Role of Erythropoietin in the Anemia of Renal Insufficiency in Man and in an Experimental Uremic Rabbit Model

2015 ◽  
pp. 69-80 ◽  
Author(s):  
E. Schulz ◽  
B. M�dder ◽  
J. W. Fisher
Keyword(s):  
Renal Insufficiency ◽  
Rabbit Model

The role of NT-proBNP in chronic heart failure and renal insufficiency

2005 ◽  
Vol 53 (S 01) ◽  
Author(s):  
M Rothenburger ◽  
J Stypmann ◽  
T Wichter ◽  
A Löher ◽  
E Berendes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Renal Insufficiency

Immune complex binding Streptococcus pyogenes type M12/emm12 in experimental glomerulonephritis

2013 ◽  
Vol 62 (9) ◽  
pp. 1272-1280 ◽  
Author(s):  
Larissa Burova ◽  
Peter Pigarevsky ◽  
Nadezhda Duplik ◽  
Vlada Snegova ◽  
Alexander Suvorov ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Complement C3 ◽  
Poststreptococcal Glomerulonephritis ◽  
Tnf Α ◽  
Rabbit Igg ◽  
Renal Changes ◽  
Group A ◽  
Study Type ◽  
Binding Component

In a rabbit model, we have previously reported evidence for a pathogenic role of streptococcal IgG Fc-binding proteins (IgGFcBP) in poststreptococcal glomerulonephritis (PSGN). These proteins, of the M protein family, were shown to trigger anti-IgG production and enhance renal deposition of IgG and/or immune complexes (ICs), with resulting activation of complement and cytokine cascades. In the present study, type M12/emm12, group A streptococci (GAS) were found often to bind artificial ICs, viz. peroxidase–anti-peroxidase rabbit IgG (PAP) or tetanus toxoid–anti-tetanus human IgG (TAT), rather than monomeric IgG. Animals injected with each of four IC binding clinical isolates (from patients with scarlet fever or PSGN) showed pronounced inflammatory and degenerative glomerular changes, morphologically similar to human PSGN, with membrane thickening and IgG and complement C3 deposition, as well as secretion of IL-6 and TNF-α by mesangial and endothelial cells. In contrast, non-binding strains (two from asymptomatic carriers and one from a PSGN case) failed to trigger any renal changes. Only the IC binding strains induced elevated titres of anti-IgG. Though the streptococcal binding component(s) has not been demonstrated, the selective binding of ICs by type M12/emm12 strains appears important for the well-known, marked nephritogenic potential of this GAS type.

Hyperkalemia and Renal Insufficiency: Role of Selective Aldosterone Deficiency and Tubular Unresponsiveness to Aldosterone

1981 ◽  
Vol 1 (3-4) ◽  
pp. 160-167 ◽  
Author(s):  
Jose A.L. Arruda ◽  
Daniel C. Batlle ◽  
Timothy Sehy ◽  
Melvin K. Roseman ◽  
Robert L. Baronowski ◽  
...  
Keyword(s):  
Renal Insufficiency

scholarly journals Chronic renal insufficiency among Asian Indians with type 2 diabetes: I. Role of RAAS gene polymorphisms

2006 ◽  
Vol 7 (1) ◽  
Author(s):  
Pushplata Prasad ◽  
Arun K Tiwari ◽  
KM Prasanna Kumar ◽  
AC Ammini ◽  
Arvind Gupta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Renal Insufficiency ◽  
Chronic Renal Insufficiency ◽  
Gene Polymorphisms ◽  
Asian Indians

scholarly journals Role of Erythromycin-Regulated Histone Deacetylase-2 in Benign Tracheal Stenosis

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Zhenjie Huang ◽  
Peng Wei ◽  
Luoman Gan ◽  
Tonghua Zeng ◽  
Caicheng Qin ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Tracheal Stenosis ◽  
Type I Collagen ◽  
Rabbit Model ◽  
Immunohistochemical Method ◽  
Type Iii Collagen ◽  
Type I ◽  
Histone Deacetylase 2 ◽  
Budesonide Group

Objective. This study aims to explore the role of erythromycin-regulated histone deacetylase-2 in benign tracheal stenosis. Methods. The rabbit model of tracheal stenosis was established. The rabbits were randomly divided into 8 groups. Histone deacetylase-2 (HDAC2) expression was detected by immunofluorescence. The expression of type I collagen and type III collagen was detected by immunohistochemical method. The expression of TGF-β1, VEGF and IL-8 in serum and alveolar lavage fluid was detected by ELISA. The expression of HDAC2, TGF-β1, VEGF and IL-8 in bronchi of each group was detected by Western blotting method. Results. In Erythromycin (ERY) group, ERY + Budesonide group, ERY + Vorinostat group and ERY + Budesonide + Vorinostat group, the degree of bronchial stenosis was alleviated, and the mucosal epithelium was still slightly proliferated. The effect of ERY combined with other drugs was more obvious. The HDAC2 protein expression increased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group and decreased significantly in Vorinostat group, the expression of collagen I and III decreased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group (P<0.05). The TGF-β1, IL-8 and VEGF levels decreased significantly in ERY group, ERY + Budesonide group, ERY + Vorinostat group and ERY + Budesonide + Vorinostat group (P<0.05). Conclusions. Erythromycin inhibited inflammation and excessive proliferation of granulation tissue after tracheobronchial mucosal injury by up-regulating the expression of HDAC2, it promoted wound healing and alleviated tracheobronchial stenosis. When combined with budesonide, penicillin and other glucocorticoids and antibiotics, it had a good synergistic effect. However, vorinostat could attenuate erythromycin’s effect by down-regulating the expression of HDAC2. It may have good clinical application prospects in the treatment of tracheal stenosis.

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