TASK DEFINITION: In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.
PROBLEM: BACKGROUND Common carotid intima media thickness (CIMT) and ankle brachial pressure index (ABPI) are used as surrogate marker of atherosclerosis, and have been shown to correlate with arterial stiffness, however their correlation with global atherosclerotic burden has not been previously assessed. We compare CIMT and ABPI with atheroma burden as measured by whole body magnetic resonance angiography (WB-MRA).
METHODS 50 patients with symptomatic peripheral arterial disease were recruited. CIMT was measured using ultrasound while rest and exercise ABPI were performed. WB-MRA was performed in a 1.5T MRI scanner using 4 volume acquisitions with a divided dose of intravenous gadolinium gadoterate meglumine (Dotarem, Guerbet, FR). The WB-MRA data was divided into 31 anatomical arterial segments with each scored according to degree of luminal narrowing: 0 = normal, 1 = <50%, 2 = 50-70%, 3 = 70-99%, 4 = vessel occlusion. The segment scores were summed and from this a standardized atheroma score was calculated.
RESULTS The atherosclerotic burden was high with a standardised atheroma score of 39.511. Common CIMT showed a positive correlation with the whole body atheroma score ( 0.32, p = 0.045), however this was due to its strong correlation with the neck and thoracic segments ( 0.42 p = 0.01) with no correlation with the rest of the body. ABPI correlated with the whole body atheroma score ( -0.39, p = 0.012), which was due to a strong correlation with the ilio-femoral vessels with no correlation with the thoracic or neck vessels. On multiple linear regression, no correlation between CIMT and global atheroma burden was present ( 0.13 p = 0.45), while the correlation between ABPI and atheroma burden persisted ( -0.45 p = 0.005).
CONCLUSION ABPI but not CIMT correlates with global atheroma burden as measured by whole body contrast enhanced magnetic resonance angiography in a population with symptomatic peripheral arterial disease. However this is primarily due to a strong correlation with ilio-femoral atheroma burden.

SOLUTION: Common Carotid Intima Media Thickness and Ankle-Brachial Pressure Index Correlate with Local but Not Global Atheroma Burden: A Cross Sectional Study Using Whole Body Magnetic Resonance Angiography

PROBLEM: The discovery of microRNAs (miRNAs) provides a new and powerful tool for studying the mechanism, diagnosis and treatment of human cancers. Currently, down-regulation of tumor suppressive miRNAs by CpG island hypermethylation is emerging as a common hallmark of cancer. Here, we reported that the down-regulation of miR-33b was associated with pM stage of gastric cancer (GC) patients. Ectopic expression of miR-33b in HGC-27 and MGC-803 cells inhibited cell proliferation, migration and invasion, which might be due to miR-33b targeting oncogene c-Myc. Moreover, enhanced methylation level of the CpG island upstream of miR-33b in GC patients with down-regulated miR-33b was confirmed by methylation-specific PCR (MSP) amplification. Furthermore, re-introduction of miR-33b significantly suppressed tumorigenesis of GC cells in the nude mice. In conclusion, miR-33b acts as a tumor suppressor and hypermethylation of the CpG island upstream of miR-33b is responsible for its down-regulation in gastric cancer.

SOLUTION: DNA Methylation mediated down-regulating of MicroRNA-33b and its role in gastric cancer

PROBLEM: The N-myc downstream regulated gene 1 (NDRG1) is significantly associated with advanced tumor stages and poor survival of hepatocellular carcinoma (HCC), thereby implicating it as a potential target for HCC treatment. We aim to further understand its biological roles in hepatocarcinogenesis, as a means to exploit it for therapeutic purposes. By screening using the ProtoArray®️ Human Protein Microarrays, we identified glycogen synthase kinase 3 (GSK-3) and the orphan nuclear receptor (Nur77) as potential interaction partners of NDRG1. These interactions were confirmed in HCC cell lines in vitro by co-immunoprecipitation; and co-localizations of NDRG1 with GSK-3 and Nur77 were observed by immunofluorescence staining. Additionally, high levels of NDRG1 competitively bind to GSK-3 and Nur77 to allow -catenin to escape degradation, with consequent elevated levels of downstream oncogenic genes. In vivo, we consistently observed that NDRG1 suppression in HCC xenografts decreased -catenin levels and its downstream target Cyclin D1, with concomitant tumor growth inhibition. Clinically, the over-expression of NDRG1 in HCC patient samples is positively correlated with GSK-3-9ser (|"' R | = 0.28, p = 0.01), Nur77 (|"' R | = 0.42, p < 0.001), and -catenin (| R |= 0.32, p = 0.003) expressions. In conclusion, we identified GSK-3 and Nur77 as novel interaction partners of NDRG1. These protein-protein interactions regulate the turnover of -catenin and subsequent downstream signaling mediated by -catenin in HCC cells, and provides potential targets for future therapeutic interventions.

SOLUTION:
NDRG1 promotes growth of hepatocellular carcinoma cells by directly interacting with GSK-3 and Nur77 to prevent -catenin degradation