Molecular Biology Reports最新文献

{"title":"SIRT3 regulates CPT1a acetylation and fatty acid oxidation in renal tubular epithelial cells under diabetic condition.","authors":"Shuqing Yang, Xingyue Wang, Yu Zhang, Qingqing Ke, Weifang Su, Yang Zhou, Lei Jiang, Chunsun Dai, Ping Wen","doi":"10.1007/s11033-025-10712-y","DOIUrl":"https://doi.org/10.1007/s11033-025-10712-y","url":null,"abstract":"<p><strong>Background: </strong>The pathophysiology of renal tubular injury in diabetic kidney disease involves complex interactions between metabolic dysregulation, inflammation, and oxidative stress. Dysregulation of FAO leads to the accumulation of toxic metabolites, which may exacerbate mitochondrial dysfunction and contribute to cellular injury. CPT1a is a pivotal enzyme in FAO. Dysfunction of CPT1a impairs the translocation of long-chain fatty acyl-CoA into the mitochondria, which ultimately leads to tubular injury. Acetylation is a critical post-translational modification of proteins in essential cellular processes. In this study, we aimed to investigate the regulatory role of SIRT3 in CPT1a and its protective role against tubular injury in mice with diabetic kidney disease.</p><p><strong>Methods and results: </strong>We found that decreased SIRT3 expression was accompanied by elevated acetylation in the renal tubules of diabetic mice. Acetylome analysis using LC-MS/MS showed that mitochondrial proteins were hyper-acetylated in the tubules of diabetic mice. Specifically, CPT1a was hyperacetylated at lysines 86 and 639 in tubular epithelial cells of diabetic mice and was regulated by SIRT3. Furthermore, proximal tubular epithelial cells-specific Sirt3 knockout diabetic mice showed more pronounced lipid accumulation in the renal tubules and more significant urinary protein. The integrated optical density per area for SIRT3 was positively correlated with glomerular filtration rate and negatively correlated with urinary protein levels in humans.</p><p><strong>Conclusions: </strong>The study findings revealed that SIRT3 is downregulated in renal tubules during diabetes and interferes with the activity of CPT1a through deacetylation, disrupting fatty acid metabolism in the tubules and ultimately leading to tubular injury.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"603"},"PeriodicalIF":2.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 1357 bp deletion in β-thalassemia: molecular profiling and hematological characterization in a Guangxi cohort.","authors":"Youqiong Li, Tianjie Zhou, Lihua Ye, Liang Liang, Shufu Cheng, Lihong Zheng, Xi He, Peixing Wan, Tongfeng Huang","doi":"10.1007/s11033-025-10724-8","DOIUrl":"https://doi.org/10.1007/s11033-025-10724-8","url":null,"abstract":"<p><strong>Objective: </strong>The 1357 bp deletion is a rare type of β-thalassemia, and the literature on its characterization is very limited. This study aimed to conduct molecular diagnosis and clinical analysis of a 1357 bp deletion in the Guangxi cohort.</p><p><strong>Methods: </strong>This was a retrospective study in which all samples with Hb F > 5% and/or Hb A₂ > 3.5% suspected of β-thalassemia/hereditary persistence of fetal hemoglobin (HPFH) were enrolled in the study from 2016 to 2024. Routine genetic analysis was detected 24 common α- and β-thalassemia variants. For unresolved cases, Sanger sequencing was applied to identify novel variants in HBB and HBG genes. Additionally, Gap-PCR with specific primers and multiplex ligation-dependent probe amplification (MLPA) were utilized to screen for potential deletions. Finally, third-generation sequencing (TGS) was implemented to confirm duplicated genomic segments.</p><p><strong>Results: </strong>A cohort of 65 individuals was analyzed, revealing heterozygous β-thalassemia/HPFH/δβ-thalassemia in 83.1% (54/65) of cases. Among these, 37.0% (20/54) carried the 1357 bp deletion, 46.3% (25/54) exhibited Chinese ^Gγ(Aγδβ)⁰-thalassemia, and 16.7% (9/54) displayed SEA-HPFH. Genotypic analysis of the 1357 bp deletion showed four distinct profiles: simple heterozygotes (75%, 15/20), compound heterozygotes with α-thalassemia (15%, 3/20), compound heterozygotes with β-thalassemia (5%, 1/20), and compound heterozygotes with HPFH (5%, 1/20). Hematologically, the 1357 bp deletion presented with microcytic, hypochromic erythrocytes alongside elevated Hb A₂ and Hb F levels. Geographically, Beihai City (70%, 14/20) demonstrated the highest prevalence of this deletion within the Guangxi region.</p><p><strong>Conclusion: </strong>This study provides the first comprehensive characterization of the 1357 bp deletion, delineating its hematological profiles, molecular features, and region-specific prevalence patterns within the Guangxi Region. Accurate identification of molecular defects through phenotype-genotype correlation is important for genetic counseling and prenatal diagnosis.