自体脂肪颗粒与尿激酶联合应用预防硬膜外粘连

背景：椎板切除后,易发生硬膜外粘连。术后在硬膜外单独应用1种药品或隔离物,效果不甚理想。目的：观察自体脂肪颗粒与尿激酶联合应用预防椎板切除后硬膜外粘连的效果。方法：64只成年新西兰兔随机分为模型组、尿激酶组、自体脂肪颗粒组、尿激酶＋自体脂肪颗粒组,各16只。手术切除L5椎板造成12mm×5mm硬脊膜裸露区,探查神经根。模型组注入生理盐水,尿激酶组注入尿激酶（25U/kg）,自体脂肪颗粒组用自体游离脂肪颗粒覆盖,尿激酶＋自体脂肪颗粒组用尿激酶（25U/kg）注入后再用自体游离脂肪颗粒覆盖。术后2,4周行大体观察及组织学观察,6周时行硬膜外瘢痕面积定量分析。结果与结论：模型组椎板切除部位明显粘连,尿激酶组、自体脂肪颗粒组轻度粘连,尿激酶＋自体脂肪颗粒组无明显粘连。尿激酶组、自体脂肪颗粒组、尿激酶＋自体脂肪颗粒组成纤维细胞数显著低于模型组（P〈0.05）,尿激酶＋自体脂肪颗粒组成纤维细胞数低于尿激酶组、自体脂肪颗粒组（P〈0.05）。自体脂肪颗粒组、尿激酶＋自体脂肪颗粒组瘢痕面积显著低于模型组、尿激酶组（P〈0.05）,尿激酶＋自体脂肪颗粒组瘢痕面积低于自体脂肪颗粒组。提示脂肪颗粒及尿激酶联合应用对预防椎板切除后硬膜外粘连具有协同作用,效果显著。     

干扰素/聚乳酸-羟基乙酸共聚物及壳聚糖/聚乳酸-羟基乙酸共聚物复合膜防止椎板切除后的硬膜外瘢痕粘连（英文）

背景：应用硬膜外阻隔材料是预防椎板切除后硬膜外瘢痕粘连的一种方法,而制备既有机械阻隔能力,又有抑制成纤维细胞的能力的复合膜是其中一个重要的研究方向。目的：制备壳聚糖/聚乳酸-羟基乙酸共聚物[poly（lactic-co-glycolicacid）,PLGA]与干扰素/PLGA复合膜,观察其防止兔椎板切除后硬膜外瘢痕粘连的作用。方法：大耳白兔120只行L2椎板切除,随机分为6组：对照组硬膜外不放任何物质;自体游离脂肪移植组取皮下脂肪贴于硬膜表面;透明质酸钠组将透明质酸钠1mL滴于硬膜外;PLGA膜组、壳聚糖/PLGA及干扰素/PLGA复合膜组,分别将各种膜修剪成合适大小植于硬膜外。术后2,4,6,8周处死动物,观察L2术区的瘢痕形成及与硬膜粘连的情况并评分。术后4周,透射电镜下观察成纤维细胞的超微结构。结果与结论：随着时间的延长,对照组形成较广泛的瘢痕。游离脂肪组和PLGA膜组的瘢痕量少于对照组。透明质酸组早期瘢痕形成量明显少于自体游离脂肪组和PLGA膜组,后期无显著性差异,但优于对照组。壳聚糖/PLGA膜组与干扰素/PLGA膜组硬膜外瘢痕的形成量最少,与硬膜无或轻微粘连,其作用明显优于其他各组,但两种复合膜组间差异不明显。术后4周,对照组、游离脂肪组和PLGA膜组的成纤维细胞的状态和功能明显好于壳聚糖/PLGA膜组与干扰素/PLGA膜组。壳聚糖/PLGA复合膜与干扰素/PLGA复合膜是预防椎板切除后硬膜外瘢痕粘连的有效材料。     

