Optimization of teacher evaluation indicator system based on fuzzy-DEMATEL-BP.

The establishment of a reasonable teacher evaluation indicator system has always been a research hotspot in teacher evaluation. Simplifying and essential indicators are the foundation for maintaining the speed and accuracy of teacher evaluation. Therefore, optimizing indicators in a convincing and interpretable manner becomes highly important. Due to the complex causal relationships and fuzzy uncertainties among teacher evaluation indicators, this paper proposes a method that combines the Triangular Fuzzy Decision-making Trial and Evaluation Laboratory Model (Fuzzy-DEMATEL) with Backpropagation Neural Network (BP) to optimize the complexity of assessment systems and identify key indicators, thereby establishing a precise and rational teacher evaluation index system. DEMATEL allows us to simplify and analyze the complex causal relationships among assessment indicators, mapping them into a causal relationship diagram. Fuzzy logic effectively handles the fuzzy and uncertain relationships among the indicators, converting fuzzy information into computable forms. The BP neural network is a data training model that, from an objective data perspective, compensates for subjective errors, thereby optimizing our indicator results. In addition, we conducted empirical and comparative research using relevant data from the TIMSS 2019 dataset, and found that this method can reduce the original indicator quantity by approximately 28 %-30 %, compared to methods such as Multi-Criteria Decision Making (MCDM), the results are superior and the indicators are more accurate.

Corrigendum: Exploring the shared molecular mechanisms between systemic lupus erythematosus and primary Sjögren's syndrome based on integrated bioinformatics and single-cell RNA-seq analysis.

[This corrects the article DOI: 10.3389/fimmu.2023.1212330.].

Exploring the shared molecular mechanisms between systemic lupus erythematosus and primary Sjögren's syndrome based on integrated bioinformatics and single-cell RNA-seq analysis.

Background: Systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (pSS) are common systemic autoimmune diseases that share a wide range of clinical manifestations and serological features. This study investigates genes, signaling pathways, and transcription factors (TFs) shared between SLE and pSS. Methods: Gene expression profiles of SLE and pSS were obtained from the Gene Expression Omnibus (GEO). Weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) analysis were conducted to identify shared genes related to SLE and pSS. Overlapping genes were then subject to Gene Ontology (GO) and protein-protein interaction (PPI) network analyses. Cytoscape plugins cytoHubba and iRegulon were subsequently used to screen shared hub genes and predict TFs. In addition, gene set variation analysis (GSVA) and CIBERSORTx were used to calculate the correlations between hub genes and immune cells as well as related pathways. To confirm these results, hub genes and TFs were verified in microarray and single-cell RNA sequencing (scRNA-seq) datasets. Results: Following WGCNA and limma analysis, 152 shared genes were identified. These genes were involved in interferon (IFN) response and cytokine-mediated signaling pathway. Moreover, we screened six shared genes, namely IFI44L, ISG15, IFIT1, USP18, RSAD2 and ITGB2, out of which three genes, namely IFI44L, ISG15 and ITGB2 were found to be highly expressed in both microarray and scRNA-seq datasets. IFN response and ITGB2 signaling pathway were identified as potentially relevant pathways. In addition, STAT1 and IRF7 were identified as common TFs in both diseases. Conclusion: This study revealed IFI44L, ISG15 and ITGB2 as the shared genes and identified STAT1 and IRF7 as the common TFs of SLE and pSS. Notably, the IFN response and ITGB2 signaling pathway played vital roles in both diseases. Our study revealed common pathogenetic characteristics of SLE and pSS. The particular roles of these pivotal genes and mutually overlapping pathways may provide a basis for further mechanistic research.

Determining the Effects of Light on the Fruit Peel Quality of Photosensitive and Nonphotosensitive Eggplant.

