新型镁钙铝浇注料的脱磷作用研究

将等质量而磷含量不同的铁粉分别置于以高铝水泥为结合剂浇注成型的镁钙铝质坩埚内 ,并将坩埚埋入石墨粉中经 1 6 0 0℃保温 2h ,冷却后测定金属样中和坩埚衬表层的磷含量 ,发现金属样中磷含量显著下降而坩埚衬中磷含量增多 ,表明该浇注料有脱磷作用。采用SEM和EDAX方法探讨了浇注料脱磷机理和过程。其脱磷作用是由于镁钙砂中游离态的氧化钙能逐步吸收转化磷杂质为磷硅酸钙的固溶体存在于浇注料中     

Photoperiodic history and hypothalamic control of prolactin secretion before birth

Many neuromodulators inhibit N-type Ca2+ currents via G protein-coupled pathways in acutely isolated superior cervical ganglion (SCG) neurons. Less is known about which neuromodulators affect release of norepinephrine (NE) at varicosities and terminals of these neurons. To address this question, we used carbon fiber amperometry to measure catecholamine secretion evoked by electrical stimulation at presumed sites of high terminal density in cultures of SCG neurons. The pharmacological properties of action potential-evoked NE release paralleled those of N-type Ca2+ channels: Release was completely blocked by Cd2+ or omega-conotoxin GVIA, reduced 50% by 10 microM NE or 62% by 2 microM UK-14,304, an alpha2-adrenergic agonist, and reduced 63% by 10 microM oxotremorine M (Oxo-M), a muscarinic agonist. Consistent with action at M2 or M4 receptor subtypes, Oxo-M could be antagonized by 10 microM muscarinic antagonists methoctramine and tropicamide but not by pirenzepine. After overnight incubation with pertussis toxin, inhibition by UK-14,304 and Oxo-M was much reduced. Other neuromodulators known to inhibit Ca2+ channels in these cells, including adenosine, prostaglandin E2, somatostatin, and secretin, also depressed secretion by 34-44%. In cultures treated with omega-conotoxin GVIA, secretion dependent on L-type Ca2+ channels was evoked with long exposure to high K+ Ringer's solution. This secretion was not sensitive to UK-14,304 or Oxo-M. Evidently, many neuromodulators act on the secretory terminals of SCG neurons, and the depression of NE release at terminals closely parallels the membrane-delimited inhibition of N-type Ca2+ currents in the soma.     

Respiratory diphtheria in the United States, 1980 through 1995

OBJECTIVES: The purpose of this study was to describe the epidemiologic, laboratory, and clinical features of respiratory diphtheria cases reported in the United States during 1980 through 1995. METHODS: Respiratory diphtheria cases reported to the Centers for Disease Control and Prevention were reviewed. Cases were defined as physician-diagnosed cases with signs and symptoms compatible with respiratory diphtheria, including the presence of a pseudomembrane without other apparent cause. RESULTS: From 1980 through 1994, 41 respiratory diphtheria cases were reported; none were reported in 1995, and no secondary cases were identified. Nine (22%) case patients were 4 years of age or younger, and 28 (68%) were 15 years of age or older. None of the case patients were up to date with diphtheria vaccination; 4 unvaccinated children died. Seventeen (43%) of 40 case patients had positive culture results. CONCLUSIONS: Available surveillance data suggest that respiratory diphtheria has become a rare disease in the United States. However, importation and circulation of toxigenic strains continue to present a threat and require achieving and maintaining high coverage with diphtheria toxoid-containing vaccines in both children and adults.