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Amorphous nickel hydroxide codoped with Y and Mg was synthesized by micro-emulsion precipitation method combined with rapid freezing technique. The physical properties and micro-structural features of the prepared sample were characterized and high-temperature electrochemical performance was analyzed by cyclic voltammetry and charge/discharge tests, respectively. The results indicate that this amorphous nickel hydroxide codoped with Y and Mg has more structural defects and better thermal stability, therefore results in a relatively high specific capacity(332.46 mAh•g-1 at a charge/discharge rate of 0.2C) and a high middle discharge voltage of 1.265V at 60℃. Moreover, the Y and Mg codoped amorphous nickel hydroxide exhibits good electrochemical reaction reversibility and structural stability.

Amorphous nickel hydroxide powders codoped with Ce and Fe were synthesized by the combined chemical precipitation and rapid freezing method. The microstructure and chemical composition of the samples was characterized by XRD,SAED and EDS. The electrochemical performance of the prepared samples was analyzed by cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), and charge-discharge tests. The results showed that this amorphous nickel hydroxide codoped with Ce and Fe had more structural defects than those of Fe singly doped amorphous nickel hydroxide. These abundant structural defects with Ce and Fe codoped amorphous nickel hydroxide increased the thermal stability, decreased the charge transfer resistance, inhibited oxygen evolution reaction effectively and improved the electrochemical reversibility of the amorphous nickel hydroxide electrode.

In this paper, cathode material nickel hydroxide powder of MH-Ni battery was prepared through the method of micro emulsion deepfreeze deposition with the system of Tween-80/n-C4H9OH/c-C6H12/NiSO4 solution. By measurement of the maximum content of water of different micro-emulsion system, optimum system was determined. The effect of temprature, concentration and amount of nickel sulfate solution to the particle size of the sample powder was also discussed. The structural morphology of the sample powder were analyzed and measured by XRD, SAED, SEM, TEM and particle size distribution of the sample was also analyzed. The results showed that the sample was amorphous nano-sized particles, and the size distribution was wide.

Amorphous nickel hydroxide powder codoped with Fe3+ and PO43- was synthesized by micro-emulsion precipitation method combined with rapid freezing technique. The microstructures of the prepared samples were characterized by XRD, SEM, EDS, and Raman spectra. The electrochemical performance of the prepared samples was analyzed by cyclic voltammetry, electrochemical impedance spectroscopy, and charge-discharge tests. The results showed that this amorphous nickel hydroxide codoped with Fe3+ and PO43- resulted in more structural defects within the nickel hydroxide. The Fe3+ and PO43- codoping could increase the specific discharge capacity and improve the electrochemical reversibility of the amorphous nickel hydroxide.

Amorphous nickel hydroxide powders doped with rare earth La3+ and Al3+ were synthesized by the combined chemical precipitation and rapid freezing method. The microstructure of the samples was characterized by XRD and Raman spectra. The electrochemical performance of the prepared samples was analyzed by electrochemical impedance spectroscopy and charge-discharge tests. The results showed that this amorphous nickel hydroxide codoped with La3+ and Al3+ had more structural defects than those of the undoped amorphous nickel hydroxide and La3+ singly doped amorphous nickel hydroxide. These abundant structural defects with La3+ and Al3+ codoped amorphous nickel hydroxide decreased the electrochemical impedance spectroscopy and improved the electrochemical reversibility of the amorphous nickel hydroxide electrode.

ABSTRACTInterleukin-23 (IL-23), a member of the IL-12 family, is a heterodimeric cytokine that is composed of the p40 subunit of IL-12 plus a unique p19 subunit. IL-23 is critical for autoimmune inflammation, in part due to its stimulation of the proinflammatory cytokine IL-17A. It is less clear, however, if IL-23 is required during the immune response to pathogens. We examined the role of IL-23 during Mycobacterium bovisBCG infection. We found that IL-23 reduces the bacterial burden and promotes granuloma formation when IL-12 is absent. However, IL-23 does not contribute substantially to host resistance when IL-12 is present, as the ability to control bacterial growth and form granulomata is not affected in IL-23p19-deficient mice and mice treated with a specific anti-IL-23p19 antibody. IL-23p19-deficient mice are also able to mount an effective memory response to secondary infection with BCG. While IL-23p19-deficient mice do not produce IL-17A, this cytokine is not necessary for effective control of infection, and antibody blocking of IL-17A in both wild-type and IL-12-deficient mice also has little effect on the bacterial burden. These data suggest that IL-23 by itself does not play an essential role in the protective immune response to BCG infection; however, the presence of IL-23 can partially compensate for the absence of IL-12. Furthermore, neutralization of IL-23 or IL-17A does not increase susceptibility to mycobacterial BCG infection.

