Catalytically Active Carbon for Oxygen Reduction Reaction in Energy Conversion: Recent Advances and Future Perspectives.

The shortage and unevenness of fossil energy sources are affecting the development and progress of human civilization. The technology of efficiently converting material resources into energy for utilization and storage is attracting the attention of researchers. Environmentally friendly biomass materials are a treasure to drive the development of new-generation energy sources. Electrochemical theory is used to efficiently convert the chemical energy of chemical substances into electrical energy. In recent years, significant progress has been made in the development of green and economical electrocatalysts for oxygen reduction reaction (ORR). Although many reviews have been reported around the application of biomass-derived catalytically active carbon (CAC) catalysts in ORR, these reviews have only selected a single/partial topic (including synthesis and preparation of catalysts from different sources, structural optimization, or performance enhancement methods based on CAC catalysts, and application of biomass-derived CACs) for discussion. There is no review that systematically addresses the latest progress in the synthesis, performance enhancement, and applications related to biomass-derived CAC-based oxygen reduction electrocatalysts synchronously. This review fills the gap by providing a timely and comprehensive review and summary from the following sections: the exposition of the basic catalytic principles of ORR, the summary of the chemical composition and structural properties of various types of biomass, the analysis of traditional and the latest popular biomass-derived CAC synthesis methods and optimization strategies, and the summary of the practical applications of biomass-derived CAC-based oxidative reduction electrocatalysts. This review provides a comprehensive summary of the latest advances to provide research directions and design ideas for the development of catalyst synthesis/optimization and contributes to the industrialization of biomass-derived CAC electrocatalysis and electric energy storage.

Spatial heterogeneity of peri-tumoural lipid composition in postmenopausal patients with oestrogen receptor positive breast cancer.

Deregulation of lipid composition in adipose tissue adjacent to breast tumour is observed in ex vivo and animal models. Novel non-invasive magnetic resonance imaging (MRI) allows rapid lipid mapping of the human whole breast. We set out to elucidate the spatial heterogeneity of peri-tumoural lipid composition in postmenopausal patients with oestrogen receptor positive (ER +) breast cancer. Thirteen participants (mean age, 62 ± [SD] 6 years) with ER + breast cancer and 13 age-matched postmenopausal healthy controls were scanned on MRI. The number of double bonds in triglycerides was computed from MRI images to derive lipid composition maps of monounsaturated, polyunsaturated, and saturated fatty acids (MUFA, PUFA, SFA). The spatial heterogeneity measures (mean, median, skewness, entropy and kurtosis) of lipid composition in the peri-tumoural region and the whole breast of participants and in the whole breast of controls were computed. The Ki-67 proliferative activity marker and CD163 antibody on tumour-associated macrophages were assessed histologically. Mann Whitney U or Wilcoxon tests and Spearman's coefficients were used to assess group differences and correlations, respectively. For comparison against the whole breast in participants, peri-tumoural MUFA had a lower mean (median (IQR), 0.40 (0.02), p < .001), lower median (0.42 (0.02), p < .001), a negative skewness with lower magnitude (- 1.65 (0.77), p = .001), higher entropy (4.35 (0.64), p = .007) and lower kurtosis (5.13 (3.99), p = .001). Peri-tumoural PUFA had a lower mean (p < .001), lower median (p < .001), a positive skewness with higher magnitude (p = .005) and lower entropy (p = .002). Peri-tumoural SFA had a higher mean (p < .001), higher median (p < .001), a positive skewness with lower magnitude (p < .001) and lower entropy (p = .012). For comparison against the whole breast in controls, peri-tumoural MUFA had a negative skewness with lower magnitude (p = .01) and lower kurtosis (p = .009), however there was no difference in PUFA or SFA. CD163 moderately correlated with peri-tumoural MUFA skewness (rs = - .64), PUFA entropy (rs = .63) and SFA skewness (rs = .59). There was a lower MUFA and PUFA while a higher SFA, and a higher heterogeneity of MUFA while a lower heterogeneity of PUFA and SFA, in the peri-tumoural region in comparison with the whole breast tissue. The degree of lipid deregulation was associated with inflammation as indicated by CD163 antibody on macrophages, serving as potential marker for early diagnosis and response to therapy.

