Search

Methylammonium lead bromine (MAPbBr3) perovskites have shown great potential for a wide variety of optoelectronic applications. However, the structural and dynamic properties of MAPbBr3 have been t...

The relationship between orexin/hypocretin and rapid eye movement (REM) sleep remains elusive. Here, we find that a proportion of orexin neurons project to the sublaterodorsal tegmental nucleus (SLD) and exhibit REM sleep-related activation. In SLD, orexin directly excites orexin receptor-positive neurons (occupying ~3/4 of total-population) and increases gap junction conductance among neurons. Their interaction spreads the orexin-elicited partial-excitation to activate SLD network globally. Besides, the activated SLD network exhibits increased probability of synchronized firings. This synchronized excitation promotes the correspondence between SLD and its downstream target to enhance SLD output. Using optogenetics and fiber-photometry, we consequently find that orexin-enhanced SLD output prolongs REM sleep episodes through consolidating brain state activation/muscle tone inhibition. After chemogenetic silencing of SLD orexin signaling, a ~17% reduction of REM sleep amounts and disruptions of REM sleep muscle atonia are observed. These findings reveal a stabilization role of orexin in REM sleep., Orexin signaling is provided by diffusely distributed fibers and involved in different brain circuits that orchestrate sleep and wakefulness states. Here, the authors show that a proportion of orexin neurons project to the sublaterodorsal tegmental nucleus and exhibit rapid eye movement (REM) sleep-related actions.

Orexin/hypocretin has been implicated in central motor control. The gigantocellular reticular nucleus (Gi), a key element of the brainstem motor inhibitory system, also receives orexinergic innervations. However, the modulations of orexin on the neuronal activities and the underlying cellular mechanisms in Gi neurons remain unknown. Here, through whole-cell patch-clamp recordings, we first observed that orexin increased the firing frequency in Gi neurons. Interestingly, a postsynaptic depolarization elicited by orexin was observed in the presence of tetrodotoxin, without altering the input resistance of Gi neurons at around -60 mV. Moreover, through comparing the current-frequency curves constructed by identical current injections from equal membrane potentials, we found that orexin also increased the repetitive firing ability of Gi neurons. This action appeared to be caused by the shortening of inter-spike intervals, without altering the waveform of individual action potentials. We finally revealed that activation of the non-selective cationic conductance contributed to the orexin-elicited excitation in Gi neurons. Together, these results suggest that orexin may facilitate Gi-mediated motor functions through enhancing the neuronal activities of Gi neurons.

Cognitive behavioral therapy (CBT) is recommended as the first-line nonpharmacotherapy for sleep complaints. However, there are no studies that tested CBT for improving sleep quality and increasing quality of life (QOL) in patients with type 2 diabetes mellitus (T2DM). Therefore, this study aims to test the effect of CBT on sleep disturbances and QOL in patients with T2DM.In total, 187 participants with T2DM and comorbid poor sleep quality were included in the analysis with the control group of 93 receiving usual care (UC) only and the intervention group of 94 receiving CBT with aerobic exercise plus UC, The Pittsburgh Sleep Quality Index (PSQI), the Diabetes-Specific Quality of Life Scale (DSQLS) and the glycated hemoglobin (HbA1C) values were collected at baseline, after the 2-month intervention, and 6 months of follow-up. The CBT group had 3.03 points lower PSQI scores (95% confidence interval [CI]: 2.07-4.00, P 0.001) and 7.92 points lower total DSQLS scores (95% CI: 4.98-10.87, P 0.001) than the control group after 6-month follow-up. No difference was found in HbAlc between the two groups (t = -0.47, P = 0.64) after 2-month intervention, while the CBT group had 0.89 units lower HbAlc (95% CI: 0.49-1.28, P 0.001) than the control group after 6-month follow-up.CBT is effective for sleep disturbances and can also improve sleep quality, increase QOL, and decrease glycemic levels in participants with T2DM.Chinese Clinical Trials Registration (Practical study of the appropriate technique for improvement of quality of life of the patients with type 2 diabetes in communities: ChiCTR-IOP-16008045).

