Facet-switching of rate-determining step on copper in CO2-to-ethylene electroreduction.

Reduction of carbon dioxide (CO2) by renewable electricity to produce multicarbon chemicals, such as ethylene (C2H4), continues to be a challenge because of insufficient Faradaic efficiency, low production rates, and complex mechanistic pathways. Here, we report that the rate-determining steps (RDS) on common copper (Cu) surfaces diverge in CO2 electroreduction, leading to distinct catalytic performances. Through a combination of experimental and computational studies, we reveal that C─C bond-making is the RDS on Cu(100), whereas the protonation of *CO with adsorbed water becomes rate-limiting on Cu(111) with a higher energy barrier. On an oxide-derived Cu(100)-dominant Cu catalyst, we reach a high C2H4 Faradaic efficiency of 72%, partial current density of 359 mA cm-2, and long-term stability exceeding 100 h at 500 mA cm-2, greatly outperforming its Cu(111)-rich counterpart. We further demonstrate constant C2H4 selectivity of >60% over 70 h in a membrane electrode assembly electrolyzer with a full-cell energy efficiency of 23.4%.

Targeted photodynamic therapy of glioblastoma mediated by platelets with photo-controlled release property.

Photodynamic therapy (PDT) has recently emerged as a promising, targeted treatment modality for glioblastoma (GBM) which is the most vicious type of brain tumor. Successful GBM-PDT hinges upon light activation of a photosensitizer accumulated in the tumor. However, inadequate tumor accumulation of photosensitizer severely limits the success of PDT of GBM. To tackle this difficulty, we herein propose a drug delivery strategy of "platelets with photo-controlled release property". This strategy exploits platelets as carriers to deliver a photosensitizer which, in the current study, is a nano-composite (BNPD-Ce6) comprised of chlorine e6 (Ce6) loaded to boron nitride nanoparticles with a surface coating of polyglycerol and doxorubicin. To demonstrate the working mechanism and therapeutic advantage of this strategy, we loaded mouse platelets with BNPD-Ce6 to yield the nano-device BNPD-Ce6@Plt. In vitro experiments showed BNPD-Ce6@Plt to have a high loading capacity and efficiency. Laser irradiation (LI) at a wavelength of 808 nm induced ROS generation in BNPD-Ce6@Plt which displayed rapid activation, aggregation, and speedy discharge of BNPD-Ce6 into co-cultured GL261 mouse GBM cells which in turn, after LI, exhibited marked ROS generation, DNA damage, reduced viability, and cell death. In vivo animal experiments, mice that were intravenously injected with BNPD-Ce6@Plt exhibited rapid and extensive BNPD-Ce6 accumulation in both subcutaneous and intra-brain GL261 tumors shortly after LI of the tumors and the tumors displayed massive tissue necrosis after LI for a second time. Finally, a PDT regimen of two intravenous BNPD-Ce6@Plt injections each followed by multiple times of extracranial LI at the tumor site significantly inhibited the growth of intra-brain GL261 tumors and markedly increased the survival of the host animals. No apparent tissue damage was found in vital organs. Our findings make a compelling case for the notion that platelets are efficient carriers that can photo-controllably deliver nano-photosensitizers to achieve highly targeted and efficacious PDT of GBM. This work presents a novel approach to GBM-PDT with great translational potential.

Chylopericardium in a child with IgA nephropathy: a case report.

BACKGROUND: Chylopericardium effusion is characterized by the accumulation of milky effusion in the pericardium. It is often idiopathic but it can be secondary to trauma, chest radiation, tuberculosis and malignancy. If cardiac tamponade ensues, it becomes life-threatening. Herein we describe chylopericardium tamponade in a child with IgA nephropathy. To the best of our knowledge, this is the first reported case of chylopericardium tamponade in IgA nephropathy. CASE PRESENTATION: A 6 years old boy with IgA nephropathy presented with dyspnea, orthopnea, pretibial pitting edema, ascites and fever. Muffled heart sounds and hepatomegaly were also noted. Echocardiography and thoracic CT revealed that there was a large volume of hydropericardium. Moreover, the pericardial milky fluid by pericardiocentesis was analyzed and chylopericardium effusion was eventually confirmed. Pericardial drainage was continued and his diet was modified to low fat, rich MCT and high protein. Complete remission was achieved after 3 weeks of this combined treatment. CONCLUSION: Chylopericardial tamponade could be a rare and life-threatening complication of IgA nephropathy. Etiological analysis is critical for determining the therapeutic approach in patients with pericardial effusion.

High-Volume Hemofiltration in Critically Ill Patients With Secondary Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome: A Prospective Study in the PICU.