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"602"},"PeriodicalIF":2.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gasotransmitters and their influence on autism spectrum disorders - a systematic review.","authors":"Zhikal O Khudhur, Snur Rasool Abdullah, Bashdar Mahmud Hussen, Nyaz Abubakr Murad, Arezou Sayad, Soudeh Ghafouri-Fard","doi":"10.1007/s11033-025-10723-9","DOIUrl":"10.1007/s11033-025-10723-9","url":null,"abstract":"<p><p>Gasotransmitters, including nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S), play an important role in normal physiological processes in the body, such as neurotransmission, synaptic plasticity, and neuroinflammation. Dysregulation of signaling pathways of gasotransmitters contributes to the pathophysiology of autism spectrum disorder (ASD), which is a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behaviors. This systematic review aims to identify the potential role of gasotransmitters in ASD pathophysiology and their correlation with ASD severity. Following PRISMA guidelines, we conducted a systematic review by searching PubMed and Google Scholar databases in May 2024. We included studies that investigated the role of NO, H₂S, and CO in ASD between 2000 and 2024. We extracted data on the type of gasotransmitters, the model of the study (human or animal model), in vivo or in vitro, and the main role of these gasotransmitters as a risk factor or protective factor obtained findings. Out of 81 published papers screened from the databases, 39 reports were assessed for eligibility. After excluding studies that mentioned NO and CO as environmental pollutants, short communication, editorial letters, narrative reviews, systematic reviews, and meta-analyses, 28 original articles satisfied the inclusion and exclusion criteria. Results indicate a correlation between gasotransmitters and ASD, which contributed to the severity of ASD and its symptoms. An increase in gasotransmitters causes additional complications for individuals with ASD and can be mentioned as a risk factor or biomarker for ASD, except H₂S. The link between these endogenous gaseous molecules and ASD remains unclear; this systematic review offers strong evidence of the significant correlation between gasotransmitters and autism spectrum disorder.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"595"},"PeriodicalIF":2.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and clinical significance of autoantibodies to sulphite oxidase and glycogen phosphorylase in Chinese primary biliary cholangitis patients.","authors":"Rohil Jawed","doi":"10.1007/s11033-025-10646-5","DOIUrl":"10.1007/s11033-025-10646-5","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the prevalence and clinical significance of autoantibodies to mitochondrial sulphite oxidase (SUOX) and glycogen phosphorylase (PYGL) in Chinese PBC patients.</p><p><strong>Methods: </strong>Enzyme-linked immunosorbent assays (ELISA) were developed with purified SUOX and PYGL proteins. Serum samples from 780 PBC patients and 352 healthy controls were used for antibody detection. Statistical analysis was performed with antibody results and biochemical data from PBC patients.</p><p><strong>Results: </strong>Antibodies to SUOX and PYGL were found in 14.23% and 22.94% of PBC patients, but also in 6.53% and 9.37% of healthy controls. There is a significant positive correlation between anti-SUOX and -PYGL with anti-M2, -sp100 and -gp210. Anti-SUOX and -PYGL positivity does not correlate with ursodeoxycholic acid (UDCA) response. Time course analysis found no specific change of anti-SUOX or -PYGL antibody titers in positive patients before and after UDCA treatment.</p><p><strong>Conclusions: </strong>The data concluded that anti-SUOX and -PYGL autoantibodies are not serological markers in PBC diagnosis due to a lack of sensitivity and specificity. With the existence of PBC specific autoantibodies in PBC diagnosis and treatment, anti-SUOX and -PYGL status in PBC patients have no significant value.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"593"},"PeriodicalIF":2.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential role of PAX5 and PAX8 in regulating telomerase activity: a narrative mini-review.","authors":"Amin Abdurrahman Abdul Rashid, Marahaini Musa, Siti Norasikin Mohd Nafi, Nazia Abdul Majid, Sarina Sulong","doi":"10.1007/s11033-025-10704-y","DOIUrl":"https://doi.org/10.1007/s11033-025-10704-y","url":null,"abstract":"<p><p>The ability to express replicative immortality is one of the hallmarks of cancer. Most of these cells attain this feature by expressing the enzyme telomerase. This enzyme is responsible for maintaining the telomeres, a repeating structure at the ends of chromosomes, protecting the chromosomes from degradation. The Paired Box (PAX) genes are a family of highly conserved genes involved in various functions, including the development of diseases like cancer, in which most of them express telomerase as the mechanism to maintain telomere length. This study seeks to investigate PAX genes as potential telomerase activators and explore emerging research areas. Related literature was retrieved from PubMed, Web of Science and Scopus databases using a keyword search, where 119 records were identified. However, upon further filtering, only four reports were relevant to this topic, which addresses the role of PAX5 and PAX8 genes and their proteins' role in telomerase regulation. More studies are needed to elucidate the complex mechanism of action between the PAX genes and telomerase regulation.