Organoplatinum-Substituted Polyoxometalate Inhibits ß-amyloid Aggregation for Alzheimer's Therapy.

Aggregated ß-amyloid (Aß) is widely considered as a key factor in triggering progressive loss of neuronal function in Alzheimer's disease (AD), so targeting and inhibiting Aß aggregation has been broadly recognized as an efficient therapeutic strategy for curing AD. Herein, we designed and prepared an organic platinum-substituted polyoxometalate, (Me4 N)3 [PW11 O40 (SiC3 H6 NH2 )2 PtCl2 ] (abbreviated as PtII -PW11 ) for inhibiting Aß42 aggregation. The mechanism of inhibition on Aß42 aggregation by PtII -PW11 was attributed to the multiple interactions of PtII -PW11 with Aß42 including coordination interaction of Pt2+ in PtII -PW11 with amino group in Aß42 , electrostatic attraction, hydrogen bonding and van der Waals force. In cell-based assay, PtII -PW11 displayed remarkable neuroprotective effect for Aß42 aggregation-induced cytotoxicity, leading to increase of cell viability from 49 % to 67 % at a dosage of 8 µm. More importantly, the PtII -PW11 greatly reduced Aß deposition and rescued memory loss in APP/PS1 transgenic AD model mice without noticeable cytotoxicity, demonstrating its potential as drugs for AD treatment.

Myocardial infarction-induced hippocampal microtubule damage by cardiac originating microRNA-1 in mice.

Cardiovascular diseases are risk factors for dementia, but the mechanisms remain elusive. Here, we report that myocardial infarction (MI) generated by the ligation of the left coronary artery (LCA) could lead to increased miR-1 levels in the hippocampus and blood with neuronal microtubule damage and decreased TPPP/p25 protein expression in the hippocampus. These changes could be prevented by a knockdown of miR-1 using hippocampal stereotaxic injections of anti-miR-1 oligonucleotide fragments carried by a lentivirus vector (lenti-pre-AMO-miR-1). TPPP/p25 protein was downregulated by miR-1 overexpression, upregulated by miR-1 inhibition, and unchanged by binding-site mutations or miR-masks, indicating that the TPPP/p25 gene was a potential target for miR-1. Additionally, the pharmacological inhibition of sphingomyelinase by GW4869 to inhibit exosome generation in the heart significantly attenuated the increased miR-1 levels in the hippocampi of transgenic (Tg) and MI mice. Collectively, the present study demonstrates that MI could directly lead to neuronal microtubule damage independent of MI-induced chronic brain hypoperfusion but involving the overexpression of miR-1 in the hippocampus that was transported by exosomes from infarcted hearts. This study reveals a novel insight into the molecular mechanisms of heart-to-brain communication at the miRNA level.

Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial-Mesenchymal Transition in Glioma Cells.

BACKGROUND/AIMS: Kaiso (ZBTB33) expression is closely associated with the progression of many cancers and microRNA (miRNA) processing. MiR-181a plays critical roles in multiple cancers; however, its precise mechanisms in glioma have not been well clarified. The goal of this study was to evaluate the interaction between Kaiso and miR-181a in glioma. METHODS: Quantitative real-time PCR (qRT-PCR) was performed to detect the levels of Kaiso and miR-181a in glioma tissues and cell lines. Cell proliferation, invasion, and the epithelial-mesenchymal transition (EMT) were evaluated to analyze the biological functions of miR-181a and Kaiso in glioma cells. The mRNA and protein levels of Kaiso were measured by qRT-PCR and western blotting, respectively. Meanwhile, luciferase assays were performed to validate Kaiso as a miR-181a target in glioma cells. RESULTS: We found that the level of miR-181a was the lowest among miR-181a-d in glioma tissues and cell lines, and the low level of miR-181a was closely associated with the increased expression of Kaiso in glioma tissues. Moreover, transfection of miR-181a significantly inhibited the proliferation, invasion, and EMT of glioma cells, whereas knockdown of miR-181a had the opposite effect. Bioinformatics analysis predicted that Kaiso was a potential target gene of miR-181a, and the luciferase reporter assay demonstrated that miR-181a could directly target Kaiso. In addition, Kaiso silencing had similar effects as miR-181a overexpression in glioma cells, whereas overexpression of Kaiso in glioma cells partially reversed the inhibitory effects of the miR-181a mimic. Conclusionss: miR-181a inhibited the proliferation, invasion, and EMT of glioma cells by directly targeting and downregulating Kaiso expression.

Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation.

BACKGROUNDS/AIMS: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. METHODS: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were performed to evaluate the cognitive ability of MI mice. A theta-burst stimulation (TBS) protocol was applied to elicit long-term potentiation (LTP) of the perforant pathway-dentate gyrus synapse (PP-DG). Western blot analysis was employed to assess protein levels. RESULTS: In this study, we demonstrated that after 4 weeks of MI, C57BL/6 mice had significantly impaired memory. Compared with the sham group, in vivo physiological recording in the MI group revealed significantly decreased amplitude of population spikes (PS) with no effect on the latency and duration of the stimulus-response curve. The amplitude of LTP was markedly decreased in the MI group compared with the sham group. Further examination showed that the expression of the TBS-LTP-related proteins BDNF, GluA1 and phosphorylated GluA1 were all decreased in the MI group compared with those in the sham group. Strikingly, all these changes were prevented by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-1). CONCLUSION: MI induced cognitive decline and TBS-LTP impairment, and decreased BDNF and GluA1 phosphorylation levels from overexpression of miR-1ated were involved in this process.

Overexpression of miR-1 in the heart attenuates hippocampal synaptic vesicle exocytosis by the posttranscriptional regulation of SNAP-25 through the transportation of exosomes.

BACKGROUND: The link between cardiac diseases and cognitive deterioration has been accepted from the concept of "cardiogenic dementia", which was proposed in the late 1970s. However, the molecular mechanism is unclarified. METHODS: The two animal models used in this study were cardiac-specific overexpression of microRNA-1-2 transgenic (Tg) mice and a myocardial infarction mouse model generated by left coronary artery ligation (LCA). First, we observed the microRNA-1 (miR-1) level and synaptic vesicles (SV) distribution in the hippocampus using in situ hybridization and transmission electron microscopy (TEM) and evaluated the expression of vesicle exocytosis related proteins by western blotting. Second, we used dual luciferase reporter assay as well as antagonist and miRNA-masking techniques to identify the posttranscriptional regulatory effect of miR-1 on the Snap25 gene. Third, FM1-43 staining was performed to investigate the effect of miR-1 on synaptic vesicle exocytosis. Lastly, we used GW4869 to inhibit the biogenesis and secretion of exosomes to determine the transportation effect of exosomes for miR-1 from the heart to the brain. RESULTS: Compared with the levels in age-matched WT mice, miR-1 levels were increased in both the hearts and hippocampi of Tg mice, accompanied by the redistribution of SVs and the reduction in SV exocytosis-related protein SNAP-25 expression. In vitro studies showed that SNAP-25 protein expression was down- or upregulated by miR-1 overexpression or inhibition, respectively, however, unchanged by miRNA-masking the 3'UTR of the Snap25 gene. SV exocytosis was inhibited by miR-1 overexpression, which could be prevented by co-transfection with an anti-miR-1 oligonucleotide fragment (AMO-1). The knockdown of miR-1 by hippocampal stereotaxic injection of AMO-1 carried by a lentivirus vector (lenti-pre-AMO-1) led to the upregulation of SNAP-25 expression and prevented SV concentration in the synapses in the hippocampi of Tg mice. The application of GW4869 significantly reversed the increased miR-1 level in the blood and hippocampi as well as reduced the SNAP-25 protein levels in the hippocampi of both Tg and LCA mice. CONCLUSION: The overexpression of miR-1 in the heart attenuated SV exocytosis in the hippocampus by posttranscriptionally regulating SNAP-25 through the transportation of exosomes. This study contributes to the understanding of the relationship between cardiovascular disease and brain dysfunction.