OBJECTIVES: Hemophagocytic lymphohistiocytosis, which includes primary (familial) and secondary hemophagocytic lymphohistiocytosis, is a fatal disease in children. Macrophage activation syndrome was defined in patients who met secondary hemophagocytic lymphohistiocytosis criteria with an underlying autoimmune disease. High-volume hemofiltration has shown beneficial effects in severe sepsis and multiple organ dysfunction syndrome. Secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome shares many pathophysiologic similarities with sepsis. The present study assessed the effects of high-volume hemofiltration in children with secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome. DESIGN: A single-center nonrandomized concurrent control trial. SETTING: The PICU of Shanghai Children's Hospital, Shanghai Jiao Tong University. PATIENTS: Thirty-three critically ill secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome patients treated between January 2010 and December 2014. INTERVENTIONS: Thirty-three patients were divided into two groups: high-volume hemofiltration + hemophagocytic lymphohistiocytosis-2004 group (17 cases) or hemophagocytic lymphohistiocytosis-2004 group (16 cases). High-volume hemofiltration was defined as an ultrafiltrate flow rate of 50-70 mL/kg/hr. Clinical and biological variables were assessed before initiation and after 48 and 72 hours of high-volume hemofiltration therapy. MEASUREMENTS AND MAIN RESULTS: The total mortality rate was 42.4% (14/33), but mortality at 28 days was not significantly different between the two groups (high-volume hemofiltration + hemophagocytic lymphohistiocytosis-2004 group: five deaths, 29.4%; hemophagocytic lymphohistiocytosis-2004 group: nine deaths, 56.3%; chi-square, 2.431; p = 0.119). Children received high-volume hemofiltration for 60.2 ± 42.0 hours. After 48 and 72 hours respectively, a significant decrease in serum ferritin (p < 0.001), aspartate aminotransferase (p = 0.037 and p < 0.001), total bilirubin (p = 0.041 and p = 0.037), and serum creatinine (p = 0.006 and p = 0.004) levels were observed. Furthermore, the natural killer-cell activity up-regulated (p = 0.047) after 72 hours. Furthermore, significantly decreased levels of serum tumor necrosis factor-α (from 91.5 ± 44.7 ng/L at 48 hr to 36.7 ± 24.9 ng/L at 72 hr; p = 0.007)) and interleukin-6 (from 46.9 ± 21.1 ng/L at 48 hr to 27.7 ± 14.5 ng/L at 72 hr; p < 0.0001) were observed. After 7 days, patients receiving high-volume hemofiltration had significantly lower bilirubin, creatinine, ferritin, procalcitonin, lactate dehydrogenase level, tumor necrosis factor-α, and interleukin-6 levels, and needed less mechanical ventilation compared with hemophagocytic lymphohistiocytosis-2004 group patients. No serious adverse events were observed. CONCLUSIONS: High-volume hemofiltration may improve organ function by decreasing cytokine levels (tumor necrosis factor-α and interleukin-6). High-volume hemofiltration may be an effective adjunctive treatment in secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome.

[Study on catalytic oxidation of benzene by microwave heating].

The performance in catalytic oxidation of benzene was investigated in two different heating modes, microwave heating and conventional electric furnace heating. The effects of copper (Cu)-manganese (Mn) mass ratio, doping dose of cerium (Ce) and calcination temperature on the catalytic activity of Cu-Mn-Ce/molecular sieve catalyst were also checked in catalytic oxidation of benzene with microwave heating, and the catalysts were subsequently characterized by scanning electron microscope (SEM) and X-ray diffraction (XRD). The results showed that the catalyst had better catalytic activity for the oxidation of benzene under microwave heating than electric furnace heating, and high oxidation efficiency for benzene was reached due to the "local hot spots" and dipole polarization effect of microwave and stable bed reaction temperature. Under the conditions of Cu, Mn and Ce mass ratio 1:1:0.33 and calcination temperature 500 degrees C, the catalyst had the optimal catalytic activity for benzene oxidation, and its light-off temperature and complete combustion temperature were 165 degrees C and 230 degrees C, respectively. It was indicated by characteristics of XRD and SEM that the presence of copper and manganese oxides and Cu1.5Mn1.5O4 with spinel crystal improved the catalytic activity of the catalyst, and the doping of Ce promoted the dispersion and regularization of active components. High calcination temperature led to the sintering of the catalyst surface and agglomeration of active components, which decreased the catalytic activity of the catalyst in the catalytic oxidation

[Changes and significance of soluble CD 163 in sepsis and severe sepsis in children].

