With stricter regulation of atmospheric volatile organic compounds (VOCs) originating from fossil fuel-based vehicles and industries, the use of volatile chemical products (VCPs) and the transformation mechanism of VCPs have become increasingly important to quantify air quality. Volatile methylsiloxanes (VMS) are an important class of VCPs and high-production chemicals. Using quantum chemical calculations and kinetics modeling, we investigated the reaction mechanism of peroxy radicals of VMS, which are key intermediates in determining the atmospheric chemistry of VMS. L2-RSiCH2O2 • and D3-RSiCH2O2 • derived from hexamethyldisiloxane and hexamethylcyclotrisiloxane, respectively, were selected as representative model systems. The results indicated that L2-RSiCH2O2 • and D3-RSiCH2O2 • follow a novel Si–C–O rearrangement-driven autoxidation mechanism, leading to the formation of low volatile silanols and high yield of formaldehyde at low NO/HO2 • conditions. At high NO/HO2 • conditions, L2-RSiCH2O2 • and D3-RSiCH2O2 • react with NO/HO2 • to form organic nitrate, hydroperoxide, and active alkoxy radicals. The alkoxy radicals further follow a Si–C–O rearrangement step to finally form formate esters. The novel Si–C–O rearrangement mechanism of both peroxy and alkoxy radicals are supported by available experimental studies on the oxidation of VMS. Notably, the high yield of formaldehyde is estimated to significantly contribute to formaldehyde pollution in the indoor environment, especially during indoor cleaning.

Systemic lupus erythematosus (SLE) is a kind of chronic diffuse connective tissue illness characterized by multisystem and multiorgan involvement, repeated recurrence and remission, and the presence of a large pool of autoantibodies in the body. Although the exact cause of SLE is not thoroughly revealed, accumulating evidence has manifested that intake of probiotics alters the composition of the gut microbiome, regulating the immunomodulatory and inflammatory response, which may be linked to the disease pathogenesis. Particularly, documented experiments demonstrated that SLE patients have remarkable changes in gut microbiota compared to healthy controls, indicating that the alteration of microbiota may be implicated in different phases of SLE. In this review, the alteration of microbiota in the development of SLE is summarized, and the mechanism of intestinal microbiota on the progression of immune and inflammatory responses in SLE is also discussed. Due to limited reports on the effects of probiotics supplementation in SLE patients, we emphasize advancements made in the last few years on the function and mechanisms of probiotics in the development of SLE animal models. Besides, we follow through literature to survey whether probiotics supplements can be an adjuvant therapy for comprehensive treatment of SLE. Research has indicated that intake of probiotics alters the composition of the gut microbiome, contributing to prevent the progression of SLE. Adjustment of the gut microbiome through probiotics supplementation seems to alleviate SLE symptoms and their cardiovascular and renal complications in animal models, marking this treatment as a potentially novel approach.

Our most recent studies demonstrate that RhoGDIβ is able to promote human bladder cancer (BC) invasion and metastasis in an X‐link inhibitor of apoptosis protein‐dependent fashion accompanied by increased levels of matrix metalloproteinase (MMP)‐2 protein expression. We also found that RhoGDIβ and MMP‐2 protein expressions are consistently upregulated in both invasive BC tissues and cell lines. In the present study, we show that knockdown of RhoGDIβ inhibited MMP‐2 protein expression accompanied by a reduction of invasion in human BC cells, whereas ectopic expression of RhoGDIβ upregulated MMP‐2 protein expression and promoted invasion as well. The mechanistic studies indicated that MMP‐2 was upregulated by RhoGDIβ at the transcriptional level by increased specific binding of the transcription factor Sp1 to the mmp‐2 promoter region. Further investigation revealed that RhoGDIβ overexpression led to downregulation of miR‐200c, whereas miR‐200c was able directly to target 3′‐UTR of jnk2 mRNA and attenuated JNK2 protein translation, which resulted in attenuation of Sp1 mRNA and protein expression in turn, inhibiting Sp1‐dependent mmp‐2 transcription. Collectively, our studies demonstrate that RhoGDIβ overexpression inhibits miR‐200c abundance, which consequently results in increases of JNK2 protein translation, Sp1 expression, mmp‐2 transcription, and BC invasion. These findings, together with our previous results showing X‐link inhibitor of apoptosis protein mediating mRNA stabilization of both RhoGDIβ and mmp‐2, reveal the nature of the MMP‐2 regulatory network, which leads to MMP‐2 overexpression and BC invasion.

The atmospheric chemistry of isoprene has broad implications for regional air quality and the global climate. Allylic radicals, taking 13−17% yield in the isoprene oxidation by • Cl, can contribute as much as 3.6−4.9% to all possible formed intermediates in local regions at daytime. Considering the large quantity of isoprene emission, the chemistry of the allylic radicals is therefore highly desirable. Here, we investigated the atmospheric oxidation mechanism of the allylic radicals using quantum chemical calculations and kinetics modeling. The results indicate that the allylic radicals can barrierlessly combine with O 2 to form peroxy radicals (RO 2• ). Under ≤100 ppt NO and ≤50 ppt HO 2• conditions, the formed RO 2 • mainly undergo two times "successive cyclization and O 2 addition" to finally form the product fragments 2-alkoxy-acetaldehyde (C 2 H 3 O 2• ) and 3-hydroperoxy-2-oxopropanal (C 3 H 4 O 4 ). The presented reaction illustrates a novel successive cyclization-driven autoxidation mechanism. The formed 3-hydroperoxy-2-oxopropanal product is a new isomer of the atmospheric C 3 H 4 O 4 family and a potential aqueous-phase secondary organic aerosol precursor. Under >100 ppt NO condition, NO can mediate the cyclization-driven autoxidation process to form C 5 H 7 NO 3 , C 5 H 7 NO 7 , and alkoxy radical-related products. The proposed novel autoxidation mechanism advances our current understanding of the atmospheric chemistry of both isoprene and RO 2• .

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