Major depressive disorder (MDD) is a serious mental illness, characterized by high morbidity, which has increased in recent decades. However, the molecular mechanisms underlying MDD remain unclear. Previous studies have identified altered metabolic profiles in peripheral tissues associated with MDD. Using curated metabolic characterization data from a large sample of MDD patients, we meta-analyzed the results of metabolites in peripheral blood. Pathway and network analyses were then performed to elucidate the biological themes within these altered metabolites. We identified 23 differentially expressed metabolites between MDD patients and controls from 46 studies. MDD patients were characterized by higher levels of asymmetric dimethylarginine, tyramine, 2-hydroxybutyric acid, phosphatidylcholine (32:1), and taurochenodesoxycholic acid and lower levels of L-acetylcarnitine, creatinine, L-asparagine, L-glutamine, linoleic acid, pyruvic acid, palmitoleic acid, L-serine, oleic acid, myo-inositol, dodecanoic acid, L-methionine, hypoxanthine, palmitic acid, L-tryptophan, kynurenic acid, taurine, and 25-hydroxyvitamin D compared with controls. L-tryptophan and kynurenic acid were consistently downregulated in MDD patients, regardless of antidepressant exposure. Depression rating scores were negatively associated with decreased levels of L-tryptophan. Pathway and network analyses revealed altered amino acid metabolism and lipid metabolism, especially for the tryptophan-kynurenine pathway and fatty acid metabolism, in the peripheral system of MDD patients. Taken together, our integrated results revealed that metabolic changes in the peripheral blood were associated with MDD, particularly decreased L-tryptophan and kynurenic acid levels, and alterations in the tryptophan-kynurenine and fatty acid metabolism pathways. Our findings may facilitate biomarker development and the elucidation of the molecular mechanisms that underly MDD.

N6-methyladenosine (m6A) modulates RNA metabolism and functions in cell differentiation, tissue development, and immune response. After acute burns, skin wounds are highly susceptible to infection and poor healing. However, our understanding of the effect of burn injuries on m6A methylation and their potential mechanism is still limited. Human m6A-mRNA&lncRNA Epitranscriptomic microarray was used to obtain comprehensive mRNA and lncRNA transcriptome m6A profiling and gene expression patterns after burn injuries in human skin tissue. Bioinformatic and functional analyses were conducted to find molecular functions. Microarray profiling showed that 65 mRNAs and 39 lncRNAs were significantly hypermethylated; 5492 mRNAs and 754 lncRNAs were significantly hypomethylated. Notably, 3989 hypomethylated mRNAs were down-expressed and inhibited many wound healing biological processes and pathways including in the protein catabolic process and supramolecular fiber organization pathway; 39 hypermethylated mRNAs were up-expressed and influenced the cell surface receptor signaling pathway and inflammatory response. Moreover, we validated that m6A regulators (METTL14, METTL16, ALKBH5, FMR1, and HNRNPC) were significantly downregulated after burn injury which may be responsible for the alteration of m6A modification and gene expression. In summary, we found that homeostasis in the skin was disrupted and m6A modification may be a potential mechanism affecting trauma infection and wound healing.

N6‐methyladenosine (m6A) methylation is the most abundant mammalian mRNA modification. m6A regulates RNA processing, splicing, nucleation, translation and stability by transferring, removing and recognizing m6A methylation sites, which are critical for cancer initiation, progression, metabolism and metastasis. m6A is involved in pathophysiological tumour development by altering m6A modification and expression levels in tumour oncogenes and suppressor genes. Skin cancers are by far the most common malignancies in humans, with well over a million cases diagnosed each year. Skin cancers are grouped into two main categories: melanoma and non‐melanoma skin cancers (NMSC), based on cell origin and clinical behaviour. In this review, we summarize m6A methylation functions in different skin cancers, and discuss how m6A methylation is involved in disease development and progression. Moreover, we review potential prognostic biomarkers and molecular targets for early skin cancer diagnosis and treatment.

Background: To reveal the alterations of tRNA-derived small RNA (tsRNA) expression profiles induced by hyperbaric oxygen (HBO) treatment in diabetic foot ulcer (DFU) and investigate new therapeutic targets. Materials & methods: tsRNA sequencing was employed in normal skin tissue, in DFU, and after HBO treatment groups. A quantitative real-time PCR was used to validate tsRNA sequencing results and their targets levels. Bioinformatics analysis was performed to reveal their therapeutic functions in DFU. Results: A total of 22 tsRNAs were differentially expressed in the three groups. Three selected tsRNAs were validated by quantitative real-time PCR for further analysis, which were all significantly overexpressed in DFU while being normally expressed after HBO treatment. Bioinformatics analysis disclosed that these tsRNAs may play therapeutic roles through the regulation of the Wnt signaling pathway. Conclusion: tsRNAs may be novel useful targets for HBO to treat DFU.

INTRODUCTION Monitoring metabolic biomarkers could be used as an effective tool for post-burn patient diagnosis and repair. OBJECTIVE. Endothelial cells play an important role in repair after burns. However, little research has been done on this. We aim to discover predictive biological endothelial cell markers and study biomarker-related metabolism. METHODS After establishing a thermal injury model using endothelial cells. We examined the metabolic changes 48 and 72 h after burn using liquid-phase mass spectrometry and endothelial cell models derived from heat treatment. RESULTS A total of 365 metabolites in 12 samples were analyzed using liquid chromatography–mass spectrometry. Among these, univariate analysis after the false discovery correction showed eight concentrations in each time period changed significantly with time (P ＜0.05). The 48-h post-burn was characterized by a decreasing trend in the levels of six metabolites including deoxycholate, glucose 1-phosphate, glucose 6-phosphate, mannose 6-phosphate, histidine, and 1-methyl-2-pyrrolidone, and Metabolites with significantly increased levels were Sambucinol, Flufenacet. The levels of metabolites such as azelate, 1-methyl-2-pyrrolidone, guanosine monophosphate, xanthosine monophosphate, cytidine, and flufenacet decreased significantly, while the level of dibutyl phthalate showed an increasing trend after 72 h. Metabolic pathways such as Starch and sucrose metabolism and purine metabolism are greatly affected. CONCLUSION Our study shows that metabolomic signatures of heat-injured endothelial cells were found to correlate with their burn time, suggesting that metabolomics may have the potential to develop new diagnostic and therapeutic approaches for burns.