Background: Biodegradation is a reliable approach for efficiently eliminating persistent pollutants such as chlorpyrifos. Despite many bacteria or fungi isolated from contaminated environment and capable of degrading chlorpyrifos, limited enzymes responsible for its degradation have been identified, let alone the catalytic mechanism of the enzymes. Results: In present study, the gene cpd encoding a chlorpyrifos hydrolase was cloned by analysis of genomic sequence of Paracoccus sp. TRP. Phylogenetic analysis and BLAST indicated that CPD was a novel member of organophosphate hydrolases. The purified CPD enzyme, with conserved catalytic triad (Ser155-Asp251-His281) and motif Gly-Asp-Ser-Ala-Gly, was significantly inhibited by PMSF, a serine modifier. Molecular docking between CPD and chlorpyrifos showed that Ser155 was adjacent to chlorpyrifos, which indicated that Ser155 may be the active amino acid involved in chlorpyrifos degradation. This speculation was confirmed by site-directed mutagenesis of Ser155Ala accounting for the decreased activity of CPD towards chlorpyrifos. According to the key role of Ser155 in chlorpyrifos degradation and molecular docking conformation, the nucleophilic catalytic mechanism for chlorpyrifos degradation by CPD was proposed. Conclusion: The novel enzyme CPD was capable of hydrolyze chlorpyrifos and Ser155 played key role during degradation of chlorpyrifos.

We wanted to determine whether subjective sleep disturbance was associated with serum glycated hemoglobin (HbA1c) in people with type 2 diabetes mellitus. In total, 944 randomly-selected people with diabetes completed the Chinese version of the Pittsburgh Sleep Quality Index (PSQI). Participants’ glycaemia was assessed using HbA1c in March 2016 and September 2017. The PSQI score and the change in score(△PSQI), and the HbA1c and its change (△HbAlc) were analysed by sex and age (30–45, 46–60, 61–75, and 76–89 years). Associations between time point PSQI and △PSQI with static HbA1c and △HbA1c were analysed using multiple linear regression. The results showed subjective sleep disturbance among people with diabetes was not correlated with serum HbAlc (β coefficient = 0.032, P = 0.103). However, cross-sectional multiple linear regression showed the relationship was present in women (β coefficient = 0.163, P 61–75years 46–60years 30–45years. The strongest relationship between △PSQI and △HbA1c was in men aged 30–45 years (β = 0.452, P

We previously found that ATP synthases localize to male-specific sensory cilia and control the ciliary response by regulating polycystin signalling in Caenorhabditis elegans. Herein, we discovered that the ciliary localization of ATP synthase is evolutionarily conserved in mammals. We showed that the ATP synthase subunit F1β is colocalized with the cilia marker acetylated α-tubulin in both mammalian renal epithelial cells (MDCK) and normal mouse cholangiocytes (NMCs). Treatment with ATP synthase inhibitor oligomycin impaired ciliogenesis in MDCK cells, and F1β was co-immunoprecipitated with PKD2 in mammalian cells. Our study provides evidence for the evolutionarily conserved localization of ATP synthase in cilia from worm to mammals. Defects in ATP synthase can lead to ciliary dysfunction, which may be a potential mechanism of polycystic kidney disease.

Two zinc coordination polymers {[Zn2(TPPBDA)(oba)2]·DMF·1.5H2O}n (1), {[Zn(TPPBDA)1/2(tpdc)]·DMF}n (2) have been synthesized by zinc metal salt, nanosized tetradentate pyridine ligand with flexible or rigid V-shaped carboxylate co-ligands. These complexes were characterized by elemental analyses and X-ray single-crystal diffraction analyses. Compound 1 is a 2-fold interpenetrated 3D framework with [Zn2(CO2)4] clusters. Compound 2 can be defined as a five folded interpenetrating bbf topology with mononuclear Zn2+. These mononuclear or dinuclear cluster units are linked by mix-ligands, resulting in various degrees of interpenetration. In addition, the photoluminescent properties for TPPBDA ligand under different state and coordination polymers have been investigated in detail.

