Human Cell最新文献

{"title":"METTL14 knockdown augmented the polarization of M2-like macrophages to promote acute myeloid leukemia progression.","authors":"Meng Wang, Zhibin Xie, Yuanyuan Tan, Yan Zhou, Siyi Wang, Pingping Zhang, Jiajia Li","doi":"10.1007/s13577-025-01300-0","DOIUrl":"https://doi.org/10.1007/s13577-025-01300-0","url":null,"abstract":"<p><p>Within the m6A methyltransferase complex, methyltransferase-like 14 (METTL14) constitutes a pivotal component. This study aims to elucidate the role of METTL14 in macrophage differentiation and its involvement in the progression of acute myeloid leukemia (AML) through the modulation of programmed cell death-ligand 1 (PD-L1) expression in M2-like macrophages. The expression levels of METTL14 in M1-like and M2-like macrophages were quantified using real-time quantitative polymerase chain reaction (QRT-PCR). Macrophage differentiation in THP-1 cells was induced via treatment with phorbol 12-myristate 13-acetate (PMA), followed by lentiviral-mediated overexpression or knockdown of METTL14. Changes in the expression of CD86, iNOS, Arg-1, and CD206 were evaluated. The effects of METTL14 knockdown and overexpression on macrophage differentiation, M2 macrophage proliferation, and apoptosis was assessed. AML cells were co-cultured with M2 macrophages subjected to either METTL14 knockdown or overexpression, and subsequent changes in AML cell proliferation, apoptosis, migration, invasion, and m6A methylation levels were investigated. The expression of METTL14 mRNA was elevated in M1-like macrophages. Knockdown of METTL14 resulted in a significantly reduction in the expression of M1 markers, such as CD86 and iNOS, while concurrently increasing the expression of M2 markers, including Arg-1 and CD206. Additionally, the depletion of METTL14 facilitated the proliferation of M2-like macrophages, inhibited apoptosis, and decreased phagocytic capacity. Conversely, overexpression of METTL14 yielded opposite outcomes. Co-culture experiments demonstrated that M2-like macrophages with METTL14 knockdown significantly promoted the proliferation of AML cell, suppressed apoptosis, and enhanced migration and invasion. Concurrently, cellular m6A levels were elevated. Treatment with anti-PD-L1 partially reversed the effects of METTL14 knockdown. These findings suggest that METTL14 may enhance the proliferation of AML cells while inhibiting apoptosis by influencing macrophage differentiation and modulating macrophage function, with these effects being associated with YTHDF1 and PD-L1.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"168"},"PeriodicalIF":3.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hofbauer cell alterations and potential role in the pathophysiology of HELLP syndrome.","authors":"Ayano Ezaki, Akihito Sagara, Yoshihiro Komohara, Cheng Pan, Hiromu Yano, Shukang Zhao, Mayuko Yamamoto, Anri Imamura, Hinano Akita, Jie Su, Ren Shirotani, Tomoka Takahashi, Daiki Yoshii, Yukio Fujiwara, Masahiro Yamamoto, Munekage Yamaguchi, Eiji Kondoh","doi":"10.1007/s13577-025-01297-6","DOIUrl":"https://doi.org/10.1007/s13577-025-01297-6","url":null,"abstract":"<p><p>HELLP syndrome, a severe pregnancy complication characterized by hemolysis, elevated liver enzymes, and low platelet count, is a subtype of preeclampsia (PE). However, its rapid onset and unique clinical features suggest distinct underlying mechanisms. Although Hofbauer cells are essential for maintaining immune homeostasis, their involvement in HELLP syndrome remains unclear. We conducted transcriptomic analysis of public data sets to assess macrophage-associated gene expression in placentas from control, PE, and HELLP cases. Immunohistochemistry and image analysis were performed on formalin-fixed paraffin-embedded placental tissues to quantify macrophage density and size, and electron microscopy was conducted to evaluate ultrastructural features. Gene expression analysis revealed a significant reduction in AIF1 (Iba1) and CD163 expression in PE placentas, while CD163 expression was relatively preserved in HELLP. Immunohistochemistry confirmed decreased Hofbauer cell density in PE placentas, whereas enlarged Hofbauer cells with increased rough endoplasmic reticulum, suggesting enhanced activation status, were seen in HELLP. Hofbauer cells exhibit distinct morphological and molecular changes in HELLP syndrome compared with PE, which implicates their potential involvement in the pathophysiology of HELLP. These findings provide new insights into the fetal immune environment in pregnancy-related hypertensive disorders.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"167"},"PeriodicalIF":3.