Biology Open最新文献

A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects. 一种新的14-3-3θ拟磷小鼠模型显示社会优势缺陷。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-10 DOI: 10.1242/bio.061963

Mary A Gannon, Thanushri Srikantha, Rudradip Pattanayak, Navya Kapa, Aneesh Pathak, A Claire Roberts, William J Stone, Kasandra Scholz, Roschongporn Ekkatine, Talene A Yacoubian

{"title":"A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects.","authors":"Mary A Gannon, Thanushri Srikantha, Rudradip Pattanayak, Navya Kapa, Aneesh Pathak, A Claire Roberts, William J Stone, Kasandra Scholz, Roschongporn Ekkatine, Talene A Yacoubian","doi":"10.1242/bio.061963","DOIUrl":"10.1242/bio.061963","url":null,"abstract":"14-3-3 proteins, particularly the 14-3-3θ isoform, are neuroprotective in several models of Parkinson's disease (PD). Evidence for increased 14-3-3θ phosphorylation observed in PD and other neurodegenerative diseases points to a possible pathogenic role for 14-3-3θ phosphorylation in neurodegenerative disease. We recently created a novel conditional knock-in mouse to express the 14-3-3θ S232D phosphomimetic mutation. After crossing this conditional knock-in mouse with the Emx1-Cre mouse in order to induce expression of the S232D mutation in the cortex and hippocampus, we evaluated the effect of 14-3-3θ phosphorylation on behavior and pathology. These mice demonstrated mild motor deficits and reduced social dominance behavior but showed normal cognition and anxiety levels compared to Cre control mice. S232D mice did not show any α-synuclein or phospho-tau pathology at baseline, and dendritic arborization was normal in primary hippocampal cultures from S232D mice. Overall, this mouse model is a novel tool that can be used to look at the effect of 14-3-3θ phosphorylation at S232 in the context of neurodegenerative disease models.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109751","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}

引用次数: 0

Muscle forces and the demands of turning while walking. 肌肉力量和行走时转身的要求。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-02 DOI: 10.1242/bio.061883

Steven G Lautzenheiser, Patricia Ann Kramer

引用次数: 0

2024 Argentine Group for Extracellular Vesicles (GAVE) Workshop: promoting science in challenging times. 2024阿根廷细胞外囊泡小组（GAVE）研讨会：在充满挑战的时代促进科学。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-10 DOI: 10.1242/bio.062002

Gonzalo Germán Guendulain, Ana Lis Moyano, Vanesa Mattera, Melisa Carolina Monteleone

{"title":"2024 Argentine Group for Extracellular Vesicles (GAVE) Workshop: promoting science in challenging times.","authors":"Gonzalo Germán Guendulain, Ana Lis Moyano, Vanesa Mattera, Melisa Carolina Monteleone","doi":"10.1242/bio.062002","DOIUrl":"10.1242/bio.062002","url":null,"abstract":"The Argentine Group for Extracellular Vesicles (GAVE) was established in 2022 with the objective of bringing together researchers working in Argentina dedicated to extracellular vesicle (EV) studies. Following its successful inaugural meeting in 2023, the II GAVE Workshop was held on 12-13 September 2024, at the University of Buenos Aires, Argentina. This event brought together over 140 participants from diverse disciplines, fostering collaboration and strengthening the national EV research field. Moreover, international speakers and renowned experts in their fields shared valuable insights and experiences with the audience. Despite the challenges posed by the national government's funding cuts, the 2024 GAVE workshop showcased the Argentine scientists' strong commitment to high-quality research and the growth of local science in the field of EVs. Supported by international organizations and local companies, the II GAVE Workshop prioritized inclusivity and provided valuable networking opportunities, particularly for students and early-career researchers. This financial support was fundamental to broadening the impact of the event by promoting the assistance of underrepresented groups. This Meeting Review highlights the outcomes of our workshop and shows the advances of the Argentinian scientific community involved in EV research.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 6","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257408","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}

引用次数: 0

Generation and characterization of a DYNLT1-knockout mouse model reveals electrophysiological alterations and potential mechanistic contributors to atrial fibrillation. dynlt1敲除小鼠模型的产生和表征揭示了心房颤动的电生理改变和潜在的机制因素。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-16 DOI: 10.1242/bio.061895

Ting Chen, Ziyan Wang, Xinpeng You, Wenxing Guo, Yijin Chua, Qi Jiang, Yanhong Gao