干扰素/聚乳酸-羟基乙酸共聚物及壳聚糖/聚乳酸-羟基乙酸共聚物复合膜防止椎板切除后的硬膜外瘢痕粘连

背景:应用硬膜外阻隔材料是预防椎板切除后硬膜外瘢痕粘连的一种方法,而制备既有机械阻隔能力,又有抑制成纤维细胞的能力的复合膜是其中一个重要的研究方向.目的:制备壳聚糖/聚乳酸-羟基乙酸共聚物[poly(lactic-co-glycolic acid),PLGA]与干扰素/PLGA复合膜,观察其防止兔椎板切除后硬膜外瘢痕粘连的作用.方法:大耳白兔120只行L2椎板切除,随机分为6组:对照组硬膜外不放任何物质;自体游离脂肪移植组取皮下脂肪贴于硬膜表面;透明质酸钠组将透明质酸钠1 mL 滴于硬膜外;PLGA膜组、壳聚糖/PLGA及干扰素/PLGA复合膜组,分别将各种膜修剪成合适大小植于硬膜外.术后2,4,6,8 周处死动物,观察L2术区的瘢痕形成及与硬膜粘连的情况并评分.术后4周,透射电镜下观察成纤维细胞的超微结构.结果与结论:随着时间的延长,对照组形成较广泛的瘢痕.游离脂肪组和PLGA膜组的瘢痕量少于对照组.透明质酸组早期瘢痕形成量明显少于自体游离脂肪组和PLGA膜组,后期无显著性差异,但优于对照组.壳聚糖/PLGA膜组与干扰素/PLGA膜组硬膜外瘢痕的形成量最少,与硬膜无或轻微粘连,其作用明显优于其他各组,但两种复合膜组间差异不明显.术后4周,对照组、游离脂肪组和PLGA膜组的成纤维细胞的状态和功能明显好于壳聚糖/PLGA膜组与干扰素/ PLGA膜组.壳聚糖/PLGA复合膜与干扰素/ PLGA复合膜是预防椎板切除后硬膜外瘢痕粘连的有效材料.     

自体脂肪株移植预防硬膜外腔瘢痕粘连的临床效果

目的 比较用自体脂肪株植入和整片脂肪植入预防椎板切除术后硬膜外腔瘢痕粘连的效果。方法 选取椎板切除减压同时行内固定的病例42例，其中18例采用了整片脂肪植入预防硬膜外腔瘢痕粘连(A组，n=18)，12例采用了自体脂肪株植入预防硬膜外腔瘢痕粘连(B组，n=12)，12例没有采用措施预防硬膜外腔瘢痕粘连(C组，n=12)，在内固定物取出时进行大体标本、光镜和免疫组化观察硬膜外腔的粘连程度。结果 B组预防硬膜外腔瘢痕粘连效果优于A组和C组。结论 自体脂肪株植入预防硬膜外腔瘢痕粘连有良好的效果，应该取代整片脂肪植入。     

干扰素/聚乳酸-羟基乙酸共聚物及壳聚糖/聚乳酸-羟基乙酸共聚物复合膜防止椎板切除术后硬膜外瘢痕粘连的实验

背景: 应用硬膜外阻隔材料是预防椎板切除术后硬膜外瘢痕粘连的一种方法,而制备既有机械阻隔能力,又有抑制成纤维细胞的能力的复合膜是其研究方向.目的: 制备壳聚糖/聚乳酸-羟基乙酸共聚物[poly (lactic-co-glycolic acid), FLGA]与干扰素/PLGA复合膜,观察其防止椎板切除术后硬膜外瘢痕粘连的作用.设计、时间及地点: 2005-05/2007-04在中科院长春应用化学研究所完成材料制备,随机对照动物实验在解放军第〇八医院实验动物室完成.材料: PLGA膜、壳聚糖/PLGA及干扰素/PLGA复合膜由中科院长春应用化学研究所制备.方法: 大耳白兔120只行L2及L4椎板切除,随机分为6组,每组20只,于椎板缺损区处理如下:①空白对照组:硬膜外不放任何物质.②自体游离脂肪组:取皮下脂肪贴于硬膜表面.③透明质酸钠组:透明质酸钠1mL涂于硬膜外.④PLGA膜组、壳聚糖/PLGA及干扰素/PLGA复合膜组:分别将各种膜修剪成合适大小植于硬膜外.主要观察指标: 术后2,4,6,8周处死动物,观察L2手术区硬膜外瘢痕形成及粘连程度并评分,然后完整取下L4节段脊柱,行苏木精-伊红染色及Masson染色,光镜下观察并行组织学评分.结果: 随着时间的延长,空白对照组形成较广泛的瘢痕;自体游离脂肪组和PLGA膜组的瘢痕量少于对照组,前两者比较差异无显著性;透明质酸组早期瘢痕形成量明显少于自体游离脂肪组和PLGA膜组,后期差异无显著性,但仍优于空白对照组:壳聚糖/PLGA膜组与干扰素/PLGA膜组硬膜外瘢痕的形成量最少,与硬膜无或轻微粘连,明显优于其他各组,两种复合膜组间差异不明显.结论: 壳聚糖/PLGA与干扰素/PLGA复合膜均可预防椎板切除术后硬膜外瘢痕粘连,效果相近.     