OBJECTIVE: To investigate the changes of serum soluble CD 163 (sCD 163) level, to assess the severity of critical illness and to evaluate the immune status of sepsis or severe sepsis in children. METHOD: A prospective study was conducted. The sCD 163 was determined in 50 cases with sepsis or severe sepsis in pediatric intensive care unit (PICU) and 23 cases of age- and gender-matched healthy children were enrolled as control during the period from April 2010 to March 2011. Double-antibody sandwich ELISA was used for sCD 163 measurement. The relationship with sCD 163 level and disease severity score (pediatric critical illness score, PCIS; and pediatric risk of mortality III, PRISM III), lymphocyte subsets, C-reactive protein (CRP), tumor necrosis factor α (TNFα) were analyzed. RESULT: The sCD 163 in sepsis/severe sepsis groups (171.04 ± 177.85) mg/L was significantly higher than that in control group (44.19 ± 86.48) mg/L (P < 0.01).sCD 163 in sepsis group [(105.32 ± 145.87) mg/L] was significantly lower than that of severe sepsis group [(233.32 ± 171.78) mg/L] (P < 0.05). sCD 163 level was significantly higher in lower PCIS score patients. (P < 0.01). The sCD 163 levels was higher in PRISM III ≥ 10 than the PRISM III < 10 group. The sCD 163 levels were higher in death group than the survival group. The sCD 163 was negatively correlated with CD4 +, CD4 +/CD8 + (R = -0.820, P < 0.05; R = -0.839, P < 0.01). CONCLUSION: Detection of sCD 163 was helpful in predicting the severity of sepsis and severe sepsis, and sCD 163 may reflect the immune status of critically ill children with sepsis.

[Efficacy of continuous blood purification on rescue therapy of the critically ill children with acute lung injury and acute respiratory distress syndrome].

OBJECTIVE: To investigate the efficacy of continuous blood purification(CBP) in the treatment of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in children. METHODS: One hundred and forty seven cases of ALI/ARDS were hospitalized to our pediatric intensive care unit, and 32 cases were treated with continuous blood purification (CBP) from June, 2006 to May, 2011. The model for CBP was continuous veno-venous hemofiltration dialysis (CVVHDF). CBP treatment persisted for at least 8 hours and replacement + dialysis fluid dose was 35 - 100 ml/(kg·h). The clinical outcome measures included the mortality rate at 28th day, respiratory index (FiO2/PO2), dynamic lung compliance (Cdyn), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), mechanical ventilation parameters, vasoactive drug dose and lung X-ray changes. RESULTS: In totally 147 cases of ALI/ARDS, 89 cases (60.5%) were male and 58 (39.5%) were female, mean age was (43.4 ± 36.7) months. Death occurred in 54 cases, the total mortality was 36.7%. The cause of ALI/ARDS was mainly severe pneumonia, severe sepsis, and leukemia or tumor diseases. There were significant differences in severity of illness between the CBP treatment group and non-CBP treatment group on Pediatric risk of score mortality (PRISM) III score (15.3 vs. 12.7, P < 0.05) and pediatric critical illness score (66.8 ± 19.3 vs. 74.6 ± 17.7, P < 0.05). The average duration of CBP treatment was 52 hours (12 hours to 232 hours). PaO2/FiO2 and Cdyn were improved after 2 hours CBP treatment compared with those before CBP treatment (P < 0.05), mechanical ventilation parameters including fraction of inspired oxygen (FiO2), peak inspiratory pressure (PiP) and positive end expiratory pressure (PEEP) were reduced. The use of vasoactive drugs in patients with MODS and shock gradually declined. The average ventilator-free days of the two groups did not show significant difference (P > 0.05). The mortality on CBP treatment group and non-treatment group were 37.5% and 36.5%, respectively, the difference was not significant (P > 0.05). CONCLUSION: CBP adjuvant treatment for ALI/ ARDS could reduce pulmonary edema, improve PaO2/FiO2 and Cdyn, and improve mechanical ventilation parameters. CBP may be a very promising treatment for ALI/ARDS in children.

[Effects of vasoactive intestinal peptide on Toll-like receptor (TLR) 2 mRNA and TLR4 mRNA expression on acute lung injury induced by lipopolysaccharide in rat].

