医用钛合金在三种不同生理电解液中的耐腐蚀行为研究

利用电化学方法研究医用钛合金在0.9%NaCl生理盐水，模拟人工唾液，模拟人工体液中的腐蚀情况，分析腐蚀电位和腐蚀电流密度，扫面电镜观察腐蚀表面形貌，CA-A型接触角测试仪测试钛合金表面被腐蚀后接触角的变化。实验表明：钛合金在三种生理电解液中的腐蚀情况依次是：模拟人工唾液〉模拟人工体液〉0.9%NaCl生理盐水。扫面电镜观察表明，医用钛合金在0.9% NaCl生理盐水腐蚀后，表面出现了许多腐蚀孔，经模拟人体体液腐蚀后，表面变得粗糙不平整，腐蚀孔数目变化不大，钛合金经人工唾液腐蚀后，腐蚀孔数目增多，部分腐蚀孔孔径明显增大。经三种生理电解液腐蚀后，钛合金表面接触角都减小。结论：医用钛合金在人工唾液中的腐蚀最严重，在临床应用中应给予相应的防范措施。     

Characteristics of proton beam scanning dependent on Li target thickness from the viewpoint of heat removal and material strength for accelerator-based BNCT

This study demonstrates the characterization of proton spot scanning on a Li target assembly for accelerator-based BNCT from the viewpoint of heat removal and material strength. These characteristics are investigated as to their dependence on the Li target thickness, considering that the Cu backing plate has more suitable heat removal properties than Li. Two situations are considered in this paper, i.e. the cyclic operation of the spot scanning, and a stalled spot scanning cycle where the proton beam stays focused on a single position on the Li target.It was found that the maximum of the Li temperature and the strain of the Cu backing increase as the cycle period increases. A cycle period less than 120 ms (over 8.3 Hz of frequency) enables the Li temperature to be kept below 150 °C and a cycle of less than 115 ms (8.7 Hz) keeps the Cu strain below the critical value for a 230 μm thick Li target, though the values are evaluated conservatively. Against expectation, the Li temperature and Cu strain are larger for a 100 μm thick target than for a 230 μm target. The required cycle period in this case is 23 ms (43 Hz) for maintaining a reasonable Li temperature and 9 ms (110 Hz) to prevent Cu fatigue fracture.For a stall in the spot scanning cycle, the Cu temperature increases as the beam shutdown time increases. The time for Cu to reach its melting point is estimated to be 4.2 ms at the surface, 20 ms at 1 mm depth, for both of 100 and 230 μm thick targets. At least 34 ms is estimated to be enough to make a hole on Cu backing plate. A beam shutdown mechanism with a response time of about 20 ms is therefore required.     

Pharmacological action of Adenophora polysaccharides

Adenophora polysaccharides (AP), is an active principle extracted from the root of Adenophorae Potaninii Korsh originated in Gansu Province and isolated with boiling water(1). AP is isolated and purified from the crude drug by DEAE-cellulose and Sephadex G-200 column, with a white powder and mean molecular weight of 8.3 × 104 , and [α]D20of AP is 68(1). AP is only composed of glucose judging from the analysis of it with patina chromatography (PC) and gas chromatography-mass spectrometer (GC-MS) methods.The methylation analysis showed that AP is composed of (1→6) linked glucose residues. The measure of nuclear magnetic resonance imaging (NMR) 1H NMR and 14C NMR techniques further proved that AP is α(l→6) linked by Dglucose. The structure of AP is as follows: -[→6]α-D-Glu(1-)n→ (2).     

甘肃省妇女不同年代宫颈癌死亡状况比较分析

目的探讨甘肃省妇女不同年代宫颈癌死亡水平及其分布特征。方法利用1970-1974年、1990-1992年和2004-2005年甘肃省全死因抽样调查数据,统计分析宫颈癌在不同年代、不同地区的死亡状况及变化趋势。结果甘肃省妇女1970-1974年宫颈癌调整死亡率为13.65/10万,1990-1992年为11.88/10万,2004-2005年为5.70万/10万,2004-2005年调整死亡率比1970-1974年和1990-1992年分别下降了58.24%、52.02%,1990-1992年比1970-1974年下降了12.97%,2004-2005年较1990-1992年下降明显(P<0.001)。三个年代宫颈癌死因构成分别占全癌死因的24.86%、11.67%和5.72%,居妇女癌症位次第2、第3和第5位,呈逐年下降趋势。宫颈癌地区分布明显,高发区主要集中在甘肃陇南、陇东一带。高发年龄主要在60～70岁之间。结论甘肃省宫颈癌死亡率居全国前列,近些年有所下降,但宫颈癌仍是威胁甘肃妇女健康的主要疾病。     

健身宝对衰老模型小鼠血清SOD和MDA的影响

目的　研究健身宝补脾益肾、延缓衰老的作用机制。方法　将 60只小鼠随机分为 6组 ,除正常对照组外均每日注射对D -半乳糖造成衰老模型 ,同时给予不同剂量的健身宝和金匮肾气丸。 6周后检测小鼠血清中SOD活性、MDA含量。结果　衰老模型组与正常对照组比较 ,小鼠血清中SOD活性显著降低 ,MDA含量显著升高 (P <0 .0 1 ) ;而健身宝大、中剂量组与正常对照组相比较 ,小鼠血清中SOD活性显著升高 ,MDA含量显著降低 ,与衰老模型组相比较有显著性差异 (P <0 .0 5 )。结论　健身宝明显提升D -半乳糖拟衰小鼠血清中SOD活性 ,降低MDA含量 ,可从调节自由基代谢和提高抗氧化能力方面发挥延缓衰老的作用。     

