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.

The appropriateness of vigorous fluid resuscitation to normal blood pressure following hemorrhage in uncontrolled bleeding has recently been questioned due to the possibility of dislodging clots and exacerbating hemorrhage. To develop a rational blood pressure target that maximizes the metabolic benefits of resuscitation without causing increased blood loss, it was first necessary to determine whether there is a reproducible mean arterial pressure (MAP) at which rebleeding occurs. The purpose of this study was to explore the relationship between the rate and time of resuscitation after injury and the rebleeding MAP in an uncontrolled hemorrhage model.', "Sixty-two anesthetized pigs were instrumented with catheters and splenectomized, and suction tubes were placed in the lateral peritoneal recesses to continuously capture shed blood. With the abdomen open, an aortotomy was made in the infrarenal aorta. At either 5, 15, or 30 minutes after the end of the initial hemorrhage, resuscitation with warmed lactated Ringer's solution was begun at either 100 or 300 mL/min. The rebleeding MAP was determined at the moment blood appeared in the suction tubes.", 'The average pressure at the rebleeding point for all animals was MAP = 64 +/- 2, Systolic = 94 +/- 3, and Diastolic = 45 +/- 2 mm Hg. The pressure at which rebleeding occurred in this aortotomy model was not affected by either time of resuscitation (5-30 min), nor was the rebleeding pressure affected by the rate (100 vs. 300 mL/min) of resuscitation.
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It is largely unknown how frequently low-abundance HIV drug-resistant variants at levels under limit of detection of conventional genotyping (<20% of quasi-species) are present in antiretroviral-experienced persons experiencing virologic failure. Further, the clinical implications of low-abundance drug-resistant variants at time of virologic failure are unknown.', "Plasma samples from 22 antiretroviral-experienced subjects collected at time of virologic failure (viral load 1380 to 304,000 copies/mL) were obtained from a specimen bank (from 2004-2007). The prevalence and profile of drug-resistant mutations were determined using Sanger sequencing and ultra-deep pyrosequencing. Genotypes were interpreted using Stanford HIV database algorithm. Antiretroviral treatment histories were obtained by chart review and correlated with drug-resistant mutations. Low-abundance drug-resistant mutations were detected in all 22 subjects by deep sequencing and only in 3 subjects by Sanger sequencing. In total they accounted for 90 of 247 mutations (36%) detected by deep sequencing; the majority of these (95%) were not detected by standard genotyping. A mean of 4 additional mutations per subject were detected by deep sequencing (p<0.0001, 95%CI: 2.85-5.53). The additional low-abundance drug-resistant mutations increased a subject's genotypic resistance to one or more antiretrovirals in 17 of 22 subjects (77%). When correlated with subjects' antiretroviral treatment histories, the additional low-abundance drug-resistant mutations correlated with the failing antiretroviral drugs in 21% subjects and correlated with historical antiretroviral use in 79% subjects (OR, 13.73; 95% CI, 2.5-74.3, p = 0.0016).
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This study was aimed at understanding the effect of β-catenin and cyclin D1 on overall survival in patients with early-stage NSCLC and at evaluating if the\xa0prognostic effect can be modified by adjuvant chemotherapy.', 'We retrospectively analyzed the expression of β-catenin and cyclin D1 using immunohistochemistry in formalin-fixed paraffin-embedded tissues from 576 patients with early-stage NSCLC.', 'The median duration of follow-up was 5.1 years. Overexpression of β-catenin and cyclin D1 was found in 56% and 50% of 576 cases, respectively. Overexpression of β-catenin and cyclin D1 was significantly associated with poor overall survival (p\xa0= 0.003 and p\xa0= 0.0009, respectively; log rank test) in squamous cell carcinomas, not in adenocarcinomas. The prognostic significance of each protein in the squamous cell carcinomas was limited to stages IA, IB, and IIA. In addition, simultaneous overexpression of β-catenin and cyclin D1 in the squamous cell carcinomas synergistically increased hazard ratios (HRs) 15.79 (95% confidence interval [CI]\xa0= 1.09-51.23; p\xa0=0.04) for stage IA, 10.30 (95% CI\xa0= 2.29-46.41; p\xa0= 0.002) for stage 1B, and 3.55 (95% CI\xa0= 1.22-10.36; p\xa0= 0.02) times for stage 2A compared to those without overexpression of the two proteins, after adjusting for confounding factors. In addition, the effect was not dependent on adjuvant chemotherapy.

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