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) 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--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: This study investigated whether anxiety, fear of pain, or pain catastrophizing were predictive of pain-related outcomes after induced delayed onset muscle soreness (DOMS) at the shoulder.', 'Healthy participants (19 males and 23 females) were eligible for participation if they had (a) no history of neck or shoulder pain, (b) no sensory or motor impairments of the upper-extremity, (c) not regularly participating in upper-extremity weight training, (d) not currently or regularly taking pain medication, and (e) no history of upper-extremity surgery. Participants completed self-report measures for fear of pain, pain catastrophizing, and anxiety. Then, participants underwent a standard fatigue protocol to induce DOMS in the shoulder external rotator muscles. Participants were reassessed 24 hours after DOMS induction on clinical and evoked pressure pain reports, muscle force production, self-report of upper-extremity disability, and kinesiophobia. Stepwise regression models considered sex, anxiety, pain intensity, fear of pain, and pain catastrophizing as outcome predictors.', 'Fear of pain alone explained 16% (P=0.008) of the variance in clinical pain and 10% (P=0.047) evoked pressure pain intensity. Clinical pain intensity alone explained 11% (P<0.031) of the variance in muscle force production. Clinical pain intensity and fear of pain explained 50% (P<0.001) of the variance in upper-extremity disability, whereas fear of pain and sex accounted for 26% (P=0.005) of the variance in kinesiophobia.\Question: Does fear of pain influence outcomes after exercise-induced delayed onset muscle soreness at the shoulder?

Output: With the exception of muscle force production, fear of pain had a consistent influence on shoulder DOMS outcomes, even after controlling for pain intensity. This study suggests fear of pain may be a relevant psychologic factor to consider in clinical studies investigating the development and treatment of chronic shoulder pain.

Input: Consider Input: Context: Oxidative stress is central to the pathogenesis of Parkinson's disease (PD), but the mechanisms involved in the control of this stress in dopaminergic cells are not fully understood. There is increasing evidence that selenoproteins play a central role in the control of redox homeostasis and cell defense, but the precise contribution of members of this family of proteins during the course of neurodegenerative diseases is still elusive.", 'We demonstrated first that selenoprotein T (SelT) whose gene disruption is lethal during embryogenesis, exerts a potent oxidoreductase activity. In the SH-SY5Y cell model of dopaminergic neurons, both silencing and overexpression of SelT affected oxidative stress and cell survival. Treatment with PD-inducing neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone triggered SelT expression in the nigrostriatal pathway of wild-type mice, but provoked rapid and severe parkinsonian-like motor defects in conditional brain SelT-deficient mice. This motor impairment was associated with marked oxidative stress and neurodegeneration and decreased tyrosine hydroxylase activity and dopamine levels in the nigrostriatal system. Finally, in PD patients, we report that SelT is tremendously increased in the caudate putamen tissue.', 'These results reveal the activity of a novel selenoprotein enzyme that protects dopaminergic neurons against oxidative stress and prevents early and severe movement impairment in animal models of PD.\Question: Does selenoprotein T exert an Essential Oxidoreductase Activity That Protects Dopaminergic Neurons in Mouse Models of Parkinson 's Disease?
Output: Our findings indicate that selenoproteins such as SelT play a crucial role in the protection of dopaminergic neurons against oxidative stress and cell death, providing insight into the molecular underpinnings of this stress in PD.