語系:
繁體中文
English
說明(常見問題)
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
Molecular Mechanisms in the Pathogen...
~
Kaneko, Kazunari.
Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome/ edited by Kazunari Kaneko.
其他作者:
Kaneko, Kazunari.
面頁冊數:
VIII, 240 p. 21 illus., 16 illus. in color.online resource. :
Contained By:
Springer Nature eBook
標題:
Nephrology. -
電子資源:
https://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. - 1st ed. 2016. - VIII, 240 p. 21 illus., 16 illus. in color.online resource.
Part 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.
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:
668354
Nephrology.
LC Class. No.: RC902-918
Dewey Class. No.: 616.61
Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome
LDR
:03948nam a22003975i 4500
001
977524
003
DE-He213
005
20200701093159.0
007
cr nn 008mamaa
008
201211s2016 ja | s |||| 0|eng d
020
$a
9784431552703
$9
978-4-431-55270-3
024
7
$a
10.1007/978-4-431-55270-3
$2
doi
035
$a
978-4-431-55270-3
050
4
$a
RC902-918
072
7
$a
MJR
$2
bicssc
072
7
$a
MED055000
$2
bisacsh
072
7
$a
MJR
$2
thema
082
0 4
$a
616.61
$2
23
245
1 0
$a
Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome
$h
[electronic resource] /
$c
edited by Kazunari Kaneko.
250
$a
1st ed. 2016.
264
1
$a
Tokyo :
$b
Springer Japan :
$b
Imprint: Springer,
$c
2016.
300
$a
VIII, 240 p. 21 illus., 16 illus. in color.
$b
online resource.
336
$a
text
$b
txt
$2
rdacontent
337
$a
computer
$b
c
$2
rdamedia
338
$a
online resource
$b
cr
$2
rdacarrier
347
$a
text file
$b
PDF
$2
rda
505
0
$a
Part 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
$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
Nephrology.
$3
668354
650
0
$a
Urology.
$3
645258
650
0
$a
Molecular biology.
$3
583443
650
2 4
$a
Molecular Medicine.
$3
668353
700
1
$a
Kaneko, Kazunari.
$4
edt
$4
http://id.loc.gov/vocabulary/relators/edt
$3
1103251
710
2
$a
SpringerLink (Online service)
$3
593884
773
0
$t
Springer Nature eBook
776
0 8
$i
Printed edition:
$z
9784431552697
776
0 8
$i
Printed edition:
$z
9784431552710
776
0 8
$i
Printed edition:
$z
9784431562795
856
4 0
$u
https://doi.org/10.1007/978-4-431-55270-3
912
$a
ZDB-2-SME
912
$a
ZDB-2-SXM
950
$a
Medicine (SpringerNature-11650)
950
$a
Medicine (R0) (SpringerNature-43714)
筆 0 讀者評論
多媒體
評論
新增評論
分享你的心得
Export
取書館別
處理中
...
變更密碼[密碼必須為2種組合(英文和數字)及長度為10碼以上]
登入