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.

Q: Context: Various pathways involved in the pathogenesis of sJIA have been identified through gene expression profiling in peripheral blood mononuclear cells (PBMC), but not in neutrophils. Since neutrophils are important in tissue damage during inflammation, and are elevated as part of the acute phase response, we hypothesised that neutrophil pathways could also be important in the pathogenesis of sJIA. We therefore studied the gene profile in both PBMC and neutrophils of sJIA patients treated with tocilizumab.', 'We studied the transcriptomes of peripheral blood mononuclear cells (PBMC) and neutrophils from eight paired samples obtained from 4 sJIA patients taken before and after treatment, selected on the basis that they achieved ACR90 responses within 12 weeks of therapy initiation with tocilizumab. RNA was extracted and gene expression profiling was performed using Affymetrix GeneChip Human Genome U133 Plus 2.0 microarray platform. A longitudinal analysis using paired t-test (p\u2009<\u20090.05 and FC\u2009≥\u20091.5) was applied to identify differentially expressed genes (DEGs) between the two time points followed by ingenuity pathway analysis. Gene Set Enrichment Analysis (GSEA) and quantitative real-time PCR were then performed to verify the microarray results.', 'Gene ontology analysis in neutrophils revealed that response to tocilizumab significantly altered genes regulating mitochondrial dysfunction and oxidative stress (p\u2009=\u20094.6E-05). This was independently verified with GSEA, by identifying a set of oxidative genes whose expression correlated with response to tocilizumab. In PBMC, treatment of sJIA with tocilizumab appeared to affect genes in Oncostatin M signalling and B cell pathways.\Question: Are mitochondrial and oxidative stress genes differentially expressed in neutrophils of sJIA patients treated with tocilizumab : a pilot microarray study?

A: For the first time we demonstrate that neutrophils from sJIA patients responding to tocilizumab showed significantly different changes in gene expression. These data could highlight the importance of mitochondrial genes that modulate oxidative stress in the pathogenesis of sJIA.
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Q: Context: Glial cell line-derived neurotrophic factor (GDNF) and N-cadherin interact to transduce intracellular signals. However, the specific molecular mechanisms of this interaction are unclear. This study attempted to detect changes in GDNF-induced β-catenin phosphorylation and nuclear translocation in C6 glioma cells.', 'C6 glioma cells were treated with GDNF (70 ng/mL) and membrane and cytoplasmic proteins were extracted. A N-cadherin antibody was used for co-immunoprecipitation (co-IP). Western blot analysis using the co-IP protein was completed using antibodies for β-catenin, Src and β-actin. Immunocytochemistry was conducted with the same antibodies. To determine if Src induced phosphorylation of β-catenin Tyr-654, Western blot analysis was also performed on nuclear proteins from C6 cells treated with tyrosine kinase inhibitor PP2 using then p- β-catenin antibody.', 'After induced by GDNF, C6 cell membrane β-catenin was phosphorylated at Tyr-654 and subsequently separated from the N-cadherin/β-catenin complex. Further study confirmed that the induction by GDNF significantly increased cytoplasmic and nuclear expression of phospho-β-catenin (Tyr-654) in C6 glioma cells. There was also an increase in the binding of non-receptor protein kinase Src with N-cadherin on the inner cell membrane surface. Src induced phosphorylation of β-catenin Tyr-654 induced by GDNF decreased significantly.\Question: Does glial cell line-derived neurotrophic factor promote β-catenin phosphorylation and nuclear translocation in glioma cells?

A: The results of our study demonstrate that GDNF increases the intracellular phosphorylation level of β-catenin through N-cadherin/Src signaling, which subsequently stimulates the nuclear translocation of β-catenin. This study provides a theoretical basis for us to reveal the role of biological mechanisms on glioma cell by GDNF.
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Q: Context: To examine baseline hormonal concentrations and the pharmacokinetic response on day 0 and day 28 of 28 days of androstenedione supplementation.', 'Eight men (mean (SD) age 44.1 (3.0) years (range 40-48), weight 76.3 (9.4) kg, and percentage body fat 20.6 (6.7)) participated in a randomised, double blind, cross over, 2 x 28 day placebo controlled study. Subjects were tested on day 0 and 28 days after receiving 200 mg/day oral androstenedione and a placebo treatment with a 28 day washout period between treatments. Serum hormone concentrations were examined at baseline (time 0) and then at 30 minute intervals for 180 minutes to measure day 0 and day 28 pharmacokinetic responses. Analytes included androstenedione, total testosterone, dehydroepiandrosterone sulfate (DHEAS), oestradiol, and sex hormone binding globulin (SHBG). Lipid concentrations, weight, body composition, resting heart rate, and blood pressure were also measured.', "Analysis of integrated area under the curve (AUC) and time 0 hormonal concentrations by repeated measures multivariate analysis of variance (p<0.05) and Fisher's post hoc analysis showed a significant increase in AUC for serum androstenedione at day 0 (108.3 (27.6) nmol/l) in the supplemented condition as compared with day 28 (43.4 (13.1) nmol/l) and placebo (2.1 (0.8) nmol/l) conditions. No other significant AUC changes were noted. After 28 days of supplementation, DHEAS levels were significantly elevated (p = 0.00002) at time 0 (12.9 (1.3) micro mol/l) compared with placebo (7.0 (0.8) micro mol/l) with a trend (p = 0.08) toward elevation of time 0 androstenedione concentrations (16.4 (7.0) nmol/l) compared with placebo (5.6 (0.4) nmol/l). No changes were found for lipids, resting heart rate, or blood pressure, weight, or percentage body fat.\Question: Does four weeks of androstenedione supplementation diminish the treatment response in middle aged men?

A:
Although supplementation with 200 mg/day androstenedione increases AUC for serum androstenedione in the day 0 condition, continued supplementation is characterised by a diminished treatment response, coupled with time 0 increases in testosterone precursors but not testosterone.
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