypes were much more severe. However, the impact of OHT on retinal function was unchanged in old mice. Interestingly, the nature of these phenotypes was not equivalent among all RCPs, suggesting regional shared and distinct susceptibilities to aging and OHT. Taken together, aging causes multiple neurovascular phenotypes in mouse retinas, and OHT causes more severe effects in old mice. This suggests an interaction between aging and OHT that may help explain the increased prevalence of glaucoma in older humans.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk Factors for Oropharyngeal Dysphagia in Older Adults - Evidence from Consorci Sanitari Del Maresme and Mataró University Hospital, Catalonia, Spain.","authors":"Lucilla Guidotti, Jorge Iván Castañeda-Maldonado, Marta Santiago, Pere Clavé, Omar Ortega","doi":"10.14336/AD.2025.0345","DOIUrl":"https://doi.org/10.14336/AD.2025.0345","url":null,"abstract":"<p><p>Oropharyngeal dysphagia (OD) is a highly prevalent geriatric syndrome that remains underdiagnosed and undertreated, often resulting in severe nutritional and respiratory complications with poor clinical outcomes. Its risk factors are still not well defined, representing a critical gap in efforts to understand its pathophysiology, prevent the condition and reduce its associated complications. To analyze data from comprehensive studies conducted in a single-center setting to ascertain the major risk factors associated with OD as a geriatric syndrome. A retrospective analysis was conducted, encompassing a review of prior studies, including a cohort of 7,272 older patients with OD at Consorci Sanitari del Maresme, Catalonia, Spain, presented as a narrative review. The study presents data using odds ratios (OR) and p-values from univariate and multivariate analyses to show the association of OD with its main risk factors in different phenotypes of older patients with OD (independently living, acute hospitalized, and with pneumonia, dementia, COVID-19, stroke). Quality of studies was assessed with ROBINS-I-V2. Outcome (risk factors) quality was assessed with GRADE. Thirteen studies (2010-2022) were reviewed. OD exhibited significant associations with 8 main groups of risk factors among older patients from diverse phenotypes. The main risk factors were impaired functionality (OR:2.24-12.7), aging (OR:1.05-5.16) and malnutrition (OR:2.46-5.16). Comorbidities, respiratory disease, neurological impairments, geriatric syndromes and pharmacological treatments were also significantly associated with OD (OR:1.02-15.52). The quality of the included studies and variables was mainly moderate. OD is a geriatric syndrome associated with several risk factors across multiple phenotypes of older patients. These findings highlight the critical need for early identification and targeted prevention of key risk factors for OD to improve clinical outcomes and reduce the burden of this underdiagnosed geriatric syndrome.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Standardized Protocol for Mouse Longevity Studies in Preclinical Drug Development.","authors":"Alex Zhavoronkov, Qian Wang, Yujie Liu, Wenbin Hou, Yuelei Shen, Dominika Wilczok, Kristen Fortney, Alex Aliper, Man Zhang, Feng Ren, Richard A Miller","doi":"10.14336/AD.2025.0508","DOIUrl":"https://doi.org/10.14336/AD.2025.0508","url":null,"abstract":"<p><p>Although aging is increasingly recognized as a key factor in chronic disease management, preclinical drug development rarely incorporates direct assessments of lifespan. To date, no biotechnology company has conducted a full mouse lifespan study for a therapeutic agent prior to human clinical trials, despite widespread chronic use of many approved drugs. This oversight stems from a lack of standardized protocols for the incorporation of mouse lifespan studies, high costs, limited commercial incentives, and regulatory risks associated with long-term data. Here, we present a comprehensive and scalable protocol for conducting mouse longevity studies in the early stages of drug development. Being aware of monetary constraints in the drug discovery process, we propose a basic design for a longevity study on ~250 (176 males and 72 females) genetically heterogeneous mice (UM-HET3) per group, with survival curves as primary endpoint, and propose enhanced study design options only if budget allows. Our framework provides a standardized foundation for integrating longevity assessments into routine drug development, offering the potential to uncover long-term risks or benefits that traditional toxicology studies may overlook. Broad implementation of such protocols could support the development of safer and more effective therapeutics for chronic diseases, while opening new avenues for discovery of substances that could slow down the rate of aging, known as geroprotectors.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.","authors":"Gudimetla Susmitha Mohan, Rahul Kumar","doi":"10.14336/AD.2025.0472","DOIUrl":"https://doi.org/10.14336/AD.2025.0472","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative condition defined by the gradual impairment of cognitive functions, synaptic disarray, and extensive neuronal loss. Emerging evidence suggests that metabolic impairment, specifically within tricarboxylic acid (TCA) cycle, is instrumental in the AD pathophysiology. TCA cycle represents an indispensable pathway in metabolism that is responsible for energy production, and the maintenance of cellular homeostasis, particularly in neurons. Several in vitro, clinical, and in vivo studies reported that several TCA cycle enzymes disrupt during AD. Disruption in TCA cycle enzymes exhibits more pronounced impact on the brain owing to its high metabolic activity and continuous demand for energy, where any reduction in ATP production can severely impair neuronal function, synaptic plasticity, and overall cognitive processes. The current review explores the mechanisms underlying AD related impairment in TCA cycle, focussing on the molecular alterations of TCA enzymes. We also discussed potential activators and inhibitors of TCA cycle enzymes as a potential therapeutic intervention to restore AD related metabolic balance.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}