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: Results from GOG 178 showed a prolongation of progression-free survival (PFS) with the immediate use of chemotherapy (CT) following a complete clinical response (CR) in patients with stage III-IV ovarian cancer. We wanted to evaluate our strategy of reserving second line (2nd line) chemotherapy to the time of clinical recurrence by determining PFS intervals following first, second, and third line agents and to compare these finding to results of GOG 178.', 'We conducted a retrospective parallel study to GOG 178 using identical criteria for PFS definitions. Patients (pts) with stage III-IV cancer achieving a CR following surgery and five to eight cycles of platinum-based CT were identified. Patients not obtaining a CR and those with a CR who underwent second look surgery were excluded. Rather than immediately beginning consolidation CT after CR, second line agents were started at recurrence and were followed by a third line when pts progressed. Clinical-pathologic characteristics were abstracted, and time intervals including time to recurrence, time to use of second line CT, time to use of third line (3rd line) CT, and survival were recorded. Time intervals were studied by Kaplan-Meier method.', 'Of 217 reviewed pts (1991-2001), 59 eligible pts were identified. Forty-nine patients had stage III disease and ten had stage IV. At completion of surgery, 44 were optimally debulked. With a median follow-up of 51 months, the median PFS (from CR) of all patients was 20 months. At 5 years, 36% of pts remain disease-free, and 66% of pts are alive. Twenty-three pts have not received second line agents, and thirty-six have received them. For all pts, the median time from CR to start of second line chemotherapy was 21 months, and the median time to start of third line agents was 43 months. Recurrences occurred after 6 months from completion of first line (1st line) therapy in 87% of cases and after 12 months in 50%.

Output: Is timing n't everything : an analysis of when to start salvage chemotherapy in ovarian cancer?


Input: Consider Input: Urokinase (uPA) modulates cellular and extracellular matrix responses within the microenvironment of the vessel wall and has been shown to activate the epidermal growth factor receptor (EGFR). This study examines the role of the protease domain of uPA during EGFR activation in human vascular smooth muscle cells (VSMC).', 'Human coronary VSMC were cultured in\xa0vitro. Assays of cell proliferation and EGFR phosphorylation were examined in response to the carboxyterminal fragment of uPA (CTF) in the presence and absence of the plasmin, metalloprotease and a disintegrin and metalloproteinase (ADAM) inhibitors, heparin-bound epidermal growth factor (HB-EGF), and EGFR inhibitors, and small interfering RNA to EGFR and ADAMs.', 'CTF produced a dose-dependent increase in DNA synthesis and cell proliferation in human VSMC, which was blocked in a dose-dependent manner by both plasmin inhibitors and the EGFR inhibitor, AG1478. CTF induced time-dependent EGFR phosphorylation, which was blocked by inhibitors of plasmin and metalloproteinases activity. The presence of urokinase plasminogen activator receptor was not required. Inhibition of ADAM-10 and -12, and of HB-EGF blocked EGFR activation in response to CTF. CTF-mediated activation of EGFR was mediated through Gβγ, src, and NAD(P)H oxidase.


Output: Does protease-mediated human smooth muscle cell proliferation by urokinase require epidermal growth factor receptor transactivation by triple membrane signaling?