OBJECTIVE: Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity. Previous studies indicated that VIP can attenuate the deleterious consequences of severe sepsis and septic shock by regulating production of inflammatory cytokines in immune activated cells. The signaling induced by bacterial components occurs primarily through Toll like receptors (TLRs). TLRs have been recognized to play a key role in pathogen recognition and innate immunity. It was convincingly demonstrated that lung is one of early suffered disaster organ and may trigger multiple organ dysfunction syndrome in sepsis. The present study was conducted to investigate the effects of VIP on TLR2/4 mRNA expressions on acute lung injury of endotoxic shock induced by lipopolysaccharide (LPS) in rat. METHOD: Forty Sprague-Dawley rats were randomly divided into 3 groups, i.e., LPS shock group (n = 16), LPS + VIP group (n = 16), and control group (n = 8). LPS shock model was established by LPS (E. coli O(55)B(5) 10 mg/kg) with tail intravenous injection. The rats in LPS + VIP group were given a bolus of 5 nmol VIP intravenous injection follow by LPS. The rats in control group were given normal saline. The rats were sacrificed at 6 h, 24 h after being injected. The lung tissues were collected. The TLR2 mRNA and TLR4 mRNA expressions were detected by RT-PCR from the lung tissues. Pathological changes of the lungs were observed by light microscope and electron microscope 24 h after LPS injection. RESULT: (1) Lung histopathology: the alveolar space was full with leukocyte, necrotic cells, segmental hemorrhage and protein effusion. Partial alveolar space was enlarged, lung interstitial edema were observed in LPS shock group. However, pathological changes of LPS + VIP group were milder than those in LPS shock group. (2) The expressions of TLR2 mRNA and TLR4 mRNA were significantly higher in LPS shock group compared with those of the control group (F = 16.638, P = 0.000; t = 5.876, P = 0.000), TLR2 mRNA and TLR4 mRNA expression on 24 h was down-regulated in LPS + VIP shock subgroup than those in LPS shock subgroup (F = 16.676, P = 0.000; t = 3.946, P < 0.001). CONCLUSION: Expressions of TLR2 mRNA and TLR4 mRNA were up-regulated on LPS induced lung injury in rats. VIP mitigated lung injury induced by LPS, which may be related to TLR2 mRNA and TLR4 mRNA down-regulation of expression. The effect of VIP may suggest a protective mechanism in sepsis. VIP may play a potential protective role in severe infection.

[Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat].

OBJECTIVE: Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity in several aspects. Previous reports showed that VIP attenuates the deleterious consequences of severe infection and septic shock by regulating production of inflammatory cytokines in immune activated cells. Intestine is one of the major organ of immune system and it may trigger multiple organ dysfunction syndrome in sepsis. The present study was planned to study the change of serum TNF-alpha, IL-1beta, IL-10 level and histopathological alteration of intestinal tract, and protective effects of VIP on endotoxic shock in rat. METHODS: Twenty eight SD rats were randomly divided into 3 groups, including control group (8 rats), LPS shock group (10 rats), and LPS + VIP group (10 rats). Endotoxic shock model was established by administration of a single dose of 10 mg/kg LPS in LPS shock group, a bolus of 5 nmol VIP intravenous injection following LPS in LPS + VIP group. The rats in the control group were given the same volume of normal saline injection. Blood samples were taken at time points of 1, 2, 4, and 6 hours after intervention from each group for measuring the level of TNF-alpha, IL-1beta and IL-10 by ELISA. Pathological changes of the intestine were observed by light microscope and electron microscope at the animals death or at the end of the experiment. RESULTS: Serum TNF-alpha, IL-1beta and IL-10 levels elevated at each time point in LPS shock group and LPS + VIP group (P < 0.05 or P < 0.01). TNF-alpha concentration reached the peak level 2 h after LPS injection; IL-1beta and IL-10 increased continuously till the end of the experiment. In LPS + VIP group, TNF-alpha and IL-1beta elevated slightly and IL-10 increased significantly as compared with LPS shock group (P < 0.01). Leukocyte infiltration, ischemia, segmental hemorrhage or necrosis appeared in intestine under light microscope and cell swelling, cytoplasmic vacuoles and organelle damage were observed under electron microscope. However, pathological changes in LPS + VIP group were milder than those in LPS group. CONCLUSIONS: VIP improved endotoxic shock-associated histopathological alteration of intestine, down-regulated pro-inflammatory cytokines production and up-regulated anti-inflammatory cytokines. These effects may suggest a protective mechanism of VIP in septic shock. VIP is a potential immunoregulatory substance in treatment of septic shock.

Myocardioprotective effects of the combination of ischemic preconditioning with hypothermia and crystalloid cardioplegia in immature rabbits.

