Synergistic effect of Mn doping and hollow structure boosting Mn-CoP/Co2P nanotubes as efficient bifunctional electrocatalyst for overall water splitting.

The sluggish kinetic of hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) severely hampers the commercial application of electrochemical water splitting, promoting the urgent exploration of high-efficient bifunctional electrocatalysts. Heteroatom doping and structure engineering have been identified as the most effective strategies to boost the catalytic activity of electrocatalysts. Herein, Mn doping and hollow structure were integrated in the design of Co-based transition metal phosphide catalyst to prepare Mn-CoP/Co2P nanotubes (denoted as Mn-CP NTs) by a facile template-free method. Confirmed by characterization analysis, the introduced Mn species were in high dispersion in the regular CoP/Co2P hollow tubular framework. Such a favorable design in composition and structure effectively boosted the catalytic activity of Mn-CP NTs toward electrochemical water splitting. The Mn-CP NTs showed superior HER and OER activity demonstrated by the low overpotentials of 82 mV (vs HER) and 309 mV (vs OER) at the current density of 10 mA cm-2, as well as the satisfactory durability. When used as both cathode and anode in electrolyzer for overall water splitting, only a low cell voltage of 1.67 V was required for the Mn-CP NTs to drive 10 mA cm-2, accompanied with excellent stability confirmed by over 50 h test.

Effects of U on the growth, reactive oxygen metabolism and osmotic regulation in radish (Raphanus sativus L.).

Uranium (U) is a non-essential and toxic element, so it is necessary to study the physiological mechanism of plant response to U stress. The present study evaluated the growth status, reactive oxygen metabolism and osmotic regulation system in radish (Raphanus sativus) under U stress (0, 25, 50 and 100 µM). The results showed that U had no significant effect on the germination of radish seeds but inhibited the growth of seedlings, such as reduced root activity and increased plasma membrane permeability. U is mainly distributed in radish roots, so it poisons the roots more than the aboveground parts. When U concentration was 25 µM, superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) activities in radish were increased to cope with the oxidative stress caused by U stress, and the accumulation of proline and soluble sugar was increased to maintain cell turgor. However, under high concentration (100 µM), the damage of radish root was serious; thus, the SOD, CAT and soluble sugar could not respond to U stress. In conclusion, the identification and characterization of U-stress responses in genuine U-tolerant plants would improve our knowledge on the detoxification of this radionuclide.

Self-Exfoliated Synthesis of Transition Metal Phosphate Nanolayers for Selective Aerobic Oxidation of Ethyl Lactate to Ethyl Pyruvate.

Two-dimensional (2D) transition metal nanosheets are promising catalysts because of the enhanced exposure of the active species compared to their 3D counterparts. Here, we report a simple, scalable, and reproducible strategy to prepare 2D phosphate nanosheets by forming a layered structure in situ from phytic acid (PTA) and transition metal precursors. Controlled combustion of the organic groups of PTA results in interlayer carbon, which keeps the layers apart during the formation of phosphate, and the removal of this carbon results in ultrathin nanosheets with controllable layers. Applying this concept to vanadyl phosphate synthesis, we show that the method yields 2D ultrathin nanosheets of the orthorhombic ß-form, exposing abundant V4+/V5+ redox sites and oxygen vacancies. We demonstrate the high catalytic activity of this material in the vapor-phase aerobic oxidation of ethyl lactate to ethyl pyruvate. Importantly, these ß-VOPO4 compounds do not get hydrated, thereby reducing the competing hydrolysis reaction by water byproducts. The result has superior selectivity to ethyl pyruvate compared to analogous vanadyl phosphates. The catalysts are highly stable, maintaining a steady-state conversion of ∼90% (with >80% selectivity) for at least 80 h on stream. This "self-exfoliated" synthesis protocol opens opportunities for preparing structurally diverse metal phosphates for catalysis and other applications.

Neuroprotection of GLP-1/GIP receptor agonist via inhibition of mitochondrial stress by AKT/JNK pathway in a Parkinson's disease model.

