Mechanistic Insights into the Palladium-Catalyzed Perfluoroalkylative Carbonylation of Unactivated Alkenes to ß-Perfluoroalkyl Esters: A DFT Study.

Transition metal-catalyzed multicomponent carbonylation is an efficient synthetic strategy to access multifunctional esters in high yields with broad functional group tolerance and good chemoselectivity. Considering the development of highly efficient synthetic methods for esters, it remains significant to grasp the mechanism of constructing multifunctional esters. Herein, density functional theoretical calculations were carried out to acquire mechanistic insight into the synthesis of ß-perfluoroalkyl esters from a specific palladium-catalyzed perfluoroalkylative carbonylation of unactivated alkenes using carbon monoxide. A detailed mechanistic understanding of this reaction route includes (1) multistep radical reaction process, (2) C-C coupling and CO insertion, (3) ligand exchange, and (4) Pd-based intermediate oxidation and reductive elimination. The multistep radical process was fundamentally rationalized, including Rf· formation and radicals A and E from unactivated alkene and CO oxidation, respectively. The potential energy calculation indicated that the CO insertion into the perfluorinated alkyl radicals preceded Pd-catalyzed oxidation in the competitively multistep free radical reaction process. In addition, the I-/PhO- exchange step was predicted to be spontaneous to products. The IGMH analysis further attested to the reductive elimination process involved in the rate-determining step. Thus, a simple and valid density functional theory (DFT) approach was developed to reveal the multistep radical mechanism for the Pd-catalyzed perfluoroalkylative carbonylation of unactivated alkenes to access functional ß-perfluoroalkyl esters.

Bioinsecticide PA1b alleviates lipopolysaccharide-induced inflammation and impairment of bovine mammary epithelial cells.

Pea Albumin 1, subunit b (PA1b) is a 37 amino acid peptide. It was extracted from pea seeds and showed significant insecticidal activity against certain insects, such as the mosquitoes Culex pipiens and Aedes aegyptii, cereal weevils (genus Sitophilus), and certain species of aphids. Considering that pea seeds are regularly consumed by humans and mammals, PA1b is assumed to be a promising bioinsecticide with no allergenicity or toxicity to hosts. To clarify this aspect, PA1b was applied to bovine mammary epithelial cells challenged with lipopolysaccharide (LPS). The results revealed that LPS induced inflammatory cytokine tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL6) and monocyte chemoattractant protein 1 (MCP-1) secretion, while PA1b depressed these cytokines release via inhibiting NF-κB signaling activation. In addition, PA1b protected mammary epithelial cells from impairment caused by LPS, because it reduced cell membrane permeability and subsequently reconstructed mammary epithelial cell viability. Moreover, it inhibited cell apoptosis accompanied with alleviated oxidative stress. Furthermore, PA1b prevented opening of mitochondrial permeability transition pores, in turn up-regulated mitochondrial membrane potential and ATP production. Therefore, PA1b improved mitochondrial function, which contributed to re-construction of mammary epithelial cell viability. In conclusion, PA1b alleviates LPS-induced inflammation of bovine mammary epithelial cells via inhibiting NF-κB signaling activation and protects bovine mammary epithelial cells by improving mitochondrial function. PA1b is a good therapeutic survival factor for mammary epithelial cells.

Plaque enhancement predicts recurrence in acute ischemic stroke patients with large artery intracranial atherosclerosis.

BACKGROUND: The association between the degree of plaque enhancement and ischemic brain stroke recurrence remains unclear. We aimed to establish models to predict plaque enhancement and stroke recurrence. METHODS: Seventy-eight participants with acute ischemic brain stroke due to intracranial arterial stenosis were recruited and divided into high enhancement (HE) and non-HE groups. The relationship between imaging characteristics (degree of stenosis, minimal lumen area, intraplaque hemorrhage, and plaque burden) and the degree of plaque contrast enhancement was analyzed. Inflammatory cytokine expression was examined by flow cytometry. Independent predictors of stroke recurrence were investigated via multivariate Cox proportional hazards regression analysis. Nomogram was used to construct a prediction model. Harrell's concordance indices (c-indices) and calibration curves were used to assess the discrimination of the nomogram. A risk prediction nomogram for prognosis was constructed. RESULTS: Thirty-three participants were assigned to the HE group and 45 to the non-HE group. The degree of stenosis and plaque burden in the HE group was higher than that in the non-HE group (P<0.05). Multiple linear regression analysis showed the degree of stenosis was associated with HE (ß=0.513; P=0.000). After adjusting for confounding factors, age (HR=1.115; 95%CI=1.034-1.203, P=0.005) and HE plaques (HR=10.457; 95%CI=1.176-93.018; P=0.035) were independent risk factors of stroke recurrence, whereas cytokine levels were not statistically significant between two group. CONCLUSIONS: HE of intracranial atherosclerosis plaques is an independent factor for ischemic brain stroke recurrence.