With the development of facility agriculture, low-light stress is a prominent problem and a popular research topic currently. In this study, transcriptome analysis was used to analyze the genes in the fruit peel of photosensitive and nonphotosensitive eggplant and to explore the mechanism of changes in fruit color, texture, hormone content, aroma, and taste of these two different types of eggplant. We identified 51, 65, 66, and 66 genes involved in synthesizing anthocyanins, texture, hormone content, and aroma and flavor, respectively, in the two different types of eggplant based on the variation in gene expression trends in the fruit peel. These results provide a basis for further analysis of the molecular mechanism underlying the regulatory processes in eggplant fruits under low-light stress.

Identifying Quantitative Trait Loci for Thousand Grain Weight in Eggplant by Genome Re-Sequencing Analysis.

Eggplant (Solanum melongena L.; 2n = 24) is one of the most important Solanaceae vegetables and is primarily cultivated in China (approximately 42% of world production) and India (approximately 39%). Thousand-grain weight (TGW) is an important trait that affects eggplant breeding cost and variety promotion. This trait is controlled by quantitative trait loci (QTLs); however, no quantitative trait loci (QTL) has been reported for TGW in eggplant so far, and its potential genetic basis remain unclear. In this study, two eggplant lines, 17C01 (P1, wild resource, small seed) and 17C02 (P2, cultivar, large seed), were crossed to develop F1, F2 (308 lines), BC1P1 (44 lines), and BC1P2 (44 lines) populations for quantitative trait association analysis. The TGWs of P1, P2 and F1 were determined as 3.00, 3.98 and 3.77 g, respectively. The PG-ADI (polygene-controlled additive-dominance-epistasis) genetic model was identified as the optimal model for TGW and the polygene heritability value in the F2 generation was as high as 80.87%. A high-quality genetic linkage bin map was constructed with resequencing analysis. The map contained 3,918 recombination bins on 12 chromosomes, and the total length was 1,384.62 cM. A major QTL (named as TGW9.1) located on chromosome 9 was identified to be strongly associated with eggplant TGW, with a phenotypic variance explanation of 20.51%. A total of 45 annotated genes were identified in the genetic region of TGW9.1. Based on the annotation of Eggplant genome V3 and orthologous genes in Arabidopsis thaliana, one candidate gene SMEL_009g329850 (SmGTS1, encoding a putative ubiquitin ligase) contains 4 SNPs and 2 Indels consecutive intron mutations in the flank of the same exon in P1. SmGTS1 displayed significantly higher expression in P1 and was selected as a potential candidate gene controlling TGW in eggplant. The present results contribute to shed light on the genetic basis of the traits exploitable in future eggplant marker-assisted selection (MAS) breeding.

Bio-C (Modified Hyaluronic Acid-Coated-Collagen Tube) Implants Enable Functional Recovery after Complete Spinal Cord Injury.

Neural repair within the central nervous system (CNS) has been extremely challenging due to limited abilities of adult CNS neurons to regenerate, particularly in a highly inflammatory injury environment that is also filled with myelin debris. Spinal cord injury (SCI) is a serious medical condition that often leads to paralysis and currently has no effective treatment. Here we report the construction of a novel biocompatible and biodegradable material, Bio-C, through coating of acid-desalted-collagen (ADC) tube with pre-modified hyaluronic acid, which, after implantation, can elicit quite robust neural regeneration and functional recovery after complete spinal-cord transection with a 2 mm-spinal-cord-segment removal in mice. We combined morphological, electrophysiological, and objective transcriptomic analyses, in addition to behavioral analyses, to demonstrate neural tissue regeneration and functional recovery through the establishment of Bio-C-induced anti-inflammatory, neurogenic, and neurotrophic microenvironment. Through this study, we unveiled the underlying logic for CNS neural repair.

Index and First-Generation Cases in a COVID-19 Outbreak - Jilin Province, China, 2021.

