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.

Input: Consider Input: 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?

Output: 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.


Input: Consider Input: Context: Human breast tumors are heterogeneous and consist of phenotypically diverse cells. Breast cancer cells with a CD44+/CD24- phenotype have been suggested to have tumor-initiating properties with stem cell-like and invasive features, although it is unclear whether their presence within a tumor has clinical implications. There is also a large heterogeneity between tumors, illustrated by reproducible stratification into various subtypes based on gene expression profiles or histopathological features. We have explored the prevalence of cells with different CD44/CD24 phenotypes within breast cancer subtypes.', 'Double-staining immunohistochemistry was used to quantify CD44 and CD24 expression in 240 human breast tumors for which information on other tumor markers and clinical characteristics was available. Gene expression data were also accessible for a cohort of the material.', 'A considerable heterogeneity in CD44 and CD24 expression was seen both between and within tumors. A complete lack of both proteins was evident in 35% of the tumors, while 13% contained cells of more than one of the CD44+/CD24-, CD44-/CD24+ and CD44+/CD24+ phenotypes. CD44+/CD24- cells were detected in 31% of the tumors, ranging in proportion from only a few to close to 100% of tumor cells. The CD44+/CD24- phenotype was most common in the basal-like subgroup--characterized as negative for the estrogen and progesterone receptors as well as for HER2, and as positive for cytokeratin 5/14 and/or epidermal growth factor receptor, and particularly common in BRCA1 hereditary tumors, of which 94% contained CD44+/CD24- cells. The CD44+/CD24- phenotype was surprisingly scarce in HER2+ tumors, which had a predominantly CD24+ status. A CD44+/CD24- gene expression signature was generated, which included CD44 and alpha6-integrin (CD49f) among the top-ranked overexpressed genes.\Question: Does the CD44+/CD24- phenotype is enriched in basal-like breast tumors?

Output: We demonstrate an association between basal-like and particularly BRCA1 hereditary breast cancer and the presence of CD44+/CD24- cells. Not all basal-like tumors and very few HER2+ tumors, however, contain CD44+/CD24- cells, emphasizing that a putative tumorigenic ability may not be confined to cells of this phenotype and that other breast cancer stem cell markers remain to be identified.


Input: Consider Input: Context: Despite advances in the understanding of diabetic retinopathy, the nature and time course of molecular changes in the retina with diabetes are incompletely described. This study characterized the functional and molecular phenotype of the retina with increasing durations of diabetes.', 'Using the streptozotocin-induced rat model of diabetes, levels of retinal permeability, caspase activity, and gene expression were examined after 1 and 3 months of diabetes. Gene expression changes were identified by whole genome microarray and confirmed by qPCR in the same set of animals as used in the microarray analyses and subsequently validated in independent sets of animals. Increased levels of vascular permeability and caspase-3 activity were observed at 3 months of diabetes, but not 1 month. Significantly more and larger magnitude gene expression changes were observed after 3 months than after 1 month of diabetes. Quantitative PCR validation of selected genes related to inflammation, microvasculature and neuronal function confirmed gene expression changes in multiple independent sets of animals.\Question: Does whole genome assessment of the retinal response to diabetes reveal a progressive neurovascular inflammatory response?


Output: These changes in permeability, apoptosis, and gene expression provide further evidence of progressive retinal malfunction with increasing duration of diabetes. The specific gene expression changes confirmed in multiple sets of animals indicate that pro-inflammatory, anti-vascular barrier, and neurodegenerative changes occur in tandem with functional increases in apoptosis and vascular permeability. These responses are shared with the clinically documented inflammatory response in diabetic retinopathy suggesting that this model may be used to test anti-inflammatory therapeutics.