Interaction of air cold plasma with Saccharomyces cerevisiae in the multi-scale microenvironment for improved ethanol yield.

In this study, the long-acting mechanism of reactive species was investigated for enhanced ethanol production of Saccharomyces cerevisiae. The results indicated that short-lifetime active species from gas phase plasma dissolved into various liquid microenvironments with different media (water, buffer, medium, and cells), forming different types and amounts of reactive species in multi-scale microenvironments, such as extracellular reactive nitrogen species, endocellular reactive oxygen and nitrogen species. The sustained elevation of cytoplasm calcium concentration with treatment time depended on the activated calcium channels of Cch1p/Mid1p in cell membrane and Yvc1p in vacuole membrane by these species. Accordingly, the Ca2+ increase promoted the H+-ATPase expression. Consequently, 75.6% ATP hydrolysis induced about 5 fold NADH increase compared with the control. Ultimately, the bioethanol yield increased by 34.2% compared to the control. These results promote the development of atmospheric cold plasma as a promising bio-process enhancement technology for improved target product yields of microbes in fermentation industry.

Activation of CaMKIIδA promotes Ca2+ leak from the sarcoplasmic reticulum in cardiomyocytes of chronic heart failure rats.

Activation of the Ca2+/calmodulin-dependent protein kinase II isoform δA (CaMKIIδA) disturbs intracellular Ca2+ homeostasis in cardiomyocytes during chronic heart failure (CHF). We hypothesized that upregulation of CaMKIIδA in cardiomyocytes might enhance Ca2+ leak from the sarcoplasmic reticulum (SR) via activation of phosphorylated ryanodine receptor type 2 (P-RyR2) and decrease Ca2+ uptake by inhibition of SR calcium ATPase 2a (SERCA2a). In this study, CHF was induced in rats by ligation of the left anterior descending coronary artery. We found that CHF caused an increase in the expression of CaMKIIδA and P-RyR2 in the left ventricle (LV). The role of CaMKIIδA in regulation of P-RyR2 was elucidated in cardiomyocytes isolated from neonatal rats in vitro. Hypoxia induced upregulation of CaMKIIδA and activation of P-RyR2 in the cardiomyocytes, which both were attenuated by knockdown of CaMKIIδA. Furthermore, we showed that knockdown of CaMKIIδA significantly decreased the Ca2+ leak from the SR elicited by hypoxia in the cardiomyocytes. In addition, CHF also induced a downregulation of SERCA2a in the LV of CHF rats. Knockdown of CaMKIIδA normalized hypoxia-induced downregulation of SERCA2a in cardiomyocytes in vitro. The results demonstrate that the inhibition of CaMKIIδA may improve cardiac function by preventing SR Ca2+ leak through downregulation of P-RyR2 and upregulation of SERCA2a expression in cardiomyocytes in CHF.

(-)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway.

BACKGROUND/AIMS: Flavonol (-)-epicatechin (EPI) is present in high amounts in cocoa and tea products, and has been shown to exert beneficial effects on the cardiovascular system. However, the precise mechanism of EPI on cardiomyocyte hypertrophy has not yet been determined. In this study, we examined whether EPI could inhibit cardiac hypertrophy. METHODS: We utilised cultured neonatal mouse cardiomyocytes and mice for immunofluorescence, immunochemistry, qRT-PCR, and western blot analyses. RESULTS: 1µM EPI significantly inhibited 1µM angiotensin II (Ang II)-induced increase of cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and ß-MHC in vitro. The effects of EPI were accompanied with an up-regulation of SP1 and SIRT1, and were abolished by SP1 inhibition. Up-regulation of SP1 could block Ang II-induced increase in cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and ß-MHC, and increase the protein levels of SIRT1 in vitro. Moreover, 1 mg/kg body weight/day EPI significantly inhibited mouse cardiac hypertrophy induced by Ang II, which could be eliminated by SP1 inhibition in vivo. CONCLUSION: Our data indicated that EPI inhibited AngII-induced cardiac hypertrophy by activating the SP1/SIRT1 signaling pathway.

[Effects of UV-B radiation on the growth and reproduction of Vicia angustifolia].

A simulation experiment with supplementation and exclusion of solar ultraviolet-B (UV-B) radiation was conducted to study the effects of enhanced and near ambient UV-B radiation on the growth and reproduction of alpine annual pasture Vicia angustifolia on Qinghai-Tibet Plateau. Enhanced UV-B decreased the plant height and biomass, biomass allocation to fruit, flower number, and 100-seed mass significantly, delayed flowering stage, increased the concentration degree of flowering and success rate of reproduction, but had little effect on seed yield. Near ambient UV-B radiation made the plant height increased after an initial decrease, decreased biomass allocation to fruit and 100-seed mass, but little affected flowering duration, flower number, and seed yield. Both enhanced and near ambient UV-B radiation could inhibit the growth and production of V. angustifolia, and the effect of enhanced UV-B radiation was even larger.

