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A novel asymmetric supercapacitor device in an aqueous electrolyte is fabricated using a vanadyl phosphate/carbon nanocomposite as the positive electrode and a polypyrrole-derived carbon nanowire as the negative electrode. The vanadyl phosphate/carbon nanocomposites are synthesized by a simple two-step approach in which layered VOPO 4 ·2H 2 O is first intercalated by dodecylamine and then annealed at high temperature, leading to the in situ carbonization of the intercalated dodecylamine. It is found that the sample in which the incorporated carbon with a high degree of graphitization exhibits a high specific capacitance of 469 F g -1 at a current density of 1 A g -1 and excellent rate performance (retained 77% capacitance at 10 A g -1 ). A polypyrrole-derived carbon nanowire is synthesized by the direct carbonization of nanowire-shaped polypyrrole, revealing a rough surface of nanowire-like frameworks and good electrochemical behavior. Taking advantage of both positive and negative materials, the assembled asymmetric supercapacitor device exhibits a high energy density of 30.6 W h kg -1 at a high power density of 813 W kg -1 in a wide voltage region of 0-1.6 V, as well as a good electrochemical stability (84.3% capacitance retention after 5000 cycles). The present work can shed light on the fabrication of novel asymmetric supercapacitors with high-performance.

The S-doped mesoporous nanocomposite (S-TNT) of HTiNbO5 nanosheets (NSs) and anatase TiO2 nanoparticles (NPs) with exposed {101} facets has been successfully synthesized by first mixing freeze-dried HTiNbO5 NSs with titanium isopropoxide and then calcination with thiourea in air. The exposed anatase {101} facets can act as a possible reservoir of the photogenerated electrons, yielding a highly reactive surface for the reduction of O2 to O2˙(-). The partial substitution of Ti(4+) by S(6+) in the lattice of TiO2 NPs leads to a charge imbalance in S-TNT and the formation of Ti-O-S bonds. As a result, the formed cationic S-TNT favours adsorption of hydroxide ions (OH(-)(ads)) and thus captures the photo-induced holes to form hydroxyl radicals (˙OH). Moreover, with the formation of Ti-O-S bonds, partial electrons can be transferred from S to O atoms and hence the electron-deficient S atoms might capture photo-induced electrons. The surface-adsorbed SO4(2-) could also act as an efficient electron trapping center to promote the separation of charge carriers. In addition, the Ti(3+) species due to the removal of oxygen atoms during calcination and the associated oxygen vacancy defects on the surface of S-TNT could act as hole and electron scavengers, respectively. Besides, the closely contacted interface is formed between HTiNbO5 NSs and anatase TiO2 NPs due to the common features of TiO6 octahedra in two components, resulting in a nanoscale heterojunction structure to speed up the separation rate of photogenerated charge carriers. The formation of a nano-heterojunction and the incorporation of Ti(3+) and S dopants give rise to the visible and near-infrared light response of S-TNT. The combined effects greatly retard the charge recombination and improve the photocatalytic activity for the degradation of rhodamine B (RhB) and phenol solution under visible light irradiation. The corresponding photocatalytic mechanism was investigated via the active species capture experiments. The present work may provide an insight into the fabrication of delicate composite photocatalysts with excellent performance.

In neurons, a highly regulated microtubule cytoskeleton is essential for many cellular functions. These include axonal transport, regional specialization and synaptic function. Given the critical roles of microtubule-associated proteins (MAPs) in maintaining and regulating microtubule stability and dynamics, we sought to understand how this regulation is achieved. Here, we identify a novel LisH/WD40 repeat protein, tentatively named nemitin (neuronal enriched MAP interacting protein), as a potential regulator of MAP8-associated microtubule function. Based on expression at both the mRNA and protein levels, nemitin is enriched in the nervous system. Its protein expression is detected as early as embryonic day 11 and continues through adulthood. Interestingly, when expressed in non-neuronal cells, nemitin displays a diffuse pattern with puncta, although at the ultrastructural level it localizes along the microtubule network in vivo in sciatic nerves. These results suggest that the association of nemitin to microtubules may require an intermediary protein. Indeed, co-expression of nemitin with microtubule-associated protein 8 (MAP8) results in nemitin losing its diffuse pattern, instead decorating microtubules uniformly along with MAP8. Together, these results imply that nemitin may play an important role in regulating the neuronal cytoskeleton through an interaction with MAP8.

