ABSTRACT
Plants manage the high cost of immunity activation by suppressing the expression of defense genes during normal growth and rapidly switching them on upon pathogen invasion. TGAs are key transcription factors controlling the expression of defense genes. However, how TGAs function, especially in monocot plants like rice with continuously high levels of endogenous salicylic acid (SA) remains elusive. In this study, we characterized the role of OsTGA5 as a negative regulator of rice resistance against blast fungus by transcriptionally repressing the expression of various defense-related genes. Moreover, OsTGA5 repressed PTI responses and the accumulation of endogenous SA. Importantly, we showed that the nucleus-localized casein kinase II (CK2) complex interacts with and phosphorylates OsTGA5 on Ser-32, which reduces the affinity of OsTGA5 for the JIOsPR10 promoter, thereby alleviating the repression of JIOsPR10 transcription and increasing rice resistance. Furthermore, the in vivo phosphorylation of OsTGA5 Ser-32 was enhanced by blast fungus infection. The CK2 α subunit, depending on its kinase activity, positively regulated rice defense against blast fungus. Taken together, our results provide a mechanism for the role of OsTGA5 in negatively regulating the transcription of defense-related genes in rice and the repressive switch imposed by nuclear CK2-mediated phosphorylation during blast fungus invasion.
Subject(s)
Magnaporthe , Oryza , Casein Kinase II , Disease Resistance , Gene Expression Regulation, Plant , Phosphorylation , Plant Diseases , Plant Proteins , Salicylic Acid , Transcription, GeneticABSTRACT
Quinolone 006 is under development as an anti-methicillin-resistant Staphylococcus aureus quinolone antibiotic. A linear synthetic route was utilized to prepare the compound on a multi-kilogram scale with an overall yield of 71%. The process was optimized by controlling the temperature and the vacuum pressure. Examples of parameters examined in an effort to control the polymorphism of the 006 active pharmaceutical ingredient are described.
Subject(s)
Anti-Bacterial Agents/chemical synthesis , Quinolones/chemical synthesis , Anti-Bacterial Agents/chemistry , Chemistry Techniques, Synthetic/economics , Chemistry Techniques, Synthetic/methods , Crystallization , Humans , Methicillin-Resistant Staphylococcus aureus/drug effects , Quinolones/chemistry , Staphylococcal Infections/drug therapyABSTRACT
CONTEXT: Berberine is used in traditional Chinese medicine for thousands of years with recent reports of its anticancer activity. OBJECTIVE: To test antiangiogenic effects of berberine on human glioblastoma and clarify involvement of the VEGFR2/ERK pathway. MATERIALS AND METHODS: Cell viability, proliferation and migration assays were performed to determine in vitro antiangiogenic effects of berberine (6.25-200 µmol/L, 6-48 h). Ectopic and orthotopic xenograft models in BALB/c nude mice were induced to determine antitumour and antiangiogenic effects of berberine (50 mg/kg by oral gavage for 28 days) or vehicle control (carboxymethylcellulose sodium). RESULTS: Berberine inhibited cell viability (IC50 of 42 and 32 µmol/L, respectively) and proliferation of U87 and U251 human glioblastoma cell lines. Berberine (50 µmol/L) inhibited cell migration of HUVEC by 67.50 ± 8.14% in the Transwell assay and tube formation of HUVEC by 73.00 ± 11.12% in the Matrigel assay. In the ectopic xenograft model, tumour weight was significantly decreased by 50 mg/kg of berberine (401.2 ± 71.5 mg vs. 860.7 ± 117.1 mg in vehicle group, p Ë 0.001). Berberine significantly decreased haemoglobin content (28.81 ± 3.64 µg/mg vs. 40.84 ± 5.15 µg/mg in vehicle group, p Ë 0.001) and CD31 mRNA expression in tumour tissue. In the orthotopic xenograft model, berberine (50 mg/kg) significantly improved the survival rate of mice (p = 0.0078). Berberine inhibited (p Ë 0.001) the phosphorylation of VEGFR2 and ERK. DISCUSSION AND CONCLUSIONS: Berberine inhibited angiogenesis in glioblastoma xenografts by targeting the VEGFR2/ERK pathway. Our work sheds new light on complementary and alternative therapy for glioblastoma.
