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.

We investigated whether a computed tomography (CT)-based score could predict a large infarct (≥ 80 mL) on early diffusion-weighted magnetic resonance imaging (DWI).', 'Acute stroke patients considered for endovascular therapy within 8 hours of the onset of symptoms were included. The Alberta Stroke Program Early Computed Tomography Score (ASPECTS) was determined on noncontrast CT and computed tomography angiography source images (CTA-SI). Limited collateral flow was defined as less than 50% collateral filling on CTA-SI.', 'Fifty-six patients were analyzed. National Institutes of Health Stroke Scale score was 20 (15-24) in the large infarct group and 16 (11-20) in the small infarct group (P = .049). ASPECTS on noncontrast CT and CTA-SI was 5 (3-8) and 3 (2-6) in the large infarct group and 9 (8-10) and 8 (7-9) in the small infarct group (both P < .001), respectively. Limited collateral flow was frequent in the large infarct group than in the small infarct group (92% vs. 11%, P < .001). Multivariate analysis found that CTA-SI ASPECTS less than or equal to 5 (odds ratio [OR], 40.55; 95% confidence interval [CI], 1.10-1493.44; P = .044) and limited collateral flow (OR, 114.64; 95% CI, 1.93-6812.79; P = .023) were associated with a large infarct. Absence of ASPECTS less than or equal to 5 and limited collateral flow on CTA-SI predicted absence of a large infarct with a sensitivity of .89, specificity of 1.00, positive predictive value of 1.00, and negative predictive value of .71.
Do collateral flow and brain changes on computed tomography angiography predict infarct volume on early diffusion-weighted imaging?

This study investigated the isolated and combined effects of heat [temperate (22\xa0°C/30\xa0% rH) vs. hot (35\xa0°C/40\xa0% rH)] and hypoxia [sea level (FiO2 0.21) vs. moderate altitude (FiO2 0.15)] on exercise capacity and neuromuscular fatigue characteristics.', 'Eleven physically active subjects cycled to exhaustion at constant workload (66\xa0% of the power output associated with their maximal oxygen uptake in temperate conditions) in four different environmental conditions [temperate/sea level (control), hot/sea level (hot), temperate/moderate altitude (hypoxia) and hot/moderate altitude (hot\xa0+\xa0hypoxia)]. Torque and electromyography (EMG) responses following electrical stimulation of the tibial nerve (plantar-flexion; soleus) were recorded before and 5\xa0min after exercise.', 'Time to exhaustion was reduced (P\xa0<\xa00.05) in hot (-35\xa0±\xa015\xa0%) or hypoxia (-36\xa0±\xa014\xa0%) compared to control (61\xa0±\xa028\xa0min), while hot\xa0+\xa0hypoxia (-51\xa0±\xa020\xa0%) further compromised exercise capacity (P\xa0<\xa00.05). However, the effect of temperature or altitude on end-exercise core temperature (P\xa0=\xa00.089 and P\xa0=\xa00.070, respectively) and rating of perceived exertion (P\xa0>\xa00.05) did not reach significance. Maximal voluntary contraction torque, voluntary activation (twitch interpolation) and peak twitch torque decreased from pre- to post-exercise (-9\xa0±\xa01, -4\xa0±\xa01 and -6\xa0±\xa01\xa0% all trials compounded, respectively; P\xa0<\xa00.05), with no effect of the temperature or altitude. M-wave amplitude and root mean square activity were reduced (P\xa0<\xa00.05) in hot compared to temperate conditions, while normalized maximal EMG activity did not change. Altitude had no effect on any measured parameters.
Does combining heat stress and moderate hypoxia reduce cycling time to exhaustion without modifying neuromuscular fatigue characteristics?

Stroke is a leading cause of disability. However, there is no pharmacological therapy available for promoting recovery. Although treatment of stroke with cystamine has gained increasing interest, the detailed mechanisms underlying this process remain elusive. Thus, our aim is to examine the effect of cystamine on the function recovery after stroke and investigate further cystamine mechanisms.', 'Adult male C57BL/6J mice were subjected to photothrombotic model of focal stroke or sham operation. Cystamine or saline was administered intraperitoneally at 24\xa0h after stroke. Functional recovery was analyzed using behavioral tests; axon remodeling was analyzed using magnetic resonance diffusion tensor imaging (DTI) and histological assessment. ANA-12, an antagonist of tropomyosin-related kinase B (TrkB), was administrated to examine the mechanisms underlying the neuroprotection mediated by cystamine.', 'Treatment with cystamine resulted in amelioration of impaired function with concomitant enhancement of axonal remodeling. Cystamine treatment significantly increased brain-derived neurotrophic factor (BDNF) levels and phosphorylation of TrkB in brain after stroke. Cystamine significantly enhanced neuronal progenitor cell proliferation, neuronal survival, and plasticity through BDNF/TrkB pathway.

Does cystamine improve functional recovery via axon remodeling and neuroprotection after stroke in mice?