Dendrobine Suppresses Tumor Growth by Regulating the PD-1/PD-L1 Checkpoint Pathway in Lung Cancer.

Background: Dendrobine is a bioactive alkaloid isolated from Dendrobium nobile. Studies have evaluated the anti-tumor effect of dendrobine in cancers, including lung cancer. However, the mechanism of dendrobine inhibiting tumors requires further study.

Single-arm, phase II study of intra-arterial chemotherapy plus total neoadjuvant therapy to optimise complete response in distal rectal cancer: a study protocol.

Introduction: Organ preservation is now considered an acceptable alternative option in distal rectal cancer patients with clinical complete response (cCR) after neoadjuvant chemoradiation (CRT). But the cCR rate is low and about one-third of tumour will regrow, which requires more effective local treatment. CRT combined with intra-arterial chemotherapy (IAC) might be a promising approach.

Comprehensive bioinformatics analysis on exportins in lung adenocarcinoma and lung squamous cell carcinoma.

Background: Lung cancer is one of the most common malignant tumors in the world. Exportins are closely associated with the cellular activity and disease progression in a variety of different tumors. However, the expression level, genetic variation, immune infiltration, and biological function of different exportins in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), as well as their relationship with the prognosis of patients with LUAD and LUSC have not been fully clarified.

Small peptide LINC00511-133aa encoded by LINC00511 regulates breast cancer cell invasion and stemness through the Wnt/β-catenin pathway.

LINC00511 is an long non-coding RNA (lncRNA) of ncRNAs,This study aimed to investigate whether the lncRNA LINC00511 could encode a small peptide, LINC00511-133aa, and whether this peptide could promote breast cancer cell metastasis and stemness by activating the wnt/β-catenin pathway. The LINC00511-133aa coding sequence vector and control vector were transfected into MCF-7 and MDA-MB-231 breast cancer cells, with subsequent assessment of peptide expression using PCR, western blotting, and immunofluorescence assays. Cell proliferation, invasion, and apoptosis were evaluated using CCK8, apoptotic, wound healing, and transwell invasion assays, while the characteristic changes of tumor stem cells were detected through sphere-forming assay and western blot analyses of the stemness markers Oct4, Nanog, and SOX2.

ELF1 suppresses autophagy to reduce cisplatin resistance via the miR-152-3p/NCAM1/ERK axis in lung cancer cells.

Resistance to chemotherapeutic drugs limits the efficacy of chemotherapy in non-small cell lung cancer (NSCLC). Autophagy is an essential mechanism which involves in drug resistance. Our previous research has revealed that miR-152-3p represses NSCLC progression.

LncRNA AC098934 promotes proliferation and invasion in lung adenocarcinoma cells by combining METTL3 and m6A modifications.

Long non-coding RNA (lncRNA) regulates the tumorigenesis as well as the development of lung adenocarcinoma (LUAD), which is one of the high-mortality cancers. We explored the influence of lncRNA AC098934 on the malignant biological behavior of LUAD and potential underlying molecular mechanisms. The expression level of AC098934 in either the LUAD or the normal tissues was identified in the TCGA database.

Ferroptosis Inhibitor Regulates the Disease Progression of Systematic Lupus Erythematosus Mice Model Through Th1/Th2 Ratio.

Background: Systematic lupus erythematosus (SLE) is an autoimmunemediated disease. So far, there is no relevant report on ferroptosis in SLE research, and the role of T helper 1 (Th1) and T helper 2 (Th2) cells in SLE is still unclear.

Methods: This study employed SLE mice models with and without ferroptosis inhibitors (Liproxstatin‑1) and normal control mice.

3-hydroxy butyrate dehydrogenase 2 deficiency aggravates systemic lupus erythematosus progression in a mouse model by promoting CD40 ligand demethylation.

The implications of the CD40-CD40 ligand (CD40L) signaling pathway in systemic lupus erythematosus (SLE) were well documented, due to its important role among immune cells. Previous research found that 3-hydroxy butyrate dehydrogenase 2 (BDH2), a modulator of intracellular iron homeostasis and iron transportation promoted the pathogenic process of SLE by regulating the demethylation of , and genes among CD4 + T cells. The purpose of this study was to explore the role of BDH2 in oxidative damage-induced SLE.