OBJECTIVES: To investigate the effect of glucagon-like peptide-1 (GLP-1) receptor and glucose dependent insulinotrophic polypeptide (GIP) receptor dual agonist DA-JC4 on alleviating Parkinson's disease (PD) and unveil related cellular mechanisms. METHODS: Rotenone was injected to generate a rat PD model, on which the effect of DA-JC4 on motor functions was evaluated by rotational behavioral assay and open field test. The survival of dopaminergic neurons was analyzed, in addition to assays for mitochondrial stress and quantification of neurotransmitter levels using high performance liquid chromatography (HPLC). In cultured hippocampal neurons, the effect of DA-JC4 on mitochondrial stress and related cellular mechanism was analyzed by Flow cytometry, western blotting and reactive oxygen species (ROS). RESULTS: DA-JC4 significantly improved motor functions in PD rats, and elevated levels of major neurotransmitters. By histological analysis, DA-JC4 protected dopaminergic neurons from rotenone-induced cell death, which was associated with reduced mitochondrial stress. Experiments in cultured rat hippocampal neurons validated the neuroprotective role of DA-JC4 against cell apoptosis and mitochondrial stress induced by rotenone. The protective effect of DA-JC4 was later found to be dependent on AKT/JNK signal pathway, as treatment using AKT inhibitor or JNK activator abolished such effects. CONCLUSION: Our results showed that the dual agonist of GLP-1/GIP receptor could ameliorate motor dysfunctions of PD by protecting dopaminergic neurons which was mediated by relieved mitochondrial stress and apoptosis via AKT/JNK signal pathway.

Up-regulation of microRNA-375 ameliorates the damage of dopaminergic neurons, reduces oxidative stress and inflammation in Parkinson's disease by inhibiting SP1.

BACKGROUND: This study is conducted to investigate the protective role of elevated microRNA-375 (miR-375) in dopaminergic neurons in Parkinson's disease through down-regulating transcription factor specificity protein 1 (SP1). RESULTS: The successfully modeled rats with Parkinson's disease showed aggregated neurobehavioral change, increased neuroinflammatory response and oxidative stress, and lowered dopamine content. Parkinson's disease rats treated with overexpressed miR-375 displayed improved neurobehavioral change, ameliorated neuroinflammatory response and oxidative stress, heightened dopamine content and abated neuronal apoptosis by down-regulating SP1. Up-regulation of SP1 reversed the protective effect of upregulated miR-375 on Parkinson's disease. CONCLUSION: Up-regulation of miR-375 ameliorated the damage of dopaminergic neurons, reduced oxidative stress and inflammation in Parkinson's disease by inhibiting SP1. METHODS: Parkinson's disease rat model was established by targeted injection of 6-hydroxydopamine to damage the substantia nigra striatum. The successfully modeled Parkinson's disease rats were intracerebroventricularly injected with miR-375 mimics or pcDNA3.1-SP1. The functions of miR-375 and SP1 in neurobehavioral change, neuroinflammatory response, oxidative stress, dopamine content and expression of apoptosis-related proteins in the substantia nigra of Parkinson's disease rats were evaluated. The target relation of miR-375 and SP1 was confirmed by bioinformatics analysis and dual luciferase reporter gene assay.

Massive hemobilia due to a ruptured mycotic hepatic artery aneurysm associated with streptococcal endocarditis: case report.

Hepatic artery aneurysm rupture is a rare cause of massive hemobilia, which is potentially life-threatening, cause of upper gastrointestinal hemorrhage. Cases of mycotic hepatic artery aneurysm associated with streptococcal endocarditis have rarely been reported. In the present study, we report a case of massive hemobilia that was caused by ruptured mycotic hepatic artery aneurysm in a patient who was infected with streptococcal endocarditis 3 months previously. Transarterial embolization in the patient failed, possibly due to vascular variations. However, surgical treatment was successfully performed, and the patient completely recovered. In conclusion, surgical treatment may be useful in treating massive hemobilia under life-threatening conditions, even in cases of vascular variations and failure of transarterial embolization.

Neuroprotective effect and mechanism of baicalin on Parkinson's disease model induced by 6-OHDA.

