Tissue & cell最新文献

{"title":"Exosomes: A new perspective for radiation combined injury as biomarker and therapeutics","authors":"Kirti ,&nbsp;Ajay Kumar Sharma ,&nbsp;M.H. Yashavarddhan,&nbsp;Rishav Kumar,&nbsp;Priyanka Shaw,&nbsp;Aman Kalonia,&nbsp;Sandeep Kumar Shukla","doi":"10.1016/j.tice.2024.102563","DOIUrl":"10.1016/j.tice.2024.102563","url":null,"abstract":"<div><p>Radiation Combined Injuries (RCI) pose formidable public health risks, particularly in the context of nuclear incidents, necessitating specialized treatments and development of biomarkers. RCI encompasses instances where ionizing radiation exposure coincides with burns, wounds, or trauma. However, the limited understanding of cellular responses hinders progress in developing effective therapies. This article underscores the pivotal role of exosomes, nano-sized particles (30–120 nm) actively secreted by cells, in addressing the intricate challenges posed by RCI. Exosomes serve as vehicles for the transportation of bioactive molecules, including proteins, lipids, and miRNA, thereby facilitating processes critical to radiotherapy, burn injury, and wound healing. Exosomes hold significant promise for the transformation of RCI management by reducing inflammation, promoting wound healing, managing sepsis, altering immunological responses, and modulating signal transduction pathways. Moreover, exosomes are also being explored as biomarker for various diseases and stress conditions including radiation exposure and associated injuries. This comprehensive review highlights the burgeoning potential of exosomes in advancing the management of RCI, thereby enhancing public health preparedness and response.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142172937","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":"Biomechanical and histological evaluation of a prototype bovine pericardial patch for veterinary abdominal surgery: An approximation study","authors":"Victoria Tambella ,&nbsp;Carlos Hernán Moscuzza ,&nbsp;Adrian Lifschitz ,&nbsp;Jorge Pablo García ,&nbsp;Juan Manuel Herrera ,&nbsp;Juan Staneck ,&nbsp;Facundo Arriaga ,&nbsp;Alejandro Sala Crist ,&nbsp;Fernando Lanzini","doi":"10.1016/j.tice.2024.102565","DOIUrl":"10.1016/j.tice.2024.102565","url":null,"abstract":"<div><p>In veterinary medicine, especially within large animal medical and surgical clinics, addressing cavitary defects is a primary concern. In bovines, umbilical hernias are the most common defect, and surgical repair often necessitates the use of prosthetic materials. However, there is a high rate of recurrence with sutures or synthetic meshes, largely due to tissue contamination. The development of biological patches for such repairs is still in its early stages in veterinary medicine, with no commercially tested prototypes available in Argentina. Tissues derived from the extracellular matrix are considered for this purpose, with bovine pericardium standing out due to its architectural characteristics and mechanical properties. For an ideal membrane, the pericardium must retain its biomechanical properties while being unreactive and safe for the host. This study aimed to biomechanically and histologically characterize a bovine pericardium patch through all stages of processing. The treatment involved fixation with 0.5 % glutaraldehyde, immersion in an antibiotic/antimycotic solution, and detoxification and storage in a 98 % sterile glycerin solution, with three sodium phosphate-buffered washes between steps. Histological examinations and stress-strain tests were performed at each processing stage, using native pericardium as a control. Despite some minor modifications in the histological and mechanical properties, the final patches appear to be a viable alternative for resolving cavitary defects.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142242700","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 limelight of adipose-derived stem cells in the landscape of neural tissue engineering for peripheral nerve injury","authors":"Sun QingNing ,&nbsp;Zul Izhar Mohd Ismail ,&nbsp;Mohd Nor Azim Ab Patar ,&nbsp;Norhafiza Mat Lazim ,&nbsp;Siti Nurma Hanim Hadie ,&nbsp;Nor Farid Mohd Noor","doi":"10.1016/j.tice.2024.102556","DOIUrl":"10.1016/j.tice.2024.102556","url":null,"abstract":"<div><h3>Background and aims</h3><p>Challenges in treating peripheral nerve injury include prolonged repair time and insufficient functional recovery. Stem cell therapy coupled with neural tissue engineering has been shown to induce nerve regeneration following peripheral nerve injury. Among these stem cells, adipose-derived stem cells (ADSCs) are preferred due to their accessibility, expansion, multidirectional differentiation, and production of essential nutrient factors for nerve growth. In recent years, ADSC-laden nerve guide conduit has been utilized to enhance the therapeutic effects of tissue-engineered nerve grafts. This review explores existing research that recognizes the roles played by ADSCs in inducing peripheral nerve regeneration following injury and summarizes the different methods of application of ADSC-laden nerve conduit in neural tissue engineering.