Matthew R Hawkins, Joshua T Moeller, Ashini Kaushik, Tracey Porter, Cecilia Cesa, Landon B Gibbins, Rebecca A Wingert
{"title":"Alcohol exposure alters proximodistal nephron segmentation during zebrafish embryogenesis.","authors":"Matthew R Hawkins, Joshua T Moeller, Ashini Kaushik, Tracey Porter, Cecilia Cesa, Landon B Gibbins, Rebecca A Wingert","doi":"10.1016/j.ydbio.2026.10.006","DOIUrl":"10.1016/j.ydbio.2026.10.006","url":null,"abstract":"<p><p>Fetal alcohol spectrum disorders (FASD) encompass a broad range of effects caused by prenatal alcohol exposure. In the United States, conservative estimates place the incidence of FASD at a rate of 5 in 100 births. Children with FASD can have morphological afflictions including congenital defects of the brain, spinal cord, heart, eyes, and skeleton, as well as poor formation of facial structures such as the nose and mouth. Cognitive and behavioral abnormalities such as learning disabilities, socio-developmental delays and emotional disorders are also highly prevalent. There is no known cure for FASD and in utero detection methods are not available. In terms of urinary tract defects, kidney and renal related maladies may represent underreported aspects of FASD. To better understand the renal phenotypes associated with prenatal alcohol exposure, we employed the zebrafish, Danio rerio, a vertebrate species well suited for developmental nephrology and teratological work that has been used extensively to model FASD. We treated zebrafish embryos with ethanol then examined pattern formation and physiological activity of nephrons, which are the basic structural and functional unit of the kidney. Using whole mount in situ hybridization, we found that the formation of several cell types in the nephron blood filter and tubule, as well as renal progenitor populations, were perturbed by alcohol exposure. Interestingly, supplementation with all-trans retinoic acid, a vitamin A derivative associated with mitigating the effects of ethanol exposure in zebrafish and other animals, was sufficient to completely or partially rescue multiple ethanol induced kidney cell defects and restore nephron physiological activity. These studies have revealed several consequences of ethanol exposure that lead to the deregulation of renal ontogeny, and implicate a key role for reduced RA levels, thereby contributing useful insights relevant to the broader field of FASD research.</p>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":" ","pages":"180-193"},"PeriodicalIF":2.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180020","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}
Angeline K Chemel, Kate E McCluskey, Matthew N Tran, Michelle T Seeler, Aliza T Ehrlich, Helen Rankin Willsey
{"title":"Epilepsy-associated potassium channel KCNT1 is required for multiciliated cell specification in Xenopus.","authors":"Angeline K Chemel, Kate E McCluskey, Matthew N Tran, Michelle T Seeler, Aliza T Ehrlich, Helen Rankin Willsey","doi":"10.1016/j.ydbio.2026.10.005","DOIUrl":"https://doi.org/10.1016/j.ydbio.2026.10.005","url":null,"abstract":"<p><p>Pathogenic, presumed gain-of-function variants in the gene KCNT1, which encodes a sodium-activated potassium channel, cause a severe neurodevelopmental disorder with intractable epilepsy. In addition to seizures, affected individuals commonly present with severe respiratory issues and structural heart defects not commonly observed in other genetic pediatric epilepsies, suggesting additional developmental functions for KCNT1 in organs beyond the brain. Here we characterized the spectrum of clinical diagnoses present in a cohort of 46 individuals with genetic variants in KCNT1, ranging from 0 to 19 years of age, by medical record review. We documented the prevalence of diagnoses across organ systems, including dependence on assisted breathing, congenital structural heart defects, urinary dysfunction, and spine deformities, among others. Next, we explored the embryonic expression and function of KCNT1 in diploid frogs (Xenopus tropicalis) and observed expression in developing ciliated tissues such as the brain, heart, kidney, and epidermis. Embryonic perturbation of KCNT1 disrupted developmental signaling pathways and caused ciliogenesis defects in the mucociliary epidermis, a common model for the human airway. Loss of KCNT1 disrupted development of multiciliated cells, reminiscent of recent work on the ion channel Piezo1. Consistently, pharmacological inhibition of Piezo signaling enhanced the ciliogenesis phenotype observed following KCNT1 inhibition, while activation of Piezo1 activity partially rescued ciliogenesis in the context of KCNT1 inhibition. Finally, KCNT1 loss reduced expression of foxj1, a key transcriptional regulator of multiciliated cell specification, linking KCNT1 activity to the transcriptional programs underlying multiciliated cell formation and specification. Together, this work establishes that KCNT1 has embryonic functions in Xenopus beyond regulating neuronal activity, specifically in multiciliated cell development, and identifies an interaction with pharmacologically-tractable Piezo channels that may be productive for therapeutic efforts aimed at inhibiting KCNT1 activity.</p>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178742","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}
