胰腺癌患者外周血促血管生成因子浓度与疾病进展的关系

目的探讨胰腺癌患者外周血促血管生成因子中血管内皮细胞生长因子（VEGF）、碱性成纤维细胞生长因子（bFGF）及类胰岛素生长因子（IGF-1）浓度与临床病理学特点之间的关系。方法酶联免疫吸附试验测定32例胰腺癌可切除患者,24例胰腺癌不可切除患者和20例健康人外周血的VEGF、bFGF及IGF-1浓度,分析其与胰腺癌患者性别、年龄、病理分级、肿瘤大小、有无淋巴结及远处转移、是否侵犯血管及临床分期的关系。结果胰腺癌患者VEGF及bFGF浓度显著高于健康人（P〈0．01）,IGF-1浓度差异无统计学意义（P〉0．05）;胰腺癌不可切除组较可切除组VEGF显著升高（P〈0．05）,bFGF及IGF浓度差异无统计学意义（P〉0．05）;VEGF与胰腺癌分化、淋巴结转移、血管侵袭、远处转移及临床分期相关;bFGF与肿瘤大小及肿瘤分化相关;IGF-1与血管侵袭相关。结论胰腺癌进展过程中特有的生物学特性与胰腺癌不同时期的血管形成调控密切相关,促血管生成因子对于胰腺癌的进展发挥至关重要的作用,检测外周血促血管生成因子的表达对于胰腺癌临床筛查、诊断及治疗可能具有重要意义。     

支具治疗青少年特发性脊柱侧凸的临床随访

目的评价支具治疗青少年特发性脊柱侧凸的临床疗效,分析影响疗效的相关因素,并探讨支具治疗的适应证。方法对79例接受支具治疗的青少年特发性脊柱侧凸患者进行随访,记录患者的Cobb角,侧凸类型,女性患者初潮与否,坐高,站高,Risser征,顶椎旋转度等。结果随访12～60个月,平均23．9个月。末次随访时21例（26．6％）畸形明显进展,40例（50．6％）畸形维持或稍进展,18例（22．8％）畸形改善。初诊时原发弯Cobb角〉45°组侧凸进展率较Cobb角≤35°组高,侧凸改善率较Cobb角≤35°组低（P〈0．05）;顶椎旋转度Ⅲ°以上组侧凸进展率较0～Ⅱ°组高,侧凸改善率较0～Ⅱ°组低（P〈0．05）。侧凸类型、Risser征等参数不同的患者畸形进展和改善的比率均存在不同程度的差别,但差异不具有显著性（P〉0．05）。结论矫形支具能够有效控制或改善轻、中度特发性脊柱侧凸畸形。单独借助Risser征预测侧凸畸形变化趋势并不可靠。初始Cobb角〉45°,顶椎旋转度在Ⅲ°以上的患者,如果支具治疗的效果不佳,应考虑尽早手术矫形。     

腹腔开放患者的肠内营养支持

目的观察腹腔开放患者能否安全有效地应用肠内营养（EN）。方法回顾近3年因腹腔间室综合征行腹腔开放的患者的临床资料。通过空肠行EN支持超过3d者入选。所有患者腹腔敞开后均以聚丙烯网覆盖,根据肠功能恢复情况,决定EN开始时机和方案。采用输注泵连续输注,分别于EN前和结束时检测血浆蛋白水平和氮平衡。使用Harris—Benedict方程式计算或间接能量测定仪测定实际能量消耗和呼吸商。结果21例患者EN实施时间平均（51．5±33．6）d,开始于腹腔开放后（8．8±5．5）d,达到目标值的93％～95％。治疗前血各项蛋白水平低于正常值,但经过EN支持后均有改善,其中纤维连接蛋白增加明显,相关并发症未有增加。结论腹腔开放患者肠管虽外露,但在感染得到控制,外加聚丙烯网的覆盖情况下,及时给予EN,肠黏膜和肠壁组织获得营养和循环改善．使组织修复功能趋向健康。EN可以安全有效地应用于腹腔开放的患者。     

