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 Q]: Cancer-associated fibroblasts (CAFs) are believed to play an essential role in cancer initiation and development. However, little research has been undertaken to evaluate the role of CAFs in endometrial cancer (EC) progression. We aim to detect the functional contributions of CAFs to promote progression of EC.', 'Stromal fibroblasts were isolated from endometrioid adenocarcinomas and normal endometrial tissues. The conditioned media of cultured CAFs and normal fibroblasts (NFs) were collected to detect the level of stromal cell-derived factor-1alpha (SDF-1), macrophage chemoattractant protein-1 (MCP-1), migration inhibitory factor (MIF), colony stimulating factor-1 (CSF-1), and interleukin-1 (IL-1) by ELISA. The CAFs or NFs were cocultured with EC cell lines to determine the proliferation, migration, and invasion by MTT assays and transwell chambers. Xenograft models were used to observe tumor growth. Matrix metalloproteinases (MMP)-2 and MMP-9 activity was evaluated by zymography. AMD3100 (a chemokine receptor 4 (CXCR4) antagonist) was used to block the SDF-1/CXCR4 axis. Neutralizing antibodies were used to detect PI3K/Akt and MAPK/Erk pathways by western blotting. SDF-1 and CXCR4 expressions were analyzed in xenotransplanted tumors and 348 cases by immunohistochemistry.', 'CAFs promoted proliferation, migration, and invasion as well as in vivo tumorigenesis of admixed EC cells significantly more than NFs by secreting SDF-1. These effects were significantly inhibited by AMD3100. CAFs promoted EC progression via the SDF-1/CXCR4 axis to activate the PI3K/Akt and MAPK/Erk signalings in a paracrine-dependent manner or increase MMP-2 and MMP-9 secretion in an autocrine-dependent manner. SDF-1 and CXCR4 expression upregulation accompanied clinical EC development and progression. High SDF-1 expression levels were associated with deep myometrial invasion, lymph node metastasis, and poor prognosis in EC.
[EX A]: 0

[EX Q]: Controversy has surrounded the technique of circular stapled anopexy since an isolated report of a high incidence of persistent postdefaecation pain following the procedure. The characteristics, clinical course and management of this complication have not been described.', 'Within an ongoing multicentre randomized clinical trial comparing circular stapled anopexy with closed haemorrhoidectomy, 77 patients underwent circular stapled anopexy. Follow-up was at 6, 12, 24 and 48 weeks. Patients underwent transanal ultrasonography, anal electrosensitivity testing and manometry.', 'Of the 77 patients who had circular stapled anopexy, three men reported new-onset postdefaecation pain that compromised lifestyle, including ability to return to work. All three had sphincter hypertonicity on digital and manometric examination but were refractory to topical 0.2 per cent glyceryl trinitrate ointment. The addition of oral nifedipine 20 mg twice daily did not alter anal sphincter pressures but rapidly abolished symptoms and restored quality of life.
[EX A]: 0

[EX Q]: Cisplatin-based chemotherapy is the standard of care for patients with muscle-invasive urothelial carcinoma. Pathologic downstaging to pT0/pTis after neoadjuvant cisplatin-based chemotherapy is associated with improved survival, although molecular determinants of cisplatin response are incompletely understood. We performed whole-exome sequencing on pretreatment tumor and germline DNA from 50 patients with muscle-invasive urothelial carcinoma who received neoadjuvant cisplatin-based chemotherapy followed by cystectomy (25 pT0/pTis "responders," 25 pT2+ "nonresponders") to identify somatic mutations that occurred preferentially in responders. ERCC2, a nucleotide excision repair gene, was the only significantly mutated gene enriched in the cisplatin responders compared with nonresponders (q < 0.01). Expression of representative ERCC2 mutants in an ERCC2-deficient cell line failed to rescue cisplatin and UV sensitivity compared with wild-type ERCC2. The lack of normal ERCC2 function may contribute to cisplatin sensitivity in urothelial cancer, and somatic ERCC2 mutation status may inform cisplatin-containing regimen usage in muscle-invasive urothelial carcinoma.
[EX A]:
0