Construction of aptamer-siRNA chimera and glutamine modified carboxymethyl-ß-cyclodextrin nanoparticles for the combination therapy against lung squamous cell carcinoma.

Combination therapy has become the most important treatment for advanced non-small cell lung cancer (NSCLC), which can significantly improve the prognosis of patients. However, poor targeting and adverse reactions limited its clinical application. Here, we constructed an AS1411 aptamer-programmed cell death ligand-1 (PD-L1) siRNA chimera/polyethylenimine/glutamine/ß-cyclodextrin/doxorubicin (Chimera/ PEI/Gln/ß-CD/DOX) nanoparticle for the combination therapy (chemotherapy combined with immunotherapy). Scanning electron microscopy showed that PEI/Gln/ß-CD/DOX nanoparticle was conical, with a diameter of about 250-500 nm. AS1411 aptamer-PD-L1 siRNA chimera can effectively bind NSCLC cells and inhibit PD-L1 expression, further activating T cells and CD8+T cells. Glutamine modification effectively promoted the doxorubicin uptake by cancer cells and induced their apoptosis. Animal experiments showed that our nanoparticles effectively treated the transplanted tumor, and the adverse reactions were reduced. Compared with the Aptamer/ß-CD/DOX group, the volume and ki-67 index of transplanted tumors in the Chimera/ß-CD/DOX group were significantly decreased, while the apoptosis ratio was increased. Immunohistochemical results showed that Compared with the Aptamer/ß-CD/DOX group, the number of T cells and CD8+T cells in the Chimera/ß-CD/DOX group was increased by 1.34 and 1.41 times. Glutamine modification enhanced the chemotherapeutic efficacy and anti-tumor immune response in vivo. Our study provided a new method for the combination therapy of lung squamous cell carcinoma.

Resection of rectal metastasis after previous radical surgery for pancreatic cancer: Case report and literature review.

RATIONALE: Pancreatic ductal adenocarcinoma (PDAC) is the main type of pancreatic cancer with a poor prognosis. Rectal metastasis after radical resection of PDAC is comparatively rare, and the understanding of such cases is currently not unified. This study presents the entire process of diagnosis and treatment of a patient with PDAC metastasized to the rectal. We propose the viewpoint of exploring potential biomarkers or establishing effective predictive models to assist in the clinical decision-making of such cases. PATIENT CONCERNS: We present the case of a 71-year-old man with slight abdominal distension and dull pain. He underwent surgical treatment for a malignant tumor of the pancreatic body, which was discovered through computed tomography and magnetic resonance imaging examinations. Nine months after the pancreatectomy, a rectal mass was identified by digital rectal examination and diagnosed as a malignant lesion through a puncture biopsy. After a multidisciplinary joint consultation, the patient underwent radical surgery. It was later confirmed as rectal adenocarcinoma based on postoperative pathological results. DIAGNOSIS: The pathological result after pancreatic surgery was PDAC, which had invaded the peripheral nerves and abdominal arteries. A diagnosis of rectal metastasis was determined ultimately by combining with the medical history and immunohistochemical staining results. INTERVENTIONS AND OUTCOMES: Treatment of the PDAC included laparoscopic resection of the body and tail of the pancreas combined with splenectomy, and postoperative systemic chemotherapy. In addition, treatment of the rectal metastasis included laparoscopic radical resection and postoperative systemic chemotherapy. The patient's current living condition was good. LESSONS: As a rare metastatic site of PDAC, rectal metastasis should be avoided because of misdiagnosis and missed diagnosis. Surgical resection is still an effective treatment strategy for localized pancreatic tumors and isolated metastases. Furthermore, the mining of potential biomarkers or the establishment of predictive models for pancreatic cancer and its metastases may contribute to better clinical decision-making in the future.

Effects of tumor-infiltrating lymphocytes on nonresponse rate of neoadjuvant chemotherapy in patients with invasive breast cancer.

