Crystalline Phase Engineering to Modulate the Interfacial Interaction of the Ruthenium/Molybdenum Carbide for Acidic Hydrogen Evolution.

Ruthenium (Ru) is an ideal substitute to commercial Pt/C for the acidic hydrogen evolution reaction (HER), but it still suffers from undesirable activity due to the strong adsorption free energy of H* (ΔGH*). Herein, we propose crystalline phase engineering by loading Ru clusters on precisely prepared cubic and hexagonal molybdenum carbide (α-MoC/ß-Mo2C) supports to modulate the interfacial interactions and achieve high HER activity. Advanced spectroscopies demonstrate that Ru on ß-Mo2C shows a lower valence state and withdraws more electrons from the support than that of Ru on α-MoC, indicative of a strong interfacial interaction. Density functional theory reveals that the ΔGH* of Ru/ß-Mo2C approaches 0 eV, illuminating an enhancement mechanism at the Ru/ß-Mo2C interface. The resultant Ru/ß-Mo2C exhibits an encouraging performance in a proton exchange membrane water electrolyzer with a low cell voltage (1.58 V@ 1.0 A cm-2) and long stability (500 h@ 1.0 A cm-2).

Maize ZmHSP90 plays a role in acclimation to salt stress.

Background: Maize is sensitive to salt stress, especially during the germination and seedling stages. Methods: We conducted germination experiments on 60 maize materials under salt stress, and screened out the most salt-tolerant and salt-sensitive varieties based on germination indicators. Afterwards, transcriptome analysis was performed to screen for key regulators in the plumule and flag leaf at the germination and seedling stages, respectively. Following that, transgenic tobacco was developed to expose the roles and mechanisms of the candidate genes, enabling a deeper investigation of their functions. Results: Out of the 60 inbred lines of maize, "975-12" exhibits the highest level of salt tolerance, while "GEMS64" displays the lowest. The application of salt stress resulted in a significant increase in the levels of antioxidant enzymes in both "975-12" and "GEMS64". ABA signal transduction and jasmonic acid pathways were the pathways that mainly affected by salt stress. In addition, a significant finding has been made indicating that when exposed to high levels of salt stress, the expression of ZmHSP90 in '975-12' increased while in 'GEMS64' decreased. Furthermore, in tobacco plants overexpressing ZmHSP90, there was an increase in antioxidant enzyme activity associated with salt tolerance. ZmHSP90 enhanced the expression levels of NtSOS1, NtHKT1, and NtNHX1 as compared to those in the salt treatment, causing the maintenance of Na+ and K+ homeostasis, suggesting that high expression of ZmHSP90 was conducive to regulate Na+ transporters to maintain K+/Na+ balanced in tobacco.

Overall Design of Anode with Gradient Ordered Structure with Low Iridium Loading for Proton Exchange Membrane Water Electrolysis.

Insufficient catalyst utilization, limited mass transport, and high ohmic resistance of the conventional membrane electrode assembly (MEA) lead to significant performance losses of proton exchange membrane water electrolysis (PEMWE). Herein we propose a novel ordered MEA based on anode with a 3D membrane/catalytic layer (CL) interface and gradient tapered arrays by the nanoimprinting method, confirmed by energy dispersive spectroscopy. Benefiting from the maximized triple-phase interface, rapid mass transport, and gradient CL by overall design, such an ordered structure with Ir loading of 0.2 mg cm-2 not only greatly increases the electrochemical active area by 4.2 times but also decreases the overpotentials of both mass transport and ohmic polarization by 13.9% and 8.7%, respectively, compared with conventional MEA with an Ir loading of 2 mg cm-2, thus ensuring a superior performance (1.801 V at 2 A cm-2) and good stability. This work provides a new strategy of designing MEA for high-performance PEMWE.

Mechanism of Abnormal Coagulation Induced by Tigecycline in Cancer Patients.

