Benzoquinone-Lubricated Intercalation in Manganese Oxide for High-Capacity and High-Rate Aqueous Aluminum-Ion Battery.

Aqueous aluminum-ion batteries are attractive post-lithium battery technologies for large-scale energy storage in virtue of abundant and low-cost Al metal anode offering ultrahigh capacity via a three-electron redox reaction. However, state-of-the-art cathode materials are of low practical capacity, poor rate capability, and inadequate cycle life, substantially impeding their practical use. Here layered manganese oxide that is pre-intercalated with benzoquinone-coordinated aluminum ions (BQ-AlxMnO2) as a high-performance cathode material of rechargeable aqueous aluminum-ion batteries is reported. The coordination of benzoquinone with aluminum ions not only extends interlayer spacing of layered MnO2 framework but reduces the effective charge of trivalent aluminum ions to diminish their electrostatic interactions, substantially boosting intercalation/deintercalation kinetics of guest aluminum ions and improving structural reversibility and stability. When coupled with Zn50Al50 alloy anode in 2 m Al(OTf)3 aqueous electrolyte, the BQ-AlxMnO2 exhibits superior rate capability and cycling stability. At 1 A g-1, the specific capacity of BQ-AlxMnO2 reaches ≈300 mAh g-1 and retains ≈90% of the initial value for more than 800 cycles, along with the Coulombic efficiency of as high as ≈99%, outperforming the AlxMnO2 without BQ co-incorporation.

Molecular cloning and expression analysis of a fish specific interferon regulatory factor, IRF11, in orange spotted grouper, Epinephelus coioides.

Interferon regulatory factors (IRFs) are transcription mediators which play vital roles in multiple biological processes, such as antiviral defense, immune response, cell growth regulation and apoptosis. A fish specific IRF, termed IRF11, has been identified in previous study through searching fish genome databases. Herein, a transcript of IRF11, EcIRF11 was cloned from orange-spotted grouper, Epinephelus coioides. The EcIRF11 cDNA sequence has 1573 bp in length, encoding a putative protein of 261 amino acids, with a high degree of similarity found between EcIRF11 and its teleost counterparts. Comparative analyses in teleost genomes revealed that IRF11 may have an ancient origin at least 450 million years ago, and the locus harbouring IRF11 might have experienced chromosomal rearrangement and/or inversion during evolution. Expression analysis revealed that the other two members, IRF1 and IRF2 also in the IRF1 subgroup (SG) as IRF11, exhibited high expression levels in early experimental infection phase in response to viral stimulation of poly I:C and to bacterial stimulation of Vibrio parahaemolyticus infections in the fish, while EcIRF11 is not transcriptionally modulated at the examined time points except in kidney at 6 h following poly I:C stimulation. Taken together, the results obtained in this study indicate that IRF11 might have been originated from the same ancestor as IRF1 and IRF2, but exhibits distinct basal and induced expression, implying its different function which needs further characterization.

[Renal artery injury caused by Kawasaki disease].

OBJECTIVE: To investigate renal artery injury caused by Kawasaki disease (KD). METHODS: Forty-three children with KD were enrolled in the study. According to the blood pressure in the acute stage, these children were classified into normal blood pressure subgroup and increased blood pressure subgroup. Eighteen children with fever caused by acute upper respiratory tract infection were enrolled as the control group. The diameter of the origin of the main renal artery, hemodynamic parameters of the main renal artery and the renal interlobar artery, rennin activity, and levels of angiotensin II and aldosterone were compared between groups. RESULTS: During the acute stage of KD, both subgroups had a significantly smaller diameter of the origin of the main renal artery, a significantly higher resistance index (RI) of the main renal artery, and a significantly lower end-diastolic velocity (EDV) than the control group (P<0.05).The increased blood pressure subgroup had a significantly lower EDV of the interlobar artery than the normal blood pressure subgroup, a significantly higher RI than the normal blood pressure subgroup and the control group, as well as a significantly higher rennin activity and significantly higher levels of angiotensin II and aldosterone than the normal blood pressure subgroup (P<0.05). A significantly increased EDV and a significantly reduced RI of the renal interlobar artery were observed in the increased blood pressure subgroup in the subacute stage compared with the acute stage (P<0.05). CONCLUSIONS: KD may cause renal artery injury and early hemodynamic changes, resulting in a transient increase in blood pressure in some patients.