The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is active in both normal hematopoiesis and hematological malignancies. Moreover, Janus kinase-2 (JAK2) is the key hematopoietic kinase, and mutations together with single nucleotide polymorphisms (SNPs) of JAK2 have been thoroughly evaluated. In this study, we aimed to investigate whether the synonymous genetic polymorphism A830G in the JAK2 gene is associated with the treatment outcomes of Ara-C-based chemotherapy regimens in patients with acute myeloid leukemia (AML). A total of 152 patients with AML in a Chinese population were enrolled in our study. Peripheral blood samples drawn at the time of diagnosis were analyzed for the presence of JAK2 A830G by matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF-MS). The results showed that frequencies of the AA genotype were higher in the group 40-60 years old, higher white blood cell (WBC) patient group, homoharringtonine and Ara-C (HA) regimen group, and good therapy response group, and patients with the GG genotype were significantly associated with a higher rate of early death. We conclude that the AA and GG genotypes of JAK2 A830G might be important markers for therapy outcomes of patients with AML in a Chinese population.

While the potential impact of magnetic nanoparticles (MNPs) has been widely explored in almost all medical fields, including cardiology, one question remains; that is whether MNPs interfere with cardiac physiological processes such as the expression and function of ion channels, especially in vivo. KCNQ(1) channels are richly expressed in cardiac myocytes and are critical to the repolarization of cardiac myocytes. In this study, we evaluated the effects of Fe(3)O(4)-magnetic nanoparticles (MNPs-Fe(3)O(4)) on the expression of KCNQ(1) in cardiac muscle of mice at rest and at different times following a single bout of swimming (SBS). Firstly, we demonstrated that the expression levels of KCNQ(1) channels are significantly up-regulated in mice following a SBS by means of reverse transcription polymerase chain reaction (RT-PCR) and western-blot. After treating mice with normal saline or pure MNPs-Fe(3)O(4) separately, we studied the potential effect of MNPs-Fe(3)O(4) on the expression profile of KCNQ(1) in mouse cardiac muscle following a SBS. A SBS increased the transcription of KCNQ(1) at 3 hours post exercise (3PE) 164% +/- 24% and at 12 hours post exercise (12PE) by 159% +/- 23% (P < 0.05), and up-regulated KCNQ(1) protein 161% +/- 27% at 12PE (P < 0.05) in saline mice. In MNPs-Fe(3)O(4) mice, KCNQ(1) mRNA increased by 151% +/- 14% and 147% +/- 12% at 3 and 12 PE, respectively (P <0.05). Meanwhile, an increase of 152% +/- 14% in KCNQ(1) protein was also detected at by 12PE. These results indicated that the administration of MNPs-Fe(3)O(4) did not cause any apparent effects on the expression profile of KCNQ(1) in rested or exercised mice cardiac muscle. Our studies suggest a novel path of KCNQ(1) current adaptations in the heart during physical exercise and in addition provide some useful information for the biomedical application of MNPs which are imperative to advance nanomedicine.

In this paper we establish the xenograft leukemia model with stable multidrug resistance in nude mice and to investigate the reversal effect of 5-bromotetrandrine (5-BrTet) and magnetic nanoparticle of Fe(3)O(4) (MNP-Fe(3)O(4)) combined with daunorubicin (DNR) in vivo. Two subclones of K562 and K562/A02 cells were inoculated subcutaneously into the back of athymic nude mice (1 x 10(7) cells/each) respectively to establish leukemia xenograft models. Drug-resistant and sensitive tumor-bearing nude mice were assigned randomly into five groups which were treated with normal saline; DNR; NP-Fe(3)O(4) combined with DNR; 5-BrTet combined with DNR; 5-BrTet and MNP-Fe(3)O(4) combined with DNR, respectively. The incidence of formation, growth characteristics, weight, and volume of tumors were observed. The histopathologic examination of tumors and organs were detected. For resistant tumors, the protein levels of Bcl-2, and BAX were detected by Western blot. Bcl-2, BAX, and caspase-3 genes were also detected. For K562/A02 cells xenograft tumors, 5-BrTet and MNP-Fe(3)O(4) combined with DNR significantly suppressed growth of tumor. A histopathologic examination of tumors clearly showed necrosis of the tumors. Application of 5-BrTet and MNP-Fe(3)O(4) inhibited the expression of Bcl-2 protein and upregulated the expression of BAX and caspase-3 proteins in K562/A02 cells xenograft tumor. It is concluded that 5-BrTet and MNP-Fe(3)O(4) combined with DNR had a significant tumor-suppressing effect on a MDR leukemia cells xenograft model.

