Objective To investigate the anti-tumor effect and mechanism of Plumbagin against human large cell lung cancer cell line NL9980.Methods Plumbagin in different concentrations were set up to administrate NL9980 cell line.MTT test was performed to detect the inhibiting effects against tumor proliferation and IC50 concentration was identified.The influence of tumor apoptosis was observed by flow cytometry and the inhibiting effect against invasive ability was detected by Boyden chamber test.IC50 group and control group were set up and tumor cells were harvested 6 h,24 h and 48 h after administration.Realtime PCR was used to detect mRNA expression changes of bcl-2,bax,VEGF and CYCD1.Results MTT test showed obvious inhibiting effects of proliferation in NL9980 cell line and IC50 was 7.5 μmol/L.Plumbagin induced the apoptosis of tumor cells and showed a significant anti-invasive effect.Mean membrane-spanning cells were 161.59±47.32 and 26.58±9.07 in control group and IC50 group correspondingly.Down-regulations of bcl-2,VEGF and CYCD1 were detected and expression of bax gene increased.The effect of Plumbagin showed obvious time dependance (P ＜0.05).Conclusion Plumbagin has displayed the powerful antitumor effects against NL9980 cell line and it might work via multiple pathways.Plumbagin exhibits the prospect of being an effective drug against large cell lung cancer.

An alternative method based on an off-line solid phase extraction ( SPE ) combined with programmable temperature vaporizer-based ( PTV) large volume injection-gas chromatography-flame ionization detection ( LVI-GC-FID ) was developed. The goal of this study was to determine mineral oil saturated hydrocarbons ( MOSH ) in camellia seed oils. The purification condition of SPE columns with silver impregnated the activated silica gel and activated aluminum oxide was optimized. The optimal SPE cartridge was loaded with 10 g of Ag-activated silica gel per 10 g of activated aluminum oxide. The PTV initial temperature was set at 75℃ for 1 min (split 200:1), and heated from 75℃ to 370℃ at 250℃/min. Then the diverter valve was closed for 1 min and opened again with the split flow ratio changing to 50:1 . The injection volume was 40μL. The calibration curve of paraffin oil was liner in the range of 5-500 mg/kg with correlation coefficient of 0. 998. The detection limit (LOD) and the quantification limit (LOQ) of paraffin oils in hexane were 0. 26 mg/kg and 0. 80 mg/kg, respectively. The recoveries from spiked oil samples were between 93 . 3% and 112 . 7%, with relative standard deviation ( RSD ) of 1 . 8%-5 . 2%, the RSD of intra-day and inter-day were less than 2 . 6% . This procedure was applied to analyze the MOSH in 11 commercial camellia seed oils and the contamination was found to range from 6. 8 mg/kg to 76. 7 mg/kg. The method is simple in operation with high sensitivity, good reproducibility and low cost, and suitable for determination of MOSH in vegetable oils.

OBJECTIVETo explore seroepidemiological status and vaccine coverage of hepatitis B among drug users in Xi'an.

METHODS545 drug users in the Xi'an Compulsory Detoxification Center were asked to answer questionnaire and provide blood sample (3-5 ml) for test of HBsAg, anti-HBc and anti-HBs from March to June 2013. Totally, 545 subjects were surveyed and tested. All of them effectively completed the survey.

RESULTSThe positive rates of HBsAg, anti-HBc and anti-HBs were 29.4% (160/545), 60.0% (327/545) and 56.1% (306/545), respectively. Eighty five subjects (15.6%) were negative for all of the three markers. The prevalence of HBsAg and anti-HBc among injection drug users were 40.0% (94/235) and 65.6% (154/235), which was significantly higher than non- injection drug users' (21.6% (52/241), 58.5% (141/241)) and mixed non-injection and injection drug users ((20.3% (14/69), 46.4% (32/69)) (χ(2) = 23.518 and 9.017, respectively, P < 0.05) . The HBsAg positive rate (30.6% (153/500)) of subjects with more than once per day of drug using within one year was significantly higher than those who used drugs for 2-3 times per week (15.6% (7/45)) (χ(2) = 4.51, P < 0.05). Only 11.7% (64/545) of drug users had a clear history of hepatitis B vaccination. The vaccination rate of subjects (3.5% (5/141)) with primary education or below was significantly lower than those with high school (16.3% (45/276)) (χ(2) = 26.61, P < 0.05). The vaccination rate of subjects (7.8% (12/153)) over 45 years old was significantly lower than that of subjects below 30 years old (15.9% (21/132)) and 30-44 years old (11.9% (31/260)) (χ(2) = 30.36, P < 0.05). The vaccinees had a significantly higher positive rate of anti-HBs (73.4% (47/64)) than those who without vaccination (53.8% (259/481)) (χ(2) = 8.81, P = 0.003), but the positive rates of HBsAg (16.7% (11/64)) were lower than those who without vaccination (31.0% (149/481)) (χ(2) = 23.52 and 9.02, respectively;P > 0.05).