What is already known on this topic? Contact tracing and testing with isolated medical care of identified cases is a key strategy for interrupting chains of transmission of COVID-19 and reducing mortality associated with COVID-19. At the early phases of the COVID-19 pandemic, due to test capacity limitations, case finding often started from suspected cases. What is added by this report? The index patient infected 74 individuals who were close contacts that were identified through contact tracing, and exposed individuals were monitored in quarantine with daily polymerase chain reaction (PCR) testing. All individuals were asymptomatic initially, but all PCR-positive individuals eventually developed symptoms. Infectivity was documented up to 8 days before being confirmed as a symptomatic case, approximately 4 days before turning PCR positive. What are the implications for public health practice? During an outbreak, we suggest tracing close contacts from both PCR-positive individuals and suspected cases, rather than from suspected cases alone. Due to the long period of infectivity before turning PCR positive or developing symptoms, close contacts that had contact with a newly PCR positive case within 4 days should be judged as at risk of being infected; close contacts that had contact within 8 days of a newly symptomatic case should be judged as at risk being infected.

Identification of Quantitative Trait Loci Controlling the Development of Prickles in Eggplant by Genome Re-sequencing Analysis.

Eggplant (Solanum melongena L.) is the third most important crop in the family of Solanaceae. Prickles are considered as the undesirable traits during the plantation of eggplant and the transportation of fruits. In this study, we constructed a high-quality genetic linkage Bin map derived from the re-sequencing analysis on a cross of a prickly wild landrace, 17C01, and a cultivated variety, 17C02. The major quantitative trait locus (QTL) controlling the development of prickles on the calyx (explained 30.42% of the phenotypic variation), named as qPC.12, was identified on a ~7 kb region on chromosome 12. A gene within qPC.12, which encodes a WUSCHEL-related homeobox-like protein, with higher expression levels in 17C01 calyx and 22-bp deletion in 17C02 was probably the functional gene for prickle formation. Results from this study would ultimately facilitate uncovering the molecular regulatory mechanisms underlying the development of a prickle in eggplant.

MicroRNA-936 Targets JAG1 and Inhibits the Proliferation of Hepatocellular Carcinoma Cells.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. Investigating the underlying molecular mechanism is essential for the treatment and prognosis of HCC. Emerging evidence suggests that microRNAs (miRNAs) play pivotal roles in cancer progression. Down-regulation of miR-936 has been found in several cancers, which serves as a tumor suppressor to inhibit the development of cancers. However, the clinical significance and functional roles of miR-936 in HCC have not been determined. To explore this, the expression of miR-936 in HCC tissues and cells was detected by RT-qPCR. Cell Counting Kit-8 (CCK-8) assay, cell migration and cell cycle analysis were performed to evaluate the effects of miR-936 on the growth of HCC cells. The targets of miR-936 were predicted using the miRDB database and confirmed by luciferase reporter experiments. The protein expression of targets was determined by western blot. The results showed that miR-936 was significantly decreased in HCC tissues and cell lines. Low expression of miR-936 was associated with the advance progression and poor survival of HCC patients (P = 0.0036). Functional study revealed that overexpression of miR-936 inhibited the proliferation, migration (decreased to ∼0.26 fold) and induced cell cycle arrested in G1 phase (from 35.3% to 44.7%) of HCC cells. Additionally, miR-936 targeted the 3'-untranslated region (UTR) of jagged-1 (JAG1) and reduced the expression of JAG1 (decreased to ∼0.35 fold). JAG1 was found to be up-regulated in HCC tissues and was inversely correlated with the expression of miR-936 (Pearson r = -0.4633; P = 0.0007). The anti-cancer effects of miR-936 on the proliferation of HCC cells were partially reversed by the rescue of JAG1. Therefore, these results suggested that miR-936 might be a potential target for HCC treatment.

The Effect of Autistic Traits on Social Orienting in Typically Developing Individuals.