High level of tumor-infiltrating lymphocytes (TILs) can predict the rate of total pathological complete remission (tpCR) of breast cancer patients who receive neoadjuvant chemotherapy (NACT). This study focused on evaluating the data of patients whose primary tumor and/or lymph node metastasis show nonresponse (NR) to NACT, trying to provide a basis for the clinical decision which patients will develop NACT resistance. The study included breast cancers from 991 patients who received NACT. ROC curve analysis confirmed that TILs showed significant predictive value for NR of hormone receptor (HR)+HER2- and triple-negative breast cancer (TNBC). Among HR+HER2- breast cancer, TILs ≥ 10% was an independent predictor for low NR rate. Furthermore, positive correlation of TILs with Ki67 index and Miller-Payne grade, and negative correlation with ER and PR H-scores were only identified in this subgroup. In TNBC, TILs ≥ 17.5% was an independent predictor for low NR rate. The predictive value of low TILs on NR may facilitate to screen patients with HR+HER2- or TNBC who may not benefit from NACT. HR+HER2- breast cancer with low levels of TILs should be carefully treated with neoadjuvant chemotherapy, and other alternatives such as neoadjuvant endocrine therapy can be considered.

Effects of intrathecally administered interferon α on chronic constriction injury model rats' mechanical pain threshold and G protein expression in the spinal cord.

INTRODUCTION: The aim of the study was to explore the analgesic mechanism of effects of intrathecally administered interferon a (IFN-a) on chronic constriction injury (CCI) model rats. MATERIAL AND METHODS: 24 rats were divided into 6 groups, with 4 rats in each group, including the negative control group (Group N, no operation or treatment), the sham operation group (Group S, only the left sciatic nerve of the rats was exposed without ligation, 0.9% NaCl was intrathecally administered), and four experimental groups (CCI model was established first and then different drugs were intrathecally administered respectively), including 0.9% NaCl (Group C), IFN-a (Group CI), morphine (Group CM), and IFN-a combined with morphine (Group CIM). The mRNA levels of G proteins in both the spinal cord and dorsal root ganglia (DRG), as well as the content of amino acid and chemokine (C-X-C motif) ligand 6 (CXCL-6) in the cerebrospinal fluid were measured and analysed in each group. RESULTS: Intrathecal administration of IFN-a increased the mechanical pain threshold in CCI rats (33.32 ±1.36 vs. 21.08 ±1.59, p < 0.001), achieving the effect comparable to that of morphine (33.32 ±1.36 vs. 32.44 ±3.18, p > 0.05), increased the mRNA expression level of Gi protein (0.62 ±0.04 vs. 0.49 ±0.05, p = 0.006), and decreased the mRNA expression level of Gs protein in the spinal cord (1.80 ±0.16 vs. 2.06 ±0.15, p = 0.035) and DRG (2.11 ±0.10 vs. 2.79 ±0.13, p < 0.001). The intrathecal administration of both IFN-a and morphine can reduce the glutamate content in the cerebrospinal fluid (261.55 ±38.12 vs. 347.70 ±40.69, p = 0.012), but without any statistically significant difference in the content of CXCL-6 across all groups ( p > 0.05). CONCLUSIONS: Intrathecal injection of IFN-a improved the mechanical pain threshold in CCI rats, so we inferred that intrathecal administration of IFN-a had analgesic effects on neuropathic pain, possibly related to the activation of G-proteincoupled µ receptors in the spinal cord and the inhibition of glutamate release.

Relationship among surface electric double layer of cardiomyocyte membrane and toxicology of digoxin and opening of ion channels.