Regioselective and Enantioselective Copper-Catalyzed Hydroaminocarbonylation of Unactivated Alkenes and Alkynes.

Given the prevalence of amide backbones in marketed pharmaceuticals and their ubiquity as critical binding units in natural peptides and proteins, it remains important to develop novel methods to construct amide bonds. We report here a general method for the anti-Markovnikov hydroaminocarbonylation of unactivated alkenes under mild conditions, using copper catalysis in combination with hydroxylamine electrophile reagents and poly(methylhydrosiloxane) (PMHS) as a cheap and environmentally friendly hydride source. The reaction tolerates a variety of functional groups and efficiently converts unactivated terminal alkenes, 1,1-disubstituted alkenes, and cyclic alkenes to the corresponding amides with exclusive anti-Markovnikov selectivity (and high enantioselectivities/diastereoselectivities). Additionally, with minimal modification of the reaction conditions, alkynes can also undergo tandem hydrogenation-hydroaminocarbonylation to alkyl amides.

A DFT Study on the Binuclear Copper(I)-Catalyzed Synthesis Mechanism of 1,2,3-Triazolo[1,5-c]Pyrimidine via Interrupted Click and Ketenimine Rearrangement.

In this paper, the mechanism of the full catalytic cycle for binuclear Cu(I)-catalyzed sulfonyl azide-alkyne cycloaddition reaction for the synthesis of triazolopyrimidines was rationalized by density functional theoretical (DFT) calculations. The computed reaction route consists of: (a) formation of dicopper intermediates, including C-H activation of terminal alkyne, 3+2 ring cycloaddition and ring-reducing reaction and transmetalation, (b) interrupted CuAAC reaction, including di-copper catalyzed ring-opening of 2H-azirines and C-C bond formation to generate the copper-triazoles and -ketenimines, (c) two-step C-N cross-coupling and following (d) multi-step hydrogen transfer by the hydrogen bonding chain of water to promote the C-N formation and another C-N cleavage through the removal of p-tolyl sulfonamides. Our DFT results indicate that the multi-step hydrogen transfer process is the rate-determining step along the potential energy surface profile. The explicit water model was used for systematic determination of barrier for C-C cross-coupling, C-N bond formation and cleavage, and p-tolylsulfonamide removal. A critical insight in the interrupted CuAAC reaction was proposed. Further prediction interprets H2 O hydrogen bond chain plays an important role in C-N bond formation and cleavage, and the removal of p-tolylsulfonamide. This may have fundamental guidance on the design of 1, 5-herterocyclic functionalized triazolopyrimidines via interrupted CuAAC rearrangement reaction, as well as hydrogen bond chain of water.

Allograft inflammatory factor-1 stimulates inflammatory properties of peripheral blood leukocytes and increases cell viability via enhancing mitochondrial function in Ctenopharyngodon idellus.

Allograft inflammatory factor-1 (AIF-1) is a 17 kDa calcium-binding protein associated with numerous inflammatory diseases. The full-length cDNA of AIF-1 has been identified in grass carp, Ctenopharyngodon idellus in our previous study, and it was assumed to be a novel molecule involved in immune responses. To clarify this aspect, the level of AIF-1 expression was amplified and reduced in grass carp peripheral blood leukocytes via transfection of vector pcDNA3.1-AIF1-EGFP and pLKO.1-shRNA-EGFP-puro, respectively. Thereafter, AIF-1 stimulated cell proliferation, inhibited cell apoptosis, which might benefit from improved mitochondrial function as evidenced by increased mitochondrial membrane potential, subsequently promoted ATP production. In addition, AIF-1 induced leukocyte migration via up-regulated monocyte chemotactic protein-1(MCP-1) secretion, enhanced neutral red uptake into leukocyte, provoked pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α), interleukin 1ß (IL1ß), interleukin 6 (IL6), interleukin 8 (IL8) and suppressed anti-inflammatory cytokine interleukin 10 (IL10) production. These results indicated AIF-1 played a critical role in grass carp innate immune system.

