Current research in physiology最新文献

{"title":"An interactive, self-guided tutorial on scientific writing for first year physiology students","authors":"Alex Swainson ,&nbsp;Matthew J. Mason ,&nbsp;Frances M. MacMillan","doi":"10.1016/j.crphys.2025.100157","DOIUrl":"10.1016/j.crphys.2025.100157","url":null,"abstract":"<div><div>Most biomedical science students arriving at UK universities have very limited experience of writing scientifically and have little insight into the process involved in producing a peer-reviewed academic publication. To help support them, we created an interactive, online tutorial to help improve their scientific writing through looking at aspects including the construction of a logical argument, use of figures and referencing, as well as providing an overview of the publication process. The tutorial was delivered in an in-person teaching workshop at the University of Bristol and offered as an optional, online-only activity at the University of Cambridge, in both cases to first-year physiology students. In Bristol, 68 % of 152 students and in Cambridge, 67 % of 561 students engaged with the interactive tutorial. These students were invited to complete before-and-after surveys, with questions relating to their confidence in and understanding of the topics covered. Feedback from students in both institutions was overwhelmingly positive, with a statistically significant increase in reported confidence and understanding following completion of the tutorial. We propose the use of similar interactive tutorials as a simple, low-investment way in which training in scientific writing can be included in undergraduate science curricula, to help students prepare for what is expected in coursework, exam essays and in their postgraduate careers.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100157"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High carbohydrate diet programs metabolic enzyme gene expression modification in F2 generation wistar rat males","authors":"Joseph Chimezie ,&nbsp;Worship Odosa Agbonifo ,&nbsp;Hope Oluwabukola Francis ,&nbsp;Mercy Oluwaseun Awoleye ,&nbsp;Temitope Gabriel Adedeji","doi":"10.1016/j.crphys.2025.100154","DOIUrl":"10.1016/j.crphys.2025.100154","url":null,"abstract":"<div><div>Diets high in carbohydrates (HCD) negatively impact transgenerational metabolic health and phenotype, factors directly influenced by gene expression. This study investigates the effects of HCD feeding on gene expression of key enzymes of important metabolic pathways in the Parent (F0), first (F1) and second (F2) filial generations. Each generation consisted of a control and HCD group of male and female counterparts in the F0 and F1 generations. Female rat cohorts (F0) fed a control or high-carbohydrate diet were mated at pro-oestrous period with males fed with similar diets at a ratio of 1:1 overnight. The offspring of the F1 generation exposed to the same diet were mated (1:1) to produce the F2 generation fed on a control diet. Male animals in each generation were analysed for metabolic changes, gene expression, and phenotypic outcomes. The results indicate that HCD caused significant increases (P &lt; 0.05) in body weight in both the F1 and F2 generations, fasting blood glucose in the F2 generation, as well as serum insulin and HOMA-IR in the F1 and F2 generations. The F0 and F1 HCD-fed rats demonstrated a significant increase (P &lt; 0.05) in the expression of genes involved in glycolysis and glycogen synthesis, along with a significant decrease (P &lt; 0.05) in the expression of genes for gluconeogenic enzymes. Additionally, there was an increase (P &lt; 0.05) in the expression of genes associated with fatty acid biosynthesis and a decrease (P &lt; 0.05) in β-oxidation gene expression, a pattern similarly observed in control-fed F2 male rats. These findings suggest that a parental diet high in carbohydrates can induce modifications in the gene expression of metabolic rate-limiting enzymes in F2 offspring, regardless of their diet. However, this study did not assess the epigenetic modifications potentially responsible for the observed transgenerational effects. Future research could investigate epigenetic changes such as DNA methylation and histone modifications, and also assess these effects in female animals.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100154"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-intensity training and irisin response: A possible molecular cross-talk for irisin response","authors":"Ping Li ,&nbsp;Ligang Tong ,&nbsp;Xuecui Bi","doi":"10.1016/j.crphys.2025.100163","DOIUrl":"10.1016/j.crphys.2025.100163","url":null,"abstract":"<div><div>Physical exercise is widely recognized for its positive effect on health through alterations in genetic, molecular, or tissue-level pleiotropic effects. The extent of these advantages hinges on the intensity that elicits optimal threshold adaptation, facilitating interactions and communication within or between the cells. This requires the activation of several proteins, enzymes, and hormones. Irisin, an exercise-triggered hormone, is pivotal in converting white fat into brown fat, enhancing bone health, and optimizing brain functions. The activation of irisin is contingent upon precise exercise protocols that trigger several molecular cross-talks. However, no specific exercise protocols (types/intensity/duration) have been developed. Therefore, establishing specific exercise protocols could reveal irisin-induced benefits on bone and brain health. The present review discussed how high-intensity training (HIT) triggers the irisin response by activating its upstream and downstream molecular signaling pathways and how HIT helps to cross-talk these signaling pathways to improve irisin response.