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eucommia ulmoides (Duzhong) extract alleviates cerebral stroke by inhibiting ferroptosis-related gene DNA Damage-Inducible Transcript 4 (DDIT4) expression.","authors":"Xin Qi, Mengyuan Deng, Minhong Li, Wenjia Ma, Yangbo Zhou","doi":"10.1007/s13577-025-01298-5","DOIUrl":"https://doi.org/10.1007/s13577-025-01298-5","url":null,"abstract":"<p><p>Cerebral stroke is an acute cerebrovascular disease, which is characterized by significant morbidity, death, and disability rate. Ischemic stroke is more than hemorrhagic stroke and accounts for 60-70% of all strokes. The present study explored the mechanisms of Eucommia ulmoides extract (EUE) in the treatment of ischemic stroke. Middle cerebral artery occlusion (MCAO) mouse models and oxygen and glucose deprivation (OGD) SH-SY5Y cell models were constructed to mimic ischemic stroke, and mice and cells were treated with gradient concentrations of EUE. The neurological function and brain tissue damage in mice were assessed using multiple parameters. Then the iron contents in cerebral tissue samples and neuronal cells were examined, and the expression levels of reactive oxygen species-related indicators and iron metabolism-related proteins were detected. EUE alleviated the ferroptosis process within cerebral tissue samples of MCAO mice and OGD-triggered neuronal cells, thereby mitigating neurological function and brain tissue damage by activating PI3K/Akt pathway. The target drug genes of EUE were searched by network pharmacology and molecular docking and found that the ferroptosis-related gene DDIT4 is the potential EUE-targeted gene in the therapy of ischemic stroke. DDIT4 expression was upregulated within cerebral brain samples of MCAO mice and OGD-triggered neuronal cells, and EUE could inhibit DDIT4 expression. The protective effect of EUE on neuronal cells could be partially reversed by overexpression of DDIT4. Moreover, EUE alleviated ferroptosis and improved neurological function in MCAO mice by suppressing DDIT4 expression and modulating the PI3K/Akt pathway. In conclusion, EUE exerts its neuroprotective effect against cerebral stroke by inhibiting DDIT4 expression and ferroptosis by regulating the PI3K/Akt pathway, and DDIT4 has been predicted to be an underlying therapeutic target for the treatment of ischemic stroke.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"166"},"PeriodicalIF":3.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exportin-1 and epigenetic modifications interaction: more than nuclear transport.","authors":"Leonidas Benetatos, Eleftheria Hatzimichael, Eleni Kapsali","doi":"10.1007/s13577-025-01295-8","DOIUrl":"https://doi.org/10.1007/s13577-025-01295-8","url":null,"abstract":"<p><p>Exportin-1 (XPO1) is fundamental in the regulation of nuclear-to-cytoplasm transportation. XPO1 has the ability to transport hundreds of proteins and several different types of mRNAs responsible for proper cellular biology. Deregulation of the XPO1 transportation system aberrantly translocates transcription factors promoting the pathogenesis of diseases including cancer. However, XPO1 has transport-independent functions that involve epigenetic modifications. XPO1 associates with chromatin, recruiting oncogenic fusion proteins to target genes affecting chromatin structure and function. That intriguing association also affects transcriptional activation resulting in oncogenesis. XPO1 also regulates other epigenetic pathways and is epigenetically regulated as well. Herein, we report most recent findings on that topic, and we discuss the mechanisms and the consequences of normal and aberrant XPO1 association with the epigenetic marks.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"165"},"PeriodicalIF":3.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145132299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of human induced pluripotent stem cell lines derived from Wolf-Hirschhorn syndrome patients with chromosomal 4p deletion.","authors":"Tomoya Shimizu, Miho Takami, Mami Matsuo-Takasaki, Michiya Noguchi, Yukio Nakamura, Tadayoshi Hayata, Yohei Hayashi","doi":"10.1007/s13577-025-01292-x","DOIUrl":"10.1007/s13577-025-01292-x","url":null,"abstract":"<p><p>Wolf-Hirschhorn syndrome (WHS) is a devastating congenital disease caused by deletions on the short arm of chromosome 4 (4p), for which no curative treatments currently exist. To facilitate the development of therapeutic strategies, the development of experimental models of WHS is crucial for investigating its etiology and pathogenesis, which remain elusive. In this study, we successfully generated human induced pluripotent stem cells (hiPSCs) from three fibroblast lines from WHS patients. We then characterized these hiPSCs, along with one hiPSC line previously generated from peripheral blood mononuclear cells, as part of a Japanese nationwide project. All four hiPSC lines exhibited characteristics of self-renewal, pluripotency, and karyotypes with expected 4p deletions. Copy number variation microarray analysis revealed that these WHS-specific hiPSCs carried hemizygous deletions in p15.1-p16.3 regions, commonly encompassing 100 genes. Transcriptome analysis showed that the expression of these genes faithfully reflected hemizygous deletion in these WHS-specific hiPSCs and that these down-regulated genes were associated with the development of neural crest cells. These results indicate that WHS-specific hiPSCs can recapitulate the abnormal genomic structure genes related to and the gene expression profile observed in WHS patients. Given the limited understanding of the molecular pathogenesis of WHS, these cellular resources will be instrumental in modeling disease phenotypes and in advancing novel therapies for this syndrome.