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: In maternal trauma, the Kleihauer-Betke (KB) test has traditionally been used to detect transplacental hemorrhage (TPH), so that Rh-negative women could receive appropriate Rh immune prophylaxis. Reasoning that the magnitude of TPH would reflect uterine injury, we evaluated Kleihauer-Betke testing as an independent predictor of preterm labor (PTL) after maternal trauma.', 'Admissions to the Shock Trauma Center, University of Maryland, from January 1996 to January 2002, were reviewed. Of 30,362 trauma patients admitted, 166 were pregnant, and 93 of these underwent electronic fetal monitoring. Their records were abstracted for demographics, injury type, three separate trauma scores, documented uterine contractions, PTL (contractions with progressive cervical change), and serious perinatal complications. In 71 cases, transplacental hemorrhage was assessed by maternal KB test.', 'TPH, defined as KB-positive for greater than 0.01 mL of fetal blood in the maternal circulation, occurred in 46 women. Forty-four had documented contractions (25 had overt PTL) and 2 had no contractions. In 25 women with a negative KB test, none had uterine contractions. All patients with contractions or PTL had positive KB tests. By logistic regression, KB test result was the single risk factor associated with PTL (p < 0.001; likelihood ratio, 20.8 for positive KB test). Compared with other sites, abdominal trauma was associated more often with uterine contractions (p < 0.001), PTL (p = 0.001), and a positive KB test (p < 0.001, chi). None of the trauma scoring systems predicted PTL.\Question: Is kleihauer-betke testing important in all cases of maternal trauma?

Ex Output:
Kleihauer-Betke testing accurately predicts the risk of preterm labor after maternal trauma. Clinical assessment does not. With a negative KB test, posttrauma electronic fetal monitoring duration may be limited safely. With a positive KB test, the significant risk of PTL mandates detailed monitoring. KB testing has important advantages to all maternal trauma victims, regardless of Rh status.


Ex Input:
Context: IL-17A is a key driver of human autoimmune diseases, particularly psoriasis.', 'We sought to determine the role of IL-17A in psoriasis pathogenesis and to identify a robust and measurable biomarker of IL-17A-driven pathology.', 'We studied 8 healthy subjects and 8 patients with psoriasis before and after administration of secukinumab, a fully human anti-IL-17A mAb, and used a combination of classical techniques and a novel skin microperfusion assay to evaluate the expression of 170 proteins in blood, nonlesional skin, and lesional skin. For validation, we also tested stored sera from 601 patients with a variety of autoimmune diseases.', 'IL-17A was specifically expressed in lesional compared with nonlesional psoriatic skin (9.8 vs 0.8 pg/mL, P\xa0<\xa0.001). Proteomic and gene transcription analyses revealed dysregulated antimicrobial peptides, proinflammatory cytokines, and neutrophil chemoattractants, levels of which returned to normal after treatment with secukinumab. β-Defensin 2 (BD-2) was identified as a biomarker of IL-17A-driven pathology by comparing protein expression in patients with psoriasis versus that in healthy subjects (5746 vs 82 pg/mL in serum, P\xa0<\xa0.0001; 2747 vs\xa0<218 pg/mL in dermis, P\xa0<\xa0.001), responsiveness to secukinumab therapy, and synergistic induction by IL-17A and TNF-α in epidermal keratinocytes. In a validation set of sera from 601 patients with autoimmune diseases thought to be IL-17A driven, we found that BD-2 levels are most highly increased in patients with psoriatic skin lesions, and in patients with psoriasis, BD-2 levels correlated well with IL-17A levels (r\xa0=\xa00.70, n\xa0=\xa0199, P\xa0<\xa0.001) and Psoriasis Area and Severity Index scores (r\xa0=\xa00.53, n\xa0=\xa0281, P\xa0<\xa0.001).\Question: Is β-Defensin 2 a responsive biomarker of IL-17A-driven skin pathology in patients with psoriasis?

Ex Output:

IL-17A is a primary driver of skin pathology in patients with psoriasis, and serum BD-2 is an easily measurable biomarker of IL-17A-driven skin pathology.