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.
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Question: The tumor susceptibility gene 101 (TSG101) was originally identified as a tumor-suppressor gene that mediates many molecular and biological processes, such as ubiquitination, endosomal trafficking, cell survival, and virus budding, but its role in hepatocellular carcinoma (HCC) is currently unknown.', 'We assessed the expression of TSG101 in HCC and paracancerous tissues using qPCR. Then, we used the TSG101-specific siRNA mix to disrupt the expression of TSG101 to investigate the subsequent effect on human hepatoma-7 (Huh7) cells. Western blot was used to detect the protein expression of TSG101 and other molecules. Cell growth assay was performed using CCK8. Transwell assay was used to investigate the migration and invasion ability of Huh7 cells after transfection with of TSG101 siRNA. Flow cytometry was used to estimate the effect of TSG101 knockdown on cell cycle and apoptosis. Confocal laser scanning microscopy was used to observe the actin filaments change and the formation of autophagy.', 'TSG101 was over-expressed in HCC tissues. TSG101 silence was able to suppress Huh7 cell proliferation, migration, and invasion. Furthermore, silencing of TSG101 could induce cell cycle arrest at G1 phase and inhibit the expression of cyclin A and cyclin D, while up-regulating the expression of CDK2. The mechanism might be induction of autophagic cell death and inactivation of Akt and ERK1/2.

Answer: Does tSG101 Silencing suppress Hepatocellular Carcinoma Cell Growth by Inducing Cell Cycle Arrest and Autophagic Cell Death?


Question: Obese persons have low circulating natriuretic peptide (NP) concentrations. It has been proposed that this 'natriuretic handicap' could play a role in obesity-related hypertension. The normal physiological response of the NP system to an increase in blood pressure (BP) is an increase in NP secretion with concomitant higher circulating NP concentrations. In this study, we investigated whether higher BP would also be related to higher circulating NP concentrations in obese men; furthermore, we verified that BP had affected the hearts of our study participants, by determining left ventricular mass (LVM).", 'We examined 103 obese healthy medication-free men. We measured 24-hour ambulatory BP (ABP). LVM was calculated using the Cornell voltage-duration product method. Fasting serum concentrations of midregional proatrial NP (MR-proANP), a surrogate for active ANP, were measured. Linear regression analysis was used to calculate age-adjusted standardised regression coefficients (β).', 'LVM and BP increased across systolic ABP quartiles (mean LVM±SD: 1599.1±387.2\u2005mm\u2005ms in first vs 2188.5±551.3\u2005mm\u2005ms in fourth quartile, p<0.001; mean systolic ABP±SD: 114.5±4.2\u2005mm\u2005Hg in first vs 149.0±7.7\u2005mm\u2005Hg in fourth quartile, p<0.001). Systolic ABP was robustly associated with LVM (ß=0.48, p<0.001). Despite evidence of BP-related increases in LVM, serum MR-proANP was negatively associated with systolic ABP (ß=-0.32, p=0.004) and with diastolic ABP (ß=-0.45, p<0.001).

Answer: Does serum proatrial natriuretic peptide increase with higher systolic blood pressure in obese men?


Question: To examine whether connective tissue growth factor(CTGF) induces the production of fractalkine(FLK) by glomerular mesangial cells of rats, and explore the mechanism of signal pathway of CTGF actions.', 'The mRNA expression of FLK was analyzed by RT-PCR in cultured mesangial cells stimulated by CTGF. The protein of FLK in the supernatants of cells was determined by ELISA. The chemotactic effect of the supernatants on monocytes was assessed by the in vitro chemotaxis assay. The phosphorylation of p42/44 MAPK was assessed by Western blot.', 'Treatment of the cells with CTGF enhanced the mRNA expression of FLK and concentration of FLK in the supernatants. Pretreatment of the supernatants of CTGF-treated cells with anti-FLK antibodies partially inhibited the chemotactic effect of the supernatants on monocytes. CTGF increased the p42/44MAPK phosphorylation. Pretreatment of the cells with PD98059 or UO126, inhibitors of phosphorylated p42/44 MAKP, decreased the CTGF-induced expression of phosphorylated p42/44 MAPK and concentration of FLK in supernatants.

Answer:
Does [ p42/44 MAPK mediate synthesis of fractalkine by mesangial cells stimulated by connective tissue growth factor ]?