instruction:
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.
question:
The SARS coronavirus (SARS-CoV) 3a protein functions as an ion channel, induces apoptosis and is important for viral pathogenesis. It is expressed on the cell surface and contains a tyrosine-based sorting motif and a di-acidic motif, which may be crucial for its intracellular trafficking. However the role of these motifs is not fully understood in the case of 3a protein.', 'The subcellular distribution of the 3a protein was studied by immunofluorescence staining of cells transfected with wild type and mutant constructs along with markers for different intracellular compartments. Semi-quantitative RT-PCR was performed to estimate the mRNA where as western blotting was carried out to detect protein levels of wild type and mutant 3a proteins. In vitro transcription- translation was performed to estimate cell free protein synthesis.', 'While the wild type 3a protein is efficiently transported to the plasma membrane, the protein with mutations in the tyrosine and valine residues within the YXXV motif (ΔYXXΦ) accumulated in the Golgi compartment. However the 3a protein with mutations within the EXD di-acidic motif (ΔEXD) showed an intracellular distribution similar to the wild type protein. Increased retention of the ΔYXXΦ protein in the Golgi compartment also increased its association with lipid droplets. The ΔYXXΦ protein also expressed at significantly lower levels compared to the wild type 3a protein, which was reversed with Brefeldin A and Aprotinin.
answer:
Is the YXXΦ motif within the severe acute respiratory syndrome coronavirus ( SARS-CoV ) 3a protein crucial for its intracellular transport?


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:
Animal models suggest a genetic contribution to cerebral susceptibility to ischemia. Family history of stroke (FHxstroke) is a risk factor for ischemic stroke, but there is significant confounding by heritability of hypertension and other intermediate phenotypes, and it is uncertain whether genetic factors have a direct independent influence on cerebral susceptibility to ischemia in man.', 'We related detailed FHxstroke to baseline characteristics and subsequent risk of stroke in 2 population-based incidence studies and a consecutive hospital-referred series of patients with recent transient ischemic attack (TIA).', 'In none of the cohorts or the pooled data (757 patients; 5515 patient years follow-up; 200 ischemic strokes; 126 myocardial infarctions [MIs]) did FHxstroke predict ischemic stroke (odds ratio [OR], 0.87; 95% CI, 0.57 to 1.32). No associations were revealed by analyses stratified by age or hypertension in the proband, FHx(stroke) in parents versus siblings, number of affected relatives, or their age at stroke. FHxstroke was unrelated to presence of ischemic lesions on baseline computed tomography (OR, 0.96; 0.52 to 1.76) or risk of MI during follow-up. There was no bias attributable to any relationship between FHxstroke and risk factor control or medication.
answer:

Does family history of stroke predict risk of stroke after transient ischemic attack?