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001			86562
003			ES-MaUEC
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007			cr nn 008mamaa
008			151026s2016 ja | s |||| 0|eng d
020			_a9784431552703
040			_aES-MaUEC
050		4	_aRC918.N43 _b2016 EB
082	0	4	_a616.61
245	1	0	_aMolecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome _cedited by Kazunari Kaneko
250			_a1st ed.
260			_aTokyo _bSpringer Japan _c2016
300			_a1 recurso en línea (VIII, 240 páginas) _b21 ilustraciones, 16 ilustraciones en color
336			_aTexto _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
505	0		_aPart 1. Introduction -- 1. History of Research on Pathogenesis of Idiopathic Nephrotic Syndrome -- Part 2. Minimal-change nephrotic syndrome (MCNS) -- 2. Hemopexin in Minimal Change Nephrotic Syndrome -- 3. Angiopoietin-like-4 (Angptl4) in MCNS -- 4.�Co-stimulatory molecule CD80 (B7.1) in MCNS -- 5. Energy and Mammalian target of rapamycin complex 1 (mTORC1) in minimal change nephrotic syndrome -- 6. The role of c-mip in the pathogenesis of Minimal Change Nephrotic Syndrome -- 7.�REGULATORY T-CELLS AND OXIDATIVE STRESS IN MINIMAL CHANGE NEPHROPATHY -- 8. CYTOKINES AS ACTIVE FACTORS IN MINIMAL CHANGE NEPHROTIC SYNDROME -- Part 3. Focal segmental glomerulosclerosis (FSGS) -- 9. Soluble urokinase-type plasminogen activator receptor (suPAR) in Focal Segmental Glomerulosclerosis -- 10. CYTOKINES AS ACTIVE FACTORS IN FOCAL SEGMENTAL GLOMERULOSCLEROSIS -- Part 4. Idiopathic Membranous Nephropathy (IMN) -- 11. M-Type Phospholipase A2 Receptor (PLA2R) and Thrombospondin Type-1 Domain-Containing 7A (THSD7A) in Membranous Nephropathy -- 12. Cationic Bovine Serum Albumin as Cause of Membranous Nephropathy: From Mice to Men -- Part 5. Treatment in Idiopathic Nephrotic Syndrome -- 13. Podocytes as a direct target of drugs used in Idiopathic Nephrotic Syndrome.
520	3		_aThis comprehensive book reviews our current state of knowledge about the pathogenesis of idiopathic nephrotic syndrome (INS), which comprises a heterogeneous group of diseases with distinct histological characteristics, such as minimal-change nephrotic syndrome (MCNS), focal segmental glomerulosclerosis (FSGS), and idiopathic membranous nephropathy (IMN). As the word zidiopathicy indicates, the pathogenesis of INS remains unclear. Historically, T-cell dysfunction has been thought to play an important part in the pathogenesis of MCNS, while circulating vascular permeabilities have been believed to induce proteinuria in FSGS. The book further describes recent advances in molecular biology, which have allowed us to speculate on the interactions between visceral glomerular epithelial cells (podocytes) and the relative significance of several molecules in the pathogenesis of INS, such as reactive oxygen species, nuclear factor-kappa B, CD80, angiopoietin-like 4, cardiotrophin-like cytokine-1, and M-type phospholipase A2 receptor. The normally rapid pace of scientific progress occasionally devolves into a state of chaos, and the pathogenetic research on INS is one such case. This volume will help researchers and scientists to collaborate, share resources, and expedite the design of protocols to evaluate the putative factors.
710	2		_aSpringerLink (Online service) _0Local _9106996
942			_2lcc _cLE
650		7	_aMedicina _0comprobar BNE19900959047 _2embne _9405021
650		7	_aBiología molecular _0comprobar BNE19900968373 _2embne _9139103
700	1		_aKaneko, Kazunari. _eeditor literario _985014 _0Local
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/978-4-431-55270-3 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9784431552703
907			_a.b12958402 _b10-10-17 _c21-11-16
988			_aSpringer_Medicine_2016
998			_am _a_alco _a_vill _b - - _cm _dz _e- _feng _gja _h0
945			_aRC918.N43 M654 2016 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11600007 _z06-04-17
999			_c86562 _d86562 _x1