Plasma-Induced Selective Propylene Epoxidation Using Water as the Oxygen Source.

Propylene oxide (PO) is a critical gateway chemical used in large-scale production of plastics and many other compounds. In addition, PO is also used in many smaller-scale applications that require lower PO concentrations and volumes. These include its usage as a fumigant and disinfectant for food, a sterilizer for medical equipment, as well as in producing modified food such as starch and alginate. While PO is currently mostly produced in a large-scale propylene epoxidation chemical process, due to its toxic nature and high transport and storage costs, there is a strong incentive to develop PO production strategies that are well-suited for smaller-scale on-site applications. In this contribution, we designed a plasma-liquid interaction (PLI) catalytic process that uses only water and C3H6 as reactants to form PO. We show that hydrogen peroxide (H2O2) generated in the interactions of water with plasma serves as a critical oxidizing agent that can epoxidize C3H6 over a titanium silicate-1 (TS-1) catalyst dispersed in a water solution with a carbon-based selectivity of more than 98%. As the activity of this plasma C3H6 epoxidation system is limited by the rate of H2O2 production, strategies to improve H2O2 production were also investigated.

Adolescent Δ9-Tetrahydrocannabinol Exposure Selectively Impairs Working Memory but Not Several Other mPFC-Mediated Behaviors.

As the frequency of cannabis use by 14-16-year-olds increases, it becomes increasingly important to understand the effect of cannabis on the developing central nervous system. Using mice as a model system, we treated adolescent (28 day old) C57BL6/J mice of both sexes for 3 weeks with 3 mg/kg tetrahydrocannabinol (THC). Starting a week after the last treatment, several cognitive behaviors were analyzed. Mice treated with THC as adolescents acquired proficiency in a working memory task more slowly than vehicle-treated mice. Working memory recall in both sexes of THC-treated mice was also deficient during increasing cognitive load compared to vehicle-treated mice. Our adolescent THC treatment did not strongly affect social preference, anxiety behaviors, or decision-making behaviors on the elevated T maze task. In summary, under the conditions of this study, adolescent THC treatment of mice markedly affected the establishment, and persistence of working memory, while having little effect on decision-making, social preference or anxiety behaviors. This study provides further support that adolescent THC affects specific behavioral domains.

Stoichiometry-Controlled MoxW1-xTe2 Nanowhiskers: A Novel Electrocatalyst for Pt-Free Dye-Sensitized Solar Cells.

Novel polymorphic MoxW1-xTe2-based counter electrodes possess high carrier mobility, phase-dependent lattice distortion, and surface charge density wave to boost the charge-transfer kinetics and electrocatalytic activity in dye-sensitized solar cells (DSSCs). Here, we report the syntheses of stoichiometry-controlled binary and ternary MoxW1-xTe2 nanowhiskers directly on carbon cloth (CC), denoted by MoxW1-xTe2/CC, with an atmospheric chemical vapor deposition technique. The synthesized MoxW1-xTe2/CC samples, including 1T'-MoTe2/CC, Td-WTe2/CC, Td-Mo0.26W0.73Te2.01/CC, and 1T'- & Td-Mo0.66W0.32Te2.02/CC, were then employed as different counter electrodes to study their electrochemical activities and efficiencies in DSSCs. The photovoltaic parameter analysis manifests that MoxW1-xTe2/CCs are more stable than a standard Pt/CC in the I-/I3- electrolyte examined by cyclic voltammetry over 100 cycles. A 1T'- & Td-Mo0.66W0.32Te2.02/CC-based DSSC can achieve a photocurrent density of 16.29 mA cm-2, a maximum incident photon-to-electron conversion efficiency of 90% at 550 nm excitation, and an efficiency of 9.40%, as compared with 8.93% of the Pt/CC counterpart. Moreover, the 1T'- & Td-Mo0.66W0.32Te2.02/CC shows lower charge-transfer resistance (0.62 Ω cm2) than a standard Pt/CC (1.19 Ω cm2) in electrocatalytic reactions. Notably, MoxW1-xTe2 nanowhiskers act as an electron expressway by shortening the path of carrier transportation in the axial direction from a counter electrode to electrolytic ions to enhance the reaction kinetics in DSSCs. This work demonstrates that the nanowhisker-structured 1T'- & Td-Mo0.66W0.32Te2.02/CC with high carrier mobility and robust surface states can serve as a highly efficient counter electrode in DSSCs to replace the conventional Pt counter electrode for electrocatalytic applications.