Alice M Godden, Nicole Ward, Méghane Sittewelle, Rafeeq Mir, Aleksandr Kotov, Marco Antonaci, Anne H Monsoro-Burq, Grant N Wheeler
{"title":"MicroRNA miR-219 is required for neural border and neural crest development in Xenopus neurulas.","authors":"Alice M Godden, Nicole Ward, Méghane Sittewelle, Rafeeq Mir, Aleksandr Kotov, Marco Antonaci, Anne H Monsoro-Burq, Grant N Wheeler","doi":"10.1016/j.ydbio.2026.10.003","DOIUrl":"https://doi.org/10.1016/j.ydbio.2026.10.003","url":null,"abstract":"<p><p>At head levels, neural crest (NC) multipotent stem cells are specified in the ectoderm territory located between the anterior neural plate ectoderm and the future pre-placodal and lateral non-neural ectoderm. While the fine-tuning of NC specification is increasingly being elucidated, many questions remain, including how microRNAs may govern expression of gene programs during these processes. We have identified miR-219 as a candidate regulator of craniofacial development in the vertebrate Xenopus laevis. Here, we characterize this phenotype and explore miR-219-dependent molecular pathways by morpholino knock-down. The development of the NC and adjacent ectoderm was evaluated using whole mount in situ hybridization (WISH) of key markers (pax3, zic1, xhe2, sox10, snai2, sox2), alcian blue cartilage staining, phenotype analysis, RNA sequencing of microdissected dorsal ectoderm and microRNA rescue experiments. These complementary approaches show that while neural induction is mainly unaffected, miR-219 depletion alters gene expression programs associated with neural border development, explaining the phenotype. WISH and RNA sequencing of the miR-219 morphant tissue highlights that NC progenitor programs (pax3, zic1, pou5f3, sall3) are maintained or increased at the expense of the progression of NC development (twist1, rpe65), resulting in defective NC specification. While increased pax3 expression seems an important part of this program, reducing pax3 in miR-219 morphant embryos is not sufficient to rescue the phenotype, highlighting that other key partners remain to be identified. This study supports an important and complex role of miR-219 in the early steps of neural crest formation.</p>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148088","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}
Sapna Meena, Pooja Sagvekar, Tonatiuh Molina-Villa, Miloslav Sanda, Miguel Valle-Inclan-Cabello, Thomas Juan, Marco Tarasco, Maëlle Bellec, Nana Fukuda, Stefan Günther, João Cardeira-da-Silva, Didier Y R Stainier
{"title":"Mustn1b is required for cardiomyocyte dedifferentiation and heart regeneration in zebrafish.","authors":"Sapna Meena, Pooja Sagvekar, Tonatiuh Molina-Villa, Miloslav Sanda, Miguel Valle-Inclan-Cabello, Thomas Juan, Marco Tarasco, Maëlle Bellec, Nana Fukuda, Stefan Günther, João Cardeira-da-Silva, Didier Y R Stainier","doi":"10.1016/j.ydbio.2026.10.004","DOIUrl":"https://doi.org/10.1016/j.ydbio.2026.10.004","url":null,"abstract":"<p><p>Unlike the adult mammalian heart, the adult zebrafish heart can robustly regenerate via processes that include cardiomyocyte (CM) dedifferentiation, proliferation, and repopulation of the damaged tissue. Although CM dedifferentiation is considered indispensable for cardiac regeneration, the factors driving it remain elusive. Here, we examine the role of Mustn1b in CM dedifferentiation during zebrafish cardiac regeneration. Mustn1b is a small protein highly expressed in skeletal, smooth, and cardiac muscle tissues. Using a mustn1b:EGFP reporter line, we first find that its expression is specific to CMs during heart development, and that it peaks at early larval stages. In the regenerating adult heart, mustn1b reporter expression is re-induced in dedifferentiating CMs, establishing it as a novel marker for this subset of CMs. By evaluating two newly generated mustn1b loss-of-function mutant alleles, including a large deletion allele, we find that Mustn1b deficiency leads to decreased CM dedifferentiation and proliferation, and ultimately results in impaired cardiac regeneration. Furthermore, CM-specific overexpression of mustn1b can enhance CM dedifferentiation and proliferation after cardiac cryoinjury. Mechanistically, mass spectrometry data suggest that upon cryoinjury, Mustn1b interacts with sarcomeric and cytoskeletal proteins, pointing towards a role in structural remodeling that could facilitate CM dedifferentiation during heart regeneration. Altogether, our findings identify Mustn1b as a regulator of CM dedifferentiation during zebrafish cardiac regeneration.</p>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147795","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}