Tigecycline is a broad-spectrum active intravenous antibiotic that is active against methicillin-resistant staphylococcus aureus. In Phase 3 and 4 clinical trials, increased all-cause mortality was observed in patients treated with tigecycline compared to patients in the control group. The reason for the increase is unclear. In this study, we found that tigecycline cause abnormal coagulation in tumor patients, especially in patients with hematological malignancies. The main manifestations were decreased fibrinogen and prolonged activated prothrombin time (APTT), thrombin time (TT), and D-dimer. In addition, through functional studies, we found that tigecycline inhibit platelet adhesion and aggregation, and the coagulation function of patients gradually recover after discontinuation. Gene sequencing results suggested that tigecycline significantly regulate the expression of genes related to platelet function pathways and increase the incidence of single nucleotide polymorphisms and the number of alternative splices in the Chinese hamster ovary (CHO) cells treated with tigecycline. An abnormal function and low numbers of platelets are common in patients with hematological malignancies. Our study can explain the mechanism of abnormal coagulation caused by tigecycline. Additionally, doctors who apply tigecycline to cure infections in tumor patients should be warned.

Hemolymphangioma with multiple hemangiomas in liver of elderly woman with history of gynecological malignancy: A case report.

BACKGROUND: Hepatic hemolymphangioma is an extremely rare benign congenital malformation composed of cystically dilated lymphatic and blood vessels, and they have nonspecific clinical symptoms and laboratory results. In this study, hepatic hemolymphangioma with multiple hemangiomas in an elderly woman was initially reported and analyzed. CASE SUMMARY: A 61-year-old female patient, with a history of hysterectomy and bilateral adnexectomy, was referred to the hepatobiliary surgery department with the complaint of multiple hepatic hemangiomas that had been diagnosed 2 years prior in a preoperative contrast-enhanced computed tomography (CECT) examination. Upon entering our hospital, no abnormal physical examination and laboratory data were found. The latest CECT revealed a new 7.0 cm × 6.2 cm cystic-solid lesion with multiple internal divisions in segment II of the liver, with delayed CECT enhancement characteristics that presented as solid parts with internal division. On the positron emission tomography (PET)/CT, no significant uptake of 18F-fluorodeoxyglucse was observed. Finally, hepatic hemolymphangioma was confirmed based on the pathological and immunohistochemical results after surgery. At 1-year follow-up, her posthepatectomy evaluation was uneventful, and she had recovered full activity. In addition, no postoperative recurrent or residual lesion was found on CECT imaging. CONCLUSION: Hepatic hemolymphangioma with multiple hemangiomas was reported and observed by CECT and PET/CT imaging.

Electrochemical Reduction of CO2 to HCOOH over Copper Catalysts.

Although great progress has been made in the field of electrochemical CO2 reduction reaction (eCO2RR), inducing product selectivity is still difficult. We herein report that a thiocyanate ion (SCN-) switched the product selectivity of copper catalysts for eCO2RR in an H-cell. A cuprous thiocyanate-derived Cu catalyst was found to exhibit excellent HCOOH selectivity (faradaic efficiency = 70-88%) over a wide potential range (-0.66 to -0.95 V vs RHE). Furthermore, it was revealed that the formation of CO and C2H4 over commercial copper electrodes could be dramatically suppressed with the presence of SCN-, switching to HCOOH. Density functional theory calculations disclosed that SCN- made the formation of HCOO* easier than COOH* on Cu (211), facilitating the HCOOH generation. Our results provide a new insight into eCO2RR and will be helpful in the development of cheap electrocatalysts for specific utilization.

A sensor of liquid methanol for direct methanol fuel cells.

The methanol sensors are of significance to maintain the efficient and stable operation of direct methanol fuel cells (DMFCs). The issues, including stability, the relationship between temperature, current density and concentration need, however, urgent attention. A novel electrochemical methanol sensor which is based on current output limited by methanol diffusion is developed. The stability of sensors was lifted steeply through introducing a reference electrode, narrowing the methanol flow channel, and adding a water container. The relationship between the temperature, response current and methanol concentration was determined with the help of theoretical derivation and the validity was verified by the fitting result. Other sensors can avail of this relationship to correct the temperature effect. Application test indicated that the sensor may be of great potential for the accurate monitoring of methanol concentration at the levels of DMFCs application.

Ozone induces tolerance against cardiomyocytes oxygen-glucose deprivation/reperfusion through inhibition of autophagy pathway.

