Levels of STING were increased in liver tissues from patients with NAFLD and mice with HFD-induced steatosis. In mice, loss of STING from macrophages decreased the severity of liver fibrosis and the inflammatory response. STING might be a therapeutic target for NAFLD.

Taken together, our results demonstrate that disruption of A R in both macrophage and hepatocytes accounts for increased severity of NAFLD, likely through increasing inflammation and through elevating lipogenic events due to stimulation of SREBP1c expression and transcription activity. (Hepatology 2018;68:48-61).

A tubular molecular rotor B-Ta@B (1) and boron drum Ta@B (2) with the highest coordination number of twenty in chemistry are observed via a joint photoelectron spectroscopy and first-principles theory investigation.

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Size-selected boron clusters have been found to be predominantly planar or quasi-planar (2D) in the small size regime with the appearance of three-dimensional (3D) borospherene cages of larger sizes. A seashell-like B cluster was previously shown to be the smallest borospherene, which competes with a quasi-planar isomer for the global minimum. Here we report a study on the structures and bonding of the B and B clusters using photoelectron spectroscopy (PES) and first-principles calculations and demonstrate the continued competition between the 2D and borospherene structures. The PES spectrum of B displays a complex pattern with evidence of low-lying isomers. Global-minimum searches and extensive theoretical calculations revealed a complicated potential energy surface for B with five low-lying isomers, among which the lowest three were shown to contribute to the experimental spectrum. A 3D seashell-like C (2, A') isomer, featuring two heptagons on the waist and one octagon at the bottom, is the global minimum for B, followed by a 2D C (3, A) isomer with a hexagonal hole and a stingray-shaped 2D C (1, A') isomer with a pentagonal hole. However, by taking into account the entropic effects, the stingray-shaped isomer 1 was shown to be the lowest in energy at room temperature and was found to dominate the PES spectrum. Isomers 2 and 3, which have lower electron binding energies, were also found to be present in the experiment. Chemical bonding analyses showed that isomer 1 is an all-boron analogue of benzo[ghi]fluoranthene (CH), whereas the borospherene isomer 2 possesses 18π electrons, conforming to the 2(N + 1) electron counting rule for spherical aromaticity. For the B neutral cluster, the seashell-like borospherene isomer is the global minimum, significantly lower in energy than the stingray-shaped quasi-planar structure.

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Electrospray ionization mass spectrometry (ESI-MS) and tandem MS in an ion trap were used to explore the reduction of a PdCl(2) solution and the role of the metal in the formation of organosulfur radical cations. For tandem MS experiments, a 32 Da neutral loss (M - S), was observed for dibenzothiophene, thianthrene and benzonaphthothiophene, whereas both 32 and 33 Da neutral losses were observed for 2-methyldibenzothiophene and 4,6-dimethyldibenzothiophene. The effects of several variables on the formation of molecular ions or molecular fragments were studied to optimize radical cation formation, including the concentration ratio between PdCl(2) and sulfur and the collision energy. Electrochemical and chromatographic data were used to provide an explanation for the relative sensitivity observed for a mixture of polyaromatic sulfur heterocycles.

Adenosine 2A receptor (A2AR) exerts anti-inflammatory effects. However, the role for A2AR in obesity-associated adipose tissue inflammation remains to be elucidated. The present study examined the expression of A2AR in adipose tissue of mice with diet-induced obesity, and determined the effect of A2AR disruption on the status of obesity-associated adipose tissue inflammation. Wild-type C57BL/6J mice and A2AR-disrupted mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity and adipose tissue inflammation. In vitro, bone marrow-derived macrophages from A2AR-disrupted mice and wild-type control mice were treated with palmitate and examined for macrophage proinflammatory activation. Compared with that of low-fat diet (LFD)-fed wild-type mice, A2AR expression in adipose tissue of HFD-fed wild-type mice was increased significantly and was present predominantly in adipose tissue macrophages. The increase in adipose tissue A2AR expression in HFD-fed mice was accompanied with increased phosphorylation states of c-Jun N-terminal kinase 1 p46 and nuclear factor kappa B p65 and mRNA levels of interleukin (Il)-1beta, Il6, and tumor necrosis factor alpha. In A2AR-disrupted mice, HFD feeding induced significant increases in adipose tissue inflammation, indicated by enhanced proinflammatory signaling and increased proinflammatory cytokine expression, and adipose tissue insulin resistance, indicated by a decrease in insulin-stimulated Akt phosphorylation relative to those in wild-type mice. Lastly, A2AR disruption enhanced palmitate-induced macrophage proinflammatory activation. Taken together, these results suggest that A2AR plays a protective role in obesity-associated adipose tissue inflammation, which is attributable to, in large part, A2AR suppression of macrophage proinflammatory activation.