U@Cs(4)-C82: A Different Cage Isomer with Reactivity Controlled by U-Sumanene Interaction.

Actinide endohedral metallofullerenes (EMFs) are a fullerene family that possess unique actinide-carbon cage host-guest molecular and electronic structures. In this work, a novel actinide EMF, U@Cs(4)-C82, was successfully synthesized and characterized, and its chemical reactivity was investigated. Crystallographic analysis shows that U@Cs(4)-C82, a new isomer of U@C82, has a Cs(4)-C82 cage, which has never been discovered in the form of empty or endohedral fullerenes. Its unique chemical reactivities were further revealed through the Bingel-Hirsch reaction and carbene addition reaction studies. The Bingel-Hirsch reaction of U@Cs(4)-C82 shows exceptionally high selectivity and product yield, yielding only one major addition adduct. Moreover, the addition sites for both reactions are unexpectedly located on adjacent carbon atoms far away from the actinide metal, despite the nucleophilic (Bingel-Hirsch) and electrophilic (carbene addition) nature of either reactant. Density functional theory (DFT) calculations suggest that this chemical behavior, unprecedented for EMFs, is directed by the unusually strong interaction between U and the sumanene motif of the carbon cage in U@Cs(4)-C82, which makes the energy increase when it is disrupted. This work reveals remarkable chemical properties of actinide EMFs originating from their unique electronic structures and highlights the key role of actinide-cage interactions in the determination of their chemical behaviors.

Hyperacute hyponatremia mimicking acute ischemic stroke.

We present a case of hyperacute hyponatremia with stroke like symptoms on presentation. Symptoms included confusion, left-sided facial droop, right-sided hemiparesis, dysarthria and aphasia, with an NIH stroke score of 5. Sodium level at the time of presentation was 119 mmol/L which dropped acutely from 138 mmol/L seven hours prior. Symptoms improved after treatment with 3% saline and no evidence of stroke, intracranial hemorrhage or space-occupying lesion was seen on imaging. The most likely cause of the hyponatremia was increased free water consumption and ADH surge. The patient remained symptom free after discharge with resolution of hyponatremia. Acute hyponatremia can cause focal neurological complaints and deficits, mimicking acute ischemic stroke. We advise clinicians to be aware of this entity when considering interventions for possible acute ischemic stroke and evaluating a patient with focal neurological deficits.