Subject(s)
Angiogenesis Inhibitors/therapeutic use , Berberine/administration & dosage , Drug Delivery Systems/methods , Glioblastoma/drug therapy , MAP Kinase Signaling System/drug effects , Vascular Endothelial Growth Factor Receptor-2/antagonists & inhibitors , Angiogenesis Inhibitors/pharmacology , Animals , Cell Line, Tumor , Cell Survival/drug effects , Cell Survival/physiology , Dose-Response Relationship, Drug , Glioblastoma/metabolism , Human Umbilical Vein Endothelial Cells/drug effects , Human Umbilical Vein Endothelial Cells/metabolism , Humans , MAP Kinase Signaling System/physiology , Mice , Mice, Inbred BALB C , Mice, Nude , Random Allocation , Vascular Endothelial Growth Factor Receptor-2/metabolism , Xenograft Model Antitumor Assays/methodsABSTRACT
A series of C10 non-basic building block-substituted, levofloxacin core-based derivatives were synthesized in 43-86% yield. The antibacterial activity of these new fluoroquinolones was evaluated using a standard broth microdilution technique. The quinolone (S)-9-fluoro-10-(4-hydroxypiperidin-1-yl)-3-methyl-7-oxo-3,7-dihydro-2H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid L-arginine tetrahydrate exhibited superior antibacterial activity against quinolone-susceptible and resistant strains compared with the clinically used fluoroquinolones ciprofloxacin, levofloxacin, moxifloxacin, penicillin, and vancomycin, especially to the methicillin-resistant Staphylococcus aureus clinical isolates, penicillin-resistant Streptococcus pneumoniae clinical isolates, and Streptococcus pyogenes.
Subject(s)
Anti-Bacterial Agents/chemical synthesis , Anti-Bacterial Agents/pharmacology , Levofloxacin/analogs & derivatives , Levofloxacin/pharmacology , Methicillin-Resistant Staphylococcus aureus/drug effects , Streptococcus pneumoniae/drug effects , Streptococcus pyogenes/drug effects , Anti-Bacterial Agents/chemistry , Dose-Response Relationship, Drug , Levofloxacin/chemical synthesis , Levofloxacin/chemistry , Microbial Sensitivity Tests , Molecular Structure , Penicillin Resistance/drug effects , Structure-Activity RelationshipABSTRACT
Reactive oxygen species (ROS) play a critical role in renal ischemia-reperfusion injury (IRI). Intermedin (IMD) reportedly protected against myocardial IRI via its antioxidant effects; however, its protective role in renal IRI has not been investigated. We overexpressed IMD in rat kidneys and examined how the kidneys respond to renal IRI. Eukaryotic expression plasmid encoding the rat IMD gene or control empty vector was transfected into the left kidney using an ultrasound-microbubble-mediated delivery system. This method yielded high expression of IMD in kidney cells. Renal IRI was induced by clamping the left renal artery followed by reperfusion. In response to IRI, overexpression of IMD in the kidney significantly improved renal function and pathology compared with the kidney transfected with control plasmid. We investigated the mechanisms by which IMD protects against renal IRI. We examined renal superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and found SOD activity was significantly increased, while MDA level was markedly decreased in kidneys transfected with IMD, suggesting ROS production and oxidative stress were reduced by IMD overexpression. We also measured myeloperoxidase (MPO) activity, tubular cell apoptosis, and the expression of intercellular adhesion molecule-1 (ICAM-1), P-selectin, and endothelin-1 (ET-1) in the kidney. Renal MPO activity and the expression of ICAM-1, P-selectin, and ET-1 stimulated by IRI were significantly inhibited by IMD overexpression. Moreover, IMD overexpression prevented kidney cells from apoptosis caused by IRI. Our results demonstrate that overexpression of IMD in the kidney protects against renal IRI, apparently by reducing oxidative stress, consequently suppressing inflammation and vasoconstrictor production and apoptosis.