{"title":"Generation and characterization of a DYNLT1-knockout mouse model reveals electrophysiological alterations and potential mechanistic contributors to atrial fibrillation.","authors":"Ting Chen, Ziyan Wang, Xinpeng You, Wenxing Guo, Yijin Chua, Qi Jiang, Yanhong Gao","doi":"10.1242/bio.061895","DOIUrl":"10.1242/bio.061895","url":null,"abstract":"Atrial fibrillation (AF) is a common arrhythmia that increases the risk of stroke and heart failure and is associated with high morbidity and mortality. However, its molecular pathogenesis remains incompletely understood. In this study, we generated a DYNLT1 knockout (KO) mouse model using CRISPR/Cas9 technology. Through electrocardiography, echocardiography, and histological analysis, we found that DYNLT1 deletion induced spontaneous AF. The KO mice exhibited not only surface electrophysiological remodeling and atrial structural changes but also increased atrial cardiomyocyte apoptosis, downregulation of gap junction proteins, and elevated inflammatory markers at the molecular level. Furthermore, using mass spectrometry, immunofluorescence, and other molecular techniques, we observed that DYNLT1 deletion reduced the distribution of its interacting protein TMCO1 in the endoplasmic reticulum (ER) of atrial cardiomyocytes, leading to ER calcium overload and potentially triggering the onset of AF. This study establishes a novel animal model for AF research, advances our understanding of the molecular mechanisms underlying AF, and provides a theoretical basis for the development of targeted molecular therapies.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207736","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}

引用次数: 0

Filtration and respiration of filter-feeding marine invertebrates are linked through allometric power-law functions. 滤食性海洋无脊椎动物的过滤和呼吸是通过异速幂律函数联系起来的——假设的验证。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-13 DOI: 10.1242/bio.062024

Hans Ulrik Riisgård, Poul S Larsen

{"title":"Filtration and respiration of filter-feeding marine invertebrates are linked through allometric power-law functions.","authors":"Hans Ulrik Riisgård, Poul S Larsen","doi":"10.1242/bio.062024","DOIUrl":"10.1242/bio.062024","url":null,"abstract":"Filter feeding in marine invertebrates is a secondary adaptation where the filtration rate (F) that provides the food energy to cover the respiration (R) increases with increasing body dry weight (W), and therefore it may be suggested that the exponents in the equations F=a1Wb1 and R=a2Wb2 have, during evolution, become near equal, b1≈b2, ensuring that the F/R-ratio=a1/a2 is nearly constant. Based on published data, we verify the hypothesis of equal allometric power-law exponents and test to what degree the F/R-ratio may be used to characterize various adaptations to filter feeding. The available b-values for very different taxonomic groups of filter feeders (bivalves, ascidians, crustaceans, polychaetes, jellyfish) covering 8 decades support in most cases the hypothesis of b1≈b2. For obligate phytoplankton filter feeders where b1≈b2 the F/R-ratio was used to estimate the critical phytoplankton biomass below which the animal would starve. However, if the food-particle retention efficiency is not constant during an animal's ontogeny the F/R-ratio may change according to the size range of particles being captured at the specific stage of development.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109753","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}

引用次数: 0

Persistent enteric neuroinflammation chronically impairs colonic motility in a pyridostigmine bromide-induced mouse model of Gulf War illness. 在吡哆斯的明溴诱导的海湾战争病小鼠模型中，持续的肠道神经炎症慢性损害结肠运动。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-06 DOI: 10.1242/bio.061867

Claudia A Collier, Aelita Salikhova, Sufiyan Sabir, Shreya A Raghavan

{"title":"Persistent enteric neuroinflammation chronically impairs colonic motility in a pyridostigmine bromide-induced mouse model of Gulf War illness.","authors":"Claudia A Collier, Aelita Salikhova, Sufiyan Sabir, Shreya A Raghavan","doi":"10.1242/bio.061867","DOIUrl":"10.1242/bio.061867","url":null,"abstract":"Neuroplasticity in the adult colon enables the enteric nervous system (ENS) to adaptively remodel in response to acute inflammation, preserving motility. However, chronic inflammation may drive maladaptive neuroplasticity, resulting in gastrointestinal dysmotility, a hallmark of functional gastrointestinal disorders, including Gulf War illness (GWI). GWI affects ∼30% of Gulf War veterans and has been linked to oral toxic exposures during combat, such as pyridostigmine bromide (PB). To explore mechanisms of persistent dysmotility, we developed a PB exposure model relevant to GWI. In the colon, we observed structural and functional ENS changes, including an imbalance in excitatory and inhibitory motor neurons and altered motility patterns. These were accompanied by a sustained influx of pro-inflammatory macrophages and elevated cytokine levels, indicating persistent low-grade enteric neuroinflammation. Inflammatory macrophages were found near enteric neural stem cells (ENSCs), impairing their regenerative potential. Transcriptomic analyses corroborated the presence of chronic neuroinflammation and dysregulated repair pathways. Together, our findings suggest that persistent enteric neuroinflammation and impaired neurogenesis contribute to long-term colonic dysmotility in GWI. This model offers new insights into chronic ENS dysfunction and may guide therapeutic strategies for GWI and related disorders.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980752","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}

