Impact of digital empowerment on labor employment in manufacturing enterprises: Evidence from China.

Many studies have examined the influence of digital technologies, such as robots and artificial intelligence, on enterprise labor, but few have investigated the underlying mechanisms and impact paths of digital empowerment on labor employment. Therefore, this study uses data on manufacturing enterprises listed on China's Shanghai and Shenzhen A-share markets from 2011 to 2020, and applies a panel fixed effect model to test the relationship between digital empowerment and labor employment, and the mechanisms underlying this relationship. We find that digital empowerment increases labor employment. However, the effects are heterogeneous: firms with better corporate governance, more competitive industry, and less favorable regional business environments are more motivated to optimize the structure of their labor resources. Through robustness test and mediation effect model test, we find that digital empowerment can improve enterprise human capital by increasing economies scale and managerial efficiency, especially the employment of R&D and innovation personnel and management personnel; it can also affect the amount of human capital by improving total factor productivity.

Integrated Nursing and Psychological Intervention for Tuberculosis Complicated by Lung Cancer: Clinical Efficacy.

Context: The incidence of tuberculosis (TB) complicated by lung cancer has been increasing yearly worldwide. The overlapping effects of these two diseases leads to difficulties in clinical treatment and care. Single-care modalities fail to meet the clinical-care requirements of these complex diseases for both psychological and physical treatment. Objective: The study intended to evaluate the clinical efficacy of integrated nursing plus a psychological intervention for patients with TB complicated by lung cancer. Design: The research team conducted a randomized controlled study. Setting: The study took place at the Affiliated Hospital of Hebei University in Baoding, Hebei, China. Participants: Participants were 60 patients with pulmonary TB complicated by lung cancer who received treatment at the hospital between January 2022 and December 2022. Interventions: The research team randomly assigned participants to one of two groups, each with 30 participants: (1) the control group, who received integrated nursing and (2) the intervention group who received integrated nursing plus a psychological intervention. Outcome Measures: The research team evaluated: (1) short-term clinical efficacy; (2) quality of life, using the Medical Outcomes Study's (MOS') 36-item Short-form Health Survey (SF-36); (3) levels of anxiety and depression, using the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), respectively; and (4) nursing satisfaction. Results: No significant differences existed between the groups in demographic or clinical characteristics at baseline (P > .05). Compared to the control group, the intervention group's; (1) short-term clinical efficacy was significantly higher (P = .035); (2) scores on the SF-36 were significantly higher (all P < .001; (3) scores on the SAS and SDS were significantly lower (both P < .001); and (4) nursing satisfaction was significantly higher (P = .000). Conclusions: Integrated nursing plus psychological intervention can improve the quality of life of patients with TB complicated by lung cancer, alleviate their negative emotions, and enhance nursing satisfaction, thereby promoting patients' recoveries.

A new integrated framework for the identification of potential virus-drug associations.

Introduction: With the increasingly serious problem of antiviral drug resistance, drug repurposing offers a time-efficient and cost-effective way to find potential therapeutic agents for disease. Computational models have the ability to quickly predict potential reusable drug candidates to treat diseases. Methods: In this study, two matrix decomposition-based methods, i.e., Matrix Decomposition with Heterogeneous Graph Inference (MDHGI) and Bounded Nuclear Norm Regularization (BNNR), were integrated to predict anti-viral drugs. Moreover, global leave-one-out cross-validation (LOOCV), local LOOCV, and 5-fold cross-validation were implemented to evaluate the performance of the proposed model based on datasets of DrugVirus that consist of 933 known associations between 175 drugs and 95 viruses. Results: The results showed that the area under the receiver operating characteristics curve (AUC) of global LOOCV and local LOOCV are 0.9035 and 0.8786, respectively. The average AUC and the standard deviation of the 5-fold cross-validation for DrugVirus datasets are 0.8856 ± 0.0032. We further implemented cross-validation based on MDAD and aBiofilm, respectively, to evaluate the performance of the model. In particle, MDAD (aBiofilm) dataset contains 2,470 (2,884) known associations between 1,373 (1,470) drugs and 173 (140) microbes. In addition, two types of case studies were carried out further to verify the effectiveness of the model based on the DrugVirus and MDAD datasets. The results of the case studies supported the effectiveness of MHBVDA in identifying potential virus-drug associations as well as predicting potential drugs for new microbes.