Macrophage migration inhibitory factor is vital for inflammatory properties and survival of peripheral blood leukocytes via enhancing mitochondrial function in Ctenopharyngodon idellus.

Macrophage migration inhibitory factor (MIF) is a pleiotropic protein implicated in a broad spectrum of inflammatory and proliferative disorders. The gene sequence of grass carp (Ctenopharyngodon idella) was identified and the expression level of it was regulated by cadmium exposure in our previous study. To further clarify the immune-regulatory activity of grass carp MIF, MIF was over-expressed and interfered in grass carp peripheral blood leukocytes via transfection of plasmids pcDNA3.1-MIF-EGFP and pLKO.1-shRNA-EGFP-puro, respectively. Subsequently, survival, phagocytic capacity, mitochondrial function and cytokine production of the transfected leukocytes were assayed. The results shown that grass carp MIF was necessary for leukocyte survival, because it enhanced leukocyte viability and inhibited cell apoptosis, while MIF interference disrupted the cell viability and induced leukocyte apoptosis. The effect might benefit from improved mitochondrial function as evidenced by increased ATP production, which was due to maintained mitochondrial trans-membrane potential. In addition, MIF is essential for neutral red uptake into leukocyte, and it provoked chemokine monocyte chemotactic protein-1 (MCP-1), pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα), interleukin 1ß (IL1ß), interleukin 6 (IL6), interleukin 8 (IL8), and suppressed anti-inflammatory cytokine interleukin 10 (IL10) production. These results indicated that grass carp MIF played a vital role in regulating inflammatory properties and survival of peripheral blood leukocytes.

Spectroscopic and mechanistic insights into solvent mediated excited-state proton transfer and aggregation-induced emission: introduction of methyl group onto 2-(o-hydroxyphenyl)benzoxazole.

Excited-state intramolecular proton transfer (ESIPT) reaction plays an important role in biology, materials, and other related fields. The ESIPT-based compounds has been proved to improve effectively fluorescence quantum yield, red-shifted emission, and wide separation between absorption and emission wavelengths (large Stokes shift, LSS). A solvatochromic benzoxazole-based probe, 2-(2-hydroxy-5-methylphenyl)benzoxazole(HBO-pCH3), exhibited a typical dual fluorescence phenomenon via the ESIPT reaction in non-polar and weakly polar solvents. The emission bands of normal* (∼370 nm) and tautomer* (∼500 nm) forms were identified and assigned, based on fluorescence spectroscopy and quantum chemical theoretical calculations. Solvatochromism confirmed ESIPT reaction inhibition by solvent polarity and intermolecular hydrogen bonding. The intramolecular reversal in combination with time-dependent density functional theoretical calculations revealed an emission-strengthening mechanism of ESIPT, coupled with aggregation-induced emission (AIE) (in mixed water/methanol solvents). Thus, this strategy provides an insight into designing potential "ESIPT + AIE" fluorescent sensors.

Excited state proton transfer of triplet state p-nitrophenylphenol to amine and alcohol: a spectroscopic and kinetic study.

Hydroxyaromatic compounds (ArOHs) have a wide range of applications in catalytic synthesis and biological processes due to their increased acidity upon photo-excitation. The proton transfer of ArOHs via the excited singlet state has been extensively studied. However, there has still been a debate on the unique type of ArOH that can undergo an ultrafast intersystem crossing. The nitro group in p-nitrophenylphenol (NO2-Bp-OH) enhances the spin-orbit coupling between excited singlet states and the triplet manifold, enabling ultrafast intersystem crossing and the formation of the long-lived lowest excited triplet state (T1) with a high yield. In this work, we used time-resolved transient absorption to investigate the excited state proton transfer of NO2-Bp-OH in its T1 state to t-butylamine, methanol, and ethanol. The T1 state of the deprotonated form NO2-Bp-O- was first observed and identified in the case of t-butylamine. Kinetic analysis demonstrates that the formation of the hydrogen-bonded complex with methanol and ethanol as proton acceptors involves their trimers. The alcohol oligomer size required in the excited state proton transfer process is dependent on the excited acidity of photoacid.

