TASK DEFINITION: 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.
PROBLEM: 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.

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

PROBLEM: Obesity and its related co-morbidities such as non-alcoholic fatty liver disease (NAFLD) are increasing dramatically worldwide. The genetic variation in Patatin-like phospholipase domain-containing protein 3 (PNPLA3), which is also called adiponutrin (ADPN), in residue 148 (I148M, rs738409) has been associated with NAFLD. However, the regulation and function of PNPLA3 in metabolic diseases remains unclear. Laparoscopic gastric banding (LAGB) of severely obese patients reduces body weight, liver and adipose tissue inflammation. In this study, we investigated whether weight loss induced by LAGB affected PNPLA3 expression in hepatic and adipose tissue.', 'Liver and subcutaneous adipose tissue samples were collected from 28 severely obese patients before and 6\xa0months after LAGB. PNPLA3 expression was assessed by quantitative real-time PCR. To understand whether inflammatory stimuli regulated PNPLA3 expression, we studied the effect of tumour necrosis factor alpha (TNFα) and lipopolysaccharide (LPS) on PNPLA3 expression in human adipocytes and hepatocytes.', 'PNPLA3 was strongly expressed in the liver and clearly detectable in subcutaneous adipose tissue of obese patients. Weight loss induced by LAGB of severely obese patients led to significantly increased adipose, but not hepatic, tissue expression of PNPLA3. Subcutaneous PNPLA3 expression negatively correlated with body-mass-index, fasting glucose and fasting insulin. TNFα potently suppressed PNPLA3 expression in adipocytes but not hepatocytes.

SOLUTION: Does weight loss induced by bariatric surgery restore adipose tissue PNPLA3 expression?

PROBLEM: Thallium-201 (201Tl) myocardial perfusion imaging has been widely used for evaluation of myocardial ischemia/viability after myocardial infarction. The 3- to 4-h early redistribution imaging has underestimated a considerable part of viable myocardium, while the 24-h late redistribution imaging may enhance the detection of myocardial ischemia/viability, but remains controversial.', 'Thirty-eighty patients with myocardial infarction underwent the initial, 3-h, and 24-h redistribution imaging after intravenous injection of 148-185 MBq 201Tl. Image quality analysis was performed using a four-grade model: excellent, good, moderate, and poor. The initial and 3-h images, the initial and 24-h images, and the 3- and 24-h images were compared double-blinded.', 'The 3- and 24-h images showed no significant differences in image quality according to the four-grade model (P=.3580). Out of the 194 abnormal segments based on the initial imaging, 60 (31%) segments improved by at least one grade on the 3-h imaging, while 86 (44%) segments improved by at least one grade on the 24-h imaging. The 24-h late imaging detected more viable myocardium than the 3-h imaging did, with a significant difference (chi2=7.4235, P=.0064). There were 164 abnormal segments on the 3-h imaging, with an average 30% (48) segments improved by at least one grade on the 24-h imaging. There were 134 initial abnormal segments without any improvement on the 3-h imaging. Out of these segments, the 24-h late redistribution imaging detected additional redistribution in 30 segments, taking up 22%. The mean global score on the 3-h imaging significantly decreased compared to that on the initial imaging (t=5.71, P<.0001), and the mean global score on the 24-h imaging further decreased significantly compared to that on the 3-h imaging (t=6.28, P<.0001).

SOLUTION:
Does twenty-four-hour thallium-201 late redistribution imaging enhance the detection of myocardial viability after myocardial infarction?