Previous studies have reported that excess activation of autophagy in cardiomyocytes is associated with an increase in myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury. Ozone therapy affords significant cardio-protection against myocardial OGD/R injury. The present study was designed to determine whether ozone-induced tolerance to myocardial OGD/R injury was mediated by inhibiting autophagy. Subsequently, the rat cardio myoblast H9C2 cell line was used in the present study. A model of H9C2 cells under OGD/R was established. The cells were incubated with different concentrations of ozone (10-60 µg/ml) during reperfusion. Furthermore, to investigate the role of autophagy in OGD/R-induced injury, the autophagy inducer and inhibitor were applied. Cell viability was detected by Cell Counting kit-8 assay. Cell apoptosis was evaluated by flow cytometry. Oxidative stress was examined by superoxide dismutase, lactate dehydrogenase and malondialdehyde levels. The expressions of apoptosis regulator B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (BAX), cleaved caspase-3, markers of autophagy microtuble-associated protein 1 light chain 3 (LC3), autophagy-related protein 5 (Atg5) and Beclin-1 were measured by western blot analysis. As a result, OGD/R notably decreased cell viability and induced apoptosis in H9C2 cells, while ozone (10-40 µg/ml) reversed the noxious effects of OGD/R on H9C2 cells, and 20 µg/ml ozone was the most effective. Ozone inhibited the decrease in the ratio of Bcl-2/BAX and the expression of cleaved caspase-3, and inhibited the increase in the ratio of LC3-II/LC3-I and the expression of Atg5 and Beclin-1 elicited by OGD/R, as well as dose-dependently preventing OGD/R-induced oxidative stress. Furthermore, rapamycin markedly reversed the effects of ozone (20 µg/ml) on OGD/R-induced expression of autophagy marker proteins and 3-methyladenine further improved the effect of ozone. Taken together, the results of the present study provided a credible mechanism by which ozone treatment at low concentrations could protect the myocardium from OGD/R-induced injury by inhibiting autophagy.

Ozone Attenuated H9c2 Cell Injury Induced by Doxorubicin.

ABSTRACT: Doxorubicin (DOX) is a commonly used drug in the treatment of cancers, whereas its application in the clinical stage is restricted because of side effects such as cardiomyocyte injury. Increasing studies indicated that ozone may protect cardiomyocytes from injuries. This study aimed to explore the effects of ozone on cardiotoxicity induced by DOX treatment. Rat heart myoblasts (H9c2) were treated with increasing concentrations of DOX (0.5, 1, 1.5, and 2 µM) to induce cell injury. 3-(4,5)-dimethylthiahiazo(-2)-3,5-diphenytetrazoliumromide assay and flow cytometry analysis were used to measure the viability and apoptosis of H9c2 cells. The mRNA and protein levels of proinflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-(IL)1ß, and IL-6, matrix metalloproteinases (MMP-2 and MMP-9), and the key factors on the TLR4/NF-kB signaling (TLR4, p-p65, and p65) were measured by reverse transcription quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, and western blot. The result showed that DOX promoted apoptosis and increased the expression of TNF-α (by 3.65-fold changes), IL-1ß (by 4.98-fold changes), IL-6 (by 3.44-fold changes), MMP-2 (by 1.98-fold changes), and MMP-9 (by 1.98-fold changes) levels in H9c2 cells. Moreover, the introduction of ozone reversed these changes in gene expression and suppressed the activation of the TLR4/NF-kB signaling, which indicated that ozone may exert protective effects on H9c2 heart myoblasts by relieving the cardiotoxicity induced by DOX. Our study provides theoretical basis for the significance of ozone in managing doxorubicin-induced H9c2 heart myoblast injury.

Evaluation of microRNAs as potential biomarkers in circulating HPV-DNA-positive non-small cell lung cancer patients.

The aim of the present study was to identify the potential risk of circulating-HPV-DNA in non-small cell lung cancer (NSCLC) and to analyze abnormally expressed miRNAs in circulating HPV-DNA-positive NSCLC. HPV universal primers were used to detect the presence of HPV-DNA in the peripheral blood of 100 patients with NSCLC. The relationship between circulating-HPV-DNA and NSCLC patients characteristics was analyzed. Then, eight differentially expressed miRNAs in NSCLC were screened based on the TCGA database. The levels of miRNAs in circulating HPV-DNA-positive NSCLC patients were detected by real-time quantitative PCR. ROC curves were generated to evaluate the diagnostic performance. Circulating-HPV-DNA was found in 16 patients. The proportion of HPV-DNA-positive patients with poorly differentiated NSCLC, advanced lung cancer and lymph node metastasis was higher than that of HPV-DNA-negative patients. The levels of miR-183, miR-210 and miR-182 were significantly higher and miR-144 was significantly lower in HPV-DNA-positive NSCLC than those in HPV-DNA-negative NSCLC patients. When using a single miRNA to identify circulating HPV-DNA-positive NSCLC patients, miR-210 had a higher area under the ROC curve (AUC) than other miRNAs, and its sensitivity and specificity were also higher. In addition, the combination of two miRNAs was more effective than a single miRNA. Among them, miR-210+ miR-144 had the highest AUC value and showed the best prediction performance. Circulating-HPV-DNA may serve as a risk factor in NSCLC. Plasma miR-183, miR-210, miR-182 and miR-144 can be used as reliable biomarkers to identify circulating HPV-DNA-positive NSCLC.

