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:
Transcranial direct current stimulation (tDCS) of the primary motor cortex has been shown to modulate pain and trigeminal nociceptive processing.', 'Ten patients with classical trigeminal neuralgia (TN) were stimulated daily for 20minutes over two weeks using anodal (1mA) or sham tDCS over the primary motor cortex (M1) in a randomized double-blind cross-over design. Primary outcome variable was pain intensity on a verbal rating scale (VRS 0-10). VRS and attack frequency were assessed for one month before, during and after tDCS. The impact on trigeminal pain processing was assessed with pain-related evoked potentials (PREP) and the nociceptive blink reflex (nBR) following electrical stimulation on both sides of the forehead before and after tDCS.', 'Anodal tDCS reduced pain intensity significantly after two weeks of treatment. The attack frequency reduction was not significant. PREP showed an increased N2 latency and decreased peak-to-peak amplitude after anodal tDCS. No severe adverse events were reported.

Ex Output:
Does patient-conducted anodal transcranial direct current stimulation of the motor cortex alleviate pain in trigeminal neuralgia?

Ex Input:
Inflammatory mediators released by nonparenchymal inflammatory cells in the liver have been implicated in the progression of acetaminophen (APAP) hepatotoxicity. Among hepatic nonparenchymal inflammatory cells, we examined the role of the abundant natural killer (NK) cells and NK cells with T-cell receptors (NKT cells) in APAP-induced liver injury.', 'C57BL/6 mice were administered a toxic dose of APAP intraperitoneally to cause liver injury with or without depletion of NK and NKT cells by anti-NK1.1 monoclonal antibody (MAb). Serum alanine transaminase (ALT) levels, liver histology, hepatic leukocyte accumulation, and cytokine/chemokine expression were assessed.', 'Compared with APAP-treated control mice, depletion of both NK and NKT cells by anti-NK1.1 significantly protected mice from APAP-induced liver injury, as evidenced by decreased serum ALT level, improved survival of mice, decreased hepatic necrosis, inhibition of messenger RNA (mRNA) expression for interferon-gamma (IFN-gamma), Fas ligand (FasL), and chemokines including KC (Keratinocyte-derived chemokine); MIP-1 alpha (macrophage inflammatory protein-1 alpha); MCP-1 (monocyte chemoattractant protein-1); IP-10 (interferon-inducible protein); Mig (monokine induced by IFN-gamma) and decreased neutrophil accumulation in the liver. Hepatic NK and NKT cells were identified as the major source of IFN-gamma by intracellular cytokine staining. APAP induced much less liver injury in Fas-deficient (lpr) and FasL-deficient (gld) mice compared with that in wild-type mice.

Ex Output:
Does innate immune system play a critical role in determining the progression and severity of acetaminophen hepatotoxicity?

Ex Input:
To compare the circulating concentrations of the acute-phase protein serum amyloid A (SAA) in lean, overweight, and obese children and adolescents and analyze the influence of body fat.', 'A total of 63 children and adolescents (65% girls) with an average age of 12.1 +/- 2.7 years (range, 6 to 18 years) were included in the study. Each child was classified on the basis of age- and sex-specific body mass index (BMI) percentile as normal weight (BMI <85th percentile; n = 17), overweight (BMI >/=85th and <95th percentiles; n = 26), or obese (BMI >/=95th percentile; n = 20). Body fat was estimated by air-displacement plethysmography.', 'Both overweight and obese children exhibited significantly increased circulating SAA concentrations (log SAA: lean, 0.66 +/- 0.20; overweight, 0.83 +/- 0.29; obese, 0.96 +/- 0.21; P = .002) compared with the lean children. Significant correlations were found between log SAA and body fat (r = 0.48; P < .0001). In multiple linear regression analysis, log C-reactive protein (CRP) (P = .014) and body fat (P = .031) emerged as significant predictors of log SAA.

Ex Output:
Is serum Amyloid A concentration increased in obese children and adolescents?