Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Example Input: Cadherins are calcium-dependent cell-to-cell adhesion glycoproteins playing a critical role in the formation and maintenance of normal tissue architecture. In normal mammary gland, E-cadherin is expressed by luminal epithelial cells, while P-cadherin is restricted to myoepithelial cells. Changes in the expression of classical E- and P-cadherins have been observed in mammary lesions and related to mammary carcinogenesis. P-cadherin and E-cadherin expressions were studied in a series of feline normal mammary glands, hyperplastic/dysplastic lesions, benign and malignant tumours by immunohistochemistry and double-label immunofluorescence.', 'In normal tissue and in the majority of hyperplastic/dysplastic lesions and benign tumours, P-cadherin was restricted to myoepithelial cells, while 80% of the malignant tumours expressed P-cadherin in luminal epithelial cells. P-cadherin expression was significantly related to high histological grade of carcinomas (p <0.0001), tumour necrosis (p = 0.001), infiltrative growth (p = 0.0051), and presence of neoplastic emboli (p = 0.0401). Moreover, P-cadherin positive carcinomas had an eightfold likelihood of developing neoplastic emboli than negative tumours. Cadherins expression profile in high grade and in infiltrative tumours was similar, the majority expressing P-cadherin, regardless of E-cadherin expression status. The two cadherins were found to be co-expressed in carcinomas with aberrant P-cadherin expression and preserved E-cadherin.
Example Output: Is aberrant P-cadherin expression associated to aggressive feline mammary carcinomas?

Example Input: Joint instability is believed to promote early osteoarthritic changes in the knee. Inflammatory reactions are associated with cartilage degradation in osteoarthritis (OA) but their possible synergistic or additive effects remain largely unexplored. The goal of the present study was to investigate the in\xa0vivo effects of Botulinum Toxin A (BTX-A) induced joint instability on intraarticular alterations in an otherwise intact rabbit knee joint model.', 'Ten 1-year-old female New Zealand White rabbits (average 5.7\xa0kg, range 4.8-6.6\xa0kg) were randomly assigned to receive three monthly unilateral intramuscular injections of BTX-A (experimental group), or no treatment (control group). After 90\xa0days, all knees were analyzed for specific mRNA levels using RT-qPCR. The synovium and cartilage tissue was assessed for histological alterations using the OARSI scoring system.', 'Cartilage and synovial histology showed significant higher OARSI scores in the BTX-A group animals compared to the untreated controls and contralateral limbs. There were no differences between the untreated control and the contralateral experimental limbs. Gene expression showed significant elevations for collagen I, collagen III, nitric oxide, TGF-β, IL-1 and IL-6 compared to the healthy controls.
Example Output: Does joint instability lead to long-term alterations to knee synovium and osteoarthritis in a rabbit model?

Example Input: To evaluate whether subjects with nonalcoholic hepatic steatosis (HS) differed in their circulating adiponectin levels compared with those in subjects without HS and, if so, to examine to what extent such differences are mediated by the adverse pattern of the metabolic syndrome variables, typically observed in these subjects.', 'In a cross-sectional study, we analysed 68 healthy, mildly obese individuals with a negative or negligible daily alcohol consumption.', 'HS (by ultrasonography), glucose tolerance status (by oral glucose load), insulin resistance [by homeostasis model assessment (HOMA)], and plasma adiponectin concentration [by enzyme-linked immunosorbent assay (ELISA)] were measured.', 'Subjects with nonalcoholic HS (n = 43) had markedly lower plasma adiponectin concentrations than those without HS (n = 25) (5.6 +/- 3 vs. 10.8 +/- 4 microg/ml; P < 0.001). In addition, the former had significantly higher values for body mass index (BMI), waist/hip ratio (WHR), HOMA-insulin resistance score, plasma insulin (at fasting and after glucose load), plasma triglyceride and liver enzyme concentrations [such as alanine aminotransferase (ALT) and gamma-glutamyltranspeptidase (GGT)], and tended to have lower high density lipoprotein (HDL) cholesterol concentration. The significant differences in plasma adiponectin levels that were observed between the groups were little affected by adjustment for potential confounding variables, such as age, sex, BMI, WHR, lipids and HOMA-insulin resistance score. Similarly, in multivariate regression analyses, hypoadiponectinaemia significantly predicted the presence of HS (P < 0.001) and the increased levels of GGT and ALT (P < 0.05), independently of potential confounders.
Example Output:
Are decreased plasma adiponectin concentrations closely associated with nonalcoholic hepatic steatosis in obese individuals?