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: Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter can result in disulfide formation between protein hetero- or homodimers that alter protein function until the local cellular redox environment has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the Forkhead Box O4 (FOXO4) transcription factor.', 'In this study, we sought to investigate whether redox signaling differentially controls the human FOXO3 and FOXO4 paralogs.', 'We present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen, we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptors Importin-7 (IPO7) and Importin-8 (IPO8) form a disulfide-dependent heterodimer with FOXO3, which is required for its reactive oxygen species-induced nuclear translocation. FOXO4 does not interact with IPO7 or IPO8.
Answer: IPO7 and IPO8 control the nuclear import of FOXO3, but not FOXO4, in a redox-sensitive and disulfide-dependent manner. Our findings suggest that evolutionary acquisition of cysteines has contributed to regulatory divergence of FOXO paralogs, and that phylogenetic analysis can aid in the identification of cysteines involved in redox signaling.

A: Does evolutionary acquisition of cysteines determine FOXO paralog-specific redox signaling?
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Q: Context: Postictal inhibition (PI) is a decrease in excitability that follows an epileptic seizure and decreases probability of new seizure occurrence. PI may involve both increased inhibition and persisting elevated excitation. Our experiments tested whether shorter trains of weak stimuli are able to unmask this residual increase of excitability during the PI.', 'Four epileptic afterdischarges (ADs) were evoked by intense electrical stimulation (20 s, 8 Hz, current intensity at 5x threshold) of the neocortex in two groups (A, B) of Wistar rats. Before the first AD and during the 10-min interictal period, 8-Hz trains of four weak pulses (half of the intensity used for the AD triggering; 4P) were applied every 20 s in group B and a single pulse with similar parameters in group A.', 'The number of interictal epileptiform events evoked by 4P in the group B was significantly higher than that in the group A (evoked by single pulses) except after the second AD. Epileptic events were triggered by 4P also immediately after the AD termination.
Answer: It is apparent that weak stimulation can trigger epileptic phenomena during PI. Our results indicate that it is no longer possible to perceive PI only as persisting extreme and active inhibition. An appropriate stimulation can reveal more subtle (but important) excitatory events contributing to the functional status during the postictal period.

A: Do short bursts of weak pulses break postictal inhibition in the neocortex of Wistar rats?
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Q: Context: Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis.', 'Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.2±27.6 and 150.1±31.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.8±1.7 and 1.0±0.2%, P<0.01, 76.2±27.5 and 32.7±7.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1α positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-β1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1α was significantly increased in the PAB group than that in the control group (2.31±0.84 and 1.0±0.18 arbitrary units, P<0.05).
Answer: Our study demonstrated that low CO and tissue hypoxia were responsible for hepatic fibrosis in right failure heart model rats.

A:
Does low Cardiac Output lead Hepatic Fibrosis in Right Heart Failure Model Rats?
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