We applied a new idea that the potential effect can change the ion adsorption structure on the cell surface to explore the mechanism of digoxin poisoning and the regulation of ion channels. The effects of digoxin on the electrophoretic mobility and behaviors (non-contraction or contraction or autorhythmicity) of cardiomyocytes were observed by single-cell electrophoresis technique (imitate the opening method of in vivo channel) and the method of decomposing surface potential components on the cells. As well as affect the association with electrical activity. The results suggested that the increase of cardiomyocytes transmembrane potential and the Na+-K+ exchange on the cell surface of the action potential phase 4 caused by the poisoning dose of digoxin, leading to the oscillation of adsorbed ions on the cell surface and the incomplete channel structure, which were the mechanism of cardiac ectopic beats. The results revealed that the opening of ion channels is regulated by the surface electric double layer of the cell membrane.

Health Effects of Probiotics on Nonalcoholic Fatty Liver in the Life Cycle Based on Data Analysis.

Objective: To observe the effect of intestinal probiotics in the treatment of nonalcoholic fatty liver disease (NAFLD) and the effect on liver function and inflammatory factors. Methods: 34 healthy rats were selected for the study and divided into 10 rats in the control group, 12 rats in the model group, and 12 rats in the treatment group according to the random number table method. The control group was given behavioral and lifestyle interventions, and the treatment group was given Bifidobacterium minus Black enteric capsules 5 g/(kg-d) by strong feeding method on the basis of the control group. The fatty liver index (FLI), liver ultrasound examination results, liver function, and inflammatory factor levels were compared among the three groups. After 8 weeks of treatment, there were statistically significant differences between the FLI values and liver ultrasound results of the three groups, and the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triacylglycerol (TG), and total cholesterol (TC) levels of the observation group were lower than those of the control group and the model group. The levels of serum high molecular weight lipocalin (HMW-APN) and interleukin 22 (IL-22) in the observation group were higher than those in the control group, and the levels of tumor necrosis factor-α (TNF-α) were lower than those in the control and model groups, and the differences were statistically significant (P < 0.05). Conclusion: Intestinal probiotics can improve the clinical efficacy of patients with NAFLD, improve liver function, and alleviate the inflammatory response, in order to provide a theoretical basis for the clinical treatment of patients with NAFLD.

Production of functional recombinant prolyl hydroxylase-2 enzyme in insect cells for small molecule inhibitor screening studies.

Prolyl hydroxylase-2 (PHD2) is a dioxygenase enzyme that specifically hydroxylates the hypoxia inducible factor (HIF) which then targets it for degradation in oxygenated cells. Inhibition of the activity of the PHD2 enzyme under hypoxic environmental conditions acts to upregulate HIF. Thus, PHD2 inhibitors may serve as a promising treatment for HIF-dependent diseases. In this study, recombinant PHD2 protein was successfully expressed using a baculovirus-insect cell expression secretory system. PHD2 was purified and in combination with bacterially expressed functional von Hippel Lindau protein-elongin B-elongin C (VBC) protein complex was used to successfully develop a fluorescence-based PHD2 activity assay. Myricetin was identified as a novel potent PHD2 inhibitor by high-throughput screening of a natural compound library. Further studies showed that treatment of human neuroblastoma SH-SY5Y cells with Myricetin increased HIF-1α protein levels. These results indicate that the insect cell expression system is capable of producing highly active recombinant PHD2 protein from which a fluorescence-based activity assay can be developed for high-throughput screening applications.

Instant hydrogelation encapsulates drugs onto implants intraoperatively against osteoarticular tuberculosis.

Osteoarticular Tuberculosis (TB) is a challenging issue because of its chronicity and recurrence. Many drug delivery systems (DDSs) have been developed for general chemotherapy. Herein, we take advantage of instant hydrogelation to in situ encapsulate drugs onto implants intraoperatively, optimizing the drug release profile against osteoarticular TB. First-line chemodrugs, i.e. rifampicin (RFP) and isoniazid (INH) are firstly loaded on tricalcium phosphate (TCP). Then, the encapsulating hydrogel is fabricated by dipping in chitosan (CS) and ß-glycerophosphate (ß-GP) solution and heating at 80 °C for 40 min. The hydrogel encapsulation inhibits explosive drug release initially, but maintains long-term drug release (INH, 158 days; RFP, 53 days) in vitro. Therefore, this technique could inhibit bone destruction and inflammation from TB effectively in vivo, better than our previous ex situ prepared DDSs. The encapsulating technology, i.e. instant hydrogelation of drug-loaded implants, shows potential for regulating the type and ratio of drugs, elastic and viscous modulus of the hydrogel according to the state of illness intraoperatively for optimal drug release.

