Korean Journal of Physiology & Pharmacology最新文献

{"title":"PAK4 as a cardiometabolic node: tissue-specific metabolic control, cardiovascular remodeling, and therapeutic trade-offs.","authors":"To Hoai Thi Nguyen, Khanh Duc Tran, Trong Kha Pham, Ju Eun Seol, Ippei Shimizu, Hyoung Kyu Kim, Jin Han","doi":"10.4196/kjpp.26.314","DOIUrl":"https://doi.org/10.4196/kjpp.26.314","url":null,"abstract":"<p><p>Cardiometabolic disease reflects interdependent dysfunction across adipose tissue, liver, skeletal muscle, vasculature, and heart. p21-activated kinase 4 (PAK4), a group II serine/threonine kinase controlling cytoskeletal organization and development, has emerged as a nutrient-responsive regulator in metabolic tissues. We position PAK4 as a candidate cardiometabolic node rather than a proven master regulator or direct energy sensor. Established mechanisms include suppression of adipocyte lipolysis and browning, hepatocyte NCoR1-PPARα-dependent fattyacid oxidation and ketogenesis, skeletal-muscle AMPKα2-GLUT4 signaling, together with promotion of hepatic stellate-cell activation via YAP phosphorylation at Thr428. These programs could alter the substrate, inflammatory, redox, and endocrine environment encountered by the cardiovascular system. We refine the hepatic ketone deficiency concept into a PAK4-ketone supply-demand mismatch hypothesis: reduced hepatic ketogenesis may limit adaptive ketone availability when myocardial demand rises, though inter-organ causality remains unproven. PAK4 is essential for embryonic cardiac morphogenesis, and limited adult endothelial studies suggest stress-protective roles in ischemic and inflammatory settings, whereas functions in adult cardiomyocytes, fibroblasts, and vascular smooth muscle cells remain largely undefined. An exploratory scan of Gene Expression Omnibus datasets identified recurrent nominal increases in PAK4 mRNA in selected failing or remodeled human myocardium and steatotic liver, but no universal cardiometabolic signature. These findings define a tissue-dependent therapeutic dilemma in which peripheral metabolic benefits of PAK4 inhibition or degradation may coexist with uncharacterized cardiac, isoform, and exposure-related risks. Resolving this paradox will require adult inducible cell-specific models, inter-organ flux studies, cardiac proteomics and phosphoproteomics, and comparison of catalytic inhibitors, degraders, and tissuedirected delivery systems.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"30 6","pages":"543-561"},"PeriodicalIF":2.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reading human physiology through adverse drug events.","authors":"Bo Ram Yang, Sang-Min Park","doi":"10.4196/kjpp.26.389","DOIUrl":"https://doi.org/10.4196/kjpp.26.389","url":null,"abstract":"","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"30 6","pages":"501-504"},"PeriodicalIF":2.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding proteomic complexity of transcript variants and homologous isoforms for precision therapeutics.","authors":"Seo A Kum, Hong Koo Ha, Sun Sik Bae","doi":"10.4196/kjpp.26.299","DOIUrl":"https://doi.org/10.4196/kjpp.26.299","url":null,"abstract":"<p><p>The traditional \"one gene, one protein\" paradigm is insufficient to capture the vast phenotypic and physiological complexity of eukaryotes. This review aims to comprehensively elucidate the molecular mechanisms of transcriptomic diversification, namely, alternative splicing, alternative usage of promoter, and alternative polyadenylation, and their profound impacts on cellular homeostasis and human disease. By synthesizing recent breakthroughs in targeted long-read RNA sequencing, single-cell isoform-specific multiomics, and AI-driven 3D structural modeling, we systematically examine how transcript variants are generated and functionally annotated. Our analysis highlights that multiple transcript variants originating from a single genetic locus are not merely redundant copies; rather, subtle sequence alterations dynamically rewire protein-protein interaction networks and dictate precise subcellular localization. The exquisite spatiotemporal regulation of these variants controls critical cell fate decisions and organ development. Consequently, the pathological dysregulation of these processes, frequently termed spliceopathies, acts as a primary driver in severe pathologies, including cancer multidrug resistance, metabolic reprogramming, and neurodegenerative disorders. In conclusion, understanding the eukaryotic proteome requires a fundamental shift from conventional gene-level to isoform-level perspectives. Decoding the complex regulatory syntax of transcript variants paves the way for next-generation precision medicine, highlighting the therapeutic potential of RNA-targeted interventions, such as antisense oligonucleotides and CRISPR-based RNA editing, to correct pathogenic isoforms.