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: del(17p), del(11q), and associated p53 dysfunction predict for short survival and chemoresistance in B-cell chronic lymphocytic leukemia (CLL). DNA-dependent protein kinase (DNA-PK) is activated by DNA damage and mediates DNA double-strand break repair. We hypothesized that inhibiting DNA-PK would sensitize CLL cells to drug-induced DNA damage and that this approach could increase the therapeutic index of agents used to treat CLL.', 'Fifty-four CLL cases were characterized for poor prognosis markers [del(17p), del(11q), CD38, and ZAP-70]. In selected cases, DNA-PK catalytic subunit (DNA-PKcs) expression and activity and p53 function were also measured. Ex vivo viability assays established sensitivity to fludarabine and chlorambucil and also tested the ability of a novel DNA-PK inhibitor (NU7441) to sensitize CLL cells to these drugs. The effects of NU7441 on fludarabine-induced DNA damage repair were also assessed (Comet assays and detection of gammaH2AX).', 'DNA-PKcs levels correlated with DNA-PK activity and varied 50-fold between cases but were consistently higher in del(17p) (P = 0.01) and del(11q) cases. NU7441 sensitized CLL cells to chlorambucil and fludarabine, including cases with del(17p), del(11q), p53 dysfunction, or high levels of DNA-PKcs. NU7441 increased fludarabine-induced double-strand breaks and abrogated drug-induced autophosphorylation of DNA-PKcs at Ser2056. High DNA-PK levels predicted for reduced treatment-free interval.

Output: 1


Input: Consider Input: To improve prostate cancer (PC) detection accuracy among patients with a prostate-specific antigen (PSA) above 4.0 ng/ml and asymptomatic prostate inflammation.', 'A total of 136 patients with PSA ranging from 4.0 to 50.0 ng/ml with asymptomatic prostatitis were included in the study cohort. All these patients underwent antibacterial therapy for 2 weeks followed by repeat PSA determination and transrectal ultrasound-guided needle prostate biopsy. The PSA, PSAD (PSA density), and f/t PSA (free/total PSA) before and after antibacterial therapy were compared using t-test. The receiver-operating characteristic (ROC) technique was used to evaluate the effectiveness of PSA, PSAD, f/t PSA, and their changes after antibacterial therapy (DeltaPSA, DeltaPSAD, and Deltaf/t PSA) on PC detection.', 'Among the 136 patients, 33 had PC and the other 103 histologically confirmed benign prostatic disease. After antibacterial therapy for 2 weeks, the PSA (mean +/- standard deviation) decreased from 14.0 +/- 7.8 ng/ml to 10.4 +/- 7.7 ng/ml (P < 0.01). The DeltaPSA, DeltaPSAD, and Deltaf/tPSA were -3.60 +/- 4.3 ng/ml, -0.1 +/- 0.1 ng/ml/ml, and -0.1 +/- 0.1 respectively. The areas under ROC curve were 0.29 for PSA, 0.64 for PSAD, and 0.50 for f/t PSA. The areas under ROC curve were 0.91 for DeltaPSA, 0.96 for DeltaPSAD, and 0.98 for Deltaf/t PSA. These values were increased significantly when compared with those for the PSA-related parameters before antibacterial therapy (P value, DeltaPSA, DeltaPSAD, and Deltaf/t PSA were <0.01).

Output: 1


Input: Consider Input: High rates of 23S rDNA mutations implicated in macrolide resistance have been identified in Treponema pallidum samples from syphilis patients in many countries. Nonetheless, some clinicians have been reluctant to abandon azithromycin as a treatment for syphilis, citing the lack of a causal association between these mutations and clinical evidence of drug resistance. Although azithromycin resistance has been demonstrated in vivo for the historical Street 14 strain, no recent T. pallidum isolates have been tested. We used the well-established rabbit model of syphilis to determine the in vivo efficacy of azithromycin against 23S rDNA mutant strains collected in 2004 to 2005 from patients with syphilis in Seattle, Wash.', 'Groups of 9 rabbits were each infected with a strain containing 23S rDNA mutation A2058G (strains UW074B, UW189B, UW391B) or A2059G (strains UW228B, UW254B, and UW330B), or with 1 wild type strain (Chicago, Bal 3, and Mexico A). After documentation of infection, 3 animals per strain were treated with azithromycin, 3 were treated with benzathine penicillin G, and 3 served as untreated control groups. Treatment efficacy was documented by darkfield microscopic evidence of T. pallidum, serological response, and rabbit infectivity test.', 'Azithromycin uniformly failed to cure rabbits infected with strains harboring either 23S rDNA mutation, although benzathine penicillin G was effective. Infections caused by wild type strains were successfully treated by either azithromycin or benzathine penicillin G.


Output: 0