Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[Q]: Hello, Listeners. Welcome to Henton Hospital Radio. Before our music programme at four, I'm going to repeat some of our hospital rules. The hospital can sleep 800 patients. There're 8 beds in each ward . The visiting hours are in the afternoon from 2:30 to 3:30 and in the evening from 7:00 to 8:00. But remember only two people can see you at the same time. Sorry about that, but you can see what would happen if we didn't have these rules. The other rules are about our hours. We start quite early---you might not be used to that. We wake you at 6 o'clock, and breakfast is at 8 o'clock, lunch is at noon. There's tea at 3:30 and supper is at 6 o'clock. You can see the non-smoking sign---we don't allow smoking in the wards. I'm sure you understand why. However, if you do need to smoke, there are some smoking rooms where it is allowed. You will find the radio switch on the wall near your bed, with your own headphones, if you want to listen. It's our own hospital radio wishing you a quick recovery.
[A]: Who do you think the listeners might be?


[Q]: The TNF family member receptor activator for NF-B ligand (RANKL) and its receptors RANK and osteoprotegerin are key regulators of bone remodeling but also influence cellular functions of tumor and immune effector cells. In this work, we studied the involvement of RANK-RANKL interaction in NK cell-mediated immunosurveillance of acute myeloid leukemia (AML). Substantial levels of RANKL were found to be expressed on leukemia cells in 53 of 78 (68%) investigated patients. Signaling via RANKL into the leukemia cells stimulated their metabolic activity and induced the release of cytokines involved in AML pathophysiology. In addition, the immunomodulatory factors released by AML cells upon RANKL signaling impaired the anti-leukemia reactivity of NK cells and induced RANK expression, and NK cells of AML patients displayed significantly upregulated RANK expression compared with healthy controls. Treatment of AML cells with the clinically available RANKL Ab Denosumab resulted in enhanced NK cell anti-leukemia reactivity. This was due to both blockade of the release of NK-inhibitory factors by AML cells and prevention of RANK signaling into NK cells. The latter was found to directly impair NK anti-leukemia reactivity with a more pronounced effect on IFN- production compared with cytotoxicity. Together, our data unravel a previously unknown function of the RANK-RANKL molecule system in AML pathophysiology as well as NK cell function and suggest that neutralization of RANKL with therapeutic Abs may serve to reinforce NK cell reactivity in leukemia patients.
[A]: To the ligand of which receptors does Denosumab (Prolia) bind?


[Q]: Transactivation response DNA-binding protein 43 (TDP-43) proteinopathies are classified based upon the extent of modified TDP-43 and include a growing number of neurodegenerative diseases such as amyotrophic lateral sclerosis, frontotemporal lobar degeneration with ubiquitin-immunoreactive, tau-negative inclusions and frontotemporal lobar degeneration with motor neuron disease. The purpose of the study was to examine whether proteolytic modifications of TDP-43 are a relevant finding in Parkinson's disease (PD) and dementia with Lewy bodies (DLB). A novel site-directed caspase cleavage antibody, termed TDP caspase cleavage product antibody (TDPccp), was utilized based upon a known caspase 3 cleavage consensus site within TDP-43 at position 219. Application of this antibody to postmortem brain sections from PD and DLB patients revealed the presence of caspase-cleaved TDP-43 in Lewy bodies and Hirano bodies in all cases examined. Colocalization of TDPccp with an antibody to alpha-synuclein (alpha-Syn), which served as a general marker for Lewy bodies, was evident within the substantia nigra in both alpha-synucleinopathies. Interestingly, the TDPccp antibody detected a greater number of Lewy bodies in PD and DLB compared to the alpha-Syn antibody. In addition, a semiquantitative analysis in both diseases confirmed this finding by indicating that the percentage of caspase-cleaved TDP-43 single-labeled Lewy bodies was approximately twice that of alpha-Syn labeling (in DLB 13.4 vs. 5.5%, while in PD 34.6 vs. 17.6%). Collectively, these data have identified caspase-cleaved TDP-43 as a primary component of Lewy and Hirano bodies in PD and DLB, and suggest that the TDPccp antibody is an effective marker for the detection of Lewy bodies in these neurodegenerative diseases.
[A]:
Which is the primary protein component of Lewy bodies?