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\"South Korea offers a timely illustration of the relationship between social media and national security. The author describes the effects of trade-offs between security and civil liberties and how narratives advanced through social media differ from those reported by traditional news outlets\"-- Provided by publisher.

Adjuvant chemotherapy after surgery improves survival of patients with stage II–III, resectable gastric cancer. However, the overall survival benefit observed after adjuvant chemotherapy is moderate, suggesting that not all patients with resectable gastric cancer treated with adjuvant chemotherapy benefit from it. We aimed to develop and validate a predictive test for adjuvant chemotherapy response in patients with resectable, stage II–III gastric cancer. In this multi-cohort, retrospective study, we developed through a multi-step strategy a predictive test consisting of two rule-based classifier algorithms with predictive value for adjuvant chemotherapy response and prognosis. Exploratory bioinformatics analyses identified biologically relevant candidate genes in gastric cancer transcriptome datasets. In the discovery analysis, a four-gene, real-time RT-PCR assay was developed and analytically validated in formalin-fixed, paraffin-embedded (FFPE) tumour tissues from an internal cohort of 307 patients with stage II–III gastric cancer treated at the Yonsei Cancer Center with D2 gastrectomy plus adjuvant fluorouracil-based chemotherapy (n=193) or surgery alone (n=114). The same internal cohort was used to evaluate the prognostic and chemotherapy response predictive value of the single patient classifier genes using associations with 5-year overall survival. The results were validated with a subset (n=625) of FFPE tumour samples from an independent cohort of patients treated in the CLASSIC trial (NCT00411229), who received D2 gastrectomy plus capecitabine and oxaliplatin chemotherapy (n=323) or surgery alone (n=302). The primary endpoint was 5-year overall survival. We identified four classifier genes related to relevant gastric cancer features (GZMB, WARS, SFRP4, and CDX1) that formed the single patient classifier assay. In the validation cohort, the prognostic single patient classifier (based on the expression of GZMB, WARS, and SFRP4) identified 79 (13%) of 625 patients as low risk, 296 (47%) as intermediate risk, and 250 (40%) as high risk, and 5-year overall survival for these groups was 83·2% (95% CI 75·2–92·0), 74·8% (69·9–80·1), and 66·0% (60·1–72·4), respectively (p=0·012). The predictive single patient classifier (based on the expression of GZMB, WARS, and CDX1) assigned 281 (45%) of 625 patients in the validation cohort to the chemotherapy-benefit group and 344 (55%) to the no-benefit group. In the predicted chemotherapy-benefit group, 5-year overall survival was significantly improved in those patients who had received adjuvant chemotherapy after surgery compared with those who received surgery only (80% [95% CI 73·5–87·1] vs 64·5% [56·8–73·3]; univariate hazard ratio 0·47 [95% CI 0·30–0·75], p=0·0015), whereas no such improvement in 5-year overall survival was observed in the no-benefit group (72·9% [66·5–79·9] in patients who received chemotherapy plus surgery vs 72·5% [65·8–79·9] in patients who only had surgery; 0·93 [0·62–1·38], p=0·71). The predictive single patient classifier groups (chemotherapy benefit vs no-benefit) could predict adjuvant chemotherapy benefit in terms of 5-year overall survival in the validation cohort (pinteraction=0·036 in univariate analysis). Similar results were obtained in the internal evaluation cohort. The single patient classifiers validated in this study provide clinically important prognostic information independent of standard risk-stratification methods and predicted chemotherapy response after surgery in two independent cohorts of patients with resectable, stage II–III gastric cancer. The single patient classifiers could complement TNM staging to optimise decision making in patients with resectable gastric cancer who are eligible for adjuvant chemotherapy after surgery. Further validation of these results in prospective studies is warranted. Ministry of ICT and Future Planning; Ministry of Trade, Industry, and Energy; and Ministry of Health and Welfare.

Seoul Station is home to Dokgo, a man shrouded in mystery with no memories of his past. Until one day his subdued existence is disrupted when he stumbles upon a lost wallet, triggering a chain of events that will change the course of his life. Enter Mrs. Yeom, a retired history teacher turned convenience store owner, who, upon discovering Dokgo's act of kindness in returning her purse, offers him a meal as a token of her gratitude. Their chance encounter blossoms into an unexpected alliance when the man's bravery saves the store from ruin, earning him not just a job but a place in the heart of the neighbourhood. But just when things are looking up for Dokgo, Mrs. Yeom's troubled son, eager to sell the store, hires a detective to dig into the mysterious man's past and unearth what he seems to be trying so hard to forget.

Sodium–glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular events in humans with type 2 diabetes (T2D); however, the underlying mechanism remains unclear. Activation of the NLR family, pyrin domain-containing 3 (NLRP3) inflammasome and subsequent interleukin (IL)-1β release induces atherosclerosis and heart failure. Here we show the effect of SGLT2 inhibitor empagliflozin on NLRP3 inflammasome activity. Patients with T2D and high cardiovascular risk receive SGLT2 inhibitor or sulfonylurea for 30 days, with NLRP3 inflammasome activation analyzed in macrophages. While the SGLT2 inhibitor’s glucose-lowering capacity is similar to sulfonylurea, it shows a greater reduction in IL-1β secretion compared to sulfonylurea accompanied by increased serum β-hydroxybutyrate (BHB) and decreased serum insulin. Ex vivo experiments with macrophages verify the inhibitory effects of high BHB and low insulin levels on NLRP3 inflammasome activation. In conclusion, SGLT2 inhibitor attenuates NLRP3 inflammasome activation, which might help to explain its cardioprotective effects. SGLT2 inhibitors, a class of type 2 diabetes medication, reduce cardiovascular events in patients beyond expectation from blood sugar control. Here the authors report a randomized controlled trial showing that SGLT2 inhibitors reduce inflammasome activation in peripheral macrophages, which may contribute to the cardiovascular protection.