DNMT3B regulates proliferation of A549 cells through the microRNA-152-3p/NCAM1 pathway.

The purpose of the present study was to examine the epigenetic mechanism by which microRNA (miR)-152-3p regulates proliferation in non-small cell lung cancer A549 cells via neural cell adhesion molecule 1 (NCAM1). Bisulfite sequencing PCR (BSP), the gold standard for methylation detection, uses bisulfite-treated DNA to determine its pattern of methylation. Treatment of DNA with bisulfite converts cytosine residues to uracil, but leaves 5-methylcytosine residues unaffected.

mRNA expression and DNA methylation analysis of the inhibitory mechanism of HO on the proliferation of A549 cells.

Reactive oxygen species, particularly hydrogen peroxide (HO), can induce proliferation inhibition and death of A549 cells via oxidative stress. Oxidative stress has effect on DNA methylation. Oxidative stress and DNA methylation feature a common denominator: The one carbon cycle.

A putative competing endogenous RNA network in cisplatin-resistant lung adenocarcinoma cells identifying potentially rewarding research targets.

Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer and has a poor 5 year survival rate (<10%). Cisplatin is one of the most effective chemotherapeutic treatments for LUAD, even though it is of limited overall utility due to acquired drug resistance. To identify possible genetic targets for the mitigation of cisplatin resistance, gene expression data from cisplatin-resistant cell lines were integrated with patient information.

[Quality control results of microbiology of provincial laboratories in China in 2014].

Objective: To get a baseline of 32 provincial center for disease control and prevention( CDC) microbiology laboratory in the aspect of quantitative test ability of Staphylococcus aureu, qualitative test ability of diarrheagenic Escherichia coli and unknown intestinal pathogen, and to comprehend the quality of microbiology testing.

Methods: Two different concentration samples of Staphylococcus aureus I and II were made. Diarrheagenic Escherichia coli and unknown intestinal pathogen samples were transported using the special semi-solid AGAR transport medium, in the form of four pure different serotypes each.

CD4(+) T cells epigenetically modified by oxidative stress cause lupus-like autoimmunity in mice.

Lupus develops when genetically predisposed people encounter environmental agents such as UV light, silica, infections and cigarette smoke that cause oxidative stress, but how oxidative damage modifies the immune system to cause lupus flares is unknown. We previously showed that oxidizing agents decreased ERK pathway signaling in human T cells, decreased DNA methyltransferase 1 and caused demethylation and overexpression of genes similar to those from patients with active lupus. The current study tested whether oxidant-treated T cells can induce lupus in mice.

[Analysis on 2011 quality control results on aerobic plate count of microbiology laboratories in China].

Objective: To test the aerobic plate count examining capability of microbiology laboratories, to ensure the accuracy and comparability of quantitative bacteria examination results, and to improve the quality of monitoring.

Methods: The 4 different concentration aerobic plate count piece samples were prepared and noted as I, II, III and IV. After homogeneity and stability tests, the samples were delivered to monitoring institutions.

Oxidative stress, T cell DNA methylation, and lupus.

Objective: Lupus develops when genetically predisposed people encounter environmental agents, such as ultraviolet light, silica, infections, and cigarette smoke, that cause oxidative stress, but how oxidative damage modifies the immune system to cause lupus flares is unknown. We previously showed that inhibiting DNA methylation in CD4+ T cells by blocking ERK pathway signaling is sufficient to alter gene expression, and that the modified cells cause lupus-like autoimmunity in mice. We also reported that T cells from patients with active lupus have decreased ERK pathway signaling, have decreased DNA methylation, and overexpress genes normally suppressed by DNA methylation.

[Comparison and anylisis on national quality control examination results of pesticides residues in food in 2009 and 2011].

Objective: To find out and compare the professionals proficiency of monitoring and inspection agencies on pesticide residue in food, and identify the main factors affecting the quality of result to provide references for improving the quality of the monitoring and inspection results.

Methods: Compare the national quality control examination results of pesticides residues in food of 2009 with 2011.

Results: The submission rates of examination results in 2011 were much higher than in 2009.

