Given a passage with a context and an answer, 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.

[EX Q]: Context: The interaction between Siglec-10 and its ligand, CD24, selectively represses tissue damage-caused immune responses. However, the nature of Siglec-10 and CD24 in human hepatocellular carcinoma (HCC) is still poorly defined. Hereon, the expression, function, and regulation of CD24 and Siglec-10 in HCC were investigated in the present study.', 'Flow cytometry was performed to examine the expression of Siglec-10 in HCC tissues and adjacent non-tumor tissues of HCC patients. To further determine whether Siglec-10 expression is associated with the clinical characteristics and survival, conventional immunohistochemistry was performed in 96 HCC patients. Additionally, the role of Siglec-10 in the regulation of natural killer (NK) cell dysfunction was evaluated. Finally, CD24 expression in HCC was also assessed.', 'Siglec-10 was expressed most on NK cells in HCC (40.7 4.5%). Compared with surrounding non-tumor tissues, tumor tissues had higher Siglec-10 expression (31.0 1.7% versus 40.7 4.5%, n = 10, P < 0.05), and the expression was negatively associated with patient survival. Siglec-10(+)CD56(+) NK cells exhibited reduced effector function, as shown by decreased granules and cytokine expressions compared with Siglec-10(-)CD56(+) NK cells. Moreover, the number of CD24(+)CD45(-) cells in HCC tissues was higher than that in adjacent non-tumor tissues (9.4 0.9% versus 3.1 0.9%, n = 15, P < 0.05).
Answer: These findings suggest that Siglec-10 is associated with decreased survival and impaired NK cell function in human HCC. This process may function via the CD24-Siglec-10 interaction, which may represent a therapeutic target in HCC patients.
[EX A]: Is siglec-10 associated with survival and natural killer cell dysfunction in hepatocellular carcinoma?

[EX Q]: Context: Cilostazol, a potent type 3 phosphodiesterase inhibitor, is found to reduce neointimal formation by inhibiting vascular smooth muscle cell (VSMC) proliferation. The aim of this study is to investigate whether the inhibitory effect of cilostazol on VSMC proliferation is operated via heme oxygenase-1 (HO-1).', 'In rat carotid arteries, cilostazol up-regulated HO-1 in the neointima of balloon-injured arteries. Treatment of human VSMCs with cilostazol enhanced the expression of HO-1, which was mainly regulated at the transcriptional level. Small interfering RNA knock-down of HO-1 attenuated the inhibitory effect of cilostazol on VSMC proliferation, suggesting the critical role of HO-1 in cilostazol effect. The transcriptional responsiveness of HO-1 to cilostazol was inversely correlated with the length of GT-repeat in human HO-1 promoter. Deletion and mutational analysis of HO-1 promoter along with chromatin immunoprecipitation showed that cyclic AMP response element (CRE)-binding protein (CREB) participated in cilostazol-induced HO-1 transcription. Furthermore, cilostazol triggered a linkage between the CRE and GT-repeat regions in the HO-1 promoter. The promoting effect of cilostazol on HO-1 expression, proliferation inhibition, and chromatin conformation in the HO-1 promoter was greater in VSMCs from subjects with shorter GT-repeat alleles than those with longer alleles.
Answer: Cilostazol inhibits VSMC proliferation involving an association between CREB and HO-1. The length polymorphism of GT-repeat in human HO-1 promoter determines the effect of cilostazol.
[EX A]: Does gT-repeat length polymorphism in heme oxygenase-1 promoter determine the effect of cilostazol on vascular smooth muscle cells?

[EX Q]: Context: Factors that influence energy metabolism and substrate oxidation, such as thyroid hormones (THs), may be important regulators of body weight.', 'We investigated associations of THs cross-sectionally with obesity, energy expenditure, and substrate oxidation and prospectively with weight change.', 'Euthyroid, nondiabetic, healthy, adult Pima Indians (n = 89; 47 M, 42 F) were studied. Percentage body fat (%BF) was measured by using dual-energy X-ray absorptiometry; sleeping metabolic rate (SMR), respiratory quotient, and substrate oxidation rates were measured in a respiratory chamber. Thyroid-stimulating hormone (TSH), free thyroxine (T(4)), free triiodothyronine (T(3)), and leptin concentrations were measured in fasting plasma samples.', 'TSH, but neither free T(3) nor free T(4), was associated with %BF and leptin concentrations (r = 0.27 and 0.29, respectively; both: P <or= 0.01). In multiple regression analyses adjusted for age, sex, fat mass, and fat-free mass, free T(3) was a positive predictor of SMR (P = 0.02). After adjustment for age, sex, %BF, and energy balance, free T(3) was a negative predictor of 24-h respiratory quotient (P < 0.05) and a positive predictor of 24-h lipid oxidation rate (P = 0.006). Prospectively, after an average follow-up of 4 +/- 2 y, the mean increase in weight was 3 +/- 9 kg. Baseline T(3) concentrations were associated with absolute and annual percentage of changes in weight (r = -0.27, P = 0.02, and r = -0.28, P = 0.009, for the age- and sex-adjusted associations, respectively).
Answer: In euthyroid Pima Indians, lower free T(3) but not free T(4) concentrations were an independent predictor of SMR and lipid oxidation and a predictor of weight gain. This finding indicates that control of T(4)-to-T(3) conversion may play a role in body weight regulation.
[EX A]:
Do plasma concentrations of free triiodothyronine predict weight change in euthyroid persons?