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.

Example Input: To determine whether cancer antigen-125 (CA-125) levels are increased in women with endometriosis, especially in those with endometriomas (OMAs), deep infiltrating lesions (DIE), and superficial endometriosis (SUP) compared with controls without endometriosis in a large cohort of operated women.', 'Cross-sectional study (Canadian Task Force classification II-2).', 'Tertiary-care university hospital.', 'Four hundred six women with histologically proven endometriosis and 279 women without endometriosis.', 'Surgical examination of the abdomino-pelvic cavity.', 'Preoperative serum CA-125 antigen levels were evaluated by electrochemoluminescence immunoassay in women with endometriosis and controls. Correlations between serum CA-125 levels and clinical and anatomical characteristics of disease severity were examined. Women with endometriosis displayed higher mean serum CA-125 levels compared with disease-free controls (50.1\xa0±\xa062.4 U/mL vs 22.5\xa0±\xa025.2 U/mL; p\xa0≤\xa0.001). CA-125 levels were significantly increased in women with OMA (60.8\xa0±\xa063.5 U/mL) and DIE (55.2\xa0±\xa068.7 U/mL) compared with women with SUP (23.2\xa0±\xa024.5 U/mL) and controls (22.5\xa0±\xa025.2 U/mL). There was no difference in CA-125 levels between patients with SUP and controls and between patients with OMA and DIE. CA-125 serum levels were correlated with DIE severity: the mean number of DIE lesions and worst DIE lesion.
Example Output: Is increased serum cancer antigen-125 a marker for severity of deep endometriosis?

Example Input: The human endometrium is an important site for contact between the host and pathogens ascending the reproductive tract, and thus plays an important role in female reproductive tract immunity. Previous work in our laboratory has suggested that Toll-like receptors (TLRs) are involved in endometrial epithelial recognition of pathogens and that ligation of endometrial TLRs results in the production of cytokines and chemokines important for both immune and reproductive functions of the endometrium. We have also demonstrated cyclic regulation of TLR3 mRNA and protein expression in human endometrium, suggesting that steroid hormones might play a role in the expression and function of TLR3. In this study, the effects of 17beta-estradiol (E2) and progesterone (P) on TLR3 expression and function in endometrial cell lines were investigated.', 'Endometrial epithelial cell lines were cultured and examined for the presence of TLR3 and hormone receptors by endpoint RT-PCR. For hormonal studies, cells were pre-treated with ethanol vehicle, 10(-8) M E2, and/or 10(-7) M P. For antagonist assays, cells were treated with the ER antagonist, ICI 182, 780, or the PR antagonist, RU486, for two hours prior to treatment with hormones. Following hormone or hormone/antagonist pre-treatment, cells were stimulated with vehicle, the synthetic TLR3 ligand, polyinosinic-polycytidylic acid (Poly I:C), a negative dsDNA control, or a positive control. Cytokine and chemokine production post-stimulation was measured by ELISA. The effects of E2 and P on TLR3 mRNA and protein expression were measured using Real Time RT-PCR and FACS analysis, respectively.', 'Stimulation of TLR3-expressing cells with the synthetic TLR3 ligand, Poly I:C, resulted in the production of cytokines and chemokines important for endometrial function and regulation. Suppression of Poly I:C-induced cytokine and chemokine production by cells treated with 10(-8) M E2, but not cells treated with 10(-7) M P, was observed in endometrial epithelial cell lines expressing TLR3 and estrogen receptor alpha (ERalpha). The effects of E2 were not observed on cells which did not express ERalpha or in cells pre-treated with the ER antagonist, ICI 182, 780. Treatment with E2 did not affect TLR3 mRNA or protein expression. However, treatment with E2 did suppress cytokine and chemokine production resulting from TLR3 stimulation with Poly I:C, suggesting that E2 modulates TLR3 function.
Example Output: Does 17Beta-estradiol suppress TLR3-induced cytokine and chemokine production in endometrial epithelial cells?

Example Input: Existing data on perfusion imaging assumes the perihemorrhagic zone (PHZ) in patients with intracerebral hemorrhage (ICH) to be size steady. This study investigates the size of the perihemorrhagic zone (PHZ) in patients with lobar ICH in relation to hematoma volume during the course of treatment using perfusion CT (PCT).', 'The present analysis is based on a previously reported cohort of 20 patients undergoing surgical evacuation for lobar SICH, with pre- and early postoperative PCT scanning. Time to peak of the residue function (T max) was measured based on the 360° cortical banding method and singular value decomposition. The size of PHZ was determined before and after treatment and correlated with hematoma volume.', 'Preoperative mean hematoma volume constituted 63.0 ml (interquartile ranges (IQR) 39.7-99.4 ml), which correlated significantly (r=0.563, p=0.010) with mean PHZ size (5.67 cm, IQR 5.44-8.17 cm). Following a surgical hematoma evacuation, mean hematoma volume was reduced to 2.5 ml IQR 0.0-9.5 ml, which also resulted in a significant reduction of PHZ size to 0.45 cm(IQR 0.0-1.36 cm; p<0.001). There was no association between postoperative hematoma volume and size of the PHZ.
Example Output:
Does the extent of the perihemorrhagic perfusion zone correlate with hematoma volume in patients with lobar intracerebral hemorrhage?