[Mycoplasma pneumoniae toxin of community-acquired respiratory distress syndrome (CARDS) promotes autophagy of THP-1 cells and activates NLRP3 inflammasomes].

Objective To study the mechanism of community-acquired respiratory distress syndrome (CARDS) toxin of Mycoplasma pneumoniae (Mp) inducing THP-1 cell autophagy and the activation of pyrin domain containing the nucleotide-binding oligomerization domain-like receptor family 3 (NLRP3). Methods The recombinant CARDS (rCARDS) Mp toxin was obtained by Escherichia coli expression system, and THP-1 cells were treated with the toxin at the concentrations of 5 and 10 µg/mL for 20, 40 minutes, 1, 2 and 3 hours. The expression of autophagy-related proteins beclin-1, LC3II and P62 of THP-1 cells were determined by Western blot; the gene expression of NLRP3, caspase-1 and interleukin 1ß (IL-1ß) were detected by real-time quantitative PCR; and the level of reactive oxygen species (ROS) of THP-1 cells was tested by DCFH-DA staining. Results Compared with the control group, when treated with rCARDS toxin for 1 hour, the expression of beclin-1, LC3 and P62 significant increased. When treated with rCARDS toxin for 2 and 3 hours, the expression of beclin-1, LC3 and P62 significant decreased. When treated with rCARDS toxin for 20 and 40 minutes, the NLRP3 gene expression had no significant difference between the groups treated with the concentration of 5 and 10 µg/mL rCARDS toxin. NLRP3 gene expression in the groups treated with rCARDS toxin was higher than that in the control group in the whole experiment. When treated with rCARDS toxin for 1 hour and 2 hours, the NLRP3 gene expression of the 10 µg/mL group was significant higher than that in the 5 µg/mL group. When treated with rCARDS toxin for 3 hours, the NLRP3 gene expression of the 10 µg/mL group and 5 µg/mL group was lower than that in the groups treated for 2 hours. When treated with rCARDS toxin for 40 minutes, 1 hour and 2 hours, the caspase-1 mRNA expression of rCARDS toxin groups was higher than that in the control group. When treated for 40 minutes, 1, 2 and 3 hours, the caspase-1 gene expression of the 10 µg/mL group was significantly higher than that in the 5 µg/mL group. Compared to the control group, when treated with rCARDS toxin for 20 and 40 minutes, IL-1ß gene expression had no significant difference. When the time prolonged to 1 hour and 3 hours, the levels of IL-1ß mRNA expression and ROS had a significant increase in a dose-dependent manner in all groups. Conclusion CARDS Mp toxin can activate NLRP3 inflammasomes and induce cell autophagy in THP-1 cells.

Carbon-Defect-Driven Electroless Deposition of Pt Atomic Clusters for Highly Efficient Hydrogen Evolution.

Pt atomic clusters (Pt-ACs) display outstanding electrocatalytic performance because of their unique electronic structure with a large number of highly exposed surface atoms. However, the small size and large specific surface area intrinsically associated with ACs pose challenges in the synthesis and stabilization of Pt-ACs without agglomeration. Herein, we report a novel one-step carbon-defect-driven electroless deposition method to produce ultrasmall but well-defined and stable Pt-ACs supported by defective graphene (Pt-AC/DG) structures. A theoretical simulation clearly revealed that the defective regions with a lower work function and hence a higher reducing capacity compared to those of normal hexagonal sites triggered the reduction of Pt ions preferentially at the defect sites. Moreover, the strong binding energy between Pt and carbon defects effectively restricted the migration of spontaneously reduced Pt atoms to immobilize/stabilize the resultant Pt-ACs. Electrochemical analyses demonstrated the high performance of Pt-ACs in catalyzing the hydrogen evolution reaction, showing a greatly enhanced mass activity, a high Pt utilization efficiency, and excellent stability compared with commercial Pt/C catalysts. The integration of proton exchange membrane water electrolysis with Pt-AC/DG as a cathode exhibited an excellent hydrogen generation activity and extraordinary stability (during 200 h of electrolysis) with a greatly reduced Pt usage compared with commercial Pt/C catalysts.