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"30 6","pages":"521-542"},"PeriodicalIF":2.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal regulation of activin, follistatin, and growth differentiation factor 15 in the liver and circulation during high-fat diet-induced fatty liver disease.","authors":"Min-Jeong Kim, Eun Bi Ma, Muhammad Arif Aslam, Gahui Lee, Christos S Mantzoros, Joo Young Huh","doi":"10.4196/kjpp.26.031","DOIUrl":"https://doi.org/10.4196/kjpp.26.031","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) develops over time, yet most hepatokine studies are cross-sectional. We investigated the temporal regulation of the activin-follistatin axis and growth differentiation factor 15 (GDF15) in high-fat diet (HFD)-induced fatty liver disease. Mice were fed an HFD or normal chow for 8, 20, or 30 weeks. Plasma, hepatic mRNA, and hepatic protein were measured by ELISA, real-time PCR, and immunoblotting. HFD increased body and liver weights and hepatic triglyceride content throughout. A central finding was discordance between compartments: hepatic <i>Inhba</i> mRNA was elevated at 8 and 30 weeks, yet plasma and hepatic activin A protein both peaked at 20 weeks, indicating post-transcriptional regulation; hepatic follistatin protein decreased at 20 and 30 weeks despite an early rise in <i>Fst</i> mRNA, while circulating follistatin and follistatin-like 3 (FSTL3) were unchanged. The activin receptors ACVR2B and ACVR1 showed distinct protein kinetics, with sustained ACVR2B elevation and a transient ACVR1 peak at 20 weeks, potentially favoring canonical activin signaling. Together these changes shifted the balance toward activin, increasing plasma activin A-to-follistatin and activin A-to-FSTL3 ratios at 20 weeks and the phospho/total-SMAD2/3 ratio at 20 and 30 weeks. Hepatic <i>Gdf15</i> mRNA was induced throughout, whereas plasma GDF15 (measured at 8 and 20 weeks) was increased at both and correlated positively with plasma activin A. These findings reveal time-dependent, level-discordant regulation of the activin-follistatin axis and GDF15 in HFD-induced fatty liver, providing a temporal reference unavailable from cross-sectional studies.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"βKlotho filters ligand-independent FGFR1/4-PLCγ signaling to prevent aberrant constitutive Ca²⁺ entry.","authors":"Bao T N Dang, Phan Anh Nguyen, Subo Lee, Hyungmin Jeong, Seung-Kuy Cha","doi":"10.4196/kjpp.26.060","DOIUrl":"https://doi.org/10.4196/kjpp.26.060","url":null,"abstract":"<p><p>Fibroblast growth factor receptors 1 and 4 (FGFR1/4) regulate diverse cellular processes, including proliferation, differentiation, and metabolic homeostasis. Although ligand-dependent FGFR signaling has been extensively characterized, the signaling properties of these receptors in their ligand-independent state remain poorly understood. Here, we investigated the intrinsic signaling outputs of FGFR1 and FGFR4 in the absence of ligands using quantitative immunoblotting and electrophysiological analyses. Overexpression of FGFR1 or FGFR4 alone robustly increased the phosphorylation of phospholipase Cγ (PLCγ) and extracellular signal-regulated kinase 1/2 (ERK1/2), whereas activation of the PI3K-Akt pathway was minimal. Strikingly, co-expression of the co-receptor βKlotho acted as a molecular switch, selectively suppressing FGFR-driven PLCγ phosphorylation while preserving ERK1/2 signaling. Functionally, this βKlotho-dependent attenuation of PLCγ signaling markedly reduced the sustained TRPC6-mediated currents observed in βKlotho-deficient cells, linking constitutive FGFR-PLCγ coupling to aberrant Ca²⁺ influx. Together, our findings identify βKlotho as a specialized signaling filter that safeguards FGFR signaling fidelity by uncoupling deleterious PLCγ-TRPC6 signaling while maintaining canonical MAPK output. These results reveal a previously unrecognized ligand-independent role of βKlotho in reconfiguring the FGFR signaling architecture.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NCAPD3 induces M2 polarization of peripheral macrophages in lung adenocarcinoma by promoting the binding of E2F1 to the FOXM1 promoter region.","authors":"Weixi Zhang, Kongjun Zou","doi":"10.4196/kjpp.26.082","DOIUrl":"https://doi.org/10.4196/kjpp.26.082","url":null,"abstract":"<p><p>Serving as a highly prevalent malignant tumor, lung adenocarcinoma (LUAD) is frequently associated with the establishment of an immunosuppressive tumor microenvironment during its initiation and progression, where M2-polarized macrophages exert pivotal effects. NCAPD3 acts as an oncogenic driver in multiple tumors; however, the mechanism underlying its regulation of macrophage M2 polarization in LUAD remains to be elucidated. TCGA-LUAD dataset was utilized to analyze the expression levels of NCAPD3 in patient samples from TCGA-LUAD. Following