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

[Q]: Context: The bradycardic agent zatebradine (UL-FS 49) reduces heart rate without negative inotropic or proarrhythmic effects. The aim was to experimentally characterize the influence of zatebradine on arterial baroreflex sensitivity (BRS) and heart rate variability (HRV) which are generally considered as estimates of vagal activity and have prognostic value in patients after myocardial infarction (MI).', 'Conscious rats were studied 3 days after left coronary artery ligation or sham-operation (SH). BRS was determined by linear regression analysis of RR-interval and mean arterial pressure changes evoked by intravenous (i.v.) injections of methoxamine and nitroprusside. HRV at rest was calculated from high-resolution electrocardiogram-recordings.', 'In MI-rats heart rate was similar to SH-rats, mean arterial pressure was lower and both BRS and HRV were markedly reduced. Zatebradine (0.5 mg/kg i.v.) reduced heart rate in MI-rats from 400 +/- 15 to 350 +/- 19 and in SH-rats from 390 +/- 19 to 324 +/- 6 beats/min without changing mean arterial pressure. Both BRS and HRV were restored in MI- and further increased in SH-rats by the drug. Effects of 0.05, 0.5 and 5 mg/kg zatebradine revealed a dose-dependency of heart rate reduction. The lowest dose enhanced reflex bradycardia despite little effect on heart rate and lack of effect on both reflex tachycardia and HRV.\Question: Does the bradycardic agent zatebradine enhance baroreflex sensitivity and heart rate variability in rats early after myocardial infarction?
[A]: Both BRS and HRV are reduced in rats early after MI, indicating a depressed reflex and tonic vagal activity. Treatment with zatebradine enhances both BRS and HRV. These data suggest that the drug has both peripheral and central effects, leading to an increase of vagal control of heart rate.

[Q]: Context: Increased arterial stiffness has been found in patients with chronic high-grade inflammatory diseases. Whether mitigation of low-grade systemic inflammation, through a low-cholesterol/low-saturated fat diet, may have a role in improving arterial stiffness is still untested.', 'We investigated whether variations in blood lipids and plasma C-reactive protein induced by low-cholesterol/low-saturated fat diet are associated with variations in large-artery stiffness in hypercholesterolaemia.', 'Thirty-five patients with primary hypercholesterolaemia and 15 normal control subjects were recruited for the study. Hypercholesterolaemic patients followed an 8-week low-cholesterol/low-saturated fat diet (30% total fat, 5% saturated fat, cholesterol <200 mg/daily). Anthropometric characteristics, blood lipids, plasma C-reactive protein and arterial stiffness were measured at baseline and after the diet.', 'Arterial stiffness and C-reactive protein levels were higher in hypercholesterolaemic patients than in controls. Significant reductions in body weight (2 kg, 3%), plasma total cholesterol (13.4 mg/dl, 5.3%), low-density lipoprotein cholesterol (11.2 mg/dl, 6.4%), C-reactive protein (0.7 mg/l, 39%) and arterial stiffness (from 8.9+/-2.0 to 8.1+/-1.9 m/s, 11%) were achieved among hypercholesterolaemic patients after the 8-week diet (P<0.05 for all). Bivariate correlations and multivariate analysis showed reduction in arterial stiffness after short-term diet to be associated with reduction of plasma C-reactive protein levels (r=0.59, beta=0.38, P<0.05 for both).\Question: Is attenuation of inflammation with short-term dietary intervention associated with a reduction of arterial stiffness in subjects with hypercholesterolaemia?
[A]:
Short-term low-cholesterol/low-saturated fat diet in hypercholesterolaemia may be effective in improving large artery stiffness, likely through the mitigation of low-grade systemic inflammation.