Herein, trifluoromethylation has proven to be an effective strategy for ultra-narrow band-gap NFAs. A PCE of 15.59% is achieved from BTIC-CF 3 -g-based devices, which is the highest value in reported ultra-narrow band-gap acceptors. A ternary device with 16.50% efficiency is also obtained, resulting from its red-shifted absorption. Meanwhile, the single-crystal structure of BTIC-CF 3 -g has been successfully presented, which gives a deep understanding of the solid-state molecular packings in these highly efficient acceptors.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by both a chronic inflammation and tissue remodelling; as indicated by extracellular matrix protein deposition, basement membrane thickening, goblet cell hyperplasia and subepithelial edema, with reduced vessels and glands. Although remodelling is generally considered to be consequence of persistent inflammation, the chronological order and relationship between inflammation and remodelling in polyp development is still not clear. The aim of our study was therefore to investigate the pathological features prevalent in the development of nasal polyps and to elucidate the chronological order and relationship between inflammation and remodelling, by comparing specific markers of inflammation and remodelling in early stage nasal polyps confined to the middle turbinate (refer to as middle turbinate CRSwNP) obtained from 5 CRSwNP patients with bilateral polyposis, mature ethmoidal polyps from 6 CRSwNP patients, and normal nasal mucosal tissue from 6 control subjects. Middle turbinate CRSwNP demonstrated significantly more severe epithelial loss compared to mature ethmoidal polyps and normal nasal mucosa. The epithelial cell junction molecules E-cadherin, ZO-1 and occludin were also expressed in significantly lower amounts in mature ethmoidal polyps compared to healthy mucosa. Middle turbinate CRSwNP were further characterized by significantly increased numbers of subepithelial eosinophils and M2 type macrophages, with a distinct lack of collagen and deposition of fibronectin in polyp part. In contrast, the turbinate area of the middle turbinate CRSwNP was characterized by an increase in TGF-β activated myofibroblasts expressing α-SMA and vimentin, an increase in the number of pSmad2 positive cells, as well as increased deposition of collagen. These findings suggest a complex network of processes in the formation of CRSwNP; including gross epithelial damage and repair reactions, eosinophil and macrophage cell infiltration, and tissue remodelling. Furthermore, remodelling appears to occur in parallel, rather than subsequent to inflammation.

Background:The utility of mesenchymal stem cells (MSCs) in the treatment of acute lung injury (ALI) is dependent on their ability to reach the sites of tissue damage. Results: Transduction of CXCR4 conferred efficient mobilization of MSCs. Conclusion: CXCR4 overexpression in MSCs facilitated treatment of ALI. Significance: Overexpression of CXCR4 may improve the therapeutic potential of MSCs for the treatment of diseases with tissue damage.

No abstract

No abstract

Luteolin, a flavonoid abundant in plants worldwide, demonstrates a spectrum of biological activities. This study is aimed at evaluating its inhibiting effects on inflammatory responses in vivo. We investigated the anti-inflammatory activity of luteolin in acute and chronic models in mice. We found that oral administration of luteolin (10 and 50 mg/kg) efficiently suppressed paw edema when induced by injecting carrageenan, and a similar tendency was also observed in the cotton pellet granuloma test. In the air pouch test, luteolin markedly reduced the number of infiltrated leukocytes and the elevated level of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) in the exudate. The results derived from the whole blood assay for cyclooxygenase (COX) and from the reverse transcription-polymerase chain reaction (RT-PCR) assay indicate that luteolin may be a potent selective inhibitor of cyclooxygenase-2 (COX-2) and that the inhibition is attributable to its down-regulation of the mRNA expression of COX-2 in inflammatory responses.

No abstract

Oxymatrine (OMT), an alkaloid derived from the root of the Sophora flavescens, has been reported to possess a significant effect on relieving UC owing to its anti-inflammatory property. But the other therapeutic mechanism of OMT remains unclear. Recent studies have found, PI3K/AKT signaling pathway is involved in the pathogenesis of UC by pro-inflammatory effects and activating T cells. Moreover, PI3K/AKT pathway is one of the most important pathways for regulating cell apoptosis. Thus, we aim to explore whether OMT protects against UC by targeting PI3K/AKT pathway. We established the UC mice models, using LY294002 (a specific inhibitor of PI3K/AKT) as a positive control, to observe the effect of low, medium and high dose of OMT on UC and its influence on PI3K/AKT signaling pathway. Our data indicated that OMT can significantly ameliorate UC through anti-inflammatory, pro-apoptotic, down-regulating the differentiation of Th1 and Th17 cells via PI3K/AKT pathway. This study reveals that PI3K/AKT signaling pathway is a potential mechanism of OMT-induced UC remission and suggests that OMT is a promising therapeutic agent for the treatment of UC.