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An overview of Sun–Sky Radiometer Observation Network (SONET) measurements in China is presented. Based on observations at 16 distributed SONET sites in China, atmospheric aerosol parameters are acquired via standardization processes of operational measurement, maintenance, calibration, inversion, and quality control implemented since 2010. A climatology study is performed focusing on total columnar atmospheric aerosol characteristics, including optical (aerosol optical depth, ÅngstrÖm exponent, fine-mode fraction, single-scattering albedo), physical (volume particle size distribution), chemical composition (black carbon; brown carbon; fine-mode scattering component, coarse-mode component; and aerosol water), and radiative properties (aerosol radiative forcing and efficiency). Data analyses show that aerosol optical depth is low in the west but high in the east of China. Aerosol composition also shows significant spatial and temporal variations, leading to noticeable diversities in optical and physical property patterns. In west and north China, aerosols are generally affected by dust particles, while monsoon climate and human activities impose remarkable influences on aerosols in east and south China. Aerosols in China exhibit strong light-scattering capability and result in significant radiative cooling effects.

Roadside air pollution is one of the serious air pollution problems in urban areas. Even though roadside air pollution has been reported to cause adverse human health impacts, the spatial distribution of roadside air pollution in a large urban agglomeration has yet to be fully assessed. This study aimed to analyse roadside fine particulate matter (PM2.5) pollution and the population exposure in 11 cities in the Pearl River Delta (PRD) region of China. We developed satellite-retrieval algorithms with dark target method, vector support machine model and random forest model to retrieve the spatial distribution of PM2.5 at an ultra-high-spatial-resolution (30 m) based on 30 m Landsat-8 L1 data. Our results show that the retrieved PM2.5 had a promising consistency with PM2.5 measurements at general and roadside stations (R2 = 0.86; RMSE = 7.72 µg m−3). Moreover, on average, the roadside PM2.5 in Dongguan, Foshan, and Guangzhou was relatively higher (up to 107.60 µg m−3) whereas that in Hong Kong was relatively lower (up to 30.40 µg m−3). The roadside PM2.5 pollution typically occurred in roads for motorized vehicles i.e. motorway, trunk, primary and secondary road. Our results also show that roadside PM2.5 was up to 17% higher in holidays than in workdays in all the PRD cities except Hong Kong that showed roadside PM2.5 higher in workdays than in holidays. The population-weighted PM2.5 decreased with increasing distances from roads in every PRD city, and population-weighted PM2.5 was estimated to be up to 22% higher at roadsides than at distances of 1500 m away from roads. This study pinpointed the seriousness of roadside air pollution in the PRD region.

Breast cancer is the most common type of cancer among women worldwide, and metastasis represents the most devastating stage of the disease. Recent studies have revealed that microRNAs (miRNA) have critical roles to regulate cancer cell invasion and metastasis. Here we present evidence to show the role of miR-182 in breast cancer metastasis. miR-182 is upregulated in the malignant cell line variants of both human MCF10 and mouse 4T1 series. Ectopic expression of miR-182 enhanced breast cancer cell motility and invasiveness, whereas miR-182 inhibition resulted in opposite changes. In nude mice, miR-182 led to increased pulmonary colonization of cancer cells. We further demonstrated that miR-182 directly targets MIM (Missing in Metastasis), which suppresses metastasis by inhibiting ras homolog family member A (RhoA) activity and stress fiber formation in breast cancer cells. Restoring MIM expression completely blocked the pro-metastasis function of miR-182, while RhoA inhibition reversed the phenotypes of both miR-182 overexpression and MIM knockdown. In breast tumor samples, miR-182 induction is linked to downregulation of MIM , RhoA activation and poor prognosis. Hence, our data delineates the molecular pathway by which miR-182 promotes breast cancer invasion and metastasis, and may have important implication for the treatment of metastatic cancers.

