锂辉石晶体结构与浮选药剂之间的作用机理研究现状

这是一篇矿物加工工程领域的论文。锂矿产是我国重要的战略资源,目前最常用浮选法来进行锂矿石的选别,本文从锂辉石晶体结构的角度出发,探讨了锂辉石的晶体结构构造特性及其与浮选药剂之间的作用机理,文中从金属阳离子活化剂、有机抑制剂、无机抑制剂、阴离子捕收剂、阳离子捕收剂、混合捕收剂、新型捕收剂七个方面分别进行阐述,对了解锂辉石与药剂之间的作用特点、研发新型高效的浮选药剂、优化选矿工艺流程等具有重要意义。

CLINICAL OBSERVATION ON 96 CASES OF PRIMARY DYSMENORRHEA TREATED BY MEDICINE-SEPARATED MOXIBUSTION AND INVESTIGATION ON ITS MECHANISMS

Objective： To observe the therapeutic effect of medicine-separated moxibustion for primary dysmenorrhea and its influence on plasma hormone level. Methods. Ninety-six patients suffering from primary dysmenorrhea were randomly and evenly divided into trealment group treated with medicine-separated moxibustion of Shenque （神阙 CV 8, 3-5 cones every time, beginning 1 week before onset of menstruation and stopping on the 3^rd day after onset, with 10 sessions being a therapeutic oourse, 3 courses all together）, and control group treated with oral administration of Yueyueshu （月月舒 menstruation-smoothing granule, 10 g/time, b.i.d, 3 courses altogether）. Menses prostaglandin E2（PGF2α） and plasma oxytocin （OT） during menstruation were determined by radioimmunoassay. Results; After the treatment, of the two 48 cases in treatment and control groups, 18 and 5 were cured, 24 and 9 had marked improvement in their symptoms, 6 and 26 had improvement, 0 and 8 failed in the treatment, with the total effective rates being 100. 096 and 83.3% respectively, the therapeutic effect of treatment group was markedly superior to that of control group （P〈0.05）. After the treatment, the contents of menses PGF2α in treatment group and plasma OT in both groups were significantly lower than those of pre-treatment （ P〈 0.01 ）. The therapeutic effect of moxibustion was significant- ly better than that of medication in lowering plasma OT. Conclusion： Medicine-separated moxibustion works well in treating primary dysmenorrhea, and moxibustion induced decrease of menses PGF2α and plasma OT may contribute to its effect in relieving dysmenorrhea.

Flotation behavior and adsorption mechanism of fine wolframite with octyl hydroxamic acid

Flotation behavior and adsorption mechanism of octyl hydroxamic acid(OHA)on wolframite were investigated through flotation experiments,adsorption tests,zeta-potential measurements,infrared spectroscopy and solution chemistry calculations.Results of flotation and adsorption experiments show that the maximum values of flotation recovery and adsorption capacity occur around p H 9.In term of the solution chemistry calculations,the concentration of metal hydroxamate is greater than that of metal tungstate and metal hydroxyl,and metal hydroxamate compounds are identified to be the main species on wolframite surface at p H region of 8-10,contributing to the increase of OHA adsorption and flotation performance.Results of zeta-potential and IR spectra demonstrate that OHA adsorbs onto wolframite surface by chemisorptions.Hydroxamate ions can bond with Mn_2+/Fe_2+cations of wolframite surface,forming metal hydroxamate compounds,which is a key factor in inducing the hydrophobicity of wolframite under the conditions of maximum flotation.

Locoregional IL-2 low dose applications for gastrointestinal tumors

AIM： To explore the feasibility of local interleukin 2 （IL-2） in patients with different forms of abdominal cancer. This required experimentation with the time interval between IL-2 applications and the methods of application. METHODS： Sixteen patients with stages Ⅲ and Ⅳ of gastrointestinal malignancies （primary or metastatic） who were admitted to our Department of Gastroenterology were treated with Iocoregionally applied IL-2 in low doses. RESULTS： No major problems applying Iocoregional IL-2 were encountered. In 6 out of 16 patients, a modest but clinically worthwhile improvement was obtained. Adverse effects were minimal. The therapeutic scheme was well tolerated, even in patients in a poor condition. CONCLUSION： This study demonstrates the feasibility of low dose Iocoregional IL-2 application in advanced abdominal cancer. Local IL-2 therapy gives only negligible adverse effects. The results suggest that it is important to apply intratumorally. Local IL-2 may be given adjunct to standard therapeutic regimes and does not imply complex surgical interventions. These initial results are encouraging.

Pathogenesis of NSAID-induced gastric damage:Importance of cyclooxygenase inhibition and gastric hypermotility

This article reviews the pathogenic mechanism of nonsteroidal anti-inflammatory drug(NSAID)-induced gastric damage,focusing on the relation between cyclooxygenase(COX) inhibition and various functional events.NSAIDs,such as indomethacin,at a dose that inhibits prostaglandin(PG) production,enhance gastric motility,resulting in an increase in mucosal permeability,neutrophil infiltration and oxyradical production,and eventually producing gastric lesions.These lesions are prevented by pretreatment with PGE 2 and antisecretory drugs,and also via an atropine-sensitive mechanism,not related to antisecretory action.Although neither rofecoxib(a selective COX-2 inhibitor) nor SC-560(a selective COX-1 inhibitor) alone damages the stomach,the combined administration of these drugs provokes gastric lesions.SC-560,but not rofecoxib,decreases prostaglandin E 2(PGE 2) production and causes gastric hypermotility and an increase in mucosal permeability.COX-2 mRNA is expressed in the stomach after administration of indomethacin and SC-560 but not rofecoxib.The up-regulation of indomethacin-induced COX-2 expression is prevented by atropine at a dose that inhibits gastric hypermotility.In addition,selective COX-2 inhibitors have deleterious influences on the stomach when COX-2 is overexpressed under various conditions,including adrenalectomy,arthritis,and Helicobacter pylori-infection.In summary,gastric hypermotility plays a primary role in the pathogenesis of NSAID-induced gastric damage,and the response,causally related with PG deficiency due to COX-1 inhibition,occurs prior to other pathogenic events such as increased mucosal permeability;and the ulcerogenic properties of NSAIDs require the inhibition of both COX-1 and COX-2,the inhibition of COX-1 upregulates COX-2 expression in association with gastric hypermotility,and PGs produced by COX-2 counteract the deleterious effect of COX-1 inhibition.