Covalent bonding of homochiral metal-organic framework in capillaries for stereoisomer separation by capillary electrochromatography.

In this work, a [Cu(mal)(bpy)]⋅H2O (mal, L-(-)-malic acid; bpy, 4,4'-bipyridyl) homochiral metal-organic frameworks (MOFs) was synthesized and used for modifying the inner walls of capillary columns by utilizing amido bonds to form covalent links between the MOFs particles and capillary inner wall. The synthesized [Cu(mal)(bpy)]⋅H2 O and MOFs-modified capillary column were characterized by X-ray diffraction, thermogravimetric analysis, particle size distribution analysis, nitrogen absorption characterization, FTIR spectroscopy, SEM, and energy-dispersive X-ray spectroscopy (EDX). The MOFs-modified capillary column was used for the stereoisomer separation of some drugs. The LODs and LOQs of six analytes were 0.1 and 0.25 µg/mL, respectively. The linear range was 0.25-250 µg/mL for ephedrine, 0.25-250 µg/mL for pseudoephedrine, 0.25-180 µg/mL for D-penicillamine, 0.25-120 µg/mL for L-penicillamine, 0.25-180 µg/mL for D-phenylalanine, and 0.25-160 µg/mL for L-phenylalanine, all with R(2) > 0.999. Finally, the MOFs-modified capillary column was applied for the analysis of active ingredients in a real sample of the traditional Chinese medicine ephedra.

Distribution and morphology of calcitonin gene-related peptide (CGRP) innervation in flat mounts of whole rat atria and ventricles.

Calcitonin gene-related peptide (CGRP) is widely used as a marker for nociceptive afferent axons. However, the distribution of CGRP-IR axons has not been fully determined in the whole rat heart. Immunohistochemically labeled flat-mounts of the right and left atria and ventricles, and the interventricular septum (IVS) in rats for CGRP were assessed with a Zeiss imager to generate complete montages of the entire atria, ventricles, and septum, and a confocal microscope was used to acquire detailed images of selected regions. We found that 1) CGRP-IR axons extensively innervated all regions of the atrial walls including the sinoatrial node region, auricles, atrioventricular node region, superior/inferior vena cava, left pre-caval vein, and pulmonary veins. 2) CGRP-IR axons formed varicose terminals around individual neurons in some cardiac ganglia but passed through other ganglia without making appositions with cardiac neurons. 3) Varicose CGRP-IR axons innervated the walls of blood vessels. 4) CGRP-IR axons extensively innervated the right/left ventricular walls and IVS. Our data shows the rather ubiquitous distribution of CGRP-IR axons in the whole rat heart at single-cell/axon/varicosity resolution for the first time. This study lays the foundation for future studies to quantify the differences in CGRP-IR axon innervation between sexes, disease models, and species.

Spinal afferent innervation in flat-mounts of the rat stomach: anterograde tracing.

The dorsal root ganglia (DRG) project spinal afferent axons to the stomach. However, the distribution and morphology of spinal afferent axons in the stomach have not been well characterized. In this study, we used a combination of state-of-the-art techniques, including anterograde tracer injection into the left DRG T7-T11, avidin-biotin and Cuprolinic Blue labeling, Zeiss M2 Imager, and Neurolucida to characterize spinal afferent axons in flat-mounts of the whole rat stomach muscular wall. We found that spinal afferent axons innervated all regions with a variety of distinct terminal structures innervating different gastric targets: (1) The ganglionic type: some axons formed varicose contacts with individual neurons within myenteric ganglia. (2) The muscle type: most axons ran in parallel with the longitudinal and circular muscles and expressed spherical varicosities. Complex terminal structures were observed within the circular muscle layer. (3) The ganglia-muscle mixed type: some individual varicose axons innervated both myenteric neurons and the circular muscle, exhibiting polymorphic terminal structures. (4) The vascular type: individual varicose axons ran along the blood vessels and occasionally traversed the vessel wall. This work provides a foundation for future topographical anatomical and functional mapping of spinal afferent axon innervation of the stomach under normal and pathophysiological conditions.

