The Role of Loading in Murine Models of Rotator Cuff Disease

Author(s):  
Adam C. Abraham ◽  
Fei Fang ◽  
Mikhail Golman ◽  
Panagiotis Oikonomou ◽  
Stavros Thomopoulos
2000 ◽  
Author(s):  
S. Thomopoulos ◽  
A. Esmail ◽  
J. D. Williamson ◽  
C. L. Flanagan ◽  
J. P. Iannotti ◽  
...  

Abstract One of the most common soft tissue injuries of the musculoskeletal system is injury to the rotator cuff tendons of the shoulder. These injuries are commonly attributed to factors such as overuse activity and extrinsic compression. Previous studies on the rotator cuff have been based on surgical reconstructive or clinical retrospective standpoints and were not designed to test hypotheses related to the causes of rotator cuff tendinosis. Our previous study has identified the rat as an appropriate in vivo animal model in which to study rotator cuff disease based on anatomic and functional similarities [1]. The current study uses this animal model to study the roles of extrinsic compression, overuse, and overuse combined with extrinsic compression, on the development of rotator cuff tendinosis. It was hypothesized that a single injury factor would be insufficient to create persistent tendinosis and a combination of injury factors would be necessary.


2015 ◽  
Vol 24 (8) ◽  
pp. 1322-1335 ◽  
Author(s):  
Damien Bachasson ◽  
Anshuman Singh ◽  
Sameer B. Shah ◽  
John G. Lane ◽  
Samuel R. Ward

2020 ◽  
Vol 71 (3) ◽  
pp. 817-826
Author(s):  
Metwaly M ◽  
Nassar N. ◽  
Khaled H. ◽  
El Mikkawy D. ◽  
Sakr H.

2009 ◽  
Vol 14 (3) ◽  
pp. 7-10
Author(s):  
Craig Uejo ◽  
Stephen Demeter

Abstract In the AMAGuides to the Evaluation of Permanent Impairment (AMA Guides), Sixth Edition, distal clavicle resection (resection arthroplasty of the acromioclavicular joint [ACJ]) results in ratable impairment, but only a single diagnosis within a region may be rated. Therefore, if another impairing condition is present in the shoulder region (eg, impingement syndrome or rotator cuff disease) only that resulting in the greatest causally related impairment is rated. In the setting of an occupational or other compensable injury or illness, causation of the impairment often is a key issue because, typically, only impairment that is causally related to the injury can be rated. For example, assume that a lifting injury at work caused a tear in a rotator cuff tendon that was already attenuated by repetitive impingement on inferiorly projecting spurs from longstanding degenerative arthritis of the ACJ. If surgery was performed for a traumatic rotator cuff tear and the distal clavicle also was resected due to preexisting ACJ arthritis, the latter surgery is not considered to be related to the injury. In other words, because the ACJ arthritis was neither caused nor worsened by the injury, this condition is not rated. The distal clavicular resection may have been warranted to diminish pain due to ACJ arthritis and/or eliminate the distal clavicle as a source of impingement.


2021 ◽  
Vol 3 (2) ◽  
pp. e373-e379
Author(s):  
Jacob Gorbaty ◽  
Susan M. Odum ◽  
Meghan K. Wally ◽  
Rachel B. Seymour ◽  
Nady Hamid ◽  
...  

2021 ◽  
Author(s):  
Xue Wang ◽  
Yuetong Wang ◽  
Zhaoyuan Fang ◽  
Hua Wang ◽  
Jian Zhang ◽  
...  

Abstract Somatic mutations of the chromatin remodeling gene ARID2 are observed in about 7% of human lung adenocarcinoma (LUAD). However, the role of ARID2 in the pathogenesis of LUAD remains largely unknown. Here we find that ARID2 expression is decreased during the malignant progression of both human and mice LUAD. Using two KrasG12D-based genetically engineered murine models (GEMM), we demonstrate that ARID2 knockout significantly promotes lung cancer malignant progression and shortens the overall survival. Consistently, ARID2 knockdown significantly promotes cell proliferation in human and mice lung cancer cells. Through integrative analyses of Chip-Seq and RNA-Seq data, we find that Hspa1a is up-regulated by Arid2 loss. Knockdown of Hspa1a specifically inhibits malignant progression of Arid2-deficient but not Arid2-wt lung cancers in both cell lines as well as animal models. Treatment with Hspa1a inhibitor could significantly inhibit the malignant progression of lung cancer with Arid2 deficiency. Together, our findings establish ARID2 as an important tumor suppressor in LUAD with novel mechanistic insights, and further identify HSPA1A as a potential therapeutic target in ARID2-deficient LUAD.


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