Nephron Physiology最新文献

{"title":"Contents Vol. 128, 2014","authors":"A. Rodríguez–Carmona, J. Spence, G. Filler, S. Huang, M. Eliasziw, W. Vezina, D. Churchill, Bonnie Richardson, A. House, Javier A. Neyra, J. Yee, John Manllo, Xilong Li, G. Jacobsen, H. Chin, S. H. Baek, Sejoong Kim, D. K. Kim, J. Park, S. Shin, Sang Ho Lee, B. Choi, Suhnggwon Kim, C. Lim, L. Yessayan, M. P. Fontán, C. R. Rodríguez, M. B. Sans, Emilio Sánchez Álvarez, Marta da Cunha Naveira, P. Q. Ganga, B. López-Calviño, C. Suárez, T. Steinman, Cristian V Riella, P. Czarnecki, O. Ortega, G. Cobo, I. Rodríguez, P. Gallar, C. Mon, J. Herrero, M. Ortiz, A. Oliet, R. Camacho, C. Gioia, A. Vigil, O. Dönmez, Okan Akacı, N. Albayrak, A. Altas, M. Furuhashi, Marenao Tanaka, Yusuke Okazaki, T. Mita, T. Fuseya, Kohei Ohno, Shutaro Ishimura, H. Yoshida, T. Miura, Yujuan Liu, H. Anders, H. Beckwith, L. Lightstone, P. Cravedi, G. Remuzzi, P. Ruggenenti, A. Kronbichler, A. Bruchfeld, R. Popat, M. Robson, A. Bomback, F. Houssiau, P. Ronco, A. Karras, D. Jayne, H. Debiec, F. Locatelli, A. D. Francisco, G. Deray, D. Fli","doi":"10.1159/000374085","DOIUrl":"https://doi.org/10.1159/000374085","url":null,"abstract":" Chronic Kidney Disease and Hypertension A. Levin, Vancouver, B.C. R. Gansevoort, Groningen  Acute Kidney Injury R. Mehta, San Diego, Calif. N. Kolhe, Derby  Dialysis J. Daugirdas, Chicago, Ill. C. Hutchison, Hawkes Bay C. Fraansen, Groningen  Patient Subjective Experience, Healthcare Delivery and Innovation in Practice R. Fluck, Derby E. Brown, London  Crossover States with Non-Renal Organ Systems C. Chan, Toronto, Ont. T. Breidthardt, Basel N. Selby, Derby  Transplantation A. Chandraker, Boston, Mass. A. Salama, London Editor-in-Chief","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"128 1","pages":"I - VI"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000374085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64770059","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":"Contents Vol. 26, 2014","authors":"L. Fine, Satz Mengensatzproduktion, Druckerei Stückle","doi":"10.1159/000365804","DOIUrl":"https://doi.org/10.1159/000365804","url":null,"abstract":"","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"126 1","pages":"XXIX - XXXII"},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000365804","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64733841","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":"Front & Back Matter","authors":"C. McIntyre, S. Beesley","doi":"10.1159/000365339","DOIUrl":"https://doi.org/10.1159/000365339","url":null,"abstract":"Each paper needs an abstract of up to 250 words. It should be structured as follows: Background/Aims: What is the major problem that prompted the study? Methods: How was the study carried out? Results: Most important findings? Conclusion: Most important conclusion? Abstracts of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review.s of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review. Footnotes: Avoid footnotes. Tables and illustrations: Tables are part of the text. Place them at the end of the text file. Illustration data must be stored as separate files. Do not integrate figures into the text. Electronically submitted b/w half-tone and color illustrations must have a final resolution of 300 dpi after scaling, line drawings one of 800–1,200 dpi. Color illustrations Online edition: Color illustrations are reproduced free of charge. In the print version, the illustrations are reproduced in black and white. Please avoid referring to the colors in the text and figure legends. Print edition: Up to 6 color illustrations per page can be integrated within the text at CHF 800.00 per page. References: In the text identify references by Arabic numerals [in square brackets]. Material submitted for publication but not yet accepted should be noted as [unpublished data] and not be included in the reference list. The list of references should include only those publications which are cited in the text. Number references in the order in which they are first mentioned in the text; do not list alphabetically. The surnames of the authors followed by initials should be given. There should be no punctuation other than a comma to separate the authors. Preferably, please cite all authors. Abbreviate journal names according to the Index Medicus system. Also see International Committee of Medical Journal Editors: Uniform requirements for manuscripts submitted to biomedical journals (www. icmje.org). Examples (a) Papers published in periodicals: Tomson C: Vascular calcification in chronic renal failure. Nephron Clin Pract 