Ruobing Li, Ti Qin, Yabo Guo, Shan Zhang, Xiaogang Guo
{"title":"CEAM is a mitochondrial-localized, amyloid-like motif-containing microprotein expressed in human cardiomyocytes.","authors":"Ruobing Li, Ti Qin, Yabo Guo, Shan Zhang, Xiaogang Guo","doi":"10.1016/j.bbrc.2024.150737","DOIUrl":"10.1016/j.bbrc.2024.150737","url":null,"abstract":"<p><p>Microproteins synthesized through non-canonical translation pathways are frequently found within mitochondria. However, the functional significance of these mitochondria-localized microproteins in energy-intensive organs such as the heart remains largely unexplored. In this study, we demonstrate that the long non-coding RNA CD63-AS1 encodes a mitochondrial microprotein. Notably, in ribosome profiling data of human hearts, there is a positive correlation between the expression of CD63-AS1 and genes associated with cardiomyopathy. We have termed this microprotein CEAM (CD63-AS1 encoded amyloid-like motif containing microprotein), reflecting its sequence characteristics. Our biochemical assays show that CEAM forms protease-resistant aggregates within mitochondria, whereas deletion of the amyloid-like motif transforms CEAM into a soluble cytosolic protein. Overexpression of CEAM triggers mitochondrial stress responses and adversely affect mitochondrial bioenergetics in cultured cardiomyocytes. In turn, the expression of CEAM is reciprocally inhibited by the activation of mitochondrial stresses induced by oligomycin. When expressed in mouse hearts via adeno-associated virus, CEAM impairs cardiac function. However, under conditions of pressure overload-induced cardiac hypertrophy, CEAM expression appears to offer a protective benefit and mitigates the expression of genes associated with cardiac remodeling, presumably through a mechanism that suppresses stress-induced translation reprogramming. Collectively, our study uncovers a hitherto unexplored amyloid-like microprotein expressed in the human cardiomyocytes, offering novel insights into myocardial hypertrophy pathophysiology.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"734 ","pages":"150737"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399169","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":"Glutathione S-transferase: A versatile and dynamic enzyme.","authors":"Chinyere Aloke, Olalekan Olugbenga Onisuru, Ikechukwu Achilonu","doi":"10.1016/j.bbrc.2024.150774","DOIUrl":"10.1016/j.bbrc.2024.150774","url":null,"abstract":"<p><p>The dynamic and versatile group of enzymes referred to as glutathione S-transferases (GSTs) play diverse roles in cellular detoxification, safeguarding hosts from oxidative damage, and performing various other functions. This review explores different classes of GST, existence of polymorphisms in GST, functions of GST and utilizations of GST inhibitors in treatment of human diseases. The study indicates that the cytosolic GSTs, mitochondrial GSTs, microsomal GSTs, and bacterial proteins that provide resistance to Fosfomycin are the major classes. Given a GST, variation in its expression and function among individuals is due to the presence of polymorphic alleles that encode it. Genetic polymorphism might result in the modification of GST activity, thereby increasing individuals' vulnerability to harmful chemical compounds. GSTs have been demonstrated to play a regulatory function in cellular signalling pathways through kinases, S-Glutathionylation, and in detoxification processes. Various applications of bacterial GSTs and their potential roles in plants were examined. Targeting GSTs, especially GSTP1-1, is considered a potential therapeutic strategy for treating cancer and diseases linked to abnormal cell proliferation. Their role in cancer cell growth, differentiation, and resistance to anticancer agents makes them promising targets for drug development, offering prospects for the future.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"734 ","pages":"150774"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375010","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}
Pankaj Pal, Monika Sharma, Sukesh Kumar Gupta, Mrugendra B Potdar, Aarti V Belgamwar
{"title":"miRNA-124 loaded extracellular vesicles encapsulated within hydrogel matrices for combating chemotherapy-induced neurodegeneration.","authors":"Pankaj Pal, Monika Sharma, Sukesh Kumar Gupta, Mrugendra B Potdar, Aarti V Belgamwar","doi":"10.1016/j.bbrc.2024.150778","DOIUrl":"10.1016/j.bbrc.2024.150778","url":null,"abstract":"<p><p>Chemotherapy-induced neurodegeneration represents a significant challenge in cancer survivorship, manifesting in cognitive impairments that severely affect patients' quality of life. Emerging neuroregenerative therapies offer promise in mitigating these adverse effects, with miRNA-124 playing a pivotal role due to its critical functions in neural differentiation, neurogenesis, and neuroprotection. This review article delves into the innovative approach of using miRNA-124-loaded extracellular vesicles (EVs) encapsulated within hydrogel matrices as a targeted strategy for combating chemotherapy-induced neurodegeneration. We explore the biological underpinnings of miR-124 in neuroregeneration, detailing its mechanisms of action and therapeutic potential. The article further examines