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100163"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144892096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acidosis enhances contribution of Ca2+-activated chloride channels to vascular tone regulation in early postnatal period","authors":"Anastasia A. Shvetsova ,&nbsp;Margarita A. Khlystova ,&nbsp;Valentina S. Shateeva ,&nbsp;Sofia D. Simonenko ,&nbsp;Anna A. Borzykh ,&nbsp;Denis V. Abramochkin ,&nbsp;Dina K. Gaynullina","doi":"10.1016/j.crphys.2025.100143","DOIUrl":"10.1016/j.crphys.2025.100143","url":null,"abstract":"<div><h3>Introduction</h3><div>Acidosis often occurs during clinical complications in newborns and can lead to changes in the mechanisms of arterial tone regulation. However, it is unknown how acidosis affects the activity of Ca²⁺-activated chloride channels (CaCC) in arteries during early ontogenesis. We hypothesized that their activity may increase during acidosis.</div></div><div><h3>Methods</h3><div>We studied isometric contractions of saphenous arteries isolated from adult and 10-13-day-old rats. Intracellular pH was measured using a fluorescent indicator BCECF-AM simultaneously with recording the contractile activity of the arterial preparation in isometric mode.</div></div><div><h3>Results</h3><div>Metabolic acidosis with pH = 6.8 caused a significant decrease in the arterial contractile responses of adult and 10-13-day-old rats. The functional contribution of CaCC was absent in the adult rat arteries both at pH = 7.4 and pH = 6.8. However, in 10-13-day-old rat pups, the functional contribution of CaCC was higher at pH = 6.8 compared to pH = 7.4.</div></div><div><h3>Conclusion</h3><div>Acidosis augments the functional role of CaCC in arteries during early postnatal ontogenesis, but not in adulthood.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100143"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice","authors":"Ozra Dehkordi ,&nbsp;Stephen Lin ,&nbsp;Safia Mohamud ,&nbsp;Richard M. Millis ,&nbsp;Paul C. Wang","doi":"10.1016/j.crphys.2025.100147","DOIUrl":"10.1016/j.crphys.2025.100147","url":null,"abstract":"<div><div>Respiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain poorly understood. G-protein-gated inwardly rectifying potassium (GIRK) channels, especially the GIRK2 subunit, are expressed in rhythm-generating neurons of the pre-Bötzinger complex and have been implicated in opioid-induced respiratory depression. Nonetheless, their specific role in morphine-induced neurochemical changes is not yet fully defined. In this study, <em>in vivo</em> proton magnetic resonance spectroscopy (¹H MRS) was used in mice to assess morphine-induced metabolite changes in ventral brainstem regions encompassing the pre-Bötzinger complex. Wild-type mice were compared with GIRK2 heterozygous (GIRK2⁺/⁻) mutants. Baseline levels of several metabolites including glutamate (Glu), myo-inositol (Ins), N-acetylaspartate plus N-acetylaspartylglutamate (NAA + NAAG), and glutamate plus glutamine (Glu + Gln) differed significantly between GIRK2⁺/⁻ and wild-type mice. Despite these baseline differences, many of morphine's effects on metabolite levels were similar in the wild-type and GIRK2⁺/⁻ mice. Morphine increased phosphocreatine (PCr) in both genotypes, while total creatine (Cr + PCr) decreased only in the wild-type mice. Glutamine levels increased significantly in both groups. Notably, NAA decreased in wild-type but increased in GIRK2⁺/⁻ mice, whereas NAA + NAAG decreased in both. These findings demonstrate that chronic morphine exposure induces substantial neurochemical changes in brainstem respiratory centers. Although the GIRK2⁺/ ^- mutation altered some of the metabolite responses, it does not fully block morphine's effects, highlighting the complexity of opioid-induced adaptations in the respiratory control networks.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100147"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex and dose differences in morphine administration on renal function, inflammatory and apoptotic markers in male and female Wistar rats","authors":"Olaoluwa Sesan Olukiran ,&nbsp;Oluwadare Joshua Ogundipe ,&nbsp;Stephen Taiye Adelodun ,&nbsp;Moses Agbomhere Hamed ,&nbsp;Olayemi Sola Babatunde ,&nbsp;Oluwole Ojo Alese ,&nbsp;Rufus Ojo Akomolafe","doi":"10.1016/j.crphys.2025.100162","DOIUrl":"10.1016/j.crphys.2025.100162","url":null,"abstract":"<div><div>This study examined the impact of morphine on renal function, antioxidant enzymes, and inflammatory and apoptotic markers in male and female Wistar rats, considering both sex- and dose-dependent effects. 