Neuroprotective effect of estrogen after chronic spinal cord injury in ovariectomized rats

BACKGROUND: At present, there is still lack of effective drugs for chronic spinal cord injury, whereas it is found recently that estrogen has a neuroprotective effect on brain and spinal cord injuries. OBJECTIVE: To observe the effect of estrogen on the apoptosis of nerve cells after gradual chronic spinal cord injury in ovariectomized rats. DESIGN: A randomized controlled animal trial. SETTING: Institute of Orthopaedics, the Second Hospital of Lanzhou University. MATERIALS: Sixty-five female Wistar rats of common degree, weighing 220–250 g, were provided by the experimental animal center of Lanzhou University. The rats were randomly divided into sham-operated group (n =5), estrogen-treated group (n =30) and saline control group (n =30), and the latter two groups were observed at 1, 3, 7, 14, 28 and 60 days respectively, and 5 rats for each time point. METHODS: All the rats were treated with bilateral oophorectomy 2 weeks before the experiment. T10 vertebral lamina was revolved into using plastic screw. The spinal canal impingement was not induced initially. After that, the original incision was opened to expose the screw every 7–10 days. MAIN OUTCOME MEASURES: The apoptosis and Caspase-3 positive cells in the damaged spinal cord were detected using terminal deoxynucleotidal transferase-mediated dUTP-biotin nick end labeling (TUNEL) method and Caspase-3 immunohistochemical staining at 1, 3, 7, 14, 28 and 60 days after chronic spinal cord injury respectively. RESULTS: Totally 65 rats were used, and the deleted ones during the experiment were supplemented by others. Changes of Caspase-3 expression after spinal cord injury: In the sham-operated group, only a small amount of Caspase-3 proteins were observed in the rat spinal cord, mainly located in motor neurons of spinal cord anterior horn. In the estrogen-treated group and saline control group, positive cells expressed occasionally at 1 day postoperatively, began to increase obviously at 7 days after injury, strongly expressed at 14 and 28 days, but decreased at 60 days, mainly located in the neurons of spinal cord gray matter anterior horn, and they expressed fewer in the motor neurons and white matter of ventral horn, and there were obvious differences between the estrogen-treated group and saline control group at 7, 14, 28 and 60 days (P < 0.05). CONCLUSION: Estrogen can reduce the apoptosis of nerve cells and promote the recovery of neurological function following gradual chronic spinal cord injury.     

医院用血液制品HCV污染情况的调查

目的调查医院治疗用血液制品ＨＣＶ污染情况．方法临床治疗所用的血液制品，在输完后留容器之残液备检．采用酶标免疫法（ＥＬＩＳＡ）检测．对ＥＬＩＳＡ检测之阳性标本及在阴性标本中随机抽取９份，采用逆转录双ＰＣＲ方法检测ＨＣＶ＿ＲＮＡ．结果血浆白蛋白抗＿ＨＣＶ阳性率４５８％，新鲜血浆阳性率２６％．两种方法检测同一标本，ＥＬＩＳＡ检测阳性的血液制品中，用ＰＣＲ证实，并非都有病毒复制；而在ＥＬＩＳＡ检测的阴性标本中，仍旧有较高的ＰＣＲ阳性检出．结论血液制品存在着ＨＣＶ污染，抗＿ＨＣＶ对于ＨＣＶ感染的诊断价值很高．检测血液制品中的抗＿ＨＣＶ，合理使用血液成份，可防止ＨＣＶ在医院内传播．     

In vivo and in vitro anti-tumour response of selenium-protein polysaccharide extracted from rich selenium Agaricus blazei

In this study, the anti-tumour activity of selenium-protein polysaccharide (SPP), a water extract of the rich selenium Agaricus blazei, was tested both in vivo and in vitro. The results of in vivo experiments show that SPP at doses of 50 and 100 mg/kg inhibits proliferation of implanted Sarcoma 180 by 22 and 37.69%, respectively, and promotes lymphocyte transformation and natural killer (NK) cells activity in tumour bearing mice. During the in vitro experiment, we treated the tumour and non-tumour bearing mice with SPP, and prepared serum treated with SPP (Serum_SPP). The results show that Serum_SPP, whether from tumour or non-tumour bearing mice, significantly inhibits K562 cells proliferation and induces their apoptosis, and also significantly increases caspase-3 activity of K562 cells. However, the difference in anti-tumour activity of Serum_SPP between tumour and non-tumour bearing mice is significantly different (p<0.01). The results, according to the studies both in vivo and in vitro, imply that SPP extracted from rich selenium A. blazei can inhibit growth of implanted Sarcoma 180 and promote lymphocyte transformation and NK cells activity in vivo. Additionally, Serum_SPP can inhibit proliferation and cause apoptotic morphological changes and the fragmentation of internucleosomal DNA, and increase caspase-3 activity of K562 cells in vitro, which indicates that apoptosis of K562 cells induced by Serum_SPP may be related to up-regulation of caspase-3.