New radio (MeerKAT and Parkes) and X-ray (XMM-Newton, Swift, Chandra, and NuSTAR) observations of PSR J1622–4950 indicate that the magnetar, in a quiescent state since at least early 2015, reactivated between 2017 March 19 and April 5. The radio flux density, while variable, is approximately 100× larger than during its dormant state. The X-ray flux one month after reactivation was at least 800× larger than during quiescence, and has been decaying exponentially on a 111 ± 19 day timescale. This high-flux state, together with a radio-derived rotational ephemeris, enabled for the first time the detection of X-ray pulsations for this magnetar. At 5%, the 0.3–6 keV pulsed fraction is comparable to the smallest observed for magnetars. The overall pulsar geometry inferred from polarized radio emission appears to be broadly consistent with that determined 6–8 years earlier. However, rotating vector model fits suggest that we are now seeing radio emission from a different location in the magnetosphere than previously. This indicates a novel way in which radio emission from magnetars can differ from that of ordinary pulsars. The torque on the neutron star is varying rapidly and unsteadily, as is common for magnetars following outburst, having changed by a factor of 7 within six months of reactivation.

Ion pair receptor 3 bearing an anion binding site and multiple cation binding sites has been synthesized and shown to function in a novel binding-release cycle that does not necessarily require displacement to effect release. The receptor forms stable complexes with the test cesium salts, CsCl and CsNO(3), in solution (10% methanol-d(4) in chloroform-d) as inferred from (1)H NMR spectroscopic analyses. The addition of KClO(4) to these cesium salt complexes leads to a novel type of cation metathesis in which the "exchanged" cations occupy different binding sites. Specifically, K(+) becomes bound at the expense of the Cs(+) cation initially present in the complex. Under liquid-liquid conditions, receptor 3 is able to extract CsNO(3) and CsCl from an aqueous D(2)O layer into nitrobenzene-d(5) as inferred from (1)H NMR spectroscopic analyses and radiotracer measurements. The Cs(+) cation of the CsNO(3) extracted into the nitrobenzene phase by receptor 3 may be released into the aqueous phase by contacting the loaded nitrobenzene phase with an aqueous KClO(4) solution. Additional exposure of the nitrobenzene layer to chloroform and water gives 3 in its uncomplexed, ion-free form. This allows receptor 3 to be recovered for subsequent use. Support for the underlying complexation chemistry came from single-crystal X-ray diffraction analyses and gas-phase energy-minimization studies.

Strategies for the design of ligands that combine with metal ions to form high-symmetry coordination assemblies are reviewed. Evaluation of crystal structure evidence reveals that prior design approaches, based on the concept of complementary bonding vector angles, fail to predict the majority of known examples. After explaining the reasons for this failure, it is shown how an alternative approach, de novo structure-based design, provides a practical method that predicts a much wider range of component shapes encoded to direct the formation of such assemblies.

On the basis of (1)H NMR spectroscopic analyses and single crystal X-ray crystal structural data, the ion-pair receptor 1, bearing a calix[4]pyrrole for anion binding and calix[4]arene crown-5 for cation recognition, was found to act as a receptor for both CsF and KF ion-pairs. Both substrates are bound strongly but via different binding modes and with different complexation dynamics. Specifically, exposure to KF in 10% CD(3)OD in CDCl(3) leads first to complexation of the K(+) cation by the calix[4]arene crown-5 moiety. As the relative concentration of KF increases, then the calix[4]pyrrole subunit binds the F(-) anion. Once bound, the K(+) cation and the F(-) anion give rise to a stable 1:1 ion-pair complex that generally precipitates from solution. In contrast to what is seen with KF, the CsF ion-pair interacts with receptor 1 in two different modes in 10% CD(3)OD in CDCl(3). In the first of these, the Cs(+) cation interacts with the calix[4]arene crown-5 ring weakly. In the second interaction mode, which is thermodynamically more stable, the Cs(+) cation and the counteranion, F(-), are simultaneously bound to the receptor framework. Further proof that system 1 acts as a viable ion-pair receptor came from the finding that receptor 1 could extract KF from an aqueous phase into nitrobenzene, overcoming the high hydration energies of the K(+) and F(-) ions. It was more effective in this regard than a 1:1 mixture of the constituent cation and anion receptors (4 and 5).

An intramolecular proton-transfer mechanism has been proposed for the carbocationic cyclization of farnesyl pyrophosphate (FPP) to (+)-aristolochene catalyzed by aristolochene synthase. This novel mechanism, which is based on results obtained by high-level ab initio molecular orbital and density functional theory calculations, differs from the previous proposal in the key step of carbocation propagation prior to the formation of the bicyclic carbon skeleton. Previously, germacrene A was proposed to be generated as an intermediate by deprotonation of germacryl cation followed by reprotonation of the C6-C7 double bond to yield eudesmane cation. In the mechanism proposed here the direct intramolecular proton transfer has a computed barrier of about 22 kcal/mol, which is further lowered to 16-20 kcal/mol by aristolochene synthase. An alternative pathway is also possible through a proton shuttle via a pyrophosphate-bound water molecule. The mechanism proposed here is consistent with the observation that germacrene A is not a substrate of aristolochene synthase. Furthermore, the modeled substrate-enzyme complex suggests that Trp 334 and Phe 178 play key roles in positioning the substrate in the reactive orientation in the binding pocket. This is consistent with experimental findings that mutations of either residue lead to pronounced generation of aborted cyclization products.