CONCLUSIONThe HBV infection status among drug users in Xi'an was in serious condition, while a low vaccination rate was also discovered among them.

Adult ; Age Factors ; China ; epidemiology ; Drug Users ; Hepatitis B ; epidemiology ; Hepatitis B Antibodies ; Hepatitis B Surface Antigens ; Hepatitis B Vaccines ; Humans ; Middle Aged ; Prevalence ; Risk Factors ; Substance Abuse, Intravenous ; epidemiology ; Vaccination

Objective:Build a research index performance model with discipline growth evaluation, to evaluate the scientific research performance level of various disciplines in hospital more objectively, fairly and dynamically.Methods:Take the research projects, papers, patents and achievements as the main evaluation indicators and establish the hierarchical and classified scoring standards, to form the weight index evaluation model for the total score, per capita score and growth of the discipline research.Results:Using the growth research index to evaluate the scientific research performance of departments and individual researcher between January 2018 and December 2020. Excellent departments were selected for the top 10% of the scientific research index, those whose scientific research scores increased by more than 20% compared with the previous year were selected as the progressive departments, and the top 1% of individual scientific research scores were selected as the advanced researchers, which were commended and encouraged. For the departments ranked in the bottom 5% or whose scientific research index significantly declined compared with previous year, early warning, guidance and supervision were implemented. Since the implementation of the evaluation system, the research performance of disciplines has been significantly improved, and many achievements were made.Conclusions:This evaluation mode can stimulate the enthusiasm of the disciplines and scientific researchers for entrepreneurship and innovation to set up the standards and promote the continuous improvement of the research capacity of the whole hospital.

Background and objective Our previous study found that nicotine could induce lung cancer cell epithelial-mesenchymal transition (EMT). The aim of this study is to explore the relationship between nicotine-induced EMT and lung cancer invasion and metastasis. Methods Real-time PCR and Western blot were used to detect the expression changes of EMT-related markers, E-cadherin and Vimentin, in A549 lung cancer cells treated with nicotine;hTe transposition ofβ-catenin protein expression was determined by immunolfuorescence;Scratch test and Transwell invasion assay were used to detect the effects of nicotine on lung cancer cell migration and invasion. Results Nicotine can signiifcantly down-regulate the expressional level of E-cadherin mRNA and protein of A549 cells in a manner of dose and time-dependent (P<0.01, P<0.01);Nicotine can signiifcantly up-regulate the expressional level of Vimentin mRNA and protein of A549 cells in a manner of dose and time-dependent (P<0.01, P<0.01);Immunolfuorescence results showed thatβ-catenin protein was signiifcantly transfered to nucleus;Scratch test and Transwell assay showed that Nicotine could remarkably increase the migration and invasion poten-tial of lung cancer cells (P<0.01, P<0.01). Conclusion Nicotine can induce cancer cells EMT, and promote the invasion and metastasis ability of lung cancer cells.

BACKGROUND: Reticulosome family gene 1 (RTN1) is a reticulosome-encoding gene associated with the endoplasmic reticulum. RTN1 plays a key role in membrane trafficking or neuroendocrine secretion of neuroendocrine cells, while RTN1 serves as a potential diagnostic/therapeutic marker for neurological diseases and cancer. However, the expression of RTN1 and its effect on the immune microenvironment in patients with lung adenocarcinoma have not been reported. In this study, we aimed to investigate the expression of RTN1 in lung adenocarcinoma and its correlation with immune infiltration and survival in lung adenocarcinoma using public databases and bioinformatics network tools. METHODS: Expression levels of RTN1 mRNA in tumor and normal tissues were analyzed using Tumor Immune Estimation Resource 2.0 (TIMER 2.0) and Gene Expression Profiling Interactive Analysis 2 (GEPIA 2). RTN1 protein expression was examined using the Human Protein Atlas. The clinical prognostic significance of RTN1 was analyzed using the GEPIA2 plotter database. To further confirm the potential function of RTN1, the data were analyzed using gene set enrichment analysis. In addition, We performed dimensionality-reduced clustering analysis at the single-cell sequencing level on two datasets from the Tumor Immune Single-cell Hub (TISCH) database to observe the cellular clustering of RTN1 in different types of immune cells. Using the TIMER online tool to analyze and predict the infiltration abundance of different types of immune cells in the immune microenvironment of lung adenocarcinoma patients in the TCGA cohort; TIMER and CIBERSORT were used to study the relationship between genes co-expressed with RTN1 and its associated tumor-infiltrating immune cells; finally, TIMER was used to analyze the relationship between RTN1 and immune correlations between immune checkpoints. RESULTS: We found that RTN1 expression was decreased in patients with lung adenocarcinoma and was closely related to patient prognosis. RTN1 is involved in the process of phagosome formation, hematopoietic cell formation and cell adhesion, and plays an important role in T cell activation. Using cBioPortal and TCGA data to analyze, it is found that RTN1 is significantly associated with BTK, CD4, ECSF1R, MNDA, NCKAP1L and SNX20. High expression of the above genes may cause significant upregulation of CD4+ T cells, mast cells, monocytes, myeloid dendritic cells and M1 macrophages. The expression of RTN1 is closely related to the common immune checkpoints CD274, CTLA4, HAVCR2, LAG3, PDCD1, PDCD1LG2, TIGIT and SIGLEC15 immune checkpoints. CONCLUSIONS RTN1 may act as a tumor suppressor gene and indicate better prognosis. Furthermore, RTN1 is associated with immune infiltration that may be involved in the immunotherapy response in LUAD. However, the related mechanism needs further research.
Adenocarcinoma of Lung/pathology* ; Biomarkers, Tumor/metabolism* ; Gene Expression Profiling ; Humans ; Lung Neoplasms/pathology* ; Mast Cells/pathology* ; Membrane Proteins/metabolism* ; Nerve Tissue Proteins/genetics* ; Prognosis ; Sorting Nexins/metabolism* ; Tumor Microenvironment/genetics*

