[Source Apportionment and Heath Risk Quantification of Heavy Metals in PM2.5 in Yangzhou, China].

Recently, a new method combining positive matrix factorization (PMF) and heavy metal health risk (HMHR) assessment was proposed to apportion sources of heavy metals in ambient particulate matter and the associated heavy metal cancer health risk (HMCR), which has been applied to data collected in Yangzhou, China. The annual average concentrations of six measured heavy metals were Pb (64.4 ng·m-3), followed by Cr (25.24 ng·m-3), As (6.36 ng·m-3), Ni (5.36 ng·m-3), Cd (3.34 ng·m-3), and Co (1.21 ng·m-3). The results showed that the major sources of PM2.5 were secondary sources (37.7%), followed by coal combustion (19.4%), resuspended dust (17.5%), vehicle emissions (16.9%), construction dust (5.2%), and industrial emissions (3.4%). As was primarily emitted from coal combustion, vehicle emissions, and resuspended dust. Co originated from industry emissions. Pb was mainly emitted from coal combustion. Ni and Cd were from industrial emissions. The major sources that contributed to HMCR were resuspended dust, coal combustion, vehicle emissions, industry emissions, and construction dust. The high contributions of resuspended dust and coal to HMCR were likely due to the high heavy metals concentrations in coal and the resuspended dust profile as well as high emissions of these sources.

PIK3CD induces cell growth and invasion by activating AKT/GSK-3ß/ß-catenin signaling in colorectal cancer.

The catalytic subunit p110δ of phosphoinositide 3-kinase (PI3K) encoded by PIK3CD has been implicated in some human solid tumors. However, its roles in colorectal cancer (CRC) remain largely unknown. Here we found that PIK3CD was overexpressed in colon cancer tissues and CRC cell lines and was an independent predictor for overall survival (OS) of patients with colon cancer. The ectopic overexpression of PIK3CD significantly promoted CRC cell growth, migration and invasion in vitro and tumor growth in vivo. In contrast, inhibition of PIK3CD by specific small-interfering RNA or idelalisib dramatically suppressed CRC cell growth, migration and invasion in vitro and tumor growth in vivo. Moreover, PIK3CD overexpression increased AKT activity, nuclear translocation of ß-catenin and T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional activity and decreased glycogen synthase kinase 3ß (GSK-3ß) activity, whereas PIK3CD inhibition exhibited the opposite effects. Furthermore, PIK3CD-mediated cell growth, migration and invasion were reversed by blockade of AKT signaling or depletion of ß-catenin. In addition, PIK3CD expression in colon cancer tissues positively correlated with ß-catenin abnormal expression, which was an independent predictor for OS of colon cancer patients. Taken together, our findings demonstrate that PIK3CD is an independent prognostic factor in CRC and that PIK3CD induces CRC cell growth, migration and invasion by activating AKT/GSK-3ß/ß-catenin signaling, suggesting that PIK3CD might be a novel prognostic biomarker and a potential therapeutic target for CRC.

Interval colorectal cancer: a challenging field in colorectal cancer.

Accumulated evidence has shown that colonoscopy may not be a perfect tool in screening and reducing the incidence of the colorectal cancer (CRC), because interval CRC (I-CRC), a specific subgroup of CRCs, has been challenging the traditional detection technology in recent years. I-CRC is accounting for an increasing proportion in CRCs. However, the effective procedures to prevent and supervise I-CRC need to be explored. In this review, we summarized the incidence, causes, risk factors, characteristics and management of I-CRC. It would promote the awareness of the special value in the education and training for the gastroenterologists, which plays an important role in conquering CRC.

The sex pheromone of a globally invasive honey bee predator, the Asian eusocial hornet, Vespa velutina.

The Asian hornet, Vespa velutina, is an invasive, globally-distributed predator of European honey bees and other insects. To better under its reproductive biology and to find a specific, effective, and low-impact control method for this species, we identified and tested the key compounds in V. velutina sex pheromone. Virgin gynes (reproductive females) produced this sex pheromone in the sixth intersegmental sternal glands of their abdomens. The active compounds were 4-oxo-octanoic acid (4-OOA, 10.4 µg bee-1) and 4-oxo-decanoic acid (4-ODA, 13.3 µg bee-1) at a 0.78 ratio of 4-OOA/4-ODA. We synthesized these compounds and showed that male antennae were highly sensitive to them. Moreover, males were only strongly attracted to a 4-OOA/4-ODA blend at the natural ratio produced by gynes. These results provide the first demonstration of an effective way to lure V. velutina males, and the first chemical identification of a sex pheromone in the eusocial hornets.

Poison and alarm: the Asian hornet Vespa velutina uses sting venom volatiles as an alarm pheromone.

