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.

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)-α. IH led to a robust increase in NF-κB DNA-binding activity in adipocytes compared with normoxic controls regardless of whether the source of adipocytes was visceral or subcutaneous. Notably, the NF-κB response of adipocytes to both IH and TNF-α 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-κB. Parallel to p65 activation, we observed a significant increase in secretion of the adipokines interleukin (IL)-8, IL-6 and TNF-α 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?
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.

Context: Women with Turner syndrome (TS) have an increased prevalence of hearing loss, with conductive (CHL) and sensorineural (SNHL) components. The association between hearing loss and clinical parameters, particularly oestrogen and previous growth hormone (GH) treatment, was investigated.', 'A cross-sectional study of pure tone audiometry tests in an adult TS population. Previous ENT history, karyotype, anthropomorphic measurements and the impact of oestrogen and childhood GH therapy were assessed. One hundred and thirty-eight women (median age 29, range 16-67 years) completed the study.', 'Normal hearing was found in 20.3% of women, CHL in 18.8%, SNHL in 57.2% and confounding factors in 3.6%. Neither CHL nor SNHL were associated with oestrogen deficiency or GH treatment independent of age. CHL but not SNHL was more common in those with a history of recurrent otitis media (p < 0.01) and monosomy 45,X (p < 0.01).\Question: Are oestrogen deficiency and growth hormone treatment in childhood associated with hearing in adults with turner syndrome?
Current regimens of oestrogen and GH therapy have no impact on adult hearing loss in TS, independent of age. The prevalence of SNHL increases with age. CHL but not SNHL is associated with ENT history and karyotype. According to present evidence, the only possible intervention to reduce hearing loss in women with TS remains assiduous treatment of ENT problems in childhood.

Context: Hepatocyte nuclear factor 4α (HNF4α) is a liver enriched transcription factor and is indispensable for liver development. However, the role of HNF4α in hepatocellular carcinoma (HCC) progression remains to be elucidated. We report that reduced HNF4α expression correlated well with the aggressive clinicopathological characteristics of HCC and predicted poor prognosis of patients. HNF4α levels were even lower in metastatic HCCs, and ectopic HNF4α expression suppressed the metastasis of hepatoma cells both in vitro and in vivo. Forced HNF4α expression attenuated the expression and nuclear translocation of RelA (p65) and impaired NF-κB activation through an IKK-independent mechanism. Blockage of RelA robustly attenuated the suppressive effect of HNF4α on hepatoma cell metastasis. MicroRNA (miR)-7 and miR-124 were transcriptionally up-regulated by HNF4α, which repressed RelA expression by way of interaction with RelA-3' untranslated region (UTR). In addition, nuclear factor kappa B (NF-κB) up-regulated the expression of miR-21 in hepatoma cells, resulting in decreased HNF4α levels through down-regulating HNF4α-3'UTR activity.\Question: Does hepatocyte nuclear factor 4α-nuclear factor-κB feedback circuit modulate liver cancer progression?

Collectively, an HNF4α-NF-κB feedback circuit including miR-124, miR-7, and miR-21 was identified in HCC, and the combination of HNF4α and NF-κB exhibited more powerful predictive efficiency of patient prognosis. These findings broaden the knowledge of hepatic inflammation and cancer initiation/progression, and also provide novel prognostic biomarkers and therapeutic targets for HCC.