A theoretical insight into excited-state decay and proton transfer of p-nitrophenylphenol in the gas phase and methanol solution.

The excited-state decay (ESD) and proton transfer (EPT) of p-nitrophenylphenol (NO2-Bp-OH), especially in the triplet states, were not characterized with high-level theoretical methods to date. Herein, the MS-CASPT2//CASSCF and QM(MS-CASPT2//CASSCF)/MM methods were employed to gain an atomic-level understanding of the ESD and EPT of NO2-Bp-OH in the gas phase and its hydrogen-bonded complex in methanol. Our calculation results revealed that the S1 and S2 states of NO2-Bp-OH are of 1ππ* and 1nπ* characters at the Franck-Condon (FC) point, which correspond to the ICT-EPT and intramolecular charge-transfer (ICT) states in spectroscopic experiments. The former state has a charge-transfer property that could facilitate the EPT reaction, while the latter one might be unfavorable for EPT. The vertical excitation energies of these states are almost degenerate at the FC region and the electronic configurations of 1ππ* and 1nπ* will exchange from the S1 FC region to the S1 minimum, which means that the 1nπ* state will participate in ESD once NO2-Bp-OH departs from the S1 FC region. Besides, we found that three triplets lie below the first bright state and will play very important roles in intersystem crossing processes. In terms of several pivotal surface crossings and relevant linearly interpolated internal coordinate (LIIC) paths, three feasible but competing ESD channels that could effectively lead the system to the ground state or the lowest triplet state were put forward. Once arrived at the T1 state, the system has enough time and internal energy to undergo the EPT reaction. The methanol solvent has a certain effect on the relative energies and spin-orbit couplings, but does not qualitatively change the ESD processes of NO2-Bp-OH. By contrast, the solvent effects will remarkably stabilize the proton-transferred product by the hydrogen bond networks and assist to form the triplet anion. Our present work would pave the road to properly understand the mechanistic photochemistry of similar hydroxyaromatic compounds.

High-efficiency water-window x-ray generation from nanowire array targets irradiated with femtosecond laser pulses.

We demonstrate the high-efficiency generation of water-window soft x-ray emissions from polyethylene nanowire array targets irradiated by femtosecond laser pulses at the intensity of 4×1019 W/cm2. The experimental results indicate more than one order of magnitude enhancement of the water-window x-ray emissions from the nanowire array targets compared to the planar targets. The highest energy conversion efficiency from laser to water-window x-rays is measured as 0.5%/sr, which comes from the targets with the longest nanowires. Supported by particle-in-cell simulations and atomic kinetic codes, the physics that leads to the high conversion efficiency is discussed.

High-efficiency generation of narrowband soft x rays from carbon nanotube foams irradiated by relativistic femtosecond lasers.

A number of applications require x rays of both high flux and narrow bandwidth. In this work, we experimentally demonstrate the high-efficiency generation of narrowband soft x rays from carbon nanotube foams irradiated by a femtosecond laser pulse at an intensity of 1019W/cm2. The building blocks of the foam, single-walled carbon nanotube bundles with diameters smaller than the laser skin length can be volumetrically heated and fully ionized on a femtosecond time scale. The three-dimensional network structure of the foam permits deep penetration and drastic absorption of the laser pulse, and results in bright line emissions without prominent Stark broadening. A single-shot yield of 3×1014photons in the carbon Lyα line at 3.37 nm was measured with a bandwidth of 0.013 nm.

The impact of payer status on hospital admissions: evidence from an academic medical center.

BACKGROUND: There are plenty of studies investigating the disparity of payer status in accessing to care. However, most studies are either disease-specific or cohort-specific. Quantifying the disparity from the level of facility through a large controlled study are rare. This study aims to examine how the payer status affects patient hospitalization from the perspective of a facility. METHODS: We extracted all patients with visiting record in a medical center between 5/1/2009-4/30/2014, and then linked the outpatient and inpatient records three year before target admission time to patients. We conduct a retrospective observational study using a conditional logistic regression methodology. To control the illness of patients with different diseases in training the model, we construct a three-dimension variable with data stratification technology. The model is validated on a dataset distinct from the one used for training. RESULTS: Patients covered by private insurance or uninsured are less likely to be hospitalized than patients insured by government. For uninsured patients, inequity in access to hospitalization is observed. The value of standardized coefficients indicates that government-sponsored insurance has the greatest impact on improving patients' hospitalization. CONCLUSION: Attention is needed on improving the access to care for uninsured patients. Also, basic preventive care services should be enhanced, especially for people insured by government. The findings can serve as a baseline from which to measure the anticipated effect of measures to reduce disparity of payer status in hospitalization.

