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.
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Context: Spinal anesthesia can be challenging in patients undergoing total joint arthroplasty because of poorly palpable surface landmarks and age-related changes in the lumbar spine. We hypothesized that pre-procedural ultrasound imaging would be effective in identifying the lumbar intervertebral spaces and would provide an accurate measure of the depth to the intrathecal space.', "Fifty patients undergoing elective total joint arthroplasty were recruited in this prospective descriptive study. Using a curved-array 2-5 MHz transducer, the lumbar spine was imaged in two views, i.e., longitudinal parasagittal (LP) and transverse midline (TM). The intervertebral levels were identified by counting upwards from the sacrum. The locations of the interlaminar spaces were identified by visualizing the ligamentum flavum-dura mater complex and the posterior aspect of the vertebral body. The needle insertion point for a midline approach was determined from the ultrasound examination and was marked on the skin of the patient's back.", 'The mean patient age was 67 +/- 10 yr, and 46% of the patients had a body mass index >30 kg . m(-2). Surface landmarks were difficult or impossible to palpate in 38% of the patients. The scan quality on the LP and TM views was adequate or better in 100 and 98% of the patients, respectively. Dural puncture was achieved with one needle insertion attempt and within two needle insertion attempts in 84% and 98% of the patients, respectively. The ultrasound-measured depth to the intrathecal space correlated well with the actual needle insertion depth (concordance correlation coefficient = 0.82, accuracy 0.95, precision 0.86), with a tendency to overestimate the depth by just 2.1 +/- 5.4 mm.
Answer: Ultrasound imaging of the lumbar spine provides clinically useful information that can facilitate spinal anesthesia in the older orthopedic patient population.
answer:
Does an ultrasound-assisted approach facilitate spinal anesthesia for total joint arthroplasty?


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?


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Context: ErbB family receptor tyrosine kinases (ErbBs) play a role in cell adhesion and migration and are frequently overexpressed in esophageal squamous cell carcinomas (ESCCs) or esophageal adenocarcinomas (EACs). Targeting ErbBs by tyrosine kinase inhibitors (TKIs) may therefore limit esophageal cancer cell migration. Here, we studied the impact of TKIs on ErbB dimerization, cell signaling pathways, and cell migration in three esophageal cell lines: OE21 (ESCC), OE33 (EAC), and Het-1A (non-neoplastic esophageal epithelium). In OE21 cells, the TKIs erlotinib, gefitinib, and lapatinib slightly affected epidermal growth factor receptor EGFR/EGFR, but not EGFR/HER2 dimerization as detected by in situ proximity ligation assay (in situ PLA). Still, TKIs inhibited ERK1/2, Akt, STAT3, and RhoA activity in OE21 cells, as assessed by Western blot, antibody arrays, and Rho GTPase effector pull-down assays. This was accompanied by reduced OE21 cell migration, induction of focal adhesions, and actin cytoskeleton reorganization, as shown by Oris™ migration assay and focal adhesion kinase (FAK)/phalloidin staining. In contrast, in OE33 cells, only lapatinib decreased STAT5, Src family kinase (SFK), and FAK activity as well as β-catenin expression. This impeded cell migration and induced morphological changes in OE33 cells. No alterations were seen for the non-neoplastic Het-1A cells. Thus, we identified the ErbB signaling network as regulator of esophageal cancer cell's actin cytoskeleton, focal adhesions, and cell migration. ErbB targeted TKIs therefore also limit ESCC and EAC cell motility and migration.
Answer: Clinical tyrosine kinase inhibitors (TKIs) reduce esophageal cancer cell migration. Loss of cell migration is linked to reduced Akt, ERK1/2, STAT (3 or 5), FAK, SFKs, and RhoA activity. Clinical TKIs act via distinct signaling in the two main histotypes of esophageal cancer.
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Do erbB targeting inhibitors repress cell migration of esophageal squamous cell carcinoma and adenocarcinoma cells by distinct signaling pathways?