Arthrobacter sp. strain CN2, capable of degrading 4-nitrophenol, was isolated from activated sludge. Degradation of 4-nitrophenol was optimized at pH 7.7, 30 °C, and 0.53% of glucose. Salt tolerance of 4-nitrophenol degradation was as high as 6% (w/v). Several biodegradation intermediates were identified and quantified by high-performance liquid chromatography and mass spectrometry. 4-Nitrocatechol is involved in the degradation of 4-nitrophenol by CN2. Scale-up of 4-nitrophenol degradation was conducted in a bioreactor with different salinity. When the salinity was below 7%, the degradation rate of 4-nitrophenol was above 90% (100 mg L−1, 3 L).

Chitosan exhibiting excellent functional properties was found to be potential in a wide variety of industrial and biomedical applications. The lack of biological activities and the poor mechanical properties somewhat limit its applications. To address these limitations, chemical modification has been proved to be an efficient method. Here, we immobilized arginine-glycine-aspartic acid (RGD) on chitosan molecules and incorporated the chitosan with Poly(L-lactide-co-glycolide)-Poly(ethylene glycol) (PLGA-PEG) and β-tricalcium phosphate (β-TCP) nanoparticles to obtain a chitosan-based scaffold with enhanced mechanical and biocompatible performance. XPS and FT-IR confirmed the successful grafting of RGD peptides onto the chitosan chain. The mechanical properties, hydrophilicity and degradation behaviors of the membrane were characterized by stress-strain, water contact angle, and weight loss, respectively. Cytotoxicity, cellular adhesion, and cellular viability of the scaffolds were studied by MTT assay, cell adhesion, and cell survival experiments, respectively. The advantageous mechanical properties and the hydrophilic surface of the chitosan-based scaffold were achieved by blending with PLGA-PEG. The preliminary biocompatibility studies revealed that all the scaffolds were cell compatible, and the hydrophilic surface was more suitable for cell adhesion. The scaffolds grafted with RGD exhibited high cell adhesion rate than the pure chitosan. The results suggested that the surface hydrophilicity and biocompatibility of the chitosan-based scaffolds play an important role in enhancing cell adhesion and growth.

Arthrobacter sp. strain YC-RL1, capable of utilizing bisphenol A (BPA) as sole carbon source for growth, was isolated from petroleum contaminated soil. YC-RL1 could rapidly degrade BPA in a wide range of pH (5.0-9.0) and temperature (20-40 °C). Substrate analysis found that YC-RL1 could also degrade bisphenol F (BPF) and tetrabromobisphenol A (TBBPA). The maximum and minimum concentrations of BPA (0.2-600 mg/L), BPF (0.2-600 mg/L), and TBBPA (0.2-300 mg/L) for efficient biodegradation were detected. The released bromide ion and metabolic intermediates of BPF and BPA/TBBPA were detected, as well as the degradation pathways for BPF and BPA/TBBPA were deduced tentatively. The present study provides important information for the investigation of BPs degrading mechanism and the application of microbial remediation in BP-contaminated environment. This study is the first report about a genus Arthrobacter bacterium which could simultaneously degrade BPA, BPF, and TBBPA.