Biomass-Derived Catalytically Active Carbon Materials for the Air Electrode of Zn-Air Batteries.

Given the growing environmental and energy problems, developing clean, renewable electrochemical energy storage devices is of great interest. Zn-air batteries (ZABs) have broad prospects in energy storage because of their high specific capacity and environmental friendliness. The unavailability of cheap air electrode materials and effective and stable oxygen electrocatalysts to catalyze air electrodes are main barriers to large-scale implementation of ZABs. Due to the abundant biomass resources, self-doped heteroatoms, and unique pore structure, biomass-derived catalytically active carbon materials (CACs) have great potential to prepare carbon-based catalysts and porous electrodes with excellent performance for ZABs. This paper reviews the research progress of biomass-derived CACs applied to ZABs air electrodes. Specifically, the principle of ZABs and the source and preparation method of biomass-derived CACs are introduced. To prepare efficient biomass-based oxygen electrocatalysts, heteroatom doping and metal modification were introduced to improve the efficiency and stability of carbon materials. Finally, the effects of electron transfer number and H2O2 yield in ORR on the performance of ZABs were evaluated. This review aims to deepen the understanding of the advantages and challenges of biomass-derived CACs in the air electrodes of ZABs, promote more comprehensive research on biomass resources, and accelerate the commercial application of ZABs.

Artemisinin Confers Neuroprotection against 6-OHDA-Induced Neuronal Injury In Vitro and In Vivo through Activation of the ERK1/2 Pathway.

Parkinson's disease (PD) is an age-related, progressive neurodegenerative disease characterized by the gradual and massive loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). We have recently reported that artemisinin, an FDA-approved first-line antimalarial drug, possesses a neuroprotective effect. However, the effects and underlying mechanisms of artemisinin on Parkinson's disease remain to be elucidated. In this study, we investigated the neuroprotective effects of artemisinin on 6-OHDA and MPP+ in neuronal cells and animal models, as well as the underlying mechanisms. Our results showed that artemisinin significantly attenuated the loss of cell viability, LDH release, elevated levels of reactive oxygen species (ROS), the collapse of the mitochondria trans-membrane potential and cell apoptosis in PC12 cells. Western blot results showed that artemisinin stimulated the phosphorylation of ERK1/2, its upstream signaling proteins c-Raf and MEK and its downstream target CREB in PC12 cells in a time- and concentration-dependent manner. In addition, the protective effect of artemisinin was significantly reduced when the ERK pathway was blocked using the ERK pathway inhibitor PD98059 or when the expression of ERK was knocked down using sgRNA. These results indicate the essential role of ERK in the protective effect of artemisinin. Similar results were obtained in SH-SY5Y cells and primary cultured neurons treated with 6-OHDA, as well as in cellular models of MPP+ injury. More interestingly, artemisinin attenuated PD-like behavior deficit in mice injected with 6-OHDA evaluated by behavioral tests including swimming test, pole-test, open field exploration and rotarod tests. Moreover, artemisinin also stimulated the phosphorylation of ERK1/2, inhibited apoptosis, and rescued dopaminergic neurons in SNc of these animals. Application of ERK pathway inhibitor PD98059 blocked the protective effect of artemisinin in mice during testing. Taking these results together, it was indicated that artemisinin preserves neuroprotective effects against 6-OHDA and MPP+ induced injury both in vitro and in vivo by the stimulation of the ERK1/2 signaling pathway. Our findings support the potential therapeutic effect of artemisinin in the prevention and treatment of Parkinson's disease.

Mechanism and Molecular Targets of a Water-Soluble Extract of Artemisia annua on the Treatment of Alzheimer's Disease Based on Network Pharmacology and Experimental Validation.

