instruction:
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.
question:
Overexpression of the human c-MYC (MYC) oncogene is one of the most frequently implicated events in the pathogenesis of hepatocellular carcinoma (HCC). Previously, we have shown in a conditional transgenic mouse model that MYC overexpression is restrained from inducing mitotic cellular division and tumorigenesis in the adult liver; whereas, in marked contrast, MYC induces robust proliferation associated with the very rapid onset of tumorigenesis in embryonic and neonatal mice.', 'Here, we show that non-genotoxic hepatotoxins induce changes in the liver cellular context associated with increased cellular proliferation and enhanced tumorigenesis. Both 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl(4)) cooperate with MYC to greatly accelerate the onset of liver cancer in an adult host to less than 7 days versus a mean latency of onset of over 35 weeks for MYC alone. These hepatotoxin-enhanced liver tumors grossly and histologically resemble embryonic and neonatal liver tumors. Importantly, we found that MYC overexpression is only capable of inducing expression of the mitotic Cyclin B1 in embryonic/neonatal hosts or adult hosts that were treated with either carcinogen.
answer:
Do hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis?

question:
Vitamin D is associated with a number of inflammatory diseases and plays a significant role in regulating bone metabolism. Serum calcifediol was demonstrated to be potentially associated with periodontal disease. The purpose of this study was to evaluate whether an association exists between plasma calcifediol concentrations and aggressive periodontitis (AgP) and whether plasma levels of bone-related biomarkers (osteocalcin, alkaline phosphatase, calcium, and phosphorus) regulated by vitamin D are related to AgP.', 'Sixty-six patients with generalized AgP, 52 patients with chronic periodontitis, and 60 healthy controls were included in this study. Periodontal examination consisted of probing depth, attachment loss, and bleeding index measurements. Hematic calcifediol and bone-related biomarker levels were detected using radioimmunity assay kits or a biochemical analyzer.', 'Plasma calcifediol levels in patients with AgP were higher than those of healthy controls (29.28 versus 21.60 nmol/l; P <0.05) and were statistically significantly correlated with bleeding index (r = 0.321; P <0.05). Plasma osteocalcin concentrations in patients with AgP were higher than those of healthy controls (0.90 versus 0.70 ng/ml; P <0.05). Serum inorganic phosphorus values of both periodontitis groups were lower than those of healthy controls (1.06 +/- 0.18 mmol/l and 1.10 +/- 0.15 mmol/l versus 1.26 +/- 0.17 mmol/l; P <0.05).
answer:
Is elevated plasma calcifediol associated with aggressive periodontitis?

question:
To determine if temporomandibular joint chondrocyte apoptosis is induced in rats with dental biomechanical stimulation and what a role TNF takes.', 'Thirty-two rats were divided into 4 groups (n = 8/group) and exposed to incisor mal-occlusion induced by unilateral anterior crossbite biomechanical stimulation. Two groups were sampled at 2 or 4 weeks. The other two groups were treated with local injections of a TNF inhibitor or PBS into the temporomandibular joints area at 2 weeks and then sampled at 4 weeks. Twenty-four rats either served as unilateral anterior crossbite mock operation controls (n = 8/group) with sampling at 2 or 4 weeks or received a local injection of the TNF inhibitor at 2 weeks with sampling at 4 weeks. Chondrocytes were isolated from the temporomandibular joints of 6 additional rats and treated with TNF in vitro. Joint samples were assessed using Hematoxylin&eosin, Safranin O, TUNEL and immunohistochemistry staining, real-time PCR, fluorogenic activity assays and Western blot analyses. The isolated chondrocytes were also analyzed by flow cytometry.', 'Unilateral anterior crossbite stimulation led to temporomandibular joint cartilage degradation, associated with an increase in TUNEL-positive chondrocytes number, caspase-9 expression levels, and the release of cytochrome c from mitochondria at 2 weeks without changes in TNF and caspase-8 levels until after 4 weeks. TNF stimulated apoptosis of the isolated chondrocytes and up-regulated caspase-8 expression, but did not change caspase-9 expression levels. Local injection of TNF inhibitor down-regulated caspase-8 expression and reduced TUNEL-positive cell number, but did not reverse cartilage thickness reduction, caspase-9 up-regulation or cytochrome c release.
answer:
Does tNF accelerate Death of Mandibular Condyle Chondrocytes in Rats with Biomechanical Stimulation-Induced Temporomandibular Joint Disease?