The aim of this study was to characterize the magnetic resonance imaging (MRI) features of PVNS. The radiographs and MR images of 23 pathologically proven cases of PVNS were retrospectively reviewed, with emphasis on MR images. There were 9 males and 14 females, mean age 36 years. Of 23 cases, 9 occurred in the hip, 8 in the knee, 3 in the ankle, 2 in the elbow and 1 in the wrist. Typical MRI findings included variable extent of nodular synovial proliferation, from mild proliferation to extensive masses, joint effusion in all cases, and multiple bony erosions in 15. Owing to the tight joint space, bone involvement was frequently seen in the hip, ankle, elbow and wrist. Although the knee joint had a loose capsule, bone involvement was rarely seen. Hemosiderin is a magnetic material, its deposit on proliferative synovial tissue resulting in a spotty low signal or extensive low signal area within the proliferative synovial masses on T(1)- (T1WI) and T(2)-weighted (T2WI) images, best seen on fast field echo (FFE) sequence MRI images. Fat-suppressed sequences obscured the deposit. This is diagnostic of PVNS. The MRI features of PVNS include variable extent of synovial proliferation, joint effusion and erosion of bone, and in particular the deposit of hemosiderin within the synovial masses. The deposit of hemosiderin, appearing as a low signal area best seen on FFE sequence, is diagnostic for PVNS.
BackgroundMounting evidences have showed the important role of transforming growth factor-β (TGF-β) in immunological surveillance of tumors. Some studies have also indicated human leukocyte antigen (HLA)-G-associated immune escape involving TGF-β management in gastric cancer (GC). However, the mechanism underlying it is unclear. This study aims to verify the correlations between HLA-G and TGF-β, involving the potential targeting of miR-152 on HLA-G.ResultsTGF-β and HLA-G levels were analyzed in blood samples from twenty GC patients with ELISA assays, while TGF-β showed directly proportional to HLA-G levels in GC patients, and TGF-β induced HLA-G up-regulation was also confirmed in GC cell lines. Furthermore, miR-152 expression could be inhibited by TGF-β, and the negative post-transcriptionally regulation of miR-152 on HLA-G was also demonstrated through gain- and loss-of-function studies. Besides, miR-152 overexpression repressed HLA-G up-regulation induced by TGF-β. And, miR-152 expression levels showed inversely proportional to both HLA-G and also TGF-β levels in GC patients.ConclusionTGF-β could induce HLA-G expression in GC by inhibiting miR-152, involving its negative regulation on HLA-G. Since TGF-β induced HLA-G up-regulation plays important role in immune escape, a potential application of miR-152 was suggested in GC treatment, or miR-152 might be one potential biomarker for GC.
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