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: The mechanism involved in AD is complex, which has prompted to develop compounds that could simultaneously interact with several potential targets. Here, we report a new synthesized compound SCR-1693 which is designed to target both AChE and calcium channels that are potential for AD therapy.', 'We investigated the effects of SCR-1693 on AChE and calcium channels, the effects of neuroprotection and anti-amnesia in icv-Aβ25-35-injected mice, and the potential mechanisms.', 'AChE activity assay, intracellular Ca(2+) content and calcium currents measurement, and Aβ25-35-induced cellular death determine were performed for validation of designed targets and neuroprotection of SCR-1693. Mice were orally administrated with SCR-1693 once daily after an Aβ25-35 injection. The Morris water maze and Y-maze test, and hippocampal protein detection were conducted on days 5-10, day 11, and day 8. The pyramidal neuron number, hippocampal AChE activity, and synaptic transmission were measured on day 12.', 'SCR-1693 acted as a selective, reversible, and noncompetitive inhibitor of AChE, and a nonselective voltage-gated calcium channel blocker. SCR-1693 also inhibited the increase of AChE activity in the mouse hippocampus. SCR-1693 was more effective than donepezil and memantine in preventing Aβ25-35-induced long-term and short-term memory impairment, maintaining the basal transmission of Schaffer collateral-CA1 synapses, and sustaining LTP in mouse hippocampus. SCR-1693 attenuated Aβ25-35-induced death of SH-SY5Y cell and the loss of hippocampal pyramidal neurons, and regulated Aβ25-35-induced signal cascade in neurons.
Answer: All these findings indicated that SCR-1693, as a double-target-direction agent, is a considerable candidate for AD therapy.

A: Does a novel acetylcholinesterase inhibitor and calcium channel blocker SCR-1693 improve Aβ25-35-impaired mouse cognitive function?
****
Q: Context: Preconditioning neurons with noninjurious hypoxia (hypoxic preconditioning, HPC) or the anesthetic isoflurane (APC) induces tolerance of severe ischemic stress. The mechanisms of both types of preconditioning in the hippocampus require moderate increases in intracellular Ca and activation of protein kinase signaling. The authors hypothesized that the expression of signal transduction genes would be similar after APC and HPC.', 'Hippocampal slice cultures prepared from 9-day-old rats were preconditioned with hypoxia (5 min of 95% nitrogen/5% carbon dioxide) or 1% isoflurane in air/5% carbon dioxide for 1 h. A day later, cultures were subjected to 10 min oxygen and glucose deprivation (simulated ischemia). Intracellular Ca, measured in CA1 neurons at the completion of preconditioning, and cell death in CA1, CA3, and dentate regions was assessed 48 h after simulated ischemia. Message RNA encoding 119 signal transduction genes was quantified with rat complimentary DNA microarrays from pre-oxygen-glucose deprivation samples.', 'Both APC and HPC increased intracellular Ca approximately 50 nm and decreased CA1, CA3, and dentate neuron death by about 50% after simulated ischemia. Many signaling genes were increased after preconditioning, with hypoxia increasing more apoptosis/survival genes (8 of 10) than isoflurane (0 of 10). In contrast, isoflurane increased more cell cycle/development/growth genes than did hypoxia (8 of 14 genes, vs. 1 of 14).
Answer: Despite sharing similar upstream signaling and neuroprotective outcomes, the genomic response to APC and HPC is different. Increased expression of antiapoptosis genes after HPC and cell development genes after APC has implications both for neuroprotection and long-term effects of anesthetics.

A: Does expression of signal transduction genes differ after hypoxic or isoflurane preconditioning of rat hippocampal slice cultures?
****
Q: Context: Although uncommon, hearing loss after spinal anesthesia has been described. Vestibulocochlear dysfunction after spinal anesthesia in which 22-gauge and 25-gauge Quincke needles were used was investigated to determine if needle size affected hearing.', 'Patients with American Society of Anesthesiologists physical status I and II, aged 20 to 40 years, who were undergoing lower extremity surgery under spinal anesthesia were randomized into 2 groups. After intravenous hydration, 3 mL of 0.5% bupivacaine was administered for spinal anesthesia, which was performed with a 22-gauge Quincke needle in group I (n=30) patients and a 25-gauge Quincke needle in group II (n=30) patients. Before surgery and 2 days after surgery, pure-tone audiometry and tympanometry were performed. Preoperative and postoperative hearing data were obtained in the right and left ears for every frequency. Headache, nausea, and vomiting and cranial nerve III, IV, V, VI, VII, and VIII function were assessed on postoperative day 2.', 'Demographic data were not different between the groups. No hypoacousis was noted at any frequency during the entire testing period in either group. Two patients from group I experienced postdural puncture headache on postoperative day 3, and neither had hearing loss. No patient had cranial nerve dysfunction.
Answer: We were unable to induce hearing loss in young patients undergoing spinal anesthesia by injecting the anesthetic with a 22-gauge or a 25-gauge Quincke needle.

A:
Does hearing loss occur in young patients undergoing spinal anesthesia?
****