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: Our aim was to investigate if: (a) authors of Biochemia Medica meet authorship criteria given by International Committee of Medical Journal Editors (ICMJE), (b) authorship violations are more frequent in submissions containing some type of scientific misconduct.', 'Self-reported authorship contributions regarding the three ICMJE criteria were analysed for all submissions to Biochemia Medica (February 2013-April 2015) which were forwarded to peer-review. To test the differences in frequencies we used Chi-squared test. P<0.05 was considered statistically significant.', '186 manuscripts were authored by 804 authors. All ICMJE criteria were met by 487/804 (61%) authors. The first and the last author met all the criteria more frequently than those authors in between (P<0.001). The degree to which ICMJE criteria was met for the first author did not differ between manuscripts authored by only one author and those authored by >1 author (P=0.859). In 9% of the manuscripts ICMJE criteria were not met by a single author. Authors of the 171/186 manuscripts declared that all persons qualify for authorship but only 49% of them satisfied all ICMJE criteria. Authors have failed to acknowledge contributors in 88/186 (47%) manuscripts; instead these contributors have been listed as authors without fulfilling ICMJE criteria. Authorship violation was not more common in 42 manuscripts with some type of scientific misconduct (P=0.135).
Example Output: Are iCMJE authorship criteria met in a substantial proportion of manuscripts submitted to Biochemia Medica?

Example Input: To clarify the effect of human umbilical cord-derived mesenchymal stem cell (hUC-MSCs) treatment on colitis and to explore the role of CD5(+) B cells in MSC therapy.', 'The trinitrobenzenesulfonic acid (TNBS)-induced colitis mouse model was used. HUC-MSCs were transferred peritoneally. Survival rates, colitis symptoms, and macroscopic and histologic scores were evaluated. CD4(+) T helper (Th) cell subgroups and CD5(+) regulatory B cell (Bregs) in lymphocytes were quantitated by flow cytometry. Cytokine levels were detected by ELISA and Bio-plex. CD5(+) B cells were isolated for in vitro co-culture and adaptive transfer.', 'HUC-MSC treatment alleviated TNBS-induced colitis by increasing survival rates, relieving symptoms, and improving macroscopic and histologic scores. Labeled hUC-MSCs were located in the inflamed areas of colitis mice. Increases in regulatory T cells (Tregs) and CD5(+) B cells and decreases in Th1 cells, Th17 cells, and several pro-inflammatory cytokines were observed with hUC-MSC treatment. After adaptive transfer, CD5(+) B cells, which were located mainly in the peritoneal lavage fluid, improved TNBS-induced colitis by correcting Treg/Th1/Th17 imbalances. CD5(+) B cells also inhibited T-cell proliferation and produced interleukin (IL)-10.
Example Output: Do human umbilical cord-derived mesenchymal stem cells protect against experimental colitis via CD5 ( + ) B regulatory cells?

Example Input: The progression of pathological left ventricular remodelling leads to cardiac dysfunction and contributes to the occurrence of malignant arrhythmias and sudden cardiac death. The underlying molecular mechanisms remain unclear, however. Our aim was to examine the role of the renin-angiotensin system (RAS) in the mechanism underlying arrhythmogenic cardiac remodelling using a transgenic mouse expressing a cardiac-specific dominant-negative form of neuron-restrictive silencer factor (dnNRSF-Tg). This mouse model exhibits progressive cardiac dysfunction leading to lethal arrhythmias.', 'Subcutaneous administration of aliskiren, a direct renin inhibitor, significantly suppressed the progression of pathological cardiac remodelling and improved survival among dnNRSF-Tg mice while reducing arrhythmogenicity. Genetic deletion of the angiotensin type 1a receptor (AT1aR) similarly suppressed cardiac remodelling and sudden death. In optical mapping analyses, spontaneous ventricular tachycardia (VT) and fibrillation (VF) initiated by breakthrough-type excitations originating from focal activation sites and maintained by functional re-entry were observed in dnNRSF-Tg hearts. Under constant pacing, dnNRSF-Tg hearts exhibited markedly slowed conduction velocity, which likely contributes to the arrhythmogenic substrate. Aliskiren treatment increased conduction velocity and reduced the incidence of sustained VT. These effects were associated with suppression of cardiac fibrosis and restoration of connexin 43 expression in dnNRSF-Tg ventricles.
Example Output:
Does the renin-angiotensin system promote arrhythmogenic substrates and lethal arrhythmias in mice with non-ischaemic cardiomyopathy?