Research progress of TiO2-based photocatalytic degradation of wastewater: bibliometric analysis.

The pollution caused by modernization and industrialization has caused serious harm to the biodiversity of the earth. TiO2-based photocatalyst has been widely studied as an effective and sustainable water environment remediation material. In this study, we analyzed the status and research trends of TiO2-based photocatalytic degradation of wastewater in depression from 2003 to 2023 to provide a reference for further research. "Doping", "Modification" and "Heterojunction" were used as keywords, and 817 related academic literatures were screened out by using Web of Science database. Through the visualization software VOSviewer and CiteSpace, the authors, institutions and literature keywords were clustered. The results show that since 2008, the annual number of published papers on TiO2-based photocatalytic degradation of wastewater has increased from 9 to 114. Among them, China has published 432 articles and made great contributions, and there are many representative research teams. Chinese universities are the main body to study TiO2-based photocatalytic degradation of wastewater, but the cooperation between universities is not as close as that abroad. This paper comprehensively analyzes the research hotspots of TiO2-based photocatalytic degradation of wastewater, such as the doping of TiO2 and the construction of different types of heterojunctions of TiO2. It is expected that these analysis results will provide new research ideas for researchers to carry out future research on related topics and let researchers know in-depth research institutions and possible collaborators to conduct academic exchanges and discussions with active institutions.

Platelets derived citrullinated proteins and microparticles are potential autoantibodies ACPA targets in RA patients.

Citrullinated neoepitopes have emerged as key triggers of autoantibodies anti-citrullinated protein antibodies (ACPA) synthesis in rheumatoid arthritis (RA) patients. Apart from their critical role in homeostasis and thrombosis, platelets have a significant contribution to inflammation as well. Although anuclear in nature, platelets have an intricate post-translational modification machinery. Till now, citrullination in platelets and its contribution to trigger autoantibodies ACPA production in RA is an unexplored research direction. Herein, we investigated the expression of peptidylarginine deiminase (PAD) enzymes and citrullinated proteins/peptides in the human platelets and platelet derived microparticles (PDP). Both PAD4 mRNA and protein, but not the other PAD isoforms, are detectable in the human platelets. With a strict filtering criterion,108 citrullination sites present on 76 proteins were identified in the human platelets, and 55 citrullinated modifications present on 37 different proteins were detected in the PDPs. Among them, some are well-known citrullinated autoantigens associated with RA. Citrullinated forms of thrombospondin-1, ß-actin, and platelet factor-4 (also known as CXCL4) are highly immunogenic and bound by autoantibodies ACPA. Furthermore, ACPA from RA sera and synovial fluids recognized citrullinated proteins from platelets and significantly activated them as evidenced by P-selectin upregulation and sCD40 L secretion. These results clearly demonstrate the presence of citrullinated autoantigens in platelets and PDPs, thus could serve as potential targets of ACPA in RA.

Identification of New Small Molecules as Apoptosis Inhibitors in Vascular Endothelial Cells.

Vascular endothelial cell (VEC) apoptosis is involved in the development of atherosclerosis and other cardiovascular diseases. We previously found that ethyl 1-(2-hydroxy-3-aroxypropyl)-3-aryl-1H-pyrazole -5-carboxylate derivatives (3a-o) play important roles in cell fate control. In this study, among the 15 compounds, we further screened 2 compounds, 3d and 3k, that suppressed VEC apoptosis induced by deprivation of serum and fibroblast growth factor 2. To clarify which chiral enantiomers of 3d and 3k functioned, we synthesized 3d-S and its enantiomer 3d-R, 3k-S, and its enantiomer 3k-R. Then, we investigated the apoptosis-inhibiting activity of the chiral compounds in VECs. Four small molecules, 3d-S, 3d-R, 3k-S, 3k-R, significantly elevated VEC viability and inhibited apoptosis. Furthermore, these small molecules could obviously decrease the level of integrin ß4 that plays a key role in the regulation of VEC apoptosis. 3k-S and 3k-R increased Bcl-2/Bax ratio and reduced reactive oxygen species levels dramatically. Therefore, we provide new VEC apoptosis inhibitors. These compounds may be potential agents in the prevention of vascular diseases associated with VEC apoptosis.