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"164"},"PeriodicalIF":3.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12449351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145088023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"tRNA-derived small RNAs: emerging regulators of ferroptosis in human diseases.","authors":"Jiqing Zhang, Mu Liu, Zhongjun Li","doi":"10.1007/s13577-025-01293-w","DOIUrl":"https://doi.org/10.1007/s13577-025-01293-w","url":null,"abstract":"<p><p>tRNA-derived small RNAs (tsRNAs) are functional non-coding RNAs that play crucial roles in transcriptional, translational, and epigenetic regulation. Ferroptosis is an iron-dependent form of programmed cell death driven by lipid peroxidation, and its core mechanisms involve dysregulated iron homeostasis, redox imbalance, and lipid peroxidation. Emerging evidence indicates that tsRNAs serve as pivotal regulators of ferroptosis by targeting key components of the ferroptosis pathway. This regulatory interplay critically influences the activation or suppression of ferroptosis in various human diseases, including non-alcoholic steatohepatitis, perioperative neurocognitive disorders, acute kidney injury, non-small cell lung cancer, gastric cancer, diabetic kidney disease, atrial fibrillation, acute pancreatitis, depression, and acute lung injury, thereby affecting disease pathogenesis, progression, and therapeutic responses. This review summarizes the mechanisms underlying the interplay between tsRNAs and ferroptosis in human diseases and highlights the potential of tsRNAs as novel regulators of ferroptosis, providing insights into disease mechanisms.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"162"},"PeriodicalIF":3.1,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145076407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ODC1 loss upon KLF6 upregulation promotes macrophage pyroptosis and acute kidney injury in sepsis.","authors":"Jiansheng Ding, Shijie Zhang, Xiangxian Zhang","doi":"10.1007/s13577-025-01290-z","DOIUrl":"https://doi.org/10.1007/s13577-025-01290-z","url":null,"abstract":"<p><p>The excessive inflammatory cascade in sepsis represents a major cause of multiorgan injuries, including sepsis-associated acute kidney injury (SAKI). Following the bioinformatics prediction, this study aims to investigate the role of ornithine decarboxylase 1 (ODC1) in macrophage phenotype in SAKI. C57BL/6 J mice and mouse bone marrow-derived macrophages or THP-1 cells were subjected to lipopolysaccharide (LPS) treatments to generate septic models. RT-qPCR and western blot assays revealed a reduced expression pattern of ODC1 in the kidney of mice and the BMDMs following LPS challenges. Upregulation of ODC1 ameliorated kidney injury, reduced M1 polarization of macrophages, and alleviated inflammatory cytokine secretion. Moreover, this upregulation inactivated the nuclear factor-kappa B signaling and enhanced macrophage autophagy while reducing pyroptosis. KLF6, highly expressed in septic mice, was found to repress ODC1 transcription by binding to its promoter. Silencing of KLF6 similarly promoted macrophage autophagy and inhibited pyroptosis, ameliorating kidney injury and inflammation in mice. These effects were, however, negated by the additional ODC1 silencing. Collectively, this study suggests that KLF6-mediated ODC1 loss inhibits macrophage autophagy while promoting pyroptosis, thus resulting in inflammation and progression of SAKI.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"163"},"PeriodicalIF":3.1,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin, ROR-α and circadian rhythm in liver.","authors":"Samanmitha Srinivasa, Shuchi Odiyanda Charmanna, Rachana Rajesh Nayak, Shreyas Hulusemane Karunakara, Prasanna Kumar Santhekadur","doi":"10.1007/s13577-025-01288-7","DOIUrl":"10.1007/s13577-025-01288-7","url":null,"abstract":"<p><p>The liver is the largest internal organ. Several critical functions are attributed to the liver which include metabolism, synthesis of serum proteins, excretion, detoxification, and various physiological processes essential for maintaining body homeostasis. Its unique regenerative capacity helps the liver to restore itself fully after injury. This process involves all hepatocytes with or without the involvement of stem cells. The function of the liver is known to be regulated by circadian rhythm, which includes feeding-fasting cycles and the maintenance of the suprachiasmatic nucleus (SCN) that regulates as a master clock. The normal functioning of the liver is critical to the overall maintenance of homeostasis as it serves as a peripheral clock, suggesting a potential link between