Background: Because of an aging population,osteoporotic vertebral fractures are becoming more frequent. Conservative therapy was considered the gold standard for treating osteoporotic vertebral compression fractures (OVCFs) in the past. Percutaneous vertebroplasty (PVP) or balloon kyphoplasty (BKP) as minimally invasive techniques are new treatments that arewidely used for painful OVCFs. However, an increase in new vertebral compression fractures at non-treated levels following augmentation is of concern. There is no convincing evidence that new fractures are inevitable after augmentation compared to after conservative treatment, and it is still unclear whether further fractures are the consequence of augmentation ora result of the natural progression of osteoporosis. Objective: The objective of this study was to evaluate the new-level fracture risk after PVP or BKP compared with conservative (non-operative) treatment and to determine the dominant risk factor associated with new OVCFs. Study Design: A meta-analysis of comparative studies was performed to evaluate the incidence of new vertebral fractures between vertebral augmentation, such as vertebroplasty and kyphoplasty, and no operation. Setting: The PubMed,ISI Web of Science, ELSEVIER ScienceDirect, and Cochrane Library databases and abstracts published in annual proceedings were systematically searched.In addition, we also retrieved data from references when titles met our inclusion criteria. Methods: Detailed searches of a number of online databases comparing operative and non-operative groups were performed. We included randomized controlled trials,clinical controlled trials,and prospective clinical studies to provide available data. All studies were reviewed by 2 reviewers independently, and all the references that met our inclusion criteria were searched for additional trials, using the guidelines set by the QUOROM (Quality of Reporting of Meta-analysis) statement. Results: We evaluated 12 studies encompassing 1,328 patients in total,including 768 who underwent operation with polymethylmethacrylateand 560 who received non-operative treatments. For new-level vertebral fractures, our meta-analysis found no significant difference between the 2 methods, including total new fractures (P = 0.55) and adjacent fractures (P = 0.5).For pre-existing vertebral fractures, there was no significant difference between the 2 groups (operative and non-operative groups) (P = 0.24). Additionally,there was no significant difference in bone mineral density, both in the lumbar (P = 0 .13) and femoral neck regions (P = 0.37), between the 2 interventions. Limitation: All studies we screened were published online except for unpublished articles. Moreover, only a few data sources could be extracted from the published studies. There were only 5 randomized clinical trials and 7 prospective studies that met our inclusion criteria. Conclusion: Vertebral augmentation techniques, such as vertebroplasty and kyphoplasty, have been widely used to treat osteoporotic vertebral fractures in order to alleviate back pain and correct the deformity, and it has been frequently reported that many new vertebral fractures occurred after this operation. Our analysis did not reveal evidence of an increased risk of fracture of vertebral bodies, especially those adjacent to the treated vertebrae, following augmentation with either method compared with conservative treatment. Key words: Vertebroplasty, kyphoplasty, new osteoporotic compression vertebral fracture, meta-analysis

ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family. Previously, we have shown that ING5 inhibits invasiveness of lung cancer cells by downregulating EMT-inducing genes. However, the underlying mechanisms remain unclear. The aim of the study was to use integrated approach involving SILAC labeling and mass spectrometry-based quantitative proteomics to quantify dynamic changes of acetylation regulated by ING5 in lung cancer cells. Here, we have found that ING5 has a profound influence on protein lysine acetylation with 163 acetylation peptides on 122 proteins significantly upregulated and 100 acetylation peptides on 72 proteins downregulated by ING5 overexpression. Bioinfomatic analysis revealed that the acetylated proteins upregulated by ING5 located preferentially in nucleus to cytoplasm and were significantly enriched in transcription cofactor activity, chromatin binding and DNA binding functions; while those downregulated by ING5 located preferentially in cytoplasm rather than nucleus and were functionally enriched in metabolism, suggesting diverse functions of ING5 through differentially regulating protein acetylation. Interestingly, we found ING5 overexpression promotes p300 autoacetylation at K1555, K1558 and K1560 within p300 HAT domain, and two novel sites K1647 and K1794, leading to activation of p300 HAT activity, which was confirmed by accelerated acetylation of p300 target proteins, p53 at k382 and histone H3 at K18. A specific p300 HAT inhibitor C646 impaired ING5-increased acetylation of H3K18 and p53K382, and subsequent expression of p21 and Bax. In conclusion, our results reveal the lysine acetylome regulated by ING5 and provide new insights into mechanisms of ING5 in the regulation of gene expression, metabolism and other cellular functions.

