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.

Input: Consider Input: Aggressive periodontitis is characterized by rapid destruction of periodontal tissue caused by Aggregatibacter actinomycetemcomitans. Interleukin (IL)-1β is a proinflammatory cytokine, and its production is tightly regulated by inflammasome activation. Xylitol, an anticaries agent, is anti-inflammatory, but its effect on inflammasome activation has not been researched. This study investigates the effect of xylitol on inflammasome activation induced by A. actinomycetemcomitans.', 'The differentiated THP-1 macrophages were stimulated by A. actinomycetemcomitans with or without xylitol and the expressions of IL-1β and inflammasome components were detected by real time PCR, ELISA, confocal microscopy and Immunoblot analysis. The effects of xylitol on the adhesion and invasion of A. actinomycetemcomitans to cells were measured by viable cell count.', 'A. actinomycetemcomitans increased pro IL-1β synthesis and IL-1β secretion in a multiplicity of infection- and time-dependent manner. A. actinomycetemcomitans also stimulated caspase-1 activation. Among inflammasome components, apoptosis-associated speck-like protein containing a CARD (ASC) and absent in melanoma 2 (AIM2) proteins were upregulated by A. actinomycetemcomitans infection. When cells were pretreated with xylitol, proIL-1β and IL-1β production by A. actinomycetemcomitans infection was significantly decreased. Xylitol also inhibited ASC and AIM2 proteins and formation of ASC puncta. Furthermore, xylitol suppressed internalization of A. actinomycetemcomitans into differentiated THP-1 macrophages without affecting viability of A. actinomycetemcomitans within cells.

Output: Does aggregatibacter actinomycetemcomitans-Induced AIM2 Inflammasome Activation be Suppressed by Xylitol in Differentiated THP-1 Macrophages?


Input: Consider Input: The clinical significance of the hepatitis B virus core-related antigen (HBcrAg) assay in monitoring the antiviral effects of lamivudine is reviewed.', 'The HBcrAg assay simultaneously measured serum levels of hepatitis B core (HBc) and e (HBe) antigens using monoclonal antibodies which recognize common epitopes of these two denatured antigens.', 'Although serum HBcrAg levels correlated linearly with those of hepatitis B virus (HBV) DNA in natural course, the decrease in HBcrAg was significantly slower than in HBV DNA after initiation of lamivudine administration. We analyzed the clinical significance of HBV DNA and HBcrAg levels to predict the occurrence of lamivudine resistance. HBV DNA measurement may be useful to identify patients who are at high risk of developing lamivudine resistance, and HBcrAg measurement may help to detect patients who are at low risk of drug resistance. The measurement of HBcrAg was also found to be a useful prognosticator for reactivation of hepatitis after cessation of lamivudine administration.

Output: Is hepatitis B core-related antigen assay useful for monitoring the antiviral effects of nucleoside analogue therapy?


Input: Consider Input: Plasminogen Activator Inhibitor-1 (PAI-1) is the most potent endogenous inhibitor of fibrinolysis which is implicated in the pathogenesis of myocardial infarction and metabolic syndrome. The formation of reactive oxygen species (ROS) plays an important role in the pathology of vascular disorders and has been shown to increase PAI-1 expression by endothelial cells. Growing evidence indicates that NADPH oxidase and in particular the constitutively active Nox4-p22(phox) complexes are major sources of ROS in endothelial cells. The aim of the present study was to characterize the role of NADPH oxidase and in particular Nox4 in the regulation of PAI-1 expression in cultured Human Umbilical Venous Endothelial Cells (HUVECs).', 'N-acetylcysteine (NAC, scavenger of ROS), diphenylene iodonium chloride (DPI, inhibitor of flavoproteins), M40403 (superoxyde dismutase mimic) and S17834 (inhibitor of NADPH oxidase) inhibited PAI-1 release and promoter activity in HUVECs. Specific knock down of Nox4 mRNA by siRNA caused a decrease in ROS production and NADPH oxidase activity. Moreover, Nox4 silencing decreased PAI-1 expression, release and activity as well as p38 MAPK pathways and NFkappaB activation. These signalling pathways are also involved in PAI-1 release.


Output: Does nox4 mediate the expression of plasminogen activator inhibitor-1 via p38 MAPK pathway in cultured human endothelial cells?