干扰素／聚乳酸-羟基乙酸共聚物及壳聚耕聚乳酸-羟基乙酸共聚物复合膜防止椎板切除术后硬膜外瘢痕粘连的实验

背景：应用硬膜外阻隔材料是预防椎板切除术后硬膜外瘢痕粘连的一种方法，而制备既有机械阻隔能力，又有抑制成纤维细胞的能力的复合膜是其研究方向。 目的：制备壳聚糖／聚乳酸-羟基乙酸共聚物[poly（lactic—co—glycolic acid），PLGA]与干扰素／PLGA复合膜，观察其防止椎板切除术后硬膜外瘢痕粘连的作用。 设计、时间及地点：2005—05／2007—04在中科院长春应用化学研究所完成材料制备，随机对照动物实验在解放军第二○八医院实验动物室完成。 材料：PLGA膜、壳聚糖／PLGA及干扰素／PLGA复合膜由中科院长春应用化学研究所制备。 方法：大耳白兔120只行L2及L4椎板切除，随机分为6组，每组20只，于椎板缺损区处理如下：①空白对照组：硬膜外不放任何物质。②自体游离脂肪组：取皮下脂肪贴于硬膜表面。③透明质酸钠组：透明质酸钠1mL涂于硬膜外。④PLGA膜组、壳聚糖／PLGA及干扰素／PLGA复合膜组：分别将各种膜修剪成合适大小植于硬膜外。 主要观察指标：术后2，4，6，8周处死动物，观察L2手术区硬膜外瘢痕形成及粘连程度并评分，然后完整取下L4节段脊柱，行苏木精-伊红染色及Masson染色，光镜下观察并行组织学评分。 结果：随着时间的延长，空白对照组形成较广泛的瘢痕；自体游离脂肪组和PLGA膜组的瘢痕量少于对照组，前两者比较差异无显著性：透明质酸组早期瘢痕形成量明显少于自体游离脂肪组和PLGA膜组，后期差异无显著性，但仍优于空白对照组；壳聚糖／PLGA膜组与干扰素／PLGA膜组硬膜外瘢痕的形成量最少，与硬膜无或轻微粘连，明显优于其他各组，两种复合膜组间差异不明显。 结论：壳聚糖／PLGA与干扰素／PLGA复合膜均可预防椎板切除术后硬膜外瘢痕粘连，效果相近。     

川芎嗪与自体骨膜植入预防椎板切除术后硬膜外粘连的实验研究

目的观察椎板切除术后用川芎嗪并在椎板缺损处植入自体骨膜预防硬膜外粘连的效果。方法48只SD大鼠随机分成A、B、C、D4组,制作L2板损伤模型。A组硬膜外涂布生理盐水,B组硬膜外涂布川芎嗪,C组硬膜外覆盖自体骨膜,D组硬膜外涂布川芎嗪的同时加自体骨膜覆盖。术后12周对椎板切除部位进行大体观察、组织学观察、生化检查比较组间瘢痕形成和粘连情况。结果B、C、D组的改良Rydell-Balazs粘连韧度评分、胶原含量、改良Nussvuaum组织学评分均明显优于A组(P0.01),D组优于B组与C组(P0.05)。结论联合运用川芎嗪和自体骨膜能有效预防硬膜外瘢痕粘连和形成,比单独应用川芎嗪和自体骨膜预防效果好。     

