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| 1 | Choice of conodont Idiognathodus simulator (sensu stricto) as the event marker for the base of the global Gzhelian Stage (Upper Pennsylvanian Series, Carboniferous System)显示文摘 | Philip H. Heckel Aleksandr S. Alekseev James E. Barrick Darwin R. Boardman Natalya V. Goreva Tatiana N. Isakova Tamara I. Nemyrovska Katsumi Ueno Elisa Villa David M. Work | 2008 | Episodes2008，31，3： | 5 |
| 2 | DMP1 prevents osteocyte alterations,FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease显示文摘During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization,but its effects in CKD are unknown.We tested the hypothesis that DMP1 supplementation in CKD would improve bone health,prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes.We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3^-/- mouse model of CKD.Col4a3^-/- mice demonstrated impaired kidney function,reduced bone DMP1 expression,reduced bone mass,altered osteocyte morphology and connectivity,increased osteocyte apoptosis,increased serum FGF23,hyperphosphatemia,left ventricular hypertrophy (LVH),and reduced survival.Genetic or pharmacological supplementation of DMP1 in Col4a3^-/- mice prevented osteocyte apoptosis,preserved osteocyte networks,corrected bone mass,partially lowered FGF23 levels by attenuating NFAT-induced FGF23 transcription,and further increased serum phosphate.Despite impaired kidney function and worsened hyperphosphatemia,DMP1 prevented development of LVH and improved Col4a3^-/- survival.Our data suggest that CKD reduces DMP1 expression,whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD. | Corey Dussold Claire Gerber Samantha White Xueyan Wang Lixin Qi Connor Francis Maralee Capella Guillaume Courbon Jingya Wang Chaoyuan Li Jian Q. Feng Tamara Isakova Myles Wolf Valentin David Aline Martin | 2019 | Bone Research2019，7，2： | 4 |
| 3 | Lipocalin 2 stimulates bone fibroblast growth factor 23 production in chronic kidney disease显示文摘Bone-produced fibroblast growth factor 23(FGF23)increases in response to inflammation and iron deficiency and contributes to cardiovascular mortality in chronic kidney disease(CKD).Neutrophil gelatinase-associated lipocalin(NGAL or lipocalin 2;LCN2 the murine homolog)is a pro-inflammatory and iron-shuttling molecule that is secreted in response to kidney injury and may promote CKD progression.We investigated bone FGF23 regulation by circulating LCN2.At 23 weeks,Col4a3KO mice showed impaired kidney function,increased levels of kidney and serum LCN2,increased bone and serum FGF23,anemia,and left ventricular hypertrophy(LVH).Deletion of Lcn2 in CKD mice did not improve kidney function or anemia but prevented the development of LVH and improved survival in association with marked reductions in serum FGF23.Lcn2 deletion specifically prevented FGF23 elevations in response to inflammation,but not iron deficiency or phosphate,and administration of LCN2 increased serum FGF23 in healthy and CKD mice by stimulating Fgf23 transcription via activation of cAMP-mediated signaling in bone cells.These results show that kidney-produced LCN2 is an important mediator of increased FGF23 production by bone in response to inflammation and in CKD.LCN2 inhibition might represent a potential therapeutic approach to lower FGF23 and improve outcomes in CKD. | Guillaume Courbon Connor Francis Claire Gerber Samantha Neuburg Xueyan Wang Emily Lynch Tamara Isakova Jodie LBabitt Myles Wolf Aline Martin Valentin David | 2021 | Bone Research2021，9，3： | 4 |
| 4 | Potential dual expansion of domesticated donkeys revealed by worldwide analysis on mitochondrial sequences显示文摘Molecular studies on donkey mitochondrial sequences have clearly defined two distinct maternal lineages involved in domestication.However,domestication histories of these two lineages remain enigmatic.We therefore compared several population characteristics between these two lineages based on global sampling,which included 171 sequences obtained in this study(including Middle Asian,East Asian,and African samples)plus 536 published sequences(including European,Asian,and African samples).The two lineages were clearly separated