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The fate of the West Antarctic Ice Sheet (WAIS) 1 is the largest cause of uncertainty in long-term sea-level projections. In the last interglacial (LIG) around 125,000 years ago, data suggest that sea level was several metres higher than today 2-4 , and required a significant contribution from Antarctic ice loss, with WAIS usually implicated. Antarctica and the Southern Ocean were warmer than today 5-8 , by amounts comparable to those expected by 2100 under moderate to high future warming scenarios. However, direct evidence about the size of WAIS in the LIG is sparse. Here we use sea salt data from an ice core from Skytrain Ice Rise, adjacent to WAIS, to show that, during most of the LIG, the Ronne Ice Shelf was still in place, and close to its current extent. Water isotope data are consistent with a retreat of WAIS 9 , but seem inconsistent with more dramatic model realizations 10 in which both WAIS and the large Antarctic ice shelves were lost. This new constraint calls for a reappraisal of other elements of the LIG sea-level budget. It also weakens the observational basis that motivated model simulations projecting the highest end of projections for future rates of sea-level rise to 2300 and beyond., Competing Interests: Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Background: Charcot–Marie–Tooth (CMT) disease is an inherited peripheral neuropathy primarily involving motor and sensory neurons. Mutations in INF2, an actin assembly factor, cause two diseases: peripheral neuropathy CMT-DIE (MIM614455) and/or focal segmental glomerulosclerosis (FSGS). These two phenotypes arise from the progressive degeneration affecting podocytes and Schwann cells. In general, nerve enlargement has been reported in 25% of the demyelinating CMT subtype (CMT1), while little is known about the CMT-DIE caused by INF2 variants. Methods: To characterize the peripheral nerve phenotype of INF2-related CMT, we studied the clinical course, imaging, histology, and germline genetic variants in two unrelated CMT-DIE patients. Results: Patient 1 (INF2 p.Gly73Asp) and patient 2 (p.Val108Asp) first noticed walking difficulties at 10 to 12 years old. Both of them were electrophysiologically diagnosed with demyelinating neuropathy. In patient 2, the sural nerve biopsy revealed an onion bulb formation. Both patients developed nephrotic syndrome almost simultaneously with CMT and progressed into renal failure at the age of 16 to 17 years. Around the age of 30 years, both patients manifested multiple hypertrophy of the trunk, plexus, and root in the cervical, brachial, lumbosacral nerves, and cauda equina. The histology of the cervical mass in patient 2 revealed Schwannoma. Exome analysis showed that patient 2 harbors a germline LZTR1 p.Arg68Gly variant, while patient 1 has no schwannomatosis-related mutations. Conclusions: Peripheral neuropathy caused by INF2 variants may lead to the development of multifocal hypertrophy with age, likely due to the initial demyelination and subsequent Schwann cell proliferation. Schwannoma could co-occur when the tissues attain additional hits in schwannomatosis-related genes (e.g., LZTR1). [ABSTRACT FROM AUTHOR]

Background and Objectives: Myoclonus is already associated with a wide variety of drugs and systemic conditions. As new components are discovered, more drugs are suspected of causing this disabling abnormal involuntary movement. This systematic review aims to assess the medications associated with drug-induced myoclonus (DIM). Materials and Methods: Two reviewers assessed the PubMed database using the search term "myoclonus", without language restriction, for articles published between 1955 and 2024. The medications found were divided into classes and sub-classes, and the subclasses were graded according to their level of evidence. Results: From 12,097 results, 1115 were found to be DIM. The subclasses of medications with level A evidence were intravenous anesthetics (etomidate), cephalosporins (ceftazidime, cefepime), fluoroquinolones (ciprofloxacin), selective serotonin reuptake inhibitors (citalopram, escitalopram, paroxetine, sertraline), tricyclic antidepressant (amitriptyline), glutamate antagonist (amantadine), atypical antipsychotics (clozapine, quetiapine), antiseizure medications (carbamazepine, oxcarbazepine, phenytoin, gabapentin, pregabalin, valproate), pure opioid agonist (fentanyl, morphine), bismuth salts, and mood stabilizers (lithium). The single medication with the highest number of reports was etomidate. Drug-induced asterixis is associated with a specific list of medications. The neurotransmitters likely involved in DIM are serotonin, dopamine, gamma-aminobutyric acid (GABA), and glutamate. Conclusions: DIM may be reversible with management that can include drug discontinuation, dose adjustment, and the prescription of a medication used to treat idiopathic myoclonus. Based on the main clinical constellation of symptoms and pathophysiological mechanisms found in this study, DIM can be categorized into three types: type 1 (serotonin syndrome), type 2 (non-serotonin syndrome), and type 3 (unknown). [ABSTRACT FROM AUTHOR]

The classical theory of homogeneous isotropic turbulence predicts that the ratio of transverse to longitudinal structure functions or power spectra is equal to 4/3 in the inertial subrange. For the typical turbulence cascade in the inertial subrange, it also predicts a power law scaling with an exponent of +2/3 and -5/3 for the structure functions and the power spectra, respectively. The goal of this study is to document the statistics of those ratios and exponents derived from aircraft observations, quantify their departures from theoretical predictions, and point out the differences among the aircraft. We estimate the transverse-to-longitudinal ratios and the scaling exponents from in situ high-rate turbulence measurements collected by three research aircraft during four field experiments in two regimes of the marine atmospheric boundary layer: shallow trade-wind convection and subtropical stratocumulus. The bulk values representing the inertial subrange were derived by fitting power law formulae to the structure functions and to the power spectra computed separately for the three components of the turbulent wind velocity measured in horizontal flight segments. The composite scale-by-scale transverse-to-longitudinal ratios were derived by averaging over the segments at common non-dimensional scales. The variability in the results can be attributed to how the wind velocity components are measured on each aircraft. The differences related to environmental conditions, e.g. between characteristic levels and regimes of the boundary layer, are of secondary importance. Experiment-averaged transverse-to-longitudinal ratios are 23 %–45 % smaller than predicted by the theory. The deviations of average scaling exponents with respect to the theoretical values range from - 34 % to + 47 % for structure functions and from - 24 % to + 22 % for power spectra, depending on experiment and velocity component. The composite scale-by-scale transverse-to-longitudinal ratios decrease and increasingly depart from 4/3 with decreasing scale, in contrast to previous experimental studies on local isotropy. The reason for the disagreement in transverse-to-longitudinal ratios between the observations and the theory remains uncertain. [ABSTRACT FROM AUTHOR]