New understanding of electrical activity brought by surface potential of cardiomyocytes.

Aiming at the problem encountered in the previous research: during the electrical activity of cardiomyocytes, the influent ions do not seem to be directly derived from the extracellular fluid. We chose to cut in from the colloidal properties of the cells, follow the basic principles of physical chemistry, and establish hypotheses along the derivation of the structural characteristics of cardiomyocytes. Through the surface ion adsorption experiment and patch clamp experiment of living cells, under the condition of sequentially reducing the concentration of Na+ in the extracellular fluid, we observed the exchange and diffusion of adsorbed ions on the cell surface; the changes of inflow INa, ICa-L and action potential; and correlation between results. The results showed that the hypothesis is true. The observed parameter changes were consistent with the fact that during depolarization of cardiomyocytes, the ions of influx were derived from the inference of adsorbed ions on the cell surface; at the same time, it also provided an objective and realistic explanation for the generation of electrocardiogram.

Esomeprazole inhibits the lysosomal cysteine protease legumain to prevent cancer metastasis.

Legumain is a newly discovered lysosomal cysteine protease that can cleave asparagine bonds and plays crucial roles in regulating immunity and cancer metastasis. Legumain has been shown to be highly expressed in various solid tumors, within the tumor microenvironment and its levels are directly related to tumor metastasis and poor prognosis. Therefore, legumain presents as a potential cancer therapeutic drug target. In this study, we have identified esomeprazole and omeprazole as novel legumain small molecule inhibitors by screening an FDA approved-drug library. These compounds inhibited enzyme activity of both recombinant and endogenous legumain proteins with esomeprazole displaying the highest inhibitory effect. Further molecular docking analysis also indicated that esomeprazole, the S- form of omeprazole had the most stable binding to legumain protein compared to R-omeprazole. Transwell assay data showed that esomeprazole and omeprazole reduced MDA-MB-231 breast cancer cell invasion without effecting cell viability. Moreover, an in vivo orthotopic transplantation nude mouse model study showed that esomeprazole reduced lung metastasis of MDA-MB-231 breast cancer cells. These results indicated that esomeprazole has the exciting potential to be used in anti-cancer therapy by preventing cancer metastasis via the inhibition of legumain enzyme activity. Graphical abstract.

Inhibition of notch enhances the anti-atherosclerotic effects of LXR agonists while reducing fatty liver development in ApoE-deficient mice.

Liver X receptor (LXR) activation can achieve satisfactory anti-atherosclerotic activity, but can also lead to the development of fatty liver and hypertriglyceridemia. In contrast, Notch inhibition can suppress both atherosclerosis and the hepatic accumulation of lipids. In the present study, we sought to assess whether combining LXR ligand agonists (T317) with Notch receptor inhibitors (DAPT) would lead to enhanced anti-atherosclerotic activity while overcoming the adverse events associated with LXR ligand agonist therapy. The impact of the combined T317 + DAPT therapeutic regimen on atherosclerosis, fatty liver development, and hypertriglyceridemia was assessed using ApoE deficient (ApoE-/-) mice. The results of this analysis suggested that DAPT was able to improve the anti-atherosclerotic activity of T317 without reducing the stability of lesion plaques while simultaneously reducing blood lipids in treated ApoE-/- mice. This combination T317 + DAPT treatment was also linked with a significant upregulation of ABCA1 and the stimulation of reverse cholesterol transport (RCT), as well as with decreases in the levels of intercellular cell adhesion molecule-1 (ICAM-1) and p-p65, and with altered M1/M2 macrophage proportions within atherosclerotic plaques. Importantly, DAPT was also able to reduce T317-mediated lipid accumulation within the liver owing to its ability to reduce SREBP-1 expression while simultaneously increasing that of Pi-AMPKα and PPARα. Together, our results suggest that administering Notch receptor inhibitors to ApoE-/- mice may be an effective means of enhancing the anti-atherosclerotic activity of LXR ligand agonists while simultaneously limiting associated fatty liver and hypertriglyceridemia development in these animals.