椎板切除模型大鼠局部应用绿原酸对硬膜外纤维化及硬脑膜粘连的影响

背景：椎板切除减压能起到有效的脊髓神经减压作用,但该操作也会发生硬膜外纤维增生并突入椎管,致医源性椎管狭窄,发生持续或复发的腰腿疼痛。绿原酸是金银花的有效药理成分之一,主要有抗炎等作用。
　　目的：观察局部应用绿原酸对椎板切除模型大鼠硬膜外纤维化及硬脑膜粘连的影响。
　　方法：选用72只健康成年Wistar大白鼠,制备椎板切除模型,随机分成3组(n=24)。绿原酸组皮肤缝合前椎板切除区域给绿原酸溶液2 mL/只;生理盐水组给予等量的生理盐水;空白对照组术后不做任何处理。各组大鼠均于造模后4周被处死,进行实验评估,包括大体评价、组织学分析、羟脯氨酸含量测定及白细胞介素6、转化生长因子β1的表达情况。
　　结果与结论：3组大白鼠均进入结果分析,解剖并取样。绿原酸组硬膜外胶原纤维增生较少,外观较为正常;生理盐水组和空白对照组硬膜外胶原纤维明显增多,外观可见明显纤维瘢痕组织。组织学评价显示,绿原酸组的组织染色切片中成纤维细胞的密度明显比其他两组的成纤维细胞密度低。绿原酸组硬膜外纤维瘢痕的羟脯氨酸含量显著低于生理盐水组和空白对照组(P <0.01)。通过RT-PCR方法测得绿原酸组白细胞介素6和转化生长因子β1的表达低于另外两组。提示椎板切除模型大鼠局部应用绿原酸可以抑制成纤维细胞增殖,同时可以降低白细胞介素6和转化生长因子β1的表达,防止硬膜外瘢痕粘连。     

持续闭式灌洗预防椎板切除后硬膜粘连

目的 观察持续闭式灌洗预防椎板切除后硬膜粘连的效果。方法 选成年健康新西兰大白兔 30 只,每只兔的背部做两处切口,分别切除L2 和L6 棘突、椎板,显露硬膜囊,其中一处直接缝合,作为对照组;另一处持续灌洗 72 h,作为冲洗组。术后4周、8周、12周取样行大体和光镜检查,12周样本增加透射电镜检查及计算机图像分析。结果 术后 4 周和 8 周样本见对照组硬膜外腔被大量瘢痕组织填充,直达肌筋膜层,瘢痕与硬膜及周围肌肉组织粘连紧密,难以剥离;冲洗组见硬膜与肌肉之间为膜性物、浸润脂肪或少量瘢痕,与硬膜无粘连或部分粘连,易于钝性分离。术后 12 周样本见对照组硬膜外瘢痕致密而广泛,与硬膜紧密粘连,难以区分;冲洗组硬膜外瘢痕形成少而疏松,与硬膜轻度粘连或无粘连,与对照组存在显著性差异( P <0.05)。透射电镜下见,对照组硬膜外组织为致密瘢痕组织;冲洗组主要为脂肪组织,脂肪细胞间夹杂少量胶原纤维。结论 兔椎板切除后持续生理盐水灌洗72 h可有效防止硬膜粘连     

