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.

Input: Consider Input: Context: Inflammation has been implicated in the initiation, progression and manifestation of hypertensive heart disease. We sought to determine the role of monocytes/macrophages in hypertension and pressure overload induced left ventricular (LV) remodeling.', 'We used two models of LV hypertrophy (LVH). First, to induce hypertension and LVH, we fed Sabra salt-sensitive rats with a high-salt diet. The number of macrophages increased in the hypertensive hearts, peaking at 10 weeks after a high-salt diet. Surprisingly, macrophage depletion, by IV clodronate (CL) liposomes, inhibited the development of hypertension. Moreover, macrophage depletion reduced LVH by 17% (p<0.05), and reduced cardiac fibrosis by 75%, compared with controls (p=0.001). Second, to determine the role of macrophages in the development and progression of LVH, independent of high-salt diet, we depleted macrophages in mice subjected to transverse aortic constriction and pressure overload. Significantly, macrophage depletion, for 3 weeks, attenuated LVH: a 12% decrease in diastolic and 20% in systolic wall thickness (p<0.05), and a 13% in LV mass (p=0.04), compared with controls. Additionally, macrophage depletion reduced cardiac fibrosis by 80% (p=0.006). Finally, macrophage depletion down-regulated the expression of genes associated with cardiac remodeling and fibrosis: transforming growth factor beta-1 (by 80%) collagen type III alpha-1 (by 71%) and atrial natriuretic factor (by 86%).\Question: Do macrophages dictate the progression and manifestation of hypertensive heart disease?

Output: Macrophages mediate the development of hypertension, LVH, adverse cardiac remodeling, and fibrosis. Macrophages, therefore, should be considered as a therapeutic target to reduce the adverse consequences of hypertensive heart disease.


Input: Consider Input: Context: To describe technical challenges encountered using the Ovation endograft for abdominal aortic aneurysms and suggest tips and maneuvers for successful management.', "Deployment of the Ovation's unsupported main body is often associated with the anteroposterior arrangement of the limb gates instead of the usual side-by-side configuration, rendering contralateral catheterization challenging. Successful catheterization of the contralateral limb can be confirmed by lateral deviation of the ipsilateral stiff guidewire caused by balloon inflation within the contralateral limb. Moreover, failure to cannulate the contralateral limb gate due to persistent impingement of the guidewire or compromise of the inflated rings can be overcome using the transbrachial antegrade approach.\Question: Does technical challenge encountered during deployment of the ovation abdominal aortic stent-graft system?

Output: Awareness of certain aspects associated with the use of the Ovation device and adoption of the adjunctive techniques herein described helps the interventionist avoid unexpected challenges or manage technical difficulties to maximize the device's safety and effectiveness.


Input: Consider Input: Context: Dystrophic epidermolysis bullosa pruriginosa (DEB-Pr; OMIM 604129) is a rare manifestation of dystrophic epidermolysis bullosa (DEB), characterized by pruritus, nodular prurigo-like lesions and fragility of the skin mainly in the extremities. Fewer than 40 patients with autosomal dominant or recessive inheritance, or sporadic DEB-Pr, have been described in the literature.', 'To disclose mutations in DEB-Pr and to elucidate the role of other pathogenic factors which may influence the pruriginous phenotype.', 'Seven patients with typical clinical features of DEB-Pr were studied.', 'In all patients, mutations in the gene encoding collagen VII (COL7A1) were disclosed, two of them novel (p.G2623V, p.E2736K). Three mutations were dominant, three recessive and one de novo. In the families with dominant DEB there were one or more members with DEB-Pr, but also at least one affected sibling who did not develop DEB-Pr. In six of seven patients, the clinical history revealed factors that initially induced pruritus, such as atopy, pregnancy, thyroid hormone imbalance, diabetes, infections and contact sensitization. Common filaggrin mutations were ruled out in all patients and normal filaggrin staining was found in the skin samples.\Question: Is dystrophic epidermolysis bullosa pruriginosa associated with frequent FLG gene mutations?


Output: DEB-Pr develops as a result of COL7A1 gene mutations and acquired phenotype-modifying factors. Filaggrin mutations did not contribute to the pruriginous phenotype in the present patient cohort.