Synthesis of novel boron chelate complexes and proposed mechanism of new rearrangement.

We synthesized novel boron chelate complexes by the reaction of pyrazoline derivatives and boron trifluoride diethyl etherate followed by a new rearrangement. The structures of the compounds were characterized by IR, NMR and HRMS, especially, a typical compound 3c was confirmed by X-ray single crystal analysis. We proposed a mechanism of the rearrangement. Moreover, the absorption and fluorescence spectroscopy of these compounds were measured.

Novel pyrazoline-based fluorescent probe for detecting thiols and its application in cells.

A new compound, N-(4-(1,5-diphenyl-4,5-dihydro-1H-pyrazol-3-yl)phenyl)-acrylamide (probe L), was designed and synthesized as a highly sensitive and selective fluorescent probe for recognizing and detecting thiol from other amino acids. On being mixed with thiol in buffered DMSO:HEPES=1:1 solution at pH 7.4, the probe exhibited the blue emission at 474 nm. This probe is very sensitive and displayed a linear fluorescence off-on response to thiol. The fluorescence emission of the probe is pH independent in the physiological pH range. Living cell imaging of HeLa cells confirmed its cell permeability and its ability to selectively detect thiol in cells. The structure of the probe was characterized by IR, NMR and HRMS spectroscopy analysis.

Novel pyrazoline-based selective fluorescent probe for the detection of hydrazine.

A novel pyrazoline-based fluorescent probe, 2-[4-(3,5-diphenyl-4,5-dihydro-pyrazol-1-yl)-benzylidene]-malononitrile, with a simple structure and low detection limit (6.16×10(-6)M) for the detection of hydrazine is designed and synthesized. The probe responds selectively to hydrazine over other molecules with marked fluorescence enhancement. The probe can detect hydrazine effectively at pH 5.0-9.0 with a special emission wavelength at 520nm. Moreover, the probe can be used to detect hydrazine from variety of natural source water.

An activator of mTOR inhibits oxLDL-induced autophagy and apoptosis in vascular endothelial cells and restricts atherosclerosis in apolipoprotein E⁻/⁻ mice.

Oxidized low-density lipoprotein (oxLDL) inhibits mammalian target of rapamycin (mTOR) and induces autophagy and apoptosis in vascular endothelial cells (VECs) that play very critical roles for the cardiovascular homostasis. We recently defined 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one (3BDO) as a new activator of mTOR. Therefore, we hypothesized that 3BDO had a protective role in VECs and thus stabilized atherosclerotic lesions in apolipoprotein E(-/-) (apoE(-/-)) mice. Our results showed that oxLDL inhibited the activity of mTOR and increased the protein level of autophagy-related 13 (ATG13) and its dephosphorylation, thus inducing autophagy in human umbilical vein endothelial cells (HUVECs). All of these effects were strongly inhibited by 3BDO. In vivo experiments confirmed that 3BDO activated mTOR and decreased the protein level of ATG13 in the plaque endothelium of apoE(-/-) mice. Importantly, 3BDO did not affect the activity of mTOR and autophagy in macrophage cell line RAW246.7 and vascular smooth muscle cells of apoE(-/-) mice, but suppressed plaque endothelial cell death and restricted atherosclerosis development in the mice. 3BDO protected VECs by activating mTOR and thus stabilized atherosclerotic lesions in apoE(-/-) mice.

Discovery of 2'-hydroxychalcones as autophagy inducer in A549 lung cancer cells.

A series of 2'-hydroxychalcone derivatives was synthesized and the effects of all the compounds on growth of A549 lung cancer cell were investigated. The results showed that all compounds had inhibitory effects on the growth of A549 lung cancer cells and compound possessed the highest growth inhibitory effect and induced autophagy of A549 lung cancer cells.

A simple and effective coumarin-based fluorescent probe for cysteine.