Economists have long argued that a fishery that maximizes its economic potential usually will also satisfy its conservation objectives. Recently, maximum economic yield (MEY) has been identified as a primary management objective for Australian fisheries and is under consideration elsewhere. However, first attempts at estimating MEY as an actual management target for a real fishery (rather than a conceptual or theoretical exercise) have highlighted some substantial complexities generally unconsidered by fisheries economists. Here, we highlight some of the main issues encountered in our experience and their implications for estimating and transitioning to MEY. Using a bioeconomic model of an Australian fishery for which MEY is the management target, we note that unconstrained optimization may result in effort trajectories that would not be acceptable to industry or managers. Different assumptions regarding appropriate constraints result in different outcomes, each of which may be considered a valid MEY. Similarly, alternative treatments of prices and costs may result in differing estimates of MEY and their associated effort trajectories. To develop an implementable management strategy in an adaptive management framework, a set of assumptions must be agreed among scientists, economists, and industry and managers, indicating that operationalizing MEY is not simply a matter of estimating the numbers but requires strong industry commitment and involvement.

The purpose of this study was to investigate the current situation of the \"Internet + nursing service\" in Guizhou Province, China, from the perspective of service providers, and to analyze its influencing factors to provide references for further promoting the implementation of related services in the province. In this study, a questionnaire survey was conducted among nurses from 55 hospitals in Guizhou Province, China, through convenience sampling from September to December 2023. The findings showed that 85.45% of the hospitals had not yet carried out the \"Internet + nursing service\", 97.87% of the nursing staff expressed their willingness to participate in the service, but only 14.55% of the nursing staff actually participated in the service at their hospital. The participation rate of specialist nurses was just 50.00%. The findings also revealed the main issues of current concern, which included the support of relevant policy documents, the security risks of on-site services, and the pricing standards of service projects. Research data indicate that while most hospitals have not implemented the service, there is a high willingness among nursing staff to participate, yet the actual participation rate is low. The participation rate of specialized nurses is also low, and there are issues related to policy support, safety risks, and pricing standards. It is recommended that Guizhou Province strengthen policy guidance to promote the implementation of \"Internet + nursing services\". Hospitals at all levels should focus on the training of specialized nursing talents, enhance service promotion, deepen personnel awareness, and optimize the home service system to meet patients' nursing needs.

The c-Jun NH2-terminal kinase (JNK) pathway represents one subgroup of MAP kinases that are activated primarily by cytokines and exposure to environmental stress. Autophagy is a protein-degradation system characterized by the formation of double-membrane vacuoles termed autophagosomes. Autophagy-related gene beclin 1 plays a key role in autophagosome formation. However, the relationships between activation of JNK pathway, autophagy induction and Beclin 1 expression remain elusive. In this study, we used human cancer cell lines CNE2 and Hep3B to investigate the role of JNK-mediated Beclin 1 expression in ceramide-induced autophagic cell death. Ceramide-treated cells exhibited the characteristics of autophagy (that is, acidic vesicular organelle formation and the LC3-II generation). JNK was activated in these two cell lines exposed to ceramide and the phosphorylation of c-Jun also increased. In the meantime, we found that ceramide upregulated Beclin 1 expression in cancer cells. The upregulation of Beclin 1 expression could be blocked by SP600125 (a specific inhibitor of JNK) or a small interfering RNA (siRNA) directed against JNK1/2 or c-Jun. Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was involved in the regulation of beclin 1 transcription in response to ceramide treatment. In addition, inhibition of JNK activity by SP600125 could inhibit autophagy induction by ceramide. Furthermore, Beclin 1 knockdown by siRNA also inhibited ceramide-mediated autophagic cell death. JNK-mediated Beclin 1 expression was also observed in topotecan-induced autophagy. These data suggest that activation of JNK pathway can mediate Beclin 1 expression, which plays a key role in autophagic cell death in cancer cells.

We have designed and characterized a new inlet and aerodynamic lens for the Aerodyne aerosol mass spectrometer (AMS) that transmits particles between 80 nm and more than 3 μm in vacuum aerodynamic diameter. The design of the inlet and lens was optimized with computational fluid dynamics (CFD) modeling of particle trajectories. Major changes include a redesigned critical orifice holder and valve assembly, addition of a relaxation chamber behind the critical orifice, and a higher lens operating pressure. The transmission efficiency of the new inlet and lens was characterized experimentally with size-selected particles. Experimental measurements are in good agreement with the calculated transmission efficiency.

