Time-dependent Depolarization Research Articles

Effective Use of Sacrificial Zinc Anode as a Suitable Repair Method for Severely Damaged RC Members Due to Chloride Attack

In many cases, the repair strategy by using sacrificial anodes for cathodic protection in real RC structures requires additional zinc anodes after several years due to the decreasing protective area. This experimental study evaluates the effectiveness of time lag application of sacrificial anode cathodic protection applied to RC beam specimens that deteriorated severely due to chloride attack. In the experiment, sacrificial anodes and cathodic protection (SACP) were applied to 41-year-old RC beam specimens exposed to natural marine environments in which the embedded steel bars were significantly corroded. The repair work was performed in three stages. Instant-off and rest potential tests of steel bars were conducted periodically to demonstrate the time-dependent depolarization value. In the first stage, a polymer-modified mortar as a patch repair material was cast to replace the concrete in the middle tensile part with small sacrificial anodes embedded in the mortar. After the protective current reaches an equilibrium state, the sacrificial anodes are disconnected from the steel bars for a year, defined as the second stage. During the one year in the second stage, the steel bar in the patch repair area remained passive, without any sign of corrosion. As for the third stage, additional sacrificial anodes were installed in the existing concrete part to protect the steel in it. From one year of observation after applying sacrificial anodes to old concrete parts, the time lag SACP application of both in patch and non-patch repair parts was clarified to be effective in stopping the corrosion of steel bar in both parts until 20–30 years based on the service life prediction. Doi: 10.28991/CEJ-2022-08-07-015 Full Text: PDF

The electrophysiological effects of cadmium on Retzius nerve cells of the leech Haemopis sanguisuga

Cadmium is considered one of the most toxic heavy metals which can cause cytotoxicity in multiple organs including the brain. Despite many studies over the past decades, the cellular and molecular mechanisms underlying its neurotoxicity remain unclear. The present study was designed to examine the acute effects of cadmium chloride (CdCl2) on the electrical activity of the Retzius nerve cells of leech Haemopis sanguisuga using electrophysiological techniques. CdCl2, in concentrations of 10–100 μM, produced a dose- and time-dependent depolarization of Retzius neurons, paralleled by an increase in firing frequency and action potential duration. To examine potential mechanisms, we studied the effects of cadmium on the outward potassium current upon depolarization using a point microelectrode voltage-clamp technique. Reduction of the fast, and partial inhibition of the slow outward current were observed after adding 50 and 100 μM CdCl2 in the external fluid. The present results support the view that the effect of cadmium on the outward potassium channel may be a potential contributing mechanism for cadmium-induced neurotoxic damage. The proposed mechanism of cadmium action on the electrical properties of leech Retzius neurons might have broader significance concerning not only the leeches but vertebrate brains as well.

Quantifying computational advantage of Grover\u2019s algorithm with the trace speed

Despite intensive research, the physical origin of the speed-up offered by quantum algorithms remains mysterious. No general physical quantity, like, for instance, entanglement, can be singled out as the essential useful resource. Here we report a close connection between the trace speed and the quantum speed-up in Grover’s search algorithm implemented with pure and pseudo-pure states. For a noiseless algorithm, we find a one-to-one correspondence between the quantum speed-up and the polarization of the pseudo-pure state, which can be connected to a wide class of quantum statistical speeds. For time-dependent partial depolarization and for interrupted Grover searches, the speed-up is specifically bounded by the maximal trace speed that occurs during the algorithm operations. Our results quantify the quantum speed-up with a physical resource that is experimentally measurable and related to multipartite entanglement and quantum coherence.

Different orders of scattering through time-resolved Mueller matrix imaging estimates of pre-malignancy in human cervical tissues.

