Given an abstract, indicate which of the provided candidate titles (Option1 and Option2) best describes it (respond with the text of the title, not option1/2).

Example Input: Abstract: Two patients had heavy metal intoxication resulting from industrial exposure to mercury vapors. One patient remained asymptomatic despite high urinary mercury levels. The second presented with a documented toxic reaction, including abnormal electromyograms and hematuria. Treatment was begun with 2,3-dimercaptopropane-1-sulfonate, and investigational drug used under Food and Drug Administration guidelines (IND 19,276). Use in both patients resulted in a dramatic change in excretion half-life of the mercury, from 33.1 days before treatment to 11.2 days during therapy. No significant toxic effects related to drug therapy were observed. Clearing of hematuria and reversal of electromyographic abnormalities were prompt in the symptomatic patient. Therapy with 2,3-dimercaptopropane-1-sulfonate was effective in these two patients.
Which is the apt title for the abstract? option1: The therapeutic use of 2,3-dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning. option2: American Academy of Pediatrics Task Force on Infant Mortality: Statement on infant mortality.
Example Output: The therapeutic use of 2,3-dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning.

Example Input: Abstract: Although an action of corticosteroids to inhibit glucose transport is well known, the mechanism by which this is brought about has been unclear. Some evidence has suggested an action on insulin receptors, but a postbinding or postreceptor effect has also been reported. As hydrogen peroxide acts at a postbinding site to stimulate glucose transport, studies were carried out in 3T3-L1 fibroblasts to determine whether corticosteroids would inhibit hydrogen peroxide-induced glucose transport. In this cell type, both insulin and hydrogen peroxide produced a marked increase in glucose transport after a 30-min incubation. The increase produced by hydrogen peroxide, as well as insulin, was inhibited by previous incubation of the cells with dexamethasone. These findings give further support to the conclusion that dexamethasone has effects on glucose transport at a postbinding site. As changes in membrane lipids influence the movement and/or activity of glucose transporters, and dexamethasone alters membrane lipids, dexamethasone-induced changes in the lipids of the plasma membrane may be important in the mediation of the steroid effect upon glucose transport.
Which is the apt title for the abstract? option1: Dexamethasone inhibition of hydrogen peroxide-stimulated glucose transport. option2: Effect of antibiotic therapy on the sensitivity of indium-111-labeled leukocyte scans.
Example Output: Dexamethasone inhibition of hydrogen peroxide-stimulated glucose transport.

Example Input: Abstract: Insulin may mediate the hyperandrogenism that frequently occurs in patients with insulin-resistant states. To test this hypothesis, we studied five normal women and one woman with hyperandrogenism, insulin resistance, and acanthosis nigricans with the hyperinsulinemic-euglycemic clamp technique. Each woman received a 0.1 U/kg insulin bolus dose, followed by a 10 mU/kg X min insulin infusion for 12-16 h. In the normal women, an average insulin level of 1832 +/- 292 (+/- SEM) microU/ml was achieved; serum glucose was clamped at 116 +/- 5 mg/dl. At this level, insulin may bind to the insulin-like growth factor I receptor as well as to its own receptor. Contrary to our working hypothesis, a rise in serum testosterone did not occur in any women during insulin infusion, and in one women, serum testosterone levels decreased. When analyzed as a percentage of the basal value, serum progesterone levels fell 20% in the normal women within the first 2 h of insulin infusion, but did not change thereafter. Dehydroepiandrosterone sulfate (DHEA-S) levels, however, uniformly and progressively decreased by 39% after 12 h of insulin infusion in the normal women and by 31% at 14 h in the woman with hyperandrogenism, insulin resistance, and acanthosis nigricans. The fall in serum DHEA-S levels was not due to diurnal rhythmicity, as the changes in serum DHEA-S levels did not correlated with those in serum cortisol. Suppression of PRL release also was excluded as a cause of the fall in DHEA-S levels. These results indicate that acute hyperinsulinemia of 12- to 16-h duration does not increase serum testosterone or DHEA-S concentrations and, indeed, can cause a decline in serum DHEA-S levels in both normal women and the single woman studied with hyperandrogenism, insulin resistance, and acanthosis nigricans.
Which is the apt title for the abstract? option1: The effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance, and acanthosis nigricans. option2: Duchenne dystrophic muscle develops lesions in long-term coculture with mouse spinal cord.
Example Output:
The effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance, and acanthosis nigricans.