The function of miRNA­153 against isoflurane­induced neurotoxicity via Nrf2/ARE cytoprotection.

The present study aimed to investigate the function of micro (mi)RNA­153 against isoflurane­induced neurotoxicity and its mechanism. In isoflurane­induced mice, miRNA­153 expression was downregulated compared with in the control group. Downregulation of miRNA­153 induced neurocyte apoptosis, reduced cell growth and promoted oxidative stress in an in vitro model. Overexpression of miRNA­153 reduced oxidative stress, promoted cell growth and inhibited neurocyte apoptosis within an in vitro model. Downregulation of miRNA­153 suppressed nuclear erythroid­2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway, which was induced via the overexpression of miRNA­153 in vitro. The Nrf2 agonist, dimethyl fumarate (2.5 µM), induced the Nrf2/ARE signaling pathway and reduced oxidative stress to induce neurocyte apoptosis in vitro following treatment with anti­miRNA­153. The results of the present study suggested the function of miRNA­153 against neurotoxicity via Nrf2/ARE­mediated cytoprotection.

Controllable synthesis of titanium nitride nanotubes by coaxial electrospinning and their application as a durable support for oxygen reduction reaction electrocatalysts.

Chemical and electrochemical corrosion of a support limits the corresponding catalyst's performance and lifetime. In this paper, uniform TiN nanotubes are synthesized via coaxial-electrospinning, thermal oxidation and nitridation. The average diameter of nanotubes can be facilely controlled by tuning the parameters of coaxial electrospinning. The TiN nanotubes are modified further with Pt nanoparticles as Pt/TiN NT electrocatalysts. After accelerated durability tests, the electrochemical surface area (ECSA) and mass activity of the Pt/TiN decrease by only 6% and 14% respectively, while those of the Pt/C decrease by 44% and 46.2% respectively. The enhanced activity is attributed to the strong interaction between the Pt nanoparticles and the TiN support, which is confirmed by the X-ray dispersive spectra of Pt 4f.

Study on the Mechanism of mTOR-Mediated Autophagy during Electroacupuncture Pretreatment against Cerebral Ischemic Injury.

This study is aimed at investigating the association between the electroacupuncture (EA) pretreatment-induced protective effect against early cerebral ischemic injury and autophagy. EA pretreatment can protect cerebral ischemic and reperfusion injuries, but whether the attenuation of early cerebral ischemic injury by EA pretreatment was associated with autophagy is not yet clear. This study used the middle cerebral artery occlusion model to monitor the process of ischemic injury. For rats in the EA pretreatment group, EA pretreatment was conducted at Baihui acupoint before ischemia for 30 min for 5 consecutive days. The results suggested that EA pretreatment significantly increased the expression of autophagy in the cerebral cortical area on the ischemic side of rats. But the EA pretreatment-induced protective effects on the brain could be reversed by the specific inhibitor 3-methyladenine of autophagy. Additionally, the Pearson correlation analysis indicated that the impact of EA pretreatment on p-mTOR (2481) was negatively correlated with its impact on autophagy. In conclusion, the mechanism of EA pretreatment at Baihui acupoint against cerebral ischemic injury is mainly associated with the upregulation of autophagy expression, and its regulation of autophagy may depend on mTOR-mediated signaling pathways.

Plasmonic Pd Nanoparticle- and Plasmonic Pd Nanorod-Decorated BiVO4 Electrodes with Enhanced Photoelectrochemical Water Splitting Efficiency Across Visible-NIR Region.

The photoelectrochemical (PEC) water splitting performance of BiVO4 is partially hindered by insufficient photoresponse in the spectral region with energy below the band gap. Here, we demonstrate that the PEC water splitting efficiency of BiVO4 electrodes can be effectively enhanced by decorating Pd nanoparticles (NPs) and nanorods (NRs). The results indicate that the Pd NPs and NRs with different surface plasmon resonance (SPR) features delivered an enhanced PEC water splitting performance in the visible and near-infrared (NIR) regions, respectively. Considering that there is barely no absorption overlap between Pd nanostructures and BiVO4 and the finite-difference time domain (FDTD) simulation indicating there are substantial energetic hot electrons in the vicinity of Pd nanostructures, the enhanced PEC performance of Pd NP-decorated BiVO4 and Pd NR-decorated BiVO4 could both benefit from the hot electron injection mechanism instead of the plasmon resonance energy transfer process. Moreover, a combination of Pd NPs and NRs decorated on the BiVO4 electrodes leads to a broad-band enhancement across visible-NIR region.

