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.

Input: Consider Input: Hyponatraemia is a common, potentially life-threatening, complication of thiazide diuretics. The mechanism of thiazide-induced hyponatraemia is incompletely understood. Previous experiments have suggested a direct effect of thiazide diuretics on the plasma membrane expression of aquaporin (AQP)2.', 'We examined the effects of a single re-exposure to hydrochlorothiazide (HCTZ) 50\u200amg on water balance, renal sodium handling and osmoregulation in 15 elderly hypertensive patients with a history of thiazide-induced hyponatraemia and 15 matched hypertensive controls using thiazide diuretics without previous hyponatraemia.', 'Patients with thiazide-induced hyponatraemia had significantly lower body weight and lower plasma sodium and osmolality at baseline. After HCTZ administration, plasma sodium and osmolality significantly decreased and remained lower in patients compared with controls (P\u200a<\u200a0.001). Plasma antidiuretic hormone (ADH) and urine AQP2 were low or suppressed in patients, whereas solute and electrolyte-free water clearance was significantly increased compared with controls. Ad libitum water intake was significantly higher in patients (2543\u200a±\u200a925\u200aml) than in controls (1828\u200a±\u200a624\u200aml, P\u200a<\u200a0.05), whereas urinary sodium excretion did not differ. In contrast, urea excretion remained significantly lower in patients (263\u200a±\u200a69\u200ammol per 24\u200ah) compared with controls (333\u200a±\u200a97\u200ammol per 24\u200ah, P\u200a<\u200a0.05) and predicted the decrease in plasma sodium following HCTZ administration.

Output: Is thiazide-induced hyponatraemia associated with increased water intake and impaired urea-mediated water excretion at low plasma antidiuretic hormone and urine aquaporin-2?


Input: Consider Input: We recently proposed the existence of neurotoxic interactions between the cannabinoid type 1 (CB(1)) receptor and transient receptor potential vanilloid 1 (TRPV1) channels in rat mesencephalic cultures. This study seeks evidence for the mediator(s) and mechanisms underlying the neurotoxic interactions between CB(1) receptors and TRPV1 in vitro and in vivo.', 'The mediator(s) and mechanism(s) for the interactions between CB(1) receptors and TRPV1 were evaluated by cell viability assays, immunocytochemistry, Fura-2 calcium imaging, mitochondrial morphology assay, ELISA and Western blot assay in vitro in neuron-enriched mesencephalic cultures. Injections into the substantia nigra and subsequent cell counts were also used to confirm these interactions in vivo.', 'The neurotoxic interactions were mediated by 12(S)-hydroperoxyeicosatetraenoic acid (12(S)-HPETE), an endogenous TRPV1 agonist. CB(1) receptor agonists (HU210 and WIN55,212-2) increased the level of 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), a downstream metabolite of 12(S)-HPETE, which stimulates TRPV1-mediated death of mesencephalic neurons, both in vitro and in vivo. The neurotoxicity was mediated by increased intracellular Ca(2+) concentration ([Ca(2+)](i)) through TRPV1, consequently leading to mitochondrial damage and was attenuated by baicalein, a 12-lipoxygenase inhibitor.

Output: Are interactions between CB ( 1 ) receptors and TRPV1 channels mediated by 12-HPETE cytotoxic to mesencephalic dopaminergic neurons?


Input: Consider Input: To investigate whether autophagy can be induced by 1, 4-benzoquinone (1, 4-BQ) in HL60 cells, as well as the role of reactive oxygen species (ROS) in induced autophagy.', 'In order to determine a suitable 1, 4-BQ treatment concentration for autophagy detection in HL60 cells, the cell vitality were examined by CCK8 assay. Logarithmic-growth-phased cells were divided into control group, 1, 4-BQ group (10μmol/L 1, 4-BQ, 24 h) , NAC group (antioxidant n-acetyl cysteine, 5mmol/L, 24 h) and the 1, 4-BQ+NAC group (5 mmol/L NAC were preincubated for 1h prior to the treatment with 10 μmol/L 1, 4-BQ for 24 h). The autophagic acidic vesicle were inspected by acridine orange staining, LC3 were detected by immunofluorescence staining, and expressions of LC3 and Beclin1 were quantitatively detected by Western blot.', 'The results from cell viability test indicated that 1, 4-BQ exhibited a dose-dependent toxicity to HL60 cells. Compared with control group.the cell viability in 20.0、40.0μmol/L concentration were decreased obviously, and the differences had statistical significance (P<0.05). Compare with contrd group acidic vesicle, LC3II, LC3II/LC3I and Beclin1 protein expressions were increased in 1, 4-BQ group, after both respectively 12.4% and 27%, the differences had statistital significance. While 1, 4-BQ+NAC group was observed that acidic vesicle, LC3 and Beclin1 protein level were markedly lower than 1, 4-BQ group, after both decreased 12.6% and 22.6% respectively, both the difference were statistically significant (P<0.05).


Output: Do [ Benzoquinone induce autophagy in HL60 cells and the role of reactive oxygen species in induced autophagy ]?