LncRNA SNHG1 attenuates neuropathic pain following spinal cord injury by regulating CDK4 level.

OBJECTIVE: Neuropathic pain (NP) is one of the most intractable complications of spinal cord injury (SCI). This study aims to explore the role of long non-coding RNA (lncRNA) SNHG1 in influencing SCI-induced NP. MATERIALS AND METHODS: After establishment of the spinal nerve ligation (SNL) model in rats, spinal tissues were extracted. SNHG1 level in rat spinal tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The role of SNHG1 in the development of NP was explored by assessing paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in model rats. The interaction between SNHG1 and CDK4 was explored by Luciferase assay and RIP (RNA-Binding Protein Immunoprecipitation). Enzyme-linked immunosorbent assay (ELISA) and qRT-PCR were conducted to determine inflammatory factor levels in rat spinal tissues. RESULTS: SNHG1 was upregulated in rats undergoing SNL. Knockdown of SNHG1 alleviated the development of NP and overexpression of SNHG1 was capable of inducing NP symptoms in uninjured rats. SNHG1 induced NP by directly regulating CDK4 level. CONCLUSIONS: SNHG1 is a novel target in the treatment of NP associated with neuroinflammation.

MicroRNA-765 targets MTUS1 to promote the progression of osteosarcoma via mediating ERK/EMT pathway.

OBJECTIVE: Previous studies have shown that microRNA-765 (miR-765) is involved in certain biological behaviors of human cancers. However, abnormal expression and function of miR-765 have not been reported in osteosarcoma (OS). PATIENTS AND METHODS: Changes in the expression of miR-765 and MTUS1 (Microtubule-associated tumor suppressor 1) were examined via Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. The function of miR-765 was investigated through Cell Counting Kit-8 (CCK-8) and transwell assays in OS. The target of miR-765 was identified using a Dual-Luciferase reporter assay. RESULTS: MiR-765 was upregulated in OS tissues. And upregulation of miR-765 promoted cell proliferation, migration and invasion in OS. In addition, MTUS1 was confirmed as a direct target gene of miR-765. Moreover, miR-765 promoted the progression of OS through targeting MTUS1. Furthermore, miR-765 was involved in tumorigenesis of OS through activating extracellular-signal-regulated kinase/ epithelial-mesenchymal transition (ERK/EMT) pathway. CONCLUSIONS: MiR-765 targets MTUS1 to promote the progression of OS via mediating the ERK/EMT pathway. Therefore, miR-765 may be used as a novel biomarker for the diagnosis of OS.

Dietary fiber intake and stroke risk: a meta-analysis of prospective cohort studies.

BACKGROUND/OBJECTIVES: Epidemiological studies have suggested that dietary fiber intake may be associated with a decreased risk of stroke, but the findings have been inconsistent. We aimed to assess this association by conducting a meta-analysis of prospective cohort studies. SUBJECTS/METHODS: We performed a literature search on PubMed database through July 2012 to identify prospective studies of dietary fiber intake in relation to risk of stroke. We also comprehensively reviewed the reference lists of the retrieved articles to identify additional studies. We used a random-effects model to compute the summary risk estimates. RESULTS: Six prospective cohort studies containing a total of 314 864 subjects and 8920 stroke cases were included. The summary relative risk (RR) of stroke for the highest vs lowest category of dietary fiber intake was 0.87 (95% confidence interval (CI), 0.77-0.99). The corresponding RR in the subgroup analyses for men and women was 0.95 (95% CI, 0.83-1.08) and 0.80 (95% CI, 0.66-0.96), respectively; and for ischemic stroke and hemorrhagic stroke was 0.83(95% CI, 0.72-0.96) and 0.86 (95% CI, 0.70-1.06), respectively. Meta-regression indicated no significant difference between gender (P-interaction=0.18), or stroke subtypes (P-interaction =0.85). The dose-response analysis suggested a 12% (RR=0.88; 95% CI, 0.79-0.97) reduction in risk of stroke for each 10 g per day increment in dietary fiber intake. Moderate heterogeneity emerged in some of analyses, but disappeared after removing one study substantially contributing to the heterogeneity. Little evidence of publication bias was detected. CONCLUSION: Findings of this meta-analysis indicate a significant inverse dose-response relationship between dietary fiber intake and risk of stroke.

Red and processed meat consumption and risk of stroke: a meta-analysis of prospective cohort studies.

BACKGROUND/OBJECTIVES: Epidemiological evidence is suggestive, but inconclusive, for an association between consumption of red and processed meat and risk of stroke. We aimed to assess this association by conducting a meta-analysis of prospective cohort studies. SUBJECTS/METHODS: We performed a literature search on PubMed database through June 2012 to identify prospective cohort studies of red and processed meat intake in relation to risk of stroke. Reference lists of the retrieved articles were also reviewed. Both fixed-effects and random-effects model were assumed to compute the summary risk estimates. RESULTS: Five large independent prospective cohort studies were identified. These studies contained a total of 2 39 251 subjects and 9593 stroke events. Comparing the highest category of consumption with lowest category, the pooled relative risks (RRs) of total stroke were 1.15 (95% confidence interval (CI), 1.05-1.25) for total meat (red and processed meat combined) (n=4), 1.09 (95% CI, 1.01-1.18) for red meat (n=5) and 1.14 (95% CI, 1.05-1.25) for processed meat (n=5); the corresponding RRs of ischemic stroke (highest vs lowest quintile) were 1.15 (95% CI, 1.04-1.28), 1.13(95% CI, 1.01-1.25) and 1.19 (95% CI, 1.08-1.31). Consumption of red and/or processed meat was not associated with hemorrhagic stroke. In the dose-response analysis, the risk of stroke increased significantly by 10% and 13% for each 100 g per day increment in total and red meat consumption, respectively, and by 11% for each 50 g per day increment in processed meat consumption. CONCLUSION: Findings from this meta-analysis indicate that consumption of red and/or processed meat increase risk of stroke, in particular, ischemic stroke.