Time-resolved Mueller matrix (MM) imaging polarimetry in transmission mode has been implemented in both epithelium and stromal regions of cervical tissues to explore the various polarization dynamics in connection with the diagnosis of cervical precancer. The picosecond-resolved intensity patterns of various MM elements, resulting from the various orders of scattering, at different time delays provide clear demarcation between the epithelium and stroma of cervical tissue. The time dependent depolarization and retardance maps are seen to differentiate the epithelium from stroma. The average values of time dependent linear, linear-45, and circular depolarization and linear, circular, and scalar retardance parameters in different regimes of scattering from the optically anisotropic stromal region identify the pre-malignancy in cervical tissue. As the disease evolves, time dependent linear depolarization varies to larger values as compared to time dependent circular depolarization. Interestingly, the chirality of the collagen network that rotates the plane of polarized light in either direction in normal samples is limited to only the clockwise direction during the progression of the disease. These results show potential in the early detection and understanding of the mechanisms of morphological changes in cervical cancer development.

The Damaging Effects of Pedunsaponin A on Pomacea canaliculata Hemocytes.

Pomacea canaliculata hemocytes are the main functional cells in the immune defense system, and hemocyte destruction disrupts the immune response mechanism of P. canaliculata, resulting in abnormal growth, development, reproduction, and even death. Our previous study found that Pedunsaponin A significantly affects P. canaliculata hemocyte structure. This study further investigated the damaging effects of Pedunsaponin A on P. canaliculata hemocytes. The cell mortality rate results showed that the hemocyte mortality was significantly increased after treatment with Pedunsaponin A, and the mortality rate exhibited a significant positive correlation with treatment time and dose. The membrane potential results showed that the cell membranes of P. canaliculata hemocytes exhibited time-dependent membrane depolarization after 40 mg/L Pedunsaponin A treatment. At 36 h, the cell depolarization rate in the Pedunsaponin A treatment group was 41.43%, which was significantly greater than the control group (6.24%). The cytoskeleton results showed that Pedunsaponin A led to disordered and dispersed arrangement of microfilaments and changes in the cytoskeletal structure. The apoptosis and cell cycle results showed that Pedunsaponin A induced apoptosis and influenced the cell cycle to some extent. These results showed that the cell membrane and cytoskeleton of P. canaliculata hemocytes were damaged after treatment with Pedunsaponin A, which led to an increase in cell mortality, dysfunction, cell cycle abnormalities and apoptosis. This study provides a foundation for further identification of the site of Pedunsaponin A activity on hemocytes.

Reflectance and fast polarization dynamics of a GaN/Si nanowire ensemble

Optical phenomena in an ensemble of high-quality GaN nanowires (NWs) grown on a Si substrate have been studied by reflectance and time-resolved luminescence. Such NWs form a structure that acts as a virtual layer that specifically reflects and polarizes light and can be characterized by an effective refractive index. In fact we have found that the NW ensembles of high NW density (high filling fraction) behave rather like a layer of effective medium described by the Maxwell Garnett approximation. Moreover, light extinction and strong depolarization are observed that we assign to scattering and interference of light inside the NW ensemble. The wavelength range of high extinction and depolarization correlates well with transverse localization wavelength estimated for such an ensemble of NWs, so we suppose that these effects are due to Anderson localization of light.We also report results of time-resolved measurements of polarization of individual emission centers including free and bound excitons (D0XA, 3.47 eV), inversion domain boundaries (IDB, 3.45 eV) and stacking faults (SF, 3.42 eV). The emission of the D0XA and SF lines is polarized perpendicular to GaN c-axis while the 3.45 eV line is polarized along the c-axis which supports a hypothesis that this line is emitted from IDBs. Time-dependent depolarization of luminescence is observed during the first 0.1 ns after excitation and is interpreted as the result of interaction of the emission centers with hot particles existing for a short time after excitation.

Complement C5a Alters the Membrane Potential of Neutrophils during Hemorrhagic Shock.

Background Polymorphonuclear granulocytes (PMN) play a crucial role in host defense. Physiologically, exposure of PMN to the complement activation product C5a results in a protective response against pathogens, whereas in the case of systemic inflammation, excessive C5a substantially impairs neutrophil functions. To further elucidate the inability of PMN to properly respond to C5a, this study investigates the role of the cellular membrane potential of PMN in response to C5a. Methods Electrophysiological changes in cellular and mitochondrial membrane potential and intracellular pH of PMN from human healthy volunteers were determined by flow cytometry after exposure to C5a. Furthermore, PMN from male Bretoncelles-Meishan-Willebrand cross-bred pigs before and three hours after severe hemorrhagic shock were analyzed for their electrophysiological response. Results PMN showed a significant dose- and time-dependent depolarization in response to C5a with a strong response after one minute. The chemotactic peptide fMLP also evoked a significant shift in the membrane potential of PMN. Acidification of the cellular microenvironment significantly enhanced depolarization of PMN. In a clinically relevant model of porcine hemorrhagic shock, the C5a-induced changes in membrane potential of PMN were markedly diminished compared to healthy littermates. Overall, these membrane potential changes may contribute to PMN dysfunction in an inflammatory environment.