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142242699","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":"Morin promotes autophagy in human PC3 prostate cancer cells by modulating AMPK/mTOR/ULK1 signaling pathway","authors":"Fereshtesadat Fakhredini ,&nbsp;Hadis Alidadi ,&nbsp;Masoud Mahdavinia ,&nbsp;Layasadat Khorsandi","doi":"10.1016/j.tice.2024.102557","DOIUrl":"10.1016/j.tice.2024.102557","url":null,"abstract":"<div><p>AMP-activated protein kinase (AMPK) suppresses tumorigenesis by modulating autophagy and apoptosis. This study evaluated the impact of Morin on PC3 prostate cancerous cells by examining the AMPK/ mechanistic target of rapamycin (mTOR)/ ULK1 (UNC-51-like kinase 1) pathway and autophagy process. The PC3 cells were treated with Morin (50 µg/ml) and AICAR (an AMPK activator). Cell viability, apoptosis, autophagy, and level of phosphorylated and non-phosphorylated ULK1, AMPK, and mTOR, as well as LC3B/LC3A, have been investigated. Through DAPI staining, measurement of Bax/Bcl-2 ratio, Caspase activity, and Annexin V/PI method, it has been revealed that Morin induces apoptosis and reduces the growth of PC3 cells. Morin enhanced the protein level of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) and decreased the expression of phosphorylated mTOR (p-mTOR) in the PC3 cells. Morin could also increase the LC3B/LC3A ratio, Acridine Orange-positive cells, expression of Beclin-1 and ATG5 genes, and decrease the p62 protein level indicating autophagy-inducing. AICAR (an AMPK activator) enhanced the impact of Morin on apoptosis, cell growth, and expression of LC3B, p-AMPK, p-ULK1, and p-mTOR proteins in the PC3 cells. These findings suggest that Morin induces apoptotic and autophagic cell death by activating AMPK and ULK1 and suppressing mTOR pathways.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142168848","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":"L-carnitine cause to increase cell proliferation of C-Kit+ hematopoietic progenitor cells via decreasing the PI3K and FOXO-1 protein expression","authors":"Behnaz Valipour ,&nbsp;Ezzatollah Fathi ,&nbsp;Raheleh Farahzadi ,&nbsp;Elahe Naderali ,&nbsp;Hamed Behniafar","doi":"10.1016/j.tice.2024.102558","DOIUrl":"10.1016/j.tice.2024.102558","url":null,"abstract":"<div><h3>Background</h3><p>Stem cell-based therapy has emerged as an attractive approach for regenerative medicine. Poor survival and maintenance of the cells used in regenerative medicine are considered as serious barriers to enhance the efficacy of the cell therapy. Using some antioxidants has been reported to prevent the aging of stem cells, and finding effective factors to reduce the senescence of these cells has impressive potential in cell therapy. The PI3K pathway adversely regulates the transcription factors known as FOXO, which are thought to have an inhibitory influence on cell proliferation. By downregulating FOXO and other targets, PI3K signaling controls the growth of cells. For this reason, the aim of the present study is to investigate the effect of L-carnitine (LC) as antioxidant on the cell proliferation and the protein expression of PI3K and FOXO.</p></div><div><h3>Methods</h3><p>For understanding the <em>in vitro</em> effect of LC on the PI3K and FOXO-1 expression of C-kit⁺ hematopoietic progenitor cells, the bone marrow mononuclear cells were isolated, and C-kit⁺ cells was enriched by the magnetic-activated cell sorting (MACS). Next, the identification of enriched C-kit⁺ cells were done by flowcytometry and immunocytochemistry. Then, C-kit⁺ cells were treated with 0.2 mM LC, the cells were collected at the end of the treatment period (48 h), and the proteins were extracted. In the following, the protein expression of PI3K and FOXO-1 was measured by western blotting. In addition, flowcytometry was done to assess the Ki-67 expression as a key marker for cell proliferation investigation.</p></div><div><h3>Results</h3><p>0.2 mM LC cause to significantly decrease in the protein expression of PI3K and FOXO-1 (*<em>P</em>&lt;0.05 and **<em>P</em>&lt;0.01, respectively). Also, the expression of Ki-67 was significantly increased in the presence of 0.2 mM LC (***<em>P</em>&lt;0.001).</p></div><div><h3>Conclusion</h3><p>Briefly, LC can be considered an effective factor in increasing the proliferation of C-kit⁺ cells via some signaling pathways.