Hydrogen inhibition of wet AlLi alloy dust collector systems using a composite green biopolymer inhibitor based on chitosan/sodium alginate: Experimental and theoretical studies.

Aluminum­lithium (AlLi) alloy polishing and grinding processes in wet dust collector systems could cause hydrogen fire and explosion. From the fundamental perspective of preventing hydrogen explosions, a safe, nontoxic, and sustainable modified green hydrogen inhibitor based on chitosan (CS) and sodium alginate (SA) was developed in this study and was used as a hydrogen evolution inhibitor for the processing of waste dust from AlLi alloys. The structure and elemental distribution of the synthesized material were characterized through characterization experiments. Hydrogen evolution experiments and a hydrolysis kinetic model were used to explore the inhibitory effect of modified CS/SA on AlLi alloy dust, and the results revealed that the inhibitory concentration of the hydrogen explosion lower limit was 0.40 wt%, with an inhibition efficiency of 91.96 %, indicating an 11.88-61.44 % improvement over that of CS and SA. As the inhibitor concentration increased and the temperature decreased, the hydrogen inhibition effect increased. Characterization experiments and density functional theory showed that CS/SA primarily formed a dense physical protective barrier on the dust surface through chemical adsorption and complexation reactions, interrupting the hydrogen evolution reaction between the metal and water. This study introduces a novel green modified hydrogen inhibitor that fundamentally addresses hydrogen generation and explosion.

Linear and nonlinear analyses of normal and fatigue heart rate variability signals for miners in high-altitude and cold areas.

BACKGROUND AND OBJECTIVE: Fatigue is an important cause of operational errors, and human errors are the main cause of accidents. This study is an exploratory study in China. Field tests were conducted on heart rate variability (HRV) parameters and physiological indicators of fatigue among miners in high-altitude, cold and low-oxygen areas. This paper studies heart activity patterns during work fatigue in miners. METHODS: Fatigue affects both the sympathetic and parasympathetic nervous systems, and it is expressed as an abnormal pattern of HRV parameters. Thirty miners were selected as subjects for a field test, and HRV was extracted from 60 groups of electrocardiography (ECG) datasets as basic signals for fatigue analysis. Then, we analyzed the HRV signals of the miners using linear (time domain and frequency domain) and nonlinear dynamics (Poincaré plot and sample entropy (SampEn)), and a Pearson's correlation coefficient analysis and t-tests were performed on the measured indices. RESULTS: The results showed that the time-domain indices (SDNN, RMSSD, SDSD, pNN50, RRn, heart rate (HR), R-wave humps (RH)) and the coefficient of variation (CV)) and the frequency-domain indices (low frequency/high frequency (LF/HF), LFnorm and HFnorm) clearly changed after fatigue. These features were selected using a Poincaré plot, sample entropy, Pearson's correlation coefficient and a t-test for further analysis. The fatigue characteristics and sensitivity parameters of miners in a high-altitude, cold and hypoxic environment were obtained. CONCLUSIONS: This study provides deep insight into the use of linear and nonlinear fatigue characteristics to effectively and reliably identify miner fatigue. Furthermore, the study provides a reference for clinical studies of acute mountain sickness in high-altitude, cold and hypoxic environments.

Thermal decomposition characteristics of foundry sand for cast iron in nitrogen atmosphere.

Sand casting, currently the most popular approach to the casting production, has wide adaptability and low cost. The thermal decomposition characteristics of foundry sand for cast iron were determined for the first time in this study. Thermogravimetry was monitored by simultaneous thermal analyser to find that there was no obvious oxidation or combustion reaction in the foundry sand; the thermal decomposition degree increased as the heating rate increased. There was an obvious endothermic peak at about 846 K due to the transition of quartz from ß to α phase. A novel technique was established to calculate the starting temperature of volatile emission in determining the volatile release parameter of foundry sand for cast iron. Foundry sand does not readily evaporate because its volatile content is only about 2.68 wt% and its main components have high-temperature stability. The thermal decomposition kinetics parameters of foundry sand, namely activation energy and pre-exponential factor, were obtained under kinetics theory. The activation energy of foundry sand for cast iron was small, mainly due to the wide temperature range of thermal decomposition in the foundry sand.

Multiple regulation by calcium of murine homologues of transient receptor potential proteins TRPC6 and TRPC7 expressed in HEK293 cells.