Topographical organization and morphology of substance P (SP)-immunoreactive axons in the whole stomach of mice.

Nociceptive afferents innervate the stomach and send signals centrally to the brain and locally to stomach tissues. Nociceptive afferents can be detected with a variety of different markers. In particular, substance P (SP) is a neuropeptide and is one of the most commonly used markers for nociceptive nerves in the somatic and visceral organs. However, the topographical distribution and morphological structure of SP-immunoreactive (SP-IR) axons and terminals in the whole stomach have not yet been fully determined. In this study, we labeled SP-IR axons and terminals in flat mounts of the ventral and dorsal halves of the stomach of mice. Flat-mount stomachs, including the longitudinal and circular muscular layers and the myenteric ganglionic plexus, were processed with SP primary antibody followed by fluorescent secondary antibody and then scanned using confocal microscopy. We found that (1) SP-IR axons and terminals formed an extensive network of fibers in the muscular layers and within the ganglia of the myenteric plexus of the whole stomach. (2) Many axons that ran in parallel with the long axes of the longitudinal and circular muscles were also immunoreactive for the vesicular acetylcholine transporter (VAChT). (3) SP-IR axons formed very dense terminal varicosities encircling individual neurons in the myenteric plexus; many of these were VAChT immunoreactive. (4) The regional density of SP-IR axons and terminals in the muscle and myenteric plexus varied in the following order from high to low: antrum-pylorus, corpus, fundus, and cardia. (5) In only the longitudinal and circular muscles, the regional density of SP-IR axon innervation from high to low were: antrum-pylorus, corpus, cardia, and fundus. (6) The innervation patterns of SP-IR axons and terminals in the ventral and dorsal stomach were comparable. Collectively, our data provide for the first time a map of the distribution and morphology of SP-IR axons and terminals in the whole stomach with single-cell/axon/synapse resolution. This work will establish an anatomical foundation for functional mapping of the SP-IR axon innervation of the stomach and its pathological remodeling in gastrointestinal diseases.

Mapping the Organization and Morphology of Calcitonin Gene-Related Peptide (CGRP)-IR Axons in the Whole Mouse Stomach.

Nociceptive afferent axons innervate the stomach and send signals to the brain and spinal cord. Peripheral nociceptive afferents can be detected with a variety of markers [e.g., substance P (SP) and calcitonin gene-related peptide (CGRP)]. We recently examined the topographical organization and morphology of SP-immunoreactive (SP-IR) axons in the whole mouse stomach muscular layer. However, the distribution and morphological structure of CGRP-IR axons remain unclear. We used immunohistochemistry labeling and applied a combination of imaging techniques, including confocal and Zeiss Imager M2 microscopy, Neurolucida 360 tracing, and integration of axon tracing data into a 3D stomach scaffold to characterize CGRP-IR axons and terminals in the whole mouse stomach muscular layers. We found that: 1) CGRP-IR axons formed extensive terminal networks in both ventral and dorsal stomachs. 2) CGRP-IR axons densely innervated the blood vessels. 3) CGRP-IR axons ran in parallel with the longitudinal and circular muscles. Some axons ran at angles through the muscular layers. 4) They also formed varicose terminal contacts with individual myenteric ganglion neurons. 5) CGRP-IR occurred in DiI-labeled gastric-projecting neurons in the dorsal root and vagal nodose ganglia, indicating CGRP-IR axons were visceral afferent axons. 6) CGRP-IR axons did not colocalize with tyrosine hydroxylase (TH) or vesicular acetylcholine transporter (VAChT) axons in the stomach, indicating CGRP-IR axons were not visceral efferent axons. 7) CGRP-IR axons were traced and integrated into a 3D stomach scaffold. For the first time, we provided a topographical distribution map of CGRP-IR axon innervation of the whole stomach muscular layers at the cellular/axonal/varicosity scale.