Down-regulation of SENCR promotes smooth muscle cells proliferation and migration in db/db mice through up-regulation of FoxO1 and TRPC6.

BACKGROUND: The inappropriate proliferation of vascular smooth muscle cells (VSMCs) plays a crucial role in the atherosclerotic process. SENCR was reported to be associated with cell migration in human smooth muscle cells. However, the regulation role of SENCR in SMCs is still not fully understood. METHODS: qRT-PCR and Western blotting were performed to detect the mRNA and protein levels of SENCR, FOXO1 and TRPC6 in SMCs of db/db mice and SMCs exposed to high glucose. The regulation of SENCR on the expression of FoxO1 and TRPC6 were examined with luciferase report assays. Furthermore, we investigated the effect of SENCR on VSMCs proliferation and migration using MTT assay and cell migration assay, respectively. RESULTS: Here, we found that SENCR was down-regulated in db/db mice and in SMCs exposed to high glucose. According to the result of luciferase assays, it was shown that SMCs knockdown enhanced the expression of FoxO1 and FoxO1 overexpression increased the expression of TRPC6. In addition, qRT-PCR revealed that SENCR overexpression reversed the effect of high glucose on mouse VSMCs proliferation and migration. CONCLUSION: In this study, our data indicated that down-regulation of SENCR promoted smooth muscle cells proliferation and migration in db/db mice through up-regulation of FoxO1 and TRPC6.

Electroacupuncture pretreatment induces tolerance against cerebral ischemia/reperfusion injury through inhibition of the autophagy pathway.

Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment­induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule­associated protein 1A light chain 3 (LC3)­II and Beclin 1 were significantly increased 12 h post­I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3­II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.

A Study of the Effect of Heat-Treatment on the Morphology of Nafion Ionomer Dispersion for Use in the Passive Direct Methanol Fuel Cell (DMFC).

Aggregation in heat-treated Nafion ionomer dispersion and 117 membrane are investigated by 1H and 19F Nuclear Magnetic Resonance (NMR) spectra, spin-lattice relaxation time, and self-diffusion coefficient measurements. Results demonstrate that heat-treatment affects the average Nafion particle size in aqueous dispersions. Measurements on heat-treated Nafion 117 membrane show changes in the 1H isotropic chemical shift and no significant changes in ionic conductivity. Scanning electron microscopy (SEM) analysis of prepared cathode catalyst layer containing the heat-treated dispersions reveals that the surface of the electrode with the catalyst ink that has been pretreated at ca. 80 °C exhibits a compact and uniform morphology. The decrease of Nafion ionomer's size results in better contact between catalyst particles and electrolyte, higher electrochemically active surface area, as well as significant improvement in the DMFC's performance, as verified by electrochemical analysis and single cell evaluation.

Enhanced catalytic dehydrogenation of LiBH(4) by carbon-supported Pd nanoparticles.

The investigation of thermally induced dehydrogenation of LiBH(4) catalyzed by carbon-supported Pd nanoparticles (Pd/C) reveals that LiBH(4) doped with the Pd/C catalysts shows superior dehydrogenation performance, compared to dehydrogenation in the absence of catalyst, even at very low catalyst content. We have found that smaller Pd nanoparticles result in greater enhanced catalytic dehydrogenation of LiBH(4) than do larger Pd nanoparticles. For doping with 10 wt.% catalyst of an average Pd particle diameter of ca. 5.3 nm, thermal dehydrogenation of LiBH(4) is found to start at ca. 280 degrees C with a total weight loss of 15.8 wt.% for the full temperature range. With increased loading of catalyst within a LiBH(4) sample, the onset dehydrogenation temperature and the two main desorption peaks from LiBH(4) are found to decrease while the hydrogen release amount is found to increase. All the hydrogen of ca. 18.5 wt.% can be released from LiBH(4) below 580 degrees C at a catalyst doped level of 50 wt.%. Importantly, we observed a reversible hydrogenation/dehydrogenation with a capacity of approximately 4.3 wt.%. Pd nanoparticles are found to play an important role in the catalyzed dehydrogenation/rehydrogenation of LiBH(4).