碱性成纤维细胞生长因子在自体脂肪颗粒填充面部凹陷中的作用

背景:碱性成纤维细胞生长因子具有明显的促进细胞增殖、加速移植物血管化的作用,而且可以促进人前脂肪细胞向成熟脂肪细胞分化.目的:观察成纤维细胞生长因子在自体脂肪颗粒移植治疗面部凹陷中的作用,评价其治疗效果.方法:纳入武警医学院附属医院应用自体脂肪颗粒注射移植治疗面部凹陷的患者52例,患者按治疗的先后时间顺序分为对照组和碱性成纤维细胞生长因子组.对照组患者只注射自体脂肪颗粒进行治疗,碱性成纤维细胞生长因子组在注射自体脂肪颗粒的基础上加入碱性成纤维细胞生长因子.两组患者术后6个月随访,通过照相对比凹陷填充效果.结果与结论:52例患者面部凹陷均得到不同程度的改善.对照组19例患者充填效果,优4例,良6例,优良率53%,有12例患者进行了2次注射,比例为63%.成纤维细胞生长因子组33例患者充填效果,优14例,良12例,优良率79%,有11例患者进行了2次脂肪注射,比例为33%.两组优良率和二次注射率比较,有显著性差异(P<0.05).可见碱性成纤维细胞生长因子局部应用可以明显提高面部凹陷的填充效果,安全有效.     

Mammographic and ultrasonographic features after autogenous myocutaneous flap reconstruction mammoplasty.

OBJECTIVE: To present mammographic and ultrasonographic findings in various types of reconstruction using an autogenous myocutaneous flap after mastectomy or breast-conserving surgery. METHODS: Mammography and ultrasonography performed in patients who had undergone reconstruction mammoplasty using the autogenous myocutaneous flap procedure were reviewed to facilitate recognition of both normal and abnormal postoperative appearances of the various types of reconstruction using the autogenous myocutaneous flap after mastectomy or breast-conserving surgery. RESULTS: Normal mammographic and ultrasonographic findings include predominance of a fatty appearance, surgical clips, and surgical scars. Abnormal mammographic and ultrasonographic findings include fat necrosis, calcifications, and locally recurrent carcinoma. Ultrasonographic findings of fat necrosis were cystic, complex, and solid-appearing masses with circumscribed or poorly defined margins in peripheral portions of the flap. Ultrasonographic findings of locally recurrent carcinoma were poorly defined heterogeneous hypoechoic lesions in reconstructed breast, similar to those of primary breast cancer. CONCLUSIONS: Breast reconstruction using the autogenous myocutaneous flap has increased in popularity with various methods. Mammography and ultrasonography facilitated excellent visualization of normal and abnormal findings of various reconstructed breasts with the autogenous myocutaneous flap.     

纳米尿激酶的性状研究

背景:尿激酶半衰期短,需持续大量给药,并发症也不小,故有必要研制具有缓释作用的溶栓药物。目的:了解包载尿激酶的水溶性壳聚糖纳米粒子的性状。方法:将壳聚糖和三聚磷酸钠以离子凝集法制备尿激酶纳米粒子后,用透射电镜观察其形态,采用粒径仪测纳米粒子粒径,酶标仪比色法测粒子包封率,纳米粒子冻干法测其载药量,并检测体内外纳米粒子缓释特性。结果与结论:当壳聚糖、三聚磷酸钠、尿激酶的质量比为7∶1∶1时,不仅溶液稳定,形成的纳米粒子粒径小,而且包封率和载药量均合适。制备出包封率最高达94.8%的尿激酶纳米粒子,载药量为14.5%,此时平均粒径236nm,透射电镜观察示粒子形态较规则,呈球形;粒子具有较好的缓释性能;表明将尿激酶包被于纳米粒子中,避免了消化酶的直接作用,延长了半衰期,不仅在体内能保持较长时间的活性,而且具有明显的缓释效果。     

Plasmin and plasminogen activator inhibitor type 1 promote cellular motility by regulating the interaction between the urokinase receptor and vitronectin.