In colonial organisms, alarm pheromones can provide a key fitness advantage by enhancing colony defence and warning of danger. Learning which species use alarm pheromone and the key compounds involved therefore enhances our understanding of how this important signal has evolved. However, our knowledge of alarm pheromones is more limited in the social wasps and hornets compared with the social bees and ants. Vespa velutina is an economically important and widespread hornet predator that attacks honey bees and humans. This species is native to Asia and has now invaded Europe. Despite growing interest in V. velutina, it was unknown whether it possessed an alarm pheromone. We show that these hornets use sting venom as an alarm pheromone. Sting venom volatiles were strongly attractive to hornet workers and triggered attacks. Two major venom fractions, consisting of monoketones and diketones, also elicited attack. We used gas chromatography coupled to electroantennographic detection (GC-EAD) to isolate 13 known and 3 unknown aliphatic ketones and alcohols in venom that elicited conspicuous hornet antennal activity. Two of the unknown compounds may be an undecen-2-one and an undecene-2,10-dinone. Three major compounds (heptan-2-one, nonan-2-one and undecan-2-one) triggered attacks, but only nonan-2-one did so at biologically relevant levels (10 hornet equivalents). Nonan-2-one thus deserves particular attention. However, the key alarm releasers for V. velutina remain to be identified. Such identification will help to illuminate the evolution and function of alarm compounds in hornets.

MicroRNA-379-5p inhibits tumor invasion and metastasis by targeting FAK/AKT signaling in hepatocellular carcinoma.

Some microRNAs (miRNAs) have been implicated in hepatocellular carcinoma (HCC) development and progression. However, the roles and mechanisms of several miRNAs in HCC remain poorly understood. Here, we report that miR-379-5p, which is down-regulated in HCC tissues and cell lines, is associated with advanced TNM stage and metastasis in HCC. The ectopic overexpression of miR-379-5p inhibited HCC cell migration, invasion, epithelial-to-mesenchymal transition (EMT) and metastasis both in vitro and in vivo. Conversely, miR-379 knockdown increased migration, invasion and EMT in HCC cells. Moreover, miR-379-5p exerted this function by directly targeting focal adhesion kinase (FAK) 3'-UTR and repressing FAK expression, thus leading to suppression of AKT signaling. Furthermore, the tumor suppressive effects of miR-379-5p in HCC cells were reversed by activating AKT signaling or restoring FAK expression. In clinical samples of HCC, miR-379-5p negatively correlated with FAK, which was up-regulated in HCC. Taken together, our findings highlight the important role of miR-379-5p in regulating the EMT and metastasis of HCC by targeting FAK/AKT signaling, suggesting that miR-379-5p may represent a novel potential therapeutic target and prognostic marker for HCC.

[Bioimmunological characteristics of mature or immature murine dendritic cells].

OBJECTIVE: To explore the biological characteristics of immature and mature murine bone marrow-derived dendritic cells (DCs). METHODS: The murine bone marrow cells were cultured and induced in vitro into immature DCs (imDCs). Then ImDCs were incubated with TNF (tumor necrosis factor)-α to obtain mature DCs (mDCs). The DCs were purified by murine CD11c microbeads. The morphologies of DCs were observed by electron microscopy (EM). Such surface markers as MHC-II, CD80 and CD86 were tested by flow cytometry (FCM). The proliferation capacity of allogeneic T cells stimulated by DCs was examined by Cell Counting Kit-8 (CCK-8) in mixed lymphocyte reaction (MLR). The expressions of cell factors in mRNA of DCs were tested by real-time polymerase chain reaction (QPCR). The cytokines in supernatant were measured by ELISA (enzyme-linked immunosorbent assay). RESULTS: As compared with mDCs, fewer, shorter spines and more phagocytic vesicles and lysosome were observed in imDCs under EM. The expressions of cell surface molecules in imDCs were significantly lower than those of mDC by FCM, [MHC-II (27.2%) vs (97.7%); CD80 (27.6%) vs (97.2%); CD86 (29.5%) vs (96.4%)]. In MLR, the capacity of same-reaction ratio imDCs group for stimulating the proliferation of T-cells was remarkably lower than that of mDCs group,[1:5 (1.63 ± 0.04) vs (2.21 ± 0.09); 1:10 (1.50 ± 0.08) vs (1.92 ± 0.02); 1:20 (1.28 ± 0.07) vs (1.64 ± 0.01); 1:40 (1.19 ± 0.04) vs (1.45 ± 0.06), P < 0.01]. In imDCs, the relative mRNA expressions of IL12p35 (0.66 ± 0.13), IL12p40 (0.57 ± 0.10) and IFN-γ (0.74 ± 0.08) were lower than those of mDCs (1.00 ± 0.00), (P < 0.05), but the expression of TGF-ß (1.35 ± 0.09) was higher than that of mDCs by QPCR (1.00 ± 0.00), (P < 0.05). The expressions of IL12p70 and IFN-γ in supernatants from imDCs were lower than those of mDCs [IL12p70: (6 ± 4) vs (120 ± 22); IFN-γ: (56 ± 15) vs (90 ± 15), P < 0.05] while the expression of TGF (transforming growth factor)-ß was higher than that of mDCs by ELISA [TGF-ß: (176 ± 23) vs (55 ± 18), P < 0.05]. CONCLUSION: ImDCs can induce anergic T cells and immune tolerance through a down-regulation of co-stimulatory molecules, MHC-II and Th1 cytokines and an up-regulation of Th2 cytokine (TGF-ß). And MDCs may activate naive T cells and stimulate immune responses by an up-regulation of co-stimulatory molecules, MHC-II and Th1 cytokines.