the construction of NCAPD3 overexpression and knockdown cell models and verification of transfection efficiency <i>via</i> qRT-PCR, flow cytometry, colony formation, Transwell, and wound-healing assays were employed to evaluate malignant phenotypes. The indirect co-culture system, accompanied by Western blot and ELISA, was subsequently employed to systematically evaluate the polarization of macrophages. Co-IP, bioinformatics analysis, ChIP, dual-luciferase reporter assay, and rescue experiments were combined to verify the regulatory effect of the NCAPD3/E2F1/FOXM1 axis on M2 macrophage polarization in LUAD. Ultimately, the effects of the NCAPD3/E2F1/FOXM1 axis on M2 polarization of macrophages in LUAD were confirmed <i>via</i> a rescue experiment. NCAPD3 was highly expressed in LUAD cells, and its overexpression potentiated the proliferation, migration, invasion, and anti-apoptotic capacities of tumor cells, while promoting M2 phenotypic polarization. Mechanistically, NCAPD3 upregulated FOXM1 expression by recruiting E2F1 to the FOXM1 promoter, thereby inducing M2 polarization of macrophages and accelerating malignant progression in LUAD. By interacting with E2F1, NCAPD3 facilitates the binding of E2F1 to the FOXM1 promoter region to activate FOXM1 transcription, thereby accelerating LUAD progression and triggering M2 macrophage polarization.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149083015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Lactobacillus reuteri</i> ATG-F4 alleviates behavioral impairment induced by chronic stress.","authors":"So-Hee Lim, Gun-Seok Park, Tsengel Bayarsaikhan, Na-Yoon Lee, Joong Su Kim, Sun Seek Min, Jihee Kang, Jae-Ran Lee","doi":"10.4196/kjpp.25.337","DOIUrl":"https://doi.org/10.4196/kjpp.25.337","url":null,"abstract":"<p><p>Chronic stress impairs quality of life by disturbing physical and psychological functioning, and increases susceptibility to a wide range of diseases. <i>Lactobacillus reuteri</i> ATG-F4 isolated from the fecal samples of a newborn baby alleviated chronic stress-induced anhedonia by altering the expression of neurometabolites and neurotransmitter receptors. In this study, we examined whether ATG-F4 can improve behavioral deterioration induced by chronic stress using the Laboratory Animal Behavioral Observation Registration and Analysis System (LABORAS). The continuous behavior of the mice was examined in the LABORAS cage without the intervention of the researchers. Mice exposed to chronic stress displayed significantly increased frequency of immobility compared with control mice, whereas the duration of immobility remained unchanged. Interestingly, mice treated with ATGF4 during stress treatment period and two weeks prior maintained immobility frequency at control level observed in control mice. Locomotor activity and exploratory behavior of mice exposed to chronic stress were significantly attenuated, but ATG-F4 treatment restored them at control levels. Stress is known to adversely affect sleep quality. Electroencephalography analysis revealed that sleep latency enhanced in stressed mice was reduced by ATG-F4 administration. RT-PCR analysis of brain tissues demonstrated that ATG-F4 intake modulated the expression of multiple genes including GABA receptor and serotonin receptor. Alterations in gut microbiota composition and bacterial diversity induced by chronic stress were restored to levels similar to controls by ATG-F4 treatment. Taken together, these results suggest that ATG-F4 can ameliorate chronic stress-induced behavioral impairments, potentially <i>via</i> its effects on gene expression and the composition of the gut microbiota.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149082976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conduction slowing and a focal scar are jointly required for sustained ventricular reentry in diabetic cardiomyopathy.","authors":"Jae Boum Youm","doi":"10.4196/kjpp.26.198","DOIUrl":"https://doi.org/10.4196/kjpp.26.198","url":null,"abstract":"<p><p>Diabetic cardiomyopathy increases the risk of ventricular tachycardia and fibrillation through ionic and structural remodeling, but whether the reentrant substrate arises from a diffuse slow-conduction (fibrotic) substrate, a focal scar, or from repolarization remodeling remains unclear. Using a three-dimensional monodomain model (truncated-ellipsoid left ventricle; ToR-ORd ionic model with six diabetic current-scaling factors), I performed a controlled ablation study (<i>in-silico</i> knockout, not catheter ablation) in which diffuse fibrosis and connexin-43 remodeling were reduced tissue conductivity, patchy fibrosis discrete inexcitable elements, and a focal scar an inexcitable transmural wedge, with reentry tested by an S1-S2 protocol. Diabetic remodeling slowed conduction (≍60 to 13 cm/s) and prolonged the QT interval (255 to 