The synergistic effect of chemical oxidation and microbial activity on improving volatile fatty acids (VFAs) production during the animal wastewater anaerobic digestion process treated with persulfate/biochar.

Improving volatile fatty acid (VFA) production, rather than producing methane from the anaerobic digestion (AD) of waste, has become a new strategy of resource utilization. In regard to animal wastewater, the effectiveness of persulfate/biochar (potassium peroxodisulfate, PDS/BC) on the hydrolysis and acidogenesis stages and the reaction mechanisms are still unclear. In this study, the AD process on cow wastewater was controlled at the hydrolysis and acidification stages by setting the hydraulic retention time (HRT) at 25 days. The results showed that the contents of total solids (TS) and volatile solids (VS) were further reduced by PDS/BC treatment with 0.15 gPDS/gTS of PDS added. The VFAs production increased by 12.4 % from day 0 to 25 compared to the blank set. Based on our molecular analysis, the rate of increase for the dissolved organic matter with low molecular weight (0-10 kDa) was 699.5 mg/(L·d) in the first 10 days. The change rate increased nearly 2.1 times, leading to higher VFAs yield. Moreover, the activities of fermentative bacteria were enhanced and Anaerocella was determined to be the specific and critical genus. However, excessive PDS (0.3 gPDS/gTS) prolonged the acidification period and caused the inactivation of fermentative bacteria. Structural equation modeling demonstrated that PDS can directly affect VFAs yield and also had an indirect effect by influencing the decomposition of particulate matter and microbial activities. Therefore, the enhancement of VFAs production using the PDS/BC method could be due to synergistic chemical and microbial effects. Findings from this study can provide a practical strategy to enhance the VFAs production of AD technology for livestock wastewater and help reveal the reaction mechanism of PDS/BC treatment.

[Research on community promotion and application of single acupoint electroacupuncture therapy for lumbar intervertebral disc herniation].

OBJECTIVE: To observe the clinical effect of single acupoint [Yaotu (extra)] electroacupuncture (EA) therapy on lumbar intervertebral disc herniation (LIDH) and its promotion and application in community medical institutions. METHODS: This research adopted a three-level promotion model, and used multi-center collaboration topics as a platform. A total of 240 patients with LIDH were divided into a group A (top three hospital, 80 cases, 3 cases dropped off), a group B (secondary hospital, 80 cases, 8 cases dropped off), and a group C (community health center, 80 cases, 7 cases dropped off). All groups were treated with EA at a single acupoint [Yaotu (extra)] under the guidance of a unified experimental protocol. The EA was given 60 min each time and performed 3 times a week for a total of 2 weeks. The changes of visual analogue scale (VAS) scores of three groups before and after each treatment were compared, and the clinical efficacy was evaluated. RESULTS: Compared with before each treatment, the VAS scores of three groups after each treatment decreased (P<0.05). Except for the second and fifth treatments, the immediate effect in the group A was higher than that in the group B and C (P<0.05). The total effective rate of group A, group B, and group C respectively was 90.9% (70/77), 93.1% (67/72), 86.3% (63/73), and there was no statistically significant difference among the three groups (P>0.05). CONCLUSION: The single acupoint EA therapy has a significant effect in the treatment of LIDH, can quickly relieve the pain symptoms, and has the characteristics of simple operation and easy control, suitable for promotion and application in primary hospitals.

Bendable Network Built with Ultralong Silica Nanowires as a Stable Separator for High-Safety and High-Power Lithium-Metal Batteries.

Separators are key safety components for electrochemical energy storage systems. However, the intrinsic poor wettability with electrolyte and low thermal stability of commercial polyolefin separators cannot meet the requirements of the ever-expanding market for high-power, high-energy, and high-safety power systems, such as lithium-metal, lithium-sulfur, and lithium-ion batteries. In this study, scalable bendable networks built with ultralong silica nanowires (SNs) are developed as stable separators for both high-safety and high-power lithium-metal batteries. The three-dimensional porous nature (porosity of 73%) and the polar surface of the obtained SNs separators endue a much better electrolyte wettability, larger electrolyte uptake ratio (325%), higher electrolyte retention ratio (63%), and ∼7 times higher ionic conductivity than that of commercial polypropylene (PP) separators. Moreover, the pore-rich structure of the SNs separator can aid in evenly distributing lithium and, in turn, suppress the uncontrollable growth of lithium dendrites to a certain degree. Furthermore, the pure inorganic structure endows the SNs separators with excellent chemical and electrochemical stabilities even at elevated temperatures, as well as excellent thermal stability up to 700 °C. This work underpins the utilization of SNs separators as a rational choice for developing high-performance batteries with a metallic lithium anode.