多药耐药相关基因及其蛋白在介导胰腺癌细胞原发性耐药中的作用及调控

目的 检测多药耐药相关基因（MDR1）及其蛋白（P-gP）在胰腺癌细胞株的表达,初步探讨胰腺癌发生先天性耐药的机理。方法 选择8株人胰腺癌细胞株,采用RT-PCR方法检测MDR1mRNA在胰腺癌细胞中的表达;通过免疫细胞化学方法检测P-gP的表达;以流式细胞仪检测胰腺癌细胞对罗丹明的外排情况,评价P-gP泵功能;最后通过P-gP抑制物维拉帕米与化疗药物联合应用,检测其对胰腺癌细胞的杀伤作用。结果 MDR1mRNA在胰腺癌细胞株SW1990中的表达最高,除PCT-2未检测到MDR1的表达外,其余6株细胞均有MDR1的微弱表达;免疫细胞化学染色结果证实P-gP在SW1990中的表达明显高于其他细胞株。57．9％±5．4％的SW1990细胞内有罗丹明蓄积,而在P-gP阴性对照细胞中,99．5％±3．3％的细胞内存在罗丹明的积聚,两者差异有统计学意义（P〈0．05）。P-gP抑制物维拉帕米与阿霉素或表阿霉素联合应用时可以部分逆转肿瘤细胞对化疗药物的耐药性。结论 MDR1及P-gP在人胰腺癌细胞中存在一定量的表达;维拉帕米联合阿霉素可以明显抑制P-gP阳性细胞的生长。     

不同脑保护方法下主动脉术后脑脊髓液S100β及IL-6的变化

目的通过对主动脉手术围手术期脑脊髓液生化指标变化的比较,评价两种不同脑保护方法的效果。方法2004年11月至2005年4月接受手术治疗的主动脉瘤患者14例,其中I型主动脉夹层11例,Ⅲ型主动脉夹层2例,假性胸腹主动脉瘤1例。在单纯深低温停循环（DHCA）下行胸降主动脉替换5例（DHCA组）;在DHCA结合选择性顺行脑灌注（ASCP）下行主动脉弓部置换9例（ASCP组）。于术前及术后0、6、12、24、48和72h检测脑脊髓液S10013蛋白（S100β）及白细胞介素6（IL-6）水平。结果ASCP组停循环时间长于DHCA组。两组脑脊髓液中S100β及IL-6的术前水平无显著差别。两组S100β于术后12h达到峰值;术后6—72h各时间点两组S100β水平差异有统计学意义（P〈0．05）。两组IL-6分别于术后12h和0h达到峰值;术后6h及12h两组IL-6水平差异有统计学意义（P〈0．05）。结论在两种脑保护方法下主动脉手术中发生的缺氧性脑损伤均属轻型。DHCA结合单侧ASCP具有比单纯DHCA更好的脑保护效果,围手术期的脑损伤较轻。     

Human osteoblasts' proliferative responses to strain and 17beta-estradiol are mediated by the estrogen receptor and the receptor for insulin-like growth factor I.

The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor.     

Preparation and degradation characteristic study of bone repair composite of DL—polylactic acid／hydroxyapatite／decalcifying bone matrix

Objective:To explore the preparative method and study the degradation characteristics of bone repair composite of DL-polyactic acid(PDLLA) /hydroxyapatite(HA)/decalcifying bone matrix(DBM) in vitro.Methods:An emulsion blend method was developed to prepare the composite of PDLLA/HA/DBM in weight ratio of PDLLA:HA:DBM=1.2-2:1.5:1.The dynamic changes of weight,biomechanical property and pH value of PDLLA/HA/DBM and PDLLA in phosphate buffered saline(PBS,pH7.4)were studied respectively through degradation tests in vitro.Results:Without being heated,PDLLA,HA and DBM could be synthesized with the emulsion blend method as bone composite of PDLLA/HA/DBM,wich had both osteoconductive and osteoinductive effects.The diameter of the aperture was 100-400μm and the gap rate was 71.3%.During degradation,the pH value of PDLLA solution decreased lightly within 2 weeks,but decreased obviously at the end of 4 weeks and the value was 4.0 .While the pH value of PDLLA/HA/DBM kept quite steady and was 6.4 at the end of 12 weeks.The weight of PDLLA changed little within 4 weeks,then changed obviously and was 50% of its initial weight at the end of 12 weeks.While the weight of PDLLA/HA/DBM changed little within 5 weeks ,then changed obviously and was 60% of the initial weight at the end of 12 weeks.The initial biomechanical strength of PDLLA was 1.33 MPa, decreased little within 3 weeks, then changed obviously and kept at 0.11 MPa at the end of 12 weeks.The initial biomechanical strength of PDLLA/HA/DBM was 1.7 MPa, decreased little within 4 weeks, then changed obviously and kept at 0.21 MPa at the end of 12 weeks.Conclusions:The emulsion blend method is a new method to prepare bone repair materials.As a new bone repair material,PDLLA/HA/DBM is more suitable for regeneration and cell implantation,and the environment during its degradation is advantageous to the growth of bone cells.     

