钙处理工艺对夹杂物变性理论分析与实践

通过钙处理的热力学分析,界定钢液中w（Al）、w（S）、φ（O）对钙处理夹杂物的变性的影响,并针对萍钢二炼钢厂冶炼的钢水条件,改变钙处理的工艺条件。从而改善钢水品质,保证了钢水的可浇注性以及材质的性能。     

关于规范和优化钙处理技术的探讨

介绍了钢水钙处理技术对夹杂物变性作用的基本原理,并分别从钙处理条件、喂线技术参数、吹氩流量控制以及最佳处理时间等方面探讨了规范和优化钙处理技术的几项措施,以求最大程度地降低夹杂物含量,提高钢水洁净度。     

钙含量对钢水流动性的影响

钙处理钢水能够在较低过热度下正常浇铸.为弄清楚钙处理影响钢水流动性的原因和确定最佳的钙含量范围,从钙含量和钢水中夹杂物固相率之间的关系方面研究了钙元素在钢水中的行为.分析不同钙含量的钙处理钢试样中的夹杂物成分并利用Al2O3-CaO-SiO2三元相图确定试样中钙铝和钙铝硅酸盐夹杂物在浇铸温度下的存在状态,由此得到钙含量和夹杂物固相率之间的关系.改善钢水流动性最佳的钙含量范围在(17～23)×10-6之间.     

浇铸钙处理钢水堵水口原因分析及工艺改进

从钢水喂钙处理机理出发,分析了浇注钙处理钢水时钢包水口堵塞的影响因素,提出了钙处理工艺的有关改进措施,解决了钢包堵水口的问题。     

钢水的实芯纯钙线钙处理工艺优势及应用

介绍了钢水钙处理工艺的基本原理及条件,分析了钢水的实芯纯钙线钙处理工艺优势,与钙铁线相比,使用实芯纯钙线喂线长度减少50%,钙的吸收率提高10%,并且减少了钢水的温降。结合宣钢炼钢厂钙吸收率和钢水增钙试验,分析了实芯纯钙线的喂线速度对钙吸收率的影响,最终确定120 m/min为最佳喂线速度。应选择在钢液下降流的中心位置喂线,尽量远离吹氩亮圈。     

钙处理钢中夹杂物行为的研究

为改善武钢CSP产线钢水的连浇性,通过工业试验对钙处理钢中夹杂物的变化进行了研究,试验结果表明,钙处理后,钢中夹杂由Al2O3和MnS转变为铝酸钙盐或CaO-Al2O3-MgO-CaS复合夹杂,由于钙处理对夹杂物的聚合变性作用,钢中夹杂物直径不小于5μm的比例增加。通过热力学计算,分析了钙处理使夹杂物变性的条件。根据试验结果对工艺进行了优化,钢水结瘤断浇次数由3.6次/月降低到1.5次/月。     

钢水的钙处理和对滑板的侵蚀分析

介绍了钙处理钢水的效果，对滑板侵蚀的原因进行分析，一定的钙含量可保证锚链钢水的流动性和避免滑板被侵蚀。     

高钙线在LF精炼炉的生产实践

文章主要研究转炉炼钢现有生产条件下高钙线钙处理的可行性、工艺技术方法及冶金效果,与原铁钙线处理做比较,并进一步优化高钙线处理工艺,提高钙回收率,改善钢水流动性、降低吨钢钙处理成本,减少烟尘的排放。     

实芯纯钙线和硅钙线钙处理效果比较及其工艺优化

主要研究在转炉炼钢厂现有生产条件下,实芯纯钙线钙处理的可行性、工艺技术方法及冶金效果,并与原硅钙线钙处理比较,以期优化钙处理工艺,提高Ca回收率,改善钢水流动性,降低吨钢钙处理成本。     

钙处理对连铸钢浇注性能的影响

分析讨论了钙处理对连铸钢浇注性能的影响。钢中加入适量钙形成液态铝酸钙 ,可以改善其浇注性能 ;如果钙处理不当不仅影响钢水浇注 ,还会影响钢水在结晶内的凝固行为     

NGF-induced cytotoxicity in PC12 cells in a hypoglycemic environment

Surprisingly, we observed that nerve growth factor (NGF) potentiated death of PC12 cells induced by glucose withdrawal, although NGF is widely believed to exert its protective role against several types of cell death. Since either glucose withdrawal or NGF treatment increases intracellular calcium levels of target cells in many cases, we hypothesized that further increase of intracellular calcium by NGF may be a determinant factor in the NGF-mediated cell death. To test this hypothesis, we examined the effect of NGF on cell death pharmacologically by measuring cell viability and traced the changes of intracellular calcium in various conditions using a confocal laser microscope. NGF promoted cell death under a glucose-deprived condition in a manner dependent on extracellular calcium, and nifedipine, but not ryanodine, could partially block the cell death. NGF treatment augmented further intracellular calcium that had been elevated by glucose withdrawal, the event that nifedipine could block. In this study, therefore, we tentatively concluded that NGF potentiates cell death of starved PC12 cells by accelerating the initial increase of intracellular calcium through activation of a dihydropyridine-sensitive calcium channel.     