the SCN and liver. Aberrations in these circadian rhythms have been linked to various chronic hepatic diseases such as metabolic dysfunction-associated steatotic liver disease (MASLD), which can lead to Hepatocellular carcinoma (HCC). This mini review explores the significance of circadian rhythm in liver function, with a focus on the role of melatonin and nuclear receptors such as Retinoic acid receptor-related orphan receptor-alpha (RORα), which is a known melatonin receptor critical to sustaining these rhythms that can influence biological functions, including immune system functioning, cell growth, and differentiation. Further, RORα is identified as one of the key regulators of inflammation and acts as a potential tumor suppressor, particularly in the context of HCC. This review explores the interplay between RORα, melatonin, and circadian rhythm and discusses the underpinnings that offer insights into the role of circadian rhythm disruption in HCC development and novel therapeutic strategies targeting circadian rhythm modulations to mitigate HCC.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"160"},"PeriodicalIF":3.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A stem cell-based toolkit to model Angelman syndrome caused by paternal uniparental disomy of chromosome 15.","authors":"Francisca Cazaux Mateus, João Camões Dos Santos, Maria Arez, Evguenia P Bekman, Simão T da Rocha","doi":"10.1007/s13577-025-01287-8","DOIUrl":"10.1007/s13577-025-01287-8","url":null,"abstract":"<p><p>Angelman syndrome is a rare neurodevelopmental disorder caused by the loss of function of the maternally inherited UBE3A gene within the chr15q11-q13 region. This gene is subjected to a tissue-specific form of genomic imprinting leading to the silencing of the paternal allele in neurons. Angelman syndrome can result from various (epi)genetic mechanisms, with paternal uniparental disomy of chromosome 15 (patUPD15) being one of the rarest and least studied due to the absence of suitable models. To address this gap, we generated three independent induced pluripotent stem cell (iPSC) lines from individuals with Angelman syndrome caused by patUPD15, alongside genetically matched unaffected familial controls. Peripheral blood mononuclear cells (PBMCs) were reprogrammed into iPSCs using a non-integrative Sendai virus-based approach expressing the Yamanaka factors. All iPSC lines underwent rigorous quality control, confirming stem cell identity, trilineage differentiation potential, and genetic and epigenetic integrity. This newly established iPSC toolkit provides a powerful platform to investigate the molecular underpinnings of Angelman syndrome caused by patUPD15, paving the way for future translational research and therapeutic development tailored for this understudied form of the disorder.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"161"},"PeriodicalIF":3.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of KGAS, a cell line derived from gastric-type adenocarcinoma of the uterine cervix.","authors":"Hiroaki Yamada, Akira Yokoi, Eri Asano-Inami, Masami Kitagawa, Kosuke Yoshida, Kazuhiro Suzuki, Shin Nishio, Hiroaki Kajiyama, Naotake Tsuda","doi":"10.1007/s13577-025-01286-9","DOIUrl":"10.1007/s13577-025-01286-9","url":null,"abstract":"<p><p>Gastric-type adenocarcinoma (GAS) of the uterine cervix is a rare and aggressive subtype of cervical adenocarcinoma characterized by intrinsic resistance to chemotherapy and poor clinical outcomes due to the lack of effective treatment options. To address this critical unmet need, we established a novel GAS-derived cell line, KGAS, from ascitic fluid collected from a patient with recurrent GAS. Short tandem repeat (STR) analysis confirmed the genetic identity between the primary tumor and the cell line. Upon transplantation into immunocompromised mice, KGAS cells formed tumors that expressed Claudin-18 and MUC6, clinically recognized markers of GAS. Furthermore, KGAS cells exhibited marked resistance to paclitaxel and carboplatin, showing significantly reduced growth inhibition compared to HeLa cells. We also established a paclitaxel- and carboplatin-resistant subline, rKGAS, and performed microRNA (miRNA) sequencing to explore the molecular basis of acquired chemoresistance. Seventeen differentially expressed miRNAs were identified between KGAS and rKGAS cells. Upregulated miRNAs in rKGAS were predicted to target oncogenes such as BCL2, MET, SIRT1, and VEGFA, whereas downregulated miRNAs were associated with tumor suppressor genes, including IGF1R, TNFAIP3, and MTOR. The KGAS and rKGAS cell lines represent valuable preclinical models for elucidating the molecular mechanisms of chemoresistance and malignant progression in cervical GAS, and may contribute to the development of novel therapeutic strategies for this challenging cancer subtype.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"159"},"PeriodicalIF":3.1,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12436518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}