ABSTRACT
OBJECTIVE: To investigate the effectiveness of focused extracorporeal shock wave therapy (FESWT) in treating postpartum sacroiliac joint (SIJ) dysfunction. METHODS: A total of 90 patients with SIJ dysfunction were included and randomly assigned to FESWT, manual therapy (MT), or combination therapy (CT) groups. Pain intensity and Oswestry Disability Index (ODI) score were measured upon admission, after 1 and 2 weeks of treatments. The treatment efficacy and adverse events of each group were also assessed. RESULTS: There were no significant differences among three groups regarding clinical data, pain intensity, and ODI score on admission (all P > 0.05). After 1 week of treatment, FESWT exhibited similar pain intensity and lower ODI score (P < 0.001) compared to MT. After 2 weeks of treatment, the pain and ODI in FESWT were similar with MT. The pain in CT was lower than MT after 1 week, but lower than FESWT after 2 weeks. Furthermore, we identified interaction effects between treatment method and duration in relation to pain intensity (Fgroup*time = 5.352, P = 0.001) and ODI score (Fgroup*time = 5.902, P < 0.001). FESWT group exhibited the highest improvement rate of 66.7%, while CT group achieved the highest cure rate of 73.3%. No adverse events were observed in any of the patients during 2 months follow-up period. CONCLUSIONS: Compared to MT, FESWT mainly reduced the ODI score rather than pain after 1 week of treatment. After 2 weeks, the effect of FESWT in relieving the pain was inferior to the MT.
Subject(s)
Joint Diseases , Low Back Pain , Musculoskeletal Manipulations , Female , Humans , Low Back Pain/therapy , Musculoskeletal Manipulations/methods , Prospective Studies , Sacroiliac Joint , Treatment OutcomeABSTRACT
MALAT1, microRNA (miR)-142-3p, and CXCR7 are critical molecules mediating endometriosis progression, and their correlation in endometriosis has been barely discussed. Thus, this research sought to survey the impact of MALAT1 on endometrial stromal cell (ESC) proliferation, apoptosis, and inflammation via miR-142-3p/CXCR7 axis to promote explorations on endometriosis. In endometrial tissues and ESCs, CXCR7 expression was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis and miR-142-3p and MALAT1 expression by qRT-PCR. Then, ESC proliferation was assessed by CCK-8 and EdU labeling assays, apoptosis by flow cytometry, and levels of inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 in ESC supernatant by enzyme linked immunosorbent assay. The interactions among CXCR7, miR-142-3p, and MALAT1 were evaluated by dual luciferase reporter gene, RNA pull-down, and Argonaute 2- RNA immunoprecipitation assays. At last, the relevance of miR-142-3p to MALAT1 and that of miR-142-3p to CXCR7 in ectopic endometrial tissues were analyzed using Pearson correlation analysis. CXCR7 and MALAT1 were overexpressed whilst miR-142-3p was lowly expressed in ectopic endometrial tissues. CXCR7 silencing or miR-142-3p overexpression reduced proliferative ability and enhanced apoptosis rate in ESCs and decreased TNF-α, IL-1ß, and IL-6 levels in cell supernatant. miR-142-3p negatively targeted CXCR7 while MALAT1 negatively targeted miR-142-3p. However, MALAT1 silencing diminished ESC proliferation and TNF-α, IL-1ß, and IL-6 levels in ESC supernatant and elevated ESC apoptosis, which was counterweighed by inhibiting miR-142-3p. Conclusively, MALAT1 promoted ESC proliferation and inflammatory factor expression and inhibited ESC apoptosis via miR-142-3p/CXCR axis.
