Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
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Question: Precursor cells have been shown to be affected by oxidative stress, in vivo and vitro, but little is known about the expression of antioxidant mechanisms in neuronal/glial differentiation. We have characterized the expression of Cu/Zn superoxide dismutase (Cu/Zn SOD), one of the main antioxidant proteins involved in the breakdown of superoxide, in the immature rat dorsolateral subventricular zone (SVZ), rostral migratory stream (RMS) and hippocampal subgranular zone (SGZ). Progenitor cells were identified immunohistochemically on cryostat sections by 5'Bromodeoxyuridine (BrdU) incorporation and expressing cells were further characterized using double labeling for progenitor markers. In the SVZ, only a subpopulation of BrdU+ cells, mostly found in the medial SVZ, expressed Cu/Zn SOD. These cells were mostly nestin+ and some were also vimentin+. In contrast, in the lateral SVZ few Cu/Zn SOD+/BrdU+ cells were found. These were primarily nestin+, vimentin-, showed some PSA-NCAM expression, but only a few were NG2+. In the RMS and SGZ virtually all BrdU+ progenitors were Cu/Zn SOD+ and expressed nestin and vimentin. Some RMS cells were also PSA-NCAM+. These findings show a heterogeneous expression of Cu/Zn SOD in restricted cell types in the germinative zones and suggest a role for antioxidant Cu/Zn SOD in progenitor cells of the immature rat brain.

Answer: Which intermediate filament (IF) protein can be used as a non-specific marker of the neuronal precursor cells of the subventricular zone?


Question: In anaesthesia and in the intensive care unit, benzodiazepines have proven safe and effective agents for the induction and maintenance of sedation for a variety of therapeutic goals. However, in these contexts, or in benzodiazepine overdose, it is often desirable to be able to terminate or interrupt sedation without waiting for the effect of the benzodiazepine to become dissipated by normal metabolism and excretion. Flumazenil, a 1,4-imidazobenzodiazepine, is a highly effective, specific benzodiazepine antagonist which is indicated for use when the effect of a benzodiazepine must be attenuated or terminated at short notice. It acts by displacing other benzodiazepines from the receptor site by competitive inhibition. The onset of effect after intravenous administration occurs within 1 to 3 minutes. The optimal dosage is determined for each patient by a dose titration procedure and lies in the range 0.2 to 1.0mg in anaesthesiology, and 0.1 to 2.0mg in intensive care use. Despite its short elimination half-life of around 1 hour, after general anaesthesia or conscious to moderate sedation for short procedures, a single dose of flumazenil is usually sufficient to attain and maintain the desired level of consciousness. After intoxication with high benzodiazepine doses, the duration of effect of a single dose of flumazenil is not expected to exceed 1 hour. In such cases, the period of wakefulness can be prolonged as necessary by repeated low intravenous doses of flumazenil or by infusion (0.1 mg/hour). Flumazenil is well tolerated both systemically and locally. The only adverse events seen with greater frequency after flumazenil compared with placebo were nausea and/or vomiting after general anaesthesia, although the incidence of actual vomiting was not significantly different between the 2 groups. Since these effects were virtually absent in studies of intensive care patients and after sedation for short procedures, and were not seen in tolerability studies in healthy volunteers receiving intravenous bolus doses of up to 100mg, there may be a link between these symptoms and the other agents used in general anaesthesia, some of which have well-known emetic properties. Thus, flumazenil provides a safe and effective means of attenuating or reversing the CNS-depressant effects of benzodiazepines whenever indicated, e.g. following benzodiazepine-induced general anaesthesia, conscious sedation, or after benzodiazepine overdose, either alone or in combination with other agents.(ABSTRACT TRUNCATED AT 400 WORDS)

Answer: Which drug should be used as an antidote in benzodiazepine overdose?


Question: At the start of World War II, the 24th Infantry was stationed at Fort Benning as school troops for the Infantry School. They participated in the Carolina Maneuvers of October - December 1941. During World War II, the 24th Infantry fought in the South Pacific Theatre as a separate regiment. Deploying on 4 April 1942 from the San Francisco Port of Embarkation, the regiment arrived in the New Hebrides Islands on 4 May 1942. The 24th moved to Guadalcanal on 28 August 1943, and was assigned to the XIV Corps. 1st Battalion deployed to Bougainville, attached to the 37th Infantry Division, from March to May 1944 for perimeter defense duty. The regiment departed Guadalcanal on 8 December 1944, and landed on Saipan and Tinian on 19 December 1944 for Garrison Duty that included mopping up the remaining Japanese forces that had yet to surrender. The regiment was assigned to the Pacific Ocean Area Command on 15 March 1945, and then to the Central Pacific Base Command on 15 May 1945, and to the Western pacific Base Command on 22 June 1945. The regiment departed Saipan and Tinian on 9 July 1945, and arrived on the Kerama Islands off Okinawa on 29 July 1945. At the end of the war, the 24th took the surrender of forces on the island of Aka-shima, the first formal surrender of a Japanese Imperial Army garrison. The regiment remained on Okinawa through 1946.

Answer:
What happened first: moved to Guadalcanal or arrived on the Kerama Islands?