Cytotoxic L-amino-acid oxidases from Amanita phalloides and Clitocybe geotropa induce caspase-dependent apoptosis.

L-amino-acid oxidases (LAO) purified from fungi induce cell death in various mammalian cells including human tumor cell lines. The mechanism, however, remains poorly understood. In this study, we aimed to define a precise mechanism of cell death induced in Jurkat and MCF7 cancer cell lines by ApLAO and CgLAO, LAOs isolated from Amanita phalloides and Clitocybe geotropa, respectively. Cell death induced by both LAOs is shown to be concentration- and time-dependent, with higher toxic effects in Jurkat cells. LAO activity is required for the cytotoxicity. Detailed study on Jurkat cells further demonstrated that ApLAO and CgLAO both induce the intrinsic mitochondrial pathway of apoptosis, accompanied by a time-dependent depolarization of the mitochondrial membrane through the generation of reactive oxygen species. Treatment with the LAOs resulted in an increased ratio of the expression of proapoptotic Bax to that of antiapoptotic Bcl-2, subsequently leading to the activation of caspase-9 and -3. However, the pancaspase inhibitor, Z-VAD-FMK, did not completely abolish the cell death induced by either ApLAO or CgLAO, suggesting an alternative pathway for LAO-induced apoptosis. Indeed, caspase-8 activity in ApLAO- and CgLAO-treated cells was increased. Further, Fas/FasL (Fas ligand) antagonist caused a slight reduction in toxin-induced cell death, supporting the involvement of ApLAO and CgLAO in death-receptor-mediated apoptosis. These results thus provide new evidence that ApLAO and CgLAO induce apoptosis in Jurkat cells via both the intrinsic and extrinsic pathways, although the significantly higher increase of caspase-9 over caspase-8 activity suggests that it is the intrinsic pathway that is the predominant mode of ApLAO- and CgLAO-induced apoptosis.

Apoptosis induction in human breast cancer (MCF-7) cells by a novel venom l-amino acid oxidase (Rusvinoxidase) is independent of its enzymatic activity and is accompanied by caspase-7 activation and reactive oxygen species production

We report the elucidation of a mechanism of apoptosis induction in breast cancer (MCF-7) cells by an L-amino acid oxidase (LAAO), Rusvinoxidase, purified from the venom of Daboia russelii russelii. Peptide mass fingerprinting analysis of Rusvinoxidase, an acidic monomeric glycoprotein with a mass of ~57kDa, confirmed its identity as snake venom LAAO. The enzymatic activity of Rusvinoxidase was completely abolished after two cycles of freezing and thawing; however, its cytotoxicity toward MCF-7 cells remained unaffected. Dose- and time-dependent induction of apoptosis by Rusvinoxidase on MCF-7 cells was evident from changes in cell morphology, cell membrane integrity, shrinkage of cells and apoptotic body formation accompanied by DNA fragmentation. Rusvinoxidase induced apoptosis in MCF-7 cells by both the extrinsic (death-receptor) and intrinsic (mitochondrial) signaling pathways. The former pathway of apoptosis operated through activation of caspase-8 that subsequently activated caspase-7 but not caspase-3. Rusvinoxidase-induced intrinsic pathway of apoptosis was accompanied by a time-dependent depolarization of the mitochondrial membrane through the generation of reactive oxygen species, followed by a decrease in cellular glutathione content and catalase activity, and down-regulation of expression of anti-apoptotic proteins Bcl-XL and heat-shock proteins (HSP-90 and HSP-70). Rusvinoxidase treatment resulted in increase of the pro-apoptotic protein Bax, subsequently leading to the release of cytochrome c from mitochondria to the cytosol and activating caspase-9, which in turn stimulated effector caspase-7. Rusvinoxidase at a dose of 4mg/kg was non-toxic in mice, indicating that it may be useful as a model for the development of peptide-based anticancer drugs.

