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.
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Question: Context: Tetrahydrocurcumin (THC) is an active metabolite of curcumin. It has been reported to have similar pharmacological activity to curcumin. The proteases that participate in extracellular matrix (ECM) degradation are involved in cancer cell metastasis. The present study investigates the effect of an ultimate metabolite of curcumin, THC, on the invasion and motility of highly-metastatic HT1080 human fibrosarcoma cells.', 'The effect of THC on HT1080 cell invasion and migration was determined using Boyden chamber assay. Cell-adhesion assay was used for examining the binding of cells to ECM molecules. Zymography assay was used to analyze the effect of THC on matrix metalloproteinase (MMP)-2, MMP-9, and urokinase plasminogen activator (uPA) secretion from HT1080 cells. Tissue inhibitor of metalloproteinase (TIMP)-2 and membrane-type 1 matrix metalloproteinase (MT1-MMP) proteins levels were analyzed by Western blotting.', 'Treatment with THC reduced HT1080 cell invasion and migration in a dose-dependent manner. THC also decreased the cell adhesion to Matrigel and laminin-coated plates. Analysis by zymography demonstrated that treatment with THC reduced the levels of MMP-2, MMP-9, and uPA. THC also inhibited the levels of MT1-MMP and TIMP-2 proteins detected by Western blot analysis.
Answer: Our findings revealed that THC reduced HT1080 cell invasion and migration. The inhibition of cancer cell invasion is associated with the downregulation of ECM degradation enzymes and the inhibition of cell adhesion to ECM proteins.

Answer: Does tetrahydrocurcumin inhibit HT1080 cell migration and invasion via downregulation of MMPs and uPA?


Question: Context: Perturbation of the endoplasmic reticulum (ER) homeostasis has emerged as one of the prominent features of obesity and diabetes. This occurs when the adaptive unfolded protein response (UPR) fails to restore ER function in key metabolic tissues. We previously reported increased inflammation and impaired heat shock response (HSR) in obese human subjects that were restored by physical exercise. Here, we investigated the status of ER stress chaperone; glucose-regulated protein 78 (GRP78) and its downstream UPR pathways in human obese, and their modulation by a supervised 3-month physical exercise.', "Subcutaneous adipose tissue (SAT) and blood samples were collected from non-diabetic adult human lean (n=40) and obese (n=40, at baseline and after 3months of physical exercise). Transcriptomic profiling was used as a primary screen to identify differentially expressed genes and it was carried out on SAT samples using the UPR RT(2) Profiler PCR Array. Conventional RT-PCR, immunohistochemistry, immunofluorescence, Western blot and ELISA were used to validate the transcriptomic data. Correlation analyses with the physical, clinical and biochemical outcomes were performed using Pearson's rank correlation coefficient.", 'Levels of GRP78 and its three downstream UPR arms; activating transcription factor-6 (ATF6), inositol-requiring enzyme-1α (IRE1α) and protein kinase RNA-like endoplasmic reticulum kinase (PERK) were increased in obese subjects. More interestingly, higher levels of circulating GRP78 protein were found in obese compared to lean subjects which correlated negatively with maximum oxygen uptake (VO2 Max) but positively with high-sensitivity C-reactive protein (hsCRP) and obesity indicators such as BMI, percentage body fat (PBF) and waist circumference. GRP78 increased secretion in obese was further confirmed in vitro using 3T3-L1 preadipocyte cells under ER stress. Finally, we showed that physical exercise significantly attenuated the expression and release of GRP78 with a concomitant reduction in the phosphorylation of IRE1α and eukaryotic initiation factor-2α (eIF2α).
Answer: Our results suggest that physical exercise alleviates ER stress in human obese through attenuation of GRP78 signaling network.

Answer: Does physical exercise alleviate ER stress in obese humans through reduction in the expression and release of GRP78 chaperone?


Question: Context: Shear stress alteration has been recognized as a predisposing factor for the impairment of endothelial function. Myocardial bridging is a congenital condition associated with alteration in shear stress, however, its impact upon vasoreactivity remains undetermined.', 'This was a case-control designed study with 29 patients with myocardial bridging and 58 patients without myocardial bridging. Endothelium-dependent and endothelium-independent changes in coronary artery diameters, blood flow and wall shear stress were determined after intracoronary infusion of acetylcholine (ACH, 10(-6)-10(-4) mol/L) and nitroglycerine (NTG, 200 microg). Coronary flow velocity reserve (CFVR) was determined after intracoronary injection of adenosine (18-36 microg). In response to ACH, there was more epicardial vasoconstriction at the myocardial bridging site compared with the proximal and distal segments (-29.6+/-21.7 vs. -9.6+/-22.5 and -17.4+/-21.5%, p<0.05) and compared with the control group (-29.6+/-21.7 vs. -5.9+/-36.5%, p<0.001). The response to NTG and CFVR was the same in the case and the control group. Wall shear rate (WSR) was higher in the MB site at baseline and in response to ACH.
Answer: MB is characterised by enhanced WSR and impairment in endothelium-dependent vasorelaxation. These functional alterations may add to the severity of structural lumen compression and thus to the clinical presentation of this congenital abnormality.

Answer:
Is myocardial bridging associated with alteration in coronary vasoreactivity?