Organization and morphology of calcitonin gene-related peptide-immunoreactive axons in the whole mouse stomach.

Nociceptive afferent axons innervate the stomach and send signals to the brain and spinal cord. Peripheral nociceptive afferents can be detected with a variety of markers (e.g., substance P [SP] and calcitonin gene-related peptide [CGRP]). We recently examined the topographical organization and morphology of SP-immunoreactive (SP-IR) axons in the whole mouse stomach muscular layer. However, the distribution and morphological structure of CGRP-IR axons remain unclear. We used immunohistochemistry labeling and applied a combination of imaging techniques, including confocal and Zeiss Imager M2 microscopy, Neurolucida 360 tracing, and integration of axon tracing data into a 3D stomach scaffold to characterize CGRP-IR axons and terminals in the whole mouse stomach muscular layers. We found that: (1) CGRP-IR axons formed extensive terminal networks in both ventral and dorsal stomachs. (2) CGRP-IR axons densely innervated the blood vessels. (3) CGRP-IR axons ran in parallel with the longitudinal and circular muscles. Some axons ran at angles through the muscular layers. (4) They also formed varicose terminal contacts with individual myenteric ganglion neurons. (5) CGRP-IR occurred in DiI-labeled gastric-projecting neurons in the dorsal root and vagal nodose ganglia, indicating CGRP-IR axons were visceral afferent axons. (6) CGRP-IR axons did not colocalize with tyrosine hydroxylase or vesicular acetylcholine transporter axons in the stomach, indicating CGRP-IR axons were not visceral efferent axons. (7) CGRP-IR axons were traced and integrated into a 3D stomach scaffold. For the first time, we provided a topographical distribution map of CGRP-IR axon innervation of the whole stomach muscular layers at the cellular/axonal/varicosity scale.

Topographical distribution and morphology of SP-IR axons in the antrum, pylorus, and duodenum of mice.

Substance-P (SP) is a commonly used marker of nociceptive afferent axons, and it plays an important role in a variety of physiological functions including the regulation of motility, gut secretion, and vascular flow. Previously, we found that SP-immunoreactive (SP-IR) axons densely innervated the pyloric antrum of the flat-mount of the mouse whole stomach muscular layer. However, the regional distribution and morphology of SP-IR axons in the submucosa and mucosa were not well documented. In this study, the mouse antrum-pylorus-duodenum (APD) were transversely and longitudinally sectioned. A Zeiss M2 imager was used to scan the serial sections of each APD (each section montage consisted of 50-100 all-in-focus maximal projection images). To determine the detailed structures of SP-IR axons and terminals, we used the confocal microscope to scan the regions of interest. We found that 1) SP-IR axons innervated the muscular, submucosal, and mucosal layers. 2) In the muscular layer, SP-IR varicose axons densely innervated the muscles and formed varicose terminals which encircled myenteric neurons. 3) In the submucosa, SP-IR axons innervated blood vessels and submucosal ganglia and formed a network in Brunner's glands. 4) In the mucosa, SP-IR axons innervated the muscularis mucosae. Some SP-IR axons entered the lamina propria. 5) The muscular layer of the antrum and duodenum showed a higher SP-IR axon density than the pyloric sphincter. 6) SP-IR axons were from extrinsic and intrinsic origins. This work provided a comprehensive view of the distribution and morphology of SP-IR axons in the APD at single cell/axon/varicosity scale. This data will be used to create a 3D scaffold of the SP-IR axon innervation of the APD.

Accurately Modeling the Resting Brain Functional Correlations Using Wave Equation With Spatiotemporal Varying Hypergraph Laplacian.