[Clinical significance of determination of serum IgE in infants with milk allergy].

OBJECTIVE: To determine the clinical significance of milk protein-specific IgE (sIgE) for infants with cow's milk protein allergy (CMPA). METHODS: Ninety-six infants with CMPA were divided into IgE+ group (n=26) and IgE- group (n=70) and clinical characteristics were compared between the two groups. Infants were denied allergy-inducing food and fed instead extensively hydrolyzed formulas or amino-acid formulas for 16 weeks before the two groups were compared. RESULTS: Twenty-seven percent of the infants were sIgE-seropositive. The first onset age of CMPA was significantly younger in the IgE+ group than in the IgE- group (P<0.05), and the family history of allergy and respiratory symptoms were significantly less common in the IgE- group than in the IgE+ group (P<0.05). Severe CMPA, gastrointestinal symptoms, underweight, growth retardation, anemia, and hypoproteinemia were significantly more common in the IgE- group than in the IgE+ group (P<0.05). Erythema, urticaria, vomiting, nasal discharge, cough, wheezing, and paroxysms of crying were major clinical symptoms of the IgE+ group, and their incidences were significantly higher in the IgE+ group than in the IgE- group (P<0.05); eczema, constipation, and diarrhea were major symptoms of the IgE- group, and their incidences were significantly higher in the IgE- group than in the IgE+ group (P<0.05). The remission rate of each symptom was as high as over 80% in the two groups after 16 weeks of intervention and there was no significant difference in the remission rates between the two groups (P>0.05). CONCLUSIONS: IgE seropositive rate is not high in infants with CMPA. Atypical signs instead of allergic symptoms are more common in the IgE seronegative infants with CMPA. Avoiding allergy-inducing food and eating extensively hydrolyzed formulas or amino-acid formulas in early age benefit infants with IgE-mediated or non-IgE-mediated CMPA.

[Expression of CysLTR-1 and CysLTR-2 in adenoid tissues from children with adenoid hypertrophy].

OBJECTIVE: To examine the expression of cysteinyl leukotriene receptor-1 (CysLTR-1) and cysteinyl leukotriene receptor-2 (CysLTR-2) in the adenoid tissues from children with adenoid hypertrophy (AH) and to explore the role of leukotrienes in the pathogenesis of AH. METHODS: Sixty children with AH who were treated by adenoidectomy and/or tonsillectomy were classified into two groups: simple AH and AH plus allergic rhinitis (n=30 each). Twenty children who underwent tonsillectomy due to recurrent purulent tonsillitis were selected as the control group. The expression of CysLTR-1 and CysLTR-2 in the excised tonsil and/or adenoid tissues was determined by immunofluorescence histochemical labeling and integrated optical density measurement. RESULTS: The expression of CysLTR-1 and CysLTR-2 in the adenoid and tonsil tissues increased significantly in both the simple AH group and AH plus allergic rhinitis group compared with the control group (P<0.01). The expression of CysLTR-1 and CysLTR-2 in the AH plus allergic rhinitis group increased more significantly compared with the simple AH group (P<0.01). CONCLUSIONS: CysLTR-1 and CysLTR-2 are highly expressed in the adenoid tissues from children with AH, suggesting that leukotrienes are involved in the pathogenesis of AH.

[Value of antiviral therapy for infectious monocytosis in children].