Oxidative stress is an important contributor to the pathogenesis of Alzheimer's disease (AD). The overproduction of reactive oxygen species observed in AD patients results in the loss of mitochondrial function, altered metal ion homeostasis, lipopolysaccharide metabolism disorder, reduced anti-oxidant defense, increased release of inflammatory factors, and the aggravation and accumulation of amyloid-beta and tau hyper-phosphorylation, which directly cause synaptic and neuronal loss and lead to cognitive dysfunction. Thus, oxidative stress proves to be a fundamental part of AD development and progression, suggesting the potential benefits of anti-oxidant-based therapies for AD. In this study, we found that a water-soluble extract of Artemisia annua (WSEAA), a traditional Chinese herbal medicine, has a strong anti-oxidant function. We also found that WSEAA is able to improve the cognitive function of 3xTg AD mice. However, the mechanisms and molecular targets underlying WSEAA action are still not known. In order to uncover the potential molecular mechanisms involved, we used a combination of network pharmacology and different experimental approaches. Obtained results revealed key genes (such as AKT1, BCL2, IL-6, TNF-[Formula: see text] and BAX) and signaling pathways (like PI3K-AKT and BCL2/BAX) are closely associated with the biological processes responding to oxidative stress. Further verification of the survival/anti-oxidant effects of WSEAA in vitro and in vivo showed that the extract has anti-oxidatant/neuronal survival action against H2O2-induced damage, and is thus able to prevent the cognitive decline and pathological changes of 3xTg transgenic (3xTg) mice via the regulation of key target-genes and pathways, such as PI3K-AKT and BCL2/BAX, related to survival/apoptosis. Our findings strongly indicate the potential of WSEAA for the prevention and treatment of AD.

Artemisia annua Extract Improves the Cognitive Deficits and Reverses the Pathological Changes of Alzheimer's Disease via Regulating YAP Signaling.

Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the occurrence of cognitive deficits. With no effective treatments available, the search for new effective therapies has become a major focus of interest. In the present study, we describe the potential therapeutic effect of Artemisia annua (A. annua) extract on AD. Nine-month-old female 3xTg AD mice were treated with A. annua extract for three months via oral administration. Animals assigned to WT and model groups were administrated with an equal volume of water for the same period. Treated AD mice significantly improved the cognitive deficits and exhibited reduced Aß accumulation, hyper-phosphorylation of tau, inflammatory factor release and apoptosis when compared with untreated AD mice. Moreover, A. annua extract promoted the survival and proliferation of neural progenitor cells (NPS) and increased the expression of synaptic proteins. Further assessment of the implicated mechanisms revealed that A. annua extract regulates the YAP signaling pathway in 3xTg AD mice. Further studies comprised the incubation of PC12 cells with Aß1-42 at a concentration of 8 µM with or without different concentrations of A. annua extract for 24 h. Obtained ROS levels, mitochondrial membrane potential, caspase-3 activity, neuronal cell apoptosis and assessment of the signaling pathways involved was performed using western blot and immunofluorescence staining. The obtained results showed that A. annua extract significantly reversed the Aß1-42-induced increase in ROS levels, caspase-3 activity and neuronal cell apoptosis in vitro. Moreover, either inhibition of the YAP signaling pathway, using a specific inhibitor or CRISPR cas9 knockout of YAP gene, reduced the neuroprotective effect of the A. annua extract. These findings suggest that A. annua extract may be a new multi-target anti-AD drug with potential use in the prevention and treatment of AD.

Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling.

The abnormal immune response is an early change in the pathogenesis of Alzheimer's disease (AD). Microglial activation is a crucial regulator of the immune response, which contributes to progressive neuronal injury by releasing neurotoxic products. Therefore, finding effective drugs to regulate microglial homeostasis and neuroinflammation has become a new AD treatment strategy. Artemisinin has potent anti-inflammatory and immune activities. However, it is unclear whether Artemisinin contributes to the regulation of microglial activation, thereby improving AD pathology. This study found that Artemisinin significantly reduced amyloid beta-peptide 1-42 (Aß1-42)-induced increases in nitric oxide and reactive oxygen species and inflammatory factors in BV2 cells. In addition, Artemisinin inhibited the migration of microglia and prevented the expansion of the inflammatory cascade. The mechanical studies showed Artemisinin inhibited neuroinflammation and exerted neuroprotective effects by regulating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-κB) signaling pathway. Similar results were obtained in AD model mice, in which Artemisinin administration attenuated Aß1-42-induced neuroinflammation and neuronal injury, reversing spatial learning and memory deficits. The anti-inflammatory effect of Artemisinin is also accompanied by the activation of the TLR4/NF-κB signaling pathway in the animal model. Our results indicate that Artemisinin attenuated Aß1-42-induced neuroinflammation and neuronal injury by stimulating the TLR4/NF-κB signaling pathway. These findings suggest that Artemisinin is a potential therapeutic agent for AD.