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by wide ranging and heterogeneous changes in social and cognitive abilities, including deficits in orienting attention during early processing of stimuli. Investigators have found that there is a continuum of autism-like traits in the general population, suggesting that these autistic traits may be examined in the absence of clinically diagnosed autism. To provide evidence for the continuum of autistic traits in terms of social attention and to provide insights into social attention deficits in people with autism, the current study was conducted to examine the effect of autistic traits of typically developing individuals on social orienting using a spatial cueing paradigm. The typically developing individuals who participated in this study were divided into high autistic traits (HA) and low autistic traits groups using the Autism Quotient scale. All participants completed a spatial cueing task in which social cues (gaze) and non-social cues (arrow) were presented under different cue predictability conditions (predictive vs. non-predictive) with different SOAs (100 ms vs. 400 ms). The results showed that compared to low autistic individuals, high autistic individuals had less benefit from non-predictive social cues but greater benefit from non-social ones, providing evidence that such spatial attention impairment in high autistic individuals is specific to the social domain. Interestingly, the smaller benefit from non-predictive social cues in high autistic individuals was shown only in the 400 ms condition, not in the 100 ms condition, suggesting that their difficulties in orienting to non-predictive social cues may be caused by a deficiency in spontaneously effortful control processing.

Regulation of mitochondrial cristae remodelling by acetylcholine alleviates palmitate-induced cardiomyocyte hypertrophy.

Mitochondrial dysfunction is associated with obesity-induced cardiac remodelling. Recent research suggests that the cristae are the true bioenergetic components of cells. Acetylcholine (ACh), the major neurotransmitter of the vagus nerve, exerts cardio-protective effects against ischaemia. This study investigated the role of cristae remodelling in palmitate (PA)-induced neonatal rat cardiomyocyte hypertrophy and explored the beneficial effects of ACh. We found loose, fragmented and even lysed cristae in PA-treated neonatal cardiomyocytes along with declines in mitochondrial network and complex expression and overproduction of mitochondrial reactive oxygen species (ROS); these changes ultimately resulted in increased myocardial size. Overexpression of mitofilin by adenoviral infection partly improved cristae shape, mitochondrial network, and ATP content and attenuated cell hypertrophy. Interestingly, siRNA-mediated AMP-activated protein kinase (AMPK) silencing increased the number of cristae with a balloon-like morphology without disturbing mitofilin expression. Furthermore, AMPK knockdown abolished the effects of mitofilin overexpression on cristae remodelling and inhibited the interaction of mitofilin with sorting and assembly machinery 50 (Sam50) and coiled-coil helix coiled-coil helix domain-containing protein 3 (CHCHD3), two core components of the mitochondrial contact site and cristae organizing system (MICOS) complex. Intriguingly, ACh upregulated mitofilin expression and AMPK phosphorylation via the muscarinic ACh receptor (MAChR). Moreover, ACh enhanced protein-protein interactions between mitofilin and other components of the MICOS complex, thereby preventing PA-induced mitochondrial dysfunction and cardiomyocyte hypertrophy; however, these effects were abolished by AMPK silencing. Taken together, our data suggest that ACh improves cristae remodelling to defend against PA-induced myocardial hypertrophy, presumably by increasing mitofilin expression and activating AMPK to form the MICOS complex through MAChR. These results suggest new and promising therapeutic approaches targeting mitochondria to prevent lipotoxic cardiomyopathy.

Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling.

AIMS: Obesity is associated with increased cardiovascular morbidity and mortality. It is accompanied by augmented O-linked ß-N-acetylglucosamine (O-GlcNAc) modification of proteins via increasing hexosamine biosynthetic pathway (HBP) flux. However, the changes and regulation of the O-GlcNAc levels induced by obesity are unclear. MAIN METHODS: High fat diet (HFD) model was induced obesity in mice with or without the cholinergic drug pyridostigmine (PYR, 3 mg/kg/d) for 22 weeks and in vitro human umbilical vein endothelial cells (HUVECs) was treated with high glucose (HG, 30 mM) with or without acetylcholine (ACh). KEY FINDINGS: PYR significantly reduced body weight, blood glucose, and O-GlcNAcylation levels and attenuated vascular endothelial cells detachment in HFD-fed mice. HG addition induced endoplasmic reticulum (ER) stress and increased O-GlcNAcylation levels and apoptosis in HUVECs in a time-dependent manner. Additionally, HG decreased levels of phosphorylated AMP-activated protein kinase (AMPK). Interestingly, ACh significantly blocked damage to HUVECs induced by HG. Furthermore, the effects of ACh on HG-induced ER stress, O-GlcNAcylation, and apoptosis were prevented by treating HUVECs with 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, a selective M3 AChR antagonist) or compound C (Comp C, an AMPK inhibitor). Treatment with 5-aminoimidazole-4-carboxamide ribose (AICAR, an AMPK activator), 4-phenyl butyric acid (4-PBA, an ER stress inhibitor), and 6-diazo-5-oxonorleucine (DON, a GFAT antagonist) reproduced a similar effect with ACh. SIGNIFICANCE: Activation of cholinergic signaling ameliorated endothelium damage, reduced levels of ER stress, O-GlcNAcylation, and apoptosis in mice and HUVECs under obese conditions, which may function through M3 AChR-AMPK signaling.