When a girl in a wheelchair calls to people far below to look up and see her, one finds a way to brighten her day.

In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis. Inflammatory diseases: Understanding mitochondrial DNA release Cytosolic DNA activates the cGAS-STING pathway which mediates inflammation and antiviral response. One source of cytosolic DNA is ‘self ‘ DNA, such as mitochondrial DNA. Studies of how mitochondria can release DNA and trigger dangerous immune responses are revealing potential treatments for inflammatory diseases. Cells isolate DNA in their nuclei and mitochondria, but if this ‘self-DNA’ leaks out, it triggers the same immune responses that the body uses to fight DNA from viruses or bacteria. Jeonghan Kim at The Catholic University of Korea College of Medicine in Seoul, South Korea, and co-workers reviewed research into the mechanism causing mitochondrial DNA release, and the resulting inflammatory pathways. Although cGAS-STING is the central driver of such inflammation, treatments targeting it may also suppress the body’s antimicrobial immunity. A safer alternative maybe to inhibit mitochondrial VDAC oligomerization, which releases mitochondrial DNA.

\"What does it mean to say that it is 'we the people' who 'ordain and establish' a constitution? Who are those sovereign people, and how can they do so? Interweaving history and theory, constitutional scholar Chaihark Hahm and political theorist Sung Ho Kim attempt to answer these perennial questions by revisiting the constitutional politics of postwar Japan and Korea. Together, these experiences demonstrate the infeasibility of the conventional assumption that there is a clearly bounded sovereign 'people' prior to constitution-making which may stand apart from both outside influence and troubled historical legacies. The authors argue that 'we the people' only emerges through a deeply transformative politics of constitutional founding and, as such, a democratic constitution and its putative author are mutually constitutive. Highly original and genuinely multidisciplinary, this book will be of interest to scholars of comparative constitutionalism as well as observers of ongoing constitutional debates in Japan and Korea\"-- Provided by publisher.

Crohn's disease (CD) and ulcerative colitis (UC) are considered rare diseases in developing countries. We have evaluated the incidence and prevalence of CD and UC over time in a district of Seoul, Korea.MethodsA population-based study was performed from 1986 to 2005 in the Songpa-Kangdong district of Seoul. To recruit patients as completely as possible, multiple information sources, including all medical facilities in the study area and 3 referral centers nearby but outside the study area, were used.ResultsDuring the 20-year study period, 138 incident cases of CD (102 men, 36 women) and 341 incident cases of UC (170 men, 171 women) were identified. For the 20-year period, the adjusted mean annual incidence rates of CD and UC per 100,000 inhabitants were 0.53 (95% CI 0.44–0.62) and 1.51 (95% CI 1.34–1.67), respectively. When analyzed by 5-year intervals, the mean annual incidence rates of CD and UC increased significantly, from 0.05 and 0.34 per 100,000 inhabitants, respectively, in 1986–1990 to 1.34 and 3.08 per 100,000 inhabitants, respectively, in 2001–2005. The adjusted prevalence rates of CD and UC per 100,000 inhabitants on December 31, 2005, were 11.24 (95% CI 9.29–13.18) and 30.87 (95% CI 27.47–34.27), respectively.ConclusionsThe incidence and prevalence of CD and UC in Seoul, Korea, are still low compared with those in Western countries, but are rapidly increasing.

Reactive oxygen species (ROS) contribute to the development of non-alcoholic fatty liver disease. ROS generation by infiltrating macrophages involves multiple mechanisms, including Toll-like receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation. Here, we show that palmitate-stimulated CD11b + F4/80 low hepatic infiltrating macrophages, but not CD11b + F4/80 high Kupffer cells, generate ROS via dynamin-mediated endocytosis of TLR4 and NOX2, independently from MyD88 and TRIF. We demonstrate that differently from LPS-mediated dimerization of the TLR4–MD2 complex, palmitate binds a monomeric TLR4–MD2 complex that triggers endocytosis, ROS generation and increases pro-interleukin-1β expression in macrophages. Palmitate-induced ROS generation in human CD68 low CD14 high macrophages is strongly suppressed by inhibition of dynamin. Furthermore, Nox2 -deficient mice are protected against high-fat diet-induced hepatic steatosis and insulin resistance. Therefore, endocytosis of TLR4 and NOX2 into macrophages might be a novel therapeutic target for non-alcoholic fatty liver disease. Reactive species of oxygen promote the development of hepatic steatosis. Here, Kim et al. demonstrate that palmitate stimulates macrophage infiltration and increases oxidative stress during steatosis by binding to the TLR4–MD2 complex, which results in the activation of NOX2.