Anti-Rheumatic Properties of Gentiopicroside Are Associated With Suppression of ROS-NF-κB-NLRP3 Axis in Fibroblast-Like Synoviocytes and NF-κB Pathway in Adjuvant-Induced Arthritis.

Rheumatoid arthritis (RA) is among the most prevalent forms of autoimmunity. Gentiopicroside (Gent) is an iridoid glucoside derived from the Gentiana Macrophylla Pall which is used in traditional Chinese medicine to treat RA. The present study was designed to explore the ability of Gent to combat RA and to explore the molecular basis for such anti-RA activity both in vitro using tumor necrosis factor alpha (TNF-α)-stimulated human RA fibroblast-like synoviocytes (RA-FLS) and in vivo using a rat adjuvant-induced arthritis (AIA) model. We found that Gent was able to significantly reduce the swelling of joints and arthritic index scores, with corresponding reductions in synovial inflammatory cell infiltration, synovial hyperplasia, and bone erosion in treated AIA rats. Importantly, Gent 200 mg/kg reduced thymus index in AIA rats, but had no effect on spleen index and body weight, it revealed that Gent was relatively safe at the dose we chose. We further found that Gent was able to suppress the TNF-α-induced proliferation and migration of RA-FLS cells. This suppression was attributed to the ability of Gent to block NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), and caspase-1, thereby disrupting the activation of the NLRP3 inflammasome. Consistent with such suppression, Gent led to a significant decrease in IL-1ß secretion by treated cells. Furthermore, this reduction in NLRP3 inflammasome activation was also associated with decreases in the activation of nuclear factor (NF-κB), the production of reactive oxygen species (ROS), and the expression of inflammatory IL-6. Together these findings indicate that Gent can suppress the ROS-NF-κB-NLRP3 axis to alleviate RA symptoms. CHEMICAL COMPOUNDS STUDIED IN THIS ARTICLE: Gentiopicroside (PubChem CID: 88708).

An intelligent vancomycin release system for preventing surgical site infections of bone tissues.

Preventing surgical site infections (SSIs) of implants has drawn significant attention in both basic and clinical research. Implants with convenient preparation methods and intelligent drug release capabilities are highly needed to resist bacterial infection. Herein, we designed an intelligent drug-release system, which can be instantly incorporated with implants during the surgical process. The drug-release system involves ß-glycerophosphate (ß-GP) and chitosan (CS) as a thermosensitive hydrogel for instant construction onto implants and hyaluronic acid (HA) as a trigger to release vancomycin hydrochloride (VH) on demand. Tertiary calcium phosphate (TCP) scaffolds (implants) are vacuum-adsorbed in a solution of the intelligent vancomycin-release system (VH-HA-CS/ß-GP), followed by heating for 40 min at 80 °C to form VH-HA-CS/ß-GP@TCP. The drug-release hydrogel intelligently releases vancomycin depending on the concentration of hyaluronidase, which is secreted by Staphylococcus aureus (S. aureus) in infection sites. Furthermore, VH-HA-CS/ß-GP@TCP showed effective antibacterial properties in vitro and in vivo. The VH-HA-CS/ß-GP drug-release system can be conveniently prepared during surgery for intelligently preventing SSIs in bone tissue.

Screening and identification of serum biomarkers of osteoarticular tuberculosis based on mass spectrometry.

