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.

Input: Consider Input: Transient tachypnea of the newborn (TTN) is a benign disorder with a variable clinical course that often leads to hospitalization. The aim of this study was to assess and validate the relationship between the serum cystatin C level and symptom duration in infants with TTN.', 'Forty newborns presenting with TTN and who had undergone serum cystatin C (Cys C) tests on the first day of admission to the Kyung Hee University Hospital (Seoul, Korea) from 2009 to 2013 were included. The serum Cys C level, creatinine (Cr) level, estimated glomerular filtration rate (eGFR), and tachypnea duration were correlated retrospectively.', 'The median gestation period was 37.8\xa0±\xa03.8 weeks and the mean birth weight was 3.2\xa0±\xa00.4\xa0kg. Tachypnea duration was 3.3\xa0±\xa02.0 days. Serum Cys C and Cr levels were 1.7\xa0±\xa00.2\xa0mg/L and 0.8\xa0±\xa01.2\xa0mg/dL, respectively. Tachypnea duration was significantly positively correlated with the serum levels of Cys C and significantly negatively correlated with Cys C-based eGFR (p\xa0=\xa00.016), but was not significantly correlated with the serum Cr level or Cr-based eGFR. When tachypnea duration was compared between infants with Cys C level <1.6\xa0mg/L (n\xa0=\xa015; Group A) and infants with Cys C level\xa0≥\xa01.6\xa0mg/L (n\xa0=\xa025; Group B), the symptom duration was significantly shorter in Group A infants (p\xa0=\xa00.011).

Output: 0


Input: Consider Input: Sepsis-induced cardiomyopathy (SIC) is thought to be the result of detrimental effects of inflammatory mediators on the cardiac muscle. Here we studied the effects of prolonged (24 ± 4 h) exposure of adult rat ventricular myocytes (ARVM) to bacterial lipopolysaccharide (LPS) and inflammatory cytokines tumor necrosis factor (TNF) and interleukins-1 (IL-1) and IL-6.', 'We measured sarcomere shortening (SS) and cellular calcium (Ca(2+)) transients (ΔCai, with fura-2 AM) in isolated cardiomyocytes externally paced at 5 Hz at 37°C.', 'SS decreased after incubation with LPS (100 μg/mL), IL-1 (100 ng/mL), and IL-6 (30 ng/mL), but not with lesser doses of these mediators, or TNF (10-100 ng/mL). A combination of LPS (100 μg/mL), TNF, IL-1, and IL-6 (each 100 ng/mL; i.e., "Cytomix-100") induced a maximal decrease in SS and ΔCai. Sarcoplasmic reticulum (SR) Ca(2+) load (CaSR, measured with caffeine) was unchanged by Cytomix-100; however, SR fractional release (ΔCai/CaSR) was decreased. Underlying these effects, Ca(2+) influx into the cell (via L-type Ca(2+) channels, LTCC) and Ca(2+) extrusion via Na(+)/Ca(2+) exchange were decreased by Cytomix-100. SR Ca(2+) pump (SERCA) (SR Ca(2+) ATPase) was not affected.

Output: 0


Input: Consider Input: Lipopolysaccharide (LPS) is closely associated with the development of infection-induced deleterious pulmonary reactions. In this study, we investigated the enhancement effects of LPS on tachykinin-mediated plasma exudation in the lungs of guinea pigs. The role of oxidants was also explored.', 'Intravenous LPS (100 mu kg-1) or its vehicle was administered 0 to 3 hours prior to bilateral electrical or sham stimulation of the cervical vagus nerves in animals anesthetized with urethane and artificially ventilated. Plasma exudation into the lungs was assessed by measurement of extravasated 125I-albumin which had been intravenously administered before stimulation.', 'The plasma exudation in the lungs increased after bilateral cervical vagal stimulation. LPS alone did not induce significant plasma exudation. The vagally-mediated plasma exudation was enhanced by LPS with the peak effect 1 hour after LPS administration. LPS also enhanced exogenous substance P (10(-8) mol kg-1, i.v.)-induced plasma exudation. The vagally-induced plasma exudation was abolished by a specific neurokinin-1 (NK-1) receptor antagonist, L-732,138. The LPS-induced enhancement response was also attenuated by L-732,138. The vagally-induced plasma exudation was not affected by superoxide dismutase (SOD, 5000 U kg-1, i.p.) pretreatment. However, SOD significantly inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-induced enhancement was not completely abolished by either L-732,138 or SOD pretreatment alone, but by a combination of both.


Output: 0