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162199","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":"Tyrobp deficiency blocks NLRP3-mediated inflammation and pyroptosis to alleviate myocardial ischemia-reperfusion injury through regulating Syk","authors":"Jie Yu ,&nbsp;Xiu’e Mu ,&nbsp;Chang Guan ,&nbsp;Yaqin Wang ,&nbsp;Hongying Li","doi":"10.1016/j.tice.2024.102555","DOIUrl":"10.1016/j.tice.2024.102555","url":null,"abstract":"<div><h3>Purpose</h3><p>The present study aims to investigate the biological function of Tyrobp in myocardial ischemia-reperfusion injury (MIRI) and to clarify its potential reaction mechanisms.</p></div><div><h3>Methods</h3><p>AC16 cells were induced by oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate the MIRI <em>in vitro</em>. The cell transfection technology was used to downregulate Tyrobp, followed by assessment of cell damage, apoptosis and cytokines production via Cell Counting Kit (CCK)-8 assay, lactate dehydrogenase (LDH) release assay, TUNEL and ELISA assays, respectively. Immunofluorescence assay was performed to assess GSDMD. Corresponding proteins were detected via western blotting, and Co-immunoprecipitation (Co-IP) assay was used to validate proteins interaction.</p></div><div><h3>Results</h3><p>Tyrobp was upregulated in OGD/R-exposed AC16 cells, and Tyrobp deficiency significantly alleviated OGD/R-caused cell viability loss, LDH release and cell apoptosis in AC16 cells. Meanwhile, Tyrobp deficiency inhibited the activation of NLRP3 inflammasome, reduced the production of cytokines and inhibited GSDMD intensity and GSDMD-N expression. Additionally, Tyrobp could interact with Syk and regulate Syk/NF-κB signaling. The rescue experiments showed that the above effects of Tyrobp deficiency on OGD/R-exposed AC16 cells were partly weakened by Syk overexpression.</p></div><div><h3>Conclusion</h3><p>Tyrobp deficiency alleviated MIRI by inhibiting NLRP3-mediated inflammation and pyroptosis through regulating Syk, providing a novel target for the treatment of MIRI.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142229402","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":"Sox2-mediated transdifferentiation of hAT-MSCs into induced neural progenitor-like cells for remyelination therapies","authors":"Hamed Shiri ,&nbsp;Mohammad Javan","doi":"10.1016/j.tice.2024.102553","DOIUrl":"10.1016/j.tice.2024.102553","url":null,"abstract":"<div><p>Mesenchymal stem cells (MSCs) are converted to neural cells using growth factors and chemicals. Although these neural cells are effective at modulating disease symptoms, they are less effective at replacing lost neural cells. Direct transdifferentiation seems to be a promising method for generating the required cells for regenerative medicine applications. Sox2 is a key transcription factor in neural progenitor (NP) fate determination and has been frequently used for transdifferentiating different cell types to NPs. Here, we demonstrated that the overexpression of a single transcription factor, Sox2, in human adipose tissue-derived mesenchymal stem cells (hAT-MSCs) led to the generation of induced NPs-like cells that were clonogenic, proliferative and passageable, and showed the potential to differentiate into three neural lineages. NPs are known as progenitors with the potential to differentiate into oligodendrocytes. In vivo, following transplantation into demyelinated adult mouse brains, they survived, differentiated and integrated into the adult brain while participating in the remyelination process and behavioral improvement. This report introduces a beneficial, low-cost and effective approach for generating NPs from an accessible adult source for autologous applications in treating neurodegenerative diseases, including remyelination therapies for multiple sclerosis and other demyelinating diseases.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162198","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":"Using hardystonite as a biomaterial in biomedical and bone tissue engineering applications","authors":"Haoyu Wang ,&nbsp;Gaurav Sanghvi ,&nbsp;Ahmadreza Arefpour ,&nbsp;Ahmad Alkhayyat ,&nbsp;Ali Soheily ,&nbsp;Saeid Jabbarzare ,&nbsp;Soheil Salahshour ,&nbsp;As'ad Alizadeh ,&nbsp;Sh. Baghaei","doi":"10.1016/j.tice.2024.102551","DOIUrl":"10.1016/j.tice.2024.102551","url":null,"abstract":"<div><p>Widespread adoption for substitutes of artificial bone grafts based on proper bioceramics has been generated in recent years. Among them, calcium-silicate-based bioceramics, which possess osteoconductive properties and can directly attach to biological organs, have attracted substantial attention for broad ranges of applications in bone tissue engineering. Approaches exist for a novel strategy to promote the drawbacks of bioceramics such as the incorporation of Zn²⁺, Mg²⁺, and Zr⁴⁺ ions into calcium-silicate networks, and the improvement of their physical, mechanical, and biological properties. Recently, hardystonite (Ca₂ZnSi₂O₇) bioceramics, as one of the most proper calcium-silicate-based bioceramics, has presented excellent biocompatibility, bioactivity, and interaction. Due to its physical, mechanical, and biological behaviors and ability to be shaped utilizing a variety of fabrication techniques, hardystonite possesses the potential to be applied in biomedical and tissue engineering, mainly bone tissue engineering. A notable potential exists for the newly developed bioceramics to help therapies supply clinical outputs. The promising review paper has been presented by considering major aims to summarize and discuss the most applicable studies carried out for its physical, mechanical, and biological behaviors.