• Journal of Korean Neurosurgical Society
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• v.55 no.5
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• pp.237-243
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• 2014

Objective : Symptomatic disc degeneration develops from inflammatory reactions in the annulus fibrosus (AF). Although inflammatory mediators during annular inflammation have been studied, the roles of matrix metalloproteinases (MMPs) and their inhibitors have not been fully elucidated. In this study, we evaluated the production of MMPs and tissue inhibitors of metalloproteinase (TIMPs) during annular inflammation using an in vitro co-culture system. We also examined the effect of notochordal cells on annular inflammation. Methods : Human AF (hAF) pellet was co-cultured for 48 hours with phorbol myristate acetate-stimulated macrophage-like THP-1 cells. hAF pellet and conditioned media (CM) from co-cultured cells were assayed for MMPs, TIMPs, and insulin-like growth factor (IGF)-1 levels using real-time reverse-transcriptase polymerase chain reaction and enzyem-linked immunosorbent assay. To evaluate whether notochordal cells affected MMPs or TIMPs production on annular inflammation, hAF co-cultured with notochordal cells from adult New Zealand White rabbits, were assayed. Results : MMP-1, -3, -9; and TIMP-1 levels were significantly increased in CM of hAF co-cultured with macrophage-like cells compared with hAF alone, whereas TIMP-2 and IGF-1 levels were significantly decreased (p<0.05). After macrophage exposure, hAF produced significantly more MMP-1 and -3 and less TIMP-1 and -2. Interleukin-$1{\beta}$ stimulation enhanced MMP-1 and -3 levels, and significantly diminished TIMP-2 levels. Co-culturing with rabbit notochordal cells did not significantly influence MMPs and TIMPs production or COL1A2 gene expression. Conclusion : Our results indicate that macrophage-like cells evoke annular degeneration through the regulation of major degradative enzymes and their inhibitors, produced by hAF, suggesting that the selective regulation of these enzymes provides future targets for symptomatic disc degeneration therapy.

• Journal of Veterinary Clinics
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• v.27 no.5
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• pp.593-599
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• 2010

A seven-year-old, castrated male Basset hound weighing 21.1 kg was presented for investigation of anorexia, lethargy, weight loss, melena and vomiting for 4 months. In laboratory findings, microcytic hypochromic anemia was identified, and other results were within a normal reference range. On the plain radiographs, soft tissue opacity was increased in the descending duodenal region; and on the contrast radiographs, ulcerative changes were identified in the entire segment of descending duodenum. Ultrasonographic findings included increased duodenal wall thickness and duodenal wall layering was lost. Endoscopy revealed irregular mucosal surface and luminal narrowing of the descending duodenum. There was concentrically thickened descending duodenum on the computed tomography. And the wall of the descending duodenum showed heterogenous enhancement after contrast agent injection. On histopathological findings, both chronic inflammation with mucosal proliferation and neoplastic changes with multiple small glandslike structures invading into the submucosa were identified. Based on these findings, presented case was diagnosed as an annular form duodenal adenocarcinoma. After 13 months of supportive medical treatment, the patient was expired. The purpose of this case report was to describe the duodenal adenocarcinoma in a dog.