Enhanced and Long‐Lived Near‐Infrared Luminescence of Er3+ Ions in Lead Borate Glass‐Ceramics Containing PbWO4 Nanocrystals

Lead tungstate PbWO₄ nanocrystals in transparent lead borate glass‐ceramics containing Er³⁺ ions were fabricated. Luminescence spectra at about 1530 nm due to main ⁴I_13/2–⁴I_15/2 laser transition of Er³⁺ ions were examined for glass samples before and after heat treatment. Near‐infrared luminescence of Er³⁺ ions in glass‐ceramics is enhanced and long‐lived in comparison to precursor glasses. It suggests that the Er³⁺ ions are partially incorporated into PbWO₄ crystalline phase.     

A cross-linked conjugated metallopolymer comprised of bisaxially coordinated ruthenium tetra-t-butyl phthalocyanine connected by quaterthiophene linkers

A ruthenium tetra-t-butylphthalocyanine bisaxially ligated with 3,5-bis(2,2′-bithiophene-5-yl)pyridine was synthesized from ruthenium tetra-t-butylphthalocyanine dimer. The complex was electropolymerized (in CH₂Cl₂ and CH₃CN, with and without addition of BF₃·Et₂O) to yield an insoluble conjugated metallopolymer, which was characterized by cyclic voltammetry and UV–vis spectroelectrochemistry. The polymer combines the electrochemical and spectral properties of the phthalocyanine and of a polythiophene-type conjugated polymer. In the presence of BF₃, the polymer can be reversibly p-doped and de-doped. Materials obtained in CH₂Cl₂ (tested in the same solvent) and in CH₃CN/BF₃ (tested in CH₃CN) exhibit an unusual hysteresis of redox properties.     

UV Differentially Induces Oxidative Stress,DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib

Chronic myeloid leukemia (CML) cells express the active BCR-ABL1 protein, which has been targeted by imatinib in CML therapy, but resistance to this drug is an emerging problem. BCR-ABL1 induces endogenous oxidative stress promoting genomic instability and imatinib resistance. In the present work, we investigated the extent of oxidative stress, DNA damage, apoptosis and expression of apoptosis-related genes in BCR-ABL1 cells sensitive and resistant to imatinib. The resistance resulted either from the Y253H mutation in the BCR-ABL1 gene or incubation in increasing concentrations of imatinib (AR). UV irradiation at a dose rate of 0.12 J/(m²·s) induced more DNA damage detected by the T4 pyrimidine dimers glycosylase and hOGG1, recognizing oxidative modifications to DNA bases in imatinib-resistant than -sensitive cells. The resistant cells displayed also higher susceptibility to UV-induced apoptosis. These cells had lower native mitochondrial membrane potential than imatinib-sensitive cells, but UV-irradiation reversed that relationship. We observed a significant lowering of the expression of the succinate dehydrogenase (SDHB) gene, encoding a component of the complex II of the mitochondrial respiratory chain, which is involved in apoptosis sensing. Although detailed mechanism of imatinib resistance in AR cells in unknown, we detected the presence of the Y253H mutation in a fraction of these cells. In conclusion, imatinib-resistant cells may display a different extent of genome instability than their imatinib-sensitive counterparts, which may follow their different reactions to both endogenous and exogenous DNA-damaging factors, including DNA repair and apoptosis.