血栓闭塞性脉管炎合并动脉硬化闭塞导致下肢缺血的手术治疗

目的 探讨下肢血栓闭塞性脉管炎(thmmboangiitis obliterans,TAO)合并动脉硬化闭塞症(arteriosclerosis obliterans,ASO)手术治疗效果.方法 回顾性分析2007年治疗的TAO合并ASO 6例患者的资料.2例行腹主动脉切开取栓+内膜剥脱+腹主动脉-股深动脉人工血管旁路移植-胭动脉人工血管-小腿动脉自体大隐静脉旁路移植术,1例行腹主动脉切开取栓+内膜剥脱+腹主动脉-右股深动脉人工血管旁路移植-膝下胭动脉人工血管旁路移植术;1例行左髂总动脉-左股深动脉人工血管旁路移植一胫前动脉自体大隐静脉原位移植术,1例行左侧人工血管切开取栓+左股深动脉成形-膝下腘动脉人工血管旁路移植术,1例行右股总动脉-左股总动脉人工血管旁路移植-胫后动脉自体大隐静脉旁路移植术.结果 5例患者术后恢复顺利,1例于术后当天出现股动脉-腘动脉人工血管和远段的大隐静脉桥血栓形成,立即再次手术行人工血管和大隐静脉切开取栓术,并同时行胫后动静脉吻合.6例患者均痊愈出院,无死亡病例.5例患者的下肢远端静息痛完全缓解,1例部分缓解.足部溃疡的2例创面明显缩小,无感染发生.所有患者得到随访,平均随访为6.5个月,3例足部溃疡愈合.1例术后3个月出现左股部切口感染,最终行膝上截肢处理,残端一期愈合.其他5例患者的移植血管通畅,症状缓解.结论 对TAO合并ASO患者如果手术治疗方式恰当,可以取得比较好的疗效.     

腹部手术合并门静脉高压症患者围手术期腹水的处理

目的 探讨腹部手术合并门静脉高压症患者围手术期腹水的处理方法.方法 回顾性分析2000年1月至2007年7月93例合并门静脉高压症患者接受腹部手术的治疗结果.结果 本组术后共发生腹水21例.肝功能Child A级和B级患者同期手术的术后腹水发生率分别为7%和12%,肝功能Child A级和B级患者分期手术的术后腹水发生率分别为13%和17%,肝功能Child C级患者同期手术的术后腹水发生率则高达83%.肿瘤患者较非肿瘤患者并未增加术后腹水的发生率(P=0.21).结论 加强围手术期的处理,并正确掌握其手术适应证和时机.对于肝功能Child A级和B级的患者一期处理门静脉高压并不会增加术后腹水的发生率;对择期或限期手术者必须加强处理,尽量消减腹水以稳定病情.     

内镜腔内手术的实验研究

目的探讨内镜腔内手术的可行性. 方法 6只家猪经皮建立胃内通道,腹腔镜引导下胃内模拟缝合止血操作实验. 结果 6只家猪均很好地耐受了手术.术后开腹检查所有胃壁缝合处无渗漏及其它脏器损伤.建立胃内通道时间、胃内缝合时间及总手术时间分别为(60.5±12.2)min、(26.5±5.78)min和(92.1±15.0)min. 结论内镜腔内手术在技术上是可行的.     

后腹腔镜手术CO2气腹对脑氧供需平衡的影响

目的探讨后腹腔镜CO2气腹对脑氧供需平衡的影响. 方法选择后腹腔镜下肾及肾上腺肿瘤切除术20例,ASAⅠ～Ⅱ级,分别于气腹前,气腹后10、30、60 min和关气腹后30 min,抽取颈静脉球血和桡动脉血进行血气分析,比较不同时点动脉血PH(aPH )、颈静脉球PH(jvPH)、动脉血二氧化碳分压(PaCO2)、动脉血糖(aGS)、动脉血乳酸(aLac)、颈内静脉血氧分压(PjvO2)、颈内静脉血氧饱和度(SjvO2)、颅内动静脉氧含量差(AjvDO2)、颈内静脉血二氧化碳分压(PjvCO2)、血糖(jvGS)和乳酸(jvLac)的变化. 结果与气腹前比较,气腹后各时间点aPH、jvPH显著降低(P＜0.05);PaCO2、PjvCO2气腹后各时间点与气腹前相比显著升高(P＜0.05);AjvDO2气腹后各时点与气腹前相比显著下降(P＜0.05);jvLac气腹后各时间点与气腹前相比有降低趋势,但无统计学差异(P＞0.05);aGS、 jvGS气腹前后无显著变化(P＞0.05). 结论后腹腔镜手术期间,脑血流量显著增加,未发现脑无氧代谢增加的证据.     