OBJECTIVE: To study the value of antiviral therapy for infectious monocytosis (IM) in children by comparing the near-term therapeutic efficacies and long-term follow-up results in children with this disorder between receiving antiviral therapy or not. METHODS: The medical data of IM children between 1999 and 2009 were retrospectively reviewed. A total of 172 cases with a follow-up visit period of 1 year and more were eligible. The children were classified into three groups according to the treatment protocol: ganciclovir treatment (n=49), acyclovir treatment (n=72) and symptomatic treatment (control; n=51). The children in the ganciclovir group received an intravenous drip of 10 mg/kg per day of ganciclovir, administered in twice-daily doses; Seven days later the drip volume was changed to 5 mg/kg, administered once each day; the total course lasting 10-14 days. The children in the acyclovir group received acyclovir orally at 20 mg/kg per day, administered in three times daily doses; the total course lasting 10-14 days. The children in the control group received symptomatic treatment only. In the three groups, indicators including fever course, improvement of isthmitis symptoms, lymph node retraction, hepatic and splenic lymph node retraction time, atypical lymphocyte fallback time and alteration of granulocyte amount after drug use were observed. The long-term follow-up visits covered such indicators as blood routine reexamination, hepatic function, liver and spleen B-ultrasonography, recovery rate, recurrence rate and mortality rate. RESULTS: In the acute phase, there were no differences in terms of fever course, isthmitis improvement, hepatic and splenic lymph node retraction time and the time of atypical lymphocyte falling back to below 10% among the three groups (P>0.05). During the period of follow-up visits between 1 year and 8 years and 10 months, no significant differences were observed in the recovery rate, the recurrence rate and the mortality rate among the three groups (P>0.05). CONCLUSIONS: The efficacies of antiviral therapy for IM children appear to be similar to non-antiviral therapy, suggesting that antiviral therapy fails to be beneficial for IM children.

Template Removal and Surface Modification of an SSZ-13 Membrane with Heated Sodium Chloride for CO2/CH4 Gas Separation.

Hydrothermal synthesis with an organic template of N,N,N trimethyl-1-adamantammonium hydroxide (TMAdaOH) is the most commonly used method to prepare an SSZ-13 zeolite membrane. In this paper, the synthesized membrane was treated in heated sodium chloride to remove TMAdaOH instead of calcination in air. The surface of the membrane was modified by the heated NaCl and resulted in an improved CO2/CH4 gas separation selectivity. TMAda+ in the channels of SSZ-13 zeolite decomposed completely, and the treatment time was shortened significantly compared with calcination in air. The recrystallization of zeolite reacting with heated NaCl was the possible reason for the improved gas separation performance of the membrane.

[LY294002 blocks the effect of dexamethasone in reducing urine protein in rats by inhibiting PI3K/Akt signaling pathway].

OBJECTIVE: To investigate the involvement of PI3K/Akt signaling pathway in the changes of urine protein in adriamycin-induced nephropathic rats treated with dexamethasone and LY294002 (a PI3K inhibitor). METHODS: SD rats were randomized into normal control group, ariamycin-induced nephropathy group (ADR group), ariamycin+dexamethasone group (DEX group), and ADR+DEX+LY294002 group (LY294002 group). On days 7, 14 and 28 after the treatments, 24-h urine was collected from the rats to analyze the total urine proteins. The renal tissues were obtained on day 28 to examine the expressions of p-AKT, AKT and Bad proteins in the cortical tissues using Western blotting; the expression of Bad mRNA in the cortical tissues was measured by QPCR. RESULTS: Urine protein increased progressively in ADR group accompanied by significantly reduced p-AKT/AKT ratio and increased Bad mRNA expression in comparison with those in the normal control group (P<0.05). Urine protein was obviously reduced in DEX group with comparable p-AKT/AKT ratio and Bad mRNA expression level with those in the control group (P>0.05). Urine protein showed no significant reduction in LY294002 group, but the p-AKT/AKT ratio was significantly reduced and Bad mRNA expression was increased compared with those in DEX group (P<0.05). CONCLUSION: Dexamethasone increases the expression of Bad mRNA and reduces urine protein in adriamycin-induced nephropathic rats by activating PI3K/Akt signaling pathway. LY294002 can inhibit PI3K/Akt signaling pathway to block the effect of dexamethasone, suggesting that PI3K/Akt signaling pathway is one of the signaling pathways that mediate the effect of dexamethasone on proteinuria.