Acrylic acid 3-acetyl-2-oxo-2 H-chromen-7-yl ester (ACA) was rationally designed and synthesized as a simple and effective fluorescent probe for sensing cysteine with high selectivity and naked-eye detection. The probe can detect cysteine by fluorescence spectrometry with a detection limit of 0.657 µM and can be used with calf serum and in live cell imaging. The conjugate addition/cyclization sequence mechanism of the reaction between ACA and cysteine was confirmed by ESI-MS and fluorescence spectra.

Novel pyrazoline-based fluorescent probe for detecting glutathione and its application in cells.

A novel compound, 2-(1,5-diphenyl-4,5-dihydro-1H-pyrazol-3-yl)phenyl acrylate (probe L), was designed and synthesized as a highly sensitive and selective fluorescent probe for recognizing and detecting glutathione among cysteine, homocysteine and other amino acids. The structures of related compounds were characterized using IR, NMR and HRMS spectroscopy analysis. The probe is a non-fluorescent compound. On being mixed with glutathione in buffered EtOH:PBS=3:7 solution at pH 7.4, the probe exhibited the blue emission of the pyrazoline at 474 nm and a 83-fold enhancement in fluorescence intensity. This probe is very sensitive and displayed a linear fluorescence off-on response to glutathione with fluorometric detection limit of 8.2 × 10(-8)M. The emission of the probe is pH independent in the physiological pH range. Live-cell imaging of HeLa cells confirmed the cell permeability of the probe and its ability to selectively discriminate GSH from Cys and Hcy in cells. The toxicity of the probe was low in cultured HeLa cells.

Novel pyrazoline-based selective fluorescent sensor for Hg2+.

This paper presents the preparation of a pyrazoline compound and the properties of its UV-Vis absorption and fluorescence emission. Moreover, this compound can be used to determine Hg(2+) ion with selectivity and sensitivity in the EtOH:H2O =9:1 (v/v) solution. This sensor forms a 1:1 complex with Hg(2+) and shows a fluorescent enhancement with good tolerance of other metal ions. This sensor is very sensitive with fluorometric detection limit of 3.85 × 10(-10) M. In addition, the fluorescent probe has practical application in cells imaging.

A novel pyrazoline-based selective fluorescent probe for detecting reduced glutathione and its application in living cells and serum.

A new fluorescent probe, N-(4-(1,5-diphenyl-4,5-dihydro-1H-pyrazol-3-yl)phenyl)-2,4-dinitrobenzenesulfonamide (probe 3), was designed and synthesized as a highly sensitive and selective fluorescent probe for recognizing and detecting glutathione among biological thiols in aqueous media. Probe 3 is a nonfluorescent compound. On being mixed with biothiols under neutral aqueous conditions, the 2,4-dinitrobenzenesulfoyl moiety can be cleaved off by glutathione, and the blue emission of the pyrazoline at 464 nm is switched on, with a fluorescence enhancement of 488-fold for glutathione. Furthermore, probe 3 was highly selective for glutathione without interference from some biologically relevant analytes. The detection limit of glutathione was 4.11 × 10(-7) M. The emission of the probe is pH independent in the physiological pH range. Moreover, the probe can be used for fluorescent imaging of cellular glutathione and can be used for detecting glutathione in calf serum.

Relationship between annexin A7 and integrin ß4 in autophagy.

We recently found that both annexin A7 and integrin ß4 were involved in autophagy of vascular endothelial cells. But, their relation is not clear. In this study, we addressed this question by using a small molecule ABO that promoted autophagy by targeting annexin A7. The results showed that knockdown of integrin ß4 partly inhibited ABO-induced autophagy in vascular endothelial cells. Furthermore, in HEK293 cells that express integrin ß4 too low to detect by western blot, ABO could not induce autophagy. If integrin ß4 was overexpressed in HEK293 cells, ABO could evoke autophagy. On the other hand, knockdown of annexin A7 also blocked ABO-induced autophagy although the level of integrin ß4 was elevated. Moreover, by co-immunoprecipitation, we identified the interaction of integrin ß4 and annexin A7, and found that ABO could modulate the interaction, at the same time, the phosphorylation of Y-1494 in integrin ß4 cytoplasmic domain was inhibited significantly in vitro and in vivo. Hence, by identifying the interaction between integrin ß4 and annexin A7, we demonstrated that both annexin A7 and integrin ß4 were essential for small molecule ABO-induced autophagy and targeting annexin A7 by ABO could modulate integrin ß4 phosphorylation, while Y-1494 phosphorylation of integrin ß4 may negatively regulate autophagy.

