Functionalized galactoglucomannan‐based hydrogels for the removal of metal cations from aqueous solutions

New types of hydrogels derived from O‐acetyl galactoglucomannan (AcGGM) hemicellulose have been synthesized and characterized. The objective of this work was to analyze the sorption capacity (S) of three types of hydrogels containing AcGGM derivatives incorporated into the carboxylic groups of the polymer chain in the AA hydrogel, sulfonic groups in the APA hydrogel, and amide groups in the acrylamide (Aam) hydrogel. These hydrogels are capable of interacting and removing ions such as cadmium [Cd(II)], copper [Cu(II)], lead [Pb(II)], nickel [Ni(II)], and zinc [Zn(II)]. The results show that AA and Aam hydrogels had a lower sorption capacity of ions compared to the APA hydrogel, which had a high sorption capacity. The maximal sorption capacity was determined by the successive enrichment method, obtaining Pb(II) amount of 48.3 mg/g of AA hydrogel, 65.8 mg/g of APA hydrogel, and 40.8 mg/g of Aam hydrogel. Hence, Pb(II) ions are greatly retained by the three hydrogels. These results are promising for the development of new materials with potential applications in metal ion removal. © 2016 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2016 , 133, 44093.     

An Efficient New Pyrimidine Synthesis – a pathway to octupoles

The condensation of N,N,N′-tris(trimethylsilyl)-amidines ( 6 , 11 , 22 ) with vinamidinium salts ( 1 , 7 ) in the presence of potassium fluoride is the method of choice for the synthesis of pyrimidines ( 8 , 12 , 20 , 23 ). Octupoles comprising 1,3,5-benzene ( 8 ) and triphenylamine ( 12 , 20 ) derivatives can be prepared in high yields.     

Aurora Kinase A Is Involved in Controlling the Localization of Aquaporin-2 in Renal Principal Cells

The cAMP-dependent aquaporin-2 (AQP2) redistribution from intracellular vesicles into the plasma membrane of renal collecting duct principal cells induces water reabsorption and fine-tunes body water homeostasis. However, the mechanisms controlling the localization of AQP2 are not understood in detail. Using immortalized mouse medullary collecting duct (MCD4) and primary rat inner medullary collecting duct (IMCD) cells as model systems, we here discovered a key regulatory role of Aurora kinase A (AURKA) in the control of AQP2. The AURKA-selective inhibitor Aurora-A inhibitor I and novel derivatives as well as a structurally different inhibitor, Alisertib, prevented the cAMP-induced redistribution of AQP2. Aurora-A inhibitor I led to a depolymerization of actin stress fibers, which serve as tracks for the translocation of AQP2-bearing vesicles to the plasma membrane. The phosphorylation of cofilin-1 (CFL1) inactivates the actin-depolymerizing function of CFL1. Aurora-A inhibitor I decreased the CFL1 phosphorylation, accounting for the removal of the actin stress fibers and the inhibition of the redistribution of AQP2. Surprisingly, Alisertib caused an increase in actin stress fibers and did not affect CFL1 phosphorylation, indicating that AURKA exerts its control over AQP2 through different mechanisms. An involvement of AURKA and CFL1 in the control of the localization of AQP2 was hitherto unknown.     

SOAT1: A Suitable Target for Therapy in High-Grade Astrocytic Glioma?

Targeting molecular alterations as an effective treatment for isocitrate dehydrogenase-wildtype glioblastoma (GBM) patients has not yet been established. Sterol-O-Acyl Transferase 1 (SOAT1), a key enzyme in the conversion of endoplasmic reticulum cholesterol to esters for storage in lipid droplets (LD), serves as a target for the orphan drug mitotane to treat adrenocortical carcinoma. Inhibition of SOAT1 also suppresses GBM growth. Here, we refined SOAT1-expression in GBM and IDH-mutant astrocytoma, CNS WHO grade 4 (HGA), and assessed the distribution of LD in these tumors. Twenty-seven GBM and three HGA specimens were evaluated by multiple GFAP, Iba1, IDH1 R132H, and SOAT1 immunofluorescence labeling as well as Oil Red O staining. To a small extent SOAT1 was expressed by tumor cells in both tumor entities. In contrast, strong expression was observed in glioma-associated macrophages. Triple immunofluorescence labeling revealed, for the first time, evidence for SOAT1 colocalization with Iba1 and IDH1 R132H, respectively. Furthermore, a notable difference in the amount of LD between GBM and HGA was observed. Therefore, SOAT1 suppression might be a therapeutic option to target GBM and HGA growth and invasiveness. In addition, the high expression in cells related to neuroinflammation could be beneficial for a concomitant suppression of protumoral microglia/macrophages.