from each other based on whole mitochondrial genomes and partial non-coding displacement loop(D-loop)sequences,respectively.The Clade I lineage experienced an increase in population size more than 8000 years ago and shows a complex haplotype network.In contrast,the population size of the Clade II lineage has remained relatively constant,with a simpler haplotype network.Although the distribution of the two lineages was almost equal across the Eurasian mainland,they still presented discernible but complex geographic bias in most parts of Africa,which are known as their domestication sites.Donkeys from sub-Saharan Africa tended to descend from the Clade I lineage,whereas the Clade II lineage was dominant along the East and North coasts of Africa.Furthermore,the migration routes inferred from diversity decay suggested different expansion across China between the two lineages.Altogether,these differences indicated non-simultaneous domestication of the two lineages,which was possibly influenced by the response of pastoralists to the desertification of the Sahara and by the social expansion and trade of ancient humans in Northeast Africa,respectively. | Xi-Yao Ma Tiao Ning Adeniyi CAdeola Jie Li Ali Esmailizadeh Jacqueline KLichoti Bernard RAgwanda Jainagul Isakova Almaz AAldashev Shi-Fang Wu He-Qun Liu Najmudinov Tojiddin Abdulloevich Manilova Elena Afanasevna Khudoidodov Behruz Ibrohimovich Rahamon Akinyele Moshood Adedokun Sunday Charles Olaogun Oscar JSanke Godwin FMangbon Xi Chen Wei-Kang Yang Zhe Wang Min-Sheng Peng Sheila COmmeh Yan Li Ya-Ping Zhang | 2020 | Zoological Research2020，41，1： | 3 |
| 5 | Fibroblast growth factor 23 and mortality among patients undergoing hemodialy- sis显示文摘 | Guti6rrez OM Mannstadt M Isakova T | 2008 | N Engl J Med2008，359，： | 1 |
| 6 | Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease显示文摘 | Gutierrez O Isakova T Rhee E | | 0，，07： | 1 |
| 7 | Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis显示文摘 | Gutierrez OM Mannstadt M Isakova T | 2008 | N Engl J Med2008，359，： | 1 |
| 8 | Fibroblast growth fac- tor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease 显示文摘 | Gutierrez O Isakova T Rhee E | 2005 | J Am Soc Nephrol2005，16，： | 1 |
| 9 | Fibro- blast growth factor 23 and inflammation in CKD显示文摘 | unoz Mendoza J Isakova T Ricardo AC | 2012 | Clin J AmSoc Nephrol2012，7，： | 1 |
| 10 | Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease显示文摘 | Gutierrez O Isakova T Rhee E | 2005 | J Am Soc Nephrol2005，16，： | 1 |
| 11 | Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease显示文摘 | Gutierrez OM Januzzi JL Isakova T | 2009 | Circulation2009，119，19： | 1 |
| 12 | Mitochondrial calcium transport systems:properties,regulation,and taxonomic features显示文摘 | Deryabina Y1 Isakova EP Zvyagilskaya RA | | 0，，： | 1 |
| 13 | Fibroblast growth factor23 in patients undergoing peritoneal dialysis显示文摘 | Isakova T Xie H Barchi-Chung A | 2011 | Clin J Am Soc Nephrol2011，6，： | 1 |
| 14 | FGF23 induces left ventricular hypertrophy显示文摘 | Faul Christian Amaral Ansel P Oskouei Behzad Hu Ming-Chang Sloan Alexis Isakova Tamara Gutiérrez Orlando M Aguillon-Prada Robier Lincoln Joy Hare Joshua M Mundel Peter Morales Azorides Scialla Julia Fischer Michael Soliman Elsayed Z Chen J | 2011 | Journal of Clinical Investigation2011，，11： | 1 |
| 15 | Phosphorus binders and survival on hemodialysis显示文摘 | Isakova T Gutierrez OM Chang Y | 2009 | J Am Soc Nephro12009，20，： | 1 |
| 16 | Phosphorus binders and survival on hemodialysis显示文摘 | Isakova T Gutiérrez OM Chang Y | | 0，，： | 1 |
| 17 | Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease 显示文摘 | Isakova T Wahl P Vargas GS | 2011 | Kidney Int2011，79，12： | 1 |
| 18 | Phosphorus binders andsurvival on hemodialysis显示文摘 | Isakova T Gutierrez OM Chang Y | 2009 | J Am Soc Nephrol2009，20，2： | 1 |
| 19 | Fibroblast growth- factor 23 and mortality amdng patients undergoing hemodialysis 显示文摘 | Gutierrez OM Mannstadt M Isakova T | 2008 | N Engl J Med2008，359，6： | 1 |
| 20 | Fi- broblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease显示文摘 | GUTIERREZ O M JANUZZI J L ISAKOVA T | 2009 | Circulation2009，119，19： | 1 |
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