Practicing Scrum in Institute Course

Scrum is one of the most popular agile methods following \textit{Manifesto for Agile Software Development}, and is a value-driven software development approach which focuses on maximizing the values of the customers. Many top software companies like Amazon.com, Apple, and Microsoft directly apply Scrum and other Agile methods for developing great software products. To raise the talents required by industry, teaching agile methods in university is necessary. However, with the limits of time, space, and experts in agile development, it can be difficult for students to learn the practices of agile methods in college. In this paper, we describe an experimental course in Feng Chia University that practices Scrum for term projects among five teams composed of 34 students. To the best of our knowledge the practices is the few attempts to practically apply all the factors described in Scrum framework such as sprint planning, daily scrum, review, retrospective meetings, product owner, and scrum master in institutional agile education. In this paper, the design and the process of the term projects based on Scrum are described, and the lessons learned from practicing Scrum in college are presented as discussion

Clinical Efficacy and Post-Treatment Seromarkers Associated with the Risk of Hepatocellular Carcinoma among Chronic Hepatitis C Patients

This follow-up study enrolled chronic hepatitis C patients to evaluate the treatment efficacy and to identify post-treatment seromarkers associated with risk of hepatocellular carcinoma (HCC) among patients with a sustained virological response (SVR) or nonsustained virological response (NSVR). A total of 4639 patients who received pegylated interferon and ribavirin during 2004–2013 were followed until December 2014. HCC was confirmed through health examinations and data linkage with a national database. A total of 233 HCC cases were reported after 26,163 person-years of follow-up, indicating an incidence of 8.9 per 1000 person-years: 6.9 for SVR and 21.6 for NSVR per 1000 person-years. The associated risk of HCC in patients with SVR was 0.37 (0.22–0.63) for those without cirrhosis and 0.54 (0.31–0.92) for those with cirrhosis compared with their respective counterparts with NSVR. Among patients with SVR, advanced age, male gender, cirrhosis, decreased platelet count, and increased aspartate aminotransferase and α-fetoprotein levels were associated with HCC (p < 0.001). The treatment of chronic hepatitis C patients before they developed cirrhosis showed a higher efficacy than did the treatment of those who had already developed cirrhosis. Patients with SVR may still have a risk of HCC and need to be regularly monitored

Helicobacter pylori activates HMGB1 expression and recruits RAGE into lipid rafts to promote inflammation in gastric epithelial cells

Helicobacter pylori infection is associated with several gastrointestinal disorders in the human population worldwide. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates a variety of inflammation functions. The interaction between HMGB1 and receptor for advanced glycation end-products (RAGE) triggers nuclear factor (NF)-κB expression, which in turn stimulates the release of proinflammatory cytokines such as interleukin (IL)-8 and enhances the inflammatory response. However, how H. pylori activates HMGB1 expression and mobilizes RAGE into cholesterol-rich microdomains in gastric epithelial cells to promote inflammation has not been explored. In this study, we found that HMGB1 and RAGE expression increased significantly in H. pylori-infected cells compared to uninfected cells. Blocking HMGB1 by neutralizing antibody abrogated H. pylori-elicited RAGE, suggesting that RAGE expression follows HMGB1 production, and silenced RAGE-attenuated H. pylori-mediated NF-κB activation and IL-8 production. Furthermore, significantly more RAGE was present in detergent-resistant membranes extracted from H. pylori-infected cells than in those from uninfected cells, indicating that H. pylori exploited cholesterol to induce the HMGB1 signaling pathway. These results indicate that HMGB1 plays a crucial role in H. pylori-induced inflammation in gastric epithelial cells, which may be valuable in developing treatments for H. pylori-associated diseases

Statin decreases <i>H</i>. <i>pylori</i> CagA translocation/phosphorylation in gastric epithelial cells.

<p>Three lines of gastric epithelial cells (AGS, MKN45, and TSGH9201) were pretreated with 25 μM simvastatin, then infected with <i>H</i>. <i>pylori</i> at an MOI of 100 for 6 h. (A) Whole-cell lysates were subjected to immunoblot for analysis of CagA translocation/phosphorylation, respectively. β-actin was determined as an internal control for equal loading. The quantitative results of (B) translocated CagA and (C) phosphorylated CagA were determined using densitometric analysis and presented as means ± standard deviations for three independent experiments. Statistical analysis was performed using Student’s <i>t</i>-test. *, <i>P</i> < 0.05 compared with <i>H</i>. <i>pylori</i>-infected cells without simvastatin pretreatment.</p

The level of cellular cholesterol in gastric epithelial cells was reduced through treatment with statins.

<p>AGS cells were treated with various concentrations of simvastatin (0–50 μM) and infected with <i>H</i>. <i>pylori</i> at an MOI of 100 for 6 h. (A) Whole cell lysates were then prepared for cholesterol level analysis (open bar). (B) Bacterial suspension was plated onto Brucella blood agar plates and incubated for 3–4 days, after which the CFUs were counted for evaluation of bacterial viability (open circle). (B) Cell viability was not influenced by treatment with simvastatin, as determined by the trypan blue exclusion assay. The data are presented as means ± standard deviations for three independent experiments. Statistical significance was evaluated using Student’s <i>t</i>-test (*, <i>P</i> < 0.05).</p

Statin reduces <i>H</i>. <i>pylori</i>-induced elongation of gastric epithelial cells.

<p>(A) AGS cells were pretreated with simvastatin (25 μM) and infected with <i>H</i>. <i>pylori</i> at an MOI of 100 for 6 h. (B) The proportion of cells with the elongated (hummingbird) phenotype was evaluated as described in the materials and methods section. The quantitative results represent the means and standard deviations for three independent experiments. *, <i>P</i> < 0.05, compared with <i>H</i>. <i>pylori</i>-infected cells without simvastatin pretreatment. Scale bar, 10 μm.</p

Statin attenuates <i>H</i>. <i>pylori</i> CagA-induced pathogenesis.

<p>(A) AGS cells were transfected with κB-Luc vector and incubated for 24 h. The cells were then treated with 25 μM simvastatin, and infected with <i>H</i>. <i>pylori</i> at an MOI of 100 for 6 h. The cells were then prepared for luciferase activity assays. (B) AGS cells were pretreated with simvastatin (25 μM) prior to infection with <i>H</i>. <i>pylori</i> at an MOI of 100 for 16 h. The concentration of IL-8 in the culture supernatant was analyzed using the ELISA method. Results are expressed as means ± standard deviations. *, <i>P</i> < 0.05 was considered statistically significant.</p