Application of a novel gas phase synthesis approach to carbonyl complexes of accelerator-produced 5d transition metals

In 2014 the first synthesis of a transactinide carbonyl complex - seaborgium hexacarbonyl - was reported. This was achieved in gas-phase chemical experiments in a beam-free environment behind the recoil separator GARIS. Extending this work to heavier elements requires more efficient techniques to synthesize carbonyl complexes as production rates of transactinide elements drop with increasing atomic number. A novel approach was thus conceived, which retains the benefit of a beam-free environment but avoids the physical preseparation step. The latter reduces the yields for products of asymmetric reactions such as those used for the synthesis of suitable isotopes of Sg, Bh, Hs and Mt. For this a series of experiments with accelerator-produced radioisotopes of the lighter homologues W, Re and Os was carried out at the tandem accelerator of JAEA Tokai, Japan. A newly developed double-chamber system, which allows for a decoupled recoil ion thermalization and chemical complex formation, was used, which avoids the low-efficiency physical preseparation step. Here, we demonstrate the feasibility of this newly developed method using accelerator-produced short-lived radioisotopes of the 5d homologues of the early transactinides

Mitochondrial tumour suppressors: A genetic and biochemical update

Since the discovery 5 years ago that the D-subunit of succinate dehydrogenase ( SDHD) can behave as a classic tumour suppressor, other nuclear-encoded mitochondrial proteins (SDHB, SDHC and fumarate hydratase) have been implicated in tumour susceptibility. Mutations in these proteins are principally involved in familial predisposition to benign tumours, but the spectrum of inherited lesions is increasingly recognized to include malignant tumours, such as malignant phaeochromocytomas and renal cell carcinomas. Here we review recent advances in the field of mitochondrial tumour suppressors, the biochemical pathway that links mitochondrial dysfunction with tumorigenesis, and potential therapeutic approaches to these malignancies