Neighborhood-based inference and restricted Boltzmann machine for small molecule-miRNA associations prediction.

Background: A growing number of experiments have shown that microRNAs (miRNAs) can be used as target of small molecules (SMs) to regulate gene expression for treating diseases. Therefore, identifying SM-related miRNAs is helpful for the treatment of diseases in the domain of medical investigation. Methods: This article presents a new computational model, called NIRBMSMMA (neighborhood-based inference (NI) and restricted Boltzmann machine (RBM)), which we developed to identify potential small molecule-miRNA associations (NIRBMSMMA). First, grounded on known SM-miRNAs associations, SM similarity and miRNA similarity, NI was used to predict score of an unknown SM-miRNA pair by reckoning the sum of known associations between neighbors of the SM (miRNA) and the miRNA (SM). Second, utilizing a two-layered generative stochastic artificial neural network, RBM was used to predict SM-miRNA association by learning potential probability distribution from known SM-miRNA associations. At last, an ensemble learning model was conducted to combine NI and RBM for identifying potential SM-miRNA associations. Results: Furthermore, we conducted global leave one out cross validation (LOOCV), miRNA-fixed LOOCV, SM-fixed LOOCV and five-fold cross validation to assess performance of NIRBMSMMA based on three datasets. Results showed that NIRBMSMMA obtained areas under the curve (AUC) of 0.9912, 0.9875, 0.8376 and 0.9898 ± 0.0009 under global LOOCV, miRNA-fixed LOOCV, SM-fixed LOOCV and five-fold cross validation based on dataset 1, respectively. For dataset 2, the AUCs are 0.8645, 0.8720, 0.7066 and 0.8547 ± 0.0046 in turn. For dataset 3, the AUCs are 0.9884, 0.9802, 0.8239 and 0.9870 ± 0.0015 in turn. Also, we conducted case studies to further assess the predictive performance of NIRBMSMMA. These results illustrated the proposed model is a useful tool in predicting potential SM-miRNA associations.

Influencing pathways and toxicity changes of pre-ozonation on carcinogenic NDEA formation from greenhouse gas adsorbent DEAPA in subsequent disinfection processes.

This study was to evaluate the feasibility of controlling carcinogenic nitrosodiethylamine (NDEA) formation from greenhouse gas adsorbent 3-diethylaminopropylamine (DEAPA) by pre-O3 in subsequent chlorination/chloramination processes. The result indicated that the NDEA yields (0.4 %) during chlorination was 1.3 times of that during chloramination (0.3 %); pre-oxidation with 4 mg/L O3 significantly cut down its formation; the reduction rates were up to 67.5 and 48.5 %, respectively. OH scavenger greatly augmented the final NDEA amount from 1.86 to 5.05 µg/L during ozonation, while its roles on subsequent processes differed with disinfection methods as well as O3(g) dosages. Most of co-existed substances inhibited NDEA generation, except NO2-, CO32- and SO42-, which slightly promoted during ozonation. Basing on Gaussian calculation, GC/MS and UPLC-Q-TOF-MS analysis, the influencing mechanisms of pre-O3 on NDEA formation in subsequent disinfection processes were proposed. In addition, the calculated toxicity analysis as well as the whole toxicity was applied to evaluate the possibility of pre-O3 on risk control.

Long noncoding RNA CDKN2B-AS1 silencing protects against esophageal cancer cell invasion and migration by inactivating the TFAP2A/FSCN1 axis.