We investigated, by using the patch clamp technique, Ca2+-mediated regulation of heterologously expressed TRPC6 and TRPC7 proteins in HEK293 cells, two closely related homologues of the transient receptor potential (TRP) family and molecular candidates for native receptor-operated Ca2+ entry channels. With nystatin-perforated recording, the magnitude and time courses of activation and inactivation of carbachol (CCh; 100 microM)-activated TRPC6 currents (I(TRPC6)) were enhanced and accelerated, respectively, by extracellular Ca2+ (Ca2+(o)) whether it was continuously present or applied after receptor stimulation. In contrast, Ca2+(o) solely inhibited TRPC7 currents (I(TRPC7)). Vigorous buffering of intracellular Ca2+ (Ca2+(i)) under conventional whole-cell clamp abolished the slow potentiating (i.e. accelerated activation) and inactivating effects of Ca2+(o), disclosing fast potentiation (EC50: approximately 0.4 mM) and inhibition (IC50: approximately 4 mM) of I(TRPC6) and fast inhibition (IC50: approximately 0.4 mM) of I(TRPC7). This inhibition of I(TRPC6) and I(TRPC7) seems to be associated with voltage-dependent reductions of unitary conductance and open probability at the single channel level, whereas the potentiation of I(TRPC6) showed little voltage dependence and was mimicked by Sr2+ but not Ba2+. The activation process of I(TRPC6) or its acceleration by Ca2+(o) probably involves phosphorylation by calmodulin (CaM)-dependent kinase II (CaMKII), as pretreatment with calmidazolium (3 microM), coexpression of Ca2+-insensitive mutant CaM, and intracellular perfusion of the non-hydrolysable ATP analogue AMP-PNP and a CaMKII-specific inhibitory peptide all effectively prevented channel activation. However, this was not observed for TRPC7. Instead, single CCh-activated TRPC7 channel activity was concentration-dependently suppressed by nanomolar Ca2+(i) via CaM and conversely enhanced by IP3. In addition, the inactivation time course of I(TRPC6) was significantly retarded by pharmacological inhibition of protein kinase C (PKC). These results collectively suggest that TRPC6 and 7 channels are multiply regulated by Ca2+ from both sides of the membrane through differential Ca2+-CaM-dependent and -independent mechanisms.

Suppression of kainate-evoked AMPA receptor mediated responses by lanthanum in rat sacral dorsal commissural neurons.

The effect of lanthanum (La) on kainate (KA) responses in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) was investigated using the nystatin-perforated patch-recording configuration under voltage-clamp conditions. The responses to KA were mediated by activation of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in SDCN neurons. La(3+) reversibly inhibited KA (100 microM) activated currents (I(KA)) in a concentration-dependent manner over the range from 30 microM to 30 mM, with IC(50) values of 0.64 +/- 0.06 mM at a holding potential (V(H)) of -40 mV. Our further study indicated that the effects of La(3+) on I(KA) were voltage independent. Moreover, the inhibition was not use dependent and was not overcome by increasing the concentration of agonist. These findings indicate that La(3+) is an efficacious inhibitor of AMPA receptor mediated responses which may contribute to its cytotoxic effect.

Glycolytic ATP production regulates muscarinic cation currents in guinea-pig ileum.

We investigated the possible sources of intracellular ATP which was previously shown essential for maintaining the muscarinic cationic channel activities (or currents; I(cat)) in guinea-pig ileal myocytes, using two variants of patch clamp techniques. Deprivation of external glucose or its replacement with 2-deoxyglucose significantly reduced the magnitude of I(cat), recorded with nystatin-perforated method, with greater efficacy than for voltage-dependent Ca2+ current Intracellular dialysis of ileal myocytes with key substrates for glycolysis, oxidative metabolism and creatine-phosphocreatine system all resulted in a comparably effective maintenance of I(cat), which was abolished by inhibitors for these ATP-producing systems, 3-bromopyruvate, cyanide and 2,4-dinitrofluorobenzene (DNFB), respectively. However, amongst these inhibitors, only 3-bromopyruvate effectively reduced I(cat) recorded with the nystatin-perforated method. These results strongly suggest the exclusive physiological importance of glycolytic ATP production in maintaining I(cat), activity, and thus this mechanism may play a role in the regulation of gut motility.

Beta-alanine acts on glycine receptors in the rat sacral dorsal commissural neurons.

