Re-evaluation and modification of dehydrogenase activity tests in assessing microbial activity for wastewater treatment plant operation.

Reliable and cost-effective methods for monitoring microbial activity are critical for process control in wastewater treatment plants. The dehydrogenase activity (DHA) test has been recognized as an efficient measure of biological activity due to its simplicity and broad applicability. Nevertheless, the existing DHA test methods suffer from imperfections and are difficult to implement as routine monitoring techniques. In this work, an accurate and cost-effective modified DHA approach was developed and the procedure for the DHA test was critically evaluated with respect to the standard construction, sample pretreatment, incubation and extraction conditions. The feasibility of the modified DHA test was demonstrated by comparison with the oxygen uptake rate and adenosine triphosphate in a sequencing batch reactor. The sensitivities of the two typical tetrazolium salts to toxicant inhibition by heavy metals and antibiotics were compared, revealing that 2,3,5-triphenyltetrazolium chloride (TTC) exhibited a higher sensitivity. Furthermore, the sensitivity mechanism of the two DHA tests was elucidated through electrochemical experiments, theoretical analysis and molecular simulations. Both tetrazolium salts were found to be effective artificial electron acceptors due to their low redox potentials. Molecular docking simulations revealed that TTC could outperform other tetrazolium salts in accepting electrons and hydrogens from dehydrogenase. Overall, the modified DHA approach presents an accurate and cost-effective way to measure microbial activity, making it a practical tool for wastewater treatment plants.

Biobinder Nanocoating for Upgrading the Assembling Structures of High-Capacity Composite Electrodes with a Robust Polymeric Artificial Solid Electrolyte Interphase.

The success of next-generation lithium-ion batteries (LIBs) fundamentally depends on the rational design of not only the microstructure of an individual component but the component assembling structures on the electrode level. However, building advanced assembling structures for especially high-capacity electrodes is an urgent but a challenging task due to the lacking of in-depth understanding and effective strategies. Here, we propose a functional nanocoating biobinder using the well-known poly(lactic acid) to address the above need. It is found that the composite electrodes with this nanocoating biobinder are upgraded with uniform and robust assembling structures, including the electron-transportation network, ion-transportation network, and interfaces. Importantly, the nanocoating finally works as a new type of polymeric artificial cathode electrolyte interphase (poly-CEI) to protect the active particles. Therefore, a remarkable improvement in the electrochemical performance has been achieved for high-capacity electrodes (LiFePO4, lithium nickel cobalt manganite (NCM), and lithium nickel cobalt aluminum acid (NCA)). In particular, the LFP cathode can deliver a high discharge capacity of 74.6 mA h g-1 at 10C and a high capacity retention of 95.5% even after 850 cycles at 2C. For NCA and NCM cathodes, the cycling stability is dramatically improved due to the protection by the poly-CEI. In short, this study may reshape the essential roles of a binder in composite electrodes by highlighting its critical link to assembling structures.

Effects of PPAR-γ in the Myocardium on the Development of Ventricular Septation.

Ventricular septum defects (VSDs) are common types of congenital heart diseases caused by developmental defect; they contribute to 25%-30% of all adult congenital heart diseases. The peroxisome proliferator-activated receptor gamma (PPAR-γ) is widely expressed in mammalian tissues and in the immune system, regulating cell differentiation and immune and inflammatory responses. The PPAR-γ gene has recently been found crucial for heart development, but the mechanism of action is not clear. This study aims to investigate the effects of the PPAR-γ gene in the myocardium on the development of ventricular septation. In this study, we applied Cre-loxP recombination enzyme (CRE) technology to downregulate the expression of the PPAR-γ gene in different cardiac tissues, RT-PCR to examine the expression of the c-fos and TGF-ß1 genes, and histology staining to check the defect of embryonic heart at embryonic day 14.5 (E14.5). We found that the downregulation of the PPAR-γ gene resulted in a ventricular membranous septation defect of the embryonic heart at E14.5. Furthermore, only conversion of a Tnt:Cre, but not Mef2c:Cre, Tie2:Cre, or Wnt:Cre PPAR-γ floxed allele to a null allele resulted in VSD. PPAR-γTnt-Cre/+ embryos showed increases in atrioventricular (AV)-cushion cells and the expression of c-fos gene but no change in the expression of TGF-ß1 at E10.5. Our study demonstrates PPAR-γ in the myocardium is required for ventricular septation through regulation of AV-cushion cell proliferation by a Tnt/c-fos signal.

Cardioprotection of Rosuvastatin Pre-conditioning on Myocardial Ischemia / Reperfusion Injury in a Rat Model

Abstract This study aimed to investigate the cardioprotection of rosuvastatin pre-conditioning (R-Pre) in a rat model of myocardial ischemia / reperfusion (I/R). Male SD rats were assigned into three groups: sham group, I/R group and R-Pre group. Rats in I/R group and R-Pre group received ischemia for 30 min and reperfusion for 2 h. In R-Pre group, rats received intragastrical administration with rosuvastatin at 5 mg/kg once daily for 1 week. After 2-h reperfusion, the cardiac function was detected by ultrasonography; the blood was collected for biochemical analysis; the heart was collected for the TUNEL staining and immunohistochemistry for Bcl-2 and Bax. Our results showed rosuvastatin pre-conditioning for 1 week could significantly reduce the infarct ratio and improve the cardiac function after myocardial I/R injury, in which attenuation of oxidative stress and cell apoptosis played an important role. Our study provides evidence on the cardioprotection of rosuvastatin pre-conditioning and highlight the use of rosuvastatin before cardiopulmonary bypass.

Pharmacological Characterization of Dezocine, a Potent Analgesic Acting as a κ Partial Agonist and µ Partial Agonist.

Dezocine is becoming dominated in China market for relieving moderate to severe pain. It is believed that Dezocine's clinical efficacy and little chance to provoke adverse events during the therapeutic process are mainly attributed to its partial agonist activity at the µ opioid receptor. In the present work, we comprehensively studied the pharmacological characterization of Dezocine and identified that the analgesic effect of Dezocine was a result of action at both the κ and µ opioid receptors. We firstly found that Dezocine displayed preferential binding to µ opioid receptor over κ and δ opioid receptors. Dezocine, on its own, weakly stimulated G protein activation in cells expressing κ and µ receptors, but in the presence of full κ agonist U50,488 H and µ agonist DAMGO, Dezocine inhibited U50,488H- and DAMGO-mediated G protein activation, indicating that Dezocine was a κ partial agonist and µ partial agonist. Then the in intro results were verified by in vivo studies in mice. We observed that Dezocine-produced antinociception was significantly inhibited by κ antagonist nor-BNI and µ antagonist ß-FNA pretreatment, indicating that Dezocine-mediated antinociception was via both the κ and µ opioid receptors. When co-administrating of Dezocine with U50,488 H or morphine, Dezocine was capable of inhibiting U50,488H- or morphine-induced antinociception. Finally, κ receptor activation-associated side effect sedation was investigated. We found that Dezocine displayed limited sedative effect with a ceiling effecting at a moderate dose. Thus, our work led to a better understanding of the analgesic mechanism of action of Dezocine in vivo.