Teacher: Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.
Teacher: Now, understand the problem? If you are still confused, see the following example:
Abstract: Some patients converted from ventricular fibrillation to organized rhythms by defibrillation-trained ambulance technicians (EMT-Ds) will refibrillate before hospital arrival. The authors analyzed 271 cases of ventricular fibrillation managed by EMT-Ds working without paramedic back-up. Of 111 patients initially converted to organized rhythms, 19 (17%) refibrillated, 11 (58%) of whom were reconverted to perfusing rhythms, including nine of 11 (82%) who had spontaneous pulses prior to refibrillation. Among patients initially converted to organized rhythms, hospital admission rates were lower for patients who refibrillated than for patients who did not(53% versus 76%, P = NS), although discharge rates were virtually identical (37% and 35%, respectively). Scene-to-hospital transport times were not predictively associated with either the frequency of refibrillation or patient outcome. Defibrillation-trained EMTs can effectively manage refibrillation with additional shocks and are not at a significant disadvantage when paramedic back-up is not available.
Solution: Refibrillation managed by EMT-Ds
Reason: The abstract is about refibrillation and it is also mentioned in the abstract that it is managed by EMT-Ds. So it is an apt title.

Now, solve this instance: Abstract: The mechanism by which sickle cells and xerocytic red cells become depleted of cations in vivo has not been identified previously. Both types of cells exhibit elevated permeabilities to sodium and potassium, in the case of sickle cells, when deoxygenated. The ouabain-insensitive fluxes of sodium and potassium were equivalent, however, in both cell types under these conditions. When incubated 18 hours in vitro, sickle cells lost cations but only when deoxygenated. This cation depletion was blocked by ouabain, removal of external potassium, or pretreatment with 4,4'-diisothiocyanostilbene-2,2'-disulfonate, which blocks the increase in cation permeability induced by deoxygenation. The loss of cation exhibited by oxygenated xerocytes similarly incubated was also blocked by ouabain. These data support the hypothesis that the elevated "passive" cation fluxes of xerocytes and deoxygenated sickle cells are not directly responsible for cation depletion of these cells; rather, these pathologic leaks interact with the sodium pump to produce a net loss of cellular cation.
Student:
Cation depletion by the sodium pump in red cells with pathologic cation leaks. Sickle cells and xerocytes.