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: Thus far, live attenuated SIV has been the most successful method for vaccinating macaques against pathogenic SIV challenge; however, it is not clear what mechanisms are responsible for this protection. Adoptive transfer studies in mice have been integral to understanding live attenuated vaccine protection in models like Friend virus. Previous adoptive transfers in primates have failed as transferred cells are typically cleared within hours after transfer.', 'Here we describe adoptive transfer studies in Mauritian origin cynomolgus macaques (MCM), a non-human primate model with limited MHC diversity. Cells transferred between unrelated MHC-matched macaques persist for at least fourteen days but are rejected within 36 hours in MHC-mismatched macaques. Cells trafficked from the blood to peripheral lymphoid tissues within 12 hours of transfer.\Question: Do allogeneic lymphocytes persist and traffic in feral MHC-matched mauritian cynomolgus macaques?

Ex Output:
MHC-matched MCM provide the first viable primate model for adoptive transfer studies. Because macaques infected with SIV are the best model for HIV/AIDS pathogenesis, we can now directly study the correlates of protective immune responses to AIDS viruses. For example, plasma viral loads following pathogenic SIV challenge are reduced by several orders of magnitude in macaques previously immunized with attenuated SIV. Adoptive transfer of lymphocyte subpopulations from vaccinated donors into SIV-naïve animals may define the immune mechanisms responsible for protection and guide future vaccine development.


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: In the event of a large scale organophosphate (OP) or nerve agent exposure that depletes a hospital's atropine stores, alternative antidotes should be considered.", 'To test the effects of parenteral administration of ophthalmic antimuscarinic agents on survivability in a rat model of acute, lethal OP poisoning.', "After determining appropriate dosing for comparison, rodents were randomized to receive one of four intraperitoneal antidotes (n = 10 per group): 1) normal saline (0.3 mL), 2) atropine sulfate (10 mg/kg), 3) ophthalmic atropine sulfate (1%; 10 mg/kg), or 4) ophthalmic homatropine (5%; 20 mg/kg). Five minutes after pretreatment, dichlorvos (10 mg/kg) was administered subcutaneously. Mortality rates and time to death were compared by using Fisher's exact test and the Kaplan-Meier method with log rank test, respectively. If the animal was alive at 120 minutes, survival was assumed.", 'Survival in rats pretreated with standard atropine was 100%. Survival in rats pretreated with ophthalmic homatropine and atropine sulfate were 100% (p < 0.001; 95% CI = 0.98 to 1.02) and 90% (p < 0.01; 95% CI = 0.71 to 1.09), respectively, compared with controls (20% survival; 95% CI = 0.04 to 0.45). Time of death ranged between 7 and 19 minutes. Comparison of survival times revealed a statistically significant improvement in experimental groups compared with controls (p < 0.0001).\Question: Does pretreating rats with parenteral ophthalmic antimuscarinic agents decrease mortality from lethal organophosphate poisoning?

Ex Output:

Parenteral pretreatment with ophthalmic preparations of homatropine or atropine sulfate was equal to standard atropine in preventing lethality in this rat model of acute, lethal OP poisoning.