引用次数: 0

Maternal protein restriction affects the differentiation of cells in the epididymal epithelium lining of 44-day-old rats. 母体蛋白质限制会影响 44 天大老鼠附睾上皮细胞的分化。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-06 DOI: 10.1242/bio.060080

Fábio Colonheze, Marilia Martins Cavariani, Bruno Cesar Schimming, Talita de Mello Santos, Luiz Gustavo de Almeida Chuffa, Raquel Fantin Domeniconi

{"title":"Maternal protein restriction affects the differentiation of cells in the epididymal epithelium lining of 44-day-old rats.","authors":"Fábio Colonheze, Marilia Martins Cavariani, Bruno Cesar Schimming, Talita de Mello Santos, Luiz Gustavo de Almeida Chuffa, Raquel Fantin Domeniconi","doi":"10.1242/bio.060080","DOIUrl":"10.1242/bio.060080","url":null,"abstract":"Maternal protein restriction delays the differentiation of epididymal mesenchymal cells in newborn rats. However, it is unclear whether this delay persists until the full differentiation of the epididymal epithelium at 44 days postnatal. Thus, this study aimed to assess the impact of maternal protein reduction on 44-day-old rats' epididymal epithelium differentiation, following up on the observed delay in newborn animals. Pregnant rats were randomly divided into groups receiving normal-protein (NP: 17% protein) or low-protein (LP: 6% protein) diets during gestation and lactation. On postnatal day (PDN) 44, male offspring were euthanized, and the epididymis (NP n=10, LP n=10) was processed according to immunohistochemical techniques for the detection of aquaporin 9 (AQP9), KI-67, TP63, and ATPase. LP rats showed a decrease in the intensity of the AQP9 reaction, an increase in cellular proliferation in the initial segment and corpus of the epididymis, an increase in basal cells in the caput and corpus epididymis, and an increase in ATPase-positive clear cells in the cauda region. These findings demonstrate that maternal protein restriction impacts cell differentiation in the epididymal epithelium of 44-day-old rats, persisting even with a normal-protein diet after weaning.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139696985","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}

引用次数: 0

Ethanol downregulates gastrula gene expression and cell movement, causing symptoms of foetal alcohol spectrum disorders. 乙醇下调原肠胚基因表达和细胞运动，引起胎儿酒精谱系障碍症状。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-06 DOI: 10.1242/bio.061777

Amena Ali Alsakran, Bethany Gibson, Hoi Ying Wong, Caitlin Heaton, Rebekah Boreham, Rashid Minhas, Jonathan Ball, Tetsuhiro Kudoh

{"title":"Ethanol downregulates gastrula gene expression and cell movement, causing symptoms of foetal alcohol spectrum disorders.","authors":"Amena Ali Alsakran, Bethany Gibson, Hoi Ying Wong, Caitlin Heaton, Rebekah Boreham, Rashid Minhas, Jonathan Ball, Tetsuhiro Kudoh","doi":"10.1242/bio.061777","DOIUrl":"10.1242/bio.061777","url":null,"abstract":"Foetal alcohol spectrum disorders (FASDs) occur in embryos when they are exposed to maternally supplied alcohol. To study the mechanisms of FASDs, the zebrafish embryo can serve as an excellent model as ethanol-exposed zebrafish embryos exhibit common symptoms of human FASDs including microcephaly, incomplete neural plate closure, eye defects, craniofacial disorders and many other defects. Here, we investigated the embryo development at gastrula stage where three germ layers develop with specific gene expressions and undergo dynamic cell movement including extension, convergence and epiboly, establishing the platform to form the head and body axis in later development. Gastrula cell movement analyses using fluorescent transgenic zebrafish embryos revealed that ethanol induced dose-dependent delay of extension, convergence and epiboly cell movement and associated gene expression in all three germ layers. Our results suggest multiple targets of ethanol including gene expression and cell movement, which, consequently, delay key gene expression and cell localisation, causing irreversible developmental defects in the head and body axis formation.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959163","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}

引用次数: 0

Ammonia transport mediated by urea transporter A isoforms. 尿素转运蛋白A异构体介导的氨转运。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-15 Epub Date: 2025-06-06 DOI: 10.1242/bio.061655

