The objective of this systematic review was to identify the effectiveness of percutaneous endoscopic lumbar discectomy (PELD) in the treatment of recurrent lumbar disc herniation (rLDH) and to present its indications and techniques. We conducted a comprehensive search in MEDLINE, EMBASE, PubMed, Web of Science and Cochrane databases, searching for relevant studies of managing rLDH with PELD up to July 2015. Only papers published in English were included. Two review authors independently selected the studies, extracted relevant data and assessed their methodological quality. The Cochrane Collaboration's Revman 5.3 software was used for data analyses among the controlled studies. At last, one randomized controlled trial (RCT), two non-randomized control studies and five observational studies including a total of 579 cases were selected for this system review. The methodological quality of these studies was low to modern. The mean overall improvement of leg pain (visual analogue scale) was 66.92% (50.6%-89.87%), back pain (visual analogue scale) 54.91% (29%-67.95%), Oswestry Disability Index 60.9% (40.7%-75%), global perceived effect (MacNab/other) 75.77% (60%-95%). The mean overall of complication rate was 4.89% (0%-9.76%), dural tear rate 0.1% (0%-4.9%), recurrence rate 6.3% (4%-10%), re-operation rate 3.66% (2.33%-4.8%). We conducted a meta-analysis among the control trials. Compared with Open discectomy (OD), PELD resulted in better outcomes in terms of operative time, blood loss, lower complication rates, but with no significance differences regarding hospital stay, second recurrence rate, Macnab criteria and pain reduction. In conclusion, according to the current evidence, PELD is an effective procedure for the treatment of rLDH in terms of reducing complication and shorting hospital course, comparing with OD. Therefore, we suggested that PELD was a feasible alternative to OD in the treatment of the rLDH in the condition of proper indication. High-quality RCTs with large sample sizes are needed to further confirm these results.

G-protein coupled receptor (GPCR)-stimulated androgen-independent activation of androgen receptor (AR) contributes to acquisition of a hormone-refractory phenotype by prostate cancer. We previously reported that regulator of G-protein signaling (RGS) 2, an inhibitor of GPCRs, inhibits androgen-independent AR activation.1 Here, we show reduced RGS2 protein expression in human prostate cancer specimens compared to adjacent normal or hyperplastic tissue. Methylation-specific PCR analysis and bisulfite sequencing indicated that methylation of the CpG island in the RGS2 gene promoter correlated with RGS2 down-regulation in prostate cancer. In vitro methylation of this promoter suppressed reporter gene expression in transient transfection studies, whereas reversal of this promoter methylation with 5-aza-2′-deoxycytidine (5-Aza-dC) induced RGS2 re-expression in androgen-independent prostate cancer cells and inhibited their growth under androgen-deficient conditions. Interestingly, the inhibitory effect of 5-Aza-dC was significantly reduced by an RGS2-targeted short hairpin RNA, indicating that re-expressed RGS2 contributed to this growth inhibition. Restoration of RGS2 levels by ectopic expression in androgen-independent prostate cancer cells suppressed growth of xenografts in castrated mice. Thus, RGS2 promoter hypermethylation represses its expression and unmasks a latent pathway for AR transactivation in prostate cancer cells. Targeting this reversible process may provide a new strategy for suppressing prostate cancer progression by reestablishing its androgen-sensitivity.

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We demonstrated that the presence of GATA3-positive macrophages adversely affects remodeling of the myocardium in response to ischemia or pressure overload, whereas the absence of these macrophages led to a significant improvement in cardiac function. Targeting of signaling pathways that lead to the expression of GATA3 in macrophages may have favorable cardiac outcomes.