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: Interleukin-8 (IL-8), a CXC chemokine that induces the migration and proliferation of endothelial cells and smooth muscle cells, is a potent angiogenic factor that may play a role in atherosclerosis. Previously, IL-8 has been reported in atherosclerotic lesions and circulating macrophages from patients with atherosclerosis. Therefore, we sought to determine whether IL-8 plays a role in mediating angiogenic activity in atherosclerosis.', 'Homogenates from 16 patients undergoing directional coronary atherectomy (DCA) and control samples from the internal mammary artery (IMA) of 7 patients undergoing bypass graft surgery were assessed for IL-8 content by specific ELISA, immunohistochemistry, and in situ hybridization for IL-8 mRNA. The contribution of IL-8 to net angiogenic activity was assessed using the rat cornea micropocket assay and cultured cells. IL-8 expression was significantly elevated in DCA samples compared with IMA samples (1.71+/-0.6 versus 0.05+/-0.03 ng/mg of total protein; P<0.01). Positive immunolocalization of IL-8 was found exclusively in DCA tissue sections, and it correlated with the presence of factor VIII-related antigen. In situ reverse transcriptase polymerase chain reaction revealed the expression of IL-8 mRNA in DCA tissue. Corneal neovascular response, defined by ingrowth of capillary sprouts toward the implant, was markedly positive with DCA pellets, but no constitutive vessel ingrowth was seen with IMA specimens. Neutralizing IL-8 attenuated both the in vivo corneal neovascular response and the in vitro proliferation of cultured cells.\Question: Is iL-8 an angiogenic factor in human coronary atherectomy tissue?

A: The results suggest that, in human coronary atherosclerosis, IL-8 is an important mediator of angiogenesis and may contribute to plaque formation via its angiogenic properties.
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Q: Context: The greater omentum has been found to be immunologically competent in protecting abdominal organs from inflammation. Anastomotic omentoplasty has been used and proven effective in preventing anastomotic leaks after an esophagectomy. However, pulmonary complications are still a substantial problem after an esophagectomy. This study investigated the benefits of mediastinal transposition of the omentum, a modification of the conventional omental wrapping technique, in controlling overall postoperative intrathoracic complications.', "From January 2010 to March 2015, 208 consecutive patients receiving an open Ivor-Lewis esophagectomy at our institution were retrospectively reviewed. One hundred twenty-one patients with omentum mediastinal transposition were assigned to the transposition group and 87 patients without omental transposition were placed in the non-transposition group. The patients' demographics, postoperative short-term outcomes, and in-hospital cost were documented and analyzed.", 'Mediastinal transposition of the omentum led to a shorter postoperative hospital stay (14 vs. 16 d, P=0.038) and a lower intrathoracic infection rate (30.6% vs. 48.3%, P=0.009). Intrathoracic infection was milder in the transposition group (P=0.005), though a non-significant was found in overall complications (P=0.071). The multivariate logistic regression analyses identified omentum mediastinal transposition (P=0.007, OR=0.415) as an independent protective factor for postoperative intrathoracic infection. The total in-hospital cost was comparable in both groups (P>0.05), whereas the pharmacy cost was lower in the transposition group than in the non-transposition group (¥21,668 vs. ¥27,012, P=0.010).\Question: Does mediastinal transposition of the omentum reduce infection severity and pharmacy cost for patients undergoing esophagectomy?

A: Mediastinal transposition of the omentum decreases the rate and severity of postoperative intrathoracic infection following an open Ivor-Lewis esophagectomy. This result in decreased pharmacy costs, rather than resulting in an increased economic burden sustained by surgical patients.
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Q: Context: Adolescent intermittent alcohol exposure (AIE) has profound effects on neuronal function. We have previously shown that AIE causes aberrant hippocampal structure and function that persists into adulthood. However, the possible contributions of astrocytes and their signaling factors remain largely unexplored. We investigated the acute and enduring effects of AIE on astrocytic reactivity and signaling on synaptic expression in the hippocampus, including the impact of the thrombospondin (TSP) family of astrocyte-secreted synaptogenic factors and their neuronal receptor, alpha2delta-1 (α2δ-1). Our hypothesis is that some of the influences of AIE on neuronal function may be secondary to direct effects on astrocytes.', 'We conducted Western blot analysis on TSPs 1 to 4 and α2δ-1 from whole hippocampal lysates 24 hours after the 4th and 10th doses of AIE, then 24 days after the last dose (in adulthood). We used immunohistochemistry to assess astrocyte reactivity (i.e., morphology) and synaptogenesis (i.e., colocalization of pre- and postsynaptic puncta).', 'Adolescent AIE reduced α2δ-1 expression, and colocalized pre- and postsynaptic puncta after the fourth ethanol (EtOH) dose. By the 10th dose, increased TSP2 levels were accompanied by an increase in colocalized pre- and postsynaptic puncta, while α2δ-1 returned to control levels. Twenty-four days after the last EtOH dose (i.e., adulthood), TSP2, TSP4, and α2δ-1 expression were all elevated. Astrocyte reactivity, indicated by increased astrocytic volume and area, was also observed at that time.\Question: Are adolescent Intermittent Alcohol Exposure : Dysregulation of Thrombospondins and Synapse Formation Associated with Decreased Neuronal Density in the Adult Hippocampus?

A:
Repeated EtOH exposure during adolescence results in long-term changes in specific astrocyte signaling proteins and their neuronal synaptogenic receptor. Continued signaling by these traditionally developmental factors in adulthood may represent a compensatory mechanism whereby astrocytes reopen the synaptogenic window and repair lost connectivity, and consequently contribute to the enduring maladaptive structural and functional abnormalities previously observed in the hippocampus after AIE.
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