the roles and advantages of EVs as natural delivery systems for miRNAs and the application of hydrogel matrices in creating a sustained release environment conducive to neural tissue regeneration. By integrating these advanced materials and biological agents, we highlight a synergistic therapeutic strategy that leverages the bioactive properties of miR-124, the targeting capabilities of EVs, and the supportive framework of hydrogels. Preclinical studies and potential pathways to clinical translation are discussed, alongside the challenges, ethical considerations, and future directions in the field. This comprehensive review underscores the transformative potential of miR-124-loaded EVs in hydrogel matrices, offering insights into their development as a novel and integrative approach for addressing the complexities of chemotherapy-induced neurodegeneration.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"734 ","pages":"150778"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378977","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}
Khoula Sharif Mughal, Muhammad Ikram, Zia Uddin, Amna Rashid, Umer Rashid, Momina Khan, Naseem Zehra, Umair Sharif Mughal, Nabi Shah, Imran Amirzada
{"title":"Syringic acid improves cyclophosphamide-induced immunosuppression in a mouse model.","authors":"Khoula Sharif Mughal, Muhammad Ikram, Zia Uddin, Amna Rashid, Umer Rashid, Momina Khan, Naseem Zehra, Umair Sharif Mughal, Nabi Shah, Imran Amirzada","doi":"10.1016/j.bbrc.2024.150777","DOIUrl":"10.1016/j.bbrc.2024.150777","url":null,"abstract":"<p><p>Syringic acid (SA), a naturally occurring phenolic substance present in many edible plants and fruits, has been shown to have potential in immunoenhancement applications. In this study, we investigated the immunomodulatory effects of SA in mitigating cyclophosphamide (CYP)-induced immunosuppression in BALB/c mice using doxycycline as a positive control. SA administration prevented immune organ atrophy and morphological changes in the thymus, spleen, and bone marrow induced by CYP treatment in mice while also showing a dose-dependent enhancement of thymus and spleen indices compared to mice treated with CYP alone. Furthermore, SA improved thymocyte and splenocyte proliferation and exhibited significant antioxidant activity by reducing the elevated levels of malondialdehyde induced by CYP treatment. SA treatment effectively restored white blood cell (WBC) and lymphocyte counts to normal levels in CYP-treated animals, and the protective effects of CYP on immunological tissues were confirmed through histopathological examination. Moreover, SA treatment upregulated the expression of IL-6, IL-7, IL-15, and FoxN1. Finally, molecular docking studies revealed that binding energy values predicted minor inhibition potential toward IL-6, IL-7, FoxN1, IL-15, STAT3, STAT5, and JAK3. Overall, our findings suggest that SA treatment has the potential to reduce CYP-induced immunosuppression and may have applications as an immunologic adjuvant or functional food additive in chemotherapy.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"734 ","pages":"150777"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387579","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}
Mahintaj Dara, Mehdi Dianatpour, Negar Azarpira, Nader Tanideh, Romina Tanideh
{"title":"Integrating CRISPR technology with exosomes: Revolutionizing gene delivery systems.","authors":"Mahintaj Dara, Mehdi Dianatpour, Negar Azarpira, Nader Tanideh, Romina Tanideh","doi":"10.1016/j.bbrc.2024.151002","DOIUrl":"https://doi.org/10.1016/j.bbrc.2024.151002","url":null,"abstract":"<p><p>CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) serves as an adaptive immune system in bacteria and archaea, offering a defense mechanism against invading genetic elements such as viruses (bacteriophages) and plasmids. Today, CRISPR has evolved into a powerful gene-editing technology that enables highly specific and rapid modifications of DNA within a genome. It has a broad range of applications across various fields, including medicine, agriculture, and fundamental research. One of the significant challenges facing this technology is the efficient transfer of CRISPR constructs into target cells for gene editing. There are several methods to deliver this system into target cells, which can be classified as viral and non-viral methods. Each of these approaches has its own advantages and disadvantages. Recently, the use of extracellular vesicles for delivery has garnered particular attention. Exosomes are nano-sized extracellular vesicles that have emerged as promising carriers for drug delivery due to their unique properties. These naturally occurring vesicles, typically ranging from 30 to 150 nm in diameter, facilitate intercellular communication by transferring bioactive molecules such as proteins, lipids, and nucleic acids between cells. Exosome therapy has surfaced as a promising strategy in regenerative medicine, utilizing small extracellular vesicles to deliver therapeutic molecules to target cells. One of the emerging options for transferring the CRISPR system is exosomes. The integration of these two advanced technologies holds significant potential for developing efficient and targeted gene editing and advancing precision medicine. In contemporary medicine, there is an increasing focus on personalized and targeted treatments that cater to the distinct genetic and molecular profiles of individual patients. The synergy of CRISPR technology and exosome therapy presents a remarkable opportunity to develop highly targeted and effective therapeutic strategies customized to individual patient requirements. This review article examines the potential of incorporating CRISPR technology within exosomes for precision therapeutic applications.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"740 ","pages":"151002"},"PeriodicalIF":2.5,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680702","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}
