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The plant-derived polyphenol curcumin alleviates the inflammatory and metabolic effects of obesity, in part, by reducing adipose tissue inflammation. We hypothesized that the benefits of curcumin supplementation on diet-induced obesity and systemic inflammation in mice occur through downregulation of white adipose tissue (WAT) inflammation. The hypothesis was tested in adipose tissue from high-fat diet-induced obese mice supplemented with or without curcumin and in 3T3-L1 adipocytes treated with or without curcumin. Male B6 mice were fed a high-fat diet (HFD, 45% kcal fat) with or without 0.4% (w/w) curcumin supplementation (HFC). Metabolic changes in these mice have been previously reported. Here, we determined the serum levels of the curcumin metabolites tetrahydrocurcumin (THC) and curcumin-O-glucuronide (COG) using mass spectrometry. Moreover, we determined interleukin 6 (IL-6) levels and proteomic changes in LPS-stimulated 3T3-L1 adipocytes treated with or without curcumin by using immunoassays and mass spectrometry, respectively, to gain further insight into any altered processes. We detected both curcumin metabolites, THC and COG, in serum samples from the curcumin-fed mice. Both curcumin and its metabolites reduced LPS-induced adipocyte IL-6 secretion and mRNA levels. Proteomic analyses indicated that curcumin upregulated EIF2 and mTOR signaling pathways. Overall, curcumin exerted anti-inflammatory effects in adipocytes, in part by reducing IL-6, and these effects may be linked to the upregulation of the mTOR signaling pathway, warranting additional mechanistic studies on the effects of curcumin and its metabolites on metabolic health. [ABSTRACT FROM AUTHOR]

Lead sulfide colloidal quantum dots (PbS CQDs) are promising optoelectronic materials due to their unique properties, such as tunable band gap and strong absorption, which are of immense interest for application in photodetectors and solar cells. However, the tunable band gap of PbS CQDs would only cover visible short-wave infrared; the ability to detect longer wavelengths, such as mid- and long-wave infrared, is limited because they are restricted by the band gap of the bulk material. In this paper, a novel photodetector based on the synergistic effect of PbS CQDs and bismuth telluride (Bi2Te3) was developed for the detection of a mid-wave infrared band at room temperature. The device demonstrated good performance in the visible-near infrared band (i.e., between 660 and 850 nm) with detectivity of 1.6 × 1010 Jones at room temperature. It also exhibited photoelectric response in the mid-wave infrared band (i.e., between 4.6 and 5.1 μm). The facile fabrication process and excellent performance (with a response of up to 5.1 μm) of the hybrid Bi2Te3/PbS CQDS photodetector are highly attractive for many important applications that require high sensitivity and broadband light detection. [ABSTRACT FROM AUTHOR]

Background: Although the understanding of resistance to oxaliplatin (OXA) chemotherapy in colorectal cancer (CRC) has been sought for many years, drug tolerance remains a major challenge for cancer therapy. Revealing the molecular mechanism of OXA resistance could help to explain the poor prognosis of patients. Methods: Gene expression omnibus (GEO) database was searched, GSE83129, which contains RNA profiling in metastatic CRC patients treated first‐line with OXA, was chosen for the following analysis. Differential expressed genes (DEGs) between the adenocarcinoma and adjacent_normal team, respectively, in the OXA responders and no‐responders were analyzed. The Gene Ontology (GO) and hub genes in the protein–protein interaction (PPI) network were used for the molecular mechanism of OXA resistance. Tumor‐related databases were used for the clinical relevance of the structural maintenance of chromosomes 5 (SMC5) in CRC. The in vitro assays were used to detect the molecular function of SMC5 in CRC cells. Quantitative real‐time PCR (qRT‐PCR) and western blot were used to detect the expression of the structural maintenance of chromosomes 5/6 (SMC5/6) complex components upon OXA and raltitrexed (RTX) treatment. CCK‐8 was used to detect the cell viability of cells with different treatment. Results: SMC5 was downregulated in CRC tissues of OXA no‐response patients. Lower expression of SMC5 was correlated with a poor prognosis in CRC patients, improved this gene expression, inhibited the CRC cell growth and invasion in vitro. Furthermore, SMC5 was downregulated upon OXA treatment in CRC cells, while RTX would reverse its expression, and the combination of these two drugs restored the SMC5 level to the normal situation. Finally, RTX treatment enhanced the OXA cytotoxicity. Conclusion: SMC5 is a tumor suppressor, that low expression of this gene is benefit for the development of CRC. Combination treatment with RTX and OXA may be more suitable for those OXA no‐responders with lower SMC5. [ABSTRACT FROM AUTHOR]