TASK DEFINITION: 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.
PROBLEM: Sepsis-induced cardiomyopathy (SIC) is thought to be the result of detrimental effects of inflammatory mediators on the cardiac muscle. Here we studied the effects of prolonged (24 4 h) exposure of adult rat ventricular myocytes (ARVM) to bacterial lipopolysaccharide (LPS) and inflammatory cytokines tumor necrosis factor (TNF) and interleukins-1 (IL-1) and IL-6.', 'We measured sarcomere shortening (SS) and cellular calcium (Ca(2+)) transients (Cai, with fura-2 AM) in isolated cardiomyocytes externally paced at 5 Hz at 37C.', 'SS decreased after incubation with LPS (100 g/mL), IL-1 (100 ng/mL), and IL-6 (30 ng/mL), but not with lesser doses of these mediators, or TNF (10-100 ng/mL). A combination of LPS (100 g/mL), TNF, IL-1, and IL-6 (each 100 ng/mL; i.e., "Cytomix-100") induced a maximal decrease in SS and Cai. Sarcoplasmic reticulum (SR) Ca(2+) load (CaSR, measured with caffeine) was unchanged by Cytomix-100; however, SR fractional release (Cai/CaSR) was decreased. Underlying these effects, Ca(2+) influx into the cell (via L-type Ca(2+) channels, LTCC) and Ca(2+) extrusion via Na(+)/Ca(2+) exchange were decreased by Cytomix-100. SR Ca(2+) pump (SERCA) (SR Ca(2+) ATPase) was not affected.

SOLUTION: 0

PROBLEM: Previous studies have shown that giving other foods while breastfeeding increases the risk of mother-to-child transmission of human immunodeficiency virus (HIV) type 1. The mechanism is speculated to be increased inflammation of the gastrointestinal tract.', 'In a prospective longitudinal study, we compared fecal calprotectin, a marker of intestinal inflammatory disease, in healthy U.S. infants 0-6 months of age who were exclusively breastfed compared to those given additional liquids or solids.', 'In comparison to infants who were mixed-fed, fecal calprotectin was significantly higher in the exclusively breastfed group (p = 0.01) by a mean of 60 mg/kg (SE = 23).

SOLUTION: 0

PROBLEM: Paraquat, a quaternary nitrogen herbicide, is a highly toxic prooxidant resulting in multi-organ failure including the heart although the underlying mechanism still remains elusive. This study was designed to examine the role of the cellular fuel sensor AMP-activated protein kinase (AMPK) in paraquat-induced cardiac contractile and mitochondrial injury.', 'Wild-type and transgenic mice with overexpression of a mutant AMPK 2 subunit (kinase dead, KD), with reduced activity in both 1 and 2 subunits, were administered with paraquat (45 mg/kg) for 48 h. Paraquat elicited cardiac mechanical anomalies including compromised echocardiographic parameters (elevated left ventricular end-systolic diameter and reduced factional shortening), suppressed cardiomyocyte contractile function, intracellular Ca(2+) handling, reduced cell survival, and overt mitochondrial damage (loss in mitochondrial membrane potential). In addition, paraquat treatment promoted phosphorylation of AMPK and autophagy. Interestingly, deficiency in AMPK attenuated paraquat-induced cardiac contractile and intracellular Ca(2+) derangement. The beneficial effect of AMPK inhibition was associated with inhibition of the AMPK-TSC-mTOR-ULK1 signaling cascade. In vitro study revealed that inhibitors for AMPK and autophagy attenuated paraquat-induced cardiomyocyte contractile dysfunction.

SOLUTION:
1