Investigation of melt agglomeration process with a hydrophobic binder in combination with sucrose stearate

The melt agglomeration process of lactose powder with hydrogenated cottonseed oil (HCO) as the hydrophobic meltable binder was investigated by studying the physicochemical properties of molten HCO modified by sucrose stearates S170, S770 and S1570. The size, size distribution, micromeritic and adhesion properties of agglomerates as well as surface tension, contact angle, viscosity and specific volume of molten HCO, with and without sucrose stearates, were examined. The viscosity, specific volume and surface tension of molten HCO were found to be modified to varying extents by sucrose stearates which are available in different HLB values and melt properties. The growth of melt agglomerates was promoted predominantly by an increase in viscosity, an increase in specific volume or a decrease in surface tension of the molten binding liquid. The agglomerate growth propensity was higher with an increase in inter-particulate binding strength, agglomerate surface wetness and extent of agglomerate consolidation which enhanced the liquid migration from agglomerate core to periphery leading to an increased surface plasticity for coalescence. The inclusion of high concentrations of completely meltable sucrose stearate S170 greatly induced the growth of agglomerates through increased specific volume and viscosity of the molten binding liquid. On the other hand, the inclusion of incompletely meltable sucrose stearates S770 and S1570 promoted the agglomeration mainly via the reduction in surface tension of the molten binding liquid with declining agglomerate growth propensity at high sucrose stearate concentrations. In addition to being an agglomeration modifier, sucrose stearate demonstrated anti-adherent property in melt agglomeration process. The properties of molten HCO and melt agglomerates were dependent on the type and concentration of sucrose stearate added.     

三七总甙对人增生性瘢痕成纤维细胞TGF-β1和细胞周期的作用

目的 观察三七总甙对人增生性瘢痕成纤维细胞TGF-β1和细胞周期的作用。方法体外培养人增生性瘢痕成纤维细胞，并应用三七总甙进行干预，用免疫细胞化学染色法结合图像分析观察TGF-β1的表达变化，用流式细胞仪测定细胞周期的变化。结果与对照组相比，三七总甙能够显著抑制细胞TGF-β1的表达，并使细胞停滞于S期，而G0-G1期、G2-M期细胞明显减少（P〈0．01）。结论三七总甙改变细胞周期和抑制增生性瘢痕成纤维细胞TGF-β1的表达，可能成为防治增生性瘢痕的药物。     

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats.

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.     

Comparative study of renal sodium transport between ouabain-hypertensive rats and ouabain-nonhypertensive rats

Objective: To compare renal sodium transport, using fractional excretions of lithium(FELi) as a marker of proximal tubule sodium reabsorption, between hypertensive and non-hypertensive ouabain-treated rats and further to elucidate the role of ouabain in pathogenesis of hypertension. Methods: Thirty male Sprague-Dawley rats weighting 180-200 g were randomly divided into normal control group and ouabain treated group. Rats were infused with 1 ml/kg·d normal saline or 27. 8μg/kg·d ouabain in-traperitoneally once a day respectively. Systolic blood pressure (SBP), heart rate and body weight were recorded weekly. Rats were sacrificed 6 weeks after treatment. Blood and 24-hour urine sample were collected to measure the serum and urinary concentration of sodium, trace lithium and creatinine. Endogenous creatinine clearance rate(Ccr), fractional excretions of sodium (FENa), fractional excretions of lithium (FELi) and fractional reabsorption of sodium in the postproximal tubules (FDRNa) were calculated. Ouabain levels of plasma and renal tissue, plasma renin activity, angiotensin I and aldosterone concentration were determined. Results: 65% of the ouabain-treated rats achieved significantly higher SBP after 4 weeks, compared with that of the saline control groups or self baseline (P<0. 01). But in the other 35% of the ouabain-treated rats, their SBP was similar with control group during the experiment (P>0. 05). The body weight, heart rate and food intake between the 3 groups were no significant differences (P> 0. 05). FELi and FDRNa were significantly lower in ouabain-hypertensive group compared with ouabain-non-hypertensive group and control group(P<0. 01 and P<0. 05). The FEu and FDRn, of ouabain-nonhyper-tensive groups were similar with control group(P>0. 05). Ccr and FENa were comparable between the 3 groups (P>0. 05). Plasma and renal tissue ouabain levels, plasma renin activity, angiotensin I and aldosterone contents in ouabain-hypertensive rats were comparable with ouabain-nonhypertensive rats. Conclusion: Increase of proximal tubule sodium reabsorption play an important role in the pathogenesis of ouabain-hypertensive rats. The change of renal sodium transport may result from regulation to renal Na+ , K + -ATPase by ouabain.     