Role of the ventral tegmental area in methamphetamine extinction: AMPA receptor-mediated neuroplasticity.

The molecular mechanisms underlying drug extinction remain largely unknown, although a role for medial prefrontal cortex (mPFC) glutamate neurons has been suggested. Considering that the mPFC sends glutamate efferents to the ventral tegmental area (VTA), we tested whether the VTA is involved in methamphetamine (METH) extinction via conditioned place preference (CPP). Among various METH-CPP stages, we found that the amount of phospho-GluR1/Ser845 increased in the VTA at behavioral extinction, but not the acquisition or withdrawal stage. Via surface biotinylation, we found that levels of membrane GluR1 were significantly increased during METH-CPP extinction, while no change was observed at the acquisition stage. Specifically, the number of dendritic spines in the VTA was increased at behavioral extinction, but not during acquisition. To validate the role of the mPFC in METH-CPP extinction, we lesioned the mPFC. Ibotenic acid lesioning of the mPFC did not affect METH-CPP acquisition, however, it abolished the extinction stage and reversed the enhanced phospho-GluR1/Ser845 levels as well as increases in VTA dendritic spines during METH-CPP extinction. Overall, this study demonstrates that the mPFC plays a critical role in METH-CPP extinction and identifies the VTA as an alternative target in mediating the extinction of drug conditioning.

Mineralocorticoid receptor antagonist spironolactone prevents chronic corticosterone induced depression-like behavior.

High level of serum corticosteroid is frequently associated with depression, in which a notable HPA (hypothalamus-pituitary-adrenal) axis hyperactivity is often observed. There are two types of corticosteroid receptors expressed in the hippocampus that provide potent negative feedback regulation on the HPA axis but dysfunction during depression, i.e. the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). The balance between hippocampal MR and GR during chronic stress plays an important role in the occurrence of depression. The aim of this study is to explore if chronic corticosterone administration would induce depression-like behavior and affect the expression and function of hippocampal MR and GR, in addition to assess whether manipulation of corticosteroid receptors would modulate depressive behaviors. Hence, mice were treated with corticosterone (40 mg/kg) for 21 days followed by assessment in a battery of depression-like behaviors. The results show that chronic corticosterone-treated animals displayed an increased immobility time in a forced-swimming test, decreased preference to sucrose solution and novel object recognition performance, and enhanced hippocampal serotonin but decreased MR expression in both hippocampus and hypothalamus. On the other hand, co-administration of MR antagonist, spironolactone (25mg/kg, i.p. × 7 days) in corticosteroid-treated animals reduced immobility time in a forced-swimming test and improved performance in a novel object recognition test. In conclusion, we demonstrate that chronic corticosterone treatment triggers several depression-like behaviors, and in parallel, down-regulates MR expression in the hippocampus and hypothalamus. Administration of an MR antagonist confers an anti-depressant effect in chronic corticosterone-treated animals.

Dopamine D2 receptor-mediated Akt/PKB signalling: initiation by the D2S receptor and role in quinpirole-induced behavioural activation.

