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High-temperature and high-pressure (HTHP)-treated diamonds have attracted attention all over the world due to their vivid colors. In order to explore a new method for the rapid and non-destructive identification of HTHP-treated diamonds, in this paper, five IaAB-type diamonds yielded in Russia were selected as the research object and treated with HTHP. The HTHP-treated diamonds were investigated by DiamondViewTM, cathodoluminescence, micro-infrared spectrometry (micro-IR), low-temperature photoluminescence (PL) spectrometry, and three-dimensional (3D) fluorescence spectrometry. The results show that under DiamondViewTM and cathode rays, the five samples were all non-phosphorescent with different luminous patterns, such as regular annular bands, multiple groups of intersecting linear stripes, or jagged stripes. In the low-temperature PL spectra, most HTHP-treated diamonds exhibited stronger luminescence peaks at 637 nm compared to 575 nm. But there were also exceptions, such as the purple-red sample showing the opposite luminescence peak. In the 3D fluorescence spectrum of the HTHP-treated diamonds, the fluorescence peak mainly appeared in the range of 440–450 nm, accompanied by a broad band of 350–500 nm and even longer wavelengths. Meanwhile, some samples also exhibited fluorescence peaks at longer wavelengths, such as 353 nm, 676 nm, and 665 nm. These results make it possible to identify HTHP-treated diamonds by using luminescence characteristics, providing a new method for the non-destructive and rapid detection of HTHP-treated diamonds. [ABSTRACT FROM AUTHOR]

ObjectiveTo relate serum insulin-like growth factor-1 (IGF-1) to risk of Alzheimer disease (AD) dementia and to brain volumes in a dementia-free community sample spanning middle and older ages.MethodsDementia-free Framingham participants from generation 1 (n = 789, age 79 ± 4 years, 64% women) and generation 2 (n = 2,793, age 61 ± 9 years, 55% women; total = 3,582, age 65 ± 11 years, 57% women) had serum IGF-1 measured in 1990-1994 and 1998-2001, respectively, and were followed prospectively for incident dementia and AD dementia. Brain MRI was obtained in stroke- and dementia-free survivors of both generations 1 (n = 186) and 2 (n = 1,867) during 1999-2005. Baseline IGF-1 was related to risk of incident dementia using Cox models and to total brain and hippocampal volumes using linear regression in multivariable models adjusted for age, sex, APOE ε4, plasma homocysteine, waist-hip ratio, and physical activity.ResultsMean IGF-1 levels were 144 ± 60 μg/L in generation 1 and 114 ± 37 μg/L in generation 2. We observed 279 cases of incident dementia (230 AD dementia) over a mean follow-up of 7.4 ± 3.1 years. Persons with IGF-1 in the lowest quartile had a 51% greater risk of AD dementia (hazard ratio = 1.51, 95% confidence interval: 1.14-2.00; p = 0.004). Among persons without dementia, higher IGF-1 levels were associated with greater total brain volumes (β/SD increment in IGF-1 was 0.55 ± 0.24, p = 0.025; and 0.26 ± 0.06, p < 0.001, for generations 1 and 2, respectively).ConclusionLower serum levels of IGF-1 are associated with an increased risk of developing AD dementia and higher levels with greater brain volumes even among middle-aged community-dwelling participants free of stroke and dementia. Higher levels of IGF-1 may protect against subclinical and clinical neurodegeneration.

