Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

Example Input: Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood.', 'To define the relationship between specific viral illnesses and early childhood asthma development.', 'A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase-polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed.', 'Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age.
Example Output: 1

Example Input: Although allergic sensitization can be generated against various allergens, it is unknown how such a diversity of antigens is able to promote TH2-mediated inflammation leading to atopy. Our previous studies demonstrated that allergen-specific IgG immune complexes (ICs) and house dust mite (HDM) extract both induced dendritic cells (DCs) to drive TH2-mediated inflammation, but the mechanism by which these diverse stimuli produce similar responses is unknown.', 'We sought to identify the DC signaling pathways used by TH2 stimuli to promote TH2-mediated inflammation.', 'C57BL/6, FcγRIII(-/-), FcRγ(-/-), and ST2(-/-) mice were sensitized and challenged with HDM, and inflammation was assessed based on results of flow cytometry and histology and cytokine production. Bone marrow-derived DCs from these strains were used in signaling and adoptive transfer experiments.', 'Our findings indicate that 2 distinct TH2 stimuli, ICs and HDM, use the FcRγ-associated receptors FcγRIII and Dectin-2, respectively, to promote TH2-mediated lung inflammation. In this study we demonstrate that both ICs and HDM induce expression of IL-33, a critical mediator in asthma pathogenesis and the differentiation of TH2 cells, in DCs. Upregulation of IL-33 in DCs is dependent on FcRγ, Toll-like receptor 4, and phosphoinositide 3-kinase. Exogenous IL-33 is sufficient to restore the development of TH2 responses in FcRγ-deficient mice. Finally, adoptive transfer of allergen-pulsed FcRγ(+/-) bone-marrow derived DCs restores the development of TH2-type inflammation in FcRγ-deficient mice, demonstrating the necessity of this signaling pathway in DCs for allergen-induced inflammation.
Example Output: 1

Example Input: The objective of this study was to describe a pattern of recovery and histological nerve cell loss in Sprague-Dawley rats exposed to severe brain ischemia and to compare it to that of Wistar rats.', 'Ether- and ketamine-anesthetized Sprague-Dawley rats were exposed to 3, 5, 6 and 10 min of normothermic severe brain ischemia (4 groups) induced by hypotension and neck compression. In group No. 5, the brain temperature was rapidly lowered, after 10 min of ischemia, to 30 degrees C during 45-50 min of recirculation. Wistar rats (group No. 6) served as controls (10-min normothermic ischemia).', 'In Sprague-Dawley (S-D) rats, post-ischemic audiogenic seizures (PAS) increased with the duration of ischemia and reached 86% (6/7 rats), after 10 min of ischemia. Mortality rate was high (50% = 7/14 rats). No seizure activity was observed after 10 min of ischemia in 6 Wistar (W) rats, and all survived. In the S-D rats, 10 min of ischemia produced histopathological damage in all brain regions examined, except in the thalamus. Damage was less severe in the W rats. Post-ischemic hypothermia ameliorated hippocampal and cortical nerve cell damage, but had no effect on the incidence of PAS activity and mortality. In W rats, hippocampal nerve cell loss was much less severe than in the S-D rats and cortical damage was not observed.
Example Output:
1