The effect of corticosteroid injection in the treatment of greater trochanter pain syndrome: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: corticosteroid injection (CSI) has been used to treat greater trochanter pain syndrome (GTPS) for many years. However, so far, the efficacy of CSI in the treatment of GTPS is still controversial. Therefore, the aim of this review is to evaluate the effectiveness of CSI in comparison with sham intervention, nature history, usual care, platelet-rich plasma (PRP), physiotherapy/exercise therapy, dry needling, or other nonsurgical treatment for improvements in pain and function in GTPS. METHODS: PubMed (Medline), Embase, Cochrane Library were searched from their inception until April 2021. Randomized controlled trails (RCTs) comparing CSI to nonsurgical treatment were included. Data on the effect of CSI on pain and function were extracted and checked by two review authors independently. The treatment effect was analyzed in the short term, medium term, and long term. RESULTS: Eight RCTs (764 patients) were included. This review suggests CSI may be superior to usual care and 'wait and see,' ESWT, but may not be superior to exercise, PRP, dry needling, and sham intervention in short-term pain or function improvement. In terms of medium-term pain or function improvement, CSI may be superior to usual care and 'wait and see,' but may not be superior to PRP. In terms of long-term pain or function improvement, CSI may be inferior to PRP and ESWT, but it may be superior to usual care and 'wait and see' at 12 months. CONCLUSIONS: Due to the small sample size and lack of sufficient clinical studies, current evidence is equivocal regarding the efficacy of CSI in the treatment of GTPS. Considering the limitations, more large-sample and high-quality RCTs are needed to prove the therapeutic effect of CSI on GTPS. TRIAL REGISTRATION: PROSPERO registration number: CRD42021247991. Registered 09 May 2021.

Efficacy and safety of electroacupuncture at auricular concha region in promoting of rehabilitation of ischemic stroke patients with upper limb motor dysfunction: A study protocol for a randomized pilot trial.

INTRODUCTION: Ischemic stroke (IS) is the one of the most severe neurological disease, survivors may live with upper limb motor dysfunction (ULMD) resulting in heavy social and economic burden. Nowadays, there are few approaches to promote the rehabilitation of ULMD. Auricular acupuncture (electroacupuncture [EA]) has long been used in the treatment of neurological disorders in China. This treatment has become an attractive treatment option due to its low cost, portability, minimal side effects, and ease of use in clinical and operational environments. However, its efficacy and safety in consciousness recovery remain to be proved. METHODS: A total of 80 IS patients with single upper limb motor function impairment will be recruited in the trial and randomized into EA or control groups. Patients in the control group will receive routine conventional treatment alone while patients in the EA group will receive EA treatment for 3 consecutive weeks based on routine conventional treatment. Baseline evaluation was carried out on day of enrollment, post-treatment evaluation was carried out 14 and 21 days after enrollment, and the 2 groups were follow-ups in 3 and 6 months after the end of the trial. The efficacy will be assessed with the changes in the upper limb Fugl-Meyer assessment, Wolf motor function test, action research arm test, active range of motion, and Barthel index. The safety of EA will be estimated by monitoring the incidence of adverse events and changes in vital signs during the study period. Analysis of feasibility will be descriptive and the change in outcome measures between groups will be analyzed using an independent sample t test. DISCUSSION: This study tried to narrow the evidence gap on the efficacy of EA at the auricular on the recovery of ULMD in patients with IS. The results of this trial will provide strong evidence for the efficacy and safety of EA of auricular concha region stimulation for IS patients.Trial registration: This trial has been registered at the Chinese Clinical Trial Registry, numbered ChiCTR2100049678.

C1q/TNF-related protein 4 restores leptin sensitivity by downregulating NF-κB signaling and microglial activation.

OBJECTIVE: C1qTNF-related protein 4 (CTRP4) acts in the hypothalamus to modulate food intake in diet-induced obese mice and has been shown to exert an anti-inflammatory effect on macrophages. Since high-fat diet-induced microglial activation and hypothalamic inflammation impair leptin signaling and increase food intake, we aimed to explore the potential connection between the anorexigenic effect of CTRP4 and the suppression of hypothalamic inflammation in mice with DIO. METHODS: Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and the hypothalamic leptin signaling pathway in diet-induced obese mice. Furthermore, central and plasma proinflammatory cytokines, including TNF-α and IL-6, were measured by Western blotting and ELISA. Changes in the hypothalamic NF-κB signaling cascade and microglial activation were also examined in vivo. In addition, NF-κB signaling and proinflammatory factors were investigated in BV-2 cells after CTRP4 intervention. RESULTS: We found that food intake was decreased, while leptin signaling was significantly improved in mice with DIO after CTRP4 overexpression. Central and peripheral TNF-α and IL-6 levels were reduced by central Ad-CTRP4 administration. Hypothalamic NF-κB signaling and microglial activation were also significantly suppressed in vivo. In addition, NF-κB signaling was inhibited in BV-2 cells following CTRP4 intervention, which was consistent with the decreased production of TNF-α and IL-6. CONCLUSIONS: Our data indicate that CTRP4 reverses leptin resistance by inhibiting NF-κB-dependent microglial activation and hypothalamic inflammation.

C1q/TNF-related Protein 4 Induces Signal Transducer and Activator of Transcription 3 Pathway and Modulates Food Intake.

C1q/TNF-related protein 4 (CTRP4) has been reported to decrease food intake and regulate energy homeostasis. However, its underlying mechanism and signaling pathway remain unknown. Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and signal transducer and activator of transcription 3 (STAT3) signaling pathway in normal chow-fed mice. Expressions of neuropeptides including proopiomelanocortin (POMC) and neuropeptide Y (NPY) were studied in hypothalamus by Western blot and immunochemistry. STAT3 and suppressor of cytokine signaling 3 (SOCS3) were determined by Western blot. STAT3 signaling pathway was also investigated in Neuro 2A (N2a) cells after CTRP4 overexpression intervention. We found that food intake decreased significantly in mice under normal chow condition after CTRP4 overexpression. Both immunohistochemistry and Western blot demonstrated that POMC expression was significantly increased while NPY expression was significantly decreased. The changes of neuropeptides were accompanied by significant increased STAT3 phosphorylation and decreased SOCS3 levels. The same changes of neuropeptides and STAT3 signaling were also found in N2a cells after CTRP4 overexpression intervention. Collectively, our data reveals that CTRP4 induces the activation of STAT3 signaling and decreases food intake.