40 Wistar rats (20 male, 20 female), each weighing 120–150 g were used in this study. The control group received distilled water (0.5 mL/100 g b.w), while experimental groups were given morphine orally at 20, 40 and 60 mg/kg daily for 30 days. Renal function, inflammatory, and apoptotic markers were assessed in the plasma and tissue homogenate. Kidneys were preserved in 10 % formo-saline for histological examination. Morphine significantly increased plasma creatinine in both male and female rats, with the increase being more pronounced in males. Caspase-3 and TNF-α were also elevated in both sexes, but with no significant difference between males and females. Male rats showed significantly higher catalase activity and elevated plasma sodium, potassium, phosphate, and chloride ion concentrations compared to females. Photomicrographs revealed that low and medium doses of morphine caused more severe kidney damage in both male and female rats, leading to atrophied glomeruli, widened Bowman's space, and loss of brush border in the tubules. Conversely, high-dose resulted in less pronounced damage, with only a few atrophied glomeruli and indistinct tubules. Morphine induced more pronounced lipid peroxidation and oxidative stress in female rats compared to males, as indicated by changes in their plasma electrolytes and antioxidant enzyme activities. Interestingly, lower dose caused more significant alterations in renal function, oxidative stress and apoptotic markers compared to medium and high doses.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100162"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144917690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The story so far………- current opinion in the use and applications of interactive storytelling in physiology and clinical education","authors":"Bagley L. ,&nbsp;Wilson J. ,&nbsp;Kime A.","doi":"10.1016/j.crphys.2025.100142","DOIUrl":"10.1016/j.crphys.2025.100142","url":null,"abstract":"<div><div>Physiology and clinical practice are subjects of study which demand integration of multiple sources of systems working knowledge and information on the performance of those systems to come to meaningful conclusions. This is made more complex by the interpretation and actions as a result of this conclusion having direct impact on the sum of the component systems, the human, thereby integrating significant social and psychological considerations into an already complex situation.</div><div>As higher education educators, it is a significant challenge to provide our learners with training and most importantly, practice, in these knowledge, skills and behaviours in the classroom. There has been a significant interest in recent years in providing active learning opportunities which allow learners to apply subject knowledge to multi-faceted, immersive, continuously evolving stories which reflect a graduate's professional aspirations. This review highlights practices from the literature of storytelling education which the higher education educator can utilise in promoting “meaning making” in the classroom. Here, the case for interactive storytelling in physiology and clinical education is argued, as well as presenting commonly utilised techniques and practices with which educators can embed storytelling into their pedagogy as well as highlighting future directions in this field.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100142"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143594159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microvascular endothelial cells display organ-specific responses to extracellular matrix stiffness","authors":"Rana Haidari ,&nbsp;Wesley J. Fowler ,&nbsp;Stephen D. Robinson ,&nbsp;Robert T. Johnson ,&nbsp;Derek T. Warren","doi":"10.1016/j.crphys.2025.100140","DOIUrl":"10.1016/j.crphys.2025.100140","url":null,"abstract":"<div><div>The extracellular matrix was originally thought of as simply a cellular scaffold but is now considered a key regulator of cell function and phenotype from which cells can derive biochemical and mechanical stimuli. Age-associated changes in matrix composition drive increases in matrix stiffness. Enhanced matrix stiffness promotes the progression of numerous diseases including cardiovascular disease, musculoskeletal disease, fibrosis, and cancer. Macrovascular endothelial cells undergo endothelial dysfunction in response to enhanced matrix stiffness. However, endothelial cells are highly heterogeneous, adopting structural and gene expression profiles specific to their organ of origin. Endothelial cells isolated from different vessels (i.e. arteries, veins or capillaries) respond differently to changes in substrate stiffness. It is unknown whether microvascular endothelial cells isolated from different organs also display organ-specific responses to substrate stiffness. In this study, we compare the response of microvascular endothelial cells isolated from both the mouse lung and mammary gland to a range of