Cold-Inducible Protein RBM3 Protects UV Irradiation-Induced Apoptosis in Neuroblastoma Cells by Affecting p38 and JNK Pathways and Bcl2 Family Proteins.

Induced by hypothermia, cold-inducible protein RBM3 (RNA-binding protein motif 3), has been implicated in neuroprotection against various toxic insults such as hypoxia and ischemia. However, whether mild hypothermia and RBM3 prevent neural cells from UV irradiation-elicited apoptosis is unclear. In the present study, human neuroblastoma cell line SH-SY5Y was used as a cell model for neural cell death, and it was demonstrated that mild hypothermia protects SH-SY5Y cells from UV irradiation-induced apoptosis. However, the protective effect of mild hypothermia was abrogated when RBM3 was silenced. Conversely, the overexpression of RBM3 rescued SH-SY5Y cells from UV-induced apoptosis, as indicated by the decreased levels of cleaved caspase-3 and PARP, and increased cell survival. The analysis on the mechanism underlying RBM3-mediated neuroprotection against UV insult showed that RBM3 could substantially block the activation of p38 and JNK signaling pathways. In addition, the overexpression of RBM3 reduced the expression of pro-apoptotic proteins Bax and Bad, leaving the pro-survival protein Bcl-2 unaffected. In conclusion, RBM3 is the key mediator of mild hypothermia-related protection against UV in neuroblastoma cells, and the neuroprotective effect might be exerted through interfering with pro-apoptotic signaling pathways p38 and JNK and regulating pro-apoptotic proteins Bax and Bad.

[Effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion was observed. 32 Sprague-Dawley (SD) rats were randomly divided into four groups: the acetazolamide 200, 20, 2 mg/kg body weight and normal saline (NS) group. The animals were given intraperitoneally acetazolamide or NS, respectively, before being exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the changes in maleic dialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) were measured after acetazolamide treatment. 40 SD rats were randomly divided into five groups: NS group, 6 min with NS group, 6 min with acetazolamide group, 16 min with NS group, and 16 min with acetazolamide group. The dose of acetazolamide was 20 mg/kg body weight. After injection of NS or acetazolamide, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. The rats were decapitated and the cortex, hippocampus, and striatum of brains were dissected and homogenized. The content of MDA and the activity of GSH-PX in these tissues were determined. We found that (1) there was a significant difference in the latency of hyperbaric oxygen-induced convulsion between the acetazolamide 200 mg/kg group and the NS control group, as well as between the acetazolamide 20 mg/kg group and the NS control group (P<0.01), whereas there was no significant difference between the NS group and the acetazolamide 2 mg/kg weight group (P>0.05). The latency of these groups were listed as follows: 9.78+/-1.94 min for 200 mg/kg body weight group, 10.92+/-1.68 min for 20 mg/kg body weight group, 24.32+/-4.33 min for 2 mg/kg body weight group and 22.02+/-4.32 min for NS control group. (2) there was no significant difference between all groups in the activity of GSH-PX, though it varied with the oxidation levels. In the cortex and hippocampus, the activity of GSH-PX boosted up at first, but with the progress of the oxidation it was impaired. In the striatum, the activity of GSH-PX increased stepwise with the aggravation of the oxidation. The MDA content in the cortex increased significantly in the group of 6 min with acetazolamide (P<0.01), as well as the group of 16 min with acetazolamide group both in cortex and hippocampus (P<0.01, P<0.05). The MDA content of all groups is correlated with the dose of acetazolamide and the exposure time. These results suggest that acetazolamide which dilates the brain arteriolar obviously shortens the latency of hyperbaric oxygen-induced convulsion, and that acetazolamide dilates the vessels and increases the supply of the oxygen breaking into the brain tissues and aggravates the oxidation. The hyperbaric oxygen-induced convulsion correlates closely with the oxidation injury.