TEF3-1 (transcription enhancer factor 3 isoform 1) is a human transcriptional factor, which has a N-terminal TEA/ATTS domain supposedly for DNA binding and C-terminal PRD and STY domains for transcriptional activation. Taking advantage of the efficient reporter design of yeast two-hybrid system, we characterized the TEF3-1 domains in activating gene expression. Previously study usually mentioned that the C-terminal domain of TEF3-1 has the transcriptional activity, however, our data shows that the peptides TEF3-1 1 – 66 and TEF3-1 197 – 434 functioned as two independent activation domains, suggesting that N-terminal domain of TEF3-1 also has transcriptional activation capacity. Additionally, more deletions of amino acids 197–434 showed that only the peptides TEF3-1 197 – 265 contained the minimum sequences for the C-terminal transcriptional activation domain. The protein structure is predicted to contain a helix-turn-helix structure in TEF3-1 1 – 66 and four β sheets in TEF3-1 197 – 265 . Finally, after the truncated fragments of TEF3-1 were expressed in HUVEC cells, the whole TEF3-1 and the two activation domains could increase F-actin stress fiber, cell proliferation, migration and targeted gene expression. Further analysis and characterization of the activation domains in TEF3-1 may broaden our understanding of the gene involved in angiogenesis and other pathological processes.

Previous studies have revealed that orexin may actively participate in central motor control. The gigantocellular reticular nucleus (Gi) is a key element of the brainstem motor inhibitory system. The descending orexinergic projections also reach Gi region, and microinjection of orexin into Gi causes robust muscle tone inhibition. However, the modulation effects of orexin on Gi neurons remain unclear. In the present study, using whole-cell patch-clamp recordings, we initially observed that orexin elicited an inward current in Gi neurons at a holding potential of -70mV in a concentration-dependent manner. By combining electrophysiology with neuropharmacological methods, we further determined that the orexin-induced inward current was directly mediated by the activation of postsynaptic orexin-1 and orexin-2 receptors. Moreover, orexin did not affect the frequency and amplitude of miniature excitatory and inhibitory postsynaptic currents in Gi neurons, which suggests that orexin had no effects on neurotransmission to these neurons. Therefore, the direct excitatory effect of orexin on an inhibitory motor structure, the Gi, was reported in the present study. This modulation may be integrated into the role of orexin in central motor control.

Poly(vinylidene fluoride)/polysulfone (PVDF/PSF) blend microporous matrix of polymer electrolyte for lithium ion battery is prepared via thermally induced phase separation (TIPS) technique. Because of only one parameter, i.e., the PSF/PVDF weight ratio, the membrane microstructure is conveniently controlled. The membrane formation mechanism of PVDF/PSF blend membranes is proposed with the assistance of a binary PSF/PVDF weight ratio-temperature phase diagram. In addition to studying the microstructure and mechanical properties of PVDF/PSF blend membrane, the relationship between properties of membrane, electrochemical performances of corresponding polymer electrolyte and membrane microstructure are also discussed in this paper. It is found that the addition of PSF not only increases ionic conductivity and electrochemical stable window of polymer electrolyte, but also markedly enhances charge–discharge performances of coin cell. The results reveal that PVDF/PSF blend microporous membranes prepared via TIPS technique can be used as polymer matrices of polymer electrolytes for lithium ion batteries.

Four 3-aminoindolizines were synthesized from the substituted 2-bromopyridines and propargyl amines with the aim of obtaining potential anti-inflammatory compounds, which were characterized by NMR, IR, ESI-MS and elemental analysis. Their biological activities were evaluated by the bacterial lipopolysaccharide (LPS) stimulation of mouse cells in the RAW264.7 inflammation model. The target compounds4a-4drevealed moderate anti-inflammatory effects with the inhibitions of 45%~61% at 50 μM. The bioactive 3-aminoindolizines might be used for further optimization as potential anti-inflammatory drugs.

With the aim of obtaining potential IL-6 inhibitor for the treatment of rheumatoid arthritis, four 3-aryloxylindolizine derivatives were synthesized from the 2-bromopyridine and aryl propargyl ether through the Sonogashira coupling/5-endo-trigcycloisomerization domino strategy. These compounds were characterized by NMR, IR, EI-MS and elemental analysis. Their biological activities were evaluated by the bacterial lipopolysaccharide (LPS) stimulation of mouse cells on the RAW264.7 inflammation model. All the compounds revealed good anti-inflammatory activities with the inhibitions of 71~82% against IL-6 at 100 μM. The bioactive 3-aryloxylindolizines might be used as potential anti-inflammatory drugs.