[Quality control examination on testing pesticides residues in food for agencies in charge of food safety risk monitoring and inspection].

Objective: To find out the proficiency of professionals in monitoring and inspection agencies on the determination of pesticides residue in food, and to improve the accuracy and comparability of testing results.

Methods: Three sets of quality control samples with the same matrix but different in concentrations of pesticides were prepared; one of blind quality control samples contained chlorpyrifos, methyl parathion, methyl pirimiphos, fenitrothion or triazophos and bifenthrin was dispatched to each inspection agency. Criteria for testing results were evaluated by Z scores: [Z] = < or = 2 for satisfactory; 2 < [Z] < 3 for uncertainty and [Z] > or = 3 for unsatisfactory.

Trichostatin A sensitizes cisplatin-resistant A549 cells to apoptosis by up-regulating death-associated protein kinase.

Aim: To investigate the apoptosis-inducing effect of trichostatin A (TSA) in the human lung adenocarcinoma cisplatin-resistant cell line (A549/CDDP) and to examine whether TSA can enhance sensitivity to cisplatin treatment and the underlying molecular mechanisms of such an enhancement.

Methods: Cell viability was evaluated using the Neutral Red assay. Apoptosis was assessed using Hoechst 33258 staining and flow cytometry analysis.

Age-dependent decreases in DNA methyltransferase levels and low transmethylation micronutrient levels synergize to promote overexpression of genes implicated in autoimmunity and acute coronary syndromes.

T cell DNA methylation levels decline with age, activating genes such as KIR and TNFSF7 (CD70), implicated in lupus-like autoimmunity and acute coronary syndromes. The mechanisms causing age-dependent DNA demethylation are unclear. Maintenance of DNA methylation depends on DNA methyltransferase 1 (Dnmt1) and intracellular S-adenosylmethionine (SAM) levels, and is inhibited by S-adenosylhomocysteine (SAH).

[Different proteome of human lung adenocarcinoma cells treated with NS-398 and cisplation].

Background: Recent studies have shown that NS-398, a highly selective COX-2 inhibitor, can enhance the inhibition effects of cisplatin on adenocarcinoma cell proliferation, but the mechanism is still unknown. The aim of this study is to explore the mechanism about the synergistic effects of NS-398 and cisplatin to human lung adenocarcinoma cell line.

Methods: Differentially expressed proteins were separated in human lung adenocarcinoma cells treated with NS-398 and/or cisplatin by immobilized pH gradient-based two-dimensional gel electrophoresis (2-DE), then 19 out of obtained proteins were identified by peptide mass fingerprint (PMF) based on matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) and database searching.

[Staphylococcus aureus in food determined by polymerase chain reaction].

Objective: To establish a rapid polymerase chain reaction (PCR)method for detection of staphylococcus aureus in milk, ice cream and meat.

Methods: Two pairs of oligonucleotide primers were designed with thermo nuclease gene nuc and surfaced-associated fibrinogen-binding protein gene ClfA to detect staphylococcus aureus. Fifty-two staphylococcus aureus and thirty-one non staphylococcus aureus were amplified by PCR to verify the specificity.

[Study on immunorepressive mice model by gamma irradiation].

Objective: To establish the immunorepressive mice model by irradiation.

Methods: The 90 Kunming mice which the weight is from 30 to 34g were treated with 3Gy, 4Gy, 5Gy gamma irradiation, the delayed allergy testing, the serum haemolysin level testing, the phagocytosing functions testing and the NK cell activity testing were performed at 3th, 7th, 14th, 21th days after irradiation respectively.

Results And Conclusion: (1) All 3Gy, 4Gy, 5Gy gamma irradiation can cause mice immunorepressivestate except the NK cell activity.

[Development of methods on detection of enteropathogenic Escherichia coli by double PCR in meat and meat product].

Objective: To establish a rapid method for detecting Enteropathogenic Escherichia coli (EPEC) in meat and meat product.

Methods: Based on attaching and effacing lesion (eaeA gene) and bundle-forming pili (bfpA gene) of EPEC, two pairs of primers were designed. Then EPEC in meat and meat product were detected by double PCR.