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.

Example Input: Context: TECPR2 was first described as a disease causing gene when the c.3416delT frameshift mutation was found in five Jewish Bukharian patients with similar features. It was suggested to constitute a new subtype of complex hereditary spastic paraparesis (SPG49).', 'We report here 3 additional patients from unrelated non-Bukharian families, harboring two novel mutations (c.1319delT, c.C566T) in this gene. Accumulating clinical data clarifies that in addition to intellectual disability and evolving spasticity the main disabling feature of this unique disorder is autonomic-sensory neuropathy accompanied by chronic respiratory disease and paroxysmal autonomic events.
Answer: We suggest that the disease should therefore be classified as a new subtype of hereditary sensory-autonomic neuropathy. The discovery of additional mutations in non-Bukharian patients implies that this disease might be more common than previously appreciated and should therefore be considered in undiagnosed cases of intellectual disability with autonomic features and respiratory symptoms regardless of demographic origin.
Example Output: Do tECPR2 mutations cause a new subtype of familial dysautonomia like hereditary sensory autonomic neuropathy with intellectual disability?

Example Input: Context: To investigate the effects of quercetin, an herbal flavonoid, on LPS-induced delay in spontaneous apoptosis, adhesion molecules (CD62L, CD11b/CD18) expression of neutrophils, and superoxide (O(2)(-)) generation by LPS-primed fMLP-induced human neutrophils.', 'Neutrophils were incubated in the presence or absence of lipopolysaccharide (LPS) at a final concentration of 1 microg/ml for 24 hours. Some wells with neutrophils were pre-treated with quecetin at the final concentration ranging from 0-100 microM for 30 min and then 1 microg/ml LPS was added into the cultures for 24 hours. The apoptosis of neutrophils was evaluated by flowcytometry analysis of propidum iodide (PI)-staining of the nuclei and annexin V staining of phosphatidylserine (PS) in the cell membrane. Agarose gel electrophoresis of low molecular weight DNA was performed to analyze DNA fragmentation. The effects of quercetin on adhesion molecules were detected by using flowcytometry analysis. The generation of O(2) (-) by LPS-primed fMLP-induced neutrophils was determined by reduced cytochrome c assay.', 'LPS markedly inhibited the spontaneous apoptosis of neutrophils, but the inhibitory effect was abrogated after the pre-treatment of neutrophils with quercetin (approximately 40 microM) for 30 min. Quercetin (40 microM) also prevented LPS-induced down-regulation of CD62L expression, up-regulation of CD11b/CD18 expression, and O(2) (-) generation by fMLP-induced neutrophils.
Answer: As one of the pro-inflammatory factors, LPS aggravates inflammation through priming neutrophils to synthesize/release cytotoxic contents and prolonging functional lifespan of neutrophils by delaying the spontaneous apoptosis. Thus, our data suggest to us that quercetin might decrease the susceptibility of neutrophils to pro-inflammatory factors (e. g. LPS), which could partially explain the anti-inflammatory mechanisms of quercetin.
Example Output: Does quercetin inhibit LPS-induced delay in spontaneous apoptosis and activation of neutrophils?

Example Input: Context: The electroretinogram (ERG) is currently, together with the central visual field test, color vision test and electroculogram (EOG), an examination dedicated to prevent retinopathy due to hydroxychloroquine (HCQ) or chloroquine (CQ) intoxication.', 'Thirty-two patients on treatment with HCQ were studied. Each patient had underwent a complete clinical ophthalmological examination and a set of paraclinical examinations including at least an ERG. All the patients were requested to decrease or stop their HCQ treatment. Following this change, a second ERG was recorded for each patient. The ERGs before and after stopping HCQ treatment were compared. We noted a statistically significant increase in the amplitude of "b" wave of the ERG, following after decrease or discontinuation of HCQ treatment.
Answer: This study has demonstrated the ERG "b" wave sensitivity due to the variation of HCQ consumption. The amplitude and the culmination time of the ERG "b" wave are important parameters to monitor during long term treatment with HCQ. A decrease of the "b" wave amplitude, coupled with an increase of its culmination time in a patient on long term HCQ treatment showing for the same daily dose, shall be a sign of alert, imposing the performance of additional visual functional tests and leading a decrease or a discontinuation of the treatment with HCQ. The ERG is an objective examination, which needs almost no participation from the patient. Its usefulness has been demonstrated, for the prevention of retinopathy due to hydroxychloroquine or chloroquine intoxication in condition that successive ERGs of the same patient are precisely compared.
Example Output:
Does [ Electroretinogram `` b '' wave vary with the posology of the antimalarial treatment ]?