Ellagic acid induces a dose- and time-dependent depolarization of mitochondria and activation of caspase-9 and -3 in human neuroblastoma cells

The polyphenol ellagic acid is found in many natural food sources and has been proposed as a candidate compound for clinical applications due to its anti-oxidative capacity and as a potential anti-tumorigenic compound. The objective of the present study was to evaluate the sensitivity to and possible apoptosis mechanism induced by ellagic acid in neuronal tumor cells. As a model the human neuroblastoma SH-SY5Y cell line was used. The methods applied were bright field and phase contrast microscopy, XTT- and LDH-assays, western blot, and flow cytometric analysis of DNA degradation and mitochondrial membrane potential. Ellagic acid treatment was found to induce a reduction in cell number preceded by alterations of the mitochondrial membrane potential and activation of caspase-9 and -3, DNA-fragmentation and cell death by apoptosis. The apoptotic cell death studied was not due to anoikis since it was significant in the adherent fraction of the cells. We conclude that ellagic acid induces dose- and time-dependent apoptosis, at least partly by the mitochondrial pathway, in an embryonal neuronal tumor cell system. This finding is in agreement with previously reported data on adult carcinoma cells thus suggesting a more general effect of ellagic acid on tumor cells.

Isothermal depolarization current spectroscopy of localized states in metal oxide varistors

A new method for the processing of time-dependent isothermal depolarization current in oxide varistors is proposed. It involves (i) a new model for kinetics of the depolarization current, which is related to the parameters of the localized states, (ii) an account of the distribution of the relaxation time (which takes place due to the structure inhomogeneity of ceramics) using the Kohlrausch–Williams–Watts stretched exponential function and (iii) the determination of the most probable relaxation time. The proposed method was tested using ZnO high-voltage varistors. The ionization energy (0.06 and 0.16 eV) and the electron capture cross-section (∼10−17 and ∼10−16 cm2) of the bulk donor states in two ZnO varistor ceramics were estimated.

Ultrafast Polarization Shaping with Fano Plasmonic Crystals

Femtosecond-scale polarization state shaping is experimentally found in optical response of a plasmonic nanograting by means of time-resolved Stokes polarimetry. Simultaneous measurements of the Stokes parameters as a function of time reveal a remarkable alteration of the polarization state inside a single femtosecond pulse reflected from a plasmonic crystal due to the excitation of time-delayed polarization-sensitive surface plasmons with a highly birefringent Fano-type spectral profile. Time-dependent depolarization, indicating the sub-130-femtosecond polarization change inside the pulse, is experimentally found and described within an analytical model which predicts the fivefold enhancement of the polarization conversion effect with the use of a narrower time gate.

Assessment of neurotoxicity of monocrotaline, an alkaloid extracted from Crotalaria retusa in astrocyte/neuron co-culture system

Studies have shown cases of poisoning with plants from the genus Crotalaria (Leguminosae) mainly in animals. They induce damages in the central nervous system (CNS), which has been attributed to toxic effects of the pyrrolizidine alkaloid (PA) monocrotaline (MCT). Previously we demonstrated that both MCT and dehydromonocrotaline (DHMC), its main active metabolite, induce changes in the levels and patterns of expression of the main protein from astrocyte cytoskeleton, glial fibrillary acidic protein (GFAP). In this study we investigated the effect of MCT on rat cortical astrocyte/neuron primary co-cultures. Primary cultures were exposed to 10 or 100μM MCT. The MTT test and the measurement of LDH activity on the culture medium revealed that after 24h exposure MCT was not cytotoxic to neuron/astrocyte cells. However, the cell viability after 72h treatment decreased in 10–20%, and the LDH levels in the culture medium increased at a rate of 12% and 23%, in cultures exposed to 10 or 100μM MCT. Rosenfeld staining showed vacuolization and increase in cell body in astrocytes after MCT exposure. Immunocytochemistry and Western blot analyses revealed changes on pattern of GFAP and βIII-tubulin expression and steady state levels after MCT treatment, with a dose and time dependent intense down regulation and depolarization of neuronal βIII-tubulin. Moreover, treatment with 100μM MCT for 12h induced GSH depletion, which was not seen when cytochrome P450 enzyme system was inhibited indicating that it is involved in MCT induced cytotoxicity in CNS cells.