Interleukin-23 (IL-23), a member of the IL-12 family, is a heterodimeric cytokine that is composed of the p40 subunit of IL-12 plus a unique p19 subunit. IL-23 is critical for autoimmune inflammation, in part due to its stimulation of the proinflammatory cytokine IL-17A. It is less clear, however, if IL-23 is required during the immune response to pathogens. We examined the role of IL-23 during Mycobacterium bovis BCG infection. We found that IL-23 reduces the bacterial burden and promotes granuloma formation when IL-12 is absent. However, IL-23 does not contribute substantially to host resistance when IL-12 is present, as the ability to control bacterial growth and form granulomata is not affected in IL-23p19-deficient mice and mice treated with a specific anti-IL-23p19 antibody. IL-23p19-deficient mice are also able to mount an effective memory response to secondary infection with BCG. While IL-23p19-deficient mice do not produce IL-17A, this cytokine is not necessary for effective control of infection, and antibody blocking of IL-17A in both wild-type and IL-12-deficient mice also has little effect on the bacterial burden. These data suggest that IL-23 by itself does not play an essential role in the protective immune response to BCG infection; however, the presence of IL-23 can partially compensate for the absence of IL-12. Furthermore, neutralization of IL-23 or IL-17A does not increase susceptibility to mycobacterial BCG infection.

Atrial natriuretic peptide (ANP) has negative modulatory effects on a variety of pathophysiological mechanisms; i.e., it inhibits hypoxia-induced pulmonary vasoconstriction and vascular remodeling and facilitates natriuresis and vasorelaxation in NaCl-supplemented subjects. We have previously demonstrated organ-selective potentiation of ANP in the pulmonary circulation of hypoxia-adapted animals by local downregulation of its clearance receptor (NPR-C; Li H, Oparil S, Meng QC, Elton T, and Chen Y-F.Am J Physiol Lung Cell Mol Physiol 268: L328–L335, 1995). The present study tested the hypothesis that NPR-C expression is attenuated selectively in kidneys of NaCl-supplemented subjects. Adult male wild-type (ANP+/+) and homozygous mutant (ANP−/−) mice were studied after 5 wk of normal or high-salt diets. Mean arterial pressure (MAP) and left (LV) and right ventricular (RV) mass were greater in ANP−/− mice than in ANP+/+ mice fed the normal-salt diet; salt supplementation induced increases in plasma ANP in ANP+/+ mice and in MAP and LV, RV, and renal mass in ANP−/− mice but not in ANP+/+ mice. NPR-C mRNA levels were selectively and significantly reduced (>60%) in kidney, but not in lung, brain, LV, or RV, by dietary salt supplementation in both genotypes. NPR-A mRNA levels did not differ among diet-genotype groups in any organ studied. cGMP content was significantly increased in kidney, but not in lung or brain, by dietary salt supplementation in both genotypes. These findings suggest that selective downregulation of NPR-C in the kidney in response to dietary salt supplementation may contribute to local elevation in ANP levels and may be functionally significant in attenuating the development of salt-sensitive hypertension.

Effects of sitaxsentan (TBC11251), an orally active, highly selective antagonist of endothelin A receptors, were examined on the development and maintenance of pulmonary hypertension, pulmonary vascular remodeling, and cardiac hypertrophy in the rat. The pulmonary vasoconstrictor response to acute hypoxia (10% O2for 90 min) was prevented with sitaxsentan (5 mg/kg infused iv 10 min prior to the onset of hypoxia) while BQ-788 (a specific endothelin B receptor antagonist) was without effect. The same dose of sitaxsentan delivered iv 50 min after the onset of hypoxia reversed the established pulmonary vasoconstriction. In a 2-week model of hypoxia using 10% O2, treatment with sitaxsentan (15 mg/kg per day in drinking water) attenuated pulmonary hypertension and the associated right ventricular hypertrophy, and prevented the remodeling of small pulmonary arteries (50–100 μM) without affecting systemic arterial blood pressure or heart rate. Institution of sitaxsentan treatment (15 and 30 mg/kg per day in drinking water) for 4 weeks after 2 weeks of untreated hypoxia produced a significant, dose dependent reversal of the established pulmonary hypertension, right heart hypertrophy, and pulmonary vascular remodeling despite continued hypoxic exposure. Sitaxsentan blocked increased plasma endothelin levels in the prevention protocol but did not affect the established elevated levels in the intervention study. Sitaxsentan dose dependently (10 and 50 mg/kg per day in the drinking water) attenuated right ventricular systolic pressure, right heart hypertrophy, and pulmonary vascular remodeling observed 3 weeks after a single subcutaneous injection of monocrotaline. These findings support the hypothesis that endothelin-1 plays a significant role in the development of pulmonary hypertension, pulmonary vascular remodeling, and the associated cardiac hypertrophy, and further suggest that specific endothelin-A receptor blockade may be useful in the treatment of pulmonary hypertension of diverse etiologies.

