Impact of ambient relative humidity and acidity on chemical composition evolution for malonic acid/calcium nitrate mixed particles.

The chemical compositions in atmospheric aerosols, which often evolve with environmental factors, have significant impact on climate and human health, while our fundamental understanding of chemical process is limited owing to their sensitive to atmospheric conditions. pH and RH are critical chemical factors of aerosols, impacting reaction pathways and kinetics that ultimately govern final components in particles. Herein, we monitored the chemical composition in internally mixed malonic acid/calcium nitrate with the mole ratio of 1:1 as a function of pH and relative humidity (RH). At 30% RH, lower than efflorescence relative humidity (ERH) of pure malonic acid aerosols, malonic acid still exhibits solution feature reflected by IR spectra, which was observed to transform to malonate, along with water loss and nitrate depletion. At another RH of 54% and 80%, the similar chemical process happened with less reaction rate. The response of chemical reaction between malonic acid and calcium nitrate to pH was studied by manipulating the starting pH of the bulk solution through dropping aqueous sodium hydroxide. Due to lower H+ concentration at higher pH, the formation and liberation of HNO3 slow down, as well as water loss. After a down-up RH cycle, the water loss was obvious and grew with the decrease in pH. These measurements are improving our understanding of chemical composition evolution dependent upon pH and RH from a fundamental physical chemistry perspective and are critical for connecting chemistry and climate.

Acidosis impairs the protective role of hERG K(+) channels against premature stimulation.

INTRODUCTION: Potassium channels encoded by human ether-à-go-go-related gene (hERG) underlie the cardiac rapid delayed rectifier K(+) channel current (I(Kr)). Acidosis occurs in a number of pathological situations and modulates a range of ionic currents including I(Kr) . The aim of this study was to characterize effects of extracellular acidosis on hERG current (I(hERG)), with particular reference to quantifying effects on I(hERG) elicited by physiological waveforms and upon the protective role afforded by hERG against premature depolarizing stimuli. METHODS AND RESULTS: I(hERG) recordings were made from hERG-expressing Chinese Hamster Ovary cells using whole-cell patch-clamp at 37°C. I(hERG) during action potential (AP) waveforms was rapidly suppressed by reducing external pH from 7.4 to 6.3. Peak repolarizing current and steady state I(hERG) activation were shifted by ∼+6 mV; maximal I(hERG) conductance was reduced. The voltage-dependence of I(hERG) inactivation was little-altered. Fast and slow time-constants of I(hERG) deactivation were smaller across a range of voltages at pH 6.3 than at pH 7.4, and the contribution of fast deactivation increased. A modest acceleration of the time-course of recovery of I(hERG) from inactivation was observed, but time-course of activation was unaffected. The amplitude of outward I(hERG) transients elicited by premature stimuli following an AP command was significantly decreased at lower pH. Computer simulations showed that after AP repolarization a subthreshold stimulus at pH 7.4 could evoke an AP at pH 6.3. CONCLUSION: During acidosis the contribution of I(hERG) to action potential repolarization is reduced and hERG may be less effective in counteracting proarrhythmogenic depolarizing stimuli.

[Changes of heart rate variability and impairment of learning and memory induced by cerebral ischemia/reperfusion in rats].

The present study was designed to observe the influence of cerebral ischemia/reperfusion injury on learning and memory in hyperlipidemic rats and estimate the changes of activity of autonomic nervous system. Twenty-three male Wistar rats were randomly divided into three groups, named control group (C group, n=10), hyperlipidemia group (H group, n=6) and hyperlipidemia-ischemia group (HI group, n=7), respectively. The rats in H and HI group were fed a high-fat diet for 2 weeks and the rats in all groups were examined through Morris water maze (MWM) task. The rats in HI group underwent ischemia/reperfusion by 2-vessel occlusion (2-VO) method, and had electrocardiogram (ECG) recording simultaneously. The MWM task and ECG recording were taken again after 7 d of recuperation. The following results were obtained: (1) In the second place navigation performance and probe trial performance, the frequency of memory in quadrant of hidden-platform and memory score decreased significantly in HI group compared to that in C and H groups. (2) The heart rate in HI group decreased slowly after ischemia; the power at high frequency band (HF) reduced gradually, meanwhile the power at middle frequency band (MF) and the ratio of power at MF and HF decreased clearly compared to baseline value. (3) After 7 d of ischemia/reperfusion, the heart rate in HI group was significantly higher than that in H group (P<0.05). While there was no statistical change in the power at MF, the power at HF decreased and the ratio of MF/HF increased significantly (P<0.05). The data demonstrated that ischemia/reperfusion decreased the activity of autonomic nervous system, and the reduction of sympathetic nerve activity was much more than that of vagus nerve activity. The results suggest that the hippocampus neuron injury caused by ischemia induces cognitive disorder and imbalance of vago-sympathetic nerve activity accompanied by vagus nerve suppression.

[Effects of beta-cypermethrin on voltage-gated potassium channels in rat hippocampal CA3 neurons].

The effects of beta-cypermethrin (consisting of alpha-cypermethrin and theta-cypermethrin) on the transient outward potassium current (I(A)) and delayed rectifier potassium current (I(K)) in freshly dissociated hippocampal CA3 neurons of rats were studied using whole-cell patch-clamp technique. The results indicated that alpha-cypermethrin increased the value of I(A) and theta-cypermethrin decreased the value of I(A), though both of them shifted steady activation curve of I(A) towards negative potential. theta-cypermethrin contributed to the inactivation of I(A). The results also showed that alpha-cypermethrin and theta-cypermethrin decreased the value of I(K), and shifted the steady state activation curve of I(K) towards negative potential. Both alpha-cypermethrin and theta-cypermethrin had no obvious effects on the inactivation of I(K). theta-cypermethrin prolonged recovery process of I(K). These results imply that both transient outward potassium channels and delayed rectified potassium channels are the targets of beta-cypermethrin, which may explain the mechanism of toxical effects of beta-cypermethrin on mammalian neurons.