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.

Ex 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.

Ex Output:
Does 17Beta-estradiol suppress TLR3-induced cytokine and chemokine production in endometrial epithelial cells?


Ex Input:
An intense systemic inflammatory response is observed following reperfusion after cardiac arrest. Heparin-binding protein (HBP) is a granule protein released by neutrophils that intervenes in endothelial permeability regulation. In the present study, we investigated plasma levels of HBP in a large population of patients resuscitated from out-of-hospital cardiac arrest. We hypothesized that high circulating levels of HBP are associated with severity of post-cardiac arrest syndrome and poor outcome.', 'Plasma was obtained from 278 patients enrolled in a prospective multicenter observational study in 21 intensive care units (ICU) in Finland. HBP was assayed at ICU admission and 48\xa0h later. Multiple organ dysfunction syndrome (MODS) was defined as the 24\xa0h Sequential Organ Failure Assessment (SOFA) score\u2009≥\u200912. ICU death and 12-month Cerebral Performance Category (CPC) were evaluated. Multiple linear and logistic regression tests and receiver operating characteristic curves with area under the curve (AUC) were performed.', 'Eighty-two percent of patients (229 of 278) survived to ICU discharge and 48\xa0% (133 of 276) to 1\xa0year with a favorable neurological outcome (CPC 1 or 2). At ICU admission, median plasma levels of HBP were markedly elevated, 15.4 [9.6-31.3] ng/mL, and persisted high 48\xa0h later, 14.8 [9.8-31.1] ng/mL. Admission levels of HBP were higher in patients who had higher 24\xa0h SOFA and cardiovascular SOFA score (p\u2009<\u20090.0001) and in those who developed MODS compared to those who did not (29.3 [13.7-60.1] ng/mL vs. 13.6 [9.1-26.2] ng/mL, p\u2009<\u20090.0001; AUC\u2009=\u20090.70\u2009±\u20090.04, p\u2009=\u20090.0001). Admission levels of HBP were also higher in patients who died in ICU (31.0 [17.7-78.2] ng/mL) compared to those who survived (13.5 [9.1-25.5] ng/mL, p\u2009<\u20090.0001) and in those with an unfavorable 12-month neurological outcome compared to those with a favorable one (18.9 [11.3-44.3] ng/mL vs. 12.8 [8.6-30.4] ng/mL, p\u2009<\u20090.0001). Admission levels of HBP predicted early ICU death with an AUC of 0.74\u2009±\u20090.04 (p\u2009<\u20090.0001) and were independently associated with ICU death (OR [95 %CI] 1.607 [1.076-2.399], p\u2009=\u20090.020), but not with unfavorable 12-month neurological outcome (OR [95 %CI] 1.154 [0.834-1.596], p\u2009=\u20090.387).

Ex Output:
Is elevated plasma heparin-binding protein associated with early death after resuscitation from cardiac arrest?


Ex Input:
To examine whether the noninvasive technique of blood oxygenation level dependent magnetic resonance imaging (BOLD MRI) can detect changes in renal medullary oxygenation following administration of a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). Hypertension is associated with endothelial dysfunction and is characterized by a lack of response to endothelial-dependent vasoactive substances, including nitric oxide synthase inhibitors. We hypothesized that the magnitude of the change would be reduced in the kidneys of hypertensive subjects relative to normal controls.', 'To test this hypothesis, data were obtained in spontaneously hypertensive rats (SHR, n = 6). Wistar-Kyoto rats (WKY, n = 7) were used as normotensive controls.', 'As expected, WKY rats showed a significant response to L-NAME (R(2)* increasing from 23.6+/-1.5 Hz to 32.5+/-2.2 Hz, P < 0.05), while SHR exhibited a minimal change in medullary oxygenation (R(2)* measuring 31.9+/-2.8 Hz pre- and 35.5+/-2.2 Hz post-L-NAME). The baseline R(2)* in SHR is found to be comparable to post-L-NAME values in WKY rats, suggesting a basal deficiency of nitric oxide in SHR.

Ex Output:

Do kidneys in hypertensive rats show reduced response to nitric oxide synthase inhibition as evaluated by BOLD MRI?