The synthesis and interleukin-6 (IL-6) inhibitory activities for a series of 3-alkyloxylindolizine derivatives were described. The target products were characterized by NMR, IR, ESI-MS and elemental analysis, and two compounds revealed better IL-6 inhibitory effects on LPS-induced IL-6 expression in mouse macrophages with the corresponding inhibition ratio of 66% and 74% at 100 μM. The bioactive compounds might be a good generation for further optimization as potential anti-inflammatory agents.

The triazolo-methyl tetrahydrobenzofuran oxime ether isomers were prepared through Cu (II)-catalyzed Huisgen 1,3-dipolar cycloaddition reaction in a high-yielding three-step reaction sequence under mild conditions. All of the intermediates and target compounds were characterized by NMR, IR, ESI-MS and elemental analysis. Thein vitroanti-ulcer activity evaluation indicated the (Z)-oxime isomer of triazolo-methyl tetrahydrobenzofuran oxime ether exhibited most potent H+/K+-ATPase inhibitory effect with the IC50˰̵̱̼͆ͅ˰̶̿˰̅˾́̅˰μ̝˾ These compounds could be potentially used as anti-ulcer agents for the treatment of acid related diseases.

Mycobacterium sp. YC-RL4 is capable of utilizing a broad range of phthalic acid esters (PAEs) as sole source of carbon and energy for growth. The preliminary studies demonstrated its high degrading efficiency and good performance during the bioprocess with environmental samples. Here, we present the complete genome of Mycobacterium sp. YC-RL4, which consists of one circular chromosome (5,801,417 bp) and one plasmid (252,568 bp). The genomic analysis and gene annotation were performed and many potential genes responsible for the biodegradation of PAEs were identified from the genome. These results may advance the investigation of bioremediation of PAEs-contaminated environments by strain YC-RL4.

Bacterial strain YC-RL4, capable of utilizing phthalic acid esters (PAEs) as the sole carbon source for growth, was isolated from petroleum-contaminated soil. Strain YC-RL4 was identified as Mycobacterium sp. by 16S rRNA gene analysis and Biolog tests. Mycobacterium sp. YC-RL4 could rapidly degrade dibutyl phthalate (DBP), diethyl phthalate (DEP), dimethyl phthalate (DMP), dicyclohexyl phthalate (DCHP), and di-(2-ethylhexyl) phthalate (DEHP) under both individual and mixed conditions, and all the degradation rates were above 85.0 % within 5 days. The effects of environmental factors which might affect the degrading process were optimized as 30 °C and pH 8.0. The DEHP metabolites were detected by HPLC-MS and the degradation pathway was deduced tentatively. DEHP was transformed into phthalic acid (PA) via mono (2-ethylhexyl) phthalate (MEHP) and PA was further utilized for growth via benzoic acid (BA) degradation pathway. Cell surface hydrophobicity (CSH) assays illuminated that the strain YC-RL4 was of higher hydrophobicity while grown on DEHP and CSH increased with the higher DEHP concentration. The degradation rates of DEHP by strain YC-RL4 in different environmental samples was around 62.0 to 83.3 % and strain YC-RL4 survived well in the soil sample. These results suggested that the strain YC-RL4 could be used as a potential and efficient PAE degrader for the bioremediation of contaminated sites.

Two new iridoid glycosides, named scrophularianoids A ( 1 ) and B ( 2 ), were isolated from the roots of Scrophularia ningpoensis . The chemical structures were established on the basis of extensive analyses of spectroscopic data. Compounds 1 and 2 were inactive in our preliminary in vitro myocardial protective bioassay.

