scholarly journals The role of atorvastatin on the restenosis process post-PTA in a diabetic rabbit model

2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Xiaojun Zhou ◽  
Yaru Mou ◽  
Xue Shen ◽  
Tianshu Yang ◽  
Ju Liu ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Diabetic Rabbit

scholarly journals Hyperglycemia has no effect on development of restenosis after percutaneous transluminal angioplasty (PTA) in a diabetic rabbit model

2014 ◽  
Vol 224 (2) ◽  
pp. 119-125 ◽  
Author(s):  
Xiaojun Zhou ◽  
Jianjun Dong ◽  
Li Zhang ◽  
Ju Liu ◽  
Xiaofeng Dong ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Percutaneous Transluminal Angioplasty ◽  
Independent Risk Factor ◽  
Rabbit Model ◽  
Intima Media Thickness ◽  
Transluminal Angioplasty ◽  
Diabetic Rabbit ◽  
Patients With Diabetes ◽  
Percutaneous Transluminal

It is well known that hyperglycemia is a trigger of atherosclerosis in patients with diabetes mellitus. However, the role of hyperglycemia in restenosis remains unclear. In this study, we investigated the effects of hyperglycemia on restenosis. Stenosis was evaluated in two sets of diabetic rabbit models: i) diabetic restenosis versus nondiabetic restenosis and ii) diabetic atherosclerosis versus nondiabetic atherosclerosis. Our results indicated that there was no difference in rates of stenosis between the diabetic and the nondiabetic groups in restenosis rabbit models. However, the incidence of stenosis was significantly higher in the diabetic atherosclerosis group compared with the nondiabetic atherosclerosis group. Similarly, the intima–media thickness and cell proliferation rate were significantly increased in the diabetic atherosclerosis group compared with the nondiabetic atherosclerosis group, but there was no difference between the diabetic restenosis and the nondiabetic restenosis groups. Our results indicate that hyperglycemia is an independent risk factor for atherosclerosis, but it has no evident effect on restenosis. These findings indicate that the processes of atherosclerosis and restenosis may involve different pathological mechanisms.

404 EVALUATION OF A DIABETIC RABBIT MODEL FOR IN-STENT RESTENOSIS

2011 ◽  
Vol 12 (1) ◽  
pp. 86
Author(s):  
P.W. Radke ◽  
A. Joost ◽  
A. Kaiser ◽  
M. Basler ◽  
M. Mandapathil ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Stent Restenosis ◽  
Diabetic Rabbit ◽  
In Stent Restenosis

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.

Abstract 581: Identification on Anti-Atherosclerotic Mechanism of SGLT-2 Inhibitor in Diabetic Rabbit Model

2018 ◽  
Vol 38 (Suppl_1) ◽  
Author(s):  
Seulgee Lee ◽  
Jung-Sun Kim ◽  
Jaewon Oh ◽  
Sung-Kyung Bong ◽  
jung-jae lee
Keyword(s):  
Rabbit Model ◽  
Diabetic Rabbit

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.

scholarly journals Insulin and Glucagon Impairments in Relation with Islet Cells Morphological Modifications Following Long Term Pancreatic Duct Ligation in the Rabbit – A Model of Non-insulin-dependent Diabete

2001 ◽  
Vol 2 (2) ◽  
pp. 101-112 ◽  
Author(s):  
J. Catala ◽  
M. Daumas ◽  
A. Pham Huu Chanh ◽  
B. Lasserre ◽  
E Hollande
Keyword(s):  
Pancreatic Duct ◽  
Islet Cells ◽  
Rabbit Model ◽  
Fold Increase ◽  
Pancreatic Duct Ligation ◽  
A Cells ◽  
Duct Ligation ◽  
Insulin Dependent

Plasma levels of glucose, insulin and glucagon were measured at various time intervals after pancreatic duct ligation (PDL) in rabbits. Two hyperglycemic periods were observed: one between 15–90 days (peak at 30 days of 15.1 ± 1.2mmol/l, p < 0.01), and the other at 450 days (11.2 ± 0.5 mmol/l, p < 0.02). The first hyperglycemic episode was significantly correlated with both hypoinsulinemia (41.8 ± 8pmol/l, r= –0.94, p < 0.01) and hyperglucagonemia (232 ± 21ng/l, r=0.95, p < 0.01). However, the late hyperglycemic phase (450 days), which was not accompanied by hypoinsulinemia, was observed after the hyperglucagonemia (390 days) produced by abundant immunostained A-cells giving rise to a 3-fold increase in pancreatic glucagon stores. The insulin and glucagon responses to glucose loading at 180, 270 and 450 days reflected the insensitivity of B- and A-cells to glucose. The PDL rabbit model with chronic and severe glycemic disorders due to the predominant role of glucagon mimicked key features of the NIDDM syndrome secondary to exocrine disease.

The role of intracranial hypotension in neonatal intraventricular hemorrhage

1983 ◽  
Vol 58 (2) ◽  
pp. 204-209 ◽  
Author(s):  
E. Scott Conner ◽  
Antonio V. Lorenzo ◽  
Keasley Welch ◽  
Brent Dorval
Keyword(s):  
Preterm Infants ◽  
Premature Infants ◽  
Intracranial Hypotension ◽  
Intraventricular Hemorrhage ◽  
Rabbit Model ◽  
Germinal Matrix ◽  
Content Type ◽  
Ventricular Hemorrhage ◽  
Fine Print

✓ Most preterm infants develop transient intracranial hypotension, which reaches its lowest level on the 2nd day of life. This corresponds to the time when most neonatal intraventricular hemorrhage (IVH) occurs. In order to test the hypothesis that intracranial hypotension may have an etiological role in the development of IVH in premature infants, the authors induced intracranial hypotension in the preterm rabbit by the intraperitoneal injection of glycerol. The rabbit model is well suited for this study because this animal is at risk of developing spontaneous germinal matrix and ventricular hemorrhage. Compared to control littermates, the glycerol-treated animals exhibited a greater than 3.5-fold incidence of germinal matrix and intraventricular hemorrhage.

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