溶胶-凝胶法制备碳酸钙晶须

用溶胶-凝胶法制备碳酸钙晶须,研究恒温水浴温度、搅拌速度、热处理温度和时间对碳酸钙晶须形貌的影响,并对影响机理进行分析.制备时,首先在恒温水浴搅拌条件下把碳酸钙溶入乙酸,稍后加入柠檬酸得到含Ca中间体,最后加热保温使中间体分解获得碳酸钙晶须.研究表明,在水浴温度80℃,搅拌速度150 r/min,热处理温度700℃和保温2 h的条件下,可得到直径100～150 nm,长约4μm的碳酸钙晶须.     

A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia

Nine cases of symptomatic bradycardia are presented in which treatment with intravenous glucagon was administered when atropine failed to improve the patient's condition significantly. Although the cause often was not obvious at presentation, all nine subjects took oral medications that could have contributed to the development of symptomatic bradycardia. Eight of nine patients demonstrated clinical improvement 5 to 10 min after glucagon administration, which was consistent with its peak clinical action. Beta-blockers, calcium channel blockers, and digoxin were ultimately thought to have contributed to the majority of these presentations. This report suggests that glucagon may have a role in the treatment of symptomatic bradycardia, particularly in the presence of beta-adrenergic blockade and perhaps calcium channel blockade. Furthermore, the results in these cases suggest that future clinical trials should not be limited to drug-induced symptomatic bradycardia.     

Modulating L-type calcium current affects discontinuous cardiac action potential conduction

We have used pairs of cardiac cells (i.e., one real guinea pig ventricular cell and a real-time simulation of a numerical model of a guinea pig ventricular cell) to evaluate the effects on action potential conduction of a variable coupling conductance in combination with agents that either increase or decrease the magnitude of the L-type calcium current. For the cell pairs studied, we applied a direct repetitive stimulation to the real cell, making it the "leader" cell of the cell pair. We have demonstrated that significant delays in action potential conduction for a cell pair can occur either with a decreased value of coupling conductance or with an asymmetry in size such that the follower cell is larger than the leader cell. In both conditions we have shown that isoproterenol, applied to the real cell at very low concentrations, can reversibly decrease the critical coupling conductance (below which action potential conduction fails) for a cell pair with fixed cell sizes, or, for a fixed value of coupling conductance, increase the maximum allowable asymmetry in cell size for successful conduction. For either of these effects, we were able to show that treatment of the real cell with BayK 8644, which more specifically increases the magnitude of the L-type calcium current, was able to mimic the actions of isoproterenol. Treatment of the leader cell of the cell pair (the real cell) with nifedipine, which selectively lowers the magnitude of the L-type calcium current, had effects opposite those of isoproterenol or BayK 8644. The actions of nifedipine, isoproterenol, and BayK 8644 are all limited to conditions in which the conduction delay is on the order of 5 ms or more, whether this delay is caused by limited coupling conductance or by asymmetry in size of the cells. This limitation is consistent with the time course of the L-type calcium current and suggests that the effects of calcium channel blockers or beta-adrenergic blocking drugs, in addition to being selective for regions of the heart that depend on the L-type calcium current for the upstroke of the action potential, would also be somewhat selective for regions of the heart that have discontinuous conduction, either normally or because of some pathological condition.     

Glucocorticoid-induced osteoporosis: prevention and treatment

Glucocorticoid excess carries the risk of inducing secondary osteoporosis. In endogenous Cushing's syndrome, osteoporosis may be the presenting symptom of the underlying disease. Bone loss may reverse after the condition is cured, but often active treatment of established osteoporosis is necessary. In long-term glucocorticoid treatment at therapeutic doses, bone loss is likely and should be prevented; if prevention is ineffective, treatment is necessary. Hypercortisolism impairs calcium homeostasis and bone metabolism in a complex, multifactorial way: Glucocorticoids diminish calcium absorption and increase renal calcium excretion; this negative calcium balance leads to secondary hyperparathyroidism and osteoclast activation. Osteoblast activity is directly impaired by glucocorticoids, which lower activity of the gonadal hormone axis so that hypogonadism also contributes to bone loss. Glucocorticoids lead to muscle atrophy and decreased muscle strength with negative consequences for bone formation. For prevention and treatment, two different strategies have been used. The pathophysiological approach substitutes calcium and vitamin D in the first step; if bone loss nevertheless continues, bone formation is stimulated by fluorides. The alternative pharmaco-dynamic approach uses antiresorptives-calcitonin or, for preference, bisphosphonates. Clinically it is mandatory to monitor all patients in whom glucocorticoids are used (e.g., organ transplant recipients) before and after the initiation of treatment to stabilize bone metabolism as early as possible.     