This study was undertaken to explore the myocardioprotective effects of the combination of ischemic preconditioning (IP) with hypothermia and St.II Thomas crystalloid cardioplegic solution (CCS) on immature hearts in the rabbit. Isolated immature rabbit hearts were perfused with Krebs-Henseleit bicarbonate buffer on Langendorff apparatus. In experiment 1, 24 hearts were divided into 4 groups (n=6 in each group): Con, IP1, IP2 and IP3 group. Hearts of the four groups underwent 0, 1, 2 or 3 cycles of IP respectively. Then all the hearts were subjected to a sustained ischemia period of 2 h at 20 degrees C and a postischemic reperfusion period of 30 min at 37 degrees C. In experiment 2, 48 hearts were divided into 6 groups (n=8 in each group): SCon1, SIP1, SCon2, SIP2, SCon3 and SIP3 group, according to hypothermia and the duration of sustained ischemia (30 min at 32 degrees C; 90 min at 25 degrees C, 2 h at 20 degrees C). The SIP1, SIP2 and SIP3 groups were preconditioned twice before the sustained hypothermic ischemia, while the SCon1, SCon2 and SCon3 groups were not preconditioned. CCS was applied during sustained ischemia, all the hearts were reperfused for 30 min at 37 degrees C. Heart rate (HR), left ventricular developed pressure (LVDP) and peak rate of increase or decrease of left ventricular pressure (+/-dp/dt(max)) were recorded. Tissue concentration of adenosine triphosphate (ATP), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were measured. At the end of reperfusion, values of product of LVDP and HR, +/-dp/dt(max) in IP2 group were 96%+/-21%, 101%+/-19% and 84% +/-15% of the baseline values respectively, which were significantly higher than those of Con group and IP3 group (P<0.01, P<0.05); also, the ATP content of IP2 group was higher than that of the Con group (P<0.01). When CCS was applied during sustained period of hypothermic ischemia at 32 degrees C or 25 degrees C, recovery rates of RPP (rate product, =LVDPxHR) and +dp/dt(max) in SIP1 group were 87% +/-14% or 99% +/-26% of the baseline values respectively (P<0.05, vs SCon1 group), the values in SIP2 group changed to 87% +/-16% or 102% +/-20% respectively (P<0.05, vs SCon2 group). Contents of ATP in SIP1 and SIP2 groups were significantly higher than those of SCon1 or SCon2 groups respectively (P<0.05), but MDA content of the two groups were significantly lower than those of SCon1 or SCon2 groups (P<0.05) respectively. The study indicates that IP attenuates hypothermic ischemia/reperfusion injury to immature rabbit hearts under 20 degrees C ischemia, two cycles of IP showing better myocardioprotective effects than 1 or 3 cycles of IP. When IP was combined with CCS which were applied during hypothermic ischemia period, the beneficial effects of IP were weakened as the temperature during the hypothermic period was elevated.

[Effects of ischemic preconditioning on the hypothermic ischemia/reperfusion injury of immature rabbit hearts].

AIM: To study effects of ischemic preconditioning on the hypothermic ischemia/reperfusion injury of immature rabbit hearts. METHODS: The isolated immature rabbit (3-4 weeks) hearts were perfused on Langendorff apparatus. After 30 min perfusing with 37 degrees C K-H perfusate, the hearts in part one were yielded 0, 1, 2 or 3 times of IP respectively before 120 min ischemia at 20 degrees C hypothermia, and the hearts in part two were yielded 0 or 2 times of IP before being arrested by infusion of St. Thomas II crystalloid cardioplegic solution, then the arrested hearts were yielded ischemia for 30, 90 or 120 min at 32 degrees C, 25 degrees C and 2 degrees C hypothermia respectively. Then all the hearts were reperfused for 30 min at 37 degrees C normothermia. Heart rate (HR), left ventricular developed pressure (LVDP), +/- dp/dt(max) were recorded at baseline, preischemic and 1, 3, 5, 10, 20, 30 min after reperfusion. Also contents of ATP and MDA and activity of SOD and Ca(2+) -ATPase of myocardium were measured. RESULTS: At the end of reperfusion, the recovery rate of left ventricular function in IP2 group were significantly higher than that of control group and IP3 group (P < 0.01, P < 0.05), also the IP2 group showed a higher content of ATP and activity of Ca(2+) -ATPase than control group and IP3 group (P < 0.01, P < 0.05). When the ischemic hearts were at different hypothermia accompanied with CCS, the recovery rate of left ventricular function and contents of ATP in SIP1 and SIP2 group were significantly higher than that of SCon 1 group and SCon 2 group respectively (P < 0.01, P < 0.05), the contents of MDA in the two IP groups were lower than that of the two control groups. CONCLUSION: IP can attenuate the hypothermic ischemia/reperfusion injury of immature rabbit hearts, the cardioprotective effects are dependent on the mode of IP and the possible mechanisms may involve the following aspects: decrease the consumption of ATP, inhibit lipid peroxidation and maintain the activity of Ca(2+) -ATPase of cardiac myocyte.