Medical image encryption algorithm based on a new five-dimensional three-leaf chaotic system and genetic operation.

Current image encryption methods have many shortcomings for the medical image encryption with high resolution, strong correlation and large storage space, and it is difficult to obtain reliable clinically applicable medical images. Therefore, this paper proposes a medical image encryption algorithm based on a new five-dimensional three-leaf chaotic system and genetic operation. And the dynamic analysis of the phase diagram and bifurcation diagram of the five-dimensional three-leaf chaotic system selected in this paper is carried out, and NIST is used to test the randomness of its chaotic sequence. This algorithm follows the diffusion-scrambling framework, especially using the principle of DNA recombination combined with the five-dimensional three-leaf chaotic system to generate a chaotic matrix that participates in the operation. The bit-level DNA mutation operation is introduced in the diffusion, and the scrambling and diffusion effects have been further improved. Algorithm security and randomness have been enhanced. This paper evaluates the efficiency of this algorithm for medical image encryption in terms of security analysis and time performance. Security analysis is carried out from key space, information entropy, histogram, similarity between decrypted image and original image, PSNR, correlation, sensitivity, noise attack, cropping attack and so on. Perform time efficiency analysis from the perspective of time performance. The comparison between this algorithm and the experimental results obtained by some of the latest medical image encryption algorithms shows that this algorithm is superior to the existing medical image encryption algorithms to a certain extent in terms of security and time efficiency.

Artemisinin Reverses Glucocorticoid-Induced Injury in Bone Marrow-Derived Mesenchymal Stem Cells through Regulation of ERK1/2-CREB Signaling Pathway.

Glucocorticoids are the most common cause of secondary osteoporosis, which affects both women (pre- and postmenopausal) and men. In cases of prolonged treatment, glucocorticoids promote the loss and inactivation of the differentiational function of bone marrow mesenchymal stromal cells (BMSCs), risking the development of skeletal system diseases such as osteoporosis. This study reports for the first time the protective effect of the antimalarial artemisinin against glucocorticoid-induced insults on primary cultured rat BMSCs. At relatively low concentrations, artemisinin treatment improved BMSC survival by promoting a decline of reactive oxygen species (ROS) production that correlated with the decrease of caspase-3 activation, LDH release, mitochondrial membrane potential (Δψm) loss, and apoptosis induced by dexamethasone (DEXA). In addition, artemisinin improved the osteogenic differentiation of DEXA-damaged cells. DEXA inhibited extracellular-signal-regulated kinase 1/2 (ERK1/2) and cAMP response element binding protein (CREB) phosphorylation, and artemisinin treatment promoted their activation in a concentration-dependent manner. PD98059, the specific inhibitor of the ERK1/2 pathway, blocked ERK1/2 phosphorylation and artemisinin protection. Similarly, siCREB attenuated the protective effect of artemisinin, strongly suggesting the involvement of the ERK1/2-CREB pathway in the protective action of artemisinin against DEXA-induced damage in BMSCs. In addition, we found that the expression of antiapoptotic protein B-cell lymphoma 2 protein (BCL-2) was also upregulated by artemisinin. These studies demonstrate the therapeutic potential of artemisinin in the survival improvement of BMSCs exposed to glucocorticoid-induced apoptosis and suggest that artemisinin-mediated protection may occur via the activation of ERK1/2-CREB signaling pathway.

