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 Q]: Lipopolysaccharide (LPS)-induced preconditioning protects neurons against traumatic spinal cord injury (TSCI) in rats. This study sought to test whether Nrf2, a transcription factor, mediated LPS-induced preconditioning.', 'The TSCI model was established using a standardized NYU impactor on adult female rats. Rats were pretreated with LPS (0.2mg/kg, IP; 72h before injury). Nrf2 was silenced by injecting a lentivirus encoding RNAi against Nrf2 into injured spinal cords. Neurologic function was assessed by Basso, Beattie and Bresnahan (BBB) scores 6h, 12h, 24h, 48h, 72h, 7d and 14d after TSCI. Neuronal apoptosis was measured by a TUNEL staining. Ultrastructure was observed using transmission electron microscope (TEM). The protein expression of HO-1, NQO1 and GCLC was examined using immunohistochemistry and immunoblotting.', 'The injection of a lentivirus effectively transfected GFP into injured spinal cords. The expression of Nrf2 was significantly decreased in spinal cords receiving a lentivirus encoding RNAi against Nrf2. BBB scores showed that TSCI markedly impaired nervous function, which was markedly preserved by LPS pretreatment. Nrf2 knockdown significantly suppressed LPS pretreatment-induced protection of nervous function. TEM images and TUNEL staining showed an increase in apoptotic cells when Nrf2 was silenced. Moreover, immunohistochemistry and immunoblotting analysis exhibited that LPS pretreatment significantly upregulated the expression of anti-oxidative proteins including HO-1, NQO1 and GCLC, which was suppressed when Nrf2 expression was silenced in injured spinal cords.
[EX A]: Does lipopolysaccharide-induced preconditioning protect against traumatic spinal cord injury by upregulating Nrf2 expression in rats?

[EX Q]: Proinflammatory cytokines have the potential to activate the hypothalamo-pituitary-adrenocortical (HPA) axis, and HPA axis hyperactivity is also encountered in depression. Therefore, the induction of depressive symptoms by interferon-alpha (IFN-alpha) may be mediated by changes in the cytokine network and the HPA axis.', 'In 17 hepatitis C patients undergoing IFN-alpha treatment, depressive symptoms were measured using the Montgomery-Asberg Depression Rating Scale (MADRS). In addition, serum cytokine concentrations were measured. Saliva was collected five times over the course of a day in order to assess daily average cortisol (DAC) and awakening response. Assessments were carried out at baseline and six later time points after starting treatment.', 'During treatment, the increases in the MADRS were significantly and positively correlated with soluble interleukin (IL)-2 receptor, tumor necrosis factor alpha (TNF-alpha), and IL-6. There were no significant associations between the DAC or cortisol awakening response with the MADRS score.
[EX A]: Are interferon-alpha-induced depressive symptoms related to changes in the cytokine network but not to cortisol?

[EX Q]: Hypoxia/reoxygenation (H/R) causes oxidative stress to the cell and induces apoptotic cell death. Signal transducer and activator of transcription-3 (Stat3) is one of the most important molecules involved in the initiation of liver development and regeneration, and has recently been shown to protect cells against various pathogens. In order to investigate the hepatoprotective effects of Stat3, we examined whether it protects against H/R-induced injury in primary hepatocytes.', 'Primary cultured hepatocytes were prepared from SD rats. Adenoviruses and cytokines were added 2 days and 1h prior to the H/R insult, respectively. Hepatocytes and culture media were harvested for the assays before and after H/R insult.', 'Interleukin-6 and cardiotropin-1, which may function mainly through Stat3 activation, protected cells from H/R-induced apoptosis. Adenoviral overexpression of the constitutively activated form of Stat3 (Stat3-C) reduced H/R-induced apoptosis as well as generation of reactive oxygen species (ROS) in hepatocytes. Interestingly, Stat3-C induced Mn-SOD, but not Cu/Zn-SOD, both at the protein and mRNA levels. Overexpression of Mn-SOD significantly reduced H/R-induced ROS and apoptosis by inhibiting redox-sensitive activation of caspase-3 activity.
[EX A]:
Does stat3 confer resistance against hypoxia/reoxygenation-induced oxidative injury in hepatocytes through upregulation of Mn-SOD?