physiologically relevant substrate stiffnesses. We find that endothelial origin influences microvascular endothelial cell response to substrate stiffness in terms of both proliferation and migration speed. In lung-derived endothelial cells, proliferation is bimodal, where both physiologically soft and stiff substrates drive enhanced proliferation. Conversely, in mammary gland-derived endothelial cells, proliferation increases as substrate stiffness increases. Substrate stiffness also promotes enhanced endothelial migration. Enhanced stiffness drove greater increases in migration speed in mammary gland-derived than lung-derived endothelial cells. However, stiffness-induced changes in microvascular endothelial cell morphology were consistent between both cell lines, with substrate stiffness driving an increase in endothelial volume. Our research demonstrates the importance of considering endothelial origin in experimental design, especially when investigating how age-associated changes in matrix stiffness drive endothelial dysfunction and disease progression.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100140"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143134703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms involved in aminoacidurias: impacts of genetic and environmental factors","authors":"Joseph Abayomi Ajayi ,&nbsp;Evelyn Nnashiru Ananias ,&nbsp;Muneerah Issa-Lawal ,&nbsp;Abdulkadir Mashood Gambari ,&nbsp;Adetoun Bunmi Aribatise ,&nbsp;Lekan Sheriff Ojulari ,&nbsp;Abdullateef Isiaka Alagbonsi","doi":"10.1016/j.crphys.2025.100168","DOIUrl":"10.1016/j.crphys.2025.100168","url":null,"abstract":"<div><h3>Background</h3><div>Amino acids play vital roles in protein synthesis, energy metabolism, and cellular function. Aminoacidurias are metabolic disorders characterized by excessive urinary excretion of amino acids resulting from defects in renal tubular reabsorption or amino acid metabolism. These disorders result from a combination of genetic mutations affecting transporter proteins and environmental factors that influence disease severity. This review aims to explore the molecular mechanisms by which genetic and environmental factors disrupt amino acid homeostasis.</div></div><div><h3>Methods</h3><div>A scoping review was conducted following Arksey and O'Malley's framework. Relevant literature from 1980 to 2025 was identified using the PubMed and Google Scholar databases. Studies reporting genes or genetic variants, as well as environmental factors associated with aminoacidurias in humans and animals, were included.</div></div><div><h3>Results</h3><div>The review highlighted 9 genes associated with aminoacidurias, including SLC3A1 (rBAT), SLC7A9 (b^o,+AT), SLC6A19 (B^oAT1), SLC7A7 (y⁺LAT1), SLC7A6 (y⁺LAT2), SLC36A2 (PAT-2), SLC6A20 (SIT-1), SLC6A18 (B^oAT3), and SLC1A1 (EAAT3). Over 350 gene mutations responsible for aminoacidurias were identified. Environmental factors, including dietary intake (such as Vitamin D deficiency), gut microbiota and dysbiosis, drugs and heavy metal exposure (specifically Lead and Cadmium), were also found to cause aminoacidurias.</div></div><div><h3>Conclusion</h3><div>Understanding the genetic and environmental mechanisms underlying aminoacidurias is crucial for improving diagnostic strategies and developing targeted therapeutic approaches. Our findings reveal that aminoacidurias are largely influenced by genetic factors, with few environmental factors implicated in the pathophysiology of aminoacidurias. Future research should focus on gene-environment interactions and developing novel therapies targeting specific amino acid transport pathways to enhance treatment outcomes for affected individuals.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100168"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145265094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How PPAR-alpha mediated inflammation may affect the pathophysiology of chronic kidney disease","authors":"Sepiso K. Masenga ,&nbsp;Selam Desta ,&nbsp;Mark Hatcher ,&nbsp;Annet Kirabo ,&nbsp;Dexter L. Lee","doi":"10.1016/j.crphys.2024.100133","DOIUrl":"10.1016/j.crphys.2024.100133","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is a major risk factor for death in adults. Inflammation plays a role in the pathogenesis of CKD, but the mechanisms are poorly understood. Peroxisome proliferator-activated receptor alpha (PPAR-α) is a nuclear receptor and one of the three members (PPARα, PPARβ/δ, and PPARγ) of the PPARs that plays an important role in ameliorating pathological processes that accelerate acute and chronic kidney disease. Although other PPARs members are well studied, the role of PPAR-α is not well described and its role in inflammation-mediated chronic disease is not clear. Herein, we review the role of PPAR-α in chronic kidney disease with implications for the immune system.</div></div>","PeriodicalId":72753,"journal":{"name":"Current research in physiology","volume":"8 ","pages":"Article 100133"},"PeriodicalIF":2.1,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142722950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}