instruction:
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.
question:
Context: To evaluate whether P2X3 receptors (P2X3R) are expressed in the bladder urothelium and to determine their possible function in modulating purinergic detrusor contractions in the rat urinary bladder.', 'The expression of urothelial receptors was determined using conventional immunohistochemistry in bladders from normal Sprague-Dawley rats. The urothelial layer was removed by incubation with protamine, and disruption of the urothelium was confirmed using haematoxylin and eosin staining on bladder sections. Open cystometry was used to determine the effects of both urothelial removal as well as intravesical application of a specific P2X3R antagonist on bladder properties from intact and protamine-treated rats. Isometric contractile responses to potassium chloride (KCl) depolarization, electrical field stimulation (EFS) or chemical P2X activation were determined in normal and urothelium-denuded bladder strips, with and without application of the P2X3R antagonist.', 'Immunohistochemical staining showed high expression of P2X3R in the medial and basal layers of the urothelium. Removal of the urothelial layer disturbed normal bladder performance in vivo and eliminated the effects of the P2X3R antagonist on increasing the contractile interval and reducing the amplitude of voiding contractions. Removal of the urothelium did not affect bladder strip contractile responses to KCl depolarization or EFS. Pharmacological inhibition of P2X3R prevented desensitization to P2X-mediated detrusor muscle contractions during EFS only in the strips with an intact urothelium. A concentration-dependent, specific inhibition of P2X3R also prevented desensitization of purinergic contractile responses in intact bladder strips.
Answer: In the rat bladder, medial and basal urothelial cells express P2X3R, and specific inhibition of the receptor leads to a more hyporeflexive bladder condition. This pathway may involve P2X3R driving a paracrine amplification of ATP released from umbrella cells to increase afferent transmission in the sub-urothelial sensory plexus and desensitization of P2X1-mediated purinergic detrusor contractions.
answer:
Does inhibition of urothelial P2X3 receptors prevent desensitization of purinergic detrusor contractions in the rat bladder?

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: We sought to evaluate the incidence and nature of pulmonary stenosis after implantation of the bovine jugular vein graft (Contegra; Medtronic, Inc, Minneapolis, Minn) in the right ventricular outflow tract.', 'Between May 2000 and September 2002, 58 Contegra conduits (8-22 mm) were implanted during primary (n = 27) or redo operations (n = 31) in 57 patients, with ages ranging from 2 days to 48 years (mean, 9 years). Indications were truncus arteriosus (n = 16), tetralogy of Fallot (n = 28), pulmonary replacement in the Ross operation (n = 10), and Rastelli-type repair for double-outlet right ventricle (n = 4). Echocardiography was prospectively performed by a fixed team of investigators during follow-up (mean, 22.7 +/- 10 months). A peak gradient of greater than 50 mm Hg was considered severe stenosis.', 'Two patients died from Staphylococcus aureus -induced septicemia and enterococcal endocarditis after 12 days and 12 weeks, respectively. One patient died of heart failure caused by endocardial fibroelastosis after 1 year. Freedom from severe stenosis at the distal anastomosis was 91% +/- 3% at 3 months, 68% +/- 6% at 12 months, and 49% +/- 8% at 24 months. The risk of development of stenosis does not change over time. Younger age and its derivatives (graft size and indication) are significantly related to the occurrence of severe stenosis ( P < .0001). Seventeen (29%) conduits required an endovascular intervention (balloon dilatation or stent). Seven (12%) conduits were explanted (endocarditis, 2; stenosis, 5). Histologic analysis of the explanted conduits showed excessive proliferation of neointima at the level of the distal anastomosis. Valve regurgitation was observed in 9 (16%) conduits and was always secondary to dilatation in the presence of severe distal stenosis.
Answer: The Contegra conduit induces a neointimal proliferation at the level of the pulmonary anastomosis. This leads to a high incidence of severe stenosis at intermediate-term follow-up.
answer:
Does the Contegra conduit in the right ventricular outflow tract induce supravalvular stenosis?