The short and long isoforms of the dopamine D2 receptor (D2S and D2L respectively) are highly expressed in the striatum. Functional D2 receptors activate an intracellular signalling pathway that includes a cAMP-independent route involving Akt/GSK3 (glycogen synthase kinase 3). To investigate the Akt/GSK3 response to the seldom-studied D2S receptor, we established a rat D2S receptor-expressing cell line [HEK (human embryonic kidney)-293/rD2S]. We found that in HEK-293/rD2S cells, the D2/D3 agonists bromocriptine and quinpirole significantly induced Akt and GSK3 phosphorylation, as well as ERK1/2 (extracellular-signal-regulated kinase 1/2) activation. The D2S receptor-induced Akt signals were profoundly inhibited by the internalization blockers monodansyl cadaverine and concanavalin A. Activation of the D2S receptor in HEK-293/rD2S cells appeared to trigger Akt/phospho-Akt translocation to the cell membrane. In addition to our cell culture experiments, we studied D2 receptor-dependent Akt in vivo by systemic administration of the D2/D3 agonist quinpirole. The results show that quinpirole evoked Akt-Ser473 phosphorylation in the ventral striatum. Furthermore, intra-accumbens administration of wortmannin, a PI3K (phosphoinositide 3-kinase) inhibitor, significantly suppressed the quinpirole-evoked behavioural activation. Overall, we demonstrate that activation of the dopamine D2S receptor stimulates Akt/GSK3 signalling. In addition, in vivo Akt activity in the ventral striatum appears to play an important role in systemic D2/D3 agonist-induced behavioural activation.

2,4-Toluene diisocyanate suppressed the calcium signaling of ligand gated ion channel receptors.

Toluene diisocyanate (TDI) is widely used as a chemical intermediate in the production of polyurethane. TDI-induced asthma is related to its disturbance of acetylcholine activity in most affected workers, but the relevant mechanisms are unclear. Toluene diamine (TDA) is the main metabolite of TDI. TDI and TDA have in common the basic toluene structure. Toluene is an abused solvent affecting neuronal signal transduction by influencing the function of ligand gated ion channel receptors, including nicotinic acetylcholine receptors (nAChR), P2X purinoceptors, [gamma]-aminobutyric acid type A (GABAA) receptors, etc. To understand the actions of TDI and TDA on ligand gated ion channels, we investigated their effects on the changes of cytosolic calcium concentration ([Ca2+]c) while stimulating nAChR in human neuroblastoma SH-SY5Y cells, P2 purinoceptors in PC12 cells, and GABAA receptors in bovine adrenal chromaffin cells. Our results showed that both TDI and TDA suppressed the [Ca2+]c rise induced by the potent nicotinic ligand, epibatidine, in human SH-SY5Y cells. Similar but stronger suppression of ATP-induced [Ca2+]c rise occurred in PC12 cells. TDI and TDA also partially suppressed the [Ca2+] c rise induced by GABA in bovine adrenal chromaffin cells. We conclude that TDI and TDA can act on ligand gated ion channel receptors. Our findings suggest that TDI and TDA might have some neurotoxicity that will need to be investigated.

Inhibition by 2,4-toluene diisocyanate of the calcium signaling of neuronal nicotinic acetylcholine receptors in human neuroblastoma SH-SY5Y cells.

Toluene diisocyanate (TDI) is widely used as a chemical intermediate in the production of polyurethane products such as foams, coatings, and elastomers. In exposed workers, chronic inhalation of TDI has resulted in significant decreases in lung function. TDI-induced asthma is related to its disturbance of acetylcholine in most affected workers but the actions of TDI on nicotinic acetylcholine receptors (nAChR) are unclear. In order to understand the role of TDI acting on nAChR, we used human neuroblastoma SH-SY5Y cells to investigate the effects of TDI on cytosolic free calcium concentration ([Ca2+]c) changes under the stimulation of nAChR. The results showed that TDI was capable of inhibiting the [Ca2+]c rise induced by nicotinic ligands, epibatidine, DMPP and nicotine. The inhibition was remained, even increased after chronic treatment of TDI. Our study of TDI acting on human nAChR suggests a possibility that the human nerve system plays some role in the toxicity of TDI in the pulmonary system.