Acute hyperglycemia induces Cardiac Mitochondrial Depolarization

Mitochondrial ATP generation depends on the enormous potential across the inner mitochondrial membrane (ΔΨmito ~ −180 mV), among many other factors. Oxidative phosphorylation requires the large ΔΨmito and when the mitochondria are depolarized, oxidative phosphorylation becomes uncoupled and ATP production falls. Here we investigate the effect of hyperglycemia (30 mM versus the physiological glucose of 5 mM) on mitochondrial ΔΨmito under photonic stress in rat ventricular myocytes. Using tetra-methyl rhodamine methyl ester (TMRM) as a fluorescence monitor of ΔΨmito we examined how the time-dependent depolarization of mitochondria may be altered by hyperglycemia. Using a normal Tyrode's solution on isolated ventricular myocytes, changing the [glucose] has dramatic effect on the rate of ΔΨmito depolarization. After 3hours of hyperglycemic exposure, the rate of depolarization is reduced nearly 30% compared to controls. Antioxidant treatment protects cardiac myocytes from this hyperglycemic-induced effect while selectively inhibiting complex I causes an abrogation of the effect. These data elucidate the biophysical effects of acute hyperglycemia on cardiac myocytes.

Glucose Provides Short-Term Protection to Mitochondria in Rat Ventricular Cardiac Myocytes

Cellular ATP production depends on glycolytic and oxidative phosphorylation pathways and hence on both cytosolic and mitochondrial reactions. Mitochondrial ATP generation depends on the enormous potential across the inner mitochondrial membrane (αΨmito ∼ −180 mV), among many other factors. Using tetra-methyl rhodamine methyl ester (TMRM) as a fluorescence monitor of αΨmito we examined how the time-dependent and illumination-dependent depolarization of mitochondria may be altered by extracellular glucose. Oxidative phosphorylation requires the large αΨmito and when the mitochondria are depolarized, oxidative phosphorylation becomes uncoupled and ATP production falls. Here we investigate the effect of hyperglycemia (30 mM versus the physiological glucose of 5 mM) on mitochondrial αΨmito under photon-induced oxidative stress in rat ventricular myocytes. Using a buffered physiologic salt solution on quiescent ventricular myocytes, changing the [glucose] has dramatic effect on the rate of αΨmito depolarization. The rate of depolarization was significantly decreased in the presence of high glucose (the time-to-50% depolarization was increased from 250 s to 500s). These results were carried out in the absence of insulin. We conclude that hyperglycemia appears to protect mitochondrial function in quiescent heart cells from photon-induced oxidative stress. It is not yet clear how this apparent protection may change as metabolic load and muscle work increases, nor is it clear whether the absence of fatty acid substrates will increase or decrease this seemingly protective effect.

Nanoscale polarization relaxation of epitaxial BiFeO 3 thin film

The polarization relaxation phenomenon in a 40-nm-thick epitaxial BiFeO 3 thin film grown on a (001) SrTiO 3 substrate with SrRuO 3 bottom electrode, was studied in nanoscale using dual-frequency resonance-tracking piezoresponse force microscopy. The as-grown film shows highly irregular mosaic domain pattern. The nucleation of reversed domains followed by domain wall propagation and domain coalesce was observed during relaxations. The polarization relaxation follows a stretched exponential model f = 1 − e − k( t − t 0) n with parameters t 0 = 2894 s, n = 0.50 and k = 6.04e− 4. Local polar defects act as nucleation centers and the time-dependent depolarization field is the driving force for polarization relaxation.