Esophageal cancer (EC) is the most aggressive malignancy in the gastrointestinal tract. Long noncoding RNA cyclin-dependent kinase inhibitor 2 B antisense RNA 1 (CDKN2B-AS1) is implicated in EC development. However, the specific mechanisms involved remain poorly defined. Therefore, this research aimed to explore the mechanism of action of CDKN2B-AS1 in EC. Quantitative real-time polymerase chain reaction was conducted to measure CDKN2B-AS1 expression in EC cells and western blotting was utilized to evaluate transcription factor AP-2 alpha (TFAP2A) and fascin actin-bundling protein 1 (FSCN1) expression. After gain-of-function and loss-of-function assays, cell proliferation, migration, invasion, apoptosis, and apoptosis-related protein expression were assessed using cell counting kit-8, scratch tests, Transwell assays, flow cytometry, and western blotting, respectively. The binding relationship between CDKN2B-AS1 and TFAP2A was assessed by RNA immunoprecipitation and RNA pull-down assays. The binding relationship between TFAP2A and FSCN1 was evaluated using dual-luciferase reporter and chromatin immunoprecipitation assays. Tumor xenografts from nude mice were used for in vivo verification. CDKN2B-AS1, TFAP2A, and FSCN1 were upregulated in EC cells. Mechanistically, CDKN2B-AS1 transcriptionally activated FSCN1 by recruiting TFAP2A to the FSCN1 promoter. Silencing CDKN2B-AS1 or TFAP2A suppressed EC cell proliferative, migrating, and invasive properties and augmented apoptosis. TFAP2A was bound to CDKN2B-AS1 and the FSCN1 promoter. Overexpression of TFAP2A or FSCN1 abolished the effects of CDKN2B-AS1-silencing on EC cell function. CDKN2B-AS1 silencing curtailed tumorigenesis in nude mice, which was nullified by the upregulation of TFAP2A or FSCN1. Our findings demonstrated the antioncogenic effects of silencing CDKN2B-AS1 in EC through inactivation of the TFAP2A/FSCN1 axis.

Identification and validation of a novel prognostic model of inflammation-related gene signature of lung adenocarcinoma.

Previous literatures have suggested the importance of inflammatory response during lung adenocarcinoma (LUAD) development. This study aimed at exploring the inflammation-related genes and developing a prognostic signature for predicting the prognosis of LUAD. Survival­associated inflammation-related genes were identified by univariate Cox regression analysis in the dataset of The Cancer Genome Atlas (TCGA). The least absolute shrinkage and selection operator (LASSO) penalized Cox regression model was used to derive a risk signature which is significantly negatively correlated with OS and divide samples into high-, medium- and low-risk group. Univariate and multivariate Cox analyses suggested that the level of risk group was an independent prognostic factor of the overall survival (OS). Time-dependent receiver operating characteristic (ROC) curve indicated the AUC of 1-, 3- and 5-years of the risk signature was 0.715, 0.719, 0.699 respectively. A prognostic nomogram was constructed by integrating risk group and clinical features. The independent dataset GSE30219 of Gene Expression Omnibus (GEO) was used for verification. We further explored the differences among risk groups in Gene set enrichment analysis (GSEA), tumor mutation and tumor microenvironment. Furthermore, Single Sample Gene Set Enrichment Analysis (ssGSEA) and the results of Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) suggested the status of immune cell infiltration was highly associated with risk groups. We demonstrated the prediction effect of CTLA-4 and PD-1/PD-L1 inhibitors in the low-risk group was better than that in the high-risk group using two methods of immune score include immunophenoscore from The Cancer Immunome Atlas (TCIA) and TIDE score from Tumor Immune Dysfunction and Exclusion (TIDE). In addition, partial targeted drugs and chemotherapy drugs for lung cancer had higher drug sensitivity in the high-risk group. Our findings provide a foundation for future research targeting inflammation-related genes to predictive prognosis and some reference significance for the selection of immunotherapy and drug regimen for lung adenocarcinoma.

PEGylated Cisplatin Nanoparticles for Treating Colorectal Cancer in a pH-Responsive Manner.

Colorectal cancer (CRC) is a common malignant tumor, and its incidence ranks third and mortality rate ranks second in the world. Cisplatin cannot target CRC cells and has notable toxicity, which significantly limits its clinical application. The emerging PEGylated nanodrug delivery system can improve circulation time and enhance tumor targeting. In this study, the HA-mPEG-Cis NPs were synthesized by self-assembly, which can target CD44-positive CRC cells and dissolve the PEG hydration layer responsive to the weakly acidic tumor environment. The average hydrodynamic diameter of HA-mPEG-Cis NPs was 48 nm with the polydispersity index of 0.13. The in vitro cisplatin release was in a pH-responsive manner. The HA-mPEG-Cis NPs group showed the highest apoptosis rate (25.1%). The HA-mPEG-Cis NPs exhibited antitumor efficacy via the PI3K/AKT/mTOR signaling pathway. The HA-mPEG-Cis NPs showed the lowest tumor volume and weight among all the groups in CT26 cell-bearing mouse model. The HA-mPEG-Cis nanodrug delivery system not only increases the stability and circulation time but also reduces the side effects of loaded cisplatin. Overall, the in vitro and in vivo experiments confirmed the satisfied antitumor efficacy of HA-mPEG-Cis NPs. Therefore, this study provides a rational design for application of pH-responsive HA-mPEG-Cis nanodrug delivery system in the future.