How spontaneous brain neural activities emerge from the underlying anatomical architecture, characterized by structural connectivity (SC), has puzzled researchers for a long time. Over the past decades, much effort has been directed toward the graph modeling of SC, in which the brain SC is generally considered as relatively invariant. However, the graph representation of SC is unable to directly describe the connections between anatomically unconnected brain regions and fail to model the negative functional correlations. Here, we extend the static graph model to a spatiotemporal varying hypergraph Laplacian diffusion (STV-HGLD) model to describe the propagation of the spontaneous neural activity in human brain by incorporating the Laplacian of the hypergraph representation of the structural connectome ( h SC) into the regular wave equation. Theoretical solution shows that the dynamic functional couplings between brain regions fluctuate in the form of an exponential wave regulated by the spatiotemporal varying Laplacian of h SC. Empirical study suggests that the cortical wave might give rise to resonance with SC during the self-organizing interplay between excitation and inhibition among brain regions, which orchestrates the cortical waves propagating with harmonics emanating from the h SC while being bound by the natural frequencies of SC. Besides, the average statistical dependencies between brain regions, normally defined as the functional connectivity (FC), arises just at the moment before the cortical wave reaches the steady state after the wave spreads across all the brain regions. Comprehensive tests on four extensively studied empirical brain connectome datasets with different resolutions confirm our theory and findings.

Interfering with hyaluronic acid metabolism suppresses glioma cell proliferation by regulating autophagy.

The tumor microenvironment plays an important role in tumor progression. Hyaluronic acid (HA), an important component of the extracellular matrix in the tumor microenvironment, abnormally accumulates in a variety of tumors. However, the role of abnormal HA accumulation in glioma remains unclear. The present study indicated that HA, hyaluronic acid synthase 3 (HAS3), and a receptor of HA named CD44 were expressed at high levels in human glioma tissues and negatively correlated with the prognosis of patients with glioma. Silencing HAS3 expression or blocking CD44 inhibited glioma cell proliferation in vitro and in vivo. The underlying mechanism was attributed to the inhibition of autophagy flux and maintaining glioma cell cycle arrest in G1 phase. More importantly, 4-methylumbelliferone (4-MU), a small competitive inhibitor of Uridine diphosphate (UDP) with the ability to penetrate the blood-brain barrier (BBB), also inhibited glioma cell proliferation in vitro and in vivo. Thus, approaches that interfere with HA metabolism by altering the expression of HAS3 and CD44 and the administration of 4-MU potentially represent effective strategies for glioma treatment.

Nitazoxanide, an antiprotozoal drug, inhibits late-stage autophagy and promotes ING1-induced cell cycle arrest in glioblastoma.

Glioblastoma is the most common and aggressive primary brain tumor in adults. New drug design and development is still a major challenge for glioma treatment. Increasing evidence has shown that nitazoxanide, an antiprotozoal drug, has a novel antitumor role in various tumors and exhibits multiple molecular functions, especially autophagic regulation. However, whether nitazoxanide-associated autophagy has an antineoplastic effect in glioma remains unclear. Here, we aimed to explore the underlying molecular mechanism of nitazoxanide in glioblastoma. Our results showed that nitazoxanide suppressed cell growth and induced cell cycle arrest in glioblastoma by upregulating ING1 expression with a favorable toxicity profile. Nitazoxanide inhibited autophagy through blockage of late-stage lysosome acidification, resulting in decreased cleavage of ING1. A combination with chloroquine or Torin1 enhanced or impaired the chemotherapeutic effect of nitazoxanide in glioblastoma cells. Taken together, these findings indicate that nitazoxanide as an autophagy inhibitor induces cell cycle arrest in glioblastoma via upregulated ING1 due to increased transcription and decreased post-translational degradation by late-stage autophagic inhibition.

Estrogen deficiency is associated with hippocampal morphological remodeling of early postmenopausal mice.