Protective Mechanism of Berberine on Human Retinal Pigment Epithelial Cells against Apoptosis Induced by Hydrogen Peroxide via the Stimulation of Autophagy.

Age-related macular degeneration (AMD) is a major cause of severe and irreversible vision loss with limited effective therapies. Diminished autophagy and increased oxidative damage caused by ROS in the retinal pigment epithelium (RPE) have been implicated in the pathogenesis of AMD, and strategies aimed at enhancing autophagy are likely to protect these cells from oxidative damage. We have previously shown that berberine (BBR), an isoquinoline alkaloid isolated from Chinese herbs, was able to protect human RPE cells from H2O2-induced oxidative damage through AMPK activation. However, the precise mechanisms behind this protective effect remain unclear. Given the essential role of AMPK in autophagy activation, we postulated that BBR may confer protection against H2O2-induced oxidative damage by stimulating AMPK-dependent autophagy. Our results showed that BBR was able to induce autophagy in D407 cells, whereas autophagy inhibitor PIKIII or silencing of LC3B blocked the protective effect of BBR. Further analysis showed that BBR activated the AMPK/mTOR/ULK1 signaling pathways and that both pharmacological and genetic inhibitions of the AMPK pathway abolished the autophagy-stimulating effect of BBR. Similar results were obtained in primary cultured human RPE cells. Taken together, these results demonstrate that BBR is able to stimulate autophagy in D407 cells via the activation of AMPK pathway and that its protective effect against H2O2-induced oxidative damage relies on its autophagy-modulatory effect. Our findings also provide evidence to support the potential application of BBR in preventing and treating AMD.

Artemether confers neuroprotection on cerebral ischemic injury through stimulation of the Erk1/2-P90rsk-CREB signaling pathway.

Ischemic stroke is one of the leading causes of death and disability among adults. Despite the economic burden of the disease, available treatment options are still very limited. With the exception of anti-thrombolytics and hypothermia, current therapies fail to reduce neuronal injury, neurological deficits and mortality rates, suggesting that the development of novel and more effective therapies against ischemic stroke is urgent. In the present study, we found that artemether, which has been used in the clinic as an anti-malarial drug, was able to improve the neurological deficits, attenuate the infarction volume and the brain water content in a middle cerebral artery occlusion (MCAO) animal model. Furthermore, artemether treatment significantly suppressed cell apoptosis, stimulated cell proliferation and promoted the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), P90rsk and cAMP responsive element-binding protein (CREB). Artemether protective effect was attenuated by PD98059, an ERK1/2 inhibitor, administration. Similarly, in oxygen-glucose deprivation/reperfusion (OGD/RP) cell models, artemether pre-treatment induced the suppression of the intracellular ROS, the down-regulation of LDH activity, the reduction of caspase 3 activity and of the apoptosis cell rate and reversed the decrease of mitochondrial membrane potential. As with MCAO animal model, artemether promoted the activation of Erk1/2-P90rsk-CREB signaling pathway. This effect was blocked by the inhibition or knock-down of ERK1/2. The present study provides evidences of the neuroprotective effect of artemether unravelling its potential as a new therapeutic candidate for the prevention and treatment of stroke.

Exosomes derived from human placental mesenchymal stem cells enhanced the recovery of spinal cord injury by activating endogenous neurogenesis.