Study on seafloor hydrothermal systems circulation flow and heat transfer characteristics.

In this work, the numerical simulation study of the hydrothermal flow and heat transfer process in the porous rock under 30 MPa pressure was developed. The flow and heat transfer characteristics of hydrothermal in rocks with different porosities are studied by changing the porosity of the rock. The simulation results show that the average flow velocity decreases and the average temperature increases when the porosity decreases. The velocity field and temperature field are coupled due to the nonlinear thermophysical properties of hydrothermal. The velocity field and temperature field have strongly interacted in the range of 400-450 ℃ and the effect of temperature on velocity is gradually diminishing outside the range. Most of the fluid will be "squeezed" into the crevice and the average velocity is almost three times the no-creviced case when a crevice is present. The existence of the crevice makes the total heat flux decrease from an overall perspective, and the crevice makes a large temperature gradient at the entrance and export of the crevice from a local perspective. These results provide theoretical support for the utilization of submarine hydrothermal fluid shallow circulation heat energy.

Xanthohumol inhibits non-small cell lung cancer by activating PUMA-mediated apoptosis.

Deregulation of apoptosis signaling is an important feature of cancer cells and plays an essential role in tumorigenesis. Xanthohumol is an active ingredient in Traditional Chinese Medicines Hops (Humulus lupulus L.). Recently studies have shown the profound anti-tumor activities of Xanthohumol in multiple cancer models. However, its potency in non-small cell lung cancer (NSCLC) and the underlying mechanisms are still elusive. Here, we have investigated the potency of Xanthohumol against NSCLC cells in vitro and xenograft mouse models. Xanthohumol suppressed cell viability, colony formation and induced apoptosis in A549, H520, and H358 cells. Xanthohumol activated mitochondrial apoptosis through upregulation of (p53-upregulated modulator of apoptosis) PUMA expression. After Xanthohumol treatment, the Akt activity was inhibited, which resulted in dephosphorylation of FOXO3a and PUMA induction. Silent PUMA or FOXO3a impaired Xanthohumol-induced apoptosis in NSCLC cells. In nude mice, Xanthohumol administration suppressed NSCLC xenograft tumor growth and increased PUMA expression in tumor tissues. Briefly, our studies revealed a novel mechanism by which Xanthohumol exerted its anti-tumor activity in a PUMA-dependent manner in NSCLC cells.

NDMA formation during ozonation of DMAPA: Influencing factors, mechanisms, and new pathway exploration.

Aliphatic amines, common constituents that contribute to dissolved organic nitrogen (DON), can quickly react with ozone due to the lone electron pair on the nitrogen atom and this may produce carcinogen N-Nitrosodimethylamine (NDMA). 3-(Dimethylamino)-1-propylamine (DMAPA) was chosen as a representative to elucidate the NDMA formation characteristics, kinetic rates, reaction pathways, and influencing factors during ozonation in this study. The results demonstrated that NDMA generated directly from DMAPA during ozonation. Moreover, the NDMA yields increased with ozone dosages. The NDMA molar yield increased and then decreased when the pH raised from 5 to 9, achieving the maximum value at pH 8. Hydroxyl radical (∙OH) played a promotional role in NDMA formation, and its scavenger dramatically cut down its yields. Low levels of Br- facilitated NDMA formation, while the value significantly reduced when Br- was up to 1 mM. The NDMA amount was slightly raised by NO2-, but it was inhibited by NH4+ and NO3-. Moreover, it was also depressed by co-existing components in actual lake water. Based on the result of the Gaussian calculation, the LC-MS/MS and GC-MS analysis, four possible transformation pathways were proposed. The radical recombination was verified to be the primary pathway for ozone promoting NDMA formation from DMAPA.

Hsa_circ_0005576 promotes osimertinib resistance through the miR-512-5p/IGF1R axis in lung adenocarcinoma cells.