Zhiwen Cao , Jinwen Jiang , Yiting Wang , Yuhang Lu , Min Wu , Xin Zhen , Xinyu Cai , Haixiang Sun , Guijun Yan
{"title":"Role of PRMT5 mediated HOXA10 arginine 337 methylation in endometrial epithelial cell receptivity","authors":"Zhiwen Cao , Jinwen Jiang , Yiting Wang , Yuhang Lu , Min Wu , Xin Zhen , Xinyu Cai , Haixiang Sun , Guijun Yan","doi":"10.1016/j.bbrc.2024.151004","DOIUrl":"10.1016/j.bbrc.2024.151004","url":null,"abstract":"<div><div>A successful embryo implantation relies heavily on the receptivity of the endometrial epithelium, a process regulated by various molecular mechanisms. Evaluating endometrial receptivity in infertility patients undergoing assisted reproductive treatment, particularly those with adenomyosis related infertility, poses significant challenges due to limitations associated with conventional assessment methods. In this study, we collected residual endometrial epithelial cells from the tips of embryo transfer catheters in patients with adenomyosis related infertility. High throughput sequencing revealed a marked downregulation of protein arginine methyltransferase 5 (PRMT5) in these cells. Functional assays demonstrated that PRMT5 interacts with and methylates homeobox A10 (HOXA10), a crucial transcription factor for endometrial receptivity and implantation. The methylation of HOXA10 at arginine 337 by PRMT5 enhances its stability and promotes the transcriptional activation of genes essential for endometrial differentiation and adhesion. The downregulation of PRMT5 led to decreased HOXA10 activity, resulting in impaired endometrial receptivity and subsequent implantation failure. These findings elucidate a critical pathway where PRMT5 downregulation negatively impacts HOXA10 function, providing new insights into the molecular mechanisms underlying implantation failure in adenomyosis related infertility. This study not only advances our understanding of the regulatory mechanisms governing endometrial receptivity but also identifies potential therapeutic targets for enhancing endometrial function in affected patients.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"739 ","pages":"Article 151004"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646853","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":"Crosstalk between pancreatic cancer and adipose tissue: Molecular mechanisms and therapeutic implications.","authors":"Boyu Diao, Zhiyao Fan, Bin Zhou, Hanxiang Zhan","doi":"10.1016/j.bbrc.2024.151012","DOIUrl":"https://doi.org/10.1016/j.bbrc.2024.151012","url":null,"abstract":"<p><p>The incidence rate of pancreatic cancer, a fatal illness with a meager 5-year survival rate, has been on the rise in recent times. When individuals accumulate excessive amounts of adipose tissue, the adipose organ becomes dysfunctional due to alterations in the adipose tissue microenvironment associated with inflammation and metabolism. This phenomenon may potentially contribute to the aberrant accumulation of fat that initiates pancreatic carcinogenesis, thereby influencing the disease's progression, resistance to treatment, and metastasis. This review presents a summary of the impact of pancreatic steatosis, visceral fat, cancer-associated adipocytes and lipid diets on the advancement of pancreatic cancer, as well as the reciprocal effects of pancreatic cancer on adipose tissue. Understanding the molecular mechanisms underlying the relationship between dysfunctional adipose tissue and pancreatic cancer better may lead to the discovery of new therapeutic targets for the disease's prevention and individualized treatment. This is especially important given the rising global incidence of obesity, which will improve the pancreatic cancer treatment options that are currently insufficient.