Exposure to hypoxia is associated with increased pulmonary artery pressure and plasma endothelin (ET-1) levels and with selective enhancement of ET-1 peptide and messenger RNA (mRNA) and endothelin-A (ET-A) receptor mRNA in rat lung. Our study tested the hypothesis that A-127722, an orally active antagonist of the ET-A receptor, can prevent hypoxia-induced pulmonary hypertension and vascular remodeling in the rat. Pretreatment with A-127722 (3, 10, and 30 mg/kg/day in drinking water for 2 days) caused dose-dependent inhibition of the pulmonary vasoconstrictor response to short-term hypoxia (10% O2, 90 min). Long-term A-127722 treatment (10 mg/kg/day in drinking water for 2 weeks) instituted 48 h before hypoxic exposure attenuated the subsequent development of pulmonary hypertension, the associated right atrial hypertrophy, and pulmonary vascular remodeling. Institution of A-127722 treatment (10 mg/kg/day in drinking water for 4 weeks) after 2 weeks of hypoxia retarded the progression of established hypoxia-induced pulmonary hypertension and right atrial hypertrophy and reversed the pulmonary vascular remodeling despite continuing hypoxic exposure. These findings support the hypothesis that endogenous ET-1 plays a major role in hypoxic pulmonary vasoconstriction/hypertension, right heart hypertrophy, and pulmonary vascular remodeling and suggest that ET-A receptor blockers may be useful in the treatment and prevention of hypoxic pulmonary hypertension in humans.

Atherosclerotic vascular disease progresses more slowly in females with functional ovaries than in males. Balloon injury of the rodent carotid artery is widely used as a model for the early injury phase of atherosclerosis. The current study tested whether female Sprague-Dawley rats (SD) have a reduced (compared to males) vascular growth response to balloon injury and whether this response is estrogen dependent. 10 wk old ♂ and ♀ SD rats were either gonadectomized or studied intact. Gonadectomized rats of both sexes were implanted with (1) 15mm (empty), (2) 10mm (filled with 17-β estradiol [E]) or (3) 15 mm (filled with testosterone [T]) silastic capsules 3 days before balloon injury of the carotid artery. Two wks later, rats were perfused with 10% formalin at 120mmHg and carotid arteries were fixed and subjected to morphometric analysis. Intima/media ratios (I/M%) expressed as degree of myointimal proliferative response to vascular injury were (means ± SEM):♂+ E+TI/M%132±6 (11)132±12 (6)65±11 (6)*117±19 (7)♀+E+TI/M%82±10 (11)#133±25 (6)*38±8 (5)*#123±29 (5)*p<0.05 compared to their respective intact controls#p<0.05 compared to their respective male groups

Objective: This study tested, in ovariectomized rats, whether (1) adventitial activation plays a role in the vascular injury response, and (2) inhibition of adventitial activation and the subsequent wave of cell proliferation moving from adventitia to neointima contributes to the estrogen-induced attenuation of neointima formation in balloon injured carotid arteries. Methods: Ovariectomized Sprague-Dawley rats were treated with either 17β-estradiol or vehicle beginning 72 h prior to balloon injury of the right common carotid artery and were sacrificed at 0, 3, 7, 14 and 28 days after injury. BrdU was administered 18 h and 12 h prior to sacrifice in order to quantitate mitotic activity in adventitia, media and neointima of the damaged vessel at specified times post injury. Results: Adventitial activation, evidenced by positive BrdU staining, was evident on the day of injury, peaked on day 3 and was resolved by day 7, thus preceding neointima formation. Numbers of BrdU labeled cells in adventitia on day 3 were significantly reduced in estrogen treated rats compared to controls. BrdU labeled cells were undetectable in media on the day of injury, appeared at day 3 and disappeared by day 14. Neointima appeared at day 7 and increased in area throughout the period of observation. Neointimal area and numbers of BrdU labeled cells in neointima were significantly reduced in estrogen treated rats compared to controls. These findings suggest that there is a wave of cell proliferation moving in an adventitia-to-lumen direction following endoluminal injury of the rat carotid artery and that estrogen modulates this proliferative response to injury. Conclusion: These results support the hypothesis that adventitial activation contributes to the vascular injury response and that estrogen reduces this contribution.