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: To introduce an elastomeric continuous infusion pump for pain control after outpatient orbital implant surgery.', 'Retrospective, noncomparative consecutive case series of all patients undergoing enucleation, evisceration, or secondary orbital implantation using the On-Q pain system between August 2004 and January 2006. Postoperative pain score, need for narcotics, and adverse events were recorded. The On-Q catheter is inserted intraoperatively through the lateral lower eyelid into the muscle cone under direct visualization, prior to the orbital implant placement. The On-Q system continually infuses anesthesia (bupivacaine) to the retrobulbar site for 5 days.', 'Among 20 patients, mean postoperative period pain score, with On-Q in place, was 1.3 (scale of 0 to 10). Nine patients (45%) did not need any adjunctive oral narcotics. Two patients experienced postoperative nausea. One catheter connector leaked, thereby decreasing delivery of retrobulbar anesthetic resulting a pain level of 6, the highest level in the study. There were no postoperative infections. No systemic toxic effects from bupivacaine were observed clinically.\Question: Do on-Q pump for pain control after orbital implant surgery?
[A]: The On-Q pain pump is widely available, low cost, and requires minimal patient manipulation for the use in orbital implant surgery. The device was safe and appeared to minimize postoperative pain in the authors' case series.

[Q]: Context: Monocytes are cellular components of wound repair, arteriogenesis, and atherogenesis. Vascular endothelial growth factor (VEGF)-A and placental growth factor recruit monocytes to sites of arteriogenesis via stimulation of VEGF receptor-1 (VEGFR-1). The chemotactic response of monocytes to VEGF-A is attenuated in individuals with diabetes mellitus (DM). This VEGF resistance correlates with impaired collateral growth. The aim of this study is to elucidate the molecular basis of VEGF resistance and impaired monocyte response in DM.', 'Phosphorylation of Akt, p38, and extracellular signal-regulated kinase 1/2 (ERK1/2) could be stimulated with either placental growth factor-1 or VEGF-A in monocytes from non-DM but not DM individuals. In contrast, formyl-methionyl-leucyl-phenylalanine caused a comparable activation of these molecules in both DM and non-DM monocytes. Baseline phosphorylation of Akt, p38, and ERK1/2 was significantly elevated in monocytes from DM compared with non-DM subjects. Of note, H(2)O(2) activated Akt, p38, and ERK1/2 in non-DM monocytes ex vivo. Protein tyrosine phosphatases had stronger oxidative modifications in monocytes from DM than from non-DM individuals, which reflects functional protein tyrosine phosphatase inhibition, similar to that seen after H(2)O(2) challenge. Overall, protein tyrosine phosphatase and protein tyrosine phosphatase-1B activity were reduced in DM monocytes. DM monocytes revealed higher expression of the receptor for advanced glycation end products. Stimulation with advanced glycation end products ligands resulted in activation of non-DM monocytes and inhibition of VEGFR-1-mediated chemotaxis. The elevated baseline phosphorylation/activation of Akt, p38, and ERK1/2 in DM monocytes likely causes the resistance to further stimulation with specific stimuli such as VEGF-A, revealing a molecular explanation of the DM-related signal transduction defect.\Question: Does diabetes mellitus activate signal transduction pathways resulting in vascular endothelial growth factor resistance of human monocytes?
[A]: We propose that elevated advanced glycation end products expression and increased oxidative stress in diabetic monocytes lead to activation of VEGFR-1-related signaling pathways and to desensitization of VEGFR-1 responses. These data establish VEGF resistance as a novel molecular concept for DM-related cellular dysfunction.

[Q]: Context: We investigated whether or not fibrinogen is related to the cardiovascular risk profile and complications in hypertensive subjects.', 'Plasma fibrinogen and laboratory tests including factor VII, homocysteine and microalbuminuria were evaluated in 127 consecutive hypertensive subjects stratified according to cardiovascular risk. Parameters were age, gender, smoking, cholesterol, diabetes, target organ damage: left ventricular hypertrophy (LVH), carotid atherosclerotic complications and retinical vessels.', 'Fibrinogen levels were significantly different between patients according to risk levels (low 290+/-73, n=20, high 342+/-94 mg/dl, n=39, very high risk 350+/-72, n=29, p=0.01), hypertension grade (II-III) and organ damage. Fibrinogen was significantly higher in patients with more severe carotid atherosclerotic lesions and vascular retinal lesions (grades II-III vs 0 and I). Also in patients, matched for age and sex, without and with carotid atherosclerotic lesions, fibrinogen was significantly higher in the latter group. No significant differences were found on the basis of IVS, creatinine and microalbuminuria. In hypertensive patients, fibrinogen directly correlated with age, by multiple linear regression. In hypertensive patients with diabetes, fibrinogen was significantly higher (466+/-176 mg/dL, n=14) than in those hypertensive without diabetes (333+/-87 mg/dL, n=113, p=0.001) and in all patients there was a a significant correlation (r=0.474, p<0.001) between blood glucose and fibrinogen.\Question: Are elevated plasma fibrinogen levels in patients with essential hypertension related to vascular complications?
[A]:
Hyperfibrinogenemia is a marker of vascular damage and could be an important factor contributing to the evolution of the complications.