In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Input: Consider Input: Context: Mucus hypersecretion and neutrophil infiltration are important characteristics of airway inflammation. Epidermal growth factor receptor (EGFR) transactivation induces mucus and inflammatory cytokine secretion from airway epithelial cells. To elucidate the roles of EGFR in airway inflammation, the in vitro effects on mucin production and interleukin (IL) 8 secretion from cultured airway epithelial cells and the in vivo effects on mucus hypersecretion and neutrophil infiltration in rat nasal mucosa of the EGFR tyrosine kinase inhibitor AG1478 were examined.', 'The in vitro effects of AG1478 treatment of cultured NCI-H292 cells on lipopolysaccharide (LPS) induced or tumor necrosis factor (TNF) α induced MUC5AC mucin and IL-8 secretion were evaluated. Hypertrophic and metaplastic changes of goblet cells, mucus production and neutrophil infiltration in rat nasal epithelium were induced by intranasal instillation of LPS in vivo, and the inhibitory effects of AG1478 by intraperitoneal injection or intranasal instillation were examined.', 'AG1478 (1-1000 nM) significantly inhibited both LPS-induced and TNF-α-induced secretion of MUC5AC and IL-8 from cultured NCI-H292 cells in a dose-dependent manner. The expression of MUC5AC and IL-8 messenger RNAs was also significantly inhibited. Intranasal instillation of AG1478 one hour after intranasal LPS instillation significantly inhibited LPS-induced goblet cell metaplasia, mucus production, and neutrophil infiltration in rat nasal epithelium, as did intraperitoneal injection of AG1478 one hour before LPS instillation.\Question: Does epidermal growth factor receptor inhibitor AG1478 inhibit mucus hypersecretion in airway epithelium?

Output: These results indicated that EGFR transactivation plays an important role in mucin and IL-8 secretion from airway epithelial cells. Intranasal instillation of an EGFR tyrosine kinase inhibitor may be a new therapeutic approach for the treatment of upper airway inflammation.


Input: Consider Input: Context: To assess plantarflexion moment and hip joint moment after-effects following walking on a split-belt treadmill in healthy individuals and individuals post-stroke.', 'Cross-sectional study.', 'Ten healthy individuals (mean age 57.6 years (standard deviation; SD 17.2)) and twenty individuals post-stroke (mean age 49.3 years (SD 13.2)).', 'Participants walked on an instrumented split-belt treadmill under 3 gait periods: i) baseline (tied-belt); ii) adaptation (split-belt); and iii) post-adaptation (tied-belt). Participants post-stroke performed the protocol with the paretic and nonparetic leg on the faster belt when belts were split. Kinematic data were recorded with the Optotrak system and ground reaction forces were collected via the instrumented split-belt treadmill.', 'In both groups, the fast plantarflexion moment was reduced and the slow plantarflexion moment was increased from mid-stance to toe-off in the post-adaptation period. Significant relationships were found between the plantarflexion moment and contralateral step length.\Question: Is plantarflexion moment a contributor to step length after-effect following walking on a split-belt treadmill in individuals with stroke and healthy individuals?

Output: Split-belt treadmills could be useful for restoring step length symmetry in individuals post-stroke who present with a longer paretic step length because the use of this type of intervention increases paretic plantarflexion moments. This intervention might be less recommended for individuals post-stroke with a shorter paretic step length because it reduces the paretic plantarflexion moment.


Input: Consider Input: Context: Hyperphosphatemia, elevated calcium x phosphorus product (Ca x P), and calcium burden, major causes of vascular calcification, are correlated with increased cardiovascular morbidity and mortality in dialysis patients.', 'To address the underlying mechanisms responsible for these findings, we have utilized an in vitro human smooth muscle cell (HSMC) model of vascular calcification. Previous studies using this system demonstrated enhanced calcification of HSMC cultures treated with phosphorus levels in the hyperphosphatemic range, and implicated a sodium-dependent phosphate cotransport-dependent mechanism in this effect. In the present study, we examine the effect of increasing calcium concentrations on HSMC calcification in vitro.', 'Increasing calcium to levels observed in hypercalcemic individuals increased mineralization of HSMC cultures under normal phosphorus conditions. Importantly, at these total calcium concentrations, ionized calcium levels increased from 1.2 mmol/L to 1.7 mmol/L, consistent with levels observed physiologically in normocalcemic and hypercalcemic individuals, respectively. Furthermore, increasing both calcium and phosphorus levels led to accelerated and increased mineralization in the cultures. Calcium-induced mineralization was dependent on the function of a sodium-dependent phosphate cotransporter, since it was inhibited by phosphonoformic acid (PFA). While elevated calcium did not affect short-term phosphorus transport kinetics, long-term elevated calcium treatment of HSMCs induced expression of the sodium-dependent phosphate cotransporter, Pit-1.\Question: Do elevated extracellular calcium levels induce smooth muscle cell matrix mineralization in vitro?


Output: These studies suggest that elevated calcium may stimulate HSMC mineralization by elevating Ca x P product and enhancing the sodium-dependent phosphate cotransporter-dependent mineralization pathway previously observed in HSMCs.