BACKGROUND: Spinal cord injury (SCI) is a debilitating medical condition that can result in the irreversible loss of sensorimotor function. Current therapies fail to provide an effective recovery being crucial to develop more effective approaches. Mesenchymal stem cell (MSC) exosomes have been shown to be able to facilitate axonal growth and act as mediators to regulate neurogenesis and neuroprotection, holding great therapeutic potential in SCI conditions. This study aimed to assess the potential of human placental MSC (hpMSC)-derived exosomes on the functional recovery and reactivation of endogenous neurogenesis in an experimental animal model of SCI and to explore the possible mechanisms involved. METHODS: The hpMSC-derived exosomes were extracted and transplanted in an experimental animal model of SCI with complete transection of the thoracic segment. Functional recovery, the expression of neural stem/progenitor cell markers and the occurrence of neurogenesis, was assessed 60 days after the treatment. In vitro, neural stem cells (NSCs) were incubated with the isolated exosomes for 24 h, and the phosphorylation levels of mitogen-activated protein kinase kinase (MEK), extracellular signal-regulated kinases (ERK), and cAMP response element binding (CREB) proteins were assessed by western blot. RESULTS: Exosomes were successfully isolated and purified from hpMSCs. Intravenous injections of these purified exosomes significantly improved the locomotor activity and bladder dysfunction of SCI animals. Further study of the exosomes' therapeutic action revealed that hpMSC-derived exosomes promoted the activation of proliferating endogenous neural stem/progenitor cells as denoted by the significant increase of spinal SOX2+GFAP+, PAX6+Nestin+, and SOX1+KI67+ cells. Moreover, animals treated with exosomes exhibited a significative higher neurogenesis, as indicated by the higher percentage of DCX+MAP 2+ neurons. In vitro, hpMSC-derived exosomes promoted the proliferation of NSCs and the increase of the phosphorylated levels of MEK, ERK, and CREB. CONCLUSIONS: This study provides evidence that the use of hpMSC-derived exosomes may constitute a promising therapeutic strategy for the treatment of SCI.

Co/N-Doped hierarchical porous carbon as an efficient oxygen electrocatalyst for rechargeable Zn-air battery.

Developing efficient electrocatalysts for ORR/OER is the key issue for the large-scale application of rechargeable Zn-air batteries. The design of Co and N co-doped carbon matrices has become a promising strategy for the fabrication of bi-functional electrocatalysts. Herein, the surface-oxidized Co nanoparticles (NPs) encapsulated into N-doped hierarchically porous carbon materials (Co/NHPC) are designed as ORR/OER catalysts for rechargeable Zn-air batteries via dual-templating strategy and pyrolysis process containing Co2+. The fabricated electrocatalyst displays a core-shell structure with the surface-oxidized Co nanoparticles anchored on hierarchically porous carbon sheets. The carbon shells prevent Co NP cores from aggregating, ensuring excellent electrocatalytic properties for ORR with a half-wave potential of 0.82 V and a moderate OER performance. Notably, the obtained Co/NHPC as a cathode was further assembled in a zinc-air battery that delivered an open-circuit potential of 1.50 V, even superior to that of Pt/C (1.46 V vs. RHE), a low charge-discharge voltage gap, and long cycle life. All these results demonstrate that this study provides a simple, scalable, and efficient approach to fabricate cost-effective high-performance ORR/OER catalysts for rechargeable Zn-air batteries.

Brn2 Alone Is Sufficient to Convert Astrocytes into Neural Progenitors and Neurons.

Generating neurons or neural progenitor cells (NPCs) from astrocytes is a potential strategy for neurological repair by reprogramming. Previous study has showed that Brn2, by cooperating with other factors, participates in neurogenesis and neuronal reprogramming. However, it is still unclear whether the Brn2 alone can convert astrocytes into neurons or NPCs. Here, we explored the effect of Brn2 on reprogramming of astrocytes, and found that a single transcription factor Brn2 can convert mouse astrocytes into functional neurons. Furthermore, the Brn2-infected astrocytes can be induced into NPCs after changing culture condition. In addition, our study found that the reprogramming of astrocytes and the fate of transdifferentiated cells are closely associated with cell microenvironmental factors, such as the brain regions where the astrocytes come from, the proliferation ability of astrocytes, and culture condition of infected astrocytes. To sum up, for the first time, our results demonstrated that Brn2 alone is sufficient to convert astrocytes into neural progenitors and neurons, and the conversion is associated with cell microenvironments. This new conversion method will be a potential therapeutic approach to restore the injured diseased brain in regenerative medicine.

Simultaneously determination of trace Cd(2+) and Pb(2+) based on L-cysteine/graphene modified glassy carbon electrode.

