Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

This study was designed to determine the relevance of a proposed classification for advanced heart failure (HF). Profiles based on clinical assessment of congestion and perfusion at the time of hospitalization were compared with subsequent outcomes.', 'Optimal design of therapy and trials for advanced HF remains limited by the lack of simple clinical profiles to characterize patients.', "Prospective analysis was performed for 452 patients admitted to the cardiomyopathy service at the Brigham and Women's Hospital with a diagnosis of HF. Patients were classified by clinical assessment into four profiles: profile A, patients with no evidence of congestion or hypoperfusion (dry-warm, n = 123); profile B, congestion with adequate perfusion (wet-warm, n = 222); profile C, congestion and hypoperfusion (wet-cold, n = 91); and profile L, hypoperfusion without congestion (dry-cold, n = 16). Other standard predictors of outcome were included and patients were followed for the end points of death (n = 117) and death or urgent transplantation (n = 137) at one year.", 'Survival analysis showed that clinical profiles predict outcomes in HF. Profiles B and C increase the risk of death plus urgent transplantation by univariate (hazard ratio [HR] 1.83, p = 0.02) and multivariate analyses (HR 2.48, p = 0.003). Moreover, clinical profiles add prognostic information even when limited to patients with New York Heart Association (NYHA) class III/IV symptoms (profile B: HR 2.23, p = 0.026; profile C: HR 2.73, p = 0.009).
Does clinical assessment identify hemodynamic profiles that predict outcomes in patients admitted with heart failure?

Aggrecanase cleavage at the 392Glu-393Ala bond in the interglobular domain (IGD) of aggrecan, releasing N-terminal 393ARGS fragments, is an early key event in arthritis and joint injuries. Here, we use a quantitative immunoassay of aggrecan ARGS neoepitope fragments in human synovial fluid to determine if this cleavage-site specific method better identifies joint pathology than previously available less specific aggrecan assays.', 'Synovial fluid (SF) from 26 people with healthy knees (reference) and 269 patients were analyzed in a cross-sectional study. Patient groups were acute inflammatory arthritis, acute knee injury, chronic knee injury and knee osteoarthritis (OA). Aggrecan ARGS fragments were assayed by ELISA using the monoclonal antibody OA-1. Total aggrecan content was analyzed by an ELISA using the monoclonal antibody 1-F21, and sulfated glycosaminoglycan by Alcian blue precipitation.', 'Aggrecan ARGS fragment concentrations in all groups differed from the reference group (P < 0.001). The acute inflammatory arthritis group had the highest median level, 177-fold greater than that of the reference group. Median levels (in pmol ARGS/ml SF) were: reference 0.5, acute inflammatory arthritis 88.5, acute knee injury 53.9, chronic knee injury 0.5 and OA 4.6. In contrast, aggrecan and sulfated glycosaminoglycan concentrations varied much less between groups, and only acute inflammatory arthritis and acute knee injury were found to have a two-fold increase in median levels compared to the reference.
Is synovial fluid level of aggrecan ARGS fragments a more sensitive marker of joint disease than glycosaminoglycan or aggrecan levels : a cross-sectional study?

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.
Does blood pressure at which rebleeding occur after resuscitation in swine with aortic injury?