Subject(s)
Acute Kidney Injury/prevention & control , Adrenomedullin/pharmacology , Kidney/blood supply , Neuropeptides/pharmacology , Oxidative Stress/drug effects , Reactive Oxygen Species/antagonists & inhibitors , Reperfusion Injury/prevention & control , Animals , Kidney/pathology , Male , Models, Animal , Rats , Rats, Wistar , Transfection/methodsABSTRACT
Nano-cutting is an important development direction of the modern manufacturing technology. However, the research on the mechanism underlying nano-cutting lags far behind the practical application, which restricts the development of this advanced manufacturing technology. The chip formation process is the basic process of nano-cutting, and it is of key importance for the mechanism research of nano-cutting. In this paper, the nano-tensile behavior of single crystal copper was studied based on the molecular dynamics simulations. The toughness and brittleness characteristics of the copper at different temperatures were analyzed. Then, the molecular dynamics simulations of nano-cutting for single crystal copper with different toughness and brittleness were studied. The crystal structure, cutting force, stress-strain distribution and atomic motion characteristics were systematically investigated. The nano-chip formation mechanism of single crystal copper was revealed. The results show that the chip is formed through two ways, namely the shear and extrusion. The material near the free surface of the workpiece undergoes continuous shear slip and periodic long-distance slippage along the primary shear direction, forming the block chip in which the FCC and HCP structures are orderly distributed. The material near the tool-chip interface is extruded by the tool, block chip and stagnation zone to form the flowing chip with amorphous structure. As the temperature increases, the occurrence frequency of long-distance slippage in the block chip increases, while the slippage degree decreases. Besides, with the increase in temperature, the thickness of block chip formed by shear slip decreases, while the thickness of flowing chip formed by extrusion increases.
ABSTRACT
MTHFD2 is a folate-coupled mitochondrial metabolic enzyme which has been extensively studied in breast cancer; however, its molecular functions in this cancer remain unclear. The current study aimed to reveal the underlying mechanism of breast cancer. MTHFD2 expression status and prognostic value were determined using the Gene Expression Profiling Interactive Analysis database. To determine the function of MTHFD2 in breast cancer, MCF-7 cells with stable overexpression of Flag-MTHFD2 or depletion of MTHFD2 were generated. Cell Counting Kit-8 and colony formation assays were used to examine the effect of MTHFD2 overexpression or knockout on MCF-7 cell proliferation and clonogenicity, respectively. Luciferase reporter and an AKT inhibitor (GSK6906) analysis were carried out to investigate the effect of MTHFD2 on the AKT signaling pathway. The results demonstrated that MTHFD2 expression level was higher in breast cancer tissues compared with adjacent normal tissues. Furthermore, patients with high MTHFD2 expression had significantly poorer overall survival compared with patients with low MTHFD2 expression. In addition, ectopic expression of MTHFD2 promoted the tumorigenic properties of MCF-7 cells, including proliferation and clonogenicity. Conversely, depletion of MTHFD2 had the opposite effect on the malignant properties of MCF-7 cells. Luciferase reporter demonstrated that MTHFD2 can significantly increase the ATK luciferase density. Furthermore, the Akt inhibitor GSK690693 significantly decreased the increased clonogenicity caused by MTHFD2 overexpression in MCF-7 cells. Taken together, the findings from the present study suggested that MTHFD2 may serve a protumor role in the malignancy of breast cancer by activating the AKT signaling pathway. These results provide an alternative theoretical foundation that could help the development of MTHFD2-targeted breast cancer treatment.
