TASK DEFINITION: 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.
PROBLEM: Context: Pain intensity attenuates muscular activity, proprioception, and tactile acuity, with consequent changes of joint kinematics. People suffering from low back pain (LBP) frequently show movement control impairments of the lumbar spine in sagittal plane. This cross-sectional, observational study investigated if the intensity of LBP attenuates lumbar movement control. The hypothesis was that lumbar movement control becomes more limited with increased pain intensity.', 'The effect of LBP intensity, measured with a numeric rating scale (NRS), on lumbar movement control was tested using three movement control tests. The lumbar range of motion (ROM), the ratio of lumbar and hip ROM as indicators of direction specific movement control, and the recurrence and determinism of repetitive lumbar movement patterns were assessed in ninety-four persons suffering from LBP of different intensity and measured with an inertial measurement unit system. Generalized linear models were fitted for each outcome.', 'Lumbar ROM (+ 0.03, p = 0.24) and ratio of lumbar and hip ROM (0.01, p = 0.84) were unaffected by LBP intensity. Each one point increase on the NRS resulted in a decrease of recurrence and determinism of lumbar movement patterns (-3.11 to -0.06, p 0.05).
Answer: Our results indicate changes in movement control in people suffering from LBP. Whether decreased recurrence and determinism of lumbar movement patterns are intensifiers of LBP intensity or a consequence thereof should be addressed in a future prospective study.

SOLUTION: Does pain intensity attenuate movement control of the lumbar spine in low back pain?

PROBLEM: Context: Endoplasmic reticulum (ER) stress is induced in many forms of chronic liver disease and may promote the development of hepatocellular carcinoma. The activator protein 1 (AP-1) complex is a transcription factor that promotes hepatic carcinogenesis in response to cellular stress. The aim of this study was to determine the role of ER stress in the regulation of the hepatic AP-1 complex.', 'Human hepatocellular carcinoma (HepG2) cells and C57BL/6J mice were subjected to pharmacologic ER stress and the expression of AP-1-associated genes and proteins was assessed. To determine the role of MAPK signaling in ER stress-induced AP-1 activation, ER stress was induced in JNK- and ERK-inhibited HepG2 cells.', 'Induction of ER stress promoted the activation of both Jun- and Fos-related genes and proteins of the AP-1 complex in HepG2 cells and murine liver. Inhibition of ERK phosphorylation in HepG2 cells completely prevented ER stress-induced activation of the fos-related components of AP-1 whereas activation of Jun-related components was only partially attenuated. Conversely, inhibition of JNK phosphorylation in HepG2 cells reduced ER stress-induced activation of Jun-related components but did not prevent activation of fos-related components.
Answer: ER stress activates the hepatic AP-1 complex via MAPK-dependent signaling pathways. ER stress-induced activation of Fos-related components is dependent primarily on ERK activation whereas ER stress-induced activation of Jun-related components is dependent primarily on JNK activation, although there is interplay between these regulatory pathways. These data implicate a novel signaling pathway by which sustained ER stress, as observed in many chronic liver diseases, may promote hepatic carcinogenesis.

SOLUTION: Does endoplasmic reticulum stress activate the hepatic activator protein 1 complex via mitogen activated protein kinase-dependent signaling pathways?

PROBLEM: Context: MicroRNA-340 (miR-340) is deregulated in many human cancers in correlation with tumor progression. Recent studies have found that microRNAs play key roles in energy metabolism. This study explored the contributions of miR-340 to the metabolic shift in oral squamous cell carcinoma (OSCC).', 'MiR-340 expression was measured by real-time polymerase chain reaction. MiR-340 mimics, miR-340 inhibitor, and scramble small interfering RNA were transfected into SAS human tongue SCC cells to observe their effects on cell proliferation, colony formation, lactate secretion, and glucose uptake rate. Moreover, the relation between the level of miR-340 and glucose transporter-1 (Glut1) was investigated.', 'The expression of miR-340 was decreased and thus induced a metabolic switch in oral cancer cells. The decrease in miR-340 increased Glut1 expression, leading to an increase in lactate secretion and glucose uptake rate. The altered metabolism induced by miR-340 resulted in the rapid proliferation of oral cancer cells.
Answer: The findings suggest that miR-340 might act as a molecular switch that contributes to the regulation of glycolysis in OSCC by regulating Glut1 expression.

SOLUTION:
Does microRNA-340 mediate Metabolic Shift in Oral Squamous Cell Carcinoma by Targeting Glucose Transporter-1?