Identification and immunologic property of macrophage migration inhibitory factor (MIF) in grass carp (Ctenopharynogodon idella).

Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine, plays an important regulatory role in the activation of T cells induced by mitogenic or antigenic stimuli. However, the immunologic property of MIF in freshwater fish is limitedly known by now. In the present study, MIF gene was identified in grass carp. Bioinformatics analysis revealed that the molecular weight of grass carp MIF protein was 12.377 kDa and it could also bind to CD74. MIF gene was predominantly expressed in immune tissues including spleen and head kidney, then liver, skin, gill, intestine and blood, while a relative low level expression in heart, brain, fat and red muscle. The predicted receptor and tissues distribution of MIF implied the immunologic activity of grass carp MIF. Then grass carp MIF antigen and the polyclonal antibodies against it were prepared. Using cadmium as an immunosuppressive agent, MIF expression in spleen and head kidney was depressed in a dose-dependent manner with cadmium consumption. On the same time, white blood cell count decrease displayed a similar pattern with MIF expression, which suggested a possible positive correlation between MIF and white blood cell count. Thereafter, MIF enhanced the viability of grass carp peripheral blood leukocytes and inhibited cell apoptosis with depressed reactive oxygen species production in vitro. In addition, recombinant grass carp MIF promoted tumor necrosis factor-alpha (TNF-α), interleukin 1ß (IL1ß) and interleukin 6 (IL6) secretion from peripheral blood leukocytes. These results indicated the immunologic property of grass carp MIF.

Molecular characterization of GTP binding protein overexpressed in skeletal muscle (GEM) and its role in promoting adipogenesis in goat intramuscular preadipocytes.

GTP binding protein overexpressed in skeletal muscle (GEM) is an important gene with many functions, such as regulating the rearrangement of cytoskeleton and the activity of voltage-dependent calcium channel, and GEM was regarded as a candidate gene for obesity. However, little investigation has been carried out to explore whether GEM affected the intramuscular fat (IMF) deposition of goat. To explore the role of GEM gene in goat, this gene was cloned and its tissue and temporal expression profile were detected. Effect of GEM on adipogenesis was examined by losing function of GEM in vitro. Thereafter, several lipid metabolism-related genes were examined, including CCAAT/enhancing-binding protein α (C/EBPα), CCAAT/enhancing-binding protein ß (C/EBPß), lipoprotein lipase (LPL), preadipocyte factor 1 (Pref-1), peroxisome proliferator activated receptor γ (PPARγ) and sterol regulatory element binding protein 1 (SREBP1). We found that the goat GEM gene consisted of 936 bp, which encoded a protein of 311 amino acids. The expression of GEM was higher in spleen, lung and large intestine and it appeared sharp in the interim stage of differentiation. Furthermore, GEM knockdown blocked adipogenesis and the expression of C/EBPα, C/EBPß, LPL, PPARγ and SREBP1. These results indicated that GEM might promote lipid accumulation and adipogenesis.

Staphylococcal enterotoxin M induced inflammation and impairment of bovine mammary epithelial cells.

