Therapies targeting Immuno-moodulin may lead to a new type of treatment for mental disorders through regulation of the functions of the immune system, rather than directly acting on the nervous system. BACKGROUND Non-convulsive neurostimulation is a rapidly-developing alternative to traditional treatment approaches in depression. Modalities such as repetitive Transcranial Magnetic Stimulation (rTMS), transcranial Direct Current Stimulation (tDCS), Vagal Nerve Stimulation (VNS) and Deep Brain Stimulation (DBS) are now recognized as potential treatments. How non-convulsive neurostimulation interventions impact the neurohormonal and neuroimmune changes that accompany depression remains relatively unknown. If this type of intervention can drive endocrine, immune, as well symptom changes in depression, non-convulsive neurostimulation may represent a viable, multi-faceted treatment approach in depression. We were therefore interested to understand the state of the literature in this developing area. METHODS A systematic review of all studies that examined the impact of non-convulsive neurostimulation interventions on the hypothalamic-pituitary-adrenal (HPA) axis and immune function in the form of cytokine product measures and the limited number of studies retrieved. Animal studies generally supported the findings of those in human, but again, significant variability in methodology and study design were evident. CONCLUSIONS Non-convulsive neurostimulation interventions show promise in their ability to alter the endocrine and immune disturbances that accompany depression. Further research, which includes blinded, sham-controlled comparator designs is required. Non-damaging ultraviolet-B (UV-B) light promotes photomorphogenic development and stress acclimation in Arabidopsis through UV-B-specific signal transduction. UV-B irradiation induces monomerization and nuclear translocation of the UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8). However, it is not clear how the nuclear localization of UVR8 leads to changes in global gene expression. Here we reveal that nuclear UVR8 governs UV-B responsive transcriptional networks in concert with several previously known transcription factors, including ELONGATED HYPOCOTYL 5 (HY5) and PHYTOCHROME INTERACTING FACTOR 4 (PIF4). STC-15 Based on our transcriptomic analysis, we identify MYB13 as a novel positive regulator in UV-B-induced cotyledon expansion and stress acclimation. MYB13 is UV-B inducible and is predominantly expressed in the cotyledons. Our results demonstrate that MYB13 protein functions as a transcription factor to regulate the expression of genes involved in auxin response and flavonoid biosynthesis, and directly binds to their promoters. In addition, photoactivated UVR8 interacts with MYB13 in a UV-B dependent manner, and differentially modulates the affinity of MYB13 with its targets. Taken together, our results elucidate the cooperative function of the UV-B photoreceptor UVR8 with various transcription factors in the nucleus to orchestrate the expression of specific sets of downstream genes, and ultimately, mediate plant responses to UV-B light. Alterations in fatty acid metabolism are associated with impaired glucose uptake in skeletal muscle. Long-chain acyl-CoA synthetase (Acsl) 6 is the one of the Acsl isoforms expressed in skeletal muscle although its role in muscle energy metabolism has not been studied. Thus, the aims of this study were to investigate the role of Acsl6 in fatty acid partitioning and glucose uptake in differentiated skeletal myotubes using a siRNA-mediated knockdown approach. Compared with cells transfected with control siRNA, cells transfected with Acsl6 siRNA exhibited reduced intracellular triacylglycerol (TAG) accumulation. The initial rate of [1‑14C]‑oleic acid uptake was not altered while the incorporation of [1‑14C]‑acetic acids into total cellular lipids decreased under Acsl6 knockdown (p  less then  0.05). In a metabolic labeling study, Acsl6 suppression decreased the incorporation of [1‑14C]‑oleic acids and [1‑14C]‑acetic acids into TAG and diacylglycerol (DAG) (p  less then  0.05). During the chase period of a pulse-chase experiment, Acsl6 suppression increased the intracellular free fatty acids and decreased the fatty acid channeling toward the reacylation of TAG (p  less then  0.05). The incorporation of the labeled fatty acids into acid-soluble metabolites, β-oxidation product, was not changed under Acsl6 knockdown. Acsl6 siRNA decreased the insulin-induced uptake of [1‑14C]‑2‑deoxyglucose (p  less then  0.05) but did not change the glucose uptake in the presence of acipimox, inhibitor of lipolysis. Suppression of Acsl6 deteriorated Akt phosphorylation and Glut4 mRNA expression in response to insulin. These results suggest that Acsl6 activates and channels fatty acids toward anabolic pathways and has a role in glucose and fatty acid cycling through the re-esterification of fatty acids in skeletal muscle. V.In Barth syndrome (BTHS) mutations in tafazzin leads to changes in both the quantities and the molecular species of cardiolipin (CL), which are the hallmarks of BTHS. Contrary to the well-established alterations in CL associated with BTHS; recently a marked decrease in the plasmalogen levels in Barth specimens has been identified. To restore the plasmalogen levels, the present study reports the effect of promotion of plasmalogen biosynthesis on the lipidome of lymphoblasts derived from Barth patients as well as on cell viability, mitochondria biogenesis, and mitochondrial membrane potential. High resolution 31P NMR phospholipidomic analysis showed an increase in the levels of plasmenylethanolamine (the major plasmalogen in lymphoblasts), which reached values comparable to the control and a compensatory decrease in the levels of its diacyl-PE counterpart. Importantly, 31P NMR showed a significant increase in the levels of CL, while not altering the levels of monolysocardiolipin. Mass spectrometry measurements showed that the promotion of plasmalogen biosynthesis did not change the molecular species profile of targeted phospholipids. In addition, promotion of plasmalogen biosynthesis did not impact on cellular viability, although it significantly decrease mitochondria copy number and restored mitochondrial membrane potential. Overall, the results showed the efficacy of the promotion of plasmalogen biosynthesis on increasing the CL levels in a BTHS cell model and highlight the potential beneficial effect of a diet supplemented with plasmalogen precursors to BTHS patients.