This article studies the aerodynamic performance of a novel bypass shock-induced thrust vector nozzle. An arc-shaped bypass is innovatively designed to optimize nozzle performance and equips a variable shrinkage part. The nozzle performance is investigated numerically under diverse shrinkage area ratios. Computational results indicate that both geometry and friction choking have important effects on the nozzle performance. Normally, in the case of without any bypass shrinkage, the flow choking occurs at the bypass outlet. Very small bypass shrinkage is unable to change the flow choking location. The bypass geometry choking comes up at its throat as the shrinkage area ratio of the bypass reaches 0.06. According to computational results, the vectoring angle diminishes with the increasing shrinkage area ratio of the bypass, thrust force ratio, thrust efficiency, specific impulse ratio, and coefficient of discharge increase. As the NPR enlarges, the deflection angle and thrust efficiency decrease, and the thrust force ratio increases.

Ding P, Jin Q, Chen X, et al. Int J Nanomedicine. 2019;14:7533-7548. At the author's request, we, the Editor and Publisher of the journal International Journal of Nanomedicine have retracted the following article. During a recent review of the article, the authors identified an error in the use of the transmission electron microscopy (TEM) images for Figure 2A, which could potentially confuse readers. After discussing this issue with the editorial team and providing the original data, the authors agreed that the potential confusion could not be adequately addressed through simple correction. Although the results of TEM were independent of the in vivo and in vitro experiments and did not affect the effectiveness of the nanovaccines in the study, they could have compromised the accuracy and reliability of the findings. The authors apologize for the errors in the article and appreciate the readership's understanding in this matter. However, the authors remain confident in the results and conclusions of this study and with the original material well preserved, hope to submit a revised version of the article for republication following reevaluation. The journal has acknowledged this. In the meantime, in the interest of upholding research integrity and ensuring the trustworthiness of the scientific record, the authors believe that it is necessary to retract the article. We, the Editor and Publisher, understand and agreed with this decision. We have been informed in our decision-making by our editorial policies and COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as \"Retracted\".

Iron oxide nanoparticles coated with paclitaxel (IONP@PTX) are frequently applied to various tumor types. However, inhibitory effect and possible mechanism of IONP@ PTX on non-small-cell lung cancer (NSCLC) remain unclear. This work aimed to assess inhibitory effects and potential mechanisms of IONP@PTX on lung cancer A549 cells and further explore the nanomedicine delivery systems for applications in cancer therapies. Morphology features and qualities of IONP@PTX were directly assessed. After treatment of A549 cells with either PTX or IONP@PTX, cell viability and apoptosis were separately detected by CCK‑8 assay and flow cytometry. In addition, intracellular iron ion, lipid peroxidation (LPD) and reactive oxygen species (ROS) were identified by using an iron colorimetric assay kit, DCFH-DA and C11-BODIPY fluorescent probe, respectively. Moreover, the expression levels of autophagy-, ferroptosis-, and apoptosis-related proteins were measured by Western blot. The synthesized IONP@PTX had a core particle size of about 10 nm and a hydrated particle size of 31.01±2.47 nm. In comparison with PTX, IONP@PTX had a stronger anti-tumor effect on A549 cells, with considerably higher levels of ROS, LPD, and total iron ion concentration ( <0.05). Likewise, IONP@PTX markedly reduced the expression levels of GPX4, FTH, and SLC7A11 proteins whereas obviously increased the expression levels of LC3II/I and ACSL4 proteins ( <0.05). Furthermore, the inhibitory effects of both PTX and IONP@PTX on A549 cells could be evidently reversed by additional 3-methyladenine (3-MA) or ferrostatin-1. Interestingly, the apoptosis rates of A549 cells, together with the expression level of pro-apoptotic protein Cleaved caspase-3, were significantly higher in the IONP@PTX group than those in the control and PTX groups ( <0.05). IONP@PTX inhibits the proliferation of human lung cancer A549 cells by enhancing autophagy-dependent ferroptosis and apoptosis pathways.