instruction:
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.
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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?
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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.


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Context: No previous study has examined the comorbidity of Irritable Bowel Syndrome (IBS) and Generalized Anxiety Disorder (GAD) in a general population using standardized diagnostic methods.', 'To examine the prevalence, comorbidity and risk correlates of IBS and GAD in a general population.', 'A random community-based telephone survey was conducted. The questionnaire covered symptoms of IBS, GAD, core depressive symptoms, help-seeking behaviour and functional impairment on the Sheehan Disability Scale.', 'A total of 2005 participants completed the interview. The current prevalence of IBS was 5.4% and the 12-month prevalence of GAD was 4%. GAD was five times more common among IBS respondents than non-IBS respondents (OR: 5.84, P < 0.001), whereas IBS was 4.7 times more common among GAD respondents than among non-GAD respondents (OR: 6.32, P < 0.001). Core depressive symptoms (OR: 6.25, P < 0.01) and education level (OR: 5.918, P = 0.021) were risk correlates of GAD among IBS respondents. Comorbid respondents were more impaired than respondents having either disorder alone, but were not more likely to seek professional help than IBS-only respondents.\Question: Is irritable bowel syndrome strongly associated with generalized anxiety disorder : a community study?
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Irritable Bowel Syndrome and GAD comorbidity was common and added to impairment in the community. The strong association between psychiatric morbidity and IBS observed in referral centres was not a consequence of increased help-seeking behaviour.


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Context: Lipopolysaccharide (LPS)-induced preconditioning protects neurons against traumatic spinal cord injury (TSCI) in rats. This study sought to test whether Nrf2, a transcription factor, mediated LPS-induced preconditioning.', 'The TSCI model was established using a standardized NYU impactor on adult female rats. Rats were pretreated with LPS (0.2mg/kg, IP; 72h before injury). Nrf2 was silenced by injecting a lentivirus encoding RNAi against Nrf2 into injured spinal cords. Neurologic function was assessed by Basso, Beattie and Bresnahan (BBB) scores 6h, 12h, 24h, 48h, 72h, 7d and 14d after TSCI. Neuronal apoptosis was measured by a TUNEL staining. Ultrastructure was observed using transmission electron microscope (TEM). The protein expression of HO-1, NQO1 and GCLC was examined using immunohistochemistry and immunoblotting.', 'The injection of a lentivirus effectively transfected GFP into injured spinal cords. The expression of Nrf2 was significantly decreased in spinal cords receiving a lentivirus encoding RNAi against Nrf2. BBB scores showed that TSCI markedly impaired nervous function, which was markedly preserved by LPS pretreatment. Nrf2 knockdown significantly suppressed LPS pretreatment-induced protection of nervous function. TEM images and TUNEL staining showed an increase in apoptotic cells when Nrf2 was silenced. Moreover, immunohistochemistry and immunoblotting analysis exhibited that LPS pretreatment significantly upregulated the expression of anti-oxidative proteins including HO-1, NQO1 and GCLC, which was suppressed when Nrf2 expression was silenced in injured spinal cords.\Question: Does lipopolysaccharide-induced preconditioning protect against traumatic spinal cord injury by upregulating Nrf2 expression in rats?
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LPS preconditioning effectively alleviates TSCI-induced impairment and preserves nervous function in a Nrf2-dependent manner.