In this task, you are given an abstract of article. Your task is to generate label "True" if abstract is structured, otherwise generate "False". A structured abstract is composed of a topic sentence (or key sentence), relevant supporting sentences, and a closing (or transition) sentence. This structure is key to keeping your abstract focused on the main idea and creating a clear and concise image.
Example: RanBP type proteins have been reported to increase the catalytic efficiency of the RanGAP-mediated GTPase reaction on Ran. Since the structure of the Ran-RanBP1-RanGAP complex showed RanBP1 to be located away from the active site, we reinvestigated the reaction using fluorescence spectroscopy under pre-steady-state conditions. We can show that RanBP1 indeed does not influence the rate-limiting step of the reaction, which is the cleavage of GTP and/or the release of product P(i). It does, however, influence the dynamics of the Ran-RanGAP interaction, its most dramatic effect being the 20-fold stimulation of the already very fast association reaction such that it is under diffusion control (4.5 x 10(8) M(-1) s(-1)). Having established a valuable kinetic system for the interaction analysis, we also found, in contrast to previous findings, that the highly conserved acidic C-terminal end of RanGAP is not required for the switch-off reaction. Rather, genetic experiments in Saccharomyces cerevisiae demonstrate a profound effect of the acidic tail on microtubule organization during mitosis. We propose that the acidic tail of RanGAP is required for a process during mitosis.
Example solution: False
Example explanation: Output is appropriate for the given abstract because it is not structured.

Problem: Oncostatin M (OSM) and leukemia inhibitory factor (LIF) are members of the interleukin-6 (IL-6) subfamily of cytokines that use a common signal transducer gp130. Human OSM (hOSM) and LIF share a functional high-affinity receptor that is composed of gp130 and LIF receptor beta subunit (LIFRbeta). A second high-affinity receptor for hOSM was recently found to be formed by gp130 and the hOSM receptor beta subunit. However, the nature of murine OSM (mOSM) and its receptors has remained unknown. Using the recently cloned mOSM cDNA, we produced recombinant mOSM and studied its biological activity and receptor structure. Murine hematopoietic cell lines M1 and DA1.a, an embryonic stem cell line CCE, and Ba/F3 transfectants expressing gp130 and LIFRbeta responded to murine LIF (mLIF) and hOSM equally well, while these cells responded to mOSM only at a 30-fold to 100-fold higher concentration than those of mLIF and hOSM. In contrast, NIH3T3 cells responded to mOSM, but not to mLIF and hOSM. Scatchard plot analyses showed that mOSM bound to gp130 with low-affinity (kd = 2.8 to 4.2 nmol/L) and that the binding affinity did not increase in the presence of LIFRbeta. However, mOSM bound to NIH3T3 cells with high-affinity (kd = 660 pmol/L), whereas mLIF did not bind to NIH3T3 cells at all. These results indicate that unlike hOSM, mOSM and mLIF do not share the same functional receptor, and mOSM delivers signals only through its specific receptor complex. Further studies in mice will define the physiological roles of OSM.
Solution: False