Characterization of the physiological- and genetic phenotype of CRF-expressing neurons in the bed nucleus of the stria terminalis

Characterization of the physiological- and genetic phenotype of CRF-expressing neurons in the bed nucleus of the stria terminalis

Time-dependent depolarization of aligned D2 caused by hyperfine coupling

Molecular deuterium is prepared in the J = 2, M = 0 sublevel of ν = 1 by stimulated Raman pumping of the ν = 0 S(0) line. Following optical excitation, the degree of alignment of the rotational angular momentum J oscillates in time caused by the coupling of J to the total nuclear spin angular momentum I(T). This coupling is of two kinds, the interaction of J with the magnetic moments and the quadrupole fields of the two I = 1 deuterium nuclei. The alignment is monitored via the O(2) line of the E,F(1)Σ(g)(+)-X(1)Σ(g)(+) (0,1) band using [2+1] resonance enhanced multiphoton ionization for pump-probe delays from 0 to 20 μs. Using the hyperfine coupling constants found previously for the ν = 0 state (R. F. Code and N. F. Ramsey, Phys. Rev. A, 1971, 4, 1945), we are able to fit the time dependence essentially within our experimental error, but this requires that the presence of both I(T) = 0 and I(T) = 2 nuclear spin states for this o-deuterium level is properly weighted and taken into account.

Time-dependent depolarization of aligned HD molecules

An aligned sample of HD(v = 1, J = 2, M(J) = 0) molecules is prepared under collision-free conditions using the S(0) stimulated Raman pumping transition. Subsequent coupling to the spins of the deuteron I(D) and the proton I(H) causes the initial degree of alignment to oscillate and decrease as monitored over the time range from 0-13 mus via the O2 line of the [2 + 1] REMPI E,F(1)Sigma-X(1)Sigma (0,1) band. The time dependence of the rotational alignment is also calculated using both a hierarchical coupling scheme in which the rotational angular momentum J is regarded first to couple to I(D), and then the resultant F(i) to couple to I(H), to form the total angular momentum F and a non-hierarchical coupling scheme in which the HD energy level structure is not assumed to be diagonal in the |I(H)(JI(D))F(i)FM(F)> basis set. The experimental data is in good agreement with the non-hierarchical calculation but not with the hierarchical calculation, as expected for this system. Additionally, we calculate the time dependence of the H and D nuclear spin polarizations.

O‐acetylation of GD3 prevents its apoptotic effect and promotes survival of lymphoblasts in childhood acute lymphoblastic leukaemia

We have previously demonstrated induction of O-acetylated sialoglycoproteins on lymphoblasts of childhood acute lymphoblastic leukaemia (ALL). These molecules promote survival of lymphoblasts by preventing apoptosis. Although O-acetylated sialoglycoproteins are over expressed, the status of O-acetylation of gangliosides and their role in lymphoblasts survival remains to be explored in ALL patients. Here, we have observed enhanced levels of 9-O-acetylated GD3 (9-O-AcGD3) in the lymphoblasts of patients and leukaemic cell line versus disialoganglioside GD3 in comparison to the normal cells. Localization of GD3 and 9-O-AcGD3 on mitochondria of patient's lymphoblasts has been demonstrated by immuno-electron microscopy. The exogenous administration of GD3-induced apoptosis in lymphoblasts as evident from the nuclear fragmentation and sub G0/G1 apoptotic peak. In contrast, 9-O-AcGD3 failed to induce such apoptosis. We further explored the mitochondria-dependent pathway triggered during GD3-induced apoptosis in lymphoblasts. GD3 caused a time-dependent depolarization of mitochondrial membrane potential, release of cytochrome c and 7.4- and 8-fold increased in caspase 9 and caspase 3 activity respectively. However, under identical conditions, an equimolar concentration of 9-O-AcGD3 failed to induce similar effects. Interestingly, 9-O-AcGD3 protected the lymphoblasts from GD3-induced apoptosis when administered in equimolar concentrations simultaneously. In situ de-O-acetylation of 9-O-AcGD3 with sodium salicylate restores the GD3-responsiveness to apoptotic signals. Although both GD3 and 9-O-acetyl GD3 localize to mitochondria, these two structurally related molecules may play different roles in ALL-disease biology. Taken together, our results suggest that O-acetylation of GD3, like that of O-acetylated sialoglycoproteins, might be a general strategy adopted by leukaemic blasts towards survival in ALL.