Osimertinib is a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) for lung adenocarcinoma (LUAD) harboring activating mutations, but patients ultimately develop acquired resistance. Circular RNAs are involved in EGFR-TKI resistance, while the role of hsa_circ_0005576 in the osimertinib resistance of LUAD remains unknown. In this study, we demonstrated that hsa_circ_0005576 could facilitate osimertinib-resistant LUAD cells. Briefly, knockdown of hsa_circ_0005576 not only suppressed the proliferation and promoted the apoptosis of resistant LUAD cells, but also increased their sensitivity to osimertinib. Mechanistically, hsa_circ_0005576, serving as an miRNA sponge, could directly interact with miR-512-5p and subsequently upregulate the miR-512-5p-targeted insulin-like growth factor 1 receptor. Rescue assays indicated that miR-512-5p inhibition could reverse the effects of hsa_circ_0005576 knockdown in LUAD cells resistant to osimertinib. Overall, our study revealed that hsa_circ_0005576 regulates proliferation and apoptosis through miR-512-5p/IGF1R signaling, which contributes further to the resistance of LUAD cells to osimertinib. In addition, this study provides a novel insight into the mechanisms underlying osimertinib resistance of LUAD.

Penetration and Displacement Behavior of N2 in Porous Interlayer Structures Containing Water/Salt Component by Molecular Dynamics Simulation.

The penetration and displacement behavior of N2 molecules in porous interlayer structures containing a water/salt component with porosities of 4.29%, 4.73%, 5.17%, 7.22%, and 11.38% were explored using molecular dynamics simulations. The results demonstrated that the large porosity of the interlayer structures effectively enhanced the permeation and diffusion characteristics of N2. The water and salt in the interlayer structures were displaced during the injection of N2 in the porosity sequence of 4.29% < 4.73% < 5.17% < 7.22% < 11.38%. The high permeance of 7.12 × 10-6 indicated that the interlayer structures with a porosity of 11.38% have better movability. The strong interaction of approximately 15 kcal/mol between N2 and H2O had a positive effect on the diffusion of N2 and the displacement of H2O before it reached a stable equilibrium state. The distribution of N2 in porous interlayer structures and the relationship between the logarithm of permeability and breakthrough pressure were presented. This work highlighted the effects of porosity on the permeability and diffusion of N2/H2O in the interlayer, thus providing theoretical guidance for the development of petroleum resources.

Ultrahigh-speed graphene-based optical coherent receiver.

Graphene-based photodetectors have attracted significant attention for high-speed optical communication due to their large bandwidth, compact footprint, and compatibility with silicon-based photonics platform. Large-bandwidth silicon-based optical coherent receivers are crucial elements for large-capacity optical communication networks with advanced modulation formats. Here, we propose and experimentally demonstrate an integrated optical coherent receiver based on a 90-degree optical hybrid and graphene-on-plasmonic slot waveguide photodetectors, featuring a compact footprint and a large bandwidth far exceeding 67 GHz. Combined with the balanced detection, 90 Gbit/s binary phase-shift keying signal is received with a promoted signal-to-noise ratio. Moreover, receptions of 200 Gbit/s quadrature phase-shift keying and 240 Gbit/s 16 quadrature amplitude modulation signals on a single-polarization carrier are realized with a low additional power consumption below 14 fJ/bit. This graphene-based optical coherent receiver will promise potential applications in 400-Gigabit Ethernet and 800-Gigabit Ethernet technology, paving another route for future high-speed coherent optical communication networks.

NDMA formation during ozonation of metformin: Roles of ozone and hydroxyl radicals.

Metformin, a high-consumed pharmaceutical for diabetes, has been reported to generate carcinogenic nitroso-dimethylamine (NDMA) during treatment of its containing wastewater. However, whether it would produce NDMA during ozonation or not is unclear, let alone discriminate roles of ozone (O3) and hydroxyl radicals (OH). In this paper, effects of ozonation on NDMA formation from metformin were investigated, roles of O3 and OH were also distinguished by adding tert-butyl alcohol (tBA) as OH scavenger. Moreover, various influencing factors and reaction mechanisms were demonstrated. The results indicated that NDMA could be directly formed from metformin during ozonation, the addition of OH scavenger significantly enhanced its formation (0-46.2 ng/L vs 0-139.1 ng/L). The formation of NDMA by O3 and OH was more affected by bromide and HCO3- than those with only O3; while the impacts of pH and sulphate on the latter were more notable. No matter without/with tBA in the solution, the formed NDMA during ozonation of metformin increased with raising pH (from 5 to 9) and achieved the maximum 69.6 ng/L and 235.9 ng/L at pH 9, respectively; small amount of bromide (0.1 µM) promoted NDMA production, high levels of bromide (10 µM) inhibited its formation; the existence of HCO3- enhanced the amounts of NDMA from 44.5 to 73.5 ng/L (raised by 65.2%) by O3 and OH and from 102.9 to 130 ng/L with only O3 (raised by 26.3%); with the addition of sulphate, NDMA concentration raised by 43.8% by O3 and OH, while the value was high up to 134.6% with only O3. Based on the result of UPLC-Q-TOF and density functional theory, the oxidation intermediates were identified and possible transformation pathways of metformin during ozonation were proposed. The findings in this paper would provide reference when treating metformin-containing water in future.

