國立虎尾科技大學 |

Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome/ edited by Kazunari Kaneko.
other author:	Kaneko, Kazunari.
Published:	Tokyo :Springer Japan : : 2016.,
Description:	viii, 240 p. :ill., digital ; : 24 cm.;
Contained By:	Springer eBooks
Subject:	Nephrotic syndrome - Pathogenesis. -
Online resource:	http://dx.doi.org/10.1007/978-4-431-55270-3
ISBN:	9784431552703

Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome
Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome[electronic resource] /edited by Kazunari Kaneko. - Tokyo :Springer Japan :2016. - viii, 240 p. :ill., digital ;24 cm.

This 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 "idiopathic" 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.

ISBN: 9784431552703

Standard No.: 10.1007/978-4-431-55270-3doiSubjects--Topical Terms:

1103252
Nephrotic syndrome
--Pathogenesis.

LC Class. No.: RC918.N43

Dewey Class. No.: 616.61

Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome
LDR:02271nam a2200301 a 4500 001 861107
003 DE-He213
005 20160727151111.0
006 m d
007 cr nn 008maaau
008 170720s2016 ja s 0 eng d
020 $a 9784431552703 $q (electronic bk.)
020 $a 9784431552697 $q (paper)
024 7 $a 10.1007/978-4-431-55270-3 $2 doi
035 $a 978-4-431-55270-3
040 $a GP $c GP
041 0 $a eng
050 4 $a RC918.N43
072 7 $a MJR $2 bicssc
072 7 $a MED055000 $2 bisacsh
082 0 4 $a 616.61 $2 23
090 $a RC918.N43 $b M718 2016
245 0 0 $a Molecular mechanisms in the pathogenesis of idiopathic nephrotic syndrome $h [electronic resource] / $c edited by Kazunari Kaneko.
260 $a Tokyo : $c 2016. $b Springer Japan : $b Imprint: Springer,
300 $a viii, 240 p. : $b ill., digital ; $c 24 cm.
520 $a This 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 "idiopathic" 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.
650 0 $a Nephrotic syndrome $x Pathogenesis. $3 1103252
650 1 4 $a Medicine & Public Health. $3 593949
650 2 4 $a Nephrology. $3 668354
650 2 4 $a Urology. $3 645258
650 2 4 $a Molecular Medicine. $3 668353
700 1 $a Kaneko, Kazunari. $3 1103251
710 2 $a SpringerLink (Online service) $3 593884
773 0 $t Springer eBooks
856 4 0 $u http://dx.doi.org/10.1007/978-4-431-55270-3
950 $a Medicine (Springer-11650)