Developmental biologyPub Date : 2026-06-01Epub Date: 2026-03-04DOI: 10.1016/j.ydbio.2026.03.001
MaryJane Shimell , Robert Connacher , Sangbin Park , Aidan J. Peterson , Kavita Arora , Michael B. O'Connor
{"title":"Shrew is an essential, recently evolved, Drosophila specific gene required for formation of the embryonic BMP activity gradient","authors":"MaryJane Shimell , Robert Connacher , Sangbin Park , Aidan J. Peterson , Kavita Arora , Michael B. O'Connor","doi":"10.1016/j.ydbio.2026.03.001","DOIUrl":"10.1016/j.ydbio.2026.03.001","url":null,"abstract":"<div><div>Patterning the dorsal surface of the Drosophila blastoderm embryo requires the rapid redistribution of a BMP heterodimer (Decapentaplegic/Screw) from lateral regions of the embryo to the dorsal midline as cellularization is completed. BMP redistribution creates a steeply graded signal with peak activity in the mid-dorsal region and requires four additional secreted gene products: Short gastrulation (Sog), Twisted gastrulation (Tsg), Tolloid (Tld), and Shrew (Srw). While the functions of Sog, Tsg, Tld, and their vertebrate homologs, in generating BMP activity gradients have been well-described, the role of Drosophila Srw remains an enigma. Here we show that Srw encodes a secreted, N-terminally truncated paralog of Tsg that, like Tsg, stimulates the cleavage of Sog by Tld. However, unlike Tsg, it does not form a stable interaction with any identified component of the patterning machinery. Structural modeling and mutant analysis suggest Srw transiently binds to the Sog/Tsg/BMP complex to facilitate proteolysis of Sog. We further demonstrate that the requirement for Srw can be bypassed by providing additional Tsg in <em>srw</em> mutant embryos prior to cellularization. Phylogenetic analysis suggests that Tsg and Srw emerged from separate duplications of the Crossveinless (Cv) paralog in higher Diptera, and then Drosophilid lineages respectively, thus providing components for progressive specialization of insect embryo patterning. Taking into consideration our genetic, biochemical and phylogenetic data, we present three possible mechanistic models for how Srw might accelerate Sog cleavage by Tld, to hasten BMP gradient formation in rapidly developing Drosophila embryos.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"534 ","pages":"Pages 9-22"},"PeriodicalIF":2.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369480","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}
Developmental biologyPub Date : 2026-06-01Epub Date: 2026-02-28DOI: 10.1016/j.ydbio.2026.02.012
Arpan Parichha , Patrick Azzam , Frederic Causeret , Suranjana Pal , Elizabeth Ann Grove , Angeliki Louvi , Alessandra Pierani , Shubha Tole
{"title":"Cortical hem-like progenitors contribute pyramidal neurons to the neocortex and hippocampus","authors":"Arpan Parichha , Patrick Azzam , Frederic Causeret , Suranjana Pal , Elizabeth Ann Grove , Angeliki Louvi , Alessandra Pierani , Shubha Tole","doi":"10.1016/j.ydbio.2026.02.012","DOIUrl":"10.1016/j.ydbio.2026.02.012","url":null,"abstract":"<div><div>The cortical hem is a signaling center at the midline of the embryonic telencephalon that provides instructive cues to the adjacent cortical primordium and serves as the hippocampal organizer, inducing multiple distinct hippocampal field identities. The cortical hem consists of neuroepithelial progenitors, and gives rise to diverse neuronal and non-neuronal cell types, including Cajal-Retzius cells, hippocampal pyramidal neurons, and choroid plexus epithelial cells. Here, we use two independent Cre drivers, <em>Wnt3aCre</em> and <em>Lmx1aCre</em>, to examine the lineages from the cortical hem. We report that these lineages also contribute pyramidal neurons to the neocortex, and we describe their spatiotemporal distribution. Together, our results extend the known lineages of the cortical hem.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"534 ","pages":"Pages 1-8"},"PeriodicalIF":2.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344050","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}
Developmental biologyPub Date : 2026-05-01Epub Date: 2026-02-02DOI: 10.1016/j.ydbio.2026.02.001
Alexis Grimaldi , Muriel Rigolet , Corinne Blugeon , Nicolas Buisine , Laurent M. Sachs
