Given a passage with a context and an answer, 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.

[Q]: Context: Bradykinin is a neuropeptide released after tissue damage which plays an important role in inflammatory pain. The up-regulation of the bradykinin B1 receptor in response to inflammation makes it an attractive target for drug development. Aim was to investigate if the selective B1 receptor antagonist BI113823 reduces inflammation-induced mechanical hyperalgesia and if the effect is mediated via peripheral and/or spinal B1 receptor antagonism.', "Electrophysiological recordings of peripheral afferents and spinal neurons were combined with behavioural experiments to better understand the underlying mechanisms of B1 receptor antagonism. Experiments were performed 24\u2009h after injection of complete Freund's adjuvant (CFA) or saline into the paw of Wistar rats. A gene expression analysis for the B1 receptor was performed in different tissues. BI113823 was administered orally or intrathecally to assess effects on CFA-induced hyperalgesia. Peripheral afferents of the saphenous nerve as well as spinal wide dynamic range (WDR) and nociceptive-specific (NS) neurons were recorded, and mechanosensitivity was measured before and after BI113823 administration.", 'BI113823 reduced CFA-induced mechanical hyperalgesia when administered orally or intrathecally. An increased B1 receptor gene expression was found in peripheral and spinal neural tissue. BI113823 significantly reduced mechanosensitivity of peripheral afferents and spinal NS neurons, but had no effect on WDR neurons.
Answer: The selective bradykinin B1 receptor antagonist BI113823 reduces CFA-induced mechanical hyperalgesia which is mediated via antagonism of peripheral as well as spinal bradykinin B1 receptors. The selective modulation of CFA-sensitized spinal NS neurons by BI113823 could be a promising property for the treatment of inflammatory pain.
[A]: Does the bradykinin B1 receptor antagonist BI113823 reverse inflammatory hyperalgesia by desensitization of peripheral and spinal neurons?


[Q]: Context: To determine the mechanisms of Bacillus subtilis spore killing by and resistance to an acidic solution containing Fe(3+), EDTA, KI and ethanol termed the KMT reagent.', 'Wild-type B. subtilis spores were not mutagenized by the KMT reagent but the wild-type and recA spores were killed at the same rate. Spores (alpha(-)beta(-)) lacking most DNA-protective alpha/beta-type small, acid-soluble spore proteins were less resistant to the KMT reagent than wild-type spores but were also not mutagenized, and alpha(-)beta(-) and alpha(-)beta(-)recA spores exhibited nearly identical resistance. Spore resistance to the KMT reagent was greatly decreased if spores had defective coats. However, the level of unsaturated fatty acids in the inner membrane did not determine spore sensitivity to the KMT reagent. Survivors in spore populations killed by the KMT reagent were sensitized to killing by wet heat or nitrous acid and to high salt in plating medium. KMT reagent-killed spores had not released their dipicolinic acid (DPA), although these killed spores released their DPA more readily when germinated with dodecylamine than did untreated spores. However, KMT reagent-killed spores did not germinate with nutrients or Ca(2+)-DPA and were recovered only poorly by lysozyme treatment in a hypertonic medium.
Answer: The KMT reagent does not kill spores by DNA damage and a major factor in spore resistance to this reagent is the spore coat. KMT reagent treatment damages the spore's ability to germinate, perhaps by damaging the spore's inner membrane. However, this damage is not oxidation of unsaturated fatty acids.
[A]: Do mechanisms of Bacillus subtilis spore killing by and resistance to an acidic Fe-EDTA-iodide-ethanol formulation?


[Q]: Context: Increased arterial stiffness has been found in patients with chronic high-grade inflammatory diseases. Whether mitigation of low-grade systemic inflammation, through a low-cholesterol/low-saturated fat diet, may have a role in improving arterial stiffness is still untested.', 'We investigated whether variations in blood lipids and plasma C-reactive protein induced by low-cholesterol/low-saturated fat diet are associated with variations in large-artery stiffness in hypercholesterolaemia.', 'Thirty-five patients with primary hypercholesterolaemia and 15 normal control subjects were recruited for the study. Hypercholesterolaemic patients followed an 8-week low-cholesterol/low-saturated fat diet (30% total fat, 5% saturated fat, cholesterol <200 mg/daily). Anthropometric characteristics, blood lipids, plasma C-reactive protein and arterial stiffness were measured at baseline and after the diet.', 'Arterial stiffness and C-reactive protein levels were higher in hypercholesterolaemic patients than in controls. Significant reductions in body weight (2 kg, 3%), plasma total cholesterol (13.4 mg/dl, 5.3%), low-density lipoprotein cholesterol (11.2 mg/dl, 6.4%), C-reactive protein (0.7 mg/l, 39%) and arterial stiffness (from 8.9+/-2.0 to 8.1+/-1.9 m/s, 11%) were achieved among hypercholesterolaemic patients after the 8-week diet (P<0.05 for all). Bivariate correlations and multivariate analysis showed reduction in arterial stiffness after short-term diet to be associated with reduction of plasma C-reactive protein levels (r=0.59, beta=0.38, P<0.05 for both).
Answer: Short-term low-cholesterol/low-saturated fat diet in hypercholesterolaemia may be effective in improving large artery stiffness, likely through the mitigation of low-grade systemic inflammation.
[A]:
Is attenuation of inflammation with short-term dietary intervention associated with a reduction of arterial stiffness in subjects with hypercholesterolaemia?