[The apoptosis of mouse macrophage J774A.1 induced by oxysterol depend on NF-kappaB activation].

AIM: Investigated the relationship between NF-kappaB activation and cell apoptosis in mouse macrophages treated with 7-ketochesterol (7-KC). METHODS: Cell apoptosis was detected by MTT assay, DNA fragmentation assay and flow cytometric analysis. NF-kappaB activation was detected by western blot and immunohistochemistry. Inhibitory assay was used to show the effect of the activation of NF-kappaB on the apoptosis induced by 7-KC. RESULTS: 7-KC inhibited macrophages proliferation, and then induced apoptosis, which is associated with NF-kappaB activation. Moreover, cell apoptosis with NF-kappaB activation was inhibited by pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappaB. CONCLUSION: 7-KC induced the activation of NF-kappaB and following cell apoptosis.

GABA(A) and GABA(B) receptor-mediated inhibition of sympathetic outflow in the paraventricular nucleus is blunted in chronic heart failure.

1. Alterations in the paraventricular nucleus (PVN) are reported to be involved in sympathetic overactivity in chronic heart failure (CHF). Inhibitory inputs into the PVN contribute to sympathetic outflow. The aim of the present study was to comparatively determine the role of GABA mechanisms in the PVN in the tonic control of cardiovascular activity in anaesthetized sham and CHF rats. 2. The CHF model was induced by coronary artery ligation. Unilateral microinjection of the GABA(A) receptor agonist muscimol (0.1-0.8 nmol/200 nL) or the GABA(B) receptor agonist baclofen (0.25-2.0 nmol/200 nL) into the PVN produced similar, dose-dependent reductions in arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA). This response was significantly blunted in CHF rats. In contrast, microinjection of the GABA(A) receptor antagonist bicuculline (25-200 pmol/200 nL) or the GABA(B) receptor antagonist CGP35348 (0.25-2.0 nmol/200 nL) into the PVN caused larger, dose-dependent increases in AP, HR and RSNA in sham than in CHF rats. 3. Polymerase chain reaction data showed that mRNA expression levels of the GABA(A) receptor alpha(1)-subunit and of the GABA(B1(a)) and GABA(B1(b)) receptor subtypes in the PVN were significantly lower in CHF than in sham rats. 4. The results of the present study suggest that the tonic inhibition mediated by both GABA(A) and GABA(B) receptors in the PVN on sympathetic outflow is blunted in CHF, which may be an important mechanism responsible for sympathetic hyperactivity in CHF.

[Studies on the oxidation of LDL induced by Cu2 at different time by spectroscopic method].

Oxidized low density lipoprotein (oxLDL) is thought to be a key proatherogenic event. The oxidation of LDL induced by Cu+ at different time was studied by UV-Vis absorption spectra and circular dichroism (CD) spectra. It was shown that long oxidation time is accompanied by an increased MDA content and fluorescence intensity at 430 nm, which suggested new product. The intensity of UV absorption peak of LDL increased, while fluorescence and synchronous fluorescence intensities, which typified amino acids, decreased. CD data displayed that alpha-helical content of the protein decreased and the secondary structure changed. The results indicated that during the process of oxidation of LDL Cu2+ induced not only the product but also the change of the conformation of apoB-100.

[Allelopathic effects of Corallina pilulifera on red tide microalgae Heterosigma akashiwo].

Different concentration methanol-, acetone-, ether-, and chloroform extracts of Corallina pilulifera were used to study their growth inhibitory effects on red tide microalgae Heterosigma akashiwo. The results showed that methanol extract at relatively higher concentrations had the highest growth inhibitory activity and killed all H. akashiwo cells, while the other three kinds of organic solvent extracts had no apparent inhibitory effects, suggesting that the growth inhibitory substances in C. pilulifera had relatively high polarity. The methanol extract was partitioned to petroleum ether phase, ethyl acetate phase, butanol phase, and distilled water phase by liquid-liquid fractionation, and the bioassays on the activity of each fraction were carried out on H. akashiwo. It was found that petroleum ether phase and ethyl acetate phase had strong algicidal effects on H. akashiwo, suggesting that the fatty acids in C. pilulifera tissues might be one of the main allelochemicals.

[Effects of red tide microalgae Alexandrium tamarense on the life history of rotifer Brachionus plicatilis].

In this paper, life-table method was used to study the effects of different concentration Alexandrium tamarense on the durations of different development stages of Brachionus plicatilis and the characters of its population growth. The results showed that A. tamarense had significant effects on the growth and development of B. plicatilis via prolonging the durations of the rotifer' s pre-reproduction and generation succession, shortening the durations of its reproduction and post-reproduction and its mean lifespan, and reducing its laying eggs and fecundity. The net reproduction rate and intrinsic increasing rate of B. plicatilis decreased significantly, in comparison with those of the control. B. plicatilis could maintain definite population increase at the presence of different concentration A. tamarense.