N Pina-Lopes, J Kabutomori, R Campos, R Musa-Aziz

{"title":"Ammonia transport mediated by urea transporter A isoforms.","authors":"N Pina-Lopes, J Kabutomori, R Campos, R Musa-Aziz","doi":"10.1242/bio.061655","DOIUrl":"https://doi.org/10.1242/bio.061655","url":null,"abstract":"Urea transporters (UTs) are a family of urea-selective channel proteins that play an essential role in the urine-concentrating mechanism of the mammalian kidney. In addition to urea, UT-A2 and UT-A3 - the N- and C-terminal regions of full-length UT-A1, respectively - and UT-B transport water, and human UT-B transports water and ammonia (NH3). However, UT-A-mediated NH3 transport has not been evaluated. Given that regulated renal NH3/NH4+ transport by renal epithelial cells is essential to acid-base homeostasis and considering UT-A2 and UT-A3 localization in the inner medulla, where the transport of urea, water, and NH3 is important, it is plausible that UT-A-mediated NH3 transport could be physiologically relevant. The present study characterized the urea, water, and NH3 transport properties and solute pathways of murine UT-A2, UT-A3, and UT-B heterologously expressed in Lithobates catesbeianus oocytes. Control and UT-expressing oocytes were evaluated for surface protein expression through lysine-biotinylation and immunoblotting. Urea uptake was measured using radiolabeled urea, water permeability was assessed using video microscopy, and NH3 transport was monitored using a surface pH microelectrode. All UT-encoding cRNAs were translated, glycosylated, and inserted into the oocyte membrane. Wild-type UT-expressing oocytes displayed significantly higher urea, water, and NH3 transport than day-matched water-injected control cells. Pre-treating the oocytes with phloretin or mutating the urea pore threonines (Thr177 and Thr339 human UT-B numbering) to valines (Val) attenuated UT-mediated urea, water and NH3 transport to control oocyte values. Our study showed for the first time that UT-A2 and UT-A3 increase the membrane NH3 permeability. Thus, besides the critical role of UTs in urinary concentration, these proteins may also impact acid-base homeostasis and contribute to other processes associated with health and disease.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 6","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246532","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}

引用次数: 0

Live cell GLUT4 translocation assay reveals Per3 as a novel regulator of circadian insulin sensitivity in skeletal muscle cells. 活细胞GLUT4易位分析显示Per3是骨骼肌细胞昼夜胰岛素敏感性的一种新的调节因子。

IF 1.8 4区生物学

Biology Open Pub Date : 2025-06-11 DOI: 10.1242/bio.061941

Rashmi Sivasengh, Andrew Scott, Brendan M Gabriel

{"title":"Live cell GLUT4 translocation assay reveals Per3 as a novel regulator of circadian insulin sensitivity in skeletal muscle cells.","authors":"Rashmi Sivasengh, Andrew Scott, Brendan M Gabriel","doi":"10.1242/bio.061941","DOIUrl":"https://doi.org/10.1242/bio.061941","url":null,"abstract":"Type 2 diabetes (T2D) is a growing global health concern, with skeletal muscle playing a central role due to its contribution to postprandial glucose disposal. Insulin resistance in skeletal muscle often precedes the clinical onset of T2D and is characterised by impaired GLUT4 trafficking. Circadian disruption is increasingly recognised as a contributor to metabolic dysfunction, yet its impact on skeletal muscle insulin sensitivity remains poorly defined. We hypothesised that circadian regulators influence GLUT4 translocation and glucose uptake, contributing to the metabolic impairments observed in T2D. To investigate this, we developed a high-throughput, live-cell GLUT4 translocation assay capable of capturing circadian dynamics in skeletal muscle cells. Using publicly available transcriptomic data from primary human myotubes derived from individuals with and without T2D, our re-analysis identified altered rhythmic expression of several genes, including PER3, ARNTL, HOXB5, and TSSK6. Publicly available phenome-wide association study (PheWAS) data further supported associations between these genes and T2D-related traits. Functional validation using siRNA knockdown revealed that PER3 silencing significantly impaired GLUT4 translocation and glucose uptake in human skeletal muscle cells, while also abolishing rhythmic insulin responsiveness. ARNTL knockdown caused a moderate reduction in GLUT4 translocation, suggesting complementary roles in metabolic regulation. Our findings identify PER3 as a novel circadian regulator of GLUT4 translocation and insulin sensitivity in skeletal muscle. This work also introduces a sensitive, live-cell assay suitable for real-time assessment of GLUT4 dynamics and circadian regulation, offering a powerful platform for discovering new therapeutic targets in T2D.","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265275","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}

引用次数: 0