Wastewater, which involves easy-soluble reactive dyes, especially non-degradable dyes, is very difficult to decolor efficiently by normal processes such as coagulation process and biological treatment. The high chromaticity seriously hinders the reuse of reactive dye waste water. In this paper, a new method by bentonite adsorption and coagulation (PAC) is employed for removing color from synthetic dye waste water which contains reactive red K-2G, K-RN blue, K-GR blue, X-3B red, K-GN orange, KB-3G yellow, K-2BP red, K-RN yellow and K-6G yellow. Bentonite pretreated by 4% CTMAB and milled to 160 order screen is proven to the best decoloring agent. For a 100 mL reactive red K-2G sample (CODcr 400 mg/L, 25 000 chromaticity color), 0.5 g bentonite pretreated and 2.5 mL PAC is enough to decolor wastewater up to 99.92% and the sediment time is short. Non-degradable dyes such as active red X-3B and K-GN orange are declored completely as well. Raw sewage (low chromaticity color) is decolored completely at a bentonite dosage of 0.001g. More researches prove the high practical value of this process.

The central noradrenergic system participates in diverse nervous functions. Nevertheless, our knowledge of the action of adrenoceptors in motor regulation is still lacking. Intriguingly, reticulospinal neurons in the caudal pontine reticular nucleus (PnC) receive fairly dense noradrenergic innervation and play an important role in motor control. Here, after demonstrating the expression of α1- and α2-adrenoceptors in the PnC, we found that noradrenaline elicited a post-synaptic effect (inward or outward whole-cell current at −70 mV holding) on PnC reticulospinal neurons. The α1- and α2-adrenoceptors were co-expressed in individual PnC reticulospinal neurons to mediate an inward and an outward current component at −70 mV holding, respectively, which, when superposed, produced the overall post-synaptic effects of noradrenaline (NA). More importantly, the activation of post-synaptic α1- or α2-adrenoceptors indeed exerted opposing modulations (excitation vs. inhibition) on the firing activities of individual PnC reticulospinal neurons. Furthermore, the activation and inhibition of the Na+-permeable non-selective cationic conductance (NSCC) were demonstrated to be coupled to α1- and α2-adrenoceptors, respectively. Additionally, the activation of α2-adrenoceptors activated K+ conductance. Pre-synaptically, the α2-adrenoceptors were expressed to attenuate the miniature excitatory postsynaptic current (mEPSC) in PnC reticulospinal neurons, but not to affect the miniature inhibitory postsynaptic current (mIPSC). Consistently, the evoked EPSC in PnC reticulospinal neurons was suppressed after the activation of pre-synaptic α2-adrenoceptors. Thus, the excitatory input and post-synaptic dynamics of PnC reticulospinal neurons are indeed intricately modulated by the activation of α1- and α2-adrenoceptors, through which motor control may be regulated in an adaptive manner by the central noradrenergic system.

The two new iridoid glycosides scrophularianoids A (I) and B (II) are isolated from the roots of Scrophularia ningpoensis.

The medial entorhinal cortex (MEC) plays a crucial role in spatial learning and memory. Whereas the MEC receives a dense histaminergic innervation from the tuberomamillary nucleus of the hypothalamus, the functions of histamine in this brain region remain unclear. Here, we show that histamine acts via H1Rs to directly depolarize the principal neurons in the superficial, but not deep, layers of the MEC when recording at somata. Moreover, histamine decreases the spontaneous GABA, but not glutamate, release onto principal neurons in the superficial layers by acting at presynaptic H3Rs without effect on synaptic release in the deep layers. Histamine-induced depolarization is mediated via inhibition of Kir channels and requires the activation of protein kinase C, whereas the inhibition of spontaneous GABA release by histamine depends on voltage-gated Ca(2+) channels and extracellular Ca(2+). Furthermore, microinjection of the H1R or H3R, but not H2R, antagonist respectively into the superficial, but not deep, layers of MEC impairs rat spatial learning as assessed by water maze tasks but does not affect the motor function and exploratory activity in an open field. Together, our study indicates that histamine plays an essential role in spatial learning by selectively regulating neuronal excitability and synaptic transmission in the superficial layers of the MEC.