BACKGROUND: In view of the current difficulty of clinically diagnosing osteoarticular tuberculosis, our aim was to use mass spectrometry to establish diagnostic models and to screen and identify serum proteins which could serve as potential diagnostic biomarkers for early detection of osteoarticular tuberculosis. METHODS: Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was used to select an osteoarticular tuberculosis-specific serum peptide profile and establish diagnostic models. Further, liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to identify potential serum biomarkers that could be used for auxiliary diagnosis of osteoarticular tuberculosis, and then clinical serum samples were used to verify these biomarkers by enzyme-linked immunosorbent assay (ELISA). RESULTS: We established four diagnostic models that can distinguish osteoarticular tuberculosis from rheumatoid arthritis, ankylosing spondylitis, osteoarticular infections, and healthy adults. The models were osteoarticular tuberculosis-rheumatoid arthritis, osteoarticular tuberculosis-ankylosing spondylitis, osteoarticular tuberculosis-osteoarticular infections, and osteoarticular tuberculosis-healthy adult, and their accuracy was 76.78%, 79.02%, 83.77%, and 88.16%, respectively. Next, we selected and identified 18 proteins, including complement factor H-related protein 1 (CFHR1) and complement factor H-related protein 2 (CFHR2), which were upregulated in the tuberculosis group only. CONCLUSIONS: We successfully established four diagnostic models involving osteoarticular tuberculosis, rheumatoid arthritis, ankylosing spondylitis, osteoarticular infections, and healthy adults. Furthermore, we found that CFHR1 and CFHR2 may be two valuable auxiliary diagnostic indicators for osteoarticular tuberculosis. These results provide reference values for rapid and accurate diagnosis of osteoarticular tuberculosis.

Network Pharmacology Based Research on the Combination Mechanism Between Escin and Low Dose Glucocorticoids in Anti-rheumatoid Arthritis.

Rheumatoid arthritis (RA) is characterized by chronic progressive symmetrical synovitis and destruction of multiple joints. Glucocorticoids (GCs) are widely used in the treatment of RA. However, their adverse effects can be serious. Escin, which is isolated from Aesculus hippocastanum L., has been reported to have anti-inflammatory effects. We investigated the anti-RA effect of Escin combined with low dose GCs (dexamethasone, Dex) and the underlying mechanism. Adjuvant-induced RA rats and lipopolysaccharides (LPS)-injured RAW264.7 cells were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. The results showed that Escin combined with low-dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α levels, reduced paw swelling, and ameliorated the joint pathology and immune organ pathology. Gene chip results revealed that Nr3c1 (GR) expression was significantly altered, and that GR was activated by Escin and low dose Dex in vivo and in vitro. Additionally, Escin combined with low dose Dex also significantly increased GR mRNA expression. However, when GR expression was suppressed by its specific inhibitor, the anti-RA effect of Escin combined with low-dose Dex was abolished. The data in this study demonstrated that Escin combined with Dex reduced the dose of Dex, and exerted significant anti-RA effects, which could also reduce the adverse effects of Dex. This combination might result from GR activation. This study might provide a new combination of drugs for the treatment of RA.

Determination of the damage growth threshold of multilayer dielectric gratings by picosecond laser pulses based on saturation damage size analysis.

We propose two efficient methods of determining damage growth threshold (DGT) based on the saturation damage size analysis (SDSA) for multilayer dielectric gratings by picosecond pulsed lasers. The damage size at laser fluences above DGT increases with the shot number and finally saturates due to the Gaussian focal spot. The DGT is extracted by mapping the boundary of a saturation damage site obtained at single fluence to the beam profile, which is called the monofluence SDSA method. Meanwhile, the saturation damage size decreases when reducing laser fluence. The fitting and extrapolation of the saturation damage sizes at different fluences are also useful to accurately determine the DGT, which is called the multifluence SDSA method. Although the saturation damage site is asymmetric, the DGTs measured with two SDSA methods are almost identical for the same axis, and both are in very good agreement with those obtained with the growth probability method. The underlying mechanisms and advantages of two SDSA methods are extensively discussed. The consistence of two SDSA methods in determining DGT is attributed to the same morphology of the initial damage and the saturation damage boundary, as well as the local damage dynamics. The relation of the lifetime damage threshold and DGT obtained with the SDSA method is also revealed.

