Implantation of Scaffold-Free Engineered Cartilage Constructs in a Rabbit Model for Chondral Resurfacing

2013 ◽  
Vol 38 (2) ◽  
pp. E21-E32 ◽  
Author(s):  
Jillian M. Brenner ◽  
Nicole M. Ventura ◽  
M. Yat Tse ◽  
Andrew Winterborn ◽  
Davide D. Bardana ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Engineered Cartilage ◽  
Chondral Resurfacing

scholarly journals Pediatric laryngotracheal reconstruction with tissue-engineered cartilage in a rabbit model

2015 ◽  
Vol 126 ◽  
pp. S5-S21 ◽  
Author(s):  
Ian N. Jacobs ◽  
Robert A. Redden ◽  
Rachel Goldberg ◽  
Michael Hast ◽  
Rebecca Salowe ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Laryngotracheal Reconstruction ◽  
Engineered Cartilage

Expandable Scaffold Improves Integration of Tissue-Engineered Cartilage: An In Vivo Study in a Rabbit Model

2016 ◽  
Vol 22 (11-12) ◽  
pp. 873-884 ◽  
Author(s):  
Chen-Chie Wang ◽  
Kai-Chiang Yang ◽  
Keng-Hui Lin ◽  
Yen-Liang Liu ◽  
Ya-Ting Yang ◽  
...  
Keyword(s):  
Rabbit Model ◽  
In Vivo Study ◽  
Engineered Cartilage

The Fate of Fresh, Layered, Nonsutured and Sutured, Autogenous Cartilage in the Rabbit Model

2000 ◽  
Vol 2 (4) ◽  
pp. 256-259 ◽  
Author(s):  
Joe B. Wiseman ◽  
G. Richard Holt ◽  
Michael A. Keefe ◽  
David E. Holck ◽  
Richard L. Canaan ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Autogenous Cartilage

A new technique to visualize alveolar dynamics in a rabbit model

2009 ◽  
Vol 56 (S 01) ◽  
Author(s):  
J Bickenbach ◽  
R Rossaint ◽  
R Autschbach ◽  
R Dembinski
Keyword(s):  
Rabbit Model ◽  
New Technique ◽  
A New Technique

Healing of Circular Defects in the Rabbit Medial Meniscus Can Occur Spontaneously and Is not Improved by Intra-Articular Hyaluronic Acid

1996 ◽  
Vol 09 (02) ◽  
pp. 60-5 ◽  
Author(s):  
N. Hope ◽  
P. Ghosh ◽  
S. Collier
Keyword(s):  
Hyaluronic Acid ◽  
Medial Meniscus ◽  
Chondroitin Sulphate ◽  
Rabbit Model ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Keratan Sulphate ◽  
Meniscal Healing ◽  
Meniscus Healing ◽  
Made In

SummaryThe aim of this study was to determine the effects of intra-articular hyaluronic acid on meniscal healing. Circular defects, 1.0 mm in diameter, were made in the anterior third of the medial meniscus in rabbits. In one joint, 0.4 ml hyaluronic acid (Healon®) was instilled, and in the contralateral (control) joint, 0.4 ml Ringer’s saline. Four rabbits were killed after four, eight and 12 weeks and the menisci examined histologically. By eight weeks most of the lesions had healed by filling with hyaline-like cartilage. Healing was not improved by hyaluronic acid treatment. The repair tissue stained strongly with alcian blue, and the presence of type II collagen, keratan sulphate, and chondroitin sulphate was demonstrated by immunohistochemical localisation. In contrast to the circular defects, longitudinal incisions made in the medial menisci of a further six rabbits did not show any healing after 12 weeks, indicating that the shape of the lesion largely determined the potential for healing.The effect of hyaluronic acid on meniscal healing was tested in a rabbit model. With one millimeter circular lesions in the medial meniscus, healing by filling with hyalinelike cartilage was not significantly affected by the application of hyaluronic acid intra-articularly at the time of surgery, compared to saline controls, as assessed histologically four, eight and 12 weeks after the operation.

Inhibition of Leucocyte and Platelet Adhesion Reduces Neointimal Hyperplasia after Arterial Injury

1997 ◽  
Vol 77 (04) ◽  
pp. 783-788 ◽  
Author(s):  
Paolo Golino ◽  
Giuseppe Ambrosio ◽  
Massimo Ragni ◽  
Plinio Cirillo ◽  
Nicolino Esposito ◽  
...  
Keyword(s):  
Coronary Angioplasty ◽  
Neointimal Hyperplasia ◽  
Rabbit Model ◽  
Arterial Injury ◽  
Platelet Glycoprotein ◽  
Beneficial Effects ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Interaction ◽  
Adhesion Complex

SummaryRestenosis following coronary angioplasty is thought to result from migration and proliferation of medial smooth muscle cells. However, the factors that initiate this proliferation are still unknown. In a rabbit model of carotid artery injury, we tested the hypothesis that activated platelets and leucocytes might contribute to the development of neointimal hyperplasia. Following arterial injury, rabbits received either no treatment, R15.7, a monoclonal antibody against the leucocyte CD ll/CD 18 adhesion complex, aurintricarboxylic acid (ATA), a sub stance that inhibits platelet glycoprotein Ib-von Willebrand factor interaction, or the combination of R15.7 and ATA. After 21 days, the extent of neointimal hyperplasia was evaluated by planimetry on histological arterial sections. The area of neointima averaged 0.51 ±0.07 mm2 in control animals and it was significantly reduced by administrationof either R15.7 or ATA alone to 0.12 ± 0.05 and 0.20 ±0.01 mm2, respectively (p <0.05 vs controls for both groups). The animals that received the combination of R15.7 and ATA showed a further reduction in neointimal hyperplasia, as compared to animals that received ATA alone (p <0.05 vs ATA alone). These data indicate that platelets and leucocytes play animportant role in the pathophysi ology of neointimal hyperplasia in this experimental model. Interven tions that reduce platelet and leucocyte adhesion to vessel wall might have beneficial effects in reducing restenosis following coronary angioplasty.

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