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 Input:
Context: Myocardial infarction (MI) induces neural remodelling of the left stellate ganglion (LSG), which may contribute to ischaemia-induced arrhythmias. The neural chemorepellent Semaphorin 3a (Sema3a) has been identified as a negative regulator of sympathetic innervation in the LSG and heart. We previously reported that overexpression of Sema3a in the border zone could reduce the arrhythmogenic effects of cardiac sympathetic hyperinnervation post-MI. This study investigated whether Sema3a overexpression within the LSG confers an antiarrhythmic effect after MI through decreasing extra- and intra-cardiac neural remodelling.', 'Sprague-Dawley rats were subjected to MI, and randomly allocated to intra-LSG microinjection of either phosphate-buffered saline (PBS), adenovirus encoding green fluorescent protein (AdGFP), or adenovirus encoding Sema3a (AdSema3a). Sham-operated rats served as controls. Two weeks after infarction, MI-induced nerve sprouting and sympathetic hyperinnervation in the LSG and myocardium were significantly attenuated by intra-LSG injection with AdSema3a, as assessed by immunohistochemistry and western blot analysis of growth-associated protein 43 and tyrosine hydroxylase. This was also confirmed by sympathetic nerve function changes assessed by cardiac norepinephrine content. Additionally, intra-LSG injection with AdSema3a alleviated MI-induced accumulation of dephosphorylated connexin 43 in the infarct border zone. Furthermore, Sema3a overexpression in the LSG reduced the incidence of inducible ventricular tachyarrhythmia by programmed electrical stimulation post-MI, and arrhythmia scores were significantly lower in the AdSema3a group than in the PBS and AdGFP groups.\Question: Does semaphorin 3a transfection into the left stellate ganglion reduce susceptibility to ventricular arrhythmias after myocardial infarction in rats?

Ex Output:
Semaphorin 3a overexpression in the LSG ameliorates the inducibility of ventricular arrhythmias after MI, mainly through attenuation of neural remodelling within the cardiac-neuraxis.


Ex Input:
Context: To investigate the role of S100A3 and the effect of S100A3 inhibition on human castration-resistant prostate cancer (CRPC) cells by using in vitro and in vivo functional assays.', 'Using human CRPC cells (PC3 and DU145), S100A3 expression levels were assessed by reverse transcription-polymerase chain reaction and Western blot analysis. After S100A3-specific small interfering ribonucleic acid (RNA) treatment, cell viability was determined by Cell Counting Kit-8 assay, and apoptotic cell fractions were evaluated by flow cytometry. The invasive properties of these cells and the expression pattern of matrix metalloproteinases (MMPs) were assessed using transwell migration assays, reverse transcription-polymerase chain reaction, and gelatin zymography. Finally, the in vivo efficacy of S100A3 inhibition on human CRPC cells was investigated using human tumor xenograft models in nude mice.', 'Human CRPC cells showed overexpression of S100A3, and its suppression reduced cell viability owing to apoptotic cell death. Additionally, S100A3 inhibition decreased the invasiveness of human CRPC cells. Moreover, MMP-2 and MMP-9 were downregulated in PC3, whereas only MMP-9 was downregulated in D145 after S100A3 inhibition. In human CRPC xenograft models, we noted a marked reduction in tumor growth in mice injected with S100A3 short hairpin RNA-transfected PC3 and DU145 cells.\Question: Does s100A3 suppression inhibit in vitro and in vivo tumor growth and invasion of human castration-resistant prostate cancer cells?

Ex Output:
Human CRPC cells showed upregulation of S100A3 expression, and S100A3 inhibition reduced tumor cell viability. S100A3 inhibition reduced invasion capability with downregulation of MMP expression. More importantly, S100A3 inhibition resulted in tumor growth suppression in human CRPC xenograft models, suggesting S100A3 could serve as a novel therapeutic target for the treatment of human CRPC.


Ex Input:
Context: The prognosis of patients with severe aortic stenosis, low aortic gradient and preserved ejection fraction is controversial. Our study analyzed the prognosis of these patients and its relation to pressure gradient and aortic valve flow.', 'We performed a retrospective cohort study of 363 consecutive patients with severe aortic stenosis and preserved ejection fraction, divided into 4 groups, based on the presence of a systolic volume index greater or lower than 35 mL/m(2) and the presence of a mean aortic gradient greater or lower than 40 mmHg. Group I: normal flow, high gradient (n=169, 47%); group II: normal flow, low gradient (n=98, 27%); group III: low flow, high gradient (n=54, 15%), and group IV: low flow, low gradient (n=42, 12%). The primary endpoint was overall mortality.', 'Independent risk factors for mortality were age (hazard ratio=1.04; 95% confidence interval, 1.01-1.08) and atrial fibrillation (hazard ratio=2.21; 95% confidence interval, 1.24-3.94). Surgical treatment was associated with longer survival in all groups (hazard ratio=0.25; 95% confidence interval: 0.13-0.49). Mortality was higher in patients with low flow than in those with with normal flow (26.6% vs 13.6%; P=.004). The most favorable mean prognosis was found in group II (hazard ratio=0.4; 95% confidence interval, 0.2-0.9).\Question: Is systolic volume index by Doppler echocardiography an useful marker for stratification and prognostic evaluation in patients with severe aortic stenosis and preserved ejection fraction?

Ex Output:

Patients with severe aortic stenosis, normal ejection fraction and low aortic flow have a worse prognosis. Analysis of aortic flow by Doppler echocardiography is useful in risk stratification and therapeutic decision-making in patients with aortic stenosis.