In this work, a series of indole‐containing pyrazole‐carbohydrazide derivatives A1‐A25 were synthesized, and their biological activity on tubulin polymerization inhibition and mitotic catastrophe was evaluated. For introducing indole group to CA‐4 pattern, the carbohydrazide linker was used for the first time. As the top hit, A18 suggested notable antiproliferation efficacy and tubulin polymerization inhibitory activity. Inferring comparable antitubulin effect with the positive control Colchicine, A18 indicated obviously lower cyto‐toxicity. The cell scratch test showed that A18 could block the cell migration, while the confocal imaging depicted that A18 could induce the mitotic catastrophe via a Colchicine‐like approach. The docking simulation visualized the probable binding pattern of A18. With the information in this work, some new hints on modification might be involved in further tubulin‐related investigations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are flame-retardant chemicals that are added to many consumer products. Multiple animal studies have shown PBDEs to be thyroid hormone (TH) disruptors. Epidemiologic evidence of PBDE exposure associated with TH disruption has been inconclusive. OBJECTIVES: We used repeated measures to estimate associations between serum PBDE concentrations and THs in a North American adult cohort. METHODS: From 2010 to 2011, we collected ≤ 3 serum samples at approximately 6-month intervals from 52 healthy adult office workers from Boston, Massachusetts, for analysis of PBDE congeners and THs. RESULTS: The geometric mean sum concentrations of the most prevalent PBDE congeners (BDE-28, BDE-47, BDE-99, BDE-100, and BDE-153) were 22 ng/g lipid in winter 2010, 23 ng/g lipid in summer 2010, and 19 ng/g lipid in winter 2011. BDE-47 was the predominant congener. Based on a multivariable mixed regression model, we estimated that on average, a 1-ng/g serum increase in BDE-47 was associated with a 2.6-µg/dL decrease in total thyroxine ([T.sub.4]) (95% CI: -4.7, -0.35). Total [T.sub.4] was inversely associated with each PBDE congener. Serum concentrations of PBDEs were not strongly associated with total triiodothyronine ([T.sub.3]), free [T.sub.4], or thyroid-stimulating hormone (TSH). CONCLUSION: These results are consistent with those from animal studies showing that exposure to PBDEs is associated with a decrease in serum [T.sub.4]. Because the other TH concentrations did not appear to be associated with BDE exposures, our findings do not indicate effects on the pituitary-thyroid axis. Taken together, our findings suggest that PBDE exposure might decrease the binding of [T.sub.4] to serum [T.sub.4] binding proteins. http://dx.doi.org/10.1289/ehp.1509755, Introduction Polybrominated diphenyl ethers (PBDEs) have been used since the 1970s as additive flame retardants. The technical formulation pentabromodiphenyl ether (pentaBDE), composed of PBDE congeners containing three to six bromines, [...]

Environment-friendly approaches to directly convert atmospheric or flue gas CO2 to high-value chemicals is of great significance yet challenging. Protic ionic liquid catalysts with excellent properties are showing potential for the chemical fixation of CO2. In this work, a series of protic ionic liquids with different cationic structures have been synthesized, which bear hydrogen-bond interactions between unique N+–H bonds and the O atoms of epoxides and they are highly active catalytic sites. It was found that [AlTMG]Br shows obviously high/good catalytic activity for converting epoxides into cyclic carbonates with CO2 in the atmosphere or at even lower pressures (15% CO2 and 85% N2), outperforming the corresponding homogeneous catalyst analogues and superior to the known solvent- and metal-free catalytic systems. The results showed that under mild homogeneous catalytic reaction conditions, low-pressure CO2 can directly react with epoxides to give cyclic carbonates with excellent yields, without any co-catalysts such as metals, solvents and additives. In addition, the best catalyst [AlTMG]Br was proved to be robust with remarkable reusability, and displaying great potential for pollution reduction and industrial applications for the chemical conversion of atmospheric CO2. [ABSTRACT FROM AUTHOR]

Background: As an H3K27me3 demethylase and counteracts polycomb-mediated transcription repression, KDM6B has been implicated in the development and malignant progression in various types of cancers. However, its potential roles in esophageal squamous cell carcinoma (ESCC) have not been explored.Methods: The expression of KDM6B in human ESCC tissues and cell lines was examined using RT-qPCR, immunohistochemical staining and immunoblotting. The effects of KDM6B on the proliferation and metastasis of ESCC were examined using in vitro and in vivo functional tests. RNA-seq and ChIP-seq assay were used to demonstrate the molecular biological mechanism of KDM6B in ESCC.Results: We show that the expression level of KDM6B increased significantly in patients with lymph node metastasis. Furthermore, we confirmed that KDM6B knockdown reduces proliferation and metastasis of ESCC cells, while KDM6B overexpression has the opposite effects. Mechanistically, KDM6B regulates TNFA_SIGNALING_VIA_NFκB signalling pathways, and H3K27me3 binds to the promoter region of C/EBPβ, leading to the promotion of C/EBPβ transcription. Besides, we show that GSK-J4, a chemical inhibitor of KDM6B, markedly inhibits proliferation and metastasis of ESCC cells.Conclusions: The present study demonstrated that KDM6B promotes ESCC progression by increasing the transcriptional activity of C/EBPβ depending on its H3K27 demethylase activity. [ABSTRACT FROM AUTHOR]