大气颗粒物健康效应生物学机制研究进展

大量流行病学研究发现，大气颗粒物的污染水平与心肺系统疾病的超额发病、死亡存在密切关联，但其毒理学机制尚未阐明。本文对近年来大气颗粒物毒理学研究进行综述，包括大气颗粒物对呼吸系统、心血管系统及神经系统的毒性作用，并对氧化应激损伤、细胞钙稳态失衡及激活关键转录因子等分子毒理学机制进行了初步的阐述。     

裂解汽油在ZSM-5沸石上的芳构化

采用连续流动反应装置,考察了裂解汽油在HZSM-5与金属元素改性的HZSM-5上的芳构化反应,发现锌改性后提高了液体产物中芳烃的收率。为了克服裂解汽油中含硫含焦杂质的影响,提出了获取芳烃的有效工艺:蒸馏除焦-加氢预脱硫-氢气氛下芳构化反应-冷凝产物。用氨吸附的程序升温脱附法,将催化剂的酸性质与其催化芳构化作用进行关联,认为Zn改性后的HZSM-5催化剂具有较温和的酸中心,可能是其芳构化高活性与高选择性的原因。     

对我校重点建设课程评价结果的分析与思考

目的：加强重点课程建设．提高学校的教学质量。方法：对8门重点建设课程进行深入细致地评价并对6项指标进行统计学分析。结果：各门课程均存在显著性差异。结论：对课程建设进行评价能够发现建设中的薄弱环节，对评价结果进行分析能帮助各课程认识不足，加以改进。     

颈椎脱位的闭合复位

1985年5月～1996年3月,我们经治34例单纯颈椎脱位患者,30例行Crutchfield颅骨牵引闭合复位,20例成功,占66.6％。在成功组中,牵引重量最大为18kg,无一例出现神经损害加重。不全瘫均有不同程度恢复。尸体头颅标本测定,Crutchfield颅骨牵引承受的最大抗拨出力为60.3kg,在治疗颈椎脱位时,颅骨牵引是安全有效的闭合复位方法。     

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     

经尿道电气化切除术治疗良性前列腺增生症(附1532例报告)

目的 :总结和评价经尿道前列腺电气化切除术 (TUVP)治疗良性前列腺增生症 (BPH)的疗效。方法 :采用铲式气化切割环 ,经尿道气化切除前列腺 1 5 32例。结果 :最大尿流率 (Qmax)由手术前 (7.7± 3.8)ml/s到术后 (1 7.9± 3.2 )ml/s;国际前列腺症状评分由术前 (2 9.5± 3.6 )分到术后 (9.1± 2 .9)分 ;生活质量评分由术前 (5 .5± 0 .3)分到术后 (1 .9± 0 .3)分 ;术中前列腺包膜穿孔 2例 ;术后尿失禁 2例 ,前尿道狭窄 1 7例 ,后尿道狭窄 7例 ;无电切综合征及死亡病例。结论 :TUVP治疗BPH创伤小、出血少、疗效好、术后康复快     

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.