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0040816624002520/pdfft?md5=120ecb0c77ea7f59e29588b2467124b7&pid=1-s2.0-S0040816624002520-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162196","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}

{"title":"Impact of apoptosis and oxidative stress on pancreatic beta cell pathophysiology in streptozotocin-induced Type 1 diabetes mellitus","authors":"Orhan Yavuz ,&nbsp;Gungor Cagdas Dincel ,&nbsp;Serkan Yildirim ,&nbsp;Saeed El-Ashram ,&nbsp;Ebtesam Al‑Olayan","doi":"10.1016/j.tice.2024.102552","DOIUrl":"10.1016/j.tice.2024.102552","url":null,"abstract":"<div><h3>Aims</h3><p>Hyperglycemia plays a crucial role in the islet cells, especially pancreatic beta cell death in type 1 diabetes mellitus (T1DM). However, a few research have concentrated on the pathophysiology of apoptosis and oxidative stress in T1DM. The aim of this study was to determine the expression of Caspase 3, Caspase 9, 8-OHdG, Glutathione Reductase, endothelial and inducible nitric oxide synthase in the pancreatic tissue of streptozotocin (STZ)-induced T1DM patients and to compare the cellular mechanisms underlying this metabolic disorder.</p></div><div><h3>Methods</h3><p>For this purpose, a total of 20 Wistar albino rats were divided into two groups: Control (C) and Diabetes Mellitus (DM). In the DM group, T1DM was induced by STZ. Rats in the C group were injected intravenously with buffer solution. At the end of the day 20, rats were necropsied and immunohistochemical procedures were applied.</p></div><div><h3>Results</h3><p>The immunohistochemical examination revealed, strong positive immunoreactions were observed in the islet cells of the DM groups, particularly when all antibody stains were considered. On the other hand, the C groups showed minimal changes. The difference between the C and DM groups in terms of all antibodies was statistically significant (p&lt;0.01).</p></div><div><h3>Conclusions</h3><p>In the present study, it was concluded that apoptosis, oxidative stress and NOS expressions were involved in islet cell destruction in pancreatic tissue in STZ-induced T1DM.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162197","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":"Suppression of glomerular damage, inflammation, apoptosis, and oxidative stress of acute kidney injury induced by cyclophosphamide toxicity using resveratrol in rat models","authors":"Abdullah Alghamdi ,&nbsp;Mohammed Alissa ,&nbsp;Suad A. Alghamdi ,&nbsp;Mohammed A. Alshehri ,&nbsp;Meshari A. Alsuwat ,&nbsp;Amani Alghamdi","doi":"10.1016/j.tice.2024.102548","DOIUrl":"10.1016/j.tice.2024.102548","url":null,"abstract":"<div><p>Cyclophosphamide (CP) is a chemotherapy drug that can be used to treat different types of cancers, but its nephrotoxicity effects restrict its usage in clinical settings. Currently, we examined whether the polyphenolic antioxidant and anti-inflammatory compound, resveratrol (RES), can protect against CP-induced nephrotoxicity. Twenty male mature Sprague-Dawley rats were divided into 4 groups of equal size: control group, RES group which received RES (20 mg/kg) for 15 consecutive days, CP group which received CP as a single dose (150 mg/kg) on day 16, and CP+RES group which was similar of the RES and CP groups. Tissue samples were obtained for the stereological, immunohistochemical, biochemical, and molecular evaluations. Findings showed that the numerical density of glomerulus, total volumes and interstitial tissue volumes of kidney, antioxidative biomarkers concentrations (CAT, GSH, SOD), and expression levels of OCT2 gene were notably greater in the CP+RES group than the CP group (P&lt;0.05). During treatment, there was a significant decrease in the serum levels of the urea and creatinine, the densities of apoptotic and inflammatory cells, as well as levels of MDA and proinflammatory cytokines (IL-1β, TNF-α, and PFN1) in the CP+RES group than the CP group (P&lt;0.05). We deduce that giving RES can suppress of glomerular damage, inflammation, apoptosis, and oxidative stress of acute kidney injury induced by CP toxicity.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142128732","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}