臂丛损伤神经干细胞脊髓前角移植后分化情况及对运动神经元的保护作用

目的观察臂丛根性撕脱伤后将脊髓源性神经干细胞(neuralstemcell,NSC)移植于脊髓前角后的存活、分化情况及对脊髓前角受损运动神经元的保护作用。方法取新生鼠脊髓,分离获得脊髓源性神经干细胞,体外培养、扩增、鉴定、5溴2-脱氧尿苷(BrdU)标记。取SD大鼠60只,随机分成实验组、对照组和单纯组。从后路制备C5~C7臂丛神经根性撕脱伤动物模型。实验组移植神经干细胞于C6脊髓前角,对照组移植灭活神经干细胞,单纯组不作移植。术后1、2、4、8、12周取脊髓标本进行组织学与免疫组化染色观察。结果神经干细胞移植入脊髓后能存活、分化;臂丛根性撕脱伤后脊髓前角运动神经元数目明显减少;实验组神经干细胞移植后2、4、8、12周各个时间点运动神经元的存活率均高于对照组和单纯组。结论臂丛根性撕脱伤脊髓前角神经干细胞移植后能存活并分化为神经元及星型胶质细胞,脊髓源性神经干细胞移植能明显减少前角运动神经元的继发性死亡,对脊髓前角受损运动神经元有保护作用。     

急性肾损伤微环境上调骨髓间充质干细胞分泌肾脏保护性生长因子

目的：急性肾损伤的模型中不可忽视炎症等原因,机体在不同应激反应条件下分泌的保护性生长因子各不相同。在这种情况下,骨髓间充质干细胞分泌的肾脏保护性细胞因子不同于急性肾脏损伤的炎症因子。因此,探讨在体外模拟的急性肾衰竭微环境中上调骨髓间充质干细胞（BMSC）肾脏保护性生长因子的可能性。方法：取SD大鼠的骨髓细胞,经密度梯度离心分离,联合贴壁筛选法获取的细胞经流式细胞仪鉴定为BMSC,分别用含有胎牛血清（对照组）;胎牛血清＋缺血再灌注肾脏匀浆上清的培养基进行培养实验。培养7d后,RT—PCR检测两组BMP-7、IL-10、HGF的mRNA表达情况并进行比较。结果：培养7d后,体外模拟的急性肾衰竭微环境组BMP-7、IL-10、HGF的mRNA表达高于对照组。结论：在体外模拟的急性肾衰竭微环境中上调BMSC肾脏保护性生长因子的表达,从而对急性肾损伤发挥主要修复作用。     

肝切除术前门静脉栓塞对围手术期影响的荟萃分析

目的：探讨肝切除术（有半肝、扩大半肝切除术）前应用门静脉栓塞（portal vein embolization,PVE）对病人围手术期的影响。方法：通过电子检索Pubmed、Medline数据库,对1986～2008年有关右半肝或扩大半肝切除术前行PVE病例的对照研究资料进行荟萃分析。结果：共纳入8篇文献．423例病人。荟萃分析结果显示．PVE手术组与单纯手术组比较,术前谷草转氨酶（AST）、总胆红素（TB）、凝血酶原时间（PT）、15min吲哚氰绿储留率（ICGR-15）及肿瘤最大直径两组间均无统计学差异（19〉0．05）;术中输血、肿瘤Rn切除及手术时间两组间均无统计学差异（P〉0．05）。PVE手术组术后感染的发生率显著降低（P=0．002）,但二者在术后出血、胆瘘、肾功能衰竭及术后住院时间的差异无统计学意义（P〉0．05）。结论：术前行PVE不能提高肝脏肿瘤的R0切除率,但能降低术后感染的发生率。     

抱膝滚腰锻炼防治腰椎退行性骨关节病的 病例对照研究

目的：探讨抱膝滚腰锻炼对腰椎退行性骨关节病患者腰痛与腰椎功能的影响。方法：自2006年8月至2008年1月,150侧腰椎退行性骨关节病患者随机分为3组：对照组、抱膝滚腰锻炼组与结合组（每组50例）。3组女／男构成比分别为16／34、13／37和15／35;平均年龄分别为（58．8±10．2）岁,（60．1±8．2）岁与（59．9±11．4）岁;平均病程分别为（16．3±14．9）个月,（17．1±15.3）个月与（19．8±17．2）个月。3组分别采用美洛昔康片口服、抱膝滚腰锻炼以及上两种方法结合进行治疗,观察3组患者在治疗3周后的疗效、疼痛视觉模拟评分与腰痛指数的变化。随访6—24个月,观察患者每月腰痛指数的变化。结果：治疗3