Comparison of Clinical Efficacy of Alectinib Versus Crizotinib in ALK-Positive Non-Small Cell Lung Cancer: A Meta-Analysis.

OBJECTIVE: To systematically evaluate the efficacy and safety of alectinib versus crizotinib in the treatment of anaplastic lymphoma kinase (ALK) positive non-small-cell lung cancer. METHODS: Studies about the efficacy of alectinib versus crizotinib in the treatment of ALK-positive non-small cell lung cancer were searched in PubMed, Scopus, Embase and the Cocharane Library from inception to February 15, 2020. Two reviewers independently screened these studies, extracted the data, assessed the risk of bias in the included studies by using the Cochrane risk assessment tool, and then used review manager 5.3 software for meta-analysis. RESULTS: Three studies comprising a total of 697 patients with ALK-positive non-small cell lung cancer were included, 380 in the alectinib group and 317 in the crizotinib group. The dose of alectinib (300 mg) in J-ALEX were lower than the approved dose (600 mg), however the crizotinib group in all three studies received the recommended dose (250 mg). Performance bias was high in all three studies whereas, and the attrition bias was high in two studies (Toyoaki Hida 2017 and Solange peters 2017). The results of meta-analysis showed that: the overall response rate [OR = 2.07, 95% CI (1.41, 3.06), P = 0.0002], the progression free survival [HR = 0.34, 95% CI (0.21, 0.55), P <0.0001], the partial response [OR = 1.71, 95% CI (1.19, 2.46), P = 0.003], P = 0.001], in alectinib group were higher than that of crizotinib group. Though the total number of events in complete response and the disease control rate were more in alectinib group than that of crizotinib group, the meta-analysis results shows no significant differences between two drugs in the disease control rate [OR = 2.24, 95% CI (0.56, 8.88), P = 0.25], the complete response [OR = 1.82, 95% CI (0.75, 4.45), P = 0.19]. In addition, the number of events in the stable disease [OR = 0.45, 95% CI (0.28, O.74), P = 0.001], and the adverse events [OR = 0.50, 95% CI (0.23, 0.81), P = <0.0001] in alectinib group were lower than that of crizotinib group. CONCLUSION: Alectinib in terms of overall response rate, progression-free survival and partial response is superior to crizotinib in the treatment of ALK-positive non-small cell lung cancer and is well tolerated. Compared with crizotinib, alectinib is more effective than crizotinib and has a lower incidence of total adverse reactions. Meta-analysis results confirm the strong base for alectinib as a first-line treatment for ALK-positive NSCLC.

Validation of the promotion mechanism between bromide and UDMH to form NDMA during ozonation.

Unsymmetrical dimethylhydrazine (UDMH) is found to generate substantial carcinogenic nitroso-dimethylamine (NDMA) during ozonation, moreover, its formation is promoted by ubiquitous bromide ions (Br-) in water matrixes, but the mechanism is still unclear. In this study, effects of Br- on NDMA formation during ozonation of UDMH were studied, meanwhile, its promotion pathways were also determined. The results demonstrated that Br- promoted NDMA formation from UDMH during ozonation, the formation rate constant with Br- is over 7 times of that without Br-. NDMA amount raised from 142.5 to 327.5 µg/L when Br- dosages increased from 0 to 100 µM. No matter with or without Br-, the augment of O3 dosages facilitated NDMA formation; the maximum value was achieved at pH 8. NDMA decreased dramatically from 173.8 to 123.5 µg/L with HCO3- raising from 0 to 160 µM, while increasing remarkably to 222.5 µg/L with SO42- dosing. In addition, NOM inhibited NDMA formation from UDMH during ozonation. The mass spectrum of LC-MS/MS verified that the generation of Br-UDMH was main cause for promoting NDMA formation. Moreover, hypobromous acid (HBrO) was confirmed to be responsible for Br-UDMH formation. In addition, the position that oxidants and Br- attacked was demonstrated based on Gaussian calculation. The results of this study could provide theoretical basis for the application of ozonation in bromine-containing water matrixes.