Whole-cell current responses to bath application of beta-alanine (beta-ALA) were investigated in neurons acutely dissociated from the rat sacra! dorsal commissural nucleus (SDCN) using the nystatin perforated patch recording configuration under voltage-clamp conditions. beta-ALA activated inward currents in a concentration-dependent manner over the range of 10-3000 microM with an EC50 of 80.8 microM. The reversal potential of beta-ALA-activated currents (I beta-ALA) was close to the Cl- equilibrium potential. Strychnine and the chloride channel blocker picrotoxin suppressed the I beta-ALA in a concentration-dependent manner with the IC50 values of 0.19 microM and 343.6 microM, respectively. At the concentration of 3 microM, strychnine was sufficient to completely block 100 microM beta-ALA response, whereas it did not show a suppression of GABA response. In contrast, bicuculline, a potent GABAA receptor antagonist, at concentrations up to 10 microM, a dose that could block the GABA response completely, had little or no effect on I beta-ALA. Furthermore, the I beta-ALA was not affected by a preceding GABA response, but rather cross-desensitized with that evoked by glycine. The results indicate that beta-ALA activates the strychnine-sensitive glycine receptors in the SDCN neurons, and suggest that beta-ALA may act as a functional neurotransmitter in the mammalian SDCN.

Postnatal changes in the overall postsynaptic currents evoked in CA1 pyramidal neurons of the rat hippocampus.

Evoked fast postsynaptic currents (fPSCs) during the postnatal development of rats (postnatal day 6-70, P6-P70) were systematically examined in hippocampal CA1 pyramidal neurons using whole-cell recordings with biocytin-filled electrodes. Focal stimulation of the stratum radiatum in the CA1 region elicited fPSCs in 80% of the neurons P6-7, 90% of P9-10, and 100% of > or =P11. In neurons P6-7, the fPSCs were exclusively inward and had multiple (on average 5.6) peaks. The fPSCs increased in amplitude with the growth of dendritic arborization, but decreased in the number of peaks. A distinct outward fPSC following the inward fPSC emerged in neurons > or =P11 and was abolished by bicuculline (50 microM). Bicuculline increased the amplitude and duration of the initial inward fPSC (fEPSC) in all age groups and characteristically recruited the polysynaptic second component of fEPSCs in neurons P11-P21. No spontaneous periodic inward current was detected in any age group after blocking GABAA receptors. The coapplication of DL-2-amino-5-phosphonopentanoic acid (AP5, 100 microM) with bicuculline did not eliminate the polysynaptic second component, but the second component was only elicited in slices in which the CA3 region was kept intact. Moreover, the bicuculline- and AP5-resistant second component was due to the burst activity of CA3 pyramidal neurons, which were excited through excitatory recurrents of the Schaffer collaterals. Plausible physiological functions of the generation of the second component in vivo were discussed.

Cu(2+) inhibition of glycine-activated currents in rat sacral dorsal commissural neurons.

The effect of Cu(2+) on glycine (Gly) response was examined in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using the nystatin perforated patch clamp recording configuration under voltage-clamp conditions. Cu(2+), in the concentration range 10-1000 microM, reversibly inhibited chloride current activated by 30 microM Gly at a holding potential of -40 mV with an IC(50) of 88.4 microM. Cu(2+) shifted the Gly concentration response curve to the right in a parallel manner, which indicated that Cu(2+) decreased the apparent affinity of the receptor for Gly. Cu(2+) suppression of Gly-activated current was independent of membrane potential between -60 and +60 mV and did not involve a shift in the reversal potential of the current. Furthermore, Cu(2+) antagonized the inhibitory action of Zn(2+) in a concentration-dependent manner, suggesting a common site or mechanism of action of Cu(2+) and Zn(2+) on Gly receptors. The results show that Cu(2+) is a potent inhibitor of Gly receptor-mediated responses in rat spinal neurons.

Cu2+ suppresses GABA(A) receptor-mediated responses in rat sacral dorsal commissural neurons.

The effect of copper ions (Cu(2+)) on gamma-aminobutyric acid (GABA)-induced responses in acutely dissociated neurons from the rat sacral dorsal commissural nucleus (SDCN) was investigated using a nystatin-perforated patch recording configuration under voltage clamp conditions. The application of Cu(2+) to SDCN neurons reversibly suppressed the GABA (10 microM)-activated Cl(-) current (I(GABA)) in a concentration-dependent manner (1-1000 microM; IC(50) = 24.5 microM). In the presence of Cu(2+) (30 microM), the concentration-response curve of GABA was shifted rightward without reducing I(GABA) recorded under the maximally effective concentration of GABA, thus indicating a dependence of Cu(2+) action on GABA concentration. Inhibition of GABA (10 microM) responses by 30 microM Cu(2+) was essentially voltage independent and was not accompanied by a shift in the reversal potential of the currents. Cu(2+) antagonized the suppressive effect of Zn(2+) in a concentration-dependent manner, suggesting competition between Cu(2+) and Zn(2+) for similar binding sites. These data demonstrate that Cu(2+) is a potent inhibitor of GABA(A) receptor-mediated responses, implying a possible modulatory effect of Cu(2+) on GABAergic synaptic transmission in the mammalian SDCN.