Electroplating of nickel-cadmium alloys from alkaline solutions

The electroplating of Ni-Cd alloy coatings was carried out from alkaline baths (pH 10). For comparison, electroplating of the parent metals, Ni and Cd, was performed individually under the same conditions. The cathodic current efficiency for codeposition was high and decreased with increasing current density. The codeposition process is an anomalous type of plating with Cd being the preferentially deposited metal. The Ni content in the deposits increased with increasing current density. This increase in Ni content improves the corrosion resistance and microhardness of the deposits. X-ray diffraction analysis showed that the deposits consist of a mixture of Ni, β, γ, γ¹ phases.     

标准椅全身计数器对不同年龄组均匀体模源全能峰效率的刻度

本文介绍了用标准液体源均匀充入聚氯乙烯制的体模,刻度标准椅全身计数器〔φ8″×4″(NaI)〕的方法和结果。分别就代表6个年龄组的体模,测定了标准椅全身计数器对5种能量(364,637,898,1460和1836keV)γ射线的全能峰效率;给出了全能峰效率与γ射线能量和被测对象体重的关系曲线。     

On the mechanisms of adenosine induced pulmonary vasoconstriction in rats

The effect of adenosine on pulmonary vessels was studied in isolated perfused rat lungs. Drugs were administered intra-arterially in a fixed volume of 0.1 ml Krebs solution as bolus injections. Adenosine responses were obtained before and 10 min after drug injections. When applied in logarithmically increasing doses (1-100 micrograms/ml), adenosine caused dose-dependent increases in pulmonary perfusion pressure (e.g. pulmonary vasoconstriction) which were readily reversible. Challenging adenosine with quinidine, dihydroergocristine and cyproheptadine (2 micrograms/ml each) did not significantly alter adenosine responses. Pretreatment of lungs with 0.5 mM theophylline, 10 micrograms/ml indomethacin, 30 micrograms/ml tebokan (a PAF antagonist) or 1 microgram/ml methylene blue for 10 min, however, antagonized the vasoconstrictor effect of the drug significantly. From these experiments, it was concluded that the mechanisms underlying the pulmonary vasoconstrictor action of adenosine are complex, and that both types of purinoceptors, prostaglandins, PAF and other vascular endothelial hormones might be involved.