Staphylococcus aureus is one of the major etiological pathogens of bovine mastitis. Its invasion into mammary epithelial cells has been proven to be a key event in the pathogenesis of mastitis. However, the specific pathogenic factors have not been clearly identified. Staphylococcus aureus often triggers infections by releasing virulence factor. Recent several studies reported that staphylococcal enterotoxin M was one of the most frequently found enterotoxin genes associated with bovine mastitis. Thus, the effect of staphylococcal enterotoxin M on inflammation and damage of the bovine mammary epithelial bovine mammary gland epithelial cell line (MAC-T) cells with 48 h treatment was explored in the present study. First, staphylococcal enterotoxin M protein was purified by a Ni-NTA spin column (GE Life Science, Westborough, MA). The levels of tumor necrosis factor-α, IL-6, and monocyte chemoattractant protein 1 (MCP-1) secretion were measured with the corresponding ELISA kits (R&D Systems, Abingdon, UK). Second, cell viability was assessed with a Cell Counting Kit-8 (Bioswamp, Wuhan, China) and the apoptotic percentage of cells was determined by annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI; Beyotime, Nanjing, China) staining. Third, ATP concentration, reactive oxygen species (ROS) generation and lactate dehydrogenase (LDH) release were assayed with commercial kits, then mitochondrial membrane potential (ΔΨm) was estimated using fluorescent probe JC-1 (Beyotime). Finally, the production intercellular cell adhesion molecule-1 (ICAM-1), microtubule-associated protein 1A/1B-light chain 3 I/II (LC3 I/II), p62 (Proteintech, Rosemont, IL), and phosphorylation of IκBα, caspase 3, and mammalian target of rapamycin were detected by Western blot. The results showed that staphylococcal enterotoxin M induced inflammation of epithelial cells (upregulating tumor necrosis factor-α, IL-6, MCP-1, and ICAM-1 production) and activated NF-κB (promoting phosphorylation of IκBα). Furthermore, staphylococcal enterotoxin M impaired MAC-T cells via cell necrosis (enhancing LDH release), apoptosis (annexin V-FITC/PI stain, exacerbating oxidative stress, decreasing ΔΨm and intracellular ATP concentration, and activating caspase 3), but independent of autophagy (nonsignificantly increasing LC3-II, decreasing p62 expression, and activating mammalian target of rapamycin). Thereby, staphylococcal enterotoxin M induced the inflammatory property of bovine mammary epithelial cells by boosting cytokine, chemokine, and adhesion molecule production. Furthermore, it caused epithelial cell dysfunction via depressing cell viability and initiating cell necrosis and apoptosis. Because epithelial cells played important roles in orchestrating the inflammatory response and protecting bovine mammary tissue from mastitis, our results indicated that staphylococcal enterotoxin M may be associated with mastitis.

Simultaneous Formation of cis- and trans-CH3OCu(OH) Intermediates in Methane Activation by Cu in Solid Ar.

Understanding the mechanisms of methane activation is an important and active research area of the contemporary catalyzed conversion of hydrocarbons to shippable, valuable feedstock and has invoked close collaborations between experimentalists and theorists. This article describes the trapping of reaction intermediates in a copper-catalyzed direct methane-to-methanol conversion. Specifically, two hydroxy(methoxy)copper(I) [CH3OCu(OH)] isomeric intermediates were distinguished and characterized by matrix isolation infrared spectroscopy and 18O2, CD4, and 13CH4 isotopic substitution experiments combined with quantum chemical calculations. Initially, laser-evaporated copper reacted with oxygen to form CuO2. Upon successive broadband UV irradiation, methane activation via the insertion of CuO2 into one of the C-H bonds produced both cis- and trans-CH3OCu(OH). All possible structures of the reactants, intermediates, transition states, minimum-energy crossing points, and products were optimized. The results indicated that the two CH3OCu(OH) isomers are not thermodynamically distinguishable, although both have different frequencies, which agrees with experimental observation. The proposed reaction mechanism involved (i) O-O bond cleavage, (ii) C-H bond activation, and (iii) H and CH3 competitive transfer. The small energy barrier for cis to trans conversion accounts for the simultaneous formation of cis- and trans-CH3OCu(OH). These findings indicate that the CH3OCu(OH) species would be a potent precursor in other families of copper-cored oxidants that can trigger methanol formation.

Noble Gas-Tungsten Peroxide Complexes in Noble Gas Matrixes: Infrared Spectroscopy and Density Functional Theoretical Study.

The matrix isolation infrared spectroscopic and quantum chemical calculation results indicate that tungsten oxo and mono-superoxide, WO3 and (η2-O2)WO2, coordinate noble gas atoms in forming noble gas-tungsten oxide complexes. The results showed that both WO3 and (η2-O2)WO2 oxides can coordinate one Ar or Xe atom in solid noble gas matrixes; otherwise, tungsten mono- and dioxides cannot. Hence, the WO3 and (η2-O2)WO2 molecules trapped previously in solid argon noble gas matrixes should be regarded as the WO3(Ar) oxide and (η2-O2)WO2(Ar) peroxide complexes. When annealing, the lighter Ar atom can be replaced by a heavier xenon atom to form WO3(Xe) and (η2-O2)WO2(Xe) complexes. What's more, upon UV photolysis, both Ar and Xe atoms can be replaced by oxygen to form a tungsten disuperoxide (η2-O2)2WO2 complex. The binding energies were predicted to be 25.7, 16.6, 9.4, 14.7, and 8.1 kcal/mol for the (η2-O2)2WO2, WO3(Xe), WO3(Ar), (η2-O2)WO2(Xe), and (η2-O2)WO2(Ar) complexes at the CCSD(T)//M06-2X-D3//def2-TZVP/DGDZVP/SDD level. The substitution law, O2 > Xe > Ar, can be interpreted according to the chemical reaction energies calculated to be -6.6 and +11.0 kcal/mol, respectively, for the equation formulas Xe + (η2-O2)WO2(Ar) = (η2-O2)WO2(Xe) + Ar and O2 + (η2-O2)WO2(Xe) = (η2-O2)2WO2 + Xe at the same level.

