TASK DEFINITION: In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
PROBLEM: Context: Most hepatocellular carcinomas (HCCs) are associated with cirrhosis. Portal hypertension (PHT) and esophageal variceal bleeding (EVB) can limit the patient's treatment options. Surgical therapy in such patients is challenging. We performed devascularization plus liver resection or radiofrequency ablation (RFA) to treat HCC patients with concomitant EVB resulting from PHT secondary to cirrhosis. Such combined operations have never been reported for the management of HCC patients with variceal esophageal bleeding.", 'To evaluate two different treatment regimens for patients with HCC and EVB.', 'We evaluated 35 BCLC stage 0/A patients with HCC and EVB who underwent either devascularization plus liver resection (Group A) or devascularization plus RFA (Group B). We reviewed the safety and outcomes of the two groups and assessed risk factors for patient survival and tumor recurrence.', 'Significant factors for overall survival were surgical approach and Child-Pugh classification. Child-Pugh classification was the only independent risk factor for overall postoperative survival [hazard ratio (HR) 8.320, 95 % confidence interval (CI) 1.739-39.799, P = 0.008]. Age was the only independent risk factor for tumor recurrence (HR 4.025, 95 % CI 1.343-12.062, P = 0.013).\Question: Is radiofrequency ablation plus devascularization the preferred treatment of hepatocellular carcinoma with esophageal varices?

SOLUTION: RFA plus devascularization is the preferred treatment of HCC with EVB. RFA plus devascularization should be considered in Child-Pugh class A patients below 50 years of age.

PROBLEM: Context: In our initial attempt to identify differentiation markers for ocular surface epithelia, we observed a unique staining pattern by a commercial anti-Galphaq antibody. We further isolate and characterize the protein reactive with this anti-Galphaq antibody in human ocular surface epithelia.', 'Human donor corneoscleral buttons were sectioned and stained with a battery of commercial antibodies against Galpha proteins. Western blot analysis of cell lysates of corneal epithelial cells and HEK 293 cells transfected with Galphaq cDNA was used to determine the identity of the protein reactive with the anti-Galphaq antibody (E-17). Comparisons were made with another anti-Galphaq antibody (G4415) and an anti-cytokeratin 12C (J7) antibody. The isolated proteins reactive with E17 and J7 were then analyzed with two dimensional isoelectric focusing. Polypeptide sequences were identified using matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) after in-gel protein digestion.', 'The E-17 anti-Galphaq antibody preferentially stained the entire corneal epithelia and the suprabasal layers of the limbus with complete absence of staining in the basal limbus and conjunctiva. Western blot analysis of corneal epithelial cells showed that E-17 antibody identified a protein with a molecular weight of 55 kDa. However, the antibody did not react with the purported antigen, Galphaq protein (42 kDa) produced by Galphaq cDNA. Another anti-Galphaq antibody (G4415) did not react with the 55 kDa protein but did react with the 42 kDa Galphaq protein. Further comparison of the E-17 antibody with the J7 antibody revealed that both recognized the 55 kDa band in one and two dimensional analysis. MALDI-TOF MS analysis confirmed that the 55 kDa protein of interest was actually cytokeratin 12 (CK12), rather than Galphaq protein.\Question: Is cytokeratin 12 in human ocular surface epithelia the antigen reactive with a commercial anti-Galpha q antibody?

SOLUTION: The commercial E-17 anti-Galphaq antibody did not react with Galphaq protein, its purported antigen. Instead, it recognized a 55 kDa protein, which was characterized to be cytokeratin 12 by isoelectric focusing and peptide fingerprinting with mass spectrometry. Based on its reactivity with CK12, this commercial E-17 can be used as a differentiation marker to study ocular surface epithelia.

PROBLEM: Context: Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.', 'We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.\Question: Is altered gene expression in early atherosclerosis blocked by low level apolipoprotein E?

SOLUTION:
Atherosclerotic lesions in apoE(-/-) mice are detected as early as 4 weeks of age. Expression of low levels of apoE is shown to be both atheroprotective and to suppress these changes in key adhesion and inflammatory molecules observed in early atherosclerotic lesions.