2003;93:c124–c130. (b) Papers published only with DOI numbers: Theoharides TC, Boucher W, Spear K: Serum interleukin-6 reflects disease severity and osteoporosis in mastocytosis patients. Int Arch Allergy Immunol DOI: 10.1159/000063858. (c) Monographs: Matthews DE, Farewell VT: Using and Understanding Medical Statistics, ed 3, revised. Basel, Karger, 1996. (d) Edited b","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000365339","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64728915","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":"Front & Back Matter","authors":"","doi":"10.1159/000362513","DOIUrl":"https://doi.org/10.1159/000362513","url":null,"abstract":"Each paper needs an abstract of up to 250 words. It should be structured as follows: Background/Aims: What is the major problem that prompted the study? Methods: How was the study carried out? Results: Most important findings? Conclusion: Most important conclusion? Abstracts of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review.s of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review. Footnotes: Avoid footnotes. Tables and illustrations: Tables are part of the text. Place them at the end of the text file. Illustration data must be stored as separate files. Do not integrate figures into the text. Electronically submitted b/w half-tone and color illustrations must have a final resolution of 300 dpi after scaling, line drawings one of 800–1,200 dpi. Color illustrations Online edition: Color illustrations are reproduced free of charge. In the print version, the illustrations are reproduced in black and white. Please avoid referring to the colors in the text and figure legends. Print edition: Up to 6 color illustrations per page can be integrated within the text at CHF 800.– per page. References: In the text identify references by Arabic numerals [in square brackets]. Material submitted for publication but not yet accepted should be noted as [unpublished data] and not be included in the reference list. The list of references should include only those publications which are cited in the text. Number references in the order in which they are first mentioned in the text; do not list alphabetically. The surnames of the authors followed by initials should be given. There should be no punctuation other than a comma to separate the authors. Preferably, please cite all authors. Abbreviate journal names according to the Index Medicus system. Also see International Committee of Medical Journal Editors: Uniform requirements for manuscripts submitted to biomedical journals (www. icmje.org). Examples (a) Papers published in periodicals: Tomson C: Vascular calcification in chronic renal failure. Nephron Clin Pract 2003;93:c124–c130. (b) Papers published only with DOI numbers: Theoharides TC, Boucher W, Spear K: Serum interleukin-6 reflects disease severity and osteoporosis in mastocytosis patients. Int Arch Allergy Immunol DOI: 10.1159/000063858. (c) Monographs: Matthews DE, Farewell VT: Using and Understanding Medical Statistics, ed 3, revised. Basel, Karger, 1996. (d) Edited bo","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"126 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64716089","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":"Front & Back Matter","authors":"","doi":"10.1159/000360567","DOIUrl":"https://doi.org/10.1159/000360567","url":null,"abstract":"","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"124 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000360567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64709365","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":"Contents Vol. 124, 2013","authors":"David A. Drew, H. Tighiouart, T. Scott, Kristina V. Lou, Kamran Shaffi, D. Weiner, M. Sarnak, H. Alderson, J. Ritchie, D. Green, D. Chiu, P. Kalra, P. Grzelak, I. Kurnatowska, M. Nowicki, M. Marchwicka-Wasiak, M. Podgórski, A. Durczyński, J. Strzelczyk, L. Stefanczyk, P. Kalra, D. Green, J. Ritchie, B. Caplin, Helen Alston, A. Davenport, A. Power, D. Fogarty, D. Wheeler, Jeannet Nigten, Karina A. de Groot, D. Grootendorst, S. Koolen, M. Herruer, N. Schut, J. Clothier, J. Simpson, C. Turner, R. Dalton, P. Rasmussen, Debbie Rawlins, C. Booth, J. Peacock, M. Sinha, Do Hoon Kim, Yang-Hyun Kim, G. Nam, Kyungdo Han, Y. Park, B. Han, S. Kim, Y. Choi, Kyung-Hwan Cho, K. Lee, H. Komaba, Ryoko Tatsumi, G. Kanai, Takayo Miyakogawa, K. Sawada, T. Kakuta, M. Fukagawa, Yu-Cheng Lai, Ben-Chung Cheng, J. Hwang, Yueh‐Ting Lee, Chien-Hua Chiu, L. Kuo, Jin-Bor Chen, A. Jakes, P. Jani, S. Bhandari, P. Sarafidis, Adam