中和浓缩一体化技术在我厂的应用

中和浓缩一体化技术在我厂的应用蒋兆达洪建华（江苏泰兴市磷肥厂２２５４４２）我厂的料浆法磷铵生产装置与四川省什邡化肥总厂的生产装置基本相同，采用压力喷雾——流化床、逆流干燥制粉状磷酸一铵肥料。原流程的中和浓缩系统中配置了槽式中和反应器附搅拌桨、卫生风机...     

以湿法磷酸与碳酸氢铵为原料连续生产磷酸一铵的技术

介绍以湿法磷酸和碳酸氢铵为原料连续生产磷酸一铵的工艺流程、主要设备;比较碳酸氢铵代替液氨生产磷酸一铵的优缺点,两种工艺应根据具体情况选用。     

两种料浆法粉状磷铵流程比较

介绍了目前国内生产粉状磷铵的主要工艺流程 ,并详细比较了用于“中和料浆浓缩法磷铵工艺”的两种粉状磷铵工艺流程的各项技术经济指标 ,推荐采用“流化床逆流喷雾干燥制粉状磷铵流程     

新型无毒防锈颜料三聚磷酸二氢铝研究进展

介绍三聚磷酸二氢铝的性质、合成工艺及应用。采用湿法磷酸净化替代热法磷酸可降低成本,将成为今后此类防锈颜料的发展方向。特别提到昆明理工大学精细化工教研室,开展了肥料级磷酸一铵水溶液添加一定的净化剂,可使磷酸一铵水溶液达到合成三聚磷酸二氢铝的要求。该法称为磷酸一铵净化法,有望成为取代热法磷酸的理想方法。     

料浆法磷铵用中品位开阳磷矿的实验室评价实验

介绍开阳中品位磷矿采用“料浆浓缩”工艺制取磷酸一铵的评价实验,对湿法磷酸工艺、磷酸氧化、磷铵料浆浓缩和干燥等过程进行了研究,测定了有关的物性数据和技术经济指标,为我国中品位磷矿采用料浆浓缩法制磷酸一铵工艺提供参考数据.     

单管一步中和-转鼓造粒工艺生产粒状MAP技术的开发

介绍国内粉、粒状磷酸一铵各种生产工艺,重点介绍江西贵溪化肥有限责任公司自主创新开发的单管一步中和一转鼓造粒技术生产粒状磷酸一铵的开发依据、试车情况、试车期间存在问题、该技术的优点等.     

聚磷酸铵的合成

研究了在常压条件下以湿法磷酸生产的工业级磷酸一铵和尿素为原料生产聚磷酸铵(APP)的合成工艺条件,制备了平均聚合度为400的聚磷酸铵.研究了磷酸铵、反应温度、组分配比、反应时间对平均聚合度的影响.结果表明,高聚合度APP的优惠生产工艺条件为:尿素与磷酸一铵的摩尔比为2,聚合温度为300℃,聚合时间为3h.聚合反应完成后,冷却,即得粉末状的APP聚合物.     

甜叶菊甙的提取及应用

甜叶菊Stevia Rebaudiana(Bertoni)Hemsl 为菊科多年生草本植物。其叶含有多种甜味物质—甜叶菊甙又称斯替维甙,(Stevioside)等,其中主要成份为双萜甙类。纯品呈白色粉状结晶,甜度为蔗糖的300倍;粗制品呈淡黄色粉状物,甜度为蔗糖的100～200倍。其甜味纯正。国外进行了一系列的药理试验,均证实该糖甙是安全的,[中国农科院作物品种资源研究所译:《甜叶菊的研究     

浓缩磷酸生产工业级磷酸-铵的研究

为满足磷铵干粉灭火剂对磷铵产品的要求 ,研究以浓磷酸为原料 ,直接净化、氨中和生产磷酸一铵。阐述浓磷酸直接净化的难点及现已取得的关键技术成果 :6种专用添加剂组成的特殊高效复合净化剂 ,专利设备氨化反应结晶器。介绍利用宏福磷肥厂生产的浓磷酸 (～ 5 0 %P2 O5)直接净化生产工业级磷酸一铵的工艺流程、原料、产品及对单位产品的成本、投资估算情况。产品NH4H2 PO4质量分数 98 0 1% ,车间成本 2 12 4元 /t,按 5kt/a计 ,年创利税约 2 0 0余万元 ,投资 195万元。本技术与设备均可适用于其他磷酸盐生产。     

