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: Dexamethasone (Dex)-induced spontaneous tendon rupture and decreased self-repair capability is very common in clinical practice. The metaplasia of adipose tissue in the ruptured tendon indicates that Dex may induce tendon stem cells (TSCs) to differentiate into adipocytes, but the mechanism remains unclear. In the present study, we used in vitro methods to investigate the effects of Dex on rat TSC differentiation and the molecular mechanisms underlying this process.', 'First, we used qPCR and Western blotting to detect the expression of the adipogenic differentiation markers aP2 and C/EBPα after treating the TSCs with Dex. Oil red staining was used to confirm that high concentration Dex promoted adipogenic differentiation of rat TSCs. Next, we used qPCR and Western blotting to detect the effect of a high concentration of dexamethasone on molecules related to the canonical WNT/β-catenin pathway in TSCs.', 'Treating rat TSCs with Dex promoted the synthesis of the inhibitory molecule dickkopf1 (DKK1) at the mRNA and protein levels. Western blotting results further showed that Dex downregulated the cellular signaling molecule phosphorylated glycogen synthase kinase-3β (P-GSK-3 β (ser9)), upregulated P-GSK-3β (tyr216), and downregulated the pivotal signaling molecule β-catenin. Furthermore, DKK1 knockdown attenuated Dex-induced inhibition of the canonical WNT/β-catenin pathway and of the adipogenic differentiation of TSCs. Lithium chloride (LiCl, a GSK-3β inhibitor) reduced Dex-induced inhibition of the classical WNT/β-catenin pathway in TSCs and of the differentiation of TSCs to adipocytes.

SOLUTION: 1

PROBLEM: Previous studies regarding the outcome of laparoscopic cholecystectomy (LC) in men have reported inconsistent findings. We conducted this prospective study to test the hypothesis that the outcome of LC is worse in men than women.', 'Between 1997 and 2002, a total of 391 consecutive LCs were performed by a single surgeon at King Fahd Hospital of the University. We collected and analyzed data including age, gender, body mass index (kg/m(2)), the American Society of Anesthesiologists (ASA) class, mode of admission (elective or emergency), indication for LC (chronic or acute cholecystitis [AC]), comorbid disease, previous abdominal surgery, conversion to open cholecystectomy, complications, operation time, and length of postoperative hospital stay.', 'Bivariate analysis showed that both genders were matched for age, ASA class and mode of admission. The incidences of AC (P = 0.003) and comorbid disease (P = 0.031) were significantly higher in men. Women were significantly more obese than men (P < 0.001) and had a higher incidence of previous abdominal surgery (P = 0.017). There were no statistical differences between genders with regard to rates of conversion (P = 0.372) and complications (P = 0.647) and operation time (P = 0.063). The postoperative stay was significantly longer in men than women (P = 0.001). Logistic regression analysis showed that male gender was not an independent predictor of conversion (Odds ratio [OR] = 0.37 and P = 0.43) or complications (OR = 0.42, P = 0.42). Linear regression analysis showed that male gender was not an independent predictor of the operation time, but was associated with a longer postoperative stay (P = 0.02).

SOLUTION: 1

PROBLEM: Peroxisome proliferator-activated receptor alpha (PPARα) is a key regulator of hepatic fat oxidation that serves as an energy source during starvation. Vanin-1 has been described as a putative PPARα target gene in liver, but its function in hepatic lipid metabolism is unknown.', 'We investigated the regulation of vanin-1, and total vanin activity, by PPARα in mice and humans. Furthermore, the function of vanin-1 in the development of hepatic steatosis in response to starvation was examined in Vnn1 deficient mice, and in rats treated with an inhibitor of vanin activity.', 'Liver microarray analyses reveals that Vnn1 is the most prominently regulated gene after modulation of PPARα activity. In addition, activation of mouse PPARα regulates hepatic- and plasma vanin activity. In humans, consistent with regulation by PPARα, plasma vanin activity increases in all subjects after prolonged fasting, as well as after treatment with the PPARα agonist fenofibrate. In mice, absence of vanin-1 exacerbates the fasting-induced increase in hepatic triglyceride levels. Similarly, inhibition of vanin activity in rats induces accumulation of hepatic triglycerides upon fasting. Microarray analysis reveal that the absence of vanin-1 associates with gene sets involved in liver steatosis, and reduces pathways involved in oxidative stress and inflammation.

SOLUTION:
1