The urokinase receptor (uPAR) coordinates plasmin-mediated cell-surface proteolysis and promotes cellular adhesion via a binding site for vitronectin on uPAR. Because vitronectin also binds plasminogen activator inhibitor type 1 (PAI-1), and plasmin cleavage of vitronectin reduces PAI-1 binding, we explored the effects of plasmin and PAI-1 on the interaction between uPAR and vitronectin. PAI-1 blocked cellular binding of and adhesion to vitronectin by over 80% (IC50 approximately 5 nM), promoted detachment of uPAR-bearing cells from vitronectin, and increased cellular migration on vitronectin. Limited cleavage of vitronectin by plasmin also abolished cellular binding and adhesion and induced cellular detachment. A series of peptides surrounding a plasmin cleavage site (arginine 361) near the carboxy-terminal end of vitronectin were synthesized. Two peptides spanning res 364-380 blocked binding of uPAR to vitronectin (IC50 approximately 8-25 microM) identifying this region as an important site of uPAR-vitronectin interaction. These data illuminate a complex regulatory scheme for uPAR-dependent cellular adhesion to vitronectin: Active urokinase promotes adhesion and also subsequent detachment through activation of plasmin or complex formation with PAI-1. Excess PAI-1 may also promote migration by blocking cellular adhesion and/or promoting detachment, possibly accounting in part for the strong correlation between PAI-1 expression and tumor cell metastasis.     

四步按摩法在维持性血液透析患者内瘘血栓形成后的应用

目的 观察运用四步按摩法治疗动静脉内瘘急性血栓形成的疗效。方法 纳入前臂自体动静脉内瘘急性 血栓形成患者36例,按照治疗手法不同分为两组。对照组实行常规按摩手法,研究组采用四步按摩法,均配合尿激酶持 续静脉泵入溶栓,对比两组溶栓治疗的成功率、透析血流量、治疗时间及血肿并发症等情况。结果 研究组再通率高于 对照组,透析血流量大于对照组,而研究组治疗时间、血肿发生率低于对照组(P <0.05)。结论 对自体动静脉内瘘急 性血栓形成的血液透析患者,经四步手法按摩联合药物溶栓治疗成功率高,再通快,血肿发生率低,值得临床推广。     

Integrin-mediated leukocyte adhesive interactions: regulation by haemostatic factors

Leukocyte recruitment to sites of inflammation, infection or vascular injury is a complex event that is orchestrated by a tightly coordinated sequence of interactions between leukocytes and cells of the vessel wall, especially endothelial cells. These interactions are controlled by the expression and activation of various adhesion receptors and protease systems. This review will focus on novel aspects of the regulation of integrin-dependent leukocyte adhesion by haemostatic factors. Here, so-called non-haemostatic properties of endogenous proteins such as high molecular weight kininogen, urokinase receptor, urokinase, as well as plasminogen and its cleavage product angiostatin in leukocyte adhesion and transmigration will be summarized. The crosstalk between haemostatic factors and inflammatory reactions may contribute to a better understanding of inflammatory vascular disorders and to the development of novel therapeutical concepts.     

尿激酶胸腔内注射预防结核性渗出性胸膜炎胸膜粘连

目的 探讨胸腔内注射尿激酶用于防治结核性胸膜炎患者发生胸膜粘连的价值。方法 结核性渗出性胸膜炎患者120例随机分为治疗组59例和对照组61例,对照组给予2HRZE/4HR（异烟肼＋利福平＋吡嗪酰胺＋乙胺丁醇）方案常规抗结核和胸腔穿刺置管引流,治疗组在对照组治疗基础上于每次胸腔穿刺抽液后胸腔内注射尿激酶10万u。观察2组胸腔积液消失时间及胸膜粘连发生率。结果 治疗组胸腔积液引流量、胸腔积液消失时间、胸膜粘连发生率分别为（1 900±670）mL、（6.75±3.52）d、6.8%;对照组分别为（1 280±530）mL、（10.14±6.47）d、32.8%,2组比较差异均有统计学意义（P〈0.05）。结论 胸腔注射尿激酶辅助治疗结核性胸膜炎可缩短胸腔积液吸收时间、降低胸膜粘连发生率。     

