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.

Ex Input:
Context: Intermittent hypoxia (IH)-induced activation of pro-inflammatory pathways is a major contributing factor to the cardiovascular pathophysiology associated with obstructive sleep apnea (OSA). Obesity is commonly associated with OSA although it remains unknown whether adipose tissue is a major source of inflammatory mediators in response to IH. The aim of this study was to test the hypothesis that IH leads to augmented inflammatory responses in human adipocytes when compared to cells of non-adipocyte lineages.', 'Human primary subcutaneous and visceral adipocytes, human primary microvascular pulmonary endothelial cells (HUMEC-L) and human primary small airway epithelial cells (SAEC) were exposed to 0, 6 or 12 cycles of IH or stimulated with tumor necrosis factor (TNF)-. IH led to a robust increase in NF-B DNA-binding activity in adipocytes compared with normoxic controls regardless of whether the source of adipocytes was visceral or subcutaneous. Notably, the NF-B response of adipocytes to both IH and TNF- was significantly greater than that in HUMEC-L and SAEC. Western blotting confirmed enhanced nuclear translocation of p65 in adipocytes in response to IH, accompanied by phosphorylation of I-B. Parallel to p65 activation, we observed a significant increase in secretion of the adipokines interleukin (IL)-8, IL-6 and TNF- with IH in adipocytes accompanied by significant upregulation of mRNA expression. PCR-array suggested profound influence of IH on pro-inflammatory gene expression in adipocytes.\Question: Are human adipocytes highly sensitive to intermittent hypoxia induced NF-kappaB activity and subsequent inflammatory gene expression?

Ex Output:
Human adipocytes demonstrate strong sensitivity to inflammatory gene expression in response to acute IH and hence, adipose tissue may be a key source of inflammatory mediators in OSA.

Ex Input:
Context: To determine the role of recipient lymphopenia state in the expansion and function of leukemia specific cytotoxic T lymphocytes (CTLs).', 'C57BL/6 mice were induced to lymphopenia with 6 Gy total body irradiation. Spleen T cells or leukemia specific T cells from EGFP+ transgenic C57BL/6-EGFP mice were adoptively transferred by intravenous injection. The mice were challenged subcutaneously with 1 x 10(6) FBL3 leukemic cells at day 2 after irradiation. The peripheral WBC count, percentage of EGFP+ cells, subsets of T cells and tumor sizes were monitored.', 'Both of the spleen T cell and leukemia specific CTL proliferated efficiently with the percentage of EGFP+ cells of 28. 81% and 42.24%, respectively, after infused into lymphopenic recipients. However, spleen T cells had no anti-leukemia effect regardless of its expansion. In contrast, leukemia specific CTLs showed a more rapid and extensive expansion under the condition of lymphopenia and a enhanced anti-leukemia immunity.\Question: Does [ Recipient lymphopenia state enhance the expansion and anti-leukemia effect of leukemia specific cytotoxic T lymphocytes ]?

Ex Output:
Transfusion of leukemia specific CTLs under lymphopenia state could be a feasible strategy to expand leukemia specific CTLs and generate favorable anti-leukemia effect in vivo.

Ex Input:
Context: P53 is a key protein which controls cell cycle arrest and apoptosis in response to DNA damage. Auto-antibodies against p53 have been detected in some cancer patients and also in patients with autoimmune diseases. In these patients, the main cause of anti-p53 antibody occurrence was considered to be increased intracellular p53 protein in cancer cells and autoreactive lymphocytes, respectively. Intracellular p53 also increases with cardiomyocyte apoptosis during heart failure and autoreactive lymphocytes play a role in the course of idiopathic dilated cardiomyopathy (IDC) and ischemic cardiomyopathy (ICM). Based on these observations, we hypothesized that anti-p53 antibody response may also occur in patients with heart failure due to ICM and IDC.', 'The aim of this study was to evaluate anti-p53 antibodies in the serum of patients with heart failure due to IDC and ICM.', '70 eligible patients with heart failure and severe left ventricular systolic dysfunction (mean fractional shortening 12.03 +/- 3.93%) were included in the study. The aetiology of heart failure was IDC in 26 patients and ICM in 44 patients, according to the angiographic and echocardiographic findings.', 'Anti-p53 antibodies were not detected in any of the patients.\Question: Do serum anti-p53 antibodies occur in patients with heart failure due to idiopathic dilated and ischemic cardiomyopathies?

Ex Output:
Anti-p53 antibodies do not occur in patients with heart failure due to IDC and ICM, possible explanations are discussed in the text.