Pyridostigmine alleviates cardiac dysfunction via improving mitochondrial cristae shape in a mouse model of metabolic syndrome.

Insulin resistance and autonomic imbalance are important pathological processes in metabolic syndrome-induced cardiac remodeling. Recent studies determined that disruption of mitochondrial cristae shape is associated with myocardial ischemia; however, the change in cristae shape in metabolic syndrome-induced cardiac remodeling remains unclear. This study determined the effect of pyridostigmine (PYR), which reversibly inhibits cholinesterase to improve autonomic imbalance, on high-fat diet (HFD)-induced cardiac insulin resistance and explored the potential effect on the shape of mitochondrial cristae. Feeding of a HFD for 22 weeks led to an irregular and even lysed cristae structure in cardiac mitochondria, which contributed to decreased mitochondrial content and ATP production and increased oxygen species production, ultimately impairing insulin signaling and lipid metabolism. Interestingly, PYR enhanced vagal activity by increasing acetylcholine production and exerted mito-protective effects by activating the LKB1/AMPK/ACC signal pathway. Specifically, PYR upregulated OPA1 and Mfn1/2 expression, promoted the formation of the mitofilin/CHCHD3/Sam50 complex, and decreased p-Drp1 and Fis1 expression, resulting in tight and parallel cristae and increasing cardiac mitochondrial complex subunit expression and ATP generation as well as decreasing release of cytochrome C from mitochondria and oxidative damage. Furthermore, PYR improved glucose and insulin tolerance and insulin-stimulated Akt phosphorylation, decreased lipid toxicity, and ultimately ameliorated HFD-induced cardiac remodeling and dysfunction. In conclusion, PYR prevented cardiac and insulin insensitivity and remodeling by stimulating vagal activity to regulate mitochondrial cristae shape and function in HFD-induced metabolic syndrome in mice. These results provide novel insights for the development of a therapeutic strategy for obesity-induced cardiac dysfunction that targets mitochondrial cristae.

Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway.

AIMS: Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline. METHODS AND RESULTS: The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats. Cardiomyocyte size and cardiac fibrosis were significantly increased in hypertrophic hearts. In vitro cardiomyocyte hypertrophy was induced by exposing neonatal rat cardiomyocytes to angiotensin II (Ang II) (10-6 M, 24 h). Choline attenuated the mito-nuclear protein imbalance and activated the mitochondrial-unfolded protein response (UPRmt) in the heart, thereby preserving the ultrastructure and function of mitochondria in the context of cardiac hypertrophy. Moreover, choline inhibited myocardial metabolic dysfunction by promoting the expression of proteins involved in ketone body and fatty acid metabolism in response to pressure overload, accompanied by the activation of sirtuin 3/AMP-activated protein kinase (SIRT3-AMPK) signalling. In vitro analyses demonstrated that SIRT3 siRNA diminished choline-mediated activation of ketone body metabolism and UPRmt, as well as inhibition of hypertrophic signals. Intriguingly, serum from choline-treated abdominal aorta banding models (where ß-hydroxybutyrate was increased) attenuated Ang II-induced myocyte hypertrophy, which indicates that ß-hydroxybutyrate is important for the cardioprotective effects of choline. CONCLUSION: Choline attenuated cardiac dysfunction by modulating the expression of proteins involved in ketone body and fatty acid metabolism, and induction of UPRmt; this was likely mediated by activation of the SIRT3-AMPK pathway. Taken together, these results identify SIRT3-AMPK as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to cardiac stress. Choline treatment may represent a new therapeutic strategy for optimizing myocardial metabolism in the context of hypertrophy and heart failure.

