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https://www.selleckchem.com/products/bms-986235.html We found that LINC00662 was frequently highly expressed and related to the malignant phenotype of glioma. LINC00662 knockdown inhibited the proliferation, invasion and glioma genesis of glioma. LINC00662 acted as a ceRNA sponging miR-340-5p to protect the expression of STAT3. In addition, STAT3 was forced to the promoter region of LINC00662 and promoted its transcription. In vivo experiments demonstrated that targeting LINC00662 may be a potential strategy in glioma therapy. There was a positive regulation loop between LINC00662 and STAT3 in glioma. LINC00662 might be an oncogene in glioma. Targeting LINC00662 was a potential strategy in glioma therapy. There was a positive regulation loop between LINC00662 and STAT3 in glioma. LINC00662 might be an oncogene in glioma. Targeting LINC00662 was a potential strategy in glioma therapy.Present research aims to develop a finite element computational model to examine delamination-fretting wear behaviour that can suitably mimic actual loading conditions at HAp-Ti-6Al-4V interface of uncemented hip implant femoral stem component. A simple finite element contact configuration model based on fretting fatigue experimental arrangement subjected to different mechanical and tribological properties consist of contact pad (bone), HAp coating and Ti-6Al-4V substrate are developed using adaptive wear modelling approach adopting modified Archard wear equation to be examined under static simulation. The developed finite element model is validated and verified with reported literatures. The findings revealed that significant delamination-fretting wear is recorded at contact edge (leading edge) as a result of substantial contact pressure and contact slip driven by stress singularity effect. The delamination-fretting wear behaviour is promoted under higher delamination length, lower normal loading with higher fatigue loading, increased porous (cancellous) and cortical bone elastic modulu

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