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Abstract. We present lithium abundances for ∼50 X-ray selected candidate members of the 30-50 Myr old open clusters IC 2602 and IC 2391. These data enlarge and extend to cooler temperatures previous Li surveys of these clusters by Stauffer et al. (1989) and Randich et al. (1997). We also give for the first time an estimate of the metallicity of the two clusters which turns out to be close to solar. Radial velocity measurements together with Hα chromospheric emission and the presence/absence of other spectroscopic features are used to ascertain the membership status for the sample stars not yet confirmed as cluster members; rotational velocities have also been determined for all sample stars. Stars more massive than ∼1 M in both clusters show no sign of significant Li depletion, while lower mass stars are all lithium depleted, with the amount of Li depletion increasing to cooler temperatures. We confirm that the late-G and early-K stars in IC 2602 present a star-to-star scatter in Li abundances similar to, but not as large as the one in the Pleiades. A scatter is also seen among late-K and M dwarfs. Unlike in the Pleiades and Alpha Per clusters, the scatter among early-K stars in IC 2602 shows only marginal correlation with rotation. Our data suggest that the drop-off of lithium towards lower masses may start at an earlier color in IC 2391 than in IC 2602, but larger cluster samples are needed to confirm this result. In addition, whereas G and early K stars in the two clusters are, on average, more Li rich than their counterparts in the Pleiades, a fraction of the coolest stars, in particular in IC 2391, are as depleted as the lowest-Li Pleiades stars of the same mass. If they continue depleting Li on their way to the main sequence, they are expected to be more Li depleted than the Pleiades at the age of the latter cluster.

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.

Purpose of reviewMyotonic dystrophy type 1 (DM1) is a severe, progressive genetic disease that affects between 1 in 3,000 and 8,000 individuals globally. No evidence-based guideline exists to inform the care of these patients, and most do not have access to multidisciplinary care centers staffed by experienced professionals, creating a clinical care deficit.Recent findingsThe Myotonic Dystrophy Foundation (MDF) recruited 66 international clinicians experienced in DM1 patient care to develop consensus-based care recommendations. MDF created a 2-step methodology for the project using elements of the Single Text Procedure and the Nominal Group Technique. The process generated a 4-page Quick Reference Guide and a comprehensive, 55-page document that provides clinical care recommendations for 19 discrete body systems and/or care considerations.SummaryThe resulting recommendations are intended to help standardize and elevate care for this patient population and reduce variability in clinical trial and study environments.

The nondystrophic myotonias are rare muscle hyperexcitability disorders caused by gain-of-function mutations in the SCN4A gene or loss-of-function mutations in the CLCN1 gene. Clinically, they are characterized by myotonia, defined as delayed muscle relaxation after voluntary contraction, which leads to symptoms of muscle stiffness, pain, fatigue, and weakness. Diagnosis is based on history and examination findings, the presence of electrical myotonia on electromyography, and genetic confirmation. In the absence of genetic confirmation, the diagnosis is supported by detailed electrophysiological testing, exclusion of other related disorders, and analysis of a variant of uncertain significance if present.