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"594"},"PeriodicalIF":2.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An overview on in-vivo generation of CAR-T cells using CRISPR-loaded functionalized nanocarriers for treating B-cell lineage acute lymphoblastic leukemia.","authors":"Tushara Saha, Rudra Prasad Saha, Manoj Kumar Singh, Kanu Priya, Shareen Singh, Mithul Rajeev, Debasmita Bhattacharya, Moupriya Nag, Dibyajit Lahiri","doi":"10.1007/s11033-025-10674-1","DOIUrl":"https://doi.org/10.1007/s11033-025-10674-1","url":null,"abstract":"<p><p>Chimeric antigen receptor T (CAR-T) cell therapy has become a milestone in the management of B cell lineage acute lymphoblastic leukemia. Yet, the traditional method-dependent on ex vivo manipulation, amplification, and reinfusion of autologous T cells-is high-cost, low-scalability, and severely immune-related toxicity. Here, we report a new nano-immunoengineering platform that allows in vivo production of chimeric antigen receptor T cells through the use of functionalized nanoparticles carrying clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated protein 9 (Cas9) gene editing elements. These nanoparticles are engineered to specifically target blood circulating T lymphocytes and deliver CRISPR/Cas9 complexes that have the ability to integrate chimeric antigen receptor constructs into the TRAC locus and knock out immune checkpoint genes like programmed cell death protein 1 (PD-1) simultaneously. Targeted delivery, endosomal escape, and efficient genome editing with minimal off-target effects are ensured through gold-based and DNA nanostructure-based carriers. Preclinical models show effective in vivo programming of functional chimeric antigen receptor T cells with vigorous antitumor efficacy, improved persistence, and decreased cytokine release syndrome. This method is a revolutionary breakthrough in cancer immunotherapy that provides a scalable, economical, and clinically flexible replacement for conventional chimeric antigen receptor T cell production.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"596"},"PeriodicalIF":2.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights for lncH19, miR-9, and miR-146a expression levels and their cross-talk with pro-inflammatory cytokines, copeptin, and neopterin profile in type 1 diabetic cardiomyopathy.","authors":"Marwa A Radwan, Nabil A Hasona, Adel Abdel Moneim, Alaa M Rabea, Rehab G Khalil","doi":"10.1007/s11033-025-10672-3","DOIUrl":"https://doi.org/10.1007/s11033-025-10672-3","url":null,"abstract":"<p><strong>Background: </strong>Diabetic cardiomyopathy (DCM) have become a key long-term complication of Type 1 diabetes (T1D), is a prevalent autoimmune chronic disease that greatly raises mortality rates in T1D patients. MicroRNAs (miRNA) have been linked to the pathophysiology of T1D, oxidative stress and inflammation are acknowledged as major contributors to the development of cardiovascular problems in diabetes. In this research work, the link between oxidative stress, inflammation, and miRNA expression will be investigated in order to determine their potential as molecular biomarkers for diagnosing and tracking cardiomyopathy in T1D.</p><p><strong>Methods and results: </strong>Patients were allocated into two groups: Healthy controls (Group I) and individuals with diabetes (Group II). Group II was further split into G-IIa and G-IIb subgroups in accordance with diabetes duration (< 5 years), and (> 5 years) of diagnosis respectively. TNF-α, IL-17, and IL-23 cytokines, Neopterin, CRP, Copeptin, Creatinine, Creatine kinase, malondialdehyde, nitric oxide, total cholesterol, triglycerides, HDL, and LDL in the serum were all measured. The findings showed increased levels of oxidative stress markers, inflammatory markers, and altered lipid profiles in comparison to both diabetes groups with healthy controls, with some differences between G-IIa and G-IIb. NF-kB, lncH19, and miR-9 expressions were considerably higher in diabetic patients than in controls, but miR-146a levels were significantly lower.