Rumjon, D. Ackland, H. MacLaughlin, S. Bansal, C. Brasse-Lagnel, I. Macdougall, E. Brown, Satz Mengensatzprod","doi":"10.1159/000358277","DOIUrl":"https://doi.org/10.1159/000358277","url":null,"abstract":"Chronic Kidney Disease and Hypertension A. Levin, Vancouver, B.C. R. Gansevoort, Groningen Acute Kidney Injury R. Mehta, San Diego, Calif. N. Kolhe, Derby Dialysis J. Daugirdas, Chicago, Ill. C. Hutchison, Hawkes Bay C. Fraansen, Groningen Patient Subjective Experience, Healthcare Delivery and Innovation in Practice R. Fluck, Derby E. Brown, London Crossover States with Non-Renal Organ Systems C. Chan, Toronto, Ont. T. Breidthardt, Basel N. Selby, Derby Transplantation A. Chandraker, Boston, Mass. A. Salama, London Editor-in-Chief","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"124 1","pages":"I - IV"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000358277","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64703091","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":"Mineralocorticoid and SGK1-sensitive inflammation and tissue fibrosis.","authors":"Ferruh Artunc,&nbsp;Florian Lang","doi":"10.1159/000368267","DOIUrl":"https://doi.org/10.1159/000368267","url":null,"abstract":"<p><p>Effects of mineralocorticoids are not restricted to regulation of epithelial salt transport, extracellular volume and blood pressure; mineralocorticoids also influence a wide variety of seemingly unrelated functions such as inflammation and fibrosis. The present brief review addresses the role of mineralocorticoids in the orchestration of these latter processes. Mineralocorticoids foster inflammation as well as vascular, cardiac, renal and peritoneal fibrosis. Mechanisms involved in mineralocorticoid-sensitive inflammation and fibrosis include the serum- and glucocorticoid-inducible kinase 1 (SGK1), which is genomically upregulated by mineralocorticoids and transforming growth factor β (TGF-β), and stimulated by mineralocorticoid-sensitive phosphatidylinositide 3-kinase. SGK1 upregulates the inflammatory transcription factor nuclear factor-κB, which in turn stimulates the expression of diverse inflammatory mediators including connective tissue growth factor. Moreover, SGK1 inhibits the degradation of the TGF-β-dependent transcription factors Smad2/3. Mineralocorticoids foster the development of TH17 cells, which is compromised following SGK1 deletion. Excessive SGK1 expression is observed in a wide variety of fibrosing diseases including lung fibrosis, diabetic nephropathy, glomerulonephritis, obstructive kidney disease, experimental nephrotic syndrome, obstructive nephropathy, liver cirrhosis, fibrosing pancreatitis, peritoneal fibrosis, Crohn's disease and celiac disease. The untoward inflammatory and fibrosing effects of mineralocorticoids could be blunted or even reversed by mineralocorticoid receptor blockers, which may thus be considered in the treatment of inflammatory and/or fibrosing disease.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"128 1-2","pages":"35-9"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000368267","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32797927","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":"On the pleotropic actions of mineralocorticoids.","authors":"Florian Lang","doi":"10.1159/000368263","DOIUrl":"https://doi.org/10.1159/000368263","url":null,"abstract":"<p><p>Classical effects of mineralocorticoids include stimulation of Na(+) reabsorption and K(+) secretion in the kidney and other epithelia including colon and several glands. Moreover, mineralocorticoids enhance the excretion of Mg(2+) and renal tubular H(+) secretion. The renal salt retention following mineralocorticoid excess leads to extracellular volume expansion and hypertension. The increase of blood pressure following mineralocorticoid excess is, however, not only the result of volume expansion but may result from stiff endothelial cell syndrome impairing the release of vasodilating nitric oxide. Beyond that, mineralocorticoids are involved in the regulation of a wide variety of further functions, including cardiac fibrosis, platelet activation, neuronal function and survival, inflammation as well as vascular and tissue fibrosis and calcification. Those functions are briefly discussed in this short introduction to the special issue. Beyond that, further contributions of this special issue amplify on mineralocorticoid-induced sodium appetite and renal salt retention, the role of mineralocorticoids in the regulation of acid-base balance, the involvement of aldosterone and its receptors in major depression, the mineralocorticoid stimulation of inflammation and tissue fibrosis and the effect of aldosterone on osteoinductive signaling and vascular calcification. Clearly, still much is to be learned about the various ramifications of mineralocorticoid-sensitive physiology and pathophysiology.