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.

Ex Input:
While the incidence of inflammatory bowel disease (IBD) among African-Americans (AAs) is increasing, there is limited understanding of phenotypic differences and outcomes by race.', 'To describe disease characteristics of AA patients compared to Caucasian (Ca) patients in a tertiary care population.', "We performed a cross-sectional review of the IBD registry at the University of Chicago from January 2008 to January 2013. Data regarding race, phenotype, disease onset, disease duration, medical therapy, and surgical treatment were abstracted from the database, then compared via Pearson's chi-square analysis, Kruskal-Wallis analysis, and logistic regression with a significance level of p < 0.05.", "A total of 1,235 patients with Crohn's disease (CD) and 541 patients with ulcerative colitis (UC) included 108 AA CD patients and 28 AA UC patients. AA CD patients had an increased rate of IBD-related arthralgias (36.5 vs. 23.9 %, p < 0.01) and surgery (p < 0.01), less ileal involvement (57.8 vs. 71.0 %, p < 0.01), and no differences for other extraintestinal manifestations or disease locations compared to Ca CD patients. AA UC patients were older at diagnosis, had an increased rate of arthralgias (28.6 vs. 14.6 %, p = 0.047) and ankylosing spondylitis/sacroiliitis (7.1 vs. 1.6 %, p = 0.035), with no differences for disease extent or rate of IBD-related surgeries compared to Ca UC patients. There were no differences in medication usage by race for CD and UC patients.

Ex Output:
Does clinical presentation and disease course of inflammatory bowel disease differ by race in a large tertiary care hospital?


Ex Input:
Anal intraepithelial neoplasia precedes the development of anal squamous cell carcinoma. Detection of the lesion is essential to management. This paper describes a prospective study to detect and ablate anal squamous intraepithelial lesions (SILs) using white light narrow band imaging (NBI) and NBI with acetic acid (NBIA).', 'Sixty patients with abnormal anal cytology and risk factors for anal dysplasia underwent examination of the anoderm with a high definition gastroscope and NBIA. Targeted biopsies were taken and the lesions were ablated and characterized histopathologically. Visualization of the anal transitional zone was facilitated by retroflexion and examination through a disposable anoscope.', 'Targeted biopsies were taken from lesions in 58 patients. No lesion was seen in two patients. Histopathology showed SIL in 48 (80.0%) of 60 biopsies. One biopsy showed lymphoid aggregates. Biopsies in nine (15%) of the 60 patients showed normal mucosa. Lesions were seen in white light in 27 (45%) of the 60 cases, NBI in 39 (65%) and NBIA in 57 (95%). There was no major morbidity. Sensitivity analysis showed that all methods were significantly different from each other.

Ex Output:
Is detection of anal dysplasia enhanced by narrow band imaging and acetic acid?


Ex Input:
Sequential events of endometrial tumorigenesis can be studied by comparison of genetic lesions seen in normal, premalignant, and malignant tissues. The distribution of k-ras mutations in microsatellite stable and unstable premalignant lesions was studied to determine whether this gene is implicated in both tumorigenic pathways.', 'K-ras mutations were analysed by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and direct sequencing in matched endometrial normal, premalignant (atypical hyperplasias), and adenocarcinoma tissues from individual patients. Identification of precancers solely by their appearance as atypical endometrial hyperplasias is very subjective; therefore, in addition to histopathological assessment, we performed molecular testing (non-random X inactivation or clonal altered microsatellites) for an expected feature of precancers--that is, monoclonality.', 'Equivalent K-ras mutation frequencies were seen in microsatellite stable (six of 33) and unstable (three of 23) cancers. In both types, K-ras mutation in monoclonal precancers usually corresponded to a change from normal to an equivocal (two of 12) or hyperplastic (10 of 12) histology. Divergent K-ras genotypes among multiple neoplastic tissues of individual patients (two of six patients) are exceptions explained either by multicentric premalignant disease, or acquisition of K-ras mutation late in neoplastic progression.

Ex Output:

Do k-ras mutations appear in the premalignant phase of both microsatellite stable and unstable endometrial carcinogenesis?