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.

Ex Input:
Trans-activation Response DNA-binding Protein-43 (TDP-43) lesions are observed in Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Lobar Degeneration with ubiquitin inclusions (FTLD-TDP) and 25-50% of Alzheimer's Disease (AD) cases. These abnormal protein inclusions are composed of either amorphous TDP-43 aggregates or highly ordered filaments. The filamentous TDP-43 accumulations typically contain clean 10-12 nm filaments though wider 18-20 nm coated filaments may be observed. The TDP-43 present within these lesions is phosphorylated, truncated and ubiquitinated, and these modifications appear to be abnormal as they are linked to both a cellular heat shock response and microglial activation. The mechanisms associated with this abnormal TDP-43 accumulation are believed to result in a loss of TDP-43 function, perhaps due to the post-translational modifications or resulting from physical sequestration of the TDP-43. The formation of TDP-43 inclusions involves cellular translocation and conversion of TDP-43 into fibrillogenic forms, but the ability of these accumulations to sequester normal TDP-43 and propagate this behavior between neurons pathologically is mostly inferred. The lack of methodology to produce soluble full length TDP-43 and recapitulate this polymerization into filaments as observed in disease has limited our understanding of these pathogenic cascades.", 'The protocols described here generate soluble, full-length and untagged TDP-43 allowing for a direct assessment of the impact of various posttranslational modifications on TDP-43 function. We demonstrate that Casein Kinase II (CKII) promotes the polymerization of this soluble TDP-43 into 10 nm diameter filaments that resemble the most common TDP-43 structures observed in disease. Furthermore, these filaments are recognized as abnormal by Heat Shock Proteins (HSPs) which can inhibit TDP-43 polymerization or directly promote TDP-43 filament depolymerization.

Ex Output:
0

Ex Input:
The development of techniques that allow the imaging of animals infected with parasites expressing luciferase opens up new possibilities for following the fate of parasites in infected mammals.', 'D-luciferin potassium salt stock solution was prepared in phosphate-buffered saline (PBS) at 15 mg/ml. To produce bioluminescence, infected and control mice received an intraperitoneal injection of luciferin stock solution (150 mg/kg). All mice were immediately anesthetized with 2% isofluorane, and after 10 minutes were imaged. Ex vivo evaluation of infected tissues and organs was evaluated in a 24-well plate in 150 g/ml D-luciferin diluted in PBS. Images were captured using the IVIS Lumina image system (Xenogen). Dissected organs were also evaluated by microscopy of hematoxylin-eosin stained sections.', 'Here we describe the results obtained using a genetically modified Dm28c strain of T. cruzi expressing the firefly luciferase to keep track of infection by bioluminescence imaging. Progression of infection was observed in vivo in BALB/c mice at various intervals after infection with transgenic Dm28c-luc. The bioluminescent signal was immediately observed at the site of T. cruzi inoculation, and one day post infection (dpi) it was disseminated in the peritoneal cavity. A similar pattern in the cavity was observed on 7 dpi, but the bioluminescence was more intense in the terminal region of the large intestine, rectum, and gonads. On 14 and 21 dpi, bioluminescent parasites were also observed in the heart, snout, paws, hind limbs, and forelimbs. From 28 dpi to 180 dpi in chronically infected mice, bioluminescence declined in regions of the body but was concentrated in the gonad region. Ex vivo evaluation of dissected organs and tissues by bioluminescent imaging confirmed the in vivo bioluminescent foci. Histopathological analysis of dissected organs demonstrated parasite nests at the rectum and snout, in muscle fibers of mice infected with Dm28c-WT and with Dm28c-luc, corroborating the bioluminescent imaging.

Ex Output:
0

Ex Input:
The conventional 12-lead electrocardiogram (cECG) derived from 10 electrodes using a cardiograph is the gold standard for diagnosing myocardial ischemia. This study tested the hypothesis that a new 5-electrode 12-lead vector-based ECG (EASI; Philips Medical Systems, formerly Hewlett Packard Co, Boeblingen, Germany) patient monitoring system is equivalent to cECG in diagnosing acute coronary syndromes (ACSs).', 'Electrocardiograms (EASI and cECG) were obtained in 203 patients with chest pain on admission and 4 to 8 hours later. Both types of ECGs were graded as ST-elevation myocardial infarction if at least 1 of the 2 consecutive recordings showed ST elevation more than 0.2 mV, as ACS if one or both showed ST elevation less than 0.2 mV, T-wave inversion, or ST depression. Otherwise, the ECG was graded negative.', 'Final diagnosis was identical in 177 patients (87%; 95% confidence interval [CI], 82%-91%; kappa = 0.81; SE = 0.035). ST-elevation myocardial infarction was correctly identified or excluded by EASI with a specificity of 94% (95% CI, 89%-97%) and a sensitivity of 93% (95% CI, 86%-97%; using cECG as the gold standard). Of 118 patients with enzyme elevations, an almost identical number (72 [61% by EASI] and 73 [62% by cECG]) had ST elevations. Both techniques were equivalent in predicting subsequent enzyme elevation (identical, 108/143; 75% of ACS and ST-elevation myocardial infarction ECGs by EASI and cECG). Thus, both ECG methods had exactly the same specificity of 59% (95% CI, 48%-69%) and sensitivity of 91% (95% CI, 85%-96%) for detecting myocardial injury.

Ex Output:
1