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.

[EX Q]: Context: Thromboxane A2 (TXA2) can induce the platelet aggregation and lead to thrombosis. This will cause the low-reflow phenomenon after ischemic stroke and aggravate the damage of brain issues. Therefore, it is potential to develop the drugs inhibiting TXA2 pathway to treat cerebral ischemia.', 'This study aims to prove the protective effect of N2 (4-(2-(1H-imidazol-1-yl) ethoxy)-3-methoxybenzoic acid) on focal cerebral ischemia and reperfusion injury through platelet aggregation inhibition.', 'Middle cerebral artery occlusion/reperfusion (MCAO/R) is used as the animal model. Neurological deficit score, Morris water maze, postural reflex test, Limb-use asymmetry test, infarct volume, and water content were performed to evaluate the protective effect of N2 in MCAO/R rats. 9, 11-dieoxy-11α, 9α-methanoepoxyprostaglandin F2α (U46619) or adenosine diphosphate (ADP) was used as the inducer of platelet aggregation.\Question: Does n2 extenuate experimental ischemic stroke through platelet aggregation inhibition?
[EX A]: N2 can improve the motor function, learning and memory ability in MCAO/R rats while reducing the infarct volume. N2 can inhibit TXA2 formation but promote PGI2, and can inhibit platelet aggregation induced by U46619 and ADP. Further, N2 inhibits thrombosis with a minor adverse effect of bleeding than Clopidogrel. In conclusion, N2 can produce the protective effect on MCAO/R brain injury through inhibiting TXA2 formation, platelet aggregation and thrombosis.

[EX Q]: Context: Characteristic clinical heterogeneity and mostly slow-growing behavior of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) cause problems in finding appropriate treatments. Thus, current therapy options are not satisfactory. PKI-587 is a highly potent novel dual inhibitor of PI3K and mTORC1/C2.', 'We assessed the effects of PKI-587 in different GEP-NEN tumor models, including poorly differentiated cell line LCC-18, compared with the established mTORC1 inhibitor everolimus.', 'We treated the cell lines BON, QGP1, KRJ-I and LCC-18 with increasing concentrations of the inhibitor PKI-587, and compared with everolimus and DMSO. We assessed the impact of treatments on viability (WST-1 assay), on apoptotic processes (Caspase 3/7 assay, JC-1) and on cell cycle regulation (flow cytometry). We determined alterations of signaling mediators by phosphor-specific western blot analysis and conducted multiplexed gene expression analysis (nCounter® technology).', 'In all cell lines, PKI-587 dose-dependently inhibited proliferation whereas everolimus was less effective. Treatment with PKI-587 led to cell cycle arrest, induction of apoptosis and successfully suppressed activity of direct mTORC1 target 4E-BP1, a crucial factor for tumor genesis only partially inhibited by everolimus. Gene expression analyses revealed relevant changes of RAS, MAPK, STAT and PI3K pathway genes after treatment. Treatment dependent and cell line characteristic effects on AKT/RB/E2F signaling regarding cell cycle control and apoptosis are extensively discussed in this article.\Question: Is inhibition of mTORs Catalytic Site by PKI-587 a Promising Therapeutic Option for Gastroenteropancreatic Neuroendocrine Tumor Disease?
[EX A]: PI3K/mTOR dual targeting is a promising new therapeutic approach in neuroendocrine tumor disease that should be evaluated in further clinical trials.

[EX Q]: Context: Studies on the use of intradetrusor botulinum toxin A injection for children with neuropathic bladders are insufficient and the results are controversial. The aim of the present study was to evaluate the effect of intradetrusor botulinum toxin A injection for children with neuropathic bladders that are resistant to anticholinergic treatment, and to reveal any criteria indicating treatment success.', 'Hospital records were reviewed of 16 children with neuropathic bladders due to myelomeningocele, and who had botulinum toxin A injections between 2007 and 2010. Botulinum toxin A (10 units/kg) was injected endoscopically into various sites of the detrusor, except the trigone. The success was defined as complete dryness between clean intermittent catheterizations. Urodynamic studies before and after the application were evaluated and parameters, including bladder capacity (measured/expected) and compliance, were also analyzed. Reviewing the results, patients were then classified into two groups: as having fibrotic bladders (noncompliant, acontractile bladders with high pressures) or overactive bladders. Urodynamic findings and therapy success were then compared between the groups.', 'A total of 19 injections, including repeat injections in three patients, were performed. Results of the 16 initial injections were evaluated. Nine patients had detrusor overactivity, and five out of nine (56%) applications in this group resulted in complete dryness between clean intermittent catheterizations. In bladders with typical detrusor overactivity, there was a significant increase in both the capacity (from 0.53 to 0.74) and compliance (from 4.7 to 8.6 ml/cm H2O). Looking at the seven patients that displayed fibrotic bladders with very low compliance and no contraction at all, none of them presented with notable clinical improvement from injections. Comparing the urodynamic findings, there was no significant difference in compliance (3.1 ml/cm H2O before and 3.5 ml/cm H2O after) and bladder capacity (0.58 before and 0.52 after the treatment) in the fibrotic bladders.\Question: Is botulinum injection useless on fibrotic neuropathic bladders?
[EX A]:
Despite its worldwide usage and FDA approval, studies on the effectiveness of botulinumtoxin A on neuropathic bladders in children are controversial. There are now numerous studies attesting to the good results of BoNTA in neuropathic detrusor overactivity; however, only scarce reports comment on the specific features of the disease process among patients and reasons for failure in some. In our study, reviewing the urodynamic findings carefully, it was observed that the patients who did not respond to injections were the ones with no contractions, despite high pressures and low compliance. Therefore, describing the indications of BoNTA as neuropathic detrusor overactivity and urinary incontinence despite anticholinergic medications may lead to mistreatment of patients in the decompensated phase of a hyper-reflexive detrusor. Pretreatment urodynamic evaluation might be a good indicator, without biopsies, of estimating the degree of fibrosis and the patients who will benefit from the injection.