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.
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Question: Sigma-1 receptors are involved in the pathophysiological process of several neuropsychiatric diseases such as epilepsy, depression. Allosteric modulation represents an important mechanism for receptor functional regulation. In this study, we examined antidepressant activity of the latest identified novel and selective allosteric modulator of sigma-1 receptor 3-methyl-phenyl-2, 3, 4, 5-tetrahydro-1H-benzo[d]azepin-7-ol (SOMCL-668).', 'A single administration of SOMCL-668 decreased the immobility time in the forced swimming test (FST) and tailing suspended test in mice, which were abolished by pretreatment of sigma-1 receptor antagonist BD1047. In the chronic unpredicted mild stress (CUMS) model, chronic application of SOMCL-668 rapidly ameliorated anhedonia-like behavior (within a week), accompanying with the enhanced expression of brain-derived neurotrophic factor (BDNF) and phosphorylation of glycogen synthase kinase 3 (GSK3) (Ser-9) in the hippocampus. SOMCL-668 also rapidly promoted the phosphorylation of GSK3 (Ser-9) in an allosteric manner in vitro. In the cultured primary neurons, SOMCL-668 enhanced the sigma-1 receptor agonist-induced neurite outgrowth and the secretion of BDNF.

Answer: Does allosteric Modulation of Sigma-1 Receptors elicit Rapid Antidepressant Activity?

Question: Lipopolysaccharide (LPS)-induced preconditioning protects neurons against traumatic spinal cord injury (TSCI) in rats. This study sought to test whether Nrf2, a transcription factor, mediated LPS-induced preconditioning.', 'The TSCI model was established using a standardized NYU impactor on adult female rats. Rats were pretreated with LPS (0.2mg/kg, IP; 72h before injury). Nrf2 was silenced by injecting a lentivirus encoding RNAi against Nrf2 into injured spinal cords. Neurologic function was assessed by Basso, Beattie and Bresnahan (BBB) scores 6h, 12h, 24h, 48h, 72h, 7d and 14d after TSCI. Neuronal apoptosis was measured by a TUNEL staining. Ultrastructure was observed using transmission electron microscope (TEM). The protein expression of HO-1, NQO1 and GCLC was examined using immunohistochemistry and immunoblotting.', 'The injection of a lentivirus effectively transfected GFP into injured spinal cords. The expression of Nrf2 was significantly decreased in spinal cords receiving a lentivirus encoding RNAi against Nrf2. BBB scores showed that TSCI markedly impaired nervous function, which was markedly preserved by LPS pretreatment. Nrf2 knockdown significantly suppressed LPS pretreatment-induced protection of nervous function. TEM images and TUNEL staining showed an increase in apoptotic cells when Nrf2 was silenced. Moreover, immunohistochemistry and immunoblotting analysis exhibited that LPS pretreatment significantly upregulated the expression of anti-oxidative proteins including HO-1, NQO1 and GCLC, which was suppressed when Nrf2 expression was silenced in injured spinal cords.

Answer: Does lipopolysaccharide-induced preconditioning protect against traumatic spinal cord injury by upregulating Nrf2 expression in rats?

Question: While it is well-known that there is 18F-FDG uptake in breast tumors, clinical impact of (18)F-FDG PET in managing breast cancer patients is not well-studied.', 'One hundred and thirty-three consecutive breast cancer patients from May 1996 to June 2000 were studied. All patients were treated and being followed. Reasons of referral included equivocal conventional studies, staging/re-staging, clinical suspicion of recurrence, and elevated serum tumor markers. Clinical status at 6 months postPET is used as the gold standard in lesions of worsening versus stable or improving.', 'PET was 69% sensitive and 80% specific in predicting clinical stage at 6 months. This 69% of the patients who got worse at 6 months was PET positive and 80% of the patients who were stable or improving at 6 months were PET negative. There was a significant association between PET results and clinical outcome, after adjusting for stage of disease (P=0.04), or for the treatment patients received (P<0.01). Negative PET results changed therapy as often as positive ones did. PET influenced treatment decisions in 74% of the patients referred for study.

Answer:
Does a retrospective analysis of the impact of 18F-FDG PET scan on clinical management of 133 breast cancer patients?