Analgesic effect of extracorporeal shock-wave therapy for frozen shoulder: A randomized controlled trial protocol.

BACKGROUND: Till date only a few studies have reported the efficacy and clinical improvements obtained by extracorporeal shock-wave therapy (ESWT) on frozen shoulder. Limited by small number of studies and insufficient outcomes, it is important and necessary to conduct a new randomized controlled trial. The purpose of the present study is to determine whether ESWT could be more effective than oral steroid in treatment of frozen shoulder. METHODS: This randomized, single-blind, superiority clinical trial was approved by the institutional review board in The Third People's Hospital of Linyi. The inclusion criteria were patients aged >18 years with shoulder pain and restriction in range of motion. A symptom duration >3 months was required, with no radiographic findings on anteroposterior shoulder plain radiographs except for osteoporosis. Group 1 patients were given 30 mg of oral prednisolone daily for 2 weeks as a single morning dose and then 15 mg daily for another 2 weeks. Group 2 patients received 3 sessions of ESWT on the first, 14th, and 28th days. The primary outcome measure was shoulder pain score. The secondary outcomes included Disabilities of the Arm, Shoulder, and Hand score, range of motion, satisfaction rate, and complications. RESULTS: It was hypothesized that there would be a significant difference between ESWT and control groups in improving shoulder pain and functions in frozen shoulder. TRIAL REGISTRATION: This study protocol was registered in Research Registry (researchregistry5736).

LINC00473 contributes to the radioresistance of esophageal squamous cell carcinoma by regulating microRNA­497­5p and cell division cycle 25A.

Long non­coding RNA (lncRNA) LINC00473 plays a carcinogenic role in a variety of different tumor types. Nevertheless, the mechanisms through which LINC00473 regulates the radiosensitivity of esophageal squamous cell carcinoma (ESCC) cells remains elusive. In the present study, reverse transcription­quantitative PCR was used to quantify the expression of LINC00473, microRNA (miRNA/miR)­497­5p and cell division cycle 25A (CDC25A) in ESCC tissues. The association between LINC00473 expression and the clinicopathological characteristics of patients with ESCC was also assessed. Furthermore, Cell Counting kit­8 and colony formation assays were carried out to monitor the proliferation of ESCC cells exposed to X­ray radiation. A dual­luciferase reporter assay was also conducted to analyze the interaction between LINC00473 and miR­497­5p, as well as the interaction between CDC25A and miR­497­5p. The findings of the present study demonstrated that in ESCC tissues and cells, the expression levels of LINC00473 and CDC25A were significantly upregulated, while the expression of miR­497­5p was downregulated. The high expression level of LINC00473 was associated with a higher T stage, lymph node metastasis stage and a lower tumor differentiation grade in patients with ESCC. Following irradiation, transfection with miR­497­5p mimics reduced the promoting effect of LINC00473 overexpression on ESCC cell proliferation, and partially impeded the resistance of ESCC cells to X­ray radiation induced by LINC00473 overexpression. Moreover, transfection with miR­497­5p inhibitors partially alleviated the inhibitory effects of LINC00473 knockdown on cellular proliferation, and partly reversed the sensitivity of cells to X­ray irradiation induced by LINC00473 knockdown. Furthermore, it was confirmed that miR­497­5p was able to bind LINC00473 and the 3'­untranslated region of CDC25A. On the whole, the findings of the present study demonstrate that LINC00473 reduces the radiosensitivity of ESCC cells by modulating the miR­497­5p/CDC25A axis.

Long non-coding RNA-p21 regulates MPP+-induced neuronal injury by targeting miR-625 and derepressing TRPM2 in SH-SY5Y cells.

Parkinson's disease (PD), the second most prevalent age-related neurodegenerative disease, occurs as a result of the loss of dopaminergic neurons in the substantia nigra. Long non-coding RNA-p21 (lnc-p21) has been demonstrated to be upregulated in PD. However, its role in PD is unknown. Here, the results showed that lnc-p21 was highly expressed in human neuroblastoma SH-SY5Y cells treated with MPP+. Knockdown of lnc-p21 attenuated the cytotoxicity and cell apoptosis induced by MPP+ as shown by enhanced cell viability, decreased LDH release and cell apoptosis rate, accompanying with reduction of caspase-3 activity and Bax expression, and enhancement of Bcl-2 expression. Furthermore, knockdown of lnc-p21 mitigated MPP+-induced oxidative stress and neuroinflammation, as evidenced by the decrease in ROS generation, increase in SOD activity and decline in TNF-α, IL-1ß and IL-6 levels. Conversely, overexpression of lnc-p21 resulted in the opposite effect. miR-625 was identified as a target of lnc-p21. lnc-p21 overturned the inhibitory effect of miR-625 on MPP+-induced neuronal injury in SH-SY5Y cells. Additionally, lnc-p21 positively regulated TRPM2 expression by targeting miR-625, and knockdown of TRPM2 inhibited MPP+-induced neuronal injury. Overall, our study identified a new lnc-p21-miR-625-TRPM2 regulatory network that lnc-p21 regulated MPP + -induced neuronal injury by sponging miR-625 and upregulating TRPM2 in SH-SY5Y cells, which provide a better understanding for the pathogenesis of PD.