下蹲运动与高眼压关系及其动态观察

观察１８例３２眼下蹲运动与高眼压的关系，分为下蹲１２０次，１００次及８０次三且，每组分别观察１０眼、１１眼及１１眼，结果各组运动后眼压均见下降，平均为１．０２７±０．４８６ｋＰａ，１．３５５±０．７７０ｋＰａ及１．３２５±０．４２２ｋＰａ，运动前后有非常显著性差异，但各组之间差异不显著。同时观察３小时内眼压动态变化，下蹲１２０次组眼压下降维持时间最长，在运动后３小时与运动前眼压比较及与其余两组第３     

着色真菌蟾蜍分离株小鼠致病试验研究

目的：观察着色真菌蟾蜍分离株的致病性。方法：抽样取着色真菌蟾蜍分离株与标准人分离株对照，制成菌悬液，做小鼠腹腔接种，观察接种后小鼠的外观表现，做菌种逆培养和观察内脏病理变化。结果：蟾蜍分离株卡氏枝孢霉、疣状瓶霉、裴氏着色霉和甄氏外瓶霉与病人分离株一样，在接种28天后，均可从小鼠脏器逆培养出接种的菌种，并引起内脏病变，形成结核样肉芽肿，肉芽肿内均可查见棕黄色硬壳小体。而瓶霉和外瓶霉属菌种逆培养结果均阴性。结论：从野生蟾蜍分离出的卡氏枝孢霉、疣状瓶霉，裴氏着色霉和甄氏外瓶霉与病人分离株一样，对小鼠有致病性，故可能是人着色芽生菌病的致病菌。     

健脾降脂颗粒中绿原酸的含量测定

目的　研究健脾降脂颗粒中绿原酸的含量测定方法。方法　采用高效液相法。色谱柱YWGC18(2 5 0mm× 4 6mm ,10 μm) ,室温 ,10 %乙腈─冰醋酸 (5∶0 1)为流动相 ,流速为 1mL/min ,检测波长 32 9nm。结果　绿原酸在 0 0 2 0 8～ 0 10 4 μg范围内呈线性关系 (r =0 9994 ,n =5 ) ,平均加样回收率为 96 2 3% ,RSD为 0 798%。结论　本方法准确、可行 ,可用于健脾降脂颗粒的质量控制     

正常人口腔粘膜不同部位表面感觉的测试

目的 建立正常人口腔粘膜不同部位表面感觉的正常参考值，并测试各年龄组感觉值是否存在差异。方法 利用动静两点辨别觉试验，测试90例健康人口腔粘膜不同部位的表面感觉。结果 舌尖感觉功能最好，其次为舌背、舌腹、颊粘膜、口底和硬腭。健康人的口腔粘膜不同部位的表面感觉随着年龄增长有显著性变化。结论 口腔粘膜不同部位感觉辨别力存在差异，健康人口底、舌腹、舌背、颊和硬腭粘膜感觉功能有增龄性变化。     

血浆巨细胞病毒多聚酶链反应检测用于指导干预性治疗

目的：分析用血浆巨细胞病毒（cytomegalovirus,CMV)多聚酶链反应（plymerase chain reaction,PCR)检测结果指导抗CMV干预性治疗的临床意义。方法：1999年8月至2001年7月行异基因造血干细胞移植（hematopoietic stem cell transplantation,HSCT)的所有患者自预处理开始，常规用PCR法检测血浆的CMV－DNA（采用华美公司生产的巨细胞病毒4℃ PCR检测试剂盒），每周1次。其中尚无CMV病的临床表现而检测到血浆CMV阳性的患者89例。随机选取52例阳性患者给予干预性治疗。将上述89例患者分为3组（分别为停止治疗时血浆CMV－PCR转阴组、停止治疗时未转阴组、血浆CMV阳性未治疗组）比较各组CMV病的发生率。CMV病的发生率采用Kaplan-Meier曲线表示，曲线间的比较用Log-Rank（曲线无交叉）或Breslow（曲线交叉）检验，某时点率的比较采用RXC列联表或χ^2检验。结果：100d内CMV病的发生率，在治疗后血浆CMV－PCR由阳性转为阴性组为10．26％，治疗结束时血浆CMV－PCR仍为阳性组为66.67%，血浆CMV－PCR阳性未治疗组为36．24％（P＝0.0000)。上述3组中任两组移植后100d CMV病的发生率差异均有显著性。移植后1年时上述3例CMV病累积发生率分别为30.65%、75.00%、42.95%(P=0.0009)，治疗未转阴组与治疗转阴组和阳性未治疗组相比，CMV病的发生率明显升高。结论：血浆CMV－PCR检测结果用来指导干预性治疗有一定临床意义。干预性治疗后血浆CMV－DNA仍未转阴者，应考虑换药或联合用药治疗。     

B90催化剂上丁烯氧化脱氢的反应动力学─一一种简便的建立化学动力学方程的方法

采用简便的建立化学反应动力学方程的方法，研究了Ｂ９０催化剂上丁烯氧化脱氢制丁二烯反应的动力学，即先在一较低温度下，用微分法拟合得到化学反应动力学方程中的浓度项，然后改变反应温度，求算不同温度下的反应速率常数。采用这个简便方法，只需较少的实验，即可求得该反应体系中的丁烯转化速率方程式。     

Anti-leukemia effect of perillyl alcohol in Bcr/Abl-transformed cells indirectly inhibits signaling through Mek in a Ras- and Raf-independent fashion.

