Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

[Q]: Abstract: Body surface potential maps were recorded from 140 chest leads in 25 patients affected by the idiopathic long QT syndrome (LQTS) and in 25 healthy control subjects matched for age and sex. Potential time integrals of the QRST and ST-T intervals were calculated at each lead point and displayed as isointegral (ISOI) maps. The main abnormalities noted on the QRST and ST-T ISOI maps were one area of negative values larger than normal in the right anterior and inferior thorax and a complex multipeak distribution of the integral values. At least one abnormality was present in 19 (76%) of the patients with LQTS and four (16%) of the control subjects (p less than .001). Each ISOI map was also represented as a weighted sum of nine fundamental components (eigenvectors) to detect and quantitate the nondipolar content. The percent contribution of the nondipolar eigenvectors (all eigenvectors beyond the third) was significantly higher in the LQTS group than in the control group (p less than .005). Specifically, an abnormally high nondipolar content on the QRST ISOI maps was observed much more frequently for patients with LQTS than for control subjects (nine or 36% vs one or 4%), and this was also true on the ST-T ISOI maps (14 or 56% vs one or 4%). No correlation was found between the major abnormalities on body surface maps and syncopal episodes. However, the high prevalence (76%) of these alterations among the patients with LQTS and their infrequent occurrence in the control population strongly suggests that they may be useful markers for the diagnosis of atypical cases. The prominent electronegative area on the anterior thorax can be related to delayed repolarization of a portion of the anterior wall of the heart. This finding is in agreement with the hypothesis that lower than normal right cardiac sympathetic activity is the main pathogenetic mechanism of LQTS. Multipeak distribution and high nondipolar content suggest regional electrical disparities in the ventricular recovery process. This may in part account for the high susceptibility of patients with LQTS to malignant arrhythmias.
[A]: Mapping of body surface potentials in patients with the idiopathic long QT syndrome.


[Q]: Abstract: We examined changes in estrogen receptors (ERs) in endometrial stromal and epithelial cells in cynomolgus macaques during artificially induced menstruation and repair. We used Silastic implants filled with either estradiol (E2) or progesterone (P) to treat spayed animals for 14 days with E2 followed by 14 days of E2 plus P. We then withdrew the P (but not the E2) implants and removed uteri 0, 0.5, 1, 2, 3, 4, 5, 7, and 14 days later. Uterine tissues were assayed biochemically for ER content, fixed for histology and frozen for immunocytochemistry of ER with monoclonal antiestrophilins. On day 0, ER levels in endometrium were low [1330 +/- 201 (n = 9) fmol/mg DNA]. An increase in total receptor was evident by 3-4 days of P withdrawal 2762 +/- 190 (n = 6) fmol/mg DNA; P less than 0.001]. Total receptor concentrations increased linearly with time from 0.5-7 days of P withdrawal (r = 0.88). On day 0, staining for nuclear ER in the glandular epithelium and stroma of zones I, II, and III of the endometrium was negative. Beginning at 12-24 h and continuing through 4 days of P withdrawal, nuclear staining became detectable and increased in intensity only in endometrial stromal fibroblasts and myometrial smooth muscle cells. The glandular epithelium of the endometrium did not develop nuclear staining until 5-7 days of P withdrawal, coincident with a 10-fold increase in the mitotic index of the epithelium of the upper zones. Thus, the increase in endometrial ER levels that occurred during the first 5 days of an induced luteal-follicular transition took place almost exclusively in stromal fibroblasts.
[A]: Immunocytochemical localization of estrogen receptors in the macaque endometrium during the luteal-follicular transition.


[Q]: Abstract: Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. Laryngospasm associated with intubation and general anesthesia is a common cause of pulmonary edema in children. However, only seven cases of pulmonary edema presumably due to laryngospasm have been reported in adolescents and adults. Five of the seven had other risk factors for upper airway obstruction, and in four, the diagnosis of "laryngospasm" could be explained by other factors. Patients with underlying risk factors for upper airway obstruction, such as a forme fruste of sleep apnea or nasopharyngeal abnormalities, appear to be at increased risk for the development of pulmonary edema in the setting of intubation and anesthesia. This form of pulmonary edema usually resolves rapidly without the need for aggressive therapy or invasive monitoring.
[A]:

Show your work and conclude with the exact phrasing "Therefore, the final answer is [answer]." where [answer] is just the final number or expression that solves the problem.
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Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk?