不同剂型活性炭对急性敌敌畏中毒大鼠的疗效评价研究

目的通过观察粉状炭、片状炭和活性炭混悬液对致死量和非致死量敌敌畏染毒大鼠的解毒作用,评价不同剂型活性炭在解救急性有机磷中毒时的疗效。方法致死剂量组：将健康大鼠40只随机分为4组,3组为活性炭治疗组,1组为染毒未治疗组。全部动物一次灌胃给予敌敌畏45mg／kg染毒,灌胃容积为1ml／100g。染毒5min后开始治疗：粉状炭治疗组给予粉状炭1g／kg;混悬液组给予活性炭混悬液1g/kg;片状炭治疗组给予片状炭1g／kg;染毒未治疗组给予蒸馏水。观察各组动物死亡情况,比较4组动物病死率。非致死剂量组：健康大鼠32只随机分为4组,全部动物禁食24h后,全部动物一次灌胃给予敌敌畏15mg／kg染毒,灌胃容积为1ml／100g。染毒5min后开始治疗：粉状炭治疗组给予粉状炭1g/kg,混悬液组给予活性炭混悬液1g／kg,片状炭治疗组给予片状炭1g／kg,染毒未治疗组给予蒸馏水,以上各组均灌胃给药,给药容积为1ml／100g。4组动物分别以染毒前、染毒后0．5、2、6、24h断尾采血10μl,测定全血胆碱酯酶活性,计算胆碱酯酶抑制率[（染毒前胆碱酯酶活性-染毒后胆碱酯酶活性）／染毒前胆碱酯酶活性],比较4组不同时间胆碱酯酶抑制率。并比较4组动物中毒后肌束颤动的差异。结果与染毒未治疗组比较只有粉状炭治疗组显著减低致死量敌敌畏大鼠的病死率（P〈0．01）;3种剂型活性炭均能显著减轻非致死量敌敌畏对大鼠胆碱酯酶的抑制率（P〈0．05）,其中粉状炭的作用明显强于片状炭和活性炭混悬液（P〈0．05）;另外粉状炭能明显减轻非致死量敌敌畏致肌束颤动作用（P〈0．05）。结论粉状炭具有较好的解救急性有机磷中毒的作用。     

N-acetylcysteine attenuates TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells

1. We have previously shown that tumour necrosis factor-alpha (TNF-alpha) activates p38 mitogen-activated protein (MAP) kinase to produce interleukin-8 (IL-8) by human pulmonary vascular endothelial cells. Reactive oxygen species (ROS) including H(2)O(2) generated by TNF-alpha can act as signalling intermediates for cytokine induction; therefore, scavenging ROS by anti-oxidants is important for the regulation of cytokine production. However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined. To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production. 2. Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined. 3. Intracellular GSH levels increased in NAC-treated cells. 4. NAC attenuated TNF-alpha-induced activation of p38 MAP kinase and MKK3/MKK6. 5. NAC attenuated p38 MAP kinase-mediated IL-8 production by TNF-alpha-stimulated cells. 6. These results indicate that the cellular reduction and oxidation (redox) regulated by intracellular GSH is critical for TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells, and we emphasize that anti-oxidant therapy is an important strategy for the treatment of acute lung injury.     

200kt／a料浆法粉状MAP生产装置的技术创新

介绍采用"中和料浆浓缩法工艺"的粉状MAP装置与采用传统"磷酸浓缩工艺"的大型进口粒状DAP装置实现"联产",促进、优化后者的生产和经营的科技创意与实践效果,以及联产装置内采用的部分创新技术,如强制循环氨中和蒸发反应器、中和蒸汽二次利用节能技术.     