BackgroundMinimally invasive esophagectomy (MIE) is increasingly used for the treatment of esophageal cancer. However, the ideal approach of MIE is not yet standardized. We explore the ideal approach of MIE according to the location of the tumor and compare the clinical outcomes between patients with cancer arising in the upper third of the esophagus and those with tumors involving the middle and lower third of the esophagus.MethodsWe included patients with esophageal carcinoma and had clear indications for MIE. For cancer arising in the upper third of the esophagus, MIE McKeown approach was performed. For tumors involving the middle and lower third of the esophagus, MIE Ivor Lewis approach was adopted.ResultsOf the 251 patients included in this analysis, 200 patients underwent Ivor-Lewis MIE and 51 patients underwent McKeown MIE. The incidence of anastomotic leak, anastomotic stenosis and recurrent laryngeal nerve injury was significantly higher in the McKeown MIE group than that in the Ivor Lewis MIE group. The 30-day postoperative mortality rate was 1.2% (n = 1) in the McKeown MIE group. Lymph nodes harvested were significantly more in the MIE-McKeown group than in Ivor Lewis MIE group (P < 0.05). The median follow-up period was 15 months (1–25 months) and the overall survival rate at 1 year stratified by pathologic stage at esophagectomy was 95.9% (stage 1), 83.8% (stage II), 73.4% (stage III).ConclusionsMIE for esophageal cancer according to the location and clinical stage of the tumor will decrease all postoperative complications and may yield the greatest benefit from surgery.

Background: Acute pancreatitis is the most common serious complication of endoscopic retrograde cholangiopancreatography (ERCP). Although, somatostatin (SOM) has been used in the prevention of post-ERCP pancreatitis (PEP), the efficacy of SOM remains inconsistent.Methods: Electronic databases, including PubMed/MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library), and the Science Citation Index were searched to retrieve relevant studies. Details of the study population, including patients’ characteristics, sample size, regimen of drug administration and incidence of PEP, hyperamylasemia and abdominal pain were extracted by two investigators. Data were analyzed with Review Manager 5.3 software.Results: Eleven randomized controlled trials, enrolling a total of 4192 patients, were included in the meta-analysis. After data were pooled, we observed decreased incidence of ERCP-induced outcomes, such as PEP (RR = 0.63, 95% CI: 0.40, 0.98; P = 0.04) and hyperamylasemia (RR = 0.75, 95% CI: 0.66, 0.84; P < 0.001) in patients treated with SOM than those with placebo. Subgroup analysis by ethnicity found decreased incidence of PEP and hyperamylasemia in Asia only. Subgroup analysis by treatment schedule and dosage revealed decreased incidence of PEP and hyperamylasemia when SOM were treated with a single bolus or long-term infusion, or at dose above 3000 μg. We did not observed efficacy of SOM on abdominal pain in pooled or subgroup analysis.Conclusion: This meta-analysis of patients undergoing ERCP showed reduced incidence of PEP and hyperamylasemia when SOM was administrated with single bolus, long-term infusion, or high dosage. More data are needed to confirm our findings.

Cancer stem cells (CSCs) have been implicated in the genesis, progression and recurrence of renal cancer. The sonic hedgehog (Shh) pathway serves a critical role in maintaining the stemness of CSCs. Genistein, a major isoflavone component extracted from soybeans and soy products, has been demonstrated to possess anticancer activity. However, the effects of genistein on renal CSCs and its underlying mechanisms remain to be fully elucidated. The aim of the present study was to investigate the role of the Shh pathway in genistein inhibition of renal CSCs. The results of the present study demonstrated that expression levels of renal CSC markers were markedly upregulated in the sphere-forming cells, which were isolated and enriched from 786-O and ACHN cells in a tumor sphere formation assay, and more cells were arrested at the G 0 /G 1 phase instead of the S 1 phase compared with the adherent cells. Furthermore, the present study demonstrated that genistein could effectively diminish the activity of renal CSCs by suppressing tumor sphere formation, decreasing renal CSCs markers, inhibiting proliferation and inducing apoptosis. Additionally, the downregulation of Shh pathway activity could inhibit renal CSCs. Genistein exhibited an inhibitory effect on renal CSCs by attenuating the activation of the Shh pathway. In conclusion, the results illustrated the role of the Shh pathway in regulating renal CSC traits and the intervention of renal CSCs by genistein, which could provide novel insights into the molecular mechanisms of renal CSC intervention.