Epigenetic modulations play essential roles in diverse biological processes. During the past several years, DNA demethylation has been discovered in embryonic and postnatal development. Although some potential functions of DNA methylation have been demonstrated already, many questions remain in terms of unveiling the role of 5hmC; whether it serves either merely as an intermediate of DNA demethylation or as a stable epigenetic marker. 5-hydroxymethylcytosine (5hmC) is proved to be not merely serving as an intermediate of DNA demethylation, but also acts as a stable epigenetic marker. This review summarizes the current knowledge of the function of 5hmC in brain with the focus on the neuronal activity, neurodevelopment, aging, and neurological diseases.

SummaryLumbar laminectomy often results in failed back surgery syndrome. Most scholars support the three-dimensional theory of adhesion: Fibrosis surrounding the epidural tissues is based on the injured sacrospinalis behind, fibrous rings and posterior longitudinal ligaments. Approaches including using the minimally invasive technique, drugs, biomaterial and nonbiomaterial barriers to prevent the postoperative epidural adhesion were intensively investigated. Nevertheless, the results are far from satisfactory. Our review is based on various implant biomaterials that are used in clinical applications or are under study. We show the advantages and disadvantages of each method. The summary will help us to figure out ideas towards new techniques.The translational potential of this article: This review summarises recent biomaterials-related clinical and basic research that focuses on prevention of epidural adhesion after lumbar laminectomy. We also propose a novel possible translational method where a soft scaffold acts as a physical barrier in the early stage, engineered adipose tissue acts as a biobarrier in the later stage in the application of biomaterials and adipose-derived mesenchymal stem cells are used for prevention of epidural adhesion.

Dietary Zn(ii)-curcumin protects against doxorubicin-induced cardiomyopathy by modulation of the gut microbiota and maintenance of zinc homeostasis.

BackgroundAlzheimer’s disease (AD) is the most common form of neurodegenerative disorder that leads to a decline in cognitive function. In AD, aggregates of amyloid β peptide precede the accumulation of neurofibrillary tangles, both of which are hallmarks of the disease. The great majority (>90 %) of the AD cases are not originated from genetic defects, therefore supporting the central roles of epigenetic modifications that are acquired progressively during the life span. Strong evidences have indicated the implication of epigenetic modifications, including histone modification and DNA methylation, in AD. Recent studies revealed that 5-hydroxymethylcytosine (5hmC) is dynamically regulated during neurodevelopment and aging.ResultsWe show that amyloid peptide 1–42 (Aβ1-42) could significantly reduce the overall level of 5hmC in vitro. We found that the level of 5hmC displayed differential response to the pathogenesis in different brain regions, including the cortex, cerebellum, and hippocampus of APP-PSEN1 double transgenic (DTg) mice. We observed a significant decrease of overall 5hmC in hippocampus, but not in cortex and cerebellum, as the DTg mice aged. Genome-wide profiling identified differential hydroxymethylation regions (DhMRs) in DTg mice, which are highly enriched in introns, exons and intergenic regions. Gene ontology analyses indicated that DhMR-associated genes are highly enriched in multiple signaling pathways involving neuronal development/differentiation and neuronal function/survival.Conclusions5hmC-mediated epigenetic regulation could potentially be involved in the pathogenesis of AD.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2731-1) contains supplementary material, which is available to authorized users.

Objectives Anti-melanoma differentiation-associated gene 5 (MDA5) positive dermatomyositis (DM) is a life-threatening disease often complicated with rapidly progressive interstitial lung disease (ILD). This study aimed to establish and validate a clinical prediction model for 6-month all-cause mortality in Chinese patients with anti-MDA5 positive DM-ILD. Methods We conducted a retrospective observational study using a single-centre derivation cohort and a multi-centre validation cohort. Hospitalized DM patients with positive anti-MDA5 antibody and ILD course ≤3 months on admission were included. Patients’ baseline characteristics were described and compared between the deceased and survivors by univariable Cox regression. Optimal cut-off values were defined by the ‘survminer’ R package for significant continuous variables. Independent prognostic factors were determined by the final multivariable Cox regression model chosen by backward stepwise algorithm, which could be reproduced in both cohorts. The Kaplan-Meier survival analyses based on the derived predictor were conducted. Results A total of 184 and 81 eligible patients were included with a cumulative 40.8% and 40.7% six-month mortality in the derivation and validation cohorts, respectively. Based on multivariable Cox regression, the prognostic factor at baseline was identified and validated as three-category forced vital capacity (FVC)%: FVC% ≥ 50%, FVC% <50%, unable to perform. This significantly distinguishes three risk stages with mortalities of 15.3%, 46.8%, 97.4% in the derivation cohort, and 14.9%, 58.3%, 86.4% in the validation cohort, respectively (all p < 0.05). Conclusion The validated FVC%-based categorical predictor in anti-MDA5 positive DM-ILD is helpful for risk stratification in clinical practice and might facilitate cohort enrichment for future trials.