Identification of a small molecule targeting annexin A7.

Autophagy involves multiple membrane trafficking and fusion events. Annexin A7 (ANXA7) is postulated to play a role in membrane fusion during exocytosis, while the contribution of ANXA7 to autophagy is poorly understood. Our recent studies demonstrated that ABO could promote autophagy via elevation of ANXA7 and triggering ANXA7 subcellular redistribution. However, little is known about the molecular mechanisms how ANXA7 regulates autophagy. As molecular disruption of ANXA7 in mice results in several unwished phenotypes, small molecule modulators may be efficacious in defining the mechanisms of ANXA7 action. However, so far no compounds that selectively target ANXA7 have been identified. So, we hypothesize that ABO might be a potent modulator of ANXA7. We also have detected the colocalization of ANXA7 and microtubule-associated protein 1 light chain 3 (LC3), and ANXA7 was essential for LC3 accumulation in VEC autophagy. As a GTPase, whether ANXA7 affects the phosphorylation of LC3 or other proteins needs further investigation. In this study, we performed site-directed mutagenesis and found that ABO directly bound to Thr(286) of ANXA7 and inhibited its phosphorylation. By yeast two-hybrid screening, we found that ANXA7 could interact with grancalcin (GCA). ABO promoted the interaction and inhibited GCA phosphorylation, leading to the decrease of intracellular Ca(2+) concentration. At the same time, ABO inhibited the phosphorylation of LC3. Hence, by identifying ABO as an unprecedented modulator of ANXA7 as well as GCA and LC3 as interacting proteins of ANXA7, we demonstrated the possible mechanisms how ANXA7 regulates autophagy for the first time.

Synthesis, X-ray crystal structure and optical properties of novel 1,3,5-triarylpyrazoline derivatives and the fluorescent sensor for Cu2+.

A series of novel 1,3,5-triarylpyrazoline derivatives was synthesized by the reaction of chalcone and 5-aryl-2-hydrazinyl-1,3,4-thiadiazole in 43.3-84.7% yields. The structures of compounds were characterized using IR, (1)H NMR and HRMS spectroscopy and X-ray diffraction analysis. The absorption and fluorescence characteristics of the compounds were investigated in dichloromethane, toluene, acetonitrile, N,N-dimethylformamide and tetrahydrofuran. The results showed that the absorption maxima of the compounds vary from 366 to 370nm depending on the group bound to benzene rings. The maximum emission spectra of the compounds in dichloromethane were dependent on nature of groups in benzene ring. Furthermore, the compound 3b can be used to determine Cu(2+) ion with high selectivity and a low detection limit in the DMF:H2O=1:1 (v/v) solution.

Olive leaf extract inhibits lead poisoning-induced brain injury.

Olive leaves have an antioxidant capacity, and olive leaf extract can protect the blood, spleen and hippocampus in lead-poisoned mice. However, little is known about the effects of olive leaf extract on lead-induced brain injury. This study was designed to determine whether olive leaf extract can inhibit lead-induced brain injury, and whether this effect is associated with antioxidant capacity. First, we established a mouse model of lead poisoning by continuous intragastric administration of lead acetate for 30 days. Two hours after successful model establishment, lead-poisoned mice were given olive leaf extract at doses of 250, 500 or 1 000 mg/kg daily by intragastric administration for 50 days. Under the transmission electron microscope, olive leaf extract attenuated neuronal and capillary injury and reduced damage to organelles and the matrix around the capillaries in the frontal lobe of the cerebral cortex in the lead-poisoned mice. Olive leaf extract at a dose of 1 000 mg/kg had the greatest protective effect. Spectrophotometry showed that olive leaf extract significantly increased the activities of superoxide dismutase, catalase, alkaline phosphatase and acid phosphatase, while it reduced malondialdehyde content, in a dose-dependent manner. Furthermore, immunohistochemical staining revealed that olive leaf extract dose-dependently decreased Bax protein expression in the cerebral cortex of lead-poisoned mice. Our findings indicate that olive leaf extract can inhibit lead-induced brain injury by increasing antioxidant capacity and reducing apoptosis.

