Humans, but no other animal, make meaningful use of spoken language. What is unclear, however, is whether this capacity depends on a unique constellation of perceptual and neurobiological mechanisms, or whether a subset of such mechanisms are shared with other organisms. To explore this problem, we conducted parallel experiments on human newborns and cotton-top tamarin monkeys to assess their ability to discriminate unfamiliar languages. Using a habituation-dishabituation procedure, we show that human newborns and tamarins can discriminate sentences from Dutch and Japanese, but not if the sentences are played backwards. Moreover, the cues for discrimination are not present in backward speech. This suggests that the human newborns' tuning to certain properties of speech relies on general processes of the primate auditory system.A fundamental question in the study of language evolution and acquisition is the extent to which humans are innately endowed with specialized capacities to comprehend and produce speech. Theoretical arguments have been used to argue that language acquisition must be based on an innately specified language faculty (1, 2), but the precise nature and extent of this "language organ" is mainly an empirical matter, which notably requires studies of human newborns as well as non-human animals (3-5). With respect to studies of humans, we already know that newborns as young as four days old have the capacity to discriminate phonemes categorically (6) and perceive well-formed syllables as units (7-9); they are sensitive to the rhythm of speech, as shown in experiments where newborns distinguish sentences from languages that have different rhythmic properties, but not from languages that share the same rhythmic structure (10, 11); however newborns don't discriminate languages when speech is played backwards (10), and neurophysiological studies suggest that both infants and adults process natural speech differently from backwards speech (12, 13). All of these studies indicate that humans are born with capacities that facilitate language acquisition, and that seem well attuned to the properties of speech. Studies of non-human animals, however, show that some of these capacities may predate our hominid origins. For example, insects, birds, non-primate mammals, and primates process their own, species-typical Correspondence should be addressed to Franck Ramus. E-mail: f.ramus@ucl.ac.uk. Present address: Institute of Cognitive Neuroscience, 17 Queen Square, London WC1N 3AR, GB. sounds in a categorical manner, and some of these species perceive speech categorically (14-18).Our aim in this paper is to extend the comparative study of speech perception in three directions. First, we have conducted joint experiments on human newborns and on monkeys using the same design and the same material. Second, whereas most studies of non-human animal speech perception involve extensive training prior to testing on a generalization task, our experimental approach -the habituationdishabituation paradigm -involves no traini...

Background Among asymptomatic patients with severe carotid artery stenosis but no recent stroke or transient cerebral ischaemia, either carotid artery stenting (CAS) or carotid endarterectomy (CEA) can restore patency and reduce long-term stroke risks. However, from recent national registry data, each option causes about 1% procedural risk of disabling stroke or death. Comparison of their long-term protective effects requires large-scale randomised evidence.Methods ACST-2 is an international multicentre randomised trial of CAS versus CEA among asymptomatic patients with severe stenosis thought to require intervention, interpreted with all other relevant trials. Patients were eligible if they had severe unilateral or bilateral carotid artery stenosis and both doctor and patient agreed that a carotid procedure should be undertaken, but they were substantially uncertain which one to choose. Patients were randomly allocated to CAS or CEA and followed up at 1 month and then annually, for a mean 5 years. Procedural events were those within 30 days of the intervention. Intention-to-treat analyses are provided. Analyses including procedural hazards use tabular methods. Analyses and meta-analyses of non-procedural strokes use Kaplan-Meier and log-rank methods. The trial is registered with the ISRCTN registry, ISRCTN21144362.

Background: Supervised exercise is recommended for the management of peripheral artery disease (PAD); however, the uptake is limited. Structured home exercise programmes may be more feasible, but their effectiveness is unclear. This systematic review and meta-analysis examined the benefit of structured home exercise programmes for treating PAD in comparison to controls not receiving an exercise programme.Methods: A literature search was conducted to identify RCTs comparing structured home exercise with controls not receiving an exercise programme among patients with PAD. To be included, studies had to report outcomes from treadmill or corridor walking tests, or objective assessment of physical activity. Inverse variance-weighted meta-analysis was performed to compare changes in maximum walking distance and intermittent claudication onset distance in treadmill tests, walking distance during a 6-min walking test, and physical activity measured using a pedometer or accelerometer. Summarized results are presented in terms of standard deviation differences.Results: Eleven randomized trials involving 807 patients were included. Follow-up ranged from 2 to 24 months; only one trial included follow-up beyond 12 months. Meta-analyses showed that structured home exercise programmes led to significant improvements in maximum walking distance (mean difference (MD) 0⋅32, 95 per cent c.i. 0⋅15 to 0⋅50; P < 0⋅001), intermittent claudication onset distance (MD 0⋅45, 0⋅27 to 0⋅62; P < 0⋅001), walking distance in a 6-min walking test (MD 0⋅28, 0⋅09 to 0⋅47; P = 0⋅004) and physical activity (MD 0⋅27, 0⋅11 to 0⋅43; P = 0⋅001). Conclusion:This meta-analysis suggests that structured home exercise programmes are effective at improving walking performance and physical activity in the short term for patients with PAD.

