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[Display omitted] • The cracking speeds of oil molecules are in this order: C 17 H 36 > C 17 H 32 > C 17 H 20. • The C 2 H 4 is the initial product but the C 2 H 2 and CH 4 are the final major products. • Formic acid is unfavorable for polymerization process of molecular fragments. • Acetic acid could make the pyrolysis process faster than formic acid. • The pyrolysis mechanisms of transformer oil molecules have been proposed. The reactive force field (ReaxFF) simulations have been performed to investigate the pyrolysis process of the transformer insulating oil from 2900 to 3500 K. We selected C 17 H 36 , C 17 H 32 , and C 17 H 20 as the principal components of the oil molecules and studied the effects of formic acid (HCOOH) and acetic acid (CH 3 COOH) on the pyrolysis mechanism of insulating oils. The calculated results show that the cracking process are accelerated at high temperatures and the speeds of cracking are in this order: C 17 H 36 > C 17 H 32 > C 17 H 20. The predicted main pyrolysis products are H 2 , C 2 H 4 , CH 4 , C 2 H 2 , CH 3 , C 2 H 3 , etc. Except for H 2 molecules, the C 2 H 4 is initially the most abundant product but its number decreases gradually and finally the C 2 H 2 and CH 4 are the major products. The evolution of the number of C–C bonds suggests that the C–C bonds of oil molecules are recombined from the early stage of pyrolysis process to the final equilibration state. The pyrolysis mechanisms of transformer oil have been proposed. The typical elementary steps are H 2 C = CH 2 → H-H + H-C≡C-H, CH 4 → H-H + CH 2 , 2(H 2 C = CH 2) → H-H + 2(H 2 C = CH), and 2(H 2 C = CH) → H-H + 2(H-C≡C-H). Formic acid (HCOOH) could be decomposed into CO, H 2 O, and CO 2 by the following reactions: HCOOH → COH + O-H, COH → CO + H, H + O-H → H 2 O, and HCOOH → CO 2 + H-H. The similar steps are found for acetic acid (CH 3 COOH). Both the acetic acid and formic acid could increase the degree of unsaturation of products, which is consistent with the experimental results. [ABSTRACT FROM AUTHOR]

Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane receptor protein predominantly expressed in microglia within the central nervous system (CNS). TREM2 regulates multiple microglial functions, including lipid metabolism, immune reaction, inflammation, and microglial phagocytosis. Recent studies have found that TREM2 is highly expressed in activated microglia after ischemic stroke. However, the role of TREM2 in the pathologic response after stroke remains unclear. Herein, TREM2-deficient microglia exhibit an impaired phagocytosis rate and cholesteryl ester (CE) accumulation, leading to lipid droplet formation and upregulation of Perilipin-2 (PLIN2) expression after hypoxia. Knockdown of TREM2 results in increased lipid synthesis (PLIN2, SOAT1) and decreased cholesterol clearance and lipid hydrolysis (LIPA, ApoE, ABCA1, NECH1, and NPC2), further impacting microglial phenotypes. In these lipid droplet-rich microglia, the TGF-β1/Smad2/3 signaling pathway is downregulated, driving microglia towards a pro-inflammatory phenotype. Meanwhile, in a neuron-microglia co-culture system under hypoxic conditions, we found that microglia lost their protective effect against neuronal injury and apoptosis when TREM2 was knocked down. Under in vivo conditions, TREM2 knockdown mice express lower TGF-β1 expression levels and a lower number of anti-inflammatory M2 phenotype microglia, resulting in increased cerebral infarct size, exacerbated neuronal apoptosis, and aggravated neuronal impairment. Our work suggests that TREM2 attenuates stroke-induced neuroinflammation by modulating the TGF-β1/Smad2/3 signaling pathway. TREM2 may play a direct role in the regulation of inflammation and also exert an influence on the post-ischemic inflammation and the stroke pathology progression via regulation of lipid metabolism processes. Thus, underscoring the therapeutic potential of TREM2 agonists in ischemic stroke and making TREM2 an attractive new clinical target for the treatment of ischemic stroke and other inflammation-related diseases. [Display omitted] • TREM2 regulates multiple microglial functions including lipid metabolism, inflammation, and microglial phagocytosis. • TREM2-deficient microglia exhibit an impaired phagocytosis rate and lipid droplet accumulation. • TREM2 knockdown leads lower TGF-β1 levels and less anti-inflammatory M2 phenotype microglia. • TREM2-deficient microglia display a lower neuroprotective potential. • TREM2 regulates post-ischemic inflammation in both a direct and an indirect way by modulating lipid metabolism. [ABSTRACT FROM AUTHOR]