Short-time dynamics and decay mechanism of E,E-2,4-hexadienal in the first light-absorbing S2(ππ*) state.

The initial nonadiabatic decay dynamics of E,E-2,4-hexadienal (HAL) in the light absorbing S2(ππ*) state were studied using resonance Raman spectroscopy and complete-active space self-consistent field (CASSCF) calculations. The UV and vibrational spectra were assigned on the basis of the UV absorption, Fourier transform (FT)-Raman and FT-infrared measurements, the density-functional theory computations, and the normal mode analysis. The A-band resonance Raman spectra in cyclohexane and acetonitrile were obtained at 282.4, 273.9, 266.0, 252.7, and 245.9 nm excitation wavelengths, respectively, to probe the corresponding structural dynamics of HAL. The A-band absorption cross section and the corresponding absolute resonance Raman cross sections were simulated using a simple model based on the time-dependent wave-packet theory in a Brownian oscillator model. The geometric structures of the singlet electronic excited states and their curve-crossing points were optimized at the CASSCF level of theory. The obtained short-time structural dynamics in easy-to-visualize internal coordinates were then compared with the CASSCF-predicted structural-parameter changes of S2(ππ*)S1(nπ*)-n (n = 1-4). Our results indicate that the initial population of HAL in the S2 state ramifies in or nearby the Franck-Condon (FC) region, leading to five S2(ππ*) → S1(nπ*) internal conversion pathways due to the flexibility of the molecular chain and the different electronic resonant structures formed nearby FC of the S2 state. Then, the formed S1 transient species, which have different geometric structures and different energy partitions, undergo different photophysical processes, such as S1 → S0 internal conversion, S1 → T1 intersystem crossing, and the S1 → S'1 photoisomerization reaction. The substitution effect on the S2(ππ*) → S1(nπ*) internal conversion dynamics and the trans-cis photoisomerization reaction is proposed in terms of the p-π conjugation interaction or the p-σ superconjugation interaction.

Dl-3-n-butylphthalide inhibits phenytoin-induced neuronal apoptosis in rat hippocampus and cerebellum.

Rats were divided into six groups: sham/control , Dl-3-n-butylphthalide, P1 (low phenytoin, 100 mg/kg), P2 (high phenytoin, 200 mg/kg), NP1 (Dl-3-n-butylphthalide 80 mg/kg, phenytoin 100 mg/kg), NP2 (Dl-3-n-butylphthalide 80 mg/kg, phenytoin 200 mg/kg). Hematoxylin/eosin and Nissl staining showed that, compared to the sham/control group, the Dl-3-n-butylphthalide group had no obvious hippocampal and cerebellar neuron loss, but there was a significant neuron loss in the P1 and P2 groups (P < 0.05), which was more obvious in the P2 group (P < 0.05). The positive expression of Bax and Bcl-2 proteins in hippocampal and cerebellar neurons was not significantly different between sham and Dl-3-n-butylphthalide groups; however, compared to sham, Bax expression was significantly increased and Bcl-2 was significantly decreased in the hippocampal and cerebellar neurons of rats in both P1 and P2 groups (P < 0.05), being more obvious in the P2 group (P < 0.05). Furthermore, the administration of Dl-3-n-butylphthalide attenuated the deleterious effects of phenytoin (P < 0.05). Our results indicate that phenytoin causes apoptosis of hippocampal and cerebellar neurons in rats in a dose-dependent manner, with the effect of a higher dose being more obvious, whereas, Dl-3-n-butylphthalide inhibits the phenytoin-induced apoptosis of neurons and has a neuroprotective role.