{"title":"Crosstalk between corticosterone and triiodothyronine signaling in Xenopus tropicalis hindlimb buds","authors":"Alexis Grimaldi , Muriel Rigolet , Corinne Blugeon , Nicolas Buisine , Laurent M. Sachs","doi":"10.1016/j.ydbio.2026.02.001","DOIUrl":"10.1016/j.ydbio.2026.02.001","url":null,"abstract":"<div><div>Thyroid hormone signaling has a wide range of biological effects involved in the control of homeostasis and development. In amphibian, thyroid hormones control the onset of metamorphosis, which resemble the mammalian perinatal period. Glucocorticoids too are involved in vertebrate development but they also mediate stress response and thus act as a relay that channel environmental inputs and modulate biological processes. Despite being deeply adaptive, glucocorticoids responses may nonetheless promote more detrimental long-term effects because of sub-optimal benefit-cost balances. To date, the extent and the diversity of functional interactions between thyroid hormone and glucocorticoid signaling are supported by very little molecular data. Here, we used transcriptomic analysis to collect the molecular details of the crosstalk between triiodothyronine and corticosterone signaling during limb development, <em>in vivo</em>. We show that the transcriptional responses to the two hormones are highly archetypal and that crosstalk affect expression of a few hundred of genes, with some of them potentially involved in bone development.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"533 ","pages":"Pages 1-15"},"PeriodicalIF":2.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118070","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}
Developmental biologyPub Date : 2026-04-01Epub Date: 2026-01-06DOI: 10.1016/j.ydbio.2026.01.003
Jinxia Wang , Yue Li , Yutong Zhang , Yu Zhao , Huili Tong , Shufeng Li
{"title":"IGF-1 regulates PEAR1 through Egr1 to promote skeletal muscle post-injury regeneration","authors":"Jinxia Wang , Yue Li , Yutong Zhang , Yu Zhao , Huili Tong , Shufeng Li","doi":"10.1016/j.ydbio.2026.01.003","DOIUrl":"10.1016/j.ydbio.2026.01.003","url":null,"abstract":"<div><div>Insulin-like growth factor 1 (IGF-1) is a key regulator of skeletal muscle growth and regeneration. In this study, we demonstrate that IGF-1 promotes C2C12 myoblast proliferation in a dose- and time-dependent manner. Mechanistically, IGF-1 induces the expression of early growth response 1 (Egr1), a transcription factor that directly binds to the promoter region of platelet endothelial aggregation receptor 1 (PEAR1) and enhances its transcription. Upregulation of PEAR1 subsequently facilitates myoblast proliferation by activating the Notch signaling pathway. Furthermore, IGF-1-induced activation of the Egr1-PEAR1 cascade enhances muscle stem cell (MuSC) proliferation and accelerates skeletal muscle regeneration following injury in vivo. Collectively, this study reveals the critical role of the IGF-1-Egr1-PEAR1 regulatory axis in skeletal muscle regeneration, providing novel mechanistic insight into IGF-1-mediated muscle repair.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 52-59"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931572","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}
Developmental biologyPub Date : 2026-04-01Epub Date: 2026-01-07DOI: 10.1016/j.ydbio.2026.01.004
Manaswini Sarangi
{"title":"Introducing DevBioConnect: A new author webinar series from developmental biology","authors":"Manaswini Sarangi","doi":"10.1016/j.ydbio.2026.01.004","DOIUrl":"10.1016/j.ydbio.2026.01.004","url":null,"abstract":"","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 32-34"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942464","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":"Drosophila as a model to study autophagy during oogenesis","authors":"Mrunmayee Kulkarni , Nidhi Murmu , Minal Ayachit , Karan Selarka , Kiran Nilangekar , Bhupendra V. Shravage","doi":"10.1016/j.ydbio.2025.12.013","DOIUrl":"10.1016/j.ydbio.2025.12.013","url":null,"abstract":"<div><div>Autophagy is an evolutionarily conserved catabolic process that is essential for maintaining cellular and developmental homeostasis in eukaryotes. <em>Drosophila</em> oogenesis offers a robust model for investigating the spatial and temporal regulation of autophagy within a complex developmental framework that involves cells from both germline and somatic lineages. This tightly regulated cascade of events enables the differentiation of a germline stem cell into a mature oocyte. Autophagy contributes to cellular quality control, nutrient sensing, and the regulation of developmental cell death, all of which are critical for proper egg development and maturation. Disruption of autophagy influences oogenesis, resulting in defective egg chamber development, altered apoptotic dynamics, abnormally shaped mitochondria and compromised mitophagy. Methodological advances, including immunofluorescence-based detection, live imaging using fluorescent reporters, and ultrastructural analysis via transmission electron microscopy, have significantly enhanced the ability to monitor autophagic activity in the ovary. This review summarizes current evidence that establishes autophagy as a key regulatory mechanism during oogenesis. Additionally, it offers an opportunity to investigate the role of autophagy in various cellular processes, including cell division, gene amplification, endocycling, collective cell migration, and cytoplasmic streaming for embryonic polarity, nurse cell dumping, and programmed cell death during <em>Drosophila</em> oogenesis.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 1-19"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833347","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}