[The effect of biyuanshu oral liquid on the formation of Pseudomonas aeruginosa biofilms in vitro].

OBJECTIVE: To observe the effect of biyuanshu oral liquid on the formation of pseudomonas aeruginosa biofilms in vitro. METHOD: Pseudomonas aeruginosa biofilm was established by plate culture and detected by Scanning electron microscopy and AgNO3 staining. After treated with different dosages of biyuanshu oral liquid and erythromycin, the pseudomonas aeruginosa biofilms were observed by AgNO3 staining and the number of viable bacteria were measured by serial dilution. RESULT: The pseudomonas aeruginosa biofilms could be detected by SEM at the seventh culture day and it was consistent with the detection of AgNO3 staining. The biyuanshu oral liquid and erythromycin have the effect on inhibiting the formation of pseudomonas aeruginosa biofilms. But with the already formed pseudomonas aeruginosa biofilms the inhibition was not significant. The serial dilution method showed that the viable counts of bacteria of biyuanshu oral liquid and erythromycin treated groups were significantly lower than those untreated groups (P < 0.05). CONCLUSION: The biyuanshu oral liquid and erythromycin can inhibit the formation of pseudomonas aeruginosa biofilms in vitro.

A highly sensitive fluorescent probe based on simple pyrazoline for Zn2+ in living neuron cells.

We develop a pyrazoline-based fluorescent sensor for biological Zn(2+) detection. The sensor shows good binding selectivity for Zn(2+) over competing metal with 40-fold fluorescence enhancement in response to Zn(2+). The new probe is cell-permeable and can be used to detect intracellular zinc ions in living neuron cells.

A chemical small molecule induces mouse embryonic stem cell differentiation into functional vascular endothelial cells via Hmbox1.

Embryonic stem cells (ESCs) can differentiate to endothelial progenitor cells and vascular endothelial cells (VECs), but the mechanism is largely unknown. In this study, we synthesized 2 chiral compounds (R-ABO and S-ABO) and identified R-ABO as an effective inducer of ESC differentiation into VECs. Furthermore, we found that R-ABO induced ESC differentiation into VECs via homeobox containing 1 (Hmbox1) that acted upstream of fibroblast growth factor 2 (FGF-2). The data suggest that R-ABO is a novel tool for ESC differentiation into VECs, and Hmbox1 is a key regulator in this differentiation process. These findings provide information on a novel target and a new platform for further investigating the gene control of ESC differentiation to VECs.

Butyrolactone derivative 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one protects against amyloid-ß peptides-induced cytotoxicity in PC12 cells.

Excessive extracellular deposition of amyloid-ß peptides (Aß) is a characteristic pathologic feature of Alzheimer's disease (AD). Accumulating evidence indicates that macroautophagy is involved in the pathogenesis of AD, but the exact role of macroautophapy is still unclear. We investigated whether Aß(25-35) could cause reactive oxygen species (ROS) accumulation, decrease the activity of Na(+), K(+)-ATPase, trigger an autophagy process, and inhibit the growth of PC12 cells and examined the effect of a new autophagy modulator, butyrolactone derivative 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3 H)-one (3BDO). 3BDO could block the decrease in cell viability induced by Aß(25-35) by inhibiting ROS accumulation and the decrease in activity of Na(+), K(+)-ATPase and the autophagy process. In addition, 3BDO modulated the autophagy progress via a mammalian target of rampamycin-dependent pathway. 3BDO has a protective effect against the cytotoxicity induced by Aß(25-35) and might be a promising tool for AD research.