instruction:
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.
question:
Context: To investigate the effects of copper on permeability and P-glycoprotein (P-gp) of Caco-2 cell monolayers.', 'The differentiated Caco-2 cell model was used in this study. Permeability of cell monolayers was reflected by monitoring transepithelial electrical resistance (TEER); distribution of tight junctional protein ZO-1 was measured by immunofluorescent staining; F actin was measured by fluorescence staining; and Activity of P-gp was reflected by changes of transcellular transport and accumulation of Rho-123 in Caco-2 cells.', "Apical treatment with copper (30 - 100 micromol/L, Hanks' buffered salt solution, up to 3 hours) induced a time- and concentration-dependent increase in permeability reflected by progressive decrease of TEER of Caco-2 cell monolayers, accompanied by deorganization of F actin, but without significant effects on tight junctional protein ZO-1; at a dose without any adverse effects on viability and permeability of Caco-2 monolayers, copper treatment (300 micromol/L, complete medium, 24 hours) decreased Papp(BL-->AP) from 7.37 +/- 0.20 x 10(-6) cm/s (controls) to (6.43 +/- 0.27) x 10(-6) cm/s, the increased Papp(AP-->BL) from (1.23 +/- 0.05) x 10(-7) cm/s (controls) to (3.41 +/- 0.08) x 10(-7) cm/s, and enhanced the intracellular Rho-123 from (0.31 +/- 0.01) nmol/filter (controls) to (0.50 +/- 0.03) nmol/filter.\Question: Does [ Copper treatment alter the barrier functions of human intestinal Caco-2 cells ]?
answer:
Copper might alter the barrier functions of Caco-2 cells through increasing the permeability and inhibiting P-gp of Caco-2 cells.


question:
Context: In Crohn's disease (CD), rapid response to anti-tumor necrosis factor therapy improves short- and medium-term outcomes, but the relationship between early remission (ER) and long-term remission is unclear.", 'This exploratory analysis of PRECiSE 3 (NCT00160524) assessed whether ER after initiation of certolizumab pegol predicted long-term remission.', 'Patients enrolled in PRECiSE 3 had completed PRECiSE 1 or 2, two randomized placebo-controlled studies for moderate to severe CD, and received open-label certolizumab pegol 400\u2009mg every 4 weeks for a total treatment duration of ≤7.5 years. Time to loss of remission between patients with and without ER (Harvey-Bradshaw Index ≤4 at or before Week 6 of PRECiSE 1 or 2) was compared by log-rank test of Kaplan-Meier estimates.', 'At baseline, patients with (n\u2009=\u2009242) and without (n\u2009=\u2009148) ER had mean (standard deviation [SD]) durations of CD of 6.8 (6.6) and 7.4 (7.8) years, mean (SD) CD Activity Index scores of 280.3 (53.4) and 311.1 (55.5), with 45.5% and 41.9% of patients having ileocolonic CD, and median C-reactive protein concentrations of 8.0 and 5.0\u2009mg/L, respectively. Median certolizumab pegol plasma concentrations during the first 6 weeks of therapy were similar in both groups. Mean time to loss of remission was significantly longer in patients with versus without ER (2.77 vs. 1.14 years, p\u2009<\u20090.0001).\Question: Does early remission status predict long-term outcomes in patients with Crohn 's disease treated with certolizumab pegol?
answer:
In certolizumab pegol-treated patients with CD, ER appears to be an important predictor of long-term clinical remission. Prospective trials are needed to determine whether ER improves other long-term outcomes.


question:
Context: Defects of the mitochondrial genome (mtDNA) cause a series of rare, mainly neurological disorders. In addition, they have been implicated in more common forms of movement disorders, dementia and the ageing process. In order to try to model neuronal dysfunction associated with mitochondrial disease, we have attempted to establish a series of transmitochondrial mouse embryonic stem cells harbouring pathogenic mtDNA mutations.', 'Transmitochondrial embryonic stem cell cybrids were generated by fusion of cytoplasts carrying a variety of mtDNA mutations, into embryonic stem cells that had been pretreated with rhodamine 6G, to prevent transmission of endogenous mtDNA. Cybrids were differentiated into neurons and assessed for efficiency of differentiation and electrophysiological function.', 'Neuronal differentiation could occur, as indicated by expression of neuronal markers. Differentiation was impaired in embryonic stem cells carrying mtDNA mutations that caused severe biochemical deficiency. Electrophysiological tests showed evidence of synaptic activity in differentiated neurons carrying non-pathogenic mtDNA mutations or in those that caused a mild defect of respiratory activity. Again, however, neurons carrying mtDNA mutations that resulted in severe biochemical deficiency had marked reduction in post-synaptic events.\Question: Are transmitochondrial embryonic stem cells containing pathogenic mtDNA mutations compromised in neuronal differentiation?
answer:

Differentiated neurons carrying severely pathogenic mtDNA defects can provide a useful model for understanding how such mutations can cause neuronal dysfunction.