Regulation of histamine production in macrophages

Stimulating cells of the mouse macrophage-like cell line RAW 264.7 with the Ca(2+)-ATPase inhibitor thapsigargin increased histamine production. Thapsigargin increased the levels of histidine decarboxylase (HDC) mRNA at 4 h and the expression of 74-kDa HDC protein at 8 h. PD98059, a specific inhibitor of MEK-1 which phosphorylates p44/p42 MAP kinase, strongly suppressed the thapsigargin-induced histamine production, the increase in HDC mRNA level and 74-kDa HDC protein expression. In contrast, SB203580, an inhibitor of p38 MAP kinase, showed only a partial inhibition of histamine production. TPA and LPS also induced histamine production in RAW 264.7 cells, and the histamine production induced by TPA or LPS was also inhibited by PD98059, but the effect of SB203580 was partial. The synthetic glucocorticoid dexamethasone inhibited thapsigargin-induced histamine production, 74-kDa HDC protein expression and the activation of p44/p42 MAP kinases. In conclusion, the increase in histamine production in macrophages stimulated with inflammatory stimulants is due to the increased expression of 74-kDa HDC, which is positively regulated by activated p44/p42 MAP kinases. Dexamethasone inhibits thapsigargin-induced HDC protein expression and histamine production by inhibiting the MAP kinase activation.     

Structure-activity relationships of p38 mitogen-activated protein kinase inhibitors

Rheumatoid arthritis and other chronic inflammatory diseases constitute a major therapeutic challenge, usually not sufficiently met by the classical antiinflammatory medications. Recent research efforts provided new insights into the molecular basis of these pathologies and disclosed new opportunities for developing improved drugs directed to the chemical mediators of the disease. The enzyme p38 MAP kinase plays a central role in the signal transduction cascade that leads to the production of both the proinflammatory cytokines, TNF-alpha and IL-1 beta, thus representing an attractive therapeutic target for novel antiinflammatory therapies. A number of p38 inhibitors belonging to different structural families have been developed as potential antiinflammatory drugs, and some of them progressed into clinical trials. The initial pyridinyl imidazole inhibitors contributed to the identification and characterization of p38 MAP kinase as the molecular target of these new drugs, and were found to act as competitive inhibitors at the ATP binding site of the enzyme. A number of variations in the pyridine and imidazole rings were subsequently introduced. Other inhibitors structurally unrelated to the pyridinylimidazoles have also been developed, such as the pyridopyridazinones, diaryl ureas, aminobenzophenones and aromatic amides. One of these structural classes, the N,N'-diarylureas, has been found to interact with a distinct allosteric site of p38 MAP kinase and requires a deep conformational change prior to binding.     

Participation of mitogen-activated protein kinase in thapsigargin- and TPA-induced histamine production in murine macrophage RAW 264.7 cells

1. Stimulation of the murine macrophage cell line RAW 264.7 with thapsigargin, an endomembrane Ca(2+)-ATPase inhibitor, induced histamine production in a time- and concentration-dependent manner. 2. The protein kinase C activator, 12-O-tetradecanoylphorbol 13-acetate (TPA), also enhanced histamine production. 3. alpha-Fluoromethylhistidine, a suicide substrate of L-histidine decarboxylase (HDC), suppressed the thapsigargin (30 nM)- and TPA (30 nM)-induced histamine production. 4. Both thapsigargin (30 nM) and TPA (30 nM) induced phosphorylation of p44/p42 MAP kinase and p38 MAP kinase. 5. PD98059, a specific inhibitor of MEK-1 which phosphorylates p44/p42 MAP kinase, strongly suppressed both the thapsigargin (30 nM)- and TPA (30 nM)-induced histamine production, whereas SB203580, a specific inhibitor of p38 MAP kinase, inhibited them only partially. 6. The other MEK-1 inhibitor, U-0126, also inhibited both the thapsigargin- and TPA-induced histamine production in a concentration-dependent manner. 7. Thapsigargin (30 nM) and TPA (30 nM) increased the levels of HDC mRNA at 4 h, but PD98059 suppressed both the thapsigargin- and TPA-induced increases in the HDC mRNA level. 8. These findings indicate that thapsigargin and TPA induce histamine production in RAW 264.7 cells by increasing the level of HDC mRNA, and that both the thapsigargin- and TPA-induced histamine production are regulated largely by p44/p42 MAP kinase and partially by p38 MAP kinase.     

