Abstract:We identified a novel class of direct ion-channel blockers of ligand-gated ion channels called the gold nanoparticle-choline complex. Negatively charged gold nanoparticles (1.4 nm) block ion pores by binding to the sulfur group of the cysteine loop of nicotinic acetylcholine receptors (nAChRs), and currents evoked by acetylcholine (Ach) can break these bonds. The current evoked by ACh in nAChRs was blocked directly in ion pores by the gold nanoparticle-choline complex. In adrenal-gland perfusion studies, the complex also blocked nAChRs by diminishing catecholamine release by about 75%. An in vivo study showed muscle relaxation in rats after injection of the complex. These results will foster the application of gold nanoparticles as a direct ion-channel blocker.

No abstract

IntroductionIn our previous study, we found that negatively charged gold nanoparticles with spermidine have the potential of blocking inwardly rectifying potassium channels (Kir), both at the cellular and the tissue level.MethodsFor the purpose of the present study, we purified the cytoplasmic domain of the Kir 3.1 receptor from Escherichia coli. Using single particles with surface coating by transmission electron microscopy, we identified the gold nanoparticles at the cytoplasmic side of the human Kir channel.ResultsEnergy-dispersive X-ray spectroscopy showed the presence of the gold deposits in the cytoplasmic domain of the Kir receptor.ConclusionIn conclusion, we could identify undecagold in the ion pore of the Kir3.1 channel in order to clarify its direct blocking effect in the Kir ion pore by undecagold.Electronic supplementary materialThe online version of this article (doi:10.1007/s40119-016-0060-8) contains supplementary material, which is available to authorized users.

Infection stones are more likely to form after urinary diversion as the result of urinary stasis. To prevent urinary stasis due to encrusted pyelitis in a transplanted kidney, we describe an alternative a surgical treatment: ileo-pelvic anastomosis. In our patient with a transplanted kidney, the ileal conduit had previously been anastomosed end-to-side owing to renal tuberculosis with an atrophied bladder; the transplanted ureter was anastomosed to the ileum in the left lower abdomen with an ileal conduit on the opposite side. Routine check-up revealed hydronephrosis with infected pyelitis and ureteritis in the transplanted kidney. We performed ileo-pelvic end-to-end anastomosis to prevent urinary stasis by lengthening the ileal conduit and performed augmentation cystoplasty to support the atrophied bladder following tuberculosis. We suggest that this approach may be useful in similar cases.