MATERIALS AND METHODS: Diabetic ADSCs were treated with DFO and compared to normal and non-treated diabetic ADSCs for expression of HIF-1α, VEGF, FGF-2 and SDF-1, at mRNA and protein levels, using qRT-PCR, western blotting and ELISA assay. Activity of matrix metalloproteinases -2 and -9 were measured using a gelatin zymography assay. Angiogenic potential of conditioned media derived from normal, DFO-treated and non-treated diabetic ADSCs were determined by in vitro (in HUVECs) and in vivo experiments including scratch assay, three-dimensional tube formation testing and surgical wound healing models.
RESULTS: DFO remarkably enhanced expression of noted genes by mRNA and protein levels and restored activity of matrix metalloproteinases -2 and -9. Compromised angiogenic potential of conditioned medium derived from diabetic ADSCs was restored by DFO both in vitro and in vivo experiments.
CONCLUSION: DFO preconditioning restored neovascularization potential of ADSCs derived from diabetic rats by affecting the HIF-1α pathway.
METHOD: Several methods were employed to assess the function of LOC285629 such as gene silencing, qPCR, proliferation assay, BrdU assay, transwell migration assay, ELISA and protein profiler.
RESULTS: Via in silico analyses, we identified significant downregulation of LOC285629, a novel lncRNA, across CRC stages. LOC285629 expression was significantly downregulated in advanced stages (Stage III and IV) compared to Stage I (Kruskal-Wallis Test; p = 0.0093). Further in-house validation showed that the expression of LOC285629 was upregulated in colorectal cancer tissues and cell lines compared to the normal counterparts, but was downregulated in advanced stages. By targeting LOC285629, the viability, proliferative abilities, invasiveness and resistance of colorectal cancer cells towards 5-fluorouracil were reduced. It was also discovered that LOC285629 may regulate cancer progression by targeting several different proteins, namely survivin, BCL-xL, progranulin, PDGF-AA, enolase 2 and p70S6 K.
CONCLUSION: Our findings suggest that LOC285629 may be further developed as a potential therapeutic target for CRC treatment.
METHODS: Based on predefined eligibility criteria, the search was conducted following PRISMA-P 2015 guidelines on MEDLINE, EBSCO Host, Scopus, PubMed, and Web of Science databases in 2022 by 2 reviewers. Articles then underwent Cochrane GRADE approach and JBI critical appraisal for certainty of evidence and bias evaluation.
RESULTS: Thirty articles were included following eligibility screening. Both in vitro experiments (20%) and in vivo (80%) devices ranging from electronic axiography, electromyography, optoelectronic and ultrasonic, oral or extra-oral tracking, photogrammetry, sirognathography, digital pressure sensors, electrognathography, and computerised medical-image tracing were documented. 53.53% of the studies were rated below "moderate" certainty of evidence. Critical appraisal showed 80% case-control investigations failed to address confounding variables while 90% of the included non-randomised experimental studies failed to establish control reference.
CONCLUSION: Mandibular and condylar growth, kinematic dysfunction of the neuromuscular system, shortened dental arches, previous orthodontic treatment, variations in habitual head posture, temporomandibular joint disorders, fricative phonetics, and to a limited extent parafunctional habits and unbalanced occlusal contact were identified confounding variables that shaped jaw movement trajectories but were not highly dependent on age, gender, or diet. Realistic variations in device accuracy were found between 50 and 330 µm across the digital systems with very low interrater reliability for motion tracing from photographs. Forensic and in vitro simulation devices could not accurately recreate variations in jaw motion and muscle contractions.