TASK DEFINITION: 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.
PROBLEM: To examine the effect of TRIB3 on endoplasmic reticulum stress induced β-cell apoptosis and to investigate the mechanism with a specific emphasis on the role of NF-κB pathway.', 'We investigated the effect of TRIB3 on ER stress-induced β-cell apoptosis in INS-1 cells and primary rodent islets. The potential role of TRIB3 in ER stress inducer thapsigargin (Tg)-induced β-cell apoptosis was assessed using overexpression and siRNA knockdown approaches. Inducible TRIB3 β-cells, regulated by the tet-on system, were used for sub-renal capsule transplantation in streptozotocin (STZ)-diabetic mice, to study the effect of TRIB3 on ER stress-induced β-cell apoptosis in vivo. Apoptosis was determined by TUNEL staining both in vivo and in vitro, while the molecular mechanisms of NF-κB activation were investigated.', 'TRIB3 was induced in ER-stressed INS-1 cells and rodent islets, and its overexpression was accompanied by increased β-cell apoptosis. Specifically, TRIB3 overexpression enhanced Tg-induced INS-1 derived β-cell apoptosis both in vitro and in sub-renal capsular transplantation animal model. Additionally, knockdown of Trib3 blocked Tg-induced apoptosis. Mechanistically, the induction of TRIB3 during ER stress resulted in the activation of NF-κB and aggravated INS-1 derived β-cell apoptosis, while inhibiting the NF-κB pathway significantly abrogated this response and prevented β-cell apoptosis, both in vitro and in sub-renal capsular transplantation animal model.

SOLUTION: Does tRIB3 alter endoplasmic reticulum stress-induced β-cell apoptosis via the NF-κB pathway?

PROBLEM: To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.', 'One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.', 'Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively).

SOLUTION: Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations?

PROBLEM: The influence of the endoscopist on the polyp detection rate (PDR) is underappreciated in clinical practice. Moreover, flat lesions or lesions of the proximal colon are more difficult to detect. Here, we evaluated the differences in the PDR and the characteristics of detected polyps according to the experience of the colonoscopist.', 'We collected data on 2,549 patients who underwent screening colonoscopy performed by three fellows. The PDR was calculated according to the percentage of patients who had at least one polyp (method A) and according to the percentage of detected lesions (method B). The primary outcome included the change in the PDR, and the secondary outcome included the change in the characteristics of the detected polyps with increasing experience of the colonoscopist.', 'No proportional correlation was found between the PDR and increasing experience in colonoscopy with method A; however, with method B, the PDR increased after 400 colonoscopies (p=0.0209). With method B, the detection rates of small polyps (<5 mm) (p=0.0015) and polyps in proximal sites (p=0.0050) increased after 300 colonoscopies.

SOLUTION:
Does the Colonoscopist 's Expertise affect the Characteristics of Detected Polyps?