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.

Input: Consider Input: The proteasome is a major cellular proteinase. Its activity is modulated by cellular oxidants. Hepatitis C core protein and ethanol exposure both cause enhanced oxidant generation. The aim was to investigate whether core protein, by its ability to generate oxidants, alters proteasome activity and whether these alterations are further affected by ethanol exposure.', 'These interactions were examined in Huh-7 cell lines that expressed inducible HCV core protein and/or constitutive cytochrome P450 2E1 (CYP2E1) and as purified components in a cell-free system. Chymotrypsin-like proteasome activity was measured fluorometrically.', 'Proteasome activity in core-positive 191-20 cells was 20% higher than that in core-negative cells and was enhanced 3-fold in CYP2E1-expressing L14 cells. Exposure of core-positive cells to glutathione ethyl ester, catalase, or the CYP2E1 inhibitor diallyl sulfide partially reversed the elevation of proteasome activity in core-positive cells, whereas ethanol exposure suppressed proteasome activity. The results indicate that proteasome activity was up-regulated by low levels of core-induced oxidative stress but down-regulated by high levels of ethanol-elicited stress. These findings were partially mimicked in a cell-free system. Addition of core protein enhanced the peptidase activity of purified 20S proteasome containing the proteasome activator PA28 and was further potentiated by addition of liver mitochondrial and/or microsome fractions. However, proteasome activation was significantly attenuated when fractions were obtained from ethanol-fed animals.

Output: Is proteasome activation by hepatitis C core protein reversed by ethanol-induced oxidative stress?


Input: Consider Input: The C57BL/6J-Min/+ (Min/+) mouse bears a germline mutation in Apc and is therefore a model for familial adenomatous polyposis and sporadic colorectal cancer. Min/+ intestinal mucosa exhibits a marked tendency for spontaneous adenoma formation. Curcumin is a phenolic antioxidant known for its antitumor and immune modulatory functions in vitro. Curcumin prevents adenoma formation in Min/+ mice, through a mechanism that may be related to its immunomodulatory properties.', 'To study the relationship between intestinal immunity and curcumin-induced antitumor response, we used immunohistochemistry to characterize the effect of curcumin treatment on resident intestinal immune effector cells in Min/+ mice.

Output: Is inhibition of intestinal tumors by curcumin associated with changes in the intestinal immune cell profile?


Input: Consider Input: To investigate if diabetic patients without diabetic retinopathy despite long disease duration have different human leukocyte antigen (HLA) status vs those with an early onset of retinopathy.', 'Retrospective, nonrandomized, masked comparative study. Type 1 diabetic patients with a disease onset before age 30 were recruited to the study. The study population consisted of two groups of diabetic patients: those with normal retinopathy course (retinopathy developed during the first 20 years of diabetes onset) (23 patients) and those with postponed retinopathy (no obvious retinopathy in spite of passing 20 years of diabetes) (19 patients). These groups were matched with regard to level of glycemic control, blood pressure, and lipid profile. A group of 23 healthy patients served as controls. HLA-DQB1 typing of blood samples was done using a polymerase chain reaction with sequence-specific primer (PCR-SSP) method.', 'HLA-DQB1*0201/HLA-DQB1*0501 and HLA-DQB1*0201/HLA-DQB1*0504 haplotypes were more common among type 1 diabetic patients with normal retinopathy course than those with postponed retinopathy (26.1% vs 0.0%; p=0.019). HLA-DQB1*0301 and HLA-DQB1*0304 were less common among those diabetic patients with normal retinopathy course than those with a postponed retinopathy (63.2% vs 34.8%; p=0.067).


Output: Do hLA-DQB1 subtypes predict diabetic retinopathy in patients with type I diabetes mellitus?