Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

To investigate the inhibitory effects of adenovirus-mediated NDRG2 on the proliferation of human renal cell carcinoma cell line OS-RC-2 in vitro.', 'NDRG2 was harvested by RT-PCR, confirmed by DNA sequencing, and then cloned into the eukaryotic expression vector pIRES2-EGFP, which encodes green fluorescent protein (GFP), to construct pIRES2-EGFP-NDRG2 plasmid. OS-RC-2 cells with NDRG2 negative expression were transfected with pIRES2-EGFP-NDRG2 plasmid. The growth of transfected OS-RC-2 cells was observed under light and fluorescence microscopes. After colony-forming cell assays, cell proliferation detection and MTT assays, the growth curves of cells in each group were plotted to investigate the inhibitory effects of adenovirus-mediated NDRG2 on the proliferation of OS-RC-2 cells. Cell cycle was determined by flow cytometry. Confocal laser scanning microscopy showed that NDRG2 protein was specifically located on subcellular organelle.', 'A eukaryotic expression vector pIRES2-EGFP-NDRG2 was successfully constructed. After NDRG2 transfection, the growth of OS-RC-2 cells was inhibited. Flow cytometry showed that cells were arrested in S phase but the peak of cell apoptosis was not present, and confocal laser scanning microscopy showed that NDRG2 protein was located in mitochondrion.
Does adenovirus-mediated NDRG2 inhibit the proliferation of human renal cell carcinoma cell line OS-RC-2 in vitro?

High sensitivity C-reactive protein (Hs-CRP) and adiponectin (APN) are two critical cytokines and exert inverse effects on atherosclerosis initiation and progression. The purpose of our study was to investigate the value of Hs-CRP and ANP ratio (Hs-CRP/APN ratio) on evaluating atherosclerosis progression.', "One hundred sixty consecutive participants underwent carotid intima-media thickness (CIMT) measured by ultrasound were enrolled and drawn fasting blood samples for plasma levels Hs-CRP and APN, serum levels of lipid profiles and fasting blood glucose evaluation. Other anthropometrics and clinical status were collected by questionnaire. All participants were divided into 4 groups according to the baseline Hs-CRP/APN ratio and underwent CIMT measurement every 6 months. CIMT increment and composite cardiovascular endpoints were compared after 24 months' follow-up.", "At baseline, body mass index (BMI), smoking, diabetic mellitus, usage of statins, Hs-CRP and APN independently correlated with Hs-CRP/APN ratio as analyzed by spearman rank correlation. Smoking, serum level of LDL-C, plasma level of Hs-CRP and Hs-CRP/APN ratio were positively correlated with CIMT while usage of statins and plasma level of APN were negatively correlated with CIMT as analyzed by multiple linear regression analysis. After 24 months' follow-up, the progression of CIMT was the most prominent in the fourth quartile of baseline Hs-CRP/APN ratio. In addition, the incidence of composite cardiovascular endpoint was also higher in the fourth quartile as compared to the other 3 lower quartiles.
Is increased Hs-CRP/adiponectin ratio associated with increase carotid intima-media thickness?

Increased apoptosis may induce autoimmune conditions. Apoptosis is induced by binding of death receptor ligands, members of the tumour necrosis factor (TNF) superfamily, to their cognate receptors. The Fas-Fas ligand pathway has been studied extensively in relation to systemic lupus erythematosus (SLE). However, other death pathways are also considered important. TNF related apoptosis inducing ligand (TRAIL), another ligand of the TNF superfamily, induces apoptosis in sensitive cells.', 'To assess soluble (s) TRAIL concentrations in sera of SLE patients.', "40 SLE patients were studied (20 with active and 20 with inactive disease). Serum sTRAIL concentrations were measured by a solid phase sandwich enzyme linked immunosorbent assay. Levels in SLE patients were compared with those in patients with rheumatoid arthritis (n = 20), Wegener's granulomatosis (n = 20), and healthy controls (n = 20).", "Mean (SEM) serum sTRAIL concentration in SLE patients (936.0 (108.2) pg/ml) was higher than in healthy controls (509.4 (33.8) pg/ml; p<0.01) or in disease control patients with rheumatoid arthritis (443.8 (36.1) pg/ml, p<0.001) or Wegener's granulomatosis (357.1 (32.2) pg/ml; p<0.001). The mean serum sTRAIL concentration was 1010.2 (168.0) pg/ml for patients with inactive disease and 861.8 (138.7) pg/ml for those with active disease. sTRAIL values were not correlated with specific manifestations of the disease, such as leucopenia or lymphopenia, or with SLE disease activity index.

Are soluble TRAIL concentrations raised in patients with systemic lupus erythematosus?