Asymmetrical damage growth of multilayer dielectric gratings induced by picosecond laser pulses.

We experimentally investigated the laser damage growth behavior of multilayer dielectric gratings (MLDGs) by the picosecond pulses at 1053nm. The damage growth threshold of 2.43J/cm2 is significantly lower than the 20/1 damage threshold of 3.06 J/cm2. Once the damage site is initiated, the damage area grows linearly with shot number and saturates after sufficient shots due to the Gaussian spot. The barycenter of the growing damage site deviates from the laser spot center and their distance increases with the shot number, which indicates the asymmetry of the damage growth along the laser propagation axis. The growth rate of the damage site along the laser propagation direction is larger than that in the reverse direction by a factor of ~1.8 for various fluences. The comparison of the experimental and numerical results reveals that the asymmetrical intensity modulation induced by the damage sites causes the asymmetry in growth. The revealed characteristics and mechanisms of the damage growth can be of great significance to predict the lifetime of the MLDGs in high-power laser systems.

One-pot synthesis of single-crystal Pt nanoplates uniformly deposited on reduced graphene oxide, and their high activity and stability on the electrocalalytic oxidation of methanol.

We demonstrate a one-pot thermoreduction approach towards the preparation of single-crystal Pt nanoplates, which were uniformly deposited on the reduced graphene oxide (RGO) using polyvinylpyrrolidone (PVP) as a stabilizer. The size of Pt nanoplates can be tuned from 6.8 to 10.1 nm by controlling Pt loading. The as-prepared Pt/PVP/RGO catalysts show high stability and activity towards the methanol oxidation reaction (MOR). Their MOR current can reach up to 401 mA mg(-1) Pt and MOR current can maintain 89.4% of its initial value after 10 000 potential cycles.

Synthesis of graphene-supported one-dimensional nanoporous Pt based catalysts, and their enhanced performance on methanol electro-oxidation.

A novel approach is developed to synthesize PtIr or Pt nanowires (NWs) supported on the reduced graphene oxide (RGO) using Te NWs as template based on the replacement reaction. The resulting RGO-supported PtIr and Pt electrocatalysts are characterized by transmission electron microscopy (TEM), energy-dispersive x-ray spectroscopy and electrochemical techniques. TEM images show that these Pt based catalysts are uniformly distributed in the matrix of graphene with a characteristic of one-dimensional (1D) nanoporous structure. As one of promising anode materials used in the direct methanol fuel cells, these 1D nanoporous PtIr/RGO (or Pt/RGO) hybrids exhibit an enlarged electroactive surface and enhanced catalytic activity toward the methanol reaction relative to those PtIr or Pt NWs without graphene support.

Facile preparation of ultralong dendritic PtIrTe nanotubes and their high electrocatalytic activity on methanol oxidation.

A facile wet chemical approach was developed to prepare ultralong PtIrTe nanotubes (NTs) using Te nanowires (NWs) as template. These PtIrTe NTs were made up of Pt nanodendrites uniformly arrayed on the surface of IrTe NTs and interweaved with each other to nanopores. Their morphology, structure, and composition were investigated by transition electron microscopy, X-ray powder diffraction, and X-ray photoelectron spectroscopy. As expected, these PtIrTe NTs catalysts show a larger surface area, a stronger CO tolerance, and a higher catalytic activity toward electrochemical oxidation of methanol relative to the commercial Pt catalysts due to the 1D porous core-shell structure and the modification of the electronic effect by Ir.