PURPOSE: Perillyl alcohol (POH) displays preventive and therapeutic activity against a wide variety of tumor models, and it has been suggested that this might be associated with the ability of POH to interfere with Ras prenylation. POH also selectively induces G(1) arrest and apoptosis in Bcr/Abl-transformed hematopoietic cells. Because signaling through Ras is necessary for Bcr/Abl transformation, we examined whether POH induces its anti-leukemia effect by inhibiting Ras signaling. EXPERIMENTAL DESIGN: The ability of POH to inhibit posttranslational farnesylation and signaling from Ras as well as signaling through the Raf-Mek-Erk cascade was examined in Bcr/Abl-transformed and mock-transformed cells and related to the anti-leukemia effect of POH. RESULTS: POH does not affect Ras prenylation or Ras activity, but it blocks signaling downstream of Ras by reversing the state of activation of the Erk kinase, Mek. POH affects Mek activity only when it is added to intact cells. Treatment of either cell lysates or of purified Mek with POH has no effect on Mek activity. Inhibition of the Mek-Erk pathway seems to be related to the POH anti-leukemia effect for the following reasons: (a) the concentration of POH needed to block the Erk pathway, as well the kinetics with which POH inhibits this signaling cascade, both correlate with the anti-leukemia effect of POH; (b) both U0126 (a specific Mek inhibitor) and POH induce similar anti-leukemia effects; and (c) mock-transformed hematopoietic cells are simultaneously resistant to POH anti-leukemia effects and inhibition of the Mek-Erk pathway. CONCLUSION: Blocking Mek is sufficient to induce growth arrest and apoptosis in Bcr/Abl-transformed cells; therefore, POH represents a novel small molecule inhibitor of Mek that might be effective for treating Bcr/Abl leukemias.     

不同类型高危儿早期干预的临床研究

目的 探索早期干预对窒息、高胆、早产三类高危儿智力发育改善的效果，寻找更合适的早期干预措施。方法 将三类高危儿分为干预组及对照组，同时随机选取正常对照组进行随访。干预组采用鲍秀兰教授“0～3岁”早期干预方案训练，各组均在6个月、1岁时分别采用婴幼儿智能发育量表(CDCC)进行智力发育测评，结果用MDI、PDI表示。结果 (1)6个月龄时MDI各干预组与对照组间有显著性差异，窒息组、早产组与正常组间亦有显著性差异；高胆组与正常组间无差异；PDI窒息组中干预组与对照组之间有显著差异(P＜0．01)，高胆组、早产组均无差异(P＞0．05)。(2)1岁时MDI和PDI结果一致，干预组与对照组间比较窒息组、高胆组有显著差异，早产组无差异；窒息组、高胆组干预组与正常组比较无差异，对照组和早产组与正常组比较均有显著差异(P＜0．01)。(3)所有干预组测评分值均高于对照组，6个月与1岁之间比较有显著差异，各观察组间比较有显著性差异(P＜0．01)。结论 三类高危儿早期干预效果差异较大，干预组均较对照组分值高，早期干预有改善智力发育的作用；三类高危儿中，窒息组、高胆组效果最好，均达到或超过正常水平。所有未干预组均不及正常水平；早期干预对足月高危儿效果显著，对早产儿欠佳，远期效果尚需进一步随访观察。     

Childhood fractures are associated with decreased bone mass gain during puberty: an early marker of persistent bone fragility?

Whether peak bone mass is low among children with fractures remains uncertain. In a cohort of 125 girls followed over 8.5 years, 42 subjects reported 58 fractures. Among those, BMC gain at multiple sites and vertebral bone size at pubertal maturity were significantly decreased. Hence, childhood fractures may be markers of low peak bone mass acquisition and persistent skeletal fragility. INTRODUCTION: Fractures in childhood may result from a deficit in bone mass accrual during rapid longitudinal growth. Whether low bone mass persists beyond this period however remains unknown. MATERIALS AND METHODS: BMC at the spine, radius, hip, and femur diaphysis was prospectively measured over 8.5 years in 125 girls using DXA. Differences in bone mass and size between girls with and without fractures were analyzed using nonparametric tests. The contribution of genetic factors was evaluated by mother-daughter correlations and that of calcium intake by Cox proportional hazard models. RESULTS: Fifty-eight fractures occurred in 42 among 125 girls (cumulative incidence, 46.4%), one-half of all fractures affecting the forearm and wrist. Girls with and without fractures had similar age, height, weight. and calcium intake at all time-points. Before and during early puberty, BMC and width of the radius diaphysis was lower in the fracture compared with no-fracture group (p < 0.05), whereas aBMD and BMAD were similar in the two groups. At pubertal maturity (Tanner's stage 5, mean age +/- SD, 16.4 +/- 0.5 years), BMC at the ultradistal radius (UD Rad.), femur trochanter, and lumbar spine (LS), and LS projected bone area were all significantly lower in girls with fractures. Throughout puberty, BMC gain at these sites was also decreased in the fracture group (LS, -8.0%, p = 0.015; UD Rad., -12.0%, p = 0.004; trochanter, -8.4%, p = 0.05 versus no fractures). BMC was highly correlated between prepuberty and pubertal maturity (R = 0.54-0.81) and between mature daughters and their mothers (R = 0.32-0.46). Calcium intake was not related to fracture risk. CONCLUSIONS: Girls with fractures have decreased bone mass gain in the axial and appendicular skeleton and reduced vertebral bone size when reaching pubertal maturity. Taken together with the evidence of tracking and heritability for BMC, these observations indicate that childhood fractures may be markers for low peak bone mass and persistent bone fragility.