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:
Although trastuzumab improves the outcome of patients with human epidermal growth factor receptor2 (HER2)-overexpressing gastric or gastroesophageal junction adenocarcinoma (collectively referred to as "gastroesophageal adenocarcinoma"; GEA), no clinical response is observed in a substantial population of patients. A predictive biomarker of trastuzumab response is required. The aim of this study was to evaluate whether the hyperactivation of the downstream phosphatidylinositol 3-kinase pathway, due to phosphatase and tensin homolog (PTEN) loss or PIK3CA mutations, could provide trastuzumab resistance in GEA.', 'Expression of HER2 and PTEN, and PIK3CA gene mutations were screened in 264 surgically resected GEA specimens. The effects of PTEN knockdown on the response to trastuzumab on cell viability, HER2 downstream signaling, apoptosis, and cell cycle were evaluated in HER2-overexpressing NCI-N87 gastric adenocarcinoma and OE19 esophageal adenocarcinoma cell lines. Inhibition of xenograft tumor growth by trastuzumab was investigated in OE19 cells with or without PTEN knockdown. The PTEN expression and objective response were analyzed in 23 GEA patients who received trastuzumab-based therapy.', 'PTEN loss was identified in 34.5% of HER2-overexpressing GEA patients, whereas PIK3CA mutations were rare (5.6%). Trastuzumab-mediated growth suppression, apoptosis, and G

Ex Output:
0

Ex Input:
To investigate the effects of quercetin, an herbal flavonoid, on LPS-induced delay in spontaneous apoptosis, adhesion molecules (CD62L, CD11b/CD18) expression of neutrophils, and superoxide (O(2)(-)) generation by LPS-primed fMLP-induced human neutrophils.', 'Neutrophils were incubated in the presence or absence of lipopolysaccharide (LPS) at a final concentration of 1 microg/ml for 24 hours. Some wells with neutrophils were pre-treated with quecetin at the final concentration ranging from 0-100 microM for 30 min and then 1 microg/ml LPS was added into the cultures for 24 hours. The apoptosis of neutrophils was evaluated by flowcytometry analysis of propidum iodide (PI)-staining of the nuclei and annexin V staining of phosphatidylserine (PS) in the cell membrane. Agarose gel electrophoresis of low molecular weight DNA was performed to analyze DNA fragmentation. The effects of quercetin on adhesion molecules were detected by using flowcytometry analysis. The generation of O(2) (-) by LPS-primed fMLP-induced neutrophils was determined by reduced cytochrome c assay.', 'LPS markedly inhibited the spontaneous apoptosis of neutrophils, but the inhibitory effect was abrogated after the pre-treatment of neutrophils with quercetin (approximately 40 microM) for 30 min. Quercetin (40 microM) also prevented LPS-induced down-regulation of CD62L expression, up-regulation of CD11b/CD18 expression, and O(2) (-) generation by fMLP-induced neutrophils.

Ex Output:
1

Ex Input:
Pluripotent embryonic stem cells are considered to be an unlimited cell source for tissue regeneration and cell-based therapy. Investigating the molecular mechanism underlying the regulation of embryonic stem cell expansion is thus important. 14-3-3 proteins are implicated in controlling cell division, signaling transduction and survival by interacting with various regulatory proteins. However, the function of 14-3-3 in embryonic stem cell proliferation remains unclear.', 'In this study, we show that all seven 14-3-3 isoforms were detected in mouse embryonic stem cells. Retinoid acid suppressed selectively the expression of 14-3-3 isoform. Knockdown of 14-3-3 with siRNA reduced embryonic stem cell proliferation, while only 14-3-3 transfection increased cell growth and partially rescued retinoid acid-induced growth arrest. Since the growth-enhancing action of 14-3-3 was abrogated by -catenin knockdown, we investigated the influence of 14-3-3 overexpression on -catenin/GSK-3. 14-3-3 bound GSK-3 and increased GSK-3 phosphorylation in a PI-3K/Akt-dependent manner. It disrupted -catenin binding by the multiprotein destruction complex. 14-3-3 overexpression attenuated -catenin phosphorylation and rescued the decline of -catenin induced by retinoid acid. Furthermore, 14-3-3 enhanced Wnt3a-induced -catenin level and GSK-3 phosphorylation. DKK, an inhibitor of Wnt signaling, abolished Wnt3a-induced effect but did not interfere GSK-3/14-3-3 binding.

Ex Output:
0