Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
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Question: Hostile neck anatomy is assumed to be associated with increased surgical risk for patients undergoing carotid endarterectomy (CEA) and is often considered a reason to choose carotid stenting or medical management. This retrospective case-control study evaluated whether, and how much, anatomically hostile necks represent a condition of higher surgical risk of early and late mortality and major or minor morbidity.', 'The data for 966 homogeneous CEA patients was prospectively entered in a computer database. Seventy-seven had a hostile neck anatomy due to previous oncologic surgery or neck irradiation, restenoses after CEA, high carotid bifurcation, or bull-like and inextensible neck. A case-control matched-pair cohort study considered sex, age (5-year intervals), and year of operation. Regional anesthesia was used for all operations for atherosclerotic stenosis >or=70%, conforming to the European Carotid Surgery Trial (ECST) in symptomatic and asymptomatic patients, at a single center and by one surgeon or under his direct supervision.', 'The hostile neck patients and the control group were matched for age, sex, carotid-related symptoms, degree of stenoses, and main risk factors for cardiovascular diseases. Intraoperative variables were substantially equivalent in the two groups; however, procedure length and clamping time were, respectively, about 22 minutes (P = .0001) and 7 minutes longer (P = .01) in the hostile neck group. Rates of postoperative mortality and neurologic events were equivalent. Peripheral nerve lesions were multiple and significantly more frequent in the hostile neck patients (21% with >or=1 cranial nerve lesion vs 7% of controls, P = .03), yet all were transient and limited to a few months. The subgroups of patients with hostile neck, restenoses, and bull-like inextensible necks required the longest operative and clamping time, and those with bull-like and high bifurcation had the most frequent cranial nerve dysfunctions. At the respective follow-up of 47 and 45 months, survival curves (P = .48) and the incidence of restenoses and fatal and nonfatal strokes were similar (5 and 4, respectively).

Answer: Does the hostile neck increase the risk of carotid endarterectomy?


Question: Intracellular pathogens have developed elaborate strategies for silent infection of preferred host cells. Chlamydia pneumoniae is a common pathogen in acute infections of the respiratory tract (e.g. pneumonia) and associated with chronic lung sequelae in adults and children. Within the lung, alveolar macrophages and polymorph nuclear neutrophils (PMN) are the first line of defense against bacteria, but also preferred host phagocytes of chlamydiae.', 'We could show that C. pneumoniae easily infect and hide inside neutrophil granulocytes until these cells become apoptotic and are subsequently taken up by macrophages. C. pneumoniae infection of macrophages via apoptotic PMN results in enhanced replicative activity of chlamydiae when compared to direct infection of macrophages, which results in persistence of the pathogen. Inhibition of the apoptotic recognition of C. pneumoniae infected PMN using PS- masking Annexin A5 significantly lowered the transmission of chlamydial infection to macrophages. Transfer of apoptotic C. pneumoniae infected PMN to macrophages resulted in an increased TGF-ss production, whereas direct infection of macrophages with chlamydiae was characterized by an enhanced TNF-alpha response.

Answer: Does chlamydia pneumoniae hide inside apoptotic neutrophils to silently infect and propagate in macrophages?


Question: Cyclooxygenase-1 (COX-1) has been implicated in the pathogenesis of atherothrombosis and is expressed by the major cell types of atherosclerotic lesions. COX-1-mediated platelet thromboxane (TX) production has been proposed to promote both early atherosclerosis and thrombosis. Here, we examined the impact of COX-1 deficiency in bone marrow-derived cells on early atherogenesis in the mouse.', 'LDL receptor (LDLR)(-/-) and apolipoprotein E (apoE)(-/-) recipient mice were lethally irradiated and transplanted with COX-1(-/-) bone marrow. Mice reconstituted with COX-1(-/-) marrow had nearly complete (99.7%) loss of platelet TXA2 and significantly suppressed levels of macrophage and urinary TXA2 metabolites. Serum lipid levels and lipoprotein distributions did not differ between recipients reconstituted with COX-1(+/+) and COX-1(-/-) marrow. Surprisingly, the extent of atherosclerotic lesions in both LDLR(-/-) and apoE(-/-) mice reconstituted with COX-1(-/-) marrow was increased significantly compared with control mice transplanted with COX-1(+/+) marrow. Peritoneal macrophages isolated from LDLR(-/-) mice reconstituted with COX-1(-/-) marrow had increased lipopolysaccharide-induced levels of COX-2 mRNA and protein expression. Fetal liver cell transplantation studies revealed a 30% increase in atherosclerosis in COX-1(-/-)-->LDLR(-/-)mice compared with COX-1(+/+)-->LDLR(-/-)mice, whereas the extent of atherosclerosis was unchanged in COX-1(-/-)/COX-2(-/-)-->LDLR(-/-)mice.

Answer:
Does cyclooxygenase-1 deficiency in bone marrow cells increase early atherosclerosis in apolipoprotein E- and low-density lipoprotein receptor-null mice?