301 ms). Sustained reentry required slow conduction and a focal scar: a scar at normal conduction did not reenter, and a slow-conduction substrate without a scar did not - at any patchy-fibrosis density, nor with spatially correlated or strandlike fibrosis textures (0/14); only their combination produced scar-anchored reentry. Disabling ionic remodeling did not abolish reentry, and a conductivity sweep confined reentry to a conduction-velocity window, identifying conduction slowing, not repolarization, as the driver of reentry maintenance; findings reproduced at a finer, independent discretization, though conduction-velocity and block thresholds are effective, resolution-dependent values (coarse grid; robustness check, not mesh convergence). Because the focal scar reflects concomitant ischemic injury and the diffuse slow-conduction substrate is invisible to late-gadolinium-enhancement (LGE), detecting this two-hit substrate would require pairing LGE with diffuse-fibrosis (T1/extracellular-volume) mapping for risk stratification in diabetic patients with a scar.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148992571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of VNN1 protects cardiac myoblasts from hypoxia/reoxygenation injury <i>via</i> the PI3K/Akt pathway.","authors":"Xujiao Hu, Yu Fang","doi":"10.4196/kjpp.26.034","DOIUrl":"https://doi.org/10.4196/kjpp.26.034","url":null,"abstract":"<p><p>Myocardial ischemia/reperfusion (I/R) injury is a critical factor contributing to adverse outcomes following infarction, primarily due to oxidative stress, inflammation, and cardiomyocyte death. Vanin-1 (VNN1), a pantetheinase enzyme involved in redox regulation, has recently emerged as a potential mediator of tissue damage under stress conditions. This study aimed to investigate the role of VNN1 in hypoxia/reoxygenation (H/R)-induced injury in H9c2 cardiomyocytes and to explore the involvement of the PI3K/Akt axis. An <i>in vitro</i> H/R model was established using H9c2 cells, and VNN1 knockdown was achieved <i>via</i> shRNA. Cellular injury, inflammation, and oxidative stress were assessed using viability assays, LDH release, ELISA, ROS detection, and biochemical analysis. Results revealed that VNN1 expression was significantly upregulated in H/R-treated cells. Silencing VNN1 mitigated cell damage, reduced pro-inflammatory cytokine release, and alleviated oxidative stress. Mechanistically, these protective effects were dependent on activation of the PI3K/Akt signaling axis, as inhibition of this pathway reversed the benefits of VNN1 knockdown. In conclusion, VNN1 knockdown confers protection against H/R-induced cardiomyocyte injury <i>via</i> activating the PI3K/Akt pathway, highlighting VNN1 as a potential target for myocardial I/R injury.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148978754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α-Tocopherol rescues lipid-induced impairment of autophagy <i>via</i> mTOR/ULK1 signaling in macrophages.","authors":"Lu Kuang, Limei Wu, Zenghui Liu, Jiaxing Zhao, Qijun Chen, Huayu Yin, Xuehui Liu, Dabin Liu, Shaoguo Wu","doi":"10.4196/kjpp.25.375","DOIUrl":"https://doi.org/10.4196/kjpp.25.375","url":null,"abstract":"<p><p>Atherosclerosis is a chronic vascular disease characterized by the accumulation of lipid-filled foam cells in the arterial wall. Macrophage-derived foam cells play a key role in promoting plaque formation. α-Tocopherol (α-TOC), a common dietary antioxidant, is thought to have protective effects against atherosclerosis, but its specific mechanisms remain unclear. In this study, an <i>in vitro</i> foam cell model was established using oxidized low-density lipoprotein-induced macrophages to investigate the effects of α-TOC on foam cell formation and related mechanisms. Network pharmacology predicted that α-TOC may act through autophagy-related pathways, particularly the mTOR-mediated autophagy pathway. We demonstrated that α-TOC enhanced autophagic function in macrophages, as evidenced by increased expression of Beclin1, LC3-II, ATG5, and ATG12, along with reduced p62/SQSTM1 levels. Rapamycin reproduced, and 3-methyladenine opposed, the direction of the autophagic and mTOR/ULK1 changes observed with α-TOC, consistent with involvement of this pathway. These <i>in vitro</i> findings suggest that α-TOC reduces lipid accumulation and inhibits foam cell formation in macrophages by enhancing autophagic activity in association with reduced mTOR phosphorylation and increased ULK1 Ser555 phosphorylation. This study provides mechanistic insights into the potential anti-atherosclerotic effects of α-TOC at the cellular level, offering a theoretical basis for its further investigation as a therapeutic candidate for atherosclerosis.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148978801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}