Intracellular calcium and blood pressure: comparison between primary hyperparathyroidism and essential hypertension

Intracellular calcium has been reported to be increased in essential hypertension, and thought to play a role in its genesis through facilitation of vascular smooth muscle contraction. Since hypertension is more prevalent in primary hyperparathyroidism, intracellular calcium may also be increased in this condition. To investigate whether the hyperparathyroid condition, i.e., hypercalcemia and increased PTH per se, could be associated with high intracellular calcium, we measured intracellular calcium in platelets with the Quin-2 AM fluorometric method in 11 normotensive patients with primary hyperparathyroidism, 15 patients with essential hypertension, and 18 normal controls, all matched for age and sex. We repeated the measurements in 9 of the hyperparathyroid patients after successful surgery. We found that intracellular calcium was higher in normotensive patients with primary hyperparathyroidism than in normal controls (198 +/- 24 vs 113 +/- 11 nM, p < 0.05), but lower than in patients with essential hypertension (198 +/- 24 vs 286 +/- 38 nM, p < 0.05). Successful removal of a parathyroid adenoma decreased intracellular calcium from 215 +/- 22 to 116 +/- 19 nM, (p < 0.01). In the patients with primary hyperparathyroidism, intracellular calcium was strongly correlated with the levels of PTH (r = 0.87, p < 0.01), but not with the total serum calcium levels (r = 0.04, NS). The decrease in intracellular calcium after parathyroidectomy was also strongly correlated with the decrease in PTH (r = 0.84, P < 0.01), but not with the decrease in total serum calcium (r = 0.16, NS). In the patients with essential hypertension, intracellular calcium correlated well with systolic (r = 0.69, p < 0.01), diastolic (r = 0.76, p < 0.01) and especially mean arterial pressure (r = 0.86, P < 0.01). There was no correlation between blood pressure and intracellular calcium in the patients with primary hyperparathyroidism. We conclude that normotensive patients with primary hyperparathyroidism, as well as patients with essential hypertension, can have increased concentrations of intracellular calcium in platelets. The correction of the hyperparathyroid condition normalizes intracellular calcium concentration. The close correlation between PTH and intracellular calcium suggests that PTH may act as a ionophore for calcium entry into cells. Whether the increased levels of intracellular calcium may reflect a pre-hypertensive condition in normotensive patients with primary hyperparathyroidism remains to be determined.     

The regulation of calcium homeostasis in nerve cells

We have reviewed the major cellular elements related to the release and buffering of calcium in neurons. Voltage-operated, chemical-operated calcium channels and mechanisms of stability of intercellular calcium homeostasis (mitochondria, endoplasmic reticulum, calcium binding proteins, calcium exchange and calcium pump) are demonstrated in normal and pathological condition (105 ref.).     

The PACT model

Topical application of the vitamin D analogue calcipotriol has been found to be of clinical value in the treatment of dermatological disorders. This is considered to be safe with respect to alterations in calcium homeostasis. We report a 17-year-old female patient who developed hypercalcaemic crisis after excessive use of calcipotriol for ichthyosis. The clinical condition and serum calcium improved after cessation of calciprotiol treatment and rehydration with intravenous fluids and electrolytes. The case emphasizes the importance of limiting the topical use of calcipotriol as recommended by the manufacturer.     

电石渣为钙源的硅热法炼镁煅烧过程

电石渣是化工行业用乙炔法生产乙炔气或聚氯乙烯树脂的工业废渣,其主要成分为Ca(OH)2,是高碱性物质,属于较难处理的工业废弃物.现有处理电石渣的工艺都存在不足之处,因此电石渣的综合利用是近年来研究的重点与热点问题.本文提出以电石渣为钙源的硅热法炼镁工艺,可综合利用电石渣,将其与菱镁石、萤石和硅铁制成预制球团,用于真空热...     

钙处理对含铝冷镦钢夹杂物的影响

利用扫描电镜对80 t LF钢液喂钙处理前后的冷镦钢SWRCH22A中夹杂物形态和组成的变化进行了分析和研究,对钙处理钢中夹杂物的变性进行了热力学计算。研究表明,SWRCH22A钢液钙处理后夹杂物中的Mn被Ca置换,中间包内钢中Al₂O₃夹杂变性生成低熔点铝酸钙夹杂12CaO·7Al₂O₃;如要钢液钙处理生成易上浮排除的液态12CaO·7Al₂O₃夹杂的必要条件是[Al]_T²/[Ca]_T³≤10.58×10⁴。