阻塞性黄疸大鼠肾脏自分泌内皮素的变化及其与肾功能损害的关系

目的　探讨阻塞性黄疸时肾脏自分泌内皮素 (ET)的变化及其与肾功能损害的关系。方法　结扎胆总管(BDL)制备阻塞性黄疸大鼠模型 ,作为实验组 ,对照组鼠仅行假手术。分别于术后 5、1 0及 1 5d ,两组各取 1 0只大鼠检测其肾脏对氨基马尿酸清除率 (CPAH)、菊粉清除率 (CIN)和钠排泄分数 (FENa+) ,并用鲎试剂法测定血浆内毒素 (EX)水平 ,放射免疫法测定肾动、静脉血浆及肾组织中ET 1含量。结果　①实验组术后 5d仅FENa+明显高于对照组 (P<0 .0 1 ) ,术后 1 0d起 ,CPAH、CIN及FENa+呈进行性下降 ,术后 1 5dFENa+已较对照组低 ,与对照组比较差异有显著性 (P<0 .0 1 ) ;②实验组术后血浆EX水平呈进行性升高 ,与对照组比较差异有显著性 (P<0 .0 1 ) ;③实验组术后肾动脉血浆ET 1水平呈持续性降低 ,而肾静脉血浆及肾组织中ET 1含量呈持续性升高 ,与对照组比较差异有显著性 (P<0 .0 1 ) ;④血浆EX水平与肾组织ET 1含量呈正相关 (r =0 .762 4 ,P<0 .0 1 ) ,肾组织ET 1含量与CPAH和CIN呈负相关 (r=- 0 .883 2 ,P<0 .0 1 ;r =- 0 .945 2 ,P<0 .0 1 )、与FENa+呈正相关 (r=0 .873 4 ,P<0 .0 1 )。结论　内毒素血症及其诱导的肾内ET分泌增加在阻塞性黄疸所致大鼠肾损害中可能具有重要作用     

斑点免疫金渗滤法的改进

目的 :改进斑点免疫金渗滤法的渗滤装置 ,降低成本 ,使之更适用于现场操作。方法 :用自制的圆形渗滤片替代塑料渗滤盒 ,并比较二者的效果。结果 :自制的渗滤片体积更小 ,成本更低 ,为一次性使用材料 ;检测抗体的效果与塑料渗滤盒法一致。结论 :自制的渗滤片优于常用的塑料渗滤盒     

一种胰岛素抵抗的糖尿病特殊类型报告

报告５例对胰岛素抵抗的糖尿病特殊类型病例，其均具有胰岛素应用指征，但使用胰岛素后血糖却反而上升，逐渐增加胰岛素用量，则血糖值亦呈上升趋势。对该类病人的治疗，首先停用胰岛素，改用自制中药制剂及优降糖、降糖灵治疗，取得了良好效果。     

高血压性脑出血外科治疗体会

报告33例高血压性脑出血施行外科手术治疗的临床体会。结合术前病情分级、血肿类型、血肿量、中线结构移位程度等,对手术治疗的适应症选择、手术方式及入路、提高治疗效果、减少术后并发症等作了讨论。提出了手术治疗重要性。     

有机氮源对红霉素发酵影响的具体分析

红色糖多孢菌的摇瓶培养基中使用不同有机氮源时红霉素的效价明显不同。通过对不同有机氮源所含营养成分的逐步回归分析,我们得到有机氮源中的苏氨酸为影响红霉素效价的主要因子。最后向对照培养基中添加苏氨酸,则使红霉素的效价比对照培养基提高了22.85%。     

未破裂脑动脉瘤的治疗选择

未破裂脑动脉瘤的处理存在争议。由于其自然史尚未完全明确,因此最佳的治疗策略也不清楚。目前对未破裂脑动脉瘤处理的共识包括观察、显微手术夹闭和血管内治疗。用于随访已知未破裂脑动脉瘤的方法学也有争议,可能取决于经治医生的偏好。大多数动脉瘤由神经外科医师和介入神经放射科医师处理,但未破裂动脉瘤通常是由神经科医师在对患者进行其他神经系统疾病的筛查时首先发现的。因此,关于何时对患者进行筛查和如何对未破裂动脉瘤采取最佳处理的知识将对其日常医疗实践有直接的影响。未破裂动脉瘤经常导致包括缺血事件、癫和头痛在内的其他神经系统症状,这些症状可能促进更积极的干预治疗。由于缺乏设计完善真正基于人群的研究或随机试验,因此目前的最佳处理必须以现有文献和每例患者当时的具体情况为根据。