[Effects of ligustrazine on the Ca2+ sensitivity in carotid artery smooth muscle of simulated weightlessness rats].

OBJECTIVE: To study the effects of Ligustrazine on the Ca2+ sensitivity in carotid artery smooth muscle of simulated weightless-ness rats. METHODS: Twenty-one female SD rats were divided into control group (CON), simulated weightlessness group (TS), simulated weightlessness plus Ligustrazine administration group (LTZ) (n=7). After 4 weeks, the contractile property and the Ca2+ sensitivity in carotid artery were measured. Furthermore, the effects of ML-7(a myosin light chain kinase specific inhibitor) on above mentioned parameters were recorded. RESULTS: Compared with CON group, the contractile force induced by phenylephrine (PHE) in TS group was increased by 25.14% (P<0.01). The force in LTZ group decreased by 13.46% (P<0.01) and increased by 8.30% compared with TS and CON group, respec-tively. After the artery rings were incubated with ML-7, the force in CON, TS and LTZ group were reduced by 8.84%, 16.24% (P<0.01) and 3.40%, respectively. Compared with CON group, the contractile force induced by KCl in TS group was increased by 40.46% (P<0.01). The force in LTZ group decreased by 18.80% and increased by 14.05% compared with TS and CON group, respectively. The force in CON, TS and LTZ group were reduced by 21.97% (P<0.05), 21.88% (P<0.01) and 10.84% by ML-7, respectively. Compared with CON group, the pD2[Ca2+] in TS group was increased by 10.03% (P<0.01). The pD2[Ca2+] in LTZ group was decreased by 7.01% (P<0.01) and increased by 2.32% compared with TS and CON group, respectively. The pD2[Ca2+] in CON, TS and LTZ group was reduced by 2.42%, 7.43% (P<0.01) and 2.51% by ML-7, respectively. CONCLUSIONS: The contraction of carotid artery is strength-ened in simulated weightlessness rats, it maybe results from the Ca2+ sensitivity of contractile proteins in smooth muscle increasing. Ligus-trazine can improve the contraction of carotid artery, reducing the Ca2+ sensitivity and inhibiting myosin light chain kinase may be involved in its mechanisms.

Detailed theoretical investigation of excited-state intramolecular proton transfer mechanism of a new chromophore II.

In the present work, TDDFT has been used to investigate the excited state intramolecular proton transfer (ESIPT) mechanism of a new chromophore II [Sensors and Actuators B: Chemical. 202 (2014) 1190]. The calculated absorption and fluorescence spectra agree well with experimental results. In addition, two types of II configurations are found in the first excited state (S1), which can be ascribed to the ESIPT reaction. Based on analysis of the calculated infrared (IR) spectra of O-H stretching vibration as well as the hydrogen bonding energies, the strengthening of the hydrogen bond in the S1 state has been confirmed. The frontier molecular orbitals (MOs), Hirshfeld charge distribution and the Natural bond orbital (NBO) have also been analyzed, which displays the tendency of the ESIPT process. Finally, potential energy curves of the S0 and S1 states were constructed, demonstrating that the ESIPT reaction can be facilitated based on the photo-excitation.

Study of fluorescence probe transfer mechanism based on a new type of excited-state intramolecular proton transfer.