尿激酶胸腔注射治疗胸膜炎效果观察

目的：探讨尿激酶胸腔内注射防治结核性胸膜炎所致胸膜肥厚粘连的效果。方法：将252例患者随机分为两组,尿激酶组126例,用0．9％氯化钠注射液20ml加尿激酶5万U于每次抽液后行胸腔内注射;非尿激酶组126例,用0．9％氯化钠注射液20ml于每次抽液后行胸腔内注射,治疗结束后进行比较。结果：治疗组的胸膜厚度及胸膜粘连发生率明显低于对照组。结论：尿激酶胸腔内注射对结核性胸膜炎所致胸膜肥厚、粘连有一定的防治作用,无明显不良反应,操作简单,值得临床推广应用。     

Changes in serum levels of E-selectin correlate to improved glycaemic control and reduced obesity in subjects with the metabolic syndrome

OBJECTIVE: Inflammation plays an essential role in the atherosclerotic process. Cellular adhesion molecules (CAMs) such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are involved in the rolling, adhesion and extravasation of monocytes and T-lymphocytes into the atherosclerotic plaque. In the present study the effect of physical exercise and pravastatin (40 mg daily) on serum levels of CAMs and a possible role of adipose tissue in regulating serum levels of CAMs were investigated. MATERIAL AND METHODS: The study was designed as an unmasked randomized 2x2 factorial trial of 12 weeks duration in 32 subjects with the metabolic syndrome. Changes from baseline were studied, and correlations between changes in CAMs, anthropometric measures, regional fat distribution, glycaemic control and the adipocytokine tumour necrosis factor-a (TNF-a) and adiponectin were investigated. RESULTS: No significant changes in CAMs were observed in any of the intervention groups. However, when examining the whole study population regardless of intervention, changes in serum E-selectin were significantly correlated to changes in body mass index (r=0.48, p=0.006), waist circumference (r=0.48, p=0.006), fasting glucose (r=0.43, p=0.02) and HbA1c (r=0.45, p=0.01), but not to changes in visceral fat, subcutaneous fat, TNF-a or adiponectin. CONCLUSION: Changes in glycaemic control and obesity, rather than regional fat distribution, seem to influence the levels of E-selectin in subjects with the metabolic syndrome.     

Endothelial cell adhesion molecules in healthy adults during acute hyperhomocysteinemia and mild hypertriglyceridemia

OBJECTIVE: Hyperhomocysteinemia and hypertriglyceridemia are independently associated with atherosclerotic disease. The process of atherogenesis involves inflammation and endothelial dysfunction. We tested whether concurrent acute hyperhomocysteinemia and mild hypertriglyceridemia increase the concentrations of circulatory cellular adhesion molecules in healthy subjects. STUDY DESIGN AND METHODS: Twelve healthy volunteers aged 37.5 years (range, 25-51) participated in the present study. The concentrations of plasma total homocysteine (p-tHcy), serum triglycerides, circulatory cellular adhesion molecules (CAMs), and concentrations of nitrate were measured at 0 (fasting), 2, 4, and 6 h after loading with (1) methionine, (2) fat, (3) methionine + fat, and (4) water (control). Wash out period between each loading was >or=1 week. RESULTS: Percent relative changes from baseline in the concentrations of p-tHcy, 2, 4, and 6 h after methionine and methionine + fat were significantly different from after water and fat loading. Changes in the concentrations of serum triglycerides 2 h after fat loading were significantly different from water loading, whereas methionine + fat loading caused a significant difference after 2, 4, and 6 h. We detected a synergistic increase in the triglyceride area response to methionine + fat loading. We detected also a significant difference in percent relative changes in the concentrations of P-selectin (PSEL) (P = 0.02), E-selectin (ESEL) (P = 0.003), and vascular cell adhesion molecule-1 (VCAM-1) (P = 0.005) 6 h after methionine + fat loading as compared to water loading. There was an additive increase in the PSEL area response to methionine + fat loading. Furthermore, area response to VCAM was greater to methionine loading than water loading (P = 0.01). A decrease in the concentration of NO(3) was more pronounced after methionine + fat loading and a significantly decreased area response of nitrate to methionine + fat loading was detected than to area response to water loading (P = 0.002). CONCLUSION: Inflammatory activation of the endothelium takes place during concurrent transient hyperhomocysteinemia and mild hypertriglyceridemia.