Formation of a millimeter-sized spark discharge in ambient air is traced on a nanosecond time scale using multi-frame laser probing with an exposure time of 70 ps and spatial resolution of 3-4 μm. The discharge is initiated by a 25 kV voltage pulse with a rise time of 4 ns, with the pulse applied to the gap formed by a point cathode and flat anode. It is demonstrated that the gap breakdown is accompanied by the fast (∼1 ns) formation of a highly ionized homogeneous spark channel originating from the point cathode. We discover that the fast fine-scale filamentation of the homogeneous spark channel arises several nanoseconds after the breakdown and at some distance from the cathode, which results in a complex filamentary structure of the channel. We find that the growing spark channel, in fact, develops in the form of multiple (N 10) rapidlyevolving filaments that constitute micron-sized (∼10-50 μm) plasma channels with an electron density of -ñ 10 10 e 19 20 cm −3 and subnanosecond characteristic evolution time. First filaments appear at the top of the developing homogenous spark channel. Further, the growing filaments are split themselves, and their number is increased over time up to several tens. Our findings indicate that the fast fine-scale filamentation is one of the important mechanisms governing the spark channel resistance after the breakdown.
By employing multi-frame laser interferometry, shadow, and schlieren imaging, we trace the formation of a nanosecond spark discharge in millimeter-sized air gaps formed by a point cathode and flat anode or vice-versa. We discover that the electrical breakdown of the discharge gap is associated with extremely fast (=1 ns) explosive formation of micron-sized cathode and anode spots. We find that the characteristic delay between the instants of the anode and cathode spot initiation can be much shorter than 1ns. The spots appear as highly ionized near-electrode plasmas with an electron density n e ∼10 19 -10 20 cm −3 . The spots then give rise to highly ionized spark channels with pronounced filamentary structures. Our findings indicate that the extremely fast formation of anode spots is associated with an ultrafast gap breakdown promoted by an ultrafast ionization wave (UFIW). The role of the UFIW governed by the rapidly evolving cathode spot is discussed as a fundamental mechanism of the breakdown.
Formation of palmitic acid/Ca(2+) (PA/Ca(2+)) complexes was suggested to play a key role in the non-classical permeability transition in mitochondria (NCPT), which seems to be involved in the PA-induced apoptosis of cardiomyocytes. Our previous studies of complexation of free fatty acids (FFA) with Ca(2+) showed that long-chain (C:16-C:22) saturated FFA had an affinity to Ca(2+), which was much higher than that of other FFA and lipids. The formation of FFA/Ca(2+) complexes in the black-lipid membrane (BLM) was demonstrated to induce a nonspecific ion permeability of the membrane. In the present work, we have found that binding of Ca(2+) to PA incorporated into the membrane of sulforhodamine B (SRB)-loaded liposomes results in an instant release of a part of SRB, with the quantity of SRB released depending on the concentration of PA and Ca(2+). The pH-optimum of this phenomenon, similar to that of PA/Ca(2+) complexation, is in the alkaline range. The same picture of SRB release has been revealed for stearic, but not for linoleic acid. Along with Ca(2+), some other bivalent cations (Ba(2+), Sr(2+), Mn(2+), Ni(2+), Co(2+)) also induce SRB release upon binding to PA-containing liposomes, while Mg(2+) turns out to be relatively ineffective. As revealed by fluorescence correlation spectroscopy, the apparent size of liposomes does not alter after the addition of PA, Ca(2+) or their combination. So it has been supposed that the cause of SRB release from liposomes is the formation of lipid pores. The effect of FFA/Ca(2+)-induced permeabilization of liposomal membranes has several analogies with NCPT, suggesting that both these phenomena are of similar nature.
The initial stage of the fast electrical breakdown of an air gap with a pin-to-plane electrode geometry is studied on a nanosecond time scale using multi-frame laser probing with an exposure time of 70ps and spatial resolution as high as 3-4μm. We find that the gap breakdown is associated with the fast (1 ns) formation of a micron-sized (∼10 μm) cathode spot that appears as a plasma with an electron density of » n 10 cm e 19
Although diabetes mellitus is known to be a disease associated with mitochondrial dysfunction, not everything is clear about mitochondrial Ca2+ transport and Ca2+-induced permeability transition in diabetic cells. The objective of this work was to study the operation of MCU and Ca2+-dependent mitochondrial permeabilization in the liver cells of Sprague-Dawley rats under the streptozotocin-induced type I diabetes. It was shown that two weeks after the induction of diabetes, the rate of Ca2+ uptake by the mitochondria of diabetic animals increased ~1.4-fold. The expression of MCU and MICU1 subunits did not change, yet the quantity of dominant-negative MCUb channel subunits was almost twice as lower. The organelles also became more resistant to the induction of CsA-sensitive MPT pore and less resistant to the induction of CsA-insensitive palmitate/Ca2+-induced pore. The mitochondria of diabetic liver cells also showed changes in the lipid matrix of their membranes. The content of fatty acids in the membranes grew, and microviscosity of the lipid bilayer (assessed with laurdan) increased. At the same time, lipid peroxidation (assessed by the production of malonic dialdehyde) was stimulated. The paper discusses the consequences of the diabetes-related changes in mitochondria in the context of cell physiology.
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