A common SNP within the MMP3 promoter region, previously suggested to increase MMP3 expression, appears to be a moderate risk factor for AAA.

BackgroundPeripheral artery disease (PAD) is associated with impaired mobility and a high rate of mortality. The aim of this systematic review was to investigate whether reduced lower extremity performance was associated with an increased incidence of cardiovascular and all‐cause mortality in people with PAD.Methods and ResultsA systematic search of the MEDLINE, EMBASE, SCOPUS, Web of Science, and Cochrane Library databases was conducted. Studies assessing the association between measures of lower extremity performance and cardiovascular or all‐cause mortality in PAD patients were included. A meta‐analysis was conducted combining data from commonly assessed performance tests. The 10 identified studies assessed lower extremity performance by strength tests, treadmill walking performance, 6‐minute walk, walking velocity, and walking impairment questionnaire (WIQ). A meta‐analysis revealed that shorter maximum walking distance was associated with increased 5‐year cardiovascular (unadjusted RR=2.54, 95% CI 1.86 to 3.47, P<10−5, n=1577, fixed effects) and all‐cause mortality (unadjusted RR=2.23 95% CI 1.85 to 2.69, P<10−5, n=1710, fixed effects). Slower 4‐metre walking velocity, a lower WIQ stair‐climbing score, and poor hip extension, knee flexion, and plantar flexion strength were also associated with increased mortality. No significant associations were found for hip flexion strength, WIQ distance score, or WIQ speed score with mortality.ConclusionsA number of lower extremity performance measures are prognostic markers for mortality in PAD and may be useful clinical tools for identifying patients at higher risk of death. Further studies are needed to determine whether interventions that improve measures of lower extremity performance reduce mortality.

This study suggests that PWS is greater in symptomatic or ruptured AAA than in asymptomatic intact AAA.

These findings suggest that clinically important AAA events may be reduced in patients with diabetes who are prescribed metformin, but not those with diabetes receiving other treatments. A randomised controlled trial is needed to definitively test whether metformin reduces AAA related clinical events in patients with small AAAs who do not have diabetes.

IMPORTANCECurrently there is no drug therapy for abdominal aortic aneurysm (AAA).OBJECTIVE To test the efficacy of the angiotensin receptor blocker telmisartan in slowing AAA growth in the Telmisartan in the Management of Abdominal Aortic Aneurysm (TEDY) trial. DESIGN, SETTING, AND PARTICIPANTSA randomized, double-blind, placebo-controlled trial recruited participants between September 6, 2011, and October 5, 2016, to evaluate the efficacy of telmisartan treatment in patients with AAA. Participants with 35-to 49-mm AAAs recruited from Australia, the Netherlands, and the US were randomized 1:1 to receive telmisartan, 40 mg, or identical placebo. Analyses were conducted according to intention-to-treat principles. Final follow-up was conducted on October 11, 2018, and data analysis was performed between June and November 2019.INTERVENTION Telmisartan, 40 mg, or identical placebo. MAIN OUTCOMES AND MEASURESThe primary outcome of the difference in AAA growth, assessed on core imaging laboratory-read ultrasonographic scanning, was tested with linear mixed-effects models. Other outcomes included effects on blood pressure, computed tomographic (CT)-measured AAA diameter and volume, time to AAA-related events (AAA repair or mortality due to AAA rupture), and health-related quality of life. RESULTSOf 300 intended participants, 210 were enrolled and randomized to receive telmisartan (n = 107) or placebo (n = 103). Of patients included in the intention-to-treat analysis (telmisartan: n = 106, placebo: n = 101), 183 were men (88%); mean (SD) age was 73.5 (7.9) years. At 1 year, participants receiving telmisartan had mean lower systolic (8.9; 95% CI, 4.1-13.8 mm Hg; P < .001) and diastolic (7.0; 4.3-9.8 mm Hg; P < .001) blood pressure levels compared with participants receiving placebo. A total of 188 participants (91%) received at least 2 ultrasonographic scans and 133 participants (64%) had at least 2 CT scans. There was no significant difference in ultrasonographic-assessed AAA growth rates among those assigned telmisartan (1.68 mm/y) or placebo (1.78 mm/y): mean difference, −0.11 mm/y (95% CI, −0.60 to 0.38 mm/y; P = .66). Telmisartan had no significant effects on AAA growth assessed by CT-measured AAA diameter (mean difference, −0.01 mm/y; 95% CI, −0.02 to 0.01 mm/y; P = .23) or volume (mean difference, −0.02 cm 3 /y; 95% CI, −0.04 to 0.00 cm 3 /y; P = .11), AAA-related events (relative risk, 1.35; 95% CI, 0.54-3.35; P = .52), or health-related quality of life (mean difference in physical component score at 24 months, 0.4; 95% CI, 0.4-0.4; P = .80). Hypotensive symptoms (eg, syncope) were twice as common among participants receiving telmisartan compared with placebo (28 [26%] vs 13 [13%]; P = .02), but overall adverse event rates were otherwise similar for both groups.CONCLUSIONS AND RELEVANCE This underpowered study did not show a treatment effect for telmisartan on small AAA growth. Future trials will need to ensure adequate sample size and duration of follow-up.