Background and objective Cancer metastasis is not only the malignant marker and characteristics, but also the main cause of failure to cure and lose their life in the patients with lung cancer. Lung cancer metastasis has organ-speciifc characteristics. hTe most common sites of lung cancer metastasis are mediastinal lymph node, brain, bone, liver and adrenal gland. hTe aim of this study is to screen and establish lung cancer cell model with organ-speciifc metastasis potential with human high-metastatic large cell lung cancer cell line L9981 established by our laboratory previously, and to provide cell models for studying the mechanisms and signal regulation of organ-speciifc metastasis of lung cancer. Materials and meth-ods hTe parent lung cancer cell line, L9981-Luc, was inoculated in the armpit of nude mice. hTe live animal imaging system, IVIS-200, was used to detect the lung cancer organ-speciifc metastasis every week. When the organ-speciifc metastasis were established, the nude mices bearing the lung cancer were sacriifced when they became moribund. Under sterile conditions, the organs (mediastinal lymph nodes, lung, spinal column and brain) with lung cancer organ-speciifc metastasis were removed and the metastasized nodules were dissected free of connective tissue and blood clots, and rinsed twice with medium. hTe metas-tasized nodules were ifnely minced using sterile scalpel blades in medium, and the cells were seeded in tissue culture dishes. Then, the cells with organ-specific metastasis potential were reinoculated into the armpit of nude mice, respectively. This processes were repeated to establish the organ-speciifc metastatic sublines of L9981-Luc cell line more than 10 times. Finally, the organ-speciifc metastasis sublines of L9981-Luc were screened and established, which the four cell lines have the charac-teristics only metastasized to brian, lung, bone and mediastinal lymph node. Results A group of organ-speciifc metastasis cell lines which only metastasized to brian, lung, bone and mediastinal lymph node were successfully established through repeat-ing reinoculatation, live animal imaging in nude mice, and screening and identiifcation in vitro. We named the four cell lines as L9981-BoM, L9981-LuM, L9981-BrM and L9981-LnM, respectively. hTe L9981-BoM cell was only metastasized to bone. hTe l9981-LuM cell was only metastasized to lung. hTe L9981-BrM only metastasized to brain. hTe L9981-LnM cell was only metastasized to midiastinal lymph nodes. Conclusions A human large cell lung cancer cell model with bone, lung, brain and lymph node-speciifc metastasis potential was successfully established. It will be helpful to further study the molecular mecha-nisms and signal regulation of lung cancer organ-speciifc metastasis. It will be to also provide reliable cell model for developing new techniques and molecular targeting drugs of inhibiting or reversing lung cancer metastasis.

Background and objective Cisplatin is the ifrst-line drug for the chemotherapy of non-small cell lung cancer (NSCLC), but the acquired chemoresistance restricted the effect of its treatment. hTe aim of this study is to validate the miRNAs related to the Cisplatin resistance in lung cancer and elucidate the molecular mechanisms. Methods We performed miRNA microarray and RT-PCR to obtain the aberrant differential expressed miRNAs between A549 and its paired Cisplatin-resistant cell line A549/DDP cells, and then we investigated the biological functions of miR-192, which is the aberrant differen-tial expressed miRNA. Atfer transfection of the miR-192 into A549 cells, we measured the half inhibition concentration (IC50), cell apoptosis of the trasfectant cells, and then we used biological sotfwares and dual-luciferase report assay to explore the target gene of the miR-192, which was further validated by RT-PCR and Western blot. Result MiR-192 was highly over-expressed in A549/DDP cells , whose quantity was 37.59±0.35 fold higher than that in A549 cells. Overexpression of miR-192 in A549 cells signiifcantly conferred resistance to Cisplatin and inhibited apoptosis. By contrast, down-expression of miR-192 in A549/DDP cells remarkably restrained the Cisplatin resistance and induced apoptosis. MiR-192 binded to Bim 3’-UTR and negatively regulated Bim expression at the post-transcriptional level in lung adenocarcinoma cells. Conclusion Our data suggested that miR-192 induced Cisplatin-resistance and inhibited cell apoptosis in lung cancer via negative targeting Bim expression.