3-Hydroxyflavone (3-HF) is a typical representative of a new type of fluorescent molecular probe. The intramolecular proton transfer mechanisms of 3-HF and its derivatives have been studied theoretically based on detailed density functional theory. An optical physical cycle diagram of intramolecular proton transfer of 3-HF and its derivatives has been found based on the optimal configuration before and after proton transfer. An analysis of the absorption and fluorescence spectra of these probes explains their optical physical mechanism, which agrees well with experimental results. This correlation indicates that the adopted theory is reasonable and effective. The primary bond lengths, angles and infrared vibrational spectra indicate that the intramolecular hydrogen bonds were strengthened, which is an indication of the excited-state intramolecular proton transfer (ESIPT) processes. The constructed potential energy curves of the ground and first excited state based on these three chromophores provide the ESIPT mechanism, which demonstrates that potential barriers lower than the 6kcal/mol and justifies the ESIPT processes occur in the first excited state. The fluorescence quenching phenomenon has been explained based on the ESIPT mechanism.

A questionable excited-state double-proton transfer mechanism for 3-hydroxyisoquinoline.

Two excited state proton transfer mechanisms of 3-hydroxyisoquinoline (3HIQ) in cyclohexane and acetic acid (ACID) were investigated based on the time-dependent density functional theory (TDDFT), suggesting a different double-proton transfer mechanism from the one proposed previously (J. Phys. Chem. B, 1998, 102, 1053). Instead of the formation of keto-enol complexes for 3HIQ self-association in cyclohexane, our theoretical results predicted that 3HIQ self-association exists in two forms: the normal form (enol/enol) and the tautomer form (keto/keto) in cyclohexane. A high barrier (37.023 kcal mol(-1)) between the 3HIQ enol monomer and 3HIQ keto monomer form indicated that the 3HIQ keto monomer in the ground state should not exist. In addition, the constructed potential energy surfaces of the ground state and excited state have been used to explain the proton transfer process. Upon optical excitation, the enol/enol form is excited to the first excited state, then transfers one proton, in turn, transition to the ground state to transfer another proton. A relatively low barrier (8.98 kcal mol(-1)) demonstrates two stable structures in the ground state. In view of the acetic acid solvent effect, two protons of 3HIQ/ACID transfer along the dihydrogen bonds in the first excited state, which is a different transfer mechanism to 3HIQ self-association. In addition, the proton transfer process provides a possible explanation for the fluorescence quenching observed.

Organic nonlinear optical materials: the mechanism of intermolecular covalent bonding interactions of Kekulé hydrocarbons with significant singlet biradical character.

The ground- and excited-state properties of benzene-linked bisphenalenyl (B-LBP), naphthaline-linked bisphenalenyl (N-LBP), and anthracene-linked bisphenalenyl (A-LBP) Kekulé molecules and their respective one-dimensional (1D) stacks are investigated using time-dependent density functional theory (TD-DFT) and a range of extensive multidimensional visualization techniques. The results reveal a covalent π-π bonding interaction between overlapping phenalenyl radicals whose bond length is shorter than the van der Waals distance between carbon atoms. Increasing the linker length and/or number of molecules involved in the 1D stack decreases the HOMO-LUMO energy gap and increases the wavelength of the systems. The charge-transfer mechanism and electron coherence both differ with changes in the linker length and/or number of molecules involved in the 1D stack.

Effects of hydrogen bond on 2-aminopyridine and its derivatives complexes in methanol solvent.

In the present work, the time-dependent density functional theory (TD-DFT) method was adopted to investigate the excited state hydrogen-bond dynamics of 2-aminopyridine monomer (2AP) and its derivatives in hydrogen donating methanol solvent. The calculated steady-state absorption and fluorescence spectra agree well with the experimental results. Theoretical results state that the bond lengths of both O-H and N-H bands are lengthened, while the intermolecular hydrogen bond lengths are shortened in the excited state. Further, the intermolecular hydrogen bonds are proved to be strengthened according to the calculated binding energy. As a reasonable explanation, the hydrogen bonds binding energy increases with multiple hydrogen-bonding interactions in the electronically excited state. In addition, the hydrogen bonding dynamics in the excited state were visualized by the spectral shifts of vibrational modes. The calculated infrared spectra of both O-H and N-H stretching vibrational regions revealed that the O-H and N-H stretching bands red-shift.