Outcome after Tibial Plateau Levelling Osteotomy and Modified Maquet Procedure in Dogs with Cranial Cruciate Ligament Rupture.

OBJECTIVE: The aim of this study was to compare outcomes after tibial plateau levelling osteotomy (TPLO) and modified Maquet procedure (MMP) for the treatment of cranial cruciate ligament rupture (CCLR) in dogs using clinical and radiographic evaluation and treadmill-based force plate gait analysis. STUDY DESIGN: This study was a prospective, randomized, controlled study. MATERIALS AND METHODS: Sixty-one dogs (76 joints) with CCLR were treated with TPLO (n = 30 dogs, 41 joints) or MMP (n = 31 dogs, 35 joints) and compared with a control group of 16 healthy Labrador Retrievers. Outcomes after surgery were compared by clinical orthopaedic assessment, radiographic evaluation and force plate gait analysis performed preoperatively, and then at 6 weeks, 3 and 6 months postoperatively. For objective comparison of ground reaction forces, the data were compared with the control group. Major complications were reported. RESULTS: A significant improvement in ground reaction forces was reached in all surgically treated dogs. No significant difference was found between the surgical methods at any postoperative re-examination. With regard to peak vertical force (PVF), there were significantly more patients with TPLO within the reference range of healthy dogs at the 3 months re-examination than dogs with MMP. There was no significant difference in mean value comparisons between TPLO and control groups 6 months postoperatively. Compared with the control group, mean values of 93.9% (PVF) and 85.9% (vertical impulse [VI]) were reached by the TPLO group and 89.4% (PVF) and 79.9% (VI) by the MMP group, 6 months postoperatively.No significant differences were found regarding major complications or progression of osteoarthritis. CONCLUSIONS: Although no significant differences were found between the surgical methods, TPLO patients showed superiority with regard to clinical outcome.

Repression of transcription by TSGA/Jmjd1a, a novel interaction partner of the ETS protein ER71.

Testis-specific gene A (TSGA) was originally identified in rat and shown to be expressed within the testes. Here, we have cloned the murine homolog [also known as jumonji domain-containing 1a (Jmjd1a)] and for the first time characterized the TSGA protein and its functions. Although murine TSGA is expressed in testes, its mRNA is also present in many other tissues, including heart, thymus, liver, and skin. Immunostaining revealed that TSGA is a nuclear protein, whose N-terminus contains a putative nuclear localization signal. TSGA displays significant homology to a suspected tumor suppressor and coactivator (5qNCA), to a thyroid hormone receptor interacting protein (TRIP8) and to the corepressor Hairless, pointing at a role of TSGA in transcription regulation. Indeed, TSGA contains several functional transcription repression domains. In addition, TSGA interacts both in vitro and in vivo with ER71 (ETS related 71), a transcription factor that is expressed in the testes of adult mice and during embryogenesis. Specifically, the N-terminus of TSGA and the C-terminus of ER71 are primarily engaged in their complex formation. Furthermore, TSGA impairs the ability of ER71 to activate transcription from the matrix metalloproteinase-1 promoter. Thus, TSGA may modulate the function of ER71 and thereby affect spermatogenesis as well as embryonic development.

Delayed wound healing and epidermal hyperproliferation in mice lacking JunB in the skin.

The cutaneous response to injury and stress comprises a temporary change in the balance between epidermal proliferation and differentiation as well as an activation of the immune system. Soluble factors play an important role in the regulation of these complex processes by coordinating the intercellular communication between keratinocytes, fibroblasts, and inflammatory cells. In this study, we demonstrate that JunB, a member of the activator protein-1 transcription factor family, is an important regulator of cytokine expression and thus critically involved in the cutaneous response to injury and stress. Mice lacking JunB in the skin develop normally, indicating that JunB is neither required for cutaneous organogenesis, nor homeostasis. However, upon wounding and treatment with the phorbol ester 12-O-decanoyl-phorbol-13-acetate, JunB-deficiency in the skin likewise resulted in pronounced epidermal hyperproliferation, disturbed differentiation, and prolonged inflammation. Furthermore, delayed tissue remodelling was observed during wound healing. These phenotypic skin abnormalities were associated with JunB-dependent alterations in expression levels and kinetics of important mediators of wound repair, such as granulocyte macrophage colony-stimulating factor, growth-regulated protein-1, macrophage inflammatory protein-2, and lipocalin-2 in both the dermal and epidermal compartment of the skin, and a reduced ability of wound contraction of mutant dermal fibroblasts in vitro.