Electrochemical impedance spectroscopy (EIS) and thickness shear mode acoustic method (TSM) have been used for development of the aptamer‐based biosensor for detection leukemic Jurkat cells. Thiolated DNA aptamers specific to the cancer marker protein tyrosine kinase‐7 (PTK7) have been chemisorbed on a gold surface. Redox probe [Fe(CN)6]3−/4− has been used for monitoring changes in charge transfer resistance, Rct, in EIS experiments. Rct increased with increasing the concentration of Jurkat cells. TSM allowed label‐free detection based on decrease of resonant frequency following addition of the cells. We obtained high sensitivity of Jurkat cells determination with limit of detection (LOD) 105±10 and 463±50 cells/mL for electrochemical and acoustic sensor, respectively. Small non‐specific interactions have been observed for control U266 cells which can be particularly due to the interaction of the aptamers with lipid part of the biomembranes.

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We performed a comparative study of the detection of human cellular prions (PrPC) with a quartz crystal microbalance (QCM) immunosensor using various antibodies against PrPC. The sensing layer was formed by immobilized antibodies on a surface of polyamidoamine dendrimers (PAMAM) of fourth generation (G4) with attached protein A. The sensitivity of detection depended on the kind of antibody used and the best detection limit was 0.8 nM. PrPC detection in 10 times diluted blood plasma revealed more complicated behavior of motional resistance, which is evidence on viscosity contribution. The sensor recovery was 82.2 %, suggesting certain matrix effects on prion detection.

In eukaryotic cells, mitochondria are constantly adapting to changes in the biological activity of the cell, i.e., changes in nutrient availability and environmental stresses. We propose a model in which this adaptation is mediated by lipids.

Oncological diseases belong to the most serious illnesses with high mortality. The most common cancer in children is acute lymphoblastic leukemia (ALL). It is important to develop diagnostic methods that will be able to detect this disease in early stage. One of the possible options can be non-invasive diagnostics using the biosensors based on nucleic acid aptamers. Aptamer recognizes the surface markers on the membrane of cancer cells with the high binding affinity. Biosensors based on aptamers with redox markers are among the most sensitive experimental tools of this type. We developed and optimized the redox-labeled electrochemical aptasensors for the detection of Jurkat leukemia cells. The aptamers specific to the protein tyrosine kinase 7 (PTK7), which is important membrane protein cancer marker that is overexpressed in Jurkat cells were used. We compared the sensitivity of aptasensors for aptamers modified either by methylene blue (MB) and ferrocene carboxylic acid (Fc), respectively. Both aptasensors were tested in the presence of Jurkat cells at concentration range 50–5000 cells/mL using differential pulse voltammetry. In both cases the comparable sensitivity was obtained with limit of detection: 37 ± 6 cells/mL for Fc-labeled aptamers and 38 ± 8 cells/mL for MB-labeled aptamers based on 3.3S/N (signal to noise) rule. The interaction of the sensing surface with control U266 cells was less significant.

Absence of inositolphosphosphingolipid phospholipase C, Isc1, a yeast homologue of mammalian neutral sphingomyelinase type 2, leads to severe mitochondrial dysfunction. We show that the defect can be largely rescued by deletion of another type-C phospholipase, the phosphatidylglycerol (PG)-specific Pgc1. The reduced phosphatidylethanolamine (PE) levels, as well as reduced cytochrome c oxidase activity, observed in isc1Δ cells were restored to wild-type levels in the pgc1Δisc1Δ mutant. We found that Pgc1 substrate, PG, inhibits in vitro activity of Isc1 and phosphatidylserine decarboxylase Psd1, an enzyme crucial for PE biosynthesis. We also identified a mechanism by which the balance between the current demand for PG and its consumption is controlled. We document that the product of PG hydrolysis, diacylglycerol, competes with the substrate of PG-phosphate synthase, Pgs1, and thereby inhibits the biosynthesis of excess PG. This feedback loop does not work in the absence of Pgc1, which catalyzes PG degradation. Finally, Pgc1 activity is partially inhibited by products of Isc1-mediated hydrolysis. The described functional interconnection of the two phospholipases contributes significantly to lipid homeostasis throughout the cellular architecture.