To improve therapeutic outcome of TNBC, reliable predictive biomarkers and newer drugs against the known molecular pathways are required.

Both base excess and lactate, or the combination of the two, can be used to predict outcome in patients admitted to the intensive care unit. These variables could be utilized to identify patients who have a high risk for mortality and thus who should be admitted to the intensive care unit.

<b><i>Aim:</i></b> The aim of this study was to study the role of key epigenetic regulators pertaining to DNA methylation and histone-modification systems in <i>Helicobacter pylori</i> (HP)-associated gastritis and gastric carcinogenesis. <b><i>Methods:</i></b> The expression of DNA methyltransferase (DNMT-1, 3A, and 3B) and the catalytic subunit of polycomb repressive complex-2 (enhancer of zeste homolog 2 [EZH2]) in gastric carcinomas (<i>n</i> = 104), mucosa adjacent to carcinoma (<i>n</i> = 104), HP-associated gastritis (<i>n</i> = 95), and histologically normal mucosa (<i>n</i> = 31) was assessed by immunohistochemistry and qRT-PCR. <b><i>Results:</i></b> The expression of all 3 DNMTs and EZH2 was significantly higher in HP-associated gastritis and carcinoma cases than in those with adjacent and normal mucosa. The expression of DNMT-1 and 3B was maximum in HP-associated gastritis. DNMT-3A showed higher expression in carcinoma-adjacent mucosa than in normal mucosa. Interestingly, the expression of EZH2 was higher in cases of HP-associated gastritis with metaplasia than in those without metaplasia and also in cases of intestinal type of adenocarcinoma. Significant positive correlation of EZH2 was identified with DNMT-1, DNMT-3A, and DNMT-3B. However, none of these markers was associated with survival outcome. <b><i>Conclusion:</i></b> This study establishes an important role of the key epigenetic regulators in the pathogenesis of both HP-associated gastritis and gastric carcinoma. Higher expression of all the epigenetic markers in the gastritis and their persistence in the carcinoma point toward their implications in HP-driven gastric carcinogenesis. Further, an inter-relation between the 2 arms of epigenetics, namely, DNA methylation and histone-modification in the pathogenesis of gastric carcinoma, is also documented. Given the reversibility of epigenetic phenomenon, these molecules may be of important therapeutic use.

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Introduction Fibrinolytic shutdown plays a pivotalrole in the pathogenesis of multiple organ dysfunction syndrome (MODS) in disseminated intravascular coagulation (DIC). We tested the hypothesis that the levels of thrombin activatable fi brinolysis inhibitor (TAFI) are not suffi cient to overcome fi brinolytic shutdown, thus contributing to MODS and the poor prognosis in sepsis-induced DIC. Methods Fifty patients with sepsis, severe sepsis, or septic shock were enrolled in the study. The DIC was diagnosed based on the Japanese Association for Acute Medicine (JAAM) DIC criteria. The overt DIC scores based on the International Society on Thrombosis and Haemostasis (ISTH) were also calculated. On the day of sepsis diagnosis (day 1), and days 3 and 5, we measured TAFI, soluble fi brin, and global coagulation and fi brinolysis markers. Results The JAAM DIC scores on day 1 and maximum JAAM DIC scores were independent predictors of patient death and MODS, respectively. The JAAM DIC patients, especially those who simultaneously met the ISTH overt DIC criteria, showed lower TAFI antigen levels and activity, and higher levels of soluble fi brin in comparison with non-DIC patients. There were diff erences in the levels of soluble fi brin and TAFI activity between the patients with and without MODS. The fi ndings of stepwise logistic regression and multiple regression analyses suggested that low TAFI activity is an independent predictor of patient death and MODS. A multiple regression analysis also indicated that soluble fi brin negatively correlated with the TAFI activity in DIC patients. Conclusion Thrombin activation results in the consumption of TAFI. Low TAFI activity is involved in the pathogenesis of DIC-induced MODS and poor prognosis.