In this paper, L-cysteine/graphene-CS/GCE (L-cys/GR-CS/GCE) was prepared successfully, and its electrochemical properties were characterized by cyclic voltammetry (CV) and electrochemical AC impedance. Moreover, the electrochemical behaviors of Cd(2+) and Pb(2+) on the proposed electrode were studied by differential pulse anodic stripping voltammetry (DPASV). Experimental parameters, such as the deposition potential and time, the pH value of buffer solution, were optimized. Under the optimized conditions, the linear equations of the DPASV response current with Cd(2+) and Pb(2+) concentration were I (µA) = 0.745 C (µg/L)+4.539 (R = 0.9986), I (µA) = 0.437 C (µg/L)+2.842 (R = 0.9983), respectively, and the detection limit was 0.45 and 0.12 µg/L, respectively. Finally, L-cys/GR-CS/GCE was used to detect Cd(2+) and Pb(2+) in practical samples, and the results were compared with ICP-AES. This idea and method will provide a new approach for food security evaluation.

A facial electrochemical approach to determinate bisphenol A based on graphene-hypercrosslinked resin MN202 composite.

It first reported a novel electrochemical approach for the in situ determination of bisphenol A (BPA) in the milk and mineralised water using graphene-hypercrosslinked resin MN202 composite (MN202) modified electrode. The electrocatalytic oxidation and electroanalytical of BPA on the modified electrode were investigated by cyclic voltammetry (CV) and differential pulse voltammetry (DPV). It is notable that the oxidation peak current of BPA had enhanced remarkably and the oxidation overpotential had decreased significantly. Experimental parameters, such as the accumulation potential and time, scan rate, and the pH value of buffer solution were optimised. Under the optimised conditions, the oxidation peak current was proportional to BPA concentration in a wide range between 0.005 and 20.0 µmol/L, and the detection limit was 1.02 nmol/L (S/N=3). Moreover, the fabricated electrode also exhibited good reproducibility and stability, and employed to in situ determinate BPA in milk and mineralised water successfully.

Studies on the interaction mechanism of aminopyrene derivatives with human tumor-related DNA.

Polycyclic aromatic hydrocarbons derivatives (PAHs) have been confirmed to be carcinogenic, teratogenic and mutagenic, and have the potential to cause human malignant diseases. In this work, interactions of two selected amino-PAHs (aminopyrene derivatives) and human tumor-related DNA were evaluated using spectroscopic and polyacrylamide gel electrophoresis (PAGE) methods. Spectroscopic results demonstrated that there were remarkable interactions between PAHs and the targeted DNA with the order of the binding ability as 1-AP>1-PBA. The binding constants of 1-AP with the targeted DNA were at the level of about 10(6) L/mol, while that of 1-PBA only to about 10(3) L/mol. 1-AP with a short side-chain acted mainly as an intercalator, and its interactions with DNA were strengthened with electrostatic forces. As for 1-PBA with a flexible long side-chain, the intercalation mode was dominated with an auxiliary role of Van der Wals forces and hydrogen bonds. Besides, the binding abilities of amino-PAHs to p53 DNA seemed stronger than that for C-myc DNA. PAGE results showed that the binding of amino-PAHs could further change the conformation of DNA sequences from the duplex to the antiparallel G-quadruplex.

Investigation and comparison of bovine hemoglobin binding to Al13 and Al(III): evidences from spectroscopic studies.

The UV-vis, steady state/time resolved fluorescence spectroscopy and circular dichroism spectroscopy are employed to investigate the interaction mechanisms of Al(13)-Hb and Al(III)-Hb, respectively. The UV-vis studies represent that Al(13) and Al(III) could directly disturb the structure of Hb and induce the heme group exposed to the aqueous medium. Steady state/time resolved and synchronous fluorescence spectroscopy reveal that Al(13) and Al(III) can change the polarity around the fluorophore molecule of Hb. Al(13) makes the protein unfolding and Al(III) induces the protein buried inside the structure. The interaction processes are static quenching mechanisms and the main forces are electrostatic interactions. Moreover, circular dichroism spectra display Al(13) makes greater effect than Al(III), which is reflected on the degrees of α-helix of Hb. The comparison results suggest that Al(13) displays stronger toxicity.