An exchange for the better: X‐ray absorption spectroscopic studies show that treatment of an RuIII drug, NAMI‐A, with bovine serum albumin (BSA) results in complete replacement of the Cl− and S‐donor ligands with N‐donor and carboxylato residues of the protein (see scheme). The RuIII–BSA adduct is as active in enhancing the cell–substrate interactions as the original NAMI‐A complex (which converts into RuIII–BSA within minutes in the cell‐culture medium).

An anti-metastatic drug, NAMI-A ((ImH)[Ru(III) Cl4 (Im)(dmso)]; Im=imidazole, dmso=S-bound dimethylsulfoxide), and a cytotoxic drug, KP1019 ((IndH)[Ru(III) Cl4 (Ind)2 ]; Ind=indazole), are two Ru-based anticancer drugs in human clinical trials. Their reactivities under biologically relevant conditions, including aqueous buffers, protein solutions or gels (e.g, albumin, transferrin and collagen), undiluted blood serum, cell-culture medium and human liver (HepG2) cancer cells, were studied by Ru K-edge X-ray absorption spectroscopy (XAS). These XAS data were fitted from linear combinations of spectra of well-characterised Ru compounds. The absence of XAS data from the parent drugs in these fits points to profound changes in the coordination environments of Ru(III) . The fits point to the presence of Ru(IV/III) clusters and binding of Ru(III) to S-donor groups, amine/imine and carboxylato groups of proteins. Cellular uptake of KP1019 is approximately 20-fold higher than that of NAMI-A under the same conditions, but it diminishes drastically after the decomposition of KP1019 in cell-culture media, which indicate that the parent complex is taken in by cells through passive diffusion.

Ru‐ndum erneuert: Röntgenabsorptionsspektroskopische Studien belegen, dass der RuIII‐Wirkstoff NAMI‐A alle seine Cl−‐ und S‐Donor‐Liganden gegen N‐Donoren und Carboxylatogruppen von Rinderserumalbumin (BSA) austauschen kann (siehe Schema). Das RuIII‐BSA‐Addukt verstärkt Zell‐Substrat‐Wechselwirkungen ebenso stark wie NAMI‐A (das sich im Zellkulturmedium binnen Minuten in RuIII‐BSA umwandelt).

Nodular regenerative hyperplasia (NRH) is a rare cause of non-cirrhotic portal hypertension that should be considered in patients with no risk factors for chronic liver disease or in any unusual presentation of variceal hemorrhage. We present a case of an 82-year-old Chinese female, with a history of previous metastatic sigmoid carcinoma with oxaliplatin use, who presented with melena. A gastroscopy done revealed one column of grade 3 esophageal varix, two columns of grade 2 esophageal varices, and a type 1 gastroesophageal varix with stigmata of recent hemorrhage. Cyanoacrylate glue therapy was performed without any complications. A follow-up computed tomography (CT) imaging of the abdomen did not reveal any significant features of cirrhosis or venous thrombosis, and the decision was made for a transjugular liver biopsy with hepatic venous pressure gradient (HVPG) measurement. The measured HVPG was 6 mmHg, and the liver biopsy showed features consistent with NRH.