Effects of BD1047, a σ1 receptor antagonist, on the expression of mTOR, Camk2γ and GSK-3ß in fluvoxamine-treated N2a cells.

Fluvoxamine, a common antidepressant agent, is designed to exert its pharmacological effect by inhibiting synaptic serotonin reuptake. However, increasing evidence has demonstrated that σ1 receptors are likely to be involved in the mechanism of action of fluvoxamine. The present study aimed to observe the effects of fluvoxamine on the expression levels of mammalian target of rapamycin (mTOR), Ca2+/calmodulin-dependent protein kinase 2γ (Camk2γ) and glycogen synthase kinase-3ß (GSK-3ß) in fluvoxamine-treated N2a cells and attempted to elucidate whether σ1 receptors mediate the pharmacological effects of fluvoxamine. The N2a cells were randomly divided into three groups (each n=6): DMEM group (D group), 0.5 µmol/l fluvoxamine group (F group) and 0.2 µmol/l BD1047 (a σ1 receptor antagonist) + 0.5 µmol/l fluvoxamine group (BF group). Western blotting was used to determine the expression levels of mTOR, Camk2γ and GSK-3ß in the cultured N2a cells after two days of incubation. The F group exhibited significant increases in the expression levels of mTOR and Camk2γ and a significant reduction in the expression levels of GSK-3ß compared with those in the D group (P<0.01). By contrast, the BF group demonstrated significant reductions in the expression levels of mTOR and Camk2γ and a significant increase in the expression levels of GSK-3ß, compared with those in the F group (P<0.01). These results suggest that σ1 receptors mediate fluvoxamine-elicited changes in the expression levels of mTOR, Camk2γ and GSK-3ß in N2a cells, which indicates that σ1 receptors are likely to be involved in the pharmacological effects of fluvoxamine.

Effects of nebulized ketamine on allergen-induced airway hyperresponsiveness and inflammation in actively sensitized Brown-Norway rats.

Since airway hyperresponsiveness (AHR) and allergic inflammatory changes are regarded as the primary manifestations of asthma, the main goals of asthma treatment are to decrease inflammation and maximize bronchodilation. These goals can be achieved with aerosol therapy. Intravenous administration of the anesthetic, ketamine, has been shown to trigger bronchial smooth muscle relaxation. Furthermore, increasing evidence suggests that the anti-inflammatory properties of ketamine may protect against lung injury. However, ketamine inhalation might yield the same or better results at higher airway and lower ketamine plasma concentrations for the treatment of asthma. Here, we studied the effect of ketamine inhalation on bronchial hyperresponsiveness and airway inflammation in a Brown-Norway rat model of ovalbumin (OVA)-induced allergic asthma. Animals were actively sensitized by subcutaneous injection of OVA and challenged by repeated intermittent (thrice weekly) exposure to aerosolized OVA for two weeks. Before challenge, the sensitized rats received inhalation of aerosol of phosphate-buffered saline (PBS) or aerosol of ketamine or injection of ketamine respectivity. Airway reactivity to acetylcholine (Ach) was measured in vivo, and various inflammatory markers, including Th2 cytokines in bronchoalveolar lavage fluid (BALF), as well as inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in lungs were examined. Our results revealed that delivery of aerosolized ketamine using an ultrasonic nebulizer markedly suppressed allergen-mediated airway hyperreactivity, airway inflammation and airway inflammatory cell infiltration into the BALF, and significantly decreased the levels of interleukin-4 (IL-4) in the BALF and expression of iNOS and the concentration of NO in the inflamed airways from OVA-treated rats. These findings collectively indicate that nebulized ketamine attenuated many of the central components of inflammatory changes and AHR in OVA-provoked experimental asthma, potentially providing a new therapeutic approach against asthma.