Amantadine inhibits RANTES production by influenzavirus-infected human bronchial epithelial cells

1. Amantadine can prevent and decrease airway inflammation by inhibiting influenza virus (IV) replication; however, the effect of amantadine on RANTES production by human bronchial epithelial cells (BEC) has not been determined. In the present study, we examined the effect of amantadine on RANTES production and also analysed p38 mitogen-activated protein (MAP) kinase and c-Jun-NH2-terminal kinase (JNK) activation to clarify the mechanism in the effect of amantadine on RANTES production, since we have previously shown that p38 MAP kinase and JNK regulate RANTES production by IV-infected BEC. 2. BEC that had been preincubated with amantadine were infected with IV and then p38 MAP kinase and JNK activation in the cells and RANTES concentrations in the culture supernatants were determined. 3. Amantadine-induced inhibition of virus replication resulted in a decrease in p38 MAP kinase and JNK activity and decreased expression of RANTES in IV-infected cells. 4. Amantadine did not inhibit p38 MAP kinase and JNK activation induced by tumour necrosis factor-alpha (TNF-alpha) as a non-viral stimulus. 5. These results indicate that amantadine inhibits IV infection-induced RANTES production by human BEC and that the inhibition by amantadine of RANTES production might result from an indirect inhibitory effect of amantadine on p38 MAP kinase and JNK activation via the inhibition of virus replication, and we emphasize that amantadine may produce a beneficial effect on controlling bronchial asthma exacerbation caused by IV infection.     

Effect of tetracyclines on IgE allergic responses and asthma

There are no current therapies that specifically target IgE production in human allergic disease. We found that tetracyclines and chemically modified tetracyclines (CMT) that lack antibiotic activity prevent IgE production, making them ideal candidates for anti-allergy therapy. This is based on our findings that minocycline treatment of allergic asthmatic humans significantly improves their asthma symptoms, reduces their oral steroid requirements, and strongly suppresses their ongoing IgE responses. Tetracyclines and CMT also suppress ongoing IgE responses of BPO-KLH sensitized mice in vivo and in vitro and humans IgE responses in vitro. We also found that highly increased levels of phosphorylated p38 MAP kinase, but not phosphorylated JNK or ERK, are expressed by blood T and B cells and monocytes of allergic asthmatic humans. Levels of phosphorylated p38 MAP kinase, but not ERK or JNK, correlated with their IgE. Tetracyclines significantly suppressed expression of phosphorylated p38 MAP kinase by CD4+ and CD8+ T cells but not B cells or monocytes in vivo and in vitro. Our findings open the door to development of new drugs and patents, especially for CMTs that lack antibiotic activity (US 7649113), for treatment of human allergic disease.     

一项计算机心血管仿真实验系统的研究

目的　开发一个用于评价心血管药物给药方案的计算机仿真实验系统。方法　对Clement的犬非线性血流动力学模型加以改进 ,作为仿真实验系统的数字犬部分 ,其余部分采用VisualC ++语言以面向对象的方式构建。运用动物实验比较硝普钠多模型自适应控制 (multiplemodeladaptivecontrol,MMAC)控制性降压与等量药物匀速给药降压的平均动脉压在目标值± 0 6 6 7kPa范围内时间百分比(TMAP)、超出上述范围的积分值的均值 (SMAP)差别 ,用仿真实验系统重复动物实验过程 ,观察是否能重复出现这样的差异 ;对比模拟系统与动物实验在实行硝普钠控制性降压时的效果。结果　仿真实验系统在评价MMAC给药方案与匀速给药方案的差别时 ,结果与动物实验相同 ;在实行硝普钠MMAC方案控制性降压时 ,仿真系统的平均动脉压变化曲线与动物实验相近。结论　该仿真实验系统可用于评价心血管药物给药方案 ,并有助于建立其它相关的系统。     

Synthesis of new pyrrolo[2, 3-b]pyridines as a potent inhibitor of tumour necrosis factor alpha

The MAP kinase p38 plays a key role in the biosynthesis of the inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and 1L-1beta. Accordingly, new pyrrolo[2, 3-]pyridine derivatives 5a-d were prepared from 2-amino-3-cyanopyrroles 3a-d via the intermediate propenylaminopyrroles 4a-d. Then the compounds 5a-d were tested for their ability to inhibit the production of TNF-alpha in vivo in rats. The most potent compounds 5a and 5b possess enhanced ability to inhibit the production of TNF-alpha stimulated with bacterial lipopolysaccharide.