OBJECTIVE: This research was aimed to investigate the effects of baicalin on 6-hydroxydopamine (6-OHDA)-induced rat model of Parkinson's disease (PD) and the main mechanism of baicalin based on metabolomics. METHODS: The rat model of PD was induced by 6-OHDA. The protective effects of baicalin on rat model of PD were evaluated by open field test and rotarod test. The anti-PD efficacy of baicalin was evaluated by examining the morphologic changes of neurons and the level of monoamine neurotransmitters in the striatum, the number and morphology of tyrosine hydroxylase (TH)-positive neurons, and oxidative stress. Combined with metabolomics methods, the pharmacodynamic mechanism of baicalin on PD pathogenesis was also explored. RESULTS: Baicalin treatment improved the rod time and voluntary movement in rat model of PD (P<0.05) by the open field test and rotarod test. In addition, baicalin also protected from oxidative stress injury (P<0.05), and regulated the content of monoamine neurotransmitters dopamine, 3,4-dihydroxyphenylacetic acid, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid (P<0.05) and the number and morphology of TH-positive cells in 6-OHDA-induced PD model rats. By metabolomics, multivariate statistical analysis, and receiver operating characteristic curve analysis, we found that two metabolites N-acetyl aspartic acid and glutamic acid had a good diagnostic value. Quantitative analysis of metabolites showed a regulatory function of baicalin. CONCLUSION: Baicalin has significant protective effect on 6-OHDA-induced PD rats, which may play a protective role through an antioxidant, promoting the release of neurotransmitters and regulating the metabolism of N-acetyl aspartate and glutamate.

Bexarotene attenuates early brain injury via inhibiting micoglia activation through PPARγ after experimental subarachnoid hemorrhage.

Objectives Early brain injury (EBI) is considered to be one of the main causes of poor outcome in subarachnoid hemorrhage (SAH) patients. Bexarotene is an agonist of retinoid X receptor and plays a protective role in central nervous system diseases. However, the exact role of bexarotene in SAH has not been reported. Therefore, the present study was to determine whether bexarotene administration attenuate EBI after SAH in mice and to explore the underlying mechanism. Methods SAH was induced in C57BL/6 mice by endovascular perforation. Bexarotene was administrated intraperitoneally. Neurological score, cell death, microglia activation, and pro-inflammatory cytokines were detected at 24 h after SAH. The expression of PPARγ was measured by Western blot. Results Results showed that bexarotene significantly improved neurological score after SAH. In addition, the number of cell death and activated microglia were significantly reduced by bexarotene administration. Compared with vehicle-treated mice, bexarotene-treated mice showed reduced pro-inflammatory cytokines after SAH. The expression of PPARγ was significantly increased with bexarotene treatment compared with vehicle-treated controls. Discussion The present study demonstrats that bexarotene administration protects against EBI after SAH, inhibiting cell death, attenuating microglia activation, and alleviating neuroinflammation. The underlying mechanism may partially involve the activation of PPARγ.

[Comparison of value of GRACE, APACHEII and REMS for early prognosis of death in patients with acute myocardial infarction].

OBJECTIVE: To evaluate and compare the predictive value of short-term risk of death of global registry of acute coronary events (GRACE) risk scores, acute physiology and chronic health evaluation II (APACHEII) scores and rapid emergency medicine score (REMS) in patients with acute myocardial infarction (AMI). METHODS: A retrospective review of clinical data of 390 patients with AMI admitted from October 2012 to March 2013 in emergency department and cardiology care unit (CCU) in Guizhou People's Hospital were performed. The lowest scores within 24 hours of GRACE risk score, APACHEII risk score, and REMS risk score, respectively, for each patient were recorded. Mortality rate within 30 days after onset was calculated. Prediction of the mortality rate of AMI within 30 days as made in three scoring systems was compared. RESULTS: A total of 54 patients died from cardiovascular disease within 30 days. GRACE risk scores, APACHEII scores, and REMS risk scores were higher in non-survivors as compared with that of survivors (GRACE: 206.09±24.67 vs. 150.17±25.72, t=-4.349, P=0.000; APACHEII: 15.81±7.60 vs. 7.50±2.83, t=-4.182, P=0.000; REMS: 7.11±2.70 vs. 5.38±2.59, t=-2.345, P=0.020). Area under the receiver operator characteristic curve (ROC curve) for GRACE risk scores, APACHEII risk scores and REMS in patients with AMI died from cardiac vascular disease in 30 days were 0.862 [95% confidence interval (95%CI) 0.76-0.95, P=0.000], 0.825 (95%CI 0.71-0.93, P=0.002) and 0.615 (95%CI 0.46-0.77, P=0.192), sensitivity of three kinds of scoring system was 92.32%, 76.91%, 69.26%, respectively, with specificity of 66.23%, 77.84%, 54.02% respectively. CONCLUSIONS: GRACE and APACHEII scores for patients with AMI risk of short-term death showed more accurate in predicting early than GRACE scores, and REMS for AMI risk of short-term death did not have predictive value.