Given a passage with a context and an answer, 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.

Input: Consider Input: Context: Within Australian hospitals, cardiac and respiratory arrests result in a resuscitation attempt unless the patient is documented as not for resuscitation.', 'To examine the consistency of policies and documentation for withholding in-hospital resuscitation across health services.', 'An observational, qualitative review of hospital policy and documentation was conducted in June 2013 in three public and two private sector hospitals in metropolitan Melbourne. Not for resuscitation (NFR) forms were evaluated for physical characteristics, content, authorisation and decision-making. Hospital policies were coded for alerts, definition of futility and burden of treatment and management of discussions and dissent.', 'There was a lack of standardisation, with each site using its own unique NFR form and accompanying site-specific policies. Differences were found in who could authorise the decision, what was included on the form, the role of patients and families, and how discussions were managed and dissent resolved. Futility and burden of treatment were not defined independently. These inconsistencies across sites contribute to a lack of clarity regarding the decision to withhold resuscitation, and have implications for staff employed across multiple hospitals.
Answer: NFR forms should be reviewed and standardised so as to be clear, uniform and consistent with the legislative framework. We propose a two-stage process of documentation. Stage 1 facilitates discussion of patient-specific goals of care and consideration of limitations of treatment. Stage 2 serves to communicate a NFR order. Decisions to withhold resuscitation are inherently complex but could be aided by separating the decision-making process from the communication of the decision, resulting in improved end-of-life care.

Output: Does comparison of not for resuscitation ( NFR ) form across five Victorian health services?

Input: Consider Input: Context: Intestinal fibrosis is mainly associated with Crohn's disease and is defined as a progressive and excessive deposition of extracellular matrix components. No specific antifibrotic therapies are available. In this study, we evaluate the antifibrotic effect of a novel 5-ASA analog able to activate the peroxisome proliferator-activated receptor , named GED-0507-34 Levo.", 'Colonic fibrosis was induced in 110 C57BL/6 mice by 3 cycles of 2.5% (wt/vol) dextran sulfate sodium administration for 6 weeks. The preventive effects of oral daily GED (30 mg kg(-1) d(-1)) administration were evaluated using a macroscopic and histological score and also through biological endpoints. Expression of main markers of myofibroblasts activation was determined in transforming growth factor (TGF-)-stimulated intestinal fibroblasts and epithelial cells.', 'GED improved macroscopic and microscopic intestinal lesions in dextran sulfate sodium-treated animals and reduced the profibrotic gene expression of Acta2, COL1a1, and Fn1 by 1.48-folds (P < 0.05), 1.93-folds (P < 0.005), and 1.03-fold (P < 0.05), respectively. It reduced protein levels of main markers of fibrosis (-SMA and Collagen I-II) and the main TGF-/Smad pathway components. GED also decreased the interleukin-13 and connective tissue growth factor expression by 1.89-folds (P < 0.05) and 2.2-folds (P < 0.005), respectively. GED inhibited TGF--induced activation of both fibroblast and intestinal epithelial cell lines, by regulating mRNA expression of -SMA and fibronectin, and restoring the TGF--induced loss of intestinal epithelial cell markers. GED treatment also reduced the TGF- and ACTA1 expression in primary human intestinal fibroblasts from ulcerative colitis patients.
Answer: GED ameliorates intestinal fibrosis in dextran sulfate sodium-induced chronic colitis in mice and regulates major profibrotic cellular and molecular mechanisms.

Output: Does novel PPAR Modulator GED-0507-34 Levo ameliorate Inflammation-driven Intestinal Fibrosis?

Input: Consider Input: Context: Two different forms of vulvar intraepithelial neoplasia (VIN) are recognised: (1) usual-type (bowenoid) VIN, which is related to high-risk papillomavirus infection, and (2) differentiated (simplex) VIN, which is associated with chronic inflammation. The aim of this study was to investigate the presence of chromosome 3q26 gains in the spectrum of precancerous lesions and invasive squamous cell carcinomas (SCCs) of the vulva.', '3q26 gains were analysed using fluorescence in situ hybridisation in a series of usual-type VINs, VINs of the differentiated type and invasive squamous cell carcinomas. In addition, all cases were examined for human papillomavirus (HPV) DNA, p53 mutations, and p16 and p53 protein expression.', 'Gains of chromosome 3q26 were present in all VINs of the differentiated type and in 50% of the usual-type VIN lesions. 81% of SCCs were positive for 3q26 gains irrespective of the HPV status and of the associated precursor lesion. HPV-associated lesions exhibited the typical, strong cytoplasmic p16 accumulation while mutated p53 was only detected in HPV-negative VINs or SCCs, and was associated with an overexpression of p53 protein.
Answer: Immunohistochemical evaluation of p16 and p53 expression aids in the differential diagnosis of squamous cell alterations of the vulva. However, detection of 3q26 imbalance is of additional diagnostic value in difficult cases of HPV-unrelated usual-type VINs and VINs of the differentiated type.
Output: Are gains of chromosome region 3q26 in intraepithelial neoplasia and invasive squamous cell carcinoma of the vulva frequent and independent of HPV status?