Apoptosis is a common pathway that finally mediated the killing functions of anticancer drugs, which is an important cause of multidrug resistance (MDR). The aim of this study was to investigate the potential benefit of combination therapy with magnetic nanoparticle of Fe(3)O(4) (MNP(Fe(3)O(4))) and 5-bromotetrandrin (BrTet). Analysis of the apoptosis percentage showed that combination of daunorubicin (DNR) with either MNP(Fe(3)O(4)) or BrTet exerted a potent cytotoxic effect on K562/A02 cells, while MNP(Fe(3)O(4)) and BrTet cotreatment can synergistically enhance DNR-induced apoptosis. Importantly, we confirmed that the distinct synergism effect of that composite on reverse multidrug resistance may owe to the regulation of various proliferative and antiapoptotic gene products, including P53 and caspase-3. Thus our in vitro data strongly suggests a potential clinical application of MNP(Fe(3)O(4)) and BrTet combination on CML.

This study aims to evaluate the multidrug resistance (MDR) reversal activity by magnetic nanoparticles of Fe3O4 (MNPs-Fe3O4) and 5-bromotetrandrine (BrTet) MDR cell line K562/A02 solitarily or symphysially. The proliferation of K562 and K562/A02 cells and the cytotoxicity on peripheral blood mononuclear cells (PMBCs) were evaluated by MTT assay. Cellular accumulation of daunorubicin (DNR) was analyzed by flow cytometry. Real-time polymerase chain reaction and Western blotting analyses were performed to examine the mRNA and protein levels of mdr1, respectively. The results showed that the combination of MNPs-Fe3O4 and BrTet with effective concentrations significantly increased cytotoxicity against MDR cell line K562/A02. Both BrTet and MNPs-Fe3O4 increased the intracellular DNR accumulation in the K562/A02 cell line, and downregulated the level of mdr1 gene and expression of P-glycoprotein. Furthermore, the combination did not have significant cytotoxicity in PMBCs. We propose that MNPs-Fe3O4 conjugated with DNR and BrTet probably have synergetic effects on MDR reversal.

Drug resistance is a primary hindrance for efficiency of chemotherapy. To investigate whether Fe3O4-magnetic nanoparticles (Fe3O4-MNPs) loaded with adriamycin (ADM) and tetrandrine (Tet) would play a synergetic reverse role in multidrug resistant cell, we prepared the drug-loaded nanoparticles by mechanical absorption polymerization to act with K562 and one of its resistant cell line K562/A02. The survival of cells which were cultured with these conjugates for 48 h was observed by MTT assay. Using cells under the same condition described before, we took use of fluorescence microscope to measure fluorescence intensity of intracellular ADM at an excitation wavelength of488 nm. P-glycoprotein (P-gp) was analyzed with flow cytometer. The expression ofmdrl mRNA was measured by RT-PCR. The results showed that the growth inhibition efficacy of both the two cells increased with augmenting concentrations of Fe3O4-MNPs which were loaded with drugs. No linear correlation was found between fluorescence intensity of intracellular adriamycin and augmenting concentration of Fe3O4-MNPs. Tet could downregulate the level of mdr-1 gene and decrease the expression of P-gp. Furthermore, Tet polymerized with Fe3O4-MNPs reinforced this downregulation, causing a 100-fold more decrease in mdrl mRNA level, but did not reduce total P-gp content. Our results suggest that Fe3O4-MNPs loaded with ADM or Tet can enhance the effective accumulation of the drugs in K562/A02. We propose that Fe3O4-MNPs loaded with ADM and Tet probably have synergetic effect on reversal in multidrug resistance.