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The results of our study presented an increase in ROM, facet joint force, and ligament tension at the ADR segments. The mobile-core model showed a higher increase in segmental motion, facet force, and ligament tension, but lower stress on the PE core than the fixed-core model.

The development of heterotopic ossification (HO) is considered one of the major complications following cervical total disc replacement (TDR). Even though previous studies have identified clinical and biomechanical conditions that may stimulate HO, the mechanism of HO formation has not been fully elucidated. The objective of this study is to investigate whether mechanical loading is a biomechanical condition that plays a substantial role to decide the HO formation. A finite element model of TDR on the C5-C6 was developed, and HO formation was predicted by simulating a bone adaptation process under various physiological mechanical loadings. The distributions of strain energy on vertebrae were assessed after HO formation. For the compressive force, most of the HO formation occurred on the vertebral endplates uncovered by the implant footplate which was similar to the Type 1 HO. For the anteriorly directed shear force, the HO was predominantly formed in the anterior parts of both the upper and lower vertebrae as the Type 2 HO. For both the flexion and extension moments, the HO shapes were similar to those for the shear force. The total strain energy was reduced after HO formation for all loading conditions. Two distinct types of HO were predicted based on mechanically induced bone adaptation processes, and our findings were consistent with those of previous clinical studies. HO formation might have a role in compensating for the non-uniform strain energy distribution which is one of the mechanical parameters related to the bone remodeling after cervical TDR.

The timely diagnosis and therapeutic monitoring of human renal cell carcinoma (RCC) is limited by the lack of specific biomarkers. To identify candidate RCC biomarkers, we used 2-DE gel electrophoresis with mass spectrometry and 2-DE spot intensity-based ROC analysis to analyze 18 sets of paired normal and RCC tumor tissue including conventional, papillary, and chromophobe subtypes. Validation was performed with RCC patient plasma samples and confirmed by clustergram, shRNA, and immunohistochemistry assays. Cardinal candidates were evaluated by ELISA. The leading candidate biomarker that was upregulated in RCC samples according to the clustergram and validation analysis was nicotinamide N-methyltransferase (NNMT) (13/15, P < 0.0001). Other upregulated candidate biomarkers that were identified by this method include ferritin, hNSE, NM23, secretagogin, and L-plastin. The upregulation of NNMT in RCC was confirmed by immunoblotting and immunohistochemistry. Analysis of fractionated membrane-associated proteins identified CAP-G, mitofillin, tubulin alpha, RBBP7, and HSP27. Of these, RBBP7 and HSP27 were highly expressed in the chromophobe subtype of RCC (3/3) but were absent from conventional RCC (0/3). The triple combination of the NNMT, FTL, and hNSE biomarkers had the highest predictive capacity of 0.993, while NNMT was the single, most powerful candidate diagnostic biomarker for all types of RCC.

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