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"740 ","pages":"151012"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674790","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":"Endothelial-derived nitric oxide impacts vascular smooth muscle cell phenotypes under high wall shear stress condition.","authors":"Kaoru Sawasaki, Masanori Nakamura, Naoyuki Kimura, Koji Kawahito, Masashi Yamazaki, Hiromichi Fujie, Naoya Sakamoto","doi":"10.1016/j.bbrc.2024.151005","DOIUrl":"https://doi.org/10.1016/j.bbrc.2024.151005","url":null,"abstract":"<p><p>The Phenotypic states of vascular smooth muscle cells (SMCs) are essential to understanding vascular pathophysiology. SMCs in vessels generally express a specific set of contractile proteins, but decreased contractile protein expression, indicating a phenotypic shift, is a hallmark of vascular diseases. Recent studies have suggested the relation of abnormally high wall shear stress (WSS) of approximately 20 Pa with the aortic disease pathogenesis. However, due to the lack of appropriate experimental models to assess SMC phenotypic states, the details of the phenotypic shift under high WSS conditions remain unclear. In this study, we developed a coculture model where vascular endothelial cells (ECs) were cocultured with SMCs expressing calponin 1, a contractile protein involved in the phenotypic shift of SMCs. We investigated the effects of a pathologically high WSS condition on the phenotypic states of SMCs. Increased calponin 1 expression was found upon exposure to 20 Pa WSS compared with a physiological 2 Pa condition, whereas the expression of another contractile protein, α-smooth muscle actin (αSMA) remained unchanged. Furthermore, the inhibition of EC-derived nitric oxide (NO), which is associated with endothelial dysfunction in vascular diseases, resulted in a trend of decreasing αSMA and Calponin 1 expression under 20 Pa WSS conditions compared with 2 Pa. Our findings suggest that EC-derived NO under pathologically high WSS conditions may impact the expression of contractile proteins implicated in aortic pathophysiology.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"740 ","pages":"151005"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674797","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}
Yifan Zhang , Zhenzhong Bai , Kang Song , Ying Liu , Wenbin Zhang
{"title":"High-iron diet damages brown adipose tissue mitochondria and exacerbates metabolic hazards of a high-fat diet","authors":"Yifan Zhang , Zhenzhong Bai , Kang Song , Ying Liu , Wenbin Zhang","doi":"10.1016/j.bbrc.2024.151008","DOIUrl":"10.1016/j.bbrc.2024.151008","url":null,"abstract":"<div><div>Metabolic diseases may be prevented by reducing carbohydrate intake and replacing plant-based diets with animal-based ones low in carbohydrates but high in protein, fat, and iron. While the effects of sugars on metabolic diseases are well-known, the role of iron remains unclear. This study aimed to explore the effects of a high-fat high-iron animal diet on body metabolism in mice. Micro-PET imaging was used to assess 18-F-labelled glucose uptake in BAT, and the morphology, respiratory function, and oxidative stress of BAT mitochondria were examined. The underlying mechanisms were elucidated by analyzing the expression of UCP-1, PGC-1α and PPARα. The high-iron high-fat diet increased appetite, impaired glucose tolerance, and reduced insulin sensitivity. Additionally, the high-iron diet promoted gluconeogenesis only in the absence of high-fat levels. Both high-iron and high-fat diets suppressed BAT activity, increased mitochondrial oxidative stress, decreased mitochondrial respiratory function, and lowered thermogenic gene expression. Weight loss strategies focusing solely on reducing carbohydrates and increasing animal foods, like ketogenic diets, may have long-term detrimental effects on metabolic health. Prioritizing dietary diversity and monitoring overall caloric intake is advisable for optimal outcomes.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"739 ","pages":"Article 151008"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142661970","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":"RNA binding protein CUGBP2/ETR-3 regulates STAT3 alternative splicing","authors":"Miki Kise , So Masaki , Naoyuki Kataoka , Kenji Suzuki","doi":"10.1016/j.bbrc.2024.151000","DOIUrl":"10.1016/j.bbrc.2024.151000","url":null,"abstract":"<div><div>Signal transducer and activator of transcription 3 (STAT3) is a multifactorial regulator involved in many biological responses. Alternative splicing of STAT3 pre-mRNA leads to an internal 50-nucleotide deletion of exon 23 selecting an alternative 3’ acceptor site, resulting in the generation of two splicing isoforms, STAT3α and STAT3β. STAT3β lacks 55 amino acid-residue transactivation domain at the C-terminal of STAT3α replacing seven unique amino acids. Although STAT3β was originally thought to be a dominant negative isoform of STAT3α, accumulating evidence have shown that STAT3β possesses both its unique functions and those that overlap with STAT3α in fundamental cellular processes. However, much remains unknown about STAT3 pre-mRNA alternative splicing in determining the balance between STAT3 isoforms. In this study, we identified <em>cis</em>-regulatory elements and CUGBP2/ETR-3 as a novel <em>trans</em>-acting factor that regulates STAT3 alternative splicing. Our findings demonstrate that STAT3 splicing can be modulated by CUGBP2 via association with UG-rich elements of intron 22, providing a novel insight into the mechanism of STAT3 alternative splicing. CUGBP2 would be a crucial molecule regulating the balance of STAT3 isoform expression, thus targeting CUGBP2 and its recognition sequences in intron 22 of STAT3 might impact on various biological processes regulated by STAT3 signaling pathway.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"739 ","pages":"Article 151000"},"PeriodicalIF":2.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646851","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}