Estrogen (E2) deficiency is reported to involve in the impairment of cognition in postmenopausal women. However, the morphological basis is still unclear. In the present study, using transmission electron microscopy (TEM), we observed the ultrastructure of hippocampus in female C57BL/6 mice at the age of 18 months (18 M) which is considered as the early stage of postmenopause (n = 8). Compared with control mice aged 6 M (n = 8), we identified that the morphological changes in the hippocampus of these menopausal mice were mitochondrial damage, lipofuscin deposition and microtubule degradation. Notably, after E2 was subcutaneously injected into mice aged 16 M with a dosage of 3.5 µg/kg every three days for two months in the 18 M + E2 group (n = 8), mitochondrial damage and lipofuscin deposition in the DG region of hippocampus were prevented, but the degraded microtubules in the hippocampus of postmenopausal mice were failed to restore. These data suggest that hippocampal ultrastructure remodeling in mice can be initiated at the early stage of postmenopause, E2 supplementation could only have an effect on mitochondrial damage and lipofuscin increase.

Capillary coated with graphene oxide as stationary phase for the separation of brucine and strychnine by capillary electrophoresis.

A new capillary electrophoresis (CE) method was developed by using graphene oxide (GO) as a stationary phase for the separation of brucine and strychnine. The separation performance, reproducibility and stability of GO-coated capillary were investigated for the analysis of brucine and strychnine. After optimization of the separation conditions, a phosphate solution (40 mM, pH 7.0) containing 25% (v/v) acetonitrile was selected as the running buffer. Compared with uncoated capillary, higher separation efficiency was achieved by GO-coated capillary as a result of the increasing interactions between the analytes and the stationary phase of capillary. The linear ranges of these two alkaloids were 4.0-100.0 µg mL(-1) with a satisfied correlation coefficients (R > 0.9994), and this novel method provided an efficient separation of brucine and strychnine as well as a good reproducibility and stability. Finally, the developed method was successfully applied for the determination of these two alkaloids in a pharmaceutical formulation of traditional Chinese medicines.

Synthesis of magnetite/graphene oxide/chitosan composite and its application for protein adsorption.

In this study, a facile and novel strategy was developed to fabricate magnetite/graphene oxide/chitosan (Fe3O4/GO/CS) composite, and the composite was used as a magnetic adsorbent for the enrichment of protein, and followed by matrix-assisted laser desorption ionization mass spectrometry (MALDI-TOF MS) analysis. The phase composition, chemical structure and morphology of the composite were characterized by X-ray diffraction (XRD), Fourier transform infrared spectrometer (FTIR), transmission electron microscopy (TEM), scanning electronic microscope (SEM) and vibrating sample magnetometer (VSM). Protein cytochrome c was chosen as model target to evaluate the adsorptive property of Fe3O4/GO/CS. After enrichment procedure and magnetic separation, protein bounded with the material was analyzed by MALDI-TOF MS without desorption. The results indicated that Fe3O4/GO/CS composite exhibited a good adsorptive capacity for protein, and Fe3O4/GO/CS composite had a promising potential in magnetic separation research.

Monodisperse rutile microspheres with ultrasmall nanorods on surfaces: synthesis, characterization, luminescence, and photocatalysis.

A complex nanostructure of rutile TiO(2) microspheres with ultrasmall nanorods on surfaces was prepared by a simple solvothermal method. This complex nanostructure is different from the hierarchical structure of microspheres composed of nanorods. The obtained complex nanostructure possesses an epitaxy-like interface between the nanorod-shell and the sphere-core, which often provides superior physical and chemical properties. The size and morphology of the obtained rutile TiO(2) complex nanostructure were observed by scanning electron microscopy and transmission electron microscopy (TEM). Their intrinsic crystallography was characterized by X-ray diffraction, high-resolution TEM, and selected area electron diffraction. Controlled experiments were designed using varied temperatures and assistant reagent compositions to study their influences on the crystal phase and morphology of TiO(2). The formation process of this complex nanostructure was determined via time-dependent experiments. Its photoluminescence spectra showed the strongest emission at about 400 nm with a blue-shift. The photocatalytic experiments demonstrated the obtained complex nanostructure had the highest catalytic efficiency in the five TiO(2) samples with different morphologies.