骶骨螺钉经上终板与经前皮质固定的生物力学比较

目的测试骶骨螺钉经上终板固定技术的生物力学性能,并与经前皮质固定技术比较。方法取17具新鲜成年男性骶骨标本,两侧分别采用螺钉经上终板固定和经前皮质固定技术。经前皮质固定的螺钉指向前内侧,平行于终板;经上终板固定的螺钉指向前内侧,矢状面上向头侧成30°～35°角,钉尖对向S1上终板的前部。植入螺钉时测定最大扭矩;通过模拟生理应力进行疲劳试验,测定固定刚度变化和拔出力。结果经上终板固定组螺钉最大扭矩为(3.18±0.49)Nm,经前皮质固定组为(1.98±0.76)Nm, 差异有非常显著性(P< 0.01),经上终板固定组比经前皮质固定组高60.6%; 经上终板固定组拔出力为(1457±276)N,经前皮质固定组为(1122±364)N, 差异有显著性(P< 0.05),经上终板固定组比经前皮质固定组高29.9%;在循环负载过程中,两组刚度在负载早期(前5000个循环)均明显下降,然后趋于平稳,经上终板固定组的最后刚度高于经前皮质固定组(P< 0.05)。两组中螺钉的最大扭矩与拔出力均有显著相关性,相关系数分别为0.94和0.95(P< 0.01)。结论骶骨螺钉经上终板固定技术与经前皮质固定技术相比有一定的力学优越性。     

双波长一元线性回归分光光度法同时测定复方氨基比林注射液中三组分含量

本文依据一组含有不同比例待测和干扰组分的标准混合液的吸收值,采用一元线性回归方法,在选择最佳测定波长对的同时建立标准工作曲线方程,使其更符合实际作品测定时的情况,提高了结果的精度和可靠性,并使计算量和实验工作量得以降低。应用于复方氨基比林注射液中三组分氨基比林、安替比林和巴比妥的同时测定,其平均回收率分别为99.8%,100.4%和99.8%,变异系数分别为0.59,1.48和1.05,结果优于卡尔曼滤波法、偏最小二乘法和目标因子分析法。     

Human T cell responses against the major cysteine proteinase (cruzipain) of Trypanosoma cruzi: role of the multifunctional alpha 2- macroglobulin receptor in antigen presentation by monocytes

Chagas' disease patients (CDP) develop both humoral and cellular immune responses against the major cysteine proteinase (cruzipain) from Trypanosoma cruzi. Here we demonstrate that complexes formed by cruzipain and alpha 2-macroglobulin (alpha 2M) are efficiently internalized by human monocytes, and that this process results in enhanced presentation of cruzipain peptides to CD4+ T cells from CDP. Purified or serum alpha 2M binds to polymorphic cruzipains, but only a fraction of the proteinases become covalently linked. Once bound to alpha 2M, fluorescein-labeled cruzipain (FITC-cruzipain) or [125I]cruzipain were more efficiently internalized by normal peripheral blood mononuclear cells (PBMC) or monocytes; this effect was abolished by (I) pre-treating the cells with receptor-associated protein (rRAP), a known antagonist the of alpha 2M receptor (alpha 2MR/LRP), and (II) inactivating [125I]cruzipain's active site prior to the reaction with alpha 2M, indicating that the exposure of receptor binding sites on alpha 2M complexes required bait region cleavage. We then sought to determine if the alpha 2MR/LRP-dependent uptake of alpha 2M:cruzipain by monocytes resulted in increased CD4+ T cell responses of PBMC-CDP (n = 13). These effects were only revealed after depletion of CD19+ B lymphocytes from PBMC-CDP; the threshold of T cell stimulation was far lower in cultures stimulated with alpha 2M:cruzipain, as compared to antigen alone. Myocardial specimens from CDP with chronic myocardiopathy (three necropsies) were analyzed by immunohistochemistry with mAb anti-cruzipain or anti-alpha 2MR/LRP (CD81+). Extracellular depots of cruzipain were localized amidst inflammatory mononuclear infiltrates, part of which contained CD91+ macrophage-like cells. Ongoing studies should clarify if T. cruzi cysteinyl proteinases play a role in the pathogenesis of Chagas' heart disease.      

Oral rehydration therapy: efficacy of sodium citrate equals to sodium bicarbonate for correction of acidosis in diarrhoea.

Forty patients with moderate degrees of dehydration and acidosis because of acute watery diarrhoea were successfully treated randomly with either WHO recommended oral rehydration solution containing 2.5 g sodium bicarbonate or an oral solution containing 2.94 g sodium citrate in place of sodium bicarbonate per litre of oral rehydration rehydration solution. Efficacies were compared by measuring oral fluid intake, stool and vomitus output, change in body weight, hydration status, and rate of correction of acidosis during a period of 48 hours. Seventy five per cent (21 cases) in the citrate group and 83% (19 cases) in the bicarbonate group were successfully rehydrated (p greater than 0.05). There were no significant differences in intake, output, gain in body weight, fall in haematocrit and plasma specific gravity, and correction of acidosis between the two groups of patients within 48 hours after initiation of therapy. The solution with sodium citrate base was as effective as WHO-oral rehydration solution for management of diarrhoea. This study shows the efficacy, safety, and acceptability of citrate containing oral rehydration solution for rehydration and correction of acidosis in diarrhoea.     

Mast cell stabilization prevents ethanol-induced rat gastric mucosal injury: mechanisms of protection

INTRODUCTION: We previously demonstrated that 60% ethanol increased macromolecular leakage and induced lesion formation in areas of permanent flow stasis within gastric mucosal vessels. Mast cells and their mediators have been implicated in acute mucosal injury. Fluorescent in vivo microscopy was used to assess the effects of ketotifen, a mast cell stabilizer, and pyrilamine, a histamine (H1)-receptor antagonist, on ethanol-induced rat gastric mucosal injury. METHODS: Experiments were carried out on anaesthetized rats pretreated orally with ketotifen (1 mg/kg) or pyrilamine (30 mg/kg). Fluorescein isothiocyanate-bovine serum albumin (FITC-BSA; 0.2 mL/100 g), a marker for quantitating macromolecular leakage was administered intra-arterially. Ethanol (60%) or distilled water was applied topically to the gastric mucosa. Macromolecular leakage of FITC-BSA, vessel diameters and leucocyte activity were quantified using image analysis. RESULTS: Pretreatment with ketotifen or pyrilamine, followed by ethanol, caused no change in macromolecular leakage compared with controls. Both compounds prevented blood flow stasis in all areas and no lesion formation was observed. However, increased leucocyte activity and increases in vessel diameter were observed following pretreatment with ketotifen and pyrilamine, respectively. CONCLUSIONS: The data suggest that vasoactive substances released from mast cells may be involved in the aetiology of ethanol-induced gastric mucosal damage. The prevention of these normal physiological responses to injury may lead to the employment of other microcirculatory mechanisms of defence.