Identifying and Validating Potential Biomarkers of Early Stage Lung Adenocarcinoma Diagnosis and Prognosis.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common pathological type of lung cancer. At present, most patients with LUAD are diagnosed at an advanced stage, and the prognosis of advanced LUAD is poor. Hence, we aimed to identify novel biomarkers for the diagnosis and treatment of early stage LUAD and to explore their predictive value. METHODS: The microarray datasets GSE63459, GSE27262, and GSE33532 were searched, and the differentially expressed genes (DEGs) were obtained using GEO2R. The DEGs were subjected to gene ontology (GO) and pathway enrichment analyses using METASCAPE. A protein-protein interaction (PPI) network was plotted with STRING and visualized by Cytoscape. Module analysis of the PPI network was performed using MCODE. Overall survival (OS) analysis and analysis of the mRNA expression levels of genes identified by MCODE were performed with UALCAN. Western blot analysis of hub genes in LUAD patients, MTS assays, and clonogenic assays were performed to test the effects of the hub genes on cell proliferation in vitro. RESULTS: A total of 341 DEGs were obtained, which were mainly enriched in terms related to blood vessel development, growth factor binding, and extracellular matrix organization. A PPI network consisting of 300 nodes and 1140 edges was constructed, and a significant module including 15 genes was identified. Elevated expression of ASPM, CCNB2, CDCA5, PRC1, KIAA0101, and UBE2T was associated with poor OS in LUAD patients. In the protein level, the hub gene was overexpressed in LUAD patients. In vitro experiments showed that knockdown of the hub genes in the LUAD cell lines could promote cell proliferation. CONCLUSIONS: DEGs are potential biomarkers for early stage lung adenocarcinoma and could have utility for the diagnosis and predicting treatment efficacy.

Astragaloside alleviates alcoholic fatty liver disease by suppressing oxidative stress.

Alcoholic fatty liver disease (AFLD) is the most common liver disease and can progress to fatal liver cirrhosis and carcinoma, affecting millions of patients worldwide. The functions of astragaloside on the cardiovascular system have been elucidated. However, its role in AFLD is unclear. Ethanol-treated AML-12 cells were used as a cell model of alcoholic fatty liver. Real-time quantitative reverse transcription-PCR and Western blotting detected genes and proteins expressions. Reactive oxygen species (ROS), triglyceride, total cholesterol, low-density lipoprotein, albumin, ferritin, bilirubin, superoxide dismutase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were examined using commercial kits. Lipid accumulation was assessed by Oil red O staining. MTT and flow cytometry measured cell viability and apoptosis. JC-1 was used to analyze mitochondrial membrane potential. A rat model of AFLD was established by treating rats with ethanol. Astragaloside suppressed ethanol-induced lipid accumulation, oxidative stress, and the production of AST and ALT in AML-12 cells. Ethanol induced TNF-α and reduced IL-10 expression, which were reversed by astragaloside. Ethanol promoted Bax expression and cytochrome C release and inhibited Bcl-2 and ATP expression. Astragaloside hampered these apoptosis effects in AML-12 cells. Impaired mitochondrial membrane potential was recovered by astragaloside. However, all these astragaloside-mediated beneficial effects were abolished by the ROS inducer pyocyanin. Ethanol-induced activation of NF-κB signaling was suppressed by astragaloside in vitro and in vivo, suggesting that astragaloside inhibited oxidative stress by suppressing the activation of NF-κB signaling, thus improving liver function and alleviating AFLD in rats. Our study elucidates the pharmacological mechanism of astragaloside and provides potential therapeutic strategies for AFLD.

High-power Si-Ge photodiode assisted by doping regulation.

High-power silicon-based photodiodes are key components in many silicon photonics systems, such as microwave photonics systems, an optical interconnection system with multi-level modulation formats, etc. Usually, the saturation power of the silicon-germanium (Si-Ge) photodiode is limited by the space-charge screening (SCS) effect and the feasibility of the fabrication process. Here, we propose a high saturation power Si-Ge photodiode assisted by doping regulation. Through alleviating the SCS effect of the photodiode, we successfully demonstrate an 85.7% improvement on the saturation power and a 57% improvement on the -1 dB compression photocurrent. The proposed high-power Si-Ge photodiode requires no specific fabrication process and will promote the low-cost integrated silicon photonics systems for more applications.