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.

[Q]: The toxicity of anti-rheumatic gold compounds has limited their use and development, yet both the toxicological and therapeutic actions of these compounds remain unclear. In the current study, we tested the hypothesis that intracellular reactive oxygen species (ROS) induced by Au(I) or Au(III) compounds mediate their ability to suppress mitochondrial activity.', 'Human THP1 monocytes were exposed to HAuCl(4) x 3H(2)O (Au(III)), or the anti-rheumatic compounds auranofin (AF) or gold sodium thiomalate (GSTM) for 6-72 h, after which mitochondrial activity (succinate dehydrogenase) was measured. To assess the role of cellular redox status as a mediator of mitochondrial suppression, monocytes were pre-treated with a pro-oxidant (t-butyl hydroquinone, t-BHQ) or antioxidant (N-acetyl cysteine, NAC ). ROS levels were measured 0-24h post-gold addition to determine their role as mediators of mitochondrial activity suppression.', 'AF was the most potent inhibitor of mitochondrial activity, followed by Au(III) and GSTM. Only Au(III) induced intracellular ROS; no ROS formation was observed in response to AF or GSTM exposure. Although anti- and pro-oxidants had some effects on mitochondrial suppression of Au compounds, collectively the data do not support redox effects or ROS formation as major mediators of Au-compound mitochondrial suppression.
[A]: 0


[Q]: A limited amount of literature suggests that plasma leptin concentrations are reduced with habitual physical activity in men and non-pregnant women. We investigated the relationship between maternal physical activity and plasma leptin during early pregnancy.', 'The study population included 879 normotensive, non-diabetic pregnant women who reported physical activity type, frequency, and duration in early pregnancy. Plasma leptin, measured in blood samples collected <16 weeks gestation, were determined using enzyme immunoassays. Weekly duration (h/week) and energy expended on recreational physical activity [metabolic equivalent score (MET)-h/week] were categorized by tertiles among active women. Physical activity intensity was categorized as none, moderate (<6 MET) and vigorous (> or =6 MET). Differences in leptin concentrations across categories were estimated using linear regression procedures.', 'Mean leptin was 5.8 ng/ml lower among active versus inactive women (P=0.001). Mean leptin was lower among women in the highest levels (>12.8 h/week) of time performing physical activity (-8.1 ng/ml, P<0.001) and energy expenditure (>70.4 MET-h/week) (-8.3 ng/ml, P=0.001) compared with inactive women. Leptin was inversely associated with the intensity of physical activity.
[A]: 0


[Q]: Lipopolysaccharide (LPS) is considered a prominent pathogenic factor in inflammatory bone diseases. LPS challenge contributes to the production of reactive oxygen species (ROS) in diverse inflammatory diseases. However, its mechanism remains to be clarified in bone. Thus, we investigated the critical mechanism of ROS in LPS-induced osteoclastogenesis and bone loss.', 'Antioxidant prevented LPS-induced osteoclast formation via inhibition of nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) and c-Fos expression in preosteoclasts. Moreover, LPS-induced osteoclast formation via ROS was attenuated by treatment with c-Jun N-terminal protein kinase (JNK) inhibitor. Interestingly, LPS also activated signal transducer and activator of transcription 3 (STAT3), which is suppressed by antioxidants. We found that knockdown of STAT3 or use of a STAT3 inhibitor resulted in a significant reduction in interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and nitric oxide (NO) production, followed by decreased osteoclast formation by LPS. Peroxiredoxin II (PrxII) is a member of the antioxidant enzyme family, and it plays a protective role against oxidative damage caused by ROS. In our study, ROS production and osteoclast formation by LPS was significantly enhanced in PrxII(-/-) cells. Moreover, JNK-mediated c-Fos and NFATc1 expression was promoted in PrxII(-/-) cells. Furthermore, STAT3 activation and accompanying IL-1β, IL-6, and NO production was also increased in PrxII(-/-) cells. Consistent with the in vitro result, PrxII-deficient mice showed increased osteoclast formation and bone loss by LPS challenge compared with wild-type mice.', 'For the first time, we showed that LPS-induced ROS signaling is dependent on the coordinated mechanism of JNK and STAT3 during osteoclastogenesis, which is negatively regulated by PrxII.
[A]:
1