</p><p><strong>Conclusions: </strong>These findings suggest the involvement of pro-inflammatory cytokines, oxidative stress, and certain miRNAs in the development of T1D cardiomyopathy. These factors may also serve as potential biomarkers in light of the early identification and management of cardiovascular issues in T1D patients.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"592"},"PeriodicalIF":2.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of miR-27a-5p and miR-449a as potential serum biomarkers for breast cancer: a combined bioinformatics and experimental study.","authors":"Tahereh Barati, Zohreh Mirzaei, Amir Ebrahimi, Mahmoud Shekari Khaniani, Solmaz Hashemi, Maghsood Mehri, Sima Mansoori Derakhshan","doi":"10.1007/s11033-025-10705-x","DOIUrl":"https://doi.org/10.1007/s11033-025-10705-x","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC) is one of the most prevalent malignancies among women worldwide, and early detection is crucial for improving patient outcomes. Among the key signaling pathways involved in BC, the MAPK signaling pathway plays a significant role in tumor progression.</p><p><strong>Methods: </strong>Through bioinformatics analysis, we identified miRNAs associated with the MAPK signaling pathway. Differential expression analysis using microarray data from the GSE106817 and GSE113486 datasets further refined our selection. Based on these analyses, we identified two candidate miRNAs, hsa-miR-27a-5p and hsa-miR-449a, as potential biomarkers for BC. We then examined the expression levels of these two serum miRNAs in women with BC (n = 100) and healthy controls (n = 100) using RT-PCR.</p><p><strong>Results: </strong>Our results demonstrated that both miRNAs were significantly upregulated in women with BC compared to healthy individuals (p < 0.05). Receiver operating characteristic (ROC) curve analysis further confirmed that these miRNAs exhibit strong diagnostic potential for BC.</p><p><strong>Conclusion: </strong>Overall, our findings suggest that hsa-miR-27a-5p and hsa-miR-449a, identified through bioinformatics and microarray-based expression analyses, could serve as promising biomarkers for BC detection. Their significant association with the MAPK signaling pathway was determined through bioinformatics analysis.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"590"},"PeriodicalIF":2.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of genetic variants in the MMP and ADAM genes towards chronic obstructive pulmonary disease susceptibility and lung function in the North Indian population.","authors":"Heena Kansal, Vishal Chopra, Kranti Garg, Siddharth Sharma","doi":"10.1007/s11033-025-10695-w","DOIUrl":"https://doi.org/10.1007/s11033-025-10695-w","url":null,"abstract":"<p><strong>Background-: </strong>Chronic Obstructive (COPD)pulmonary disease is a significant global health concern, increasingly linked to genetic factors. Airway remodelling in COPD is associated with ADAM33 and MMPs.</p><p><strong>Methods-: </strong>This study selected SNPs in the protease pathway to evaluate their impact on COPD. A total of 1000 subjects (500 COPD cases and 500 controls) were recruited. Logistic regression calculated odds ratios (ORs) to assess the association between SNPs and COPD risk, and haplotype analysis was performed. SNP interactions were evaluated using Multifactor Dimensionality (MDR) Reduction, and CART analysis identified high-risk subgroups.</p><p><strong>Results-: </strong>Results indicated a strong association between COPD and MMP9 rs17576 (OR = 2.01, Pc = 0.0012) and ADAM33 rs2280091 (OR = 1.80, Pc = 0.0012). SNP combinations highlighted the significance of rs17576, rs2280091, and rs612709 in increasing COPD risk. MMP9 (rs17576) (Pc = 0.003) and ADAM33 (rs2280091) (Pc = 0.0054) are linked to disease severity and mucus production, respectively. Haplotype analysis showed a single change in rs17576 and rs2280091 SNPs increases COPD risk. MDR and CART analysis confirmed these results, indicating rs3918392, rs17576, rs2280091, and rs3918396 are strongly associated with COPD risk (p < 0.0001).</p><p><strong>Conclusion-: </strong>The study concludes that rs3918392, rs17576, rs2280091, rs612709, and rs3918396 are linked to COPD risk in the north Indian population, potentially aiding earlier detection, treatment, and prevention.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"591"},"PeriodicalIF":2.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miRNAs as biomarkers and therapeutic targets in silicosis-related lung fibrosis.","authors":"Gaurav Gupta, Ahsas Goyal, Baby Ilma, M M Rekha, Priya Priyadarshini Nayak, Mandeep Kaur, Anil Khachi, Kavita Goyal, Mohit Rana, A Rekha, Dennis Chang, Kamal Dua","doi":"10.1007/s11033-025-10687-w","DOIUrl":"10.1007/s11033-025-10687-w","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"52 1","pages":"585"},"PeriodicalIF":2.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12162749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}