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"128 1-2","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000368263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32798323","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":"Insulin Receptor and the Kidney: Nephrocalcinosis in Patients with Recessive INSR Mutations.","authors":"Arabella Simpkin, Elaine Cochran, Fergus Cameron, Mehul Dattani, Martin de Bock, David B Dunger, Gun Forsander, Tulay Guran, Julie Harris, Iona Isaac, Khalid Hussain, Robert Kleta, Catherine Peters, Velibor Tasic, Rachel Williams, Fabian Yap Kok Peng, Stephan O''Rahilly, Philipp Gorden, Robert K Semple, Detlef Bockenhauer","doi":"10.1159/000366225","DOIUrl":"10.1159/000366225","url":null,"abstract":"<p><strong>Background/aims: </strong>Donohue and Rabson-Mendenhall syndrome are rare autosomal recessive disorders caused by mutations in the insulin receptor gene, INSR. Phenotypic features include extreme insulin resistance, linear growth retardation, paucity of fat and muscle, and soft tissue overgrowth. The insulin receptor is also expressed in the kidney, where animal data suggest it plays a role in glomerular function and blood pressure (BP) regulation, yet such a role in the human kidney is untested. Patients with biallelic INSR mutations provide a rare opportunity to ascertain its role in man.</p><p><strong>Methods: </strong>Retrospective review of patients with INSR mutations. Data for BP, renal imaging, plasma creatinine and electrolyte levels, as well as urine protein, albumin and calcium excretion were sought from the treating clinicians.</p><p><strong>Results: </strong>From 33 patients with INSR mutations, data were available for 17 patients. Plasma creatinine was low (mean ± SD: 25 ± 9 μmol/l) and mean plasma electrolyte concentrations were within the normal range (n = 13). Systolic BP ranged between the 18th and 91st percentile for age, sex, height and weight (n = 9; mean ± SD: 49 ± 24). Twenty-four-hour urinary calcium data were available from 10 patients and revealed hypercalciuria in all (mean ± SD: 0.32 ± 0.17 mmol/kg/day; normal <0.1). Nephrocalcinosis was present in all patients (n = 17). Urinary albumin excretion (n = 7) ranged from 4.3-122.5 μg/min (mean ± SD: 32.4 ± 41.0 μg/min; normal <20).</p><p><strong>Conclusions: </strong>INSR dysfunction is associated with hypercalciuria and nephrocalcinosis. No other consistent abnormality of renal function was noted. Normotension and stable glomerular function with only moderate proteinuria is in contrast to genetically modified mice who have elevated BP and progressive diabetic nephropathy.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"128 3-4","pages":"55-61"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10584800","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":"Ernest Henry Starling (1866-1927) on the formation and reabsorption of lymph.","authors":"Leon G Fine","doi":"10.1159/000362620","DOIUrl":"https://doi.org/10.1159/000362620","url":null,"abstract":"<p><p>Ernest Henry Starling laid the groundwork for our modern understanding of how the interstitial fluid, which he referred to as 'lymph', is regulated. Together with his colleague, William Bayliss, he provided the crucial insight into how fluid is driven out of the capillary to form interstitial fluid. That was to measure (estimate) the capillary pressure in different parts of the circulation and to relate changes in these pressures to altered lymph formation. In addressing how interstitial fluid re-enters the circulation, he was able to show that this occurs not only via the lymphatics, but also by re-entering the capillaries, mediated by the oncotic pressure of the plasma proteins. Starling's discoveries put to rest all notions that the processes of filtration and reabsorption of fluid are mediated by the 'vital activity' of cells. They could be explained entirely on the basis of physic-chemical forces. Based upon his insights from animal experiments, he was able to explain the genesis of edema (dropsy) in a number of disease states, including venous obstruction, cardiac disease and inflammatory conditions.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"126 3","pages":"9-17"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362620","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32360872","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}