内窥镜下直接经蝶入路切除垂体腺瘤

目的 探讨内窥镜控制下直接经蝶入路切除垂体腺瘤的方法。方法 22例垂体腺瘤患者,在内窥镜控制下,经单鼻孔进入,术中不切除鼻中隔,直接自蝶窦开口打开蝶突前壁,进一步经鞍底切除垂体腺瘤。结果 22例患者中,15例肿瘤全部切除,7例肿瘤次全切除。术后随访1－12个月,17例患者内分泌功能恢复正常。4例术后发生暂时性尿崩症。结论 内窥镜控制下直接经蝶切除垂体腺瘤入路与目前常规经蝶显微手术比较,入路途径较短,且安全简捷、损伤小,手术显露良好,术后反应小,值得进一步推广。     

儿童颈椎间盘钙化的诊断和治疗

目的 探讨儿童颈椎间盘钙化诊断和治疗的有效方法。方法 回顾性分析13例儿童的颈椎间盘钙化,其中上感后颈痛5例,外伤后偶然发现2例,突发颈部疼痛3例,突发斜颈3例。所有患者均经颈椎正、侧位X片证实。伴有疼痛症状应用非甾体抗炎镇痛药类药物,对于颈部症状较重则予预围外固定或短暂牵引后颈围外固定3－4周。结果 13例患儿共发现14个椎间隙的颈椎间盘钙化。经对症处理后临床症状均消失,所有的钙化均于5个月内完全消失。结论 儿童颈椎间盘钙化是一良性自限性疾病,正确认识其病理生理过程,可避免不必要的手术创伤。     

P-Selectin Glycoprotein Ligand-1 (rPSGL-Ig)-Mediated Blockade of CD62 Selectin Molecules Protects Rat Steatotic Liver Grafts from Ischemia/Reperfusion Injury

We examined the effects of early blockade of CD62 selectin-mediated adhesive interactions in steatotic rat liver models of ex vivo cold ischemia followed by reperfusion or transplantation by administration of P-selectin glycoprotein ligand-1 (rPSGL-Ig). In the model of cold ischemia/reperfusion, livers pretreated ex vivo with rPSGL-Ig at harvesting from obese Zucker rats showed significantly decreased portal resistance, increased bile production, and diminished hepatic endothelial neutrophil infiltration, as compared with untreated controls. Pretreatment of fatty livers with rPSGL-Ig prior to transplantation extended the survival of lean Zucker rat recipients from 40% to 90%. This effect correlated with significantly improved liver function, depressed neutrophil activity, and decreased histologic features of hepatocyte injury. Intragraft expression of CD62 P-selectin was similar in both recipient groups. rPSGL-Ig treatment decreased intragraft infiltration by CD3/CD25 cells, diminished expression of pro-inflammatory TNFalpha, IL-6, iNOS, IL-2 and IFN-gamma, without significantly affecting mRNA levels coding for anti-inflammatory IL-4. Thus, rPSGL-Ig blockade of CD62-mediated adhesive interactions protects against severe ischemia/reperfusion injury suffered otherwise by steatotic rat livers. These findings document the potential utility of rPSGL-Ig in increasing the transplant donor pool through modulation of marginal steatotic livers.