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.
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Question: Context: The expression of growth-associated protein 43 (GAP-43), a marker of axonal growth, in the dorsal root ganglion (DRG) neurons innervating the lumbar intervertebral disc was assessed using the retrograde tracing method and immunohistochemistry.', 'To study whether disc inflammation affects GAP-43 expression in DRG neurons innervating the disc in rats.', 'Persistent inflammation and nerve ingrowth into the inner layer of degenerated discs can be a cause of discogenic pain. Although the presence of GAP-43-expressing nerve fibers in painful discs has been reported, the expression of GAP-43 in DRG neurons innervating the disc has not been studied.', "Seven days after the application of Fluoro-Gold to the L5-L6 disc, 50 microL of saline (n = 10, control group) or complete Freund's adjuvant (n = 10, inflammatory group) was applied to the disc in rats. Ten days after the Fluoro-Gold application, T13-L5 DRGs were double-stained with GAP-43 and either calcitonin gene-related peptide or isolectin B4 (IB4).", 'The percentage of Fluoro-Gold-labeled neurons that were positive for GAP-43 was significantly higher in the inflammatory group (44%) than in the control group (24%, P < 0.001). In both groups, the majority of GAP-43-positive neurons were small and positive for calcitonin gene-related peptide but not IB4.\Question: Does disc inflammation potentially promote axonal regeneration of dorsal root ganglion neurons innervating lumbar intervertebral disc in rats?

Answer: The present results suggest that disc inflammation potentially promotes axonal growth of DRG neurons innervating the disc. In light of the strong correlation between the expression of calcitonin gene-related peptide and nerve growth factor receptor, it is most likely that nerve growth factor-sensitive DRG neurons extend their axons following disc inflammation.


Question: Context: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.', "Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean\u2009±\u2009SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (μL/min) was similar between C57 (171\u2009±\u200917) and ApoE (140\u2009±\u200926) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112\u2009±\u20098, ~\u2009-\u200935%, p\u2009<\u20090.05) and ApoE (61\u2009±\u200910, ~\u2009-\u200956%, p\u2009<\u20090.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73\u2009±\u20097; OVX: 73\u2009±\u20098, p\u2009<\u20090.05) when compared to C57 animals (Sham: 49\u2009±\u20093; OVX: 60\u2009±\u20094), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1\u2009±\u20095.7; OVX: 33.7\u2009±\u20094.7) and ApoE sham animals (26.4\u2009±\u20093.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6\u2009±\u20095.8, p\u2009<\u20090.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2\u2009±\u20090.4; C57 OVX: 22.9\u2009±\u20091.0; ApoE Sham: 13.9\u2009±\u20090.7; ApoE OVX: 34.0\u2009±\u20091.4 au x 103, p\u2009<\u20090.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0\u2009±\u20090; C57 OVX: 0\u2009±\u20090; ApoE Sham: 6.8\u2009±\u20091.6; ApoE OVX: 5.2\u2009±\u20090.8% x 10-2, p\u2009<\u20090.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78\u2009±\u20090.04; ApoE: 0.81\u2009±\u20090.04 au, p\u2009<\u20090.05) when compared to sham animals (C57:1.00\u2009±\u20090.04; ApoE: 1.03\u2009±\u20090.03 au).\Question: Do endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice?

Answer: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.


Question: Context: Paradoxical embolism via persistent foramen ovale (PFO) is suspected to be a frequent cause of stroke in younger patients. We investigated whether the prevalence of the risk factors for venous thrombosis factor V Leiden (FVL) and prothrombin G20210A mutation (PT G20210A) is increased in this group of patients.', 'We examined FVL and PT G20210A mutation in 220 patients (group 1) with cerebral ischemia associated with a PFO and without other etiology, in 196 patients with cerebral ischemia of an etiology other than PFO (group 2), and in 362 healthy subjects (group 3) from the same region in Germany.', 'Heterozygosity for the PT G20210A mutation was more common in group 1 (5.0%) than in group 3 (1.4%; sex- and age-adjusted odds ratio 3.66; 95% CI 1.25-10.75; p = 0.01). By contrast, the mutation was not more common in group 2 (2.6%; odds ratio 1.50; 95% CI 0.42-5.41; p = 0.5). Prevalences of FVL were not different between groups.\Question: Is prothrombin G20210A mutation , but not factor V Leiden , a risk factor in patients with persistent foramen ovale and otherwise unexplained cerebral ischemia?

Answer:
We identified PT G20210A but not FVL - the strongest genetic risk factor for deep venous thrombosis - to be significantly associated with stroke attributed to PFO. These findings rise doubts about the concept of paradoxical brain embolism as the dominating mechanism in stroke associated with PFO.