ABSTRACT
A series of 4-substituted 4-(1H-1,2,3-triazol-1-yl)piperidine building blocks was synthesized and introduced to the C7 position of the quinolone core, 7-chloro-1-cyclopropyl-6-fluoro-4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid, to afford the corresponding fluoroquinolones in 40-83% yield. The antibacterial activity of these new fluoroquinolones was evaluated using a standard broth microdilution technique. Among them, the quinolone 1-cyclopropyl-6-fluoro-7-(4-(4-formyl-1H-1,2,3-triazol-1-yl)piperidin-1-yl)-4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid (34.15) exhibited comparable antibacterial activity against quinolone-susceptible and multidrug-resistant strains, especially to Staphylococcus aureus and Staphylococcus epidermidis, in comparison with ciprofloxacin and vancomycin.
Subject(s)
Anti-Bacterial Agents/chemistry , Fluoroquinolones/chemistry , Naphthyridines/chemistry , Piperidines/chemistry , Anti-Bacterial Agents/chemical synthesis , Anti-Bacterial Agents/pharmacology , Drug Resistance, Multiple, Bacterial/drug effects , Fluoroquinolones/chemical synthesis , Fluoroquinolones/pharmacology , Microbial Sensitivity Tests , Naphthyridines/chemical synthesis , Naphthyridines/pharmacology , Piperidines/chemical synthesis , Piperidines/pharmacologyABSTRACT
Protein tyrosine phosphatase receptor type A (PTPRA), one of the classic protein tyrosine phosphatases, is crucial for modulating tumorigenesis and metastasis in breast cancer; however, its functional mechanism has not fully elucidated. The present study assessed PTPRA expression and estimated its clinical impact on survival using the Gene Expression Profiling Interactive Analysis database (GEPIA). Growth curves, colony formations and Transwell assays were utilized to examine cell proliferation and migration. Additionally, luciferase reporter assays were used to examine the potential tumor signaling pathways targeted by PTPRA in HEK293T cells. Furthermore, quantitative PCR (qPCR) was utilized to confirm the transcriptional regulation of PTPRA expression. Bioinformatic analyses of data from GEPIA identified PTPRA overexpression in patients with breast cancer. The growth curve, colony formation and transwell experiments demonstrated that PTPRA upregulation significantly promoted the cell proliferation and migration of MCF-7 breast cancer cells. In contrast, PTPRA knockdown significantly attenuated cell proliferation and migration. Mechanistic experiments revealed that the transcriptional activity of NF-κB was higher compared with other classic tumor pathways when they were activated by PTPRA in HEK293T cells. Furthermore, the transcriptional activity of NF-κB was altered in a PTPRA-dose-dependent manner. Additionally, following exposure to TNF-α, PTPRA-deficient MCF-7 cells exhibited lower NF-κB transcriptional activity compared with normal control cells. The results of the present study demonstrate that PTPRA overexpression accelerates inflammatory tumor phenotypes in breast cancer and that the TNF-α-mediated PTPRA-NF-κB pathway may offer novel insight into early diagnosis and optimum treatment for breast cancer.
ABSTRACT
A series of non-basic building blocks was synthesized and introduced to the C7 position of the quinolone nucleus 7-chloro-1-cyclopropyl-6-fluoro-4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid to afford the corresponding fluoroquinolones in 46-85% yield. The antibacterial activity of these new fluoroquinolones was evaluated using a standard broth microdilution technique. The sulfur-containing quinolone, 7-(2-thia-5-azabicyclo[2.2.1]heptan-5-yl)-1-cyclopropyl-6-fluoro-4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid exhibited a superior antibacterial activity against quinolone-susceptible and multidrug-resistant strains in comparison with the clinically used fluoroquinolones ciprofloxacin and vancomycin, especially to the Streptococcus pneumonia and multidrug-resistant S. pneumonia clinical isolates.
Subject(s)
Anti-Bacterial Agents/chemical synthesis , Anti-Bacterial Agents/pharmacology , Chemistry, Pharmaceutical/methods , Fluoroquinolones/chemical synthesis , Fluoroquinolones/pharmacology , Ciprofloxacin/chemical synthesis , Ciprofloxacin/pharmacology , Drug Design , Drug Resistance, Multiple, Bacterial , Microbial Sensitivity Tests , Models, Chemical , Molecular Structure , Stereoisomerism , Streptococcus pneumoniae/metabolism , Structure-Activity Relationship , Vancomycin/chemical synthesis , Vancomycin/pharmacologyABSTRACT
This paper presents a corrosion fatigue cyclic failure test for X80 steel, which has arc sprayed with an Al-Zn coating in natural seawater under different stress levels. We found that the Al-Zn coating can significantly improve the corrosion fatigue resistance and slow the crack initiation of X80 steel. The effect of the Al-Zn coating on the corrosion fatigue crack initiation is mainly attributed to its physical isolation, cathodic protection and residual prestress while the effect on crack propagation is due to its inhibition of the formation and evolution of secondary cracks. Moreover, according to the test results, a new life prediction model for corrosion fatigue based on the damage evolution law is proposed and the effect of corrosion-fatigue coupling damage in the proposed model is also considered.
ABSTRACT
Renal fibrosis is a significant characteristic of chronic kidney diseases. Surfactant protein A (SP-A) is a recently identified fibrosis-associated factor in lung fibrosis; however, whether SP-A has the same role in renal fibrosis has remained elusive. The aim of the present study was to investigate the role of SP-A and its receptor calreticulin (CRT) in the pathogenesis of kidney fibrosis. The HK-2 human tubular epithelial cell line was cultured and treated with SP-A and SP-A + anti-CRT. The production of reactive oxygen species (ROS) at 30, 60 and 120 min was examined. Furthermore, cell apoptosis was assessed using an Annexin V assay and the expression of various proteins was measured using western blot analysis. In addition, the cell culture supernatants were collected and the expression of type I collagen was examined using ELISA. Compared with the control group, SP-A treatment significantly increased the ROS production, type I collagen secretion and cell apoptosis, which was partially inhibited by addition of anti-CRT. Furthermore, downregulation of matrix metalloproteinase (MMP)2 and -9 as well as upregulation of tissue inhibitor of metalloproteinase 1 indicated that SP-A treatment increased the degree of fibrosis in HK-2 cells, while addition of anti-CRT alleviated the fibrotic conditions. Finally, SP-A treatment significantly increased the expression of phosphorylated (p)-p38, p-p-65 and NADPH oxidase 2, which was partially inhibited by addition of anti-CRT. In conclusion, SP-A may participate in the pathogenesis of kidney fibrosis through binding to CRT and activate the mitogen-activated protein kinase/nuclear factor-κB-associated oxidative stress signaling pathway.
ABSTRACT
The photoluminescence quantum yield (PLQY) and charge carrier mobility of organic-inorganic perovskite QDs were enhanced by the optimization of crystallinity and surface passivation as well as solid-state ligand exchange. The crystallinity of perovskite QDs was determined by the Effective solvent field (Esol) of various solvents for precipitation. The solvent with high Esol could more quickly countervail the localized field generated by the polar solvent, and it causes fast crystallization of the dissolved precursor, which results in poor crystallinity. The post-ligand adding process (PLAP) and post-ligand exchange process (PLEP) increase the PLQY of perovskite QDs by reducing non-radiative recombination and the density of surface defect states through surface passivation. Particularly, the post ligand exchange process (PLEP) in the solid-state improved the charge carrier mobility of perovskite QDs in addition to the PLQY enhancement. The ligand exchange with short alkyl chain length ligands could improve the packing density of perovskite QDs in films by reducing the inter-particle distance between perovskite QDs. The maximum hole mobility of 6.2 × 10-3 cm2 V-1 s-1, one order higher than that of pristine QDs without the PLEP, is obtained at perovskite QDs with hexyl ligands. By using PLEP treatment, compared to the pristine device, a 2.5 times higher current efficiency in perovskite QD-LEDs was achieved due to the improved charge carrier mobility and PLQY.
ABSTRACT
The existing three-dimensional (3D) x-ray reconstruction methods for lung cancer tissue reconstruct the investigated objects based on a series of two-dimensional (2D) image sections and a chosen 3D reconstruction algorithm. However, because these procedures apply the same segmentation method for all 2D image sections, they may not achieve the optimal segmentation for each section. As a result, the reconstructed 3D images have limited spatial resolution. Furthermore, the existing 3D reconstruction method is time-consuming and results in a limited time resolution. This research presents an innovation of 3D reconstruction by reformulating two main components of the method. First, a validity index for fuzzy clustering is used to obtain the optimal segmentations of any 2D x-ray image. The process is realized by automatically determining the optimal number of clusters for the image. Second, unlike the existing 3D reconstruction methods, a fast-FCM algorithm is used to speed up the 2D image segmenting process, thereby raising the time resolution of the 3D reconstruction process. With the aid of commonly used VTK software, the proposed method has been used to visualize four classes of typical lung cancer tissues: adenocarcinoma, large cell carcinoma, small cell carcinoma, and squamous cell carcinoma. Experimental results validate the effectiveness and efficiency of the proposed algorithm. Thus, the method contributes a useful tool for x-ray-based 3D image reconstruction.
Subject(s)
Image Processing, Computer-Assisted/methods , Lung Neoplasms/pathology , Algorithms , Fuzzy Logic , Humans , Imaging, Three-Dimensional , Lung/pathology , Lung Neoplasms/diagnostic imaging , Models, Statistical , Tomography, X-Ray ComputedABSTRACT
A simple, low cost, non-toxic and eco-friendly pathway for synthesizing efficient sunlight-driven tin sulfide photocatalyst was studied. SnS nanocrystals were prepared by using mechanical method. The bulk SnS was obtained by evaporation of SnS nanocrystal solution. The synthesized samples were characterized by using XRD, SEM, TEM, UV-vis, and Raman analyses. Well crystallized SnS nanocrystals were verified and the electrochemical characterization was also performed under visible light irradiation. The SnS nanocrystals have shown remarkable photocurrent density of 7.6 mA cm-2 under 100 mW cm-2 which is about 10 times larger than that of the bulk SnS under notably stable operation conditions. Furthermore, the SnS nanocrystals presented higher stability than the bulk form. The IPCE(Incident photon to current conversion efficiency) of 9.3% at 420 nm was obtained for SnS nanocrystal photoanode which is strikingly higher than that of bulk SnS, 0.78%. This work suggests that the enhancement of reacting area by using SnS nanocrystal absorbers could give rise to the improvement of photoelectrochemical cell efficiency.
ABSTRACT
OBJECTIVE: To investigate the need for elective neck irradiation (ENI) to nodal Level IB in patients with nasopharyngeal carcinoma (NPC) with negative Level IB lymph nodes (IB-negative) treated by intensity-modulated radiotherapy (IMRT). METHODS: We conducted a Phase 2 prospective study in 123 newly diagnosed IB-negative patients with NPC treated by IMRT, who met at least 1 of the following criteria: (1) unilateral or bilateral Level II involvement with 1 of the following: Level IIA involvement or any Level II node ≥2 cm/with extracapsular spread; (2) ≥2 unilateral node-positive regions. Bilateral Level IB nodes were not contoured as part of the treatment target and treated electively. Level IB regional recurrence rate; pattern of treatment failure; 3-year overall survival (3y-OS), 3-year local control (3y-LC) and 3-year regional control (3y-RC) rates; toxicities; and dosimetric data for planning target volumes, organs at risk, Level IB and submandibular glands (SMGs) were evaluated. RESULTS: Two patients developed failures at Level IB (1.6%). The 3y-LC, 3y-RC and 3y-OS rates were 93.5%, 93.5% and 78.0%, respectively. Bilateral Level IB received unplanned high-dose irradiation with a mean dose (Dmean) ≥50 Gy in 60% of patients. The average Dmean of bilateral SMGs was approximately 53 Gy. CONCLUSION: ENI to Level IB may be unnecessary in IB-negative patients with NPC treated by IMRT. A further Phase 3 study is warranted. ADVANCES IN KNOWLEDGE: Based on the results of this first Phase 2 study, we suggest omitting ENI to Level IB in Ib-negative patients with NPC with extensive nodal disease treated by IMRT.
Subject(s)
Nasopharyngeal Neoplasms/radiotherapy , Radiotherapy, Intensity-Modulated/methods , Adult , Aged , Carcinoma , Female , Humans , Lymphatic Metastasis , Male , Middle Aged , Nasopharyngeal Carcinoma , Nasopharyngeal Neoplasms/drug therapy , Nasopharyngeal Neoplasms/mortality , Neck , Neoplasm Recurrence, Local/etiology , Neoplasm Recurrence, Local/mortality , Prospective Studies , Radiotherapy Dosage , Radiotherapy, Intensity-Modulated/mortality , Survival Analysis , Treatment FailureABSTRACT
To explore the effect of terminal groups of tripodal ligands on the photoluminescence behaviors of the complexes, lanthanide (Eu(III), Tb(III)) nitrate complexes with two flexible amide-type tripodal ligands, 2,2',2''-nitrilotris-(N-phenylmethyl)-acetamide (L(I)) and 2,2',2''-nitrilotris-(N-naphthalenemethyl)-acetamide (L(II)) were synthesized and characterized. The general formulas of the complexes are [EuL(I)(2)(C(3)H(6)O)]·(NO(3))(3)·(HCCl(3))·(H(2)O)(4) (1), TbL(I)(2)(NO(3))(3)·2H(2)O (2), EuL(II)(NO(3))(3) (3), and TbL(II)(NO(3))(3) (4). Among them, 1, 3, and 4 were characterized by single-crystal X-ray diffraction. Complex 1 demonstrates a 1 : 2 (ML(2)) capsule type stoichiometry, and the complexes 3 and 4 confirm 1 : 1 (ML) type coordination structures. What is more, the triplet energy levels of L(I) and L(II) are 24,331 and 19,802 cm(-1), which were determined from the phosphorescence spectra of the Gd(III) complexes. Ligand modification by changing the terminal groups alters their triplet energy, and results in a different sensitizing ability towards lanthanide ions. The density functional theory (DFT) calculations of energy levels including HOMO, LUMO, singlet, and triplet energies tuned by the different terminal groups are also discussed in detail, and the trends are almost consistent with the experimental conclusions.
Subject(s)
Amides/chemistry , Lanthanoid Series Elements/chemistry , Luminescence , Organometallic Compounds/chemical synthesis , Crystallography, X-Ray , Ligands , Models, Chemical , Molecular StructureABSTRACT
Two fluorescent chemosensors for cadmium ions, 2-(2-formylquinolin-8-yloxy)-N,N-diisopropylacetamide (FQDIPA) and 2-(2-formylquinolin-8-yloxy)-N,N-diphenylacetamide (FQDPA), were first assessed in 99% aqueous solutions. The sensor FQDIPA with an end group of an aliphatic amine can recognize Cd(2+) from other metal ions more selectively and sensitively than FQDPA with that of aromatic amines, which was further demonstrated by DFT calculations that were comparable to the experimental results. It is indeed the distinction between the end groups of these chemosensors that results in the variation of the energy difference between the LUMOs and HOMOs and the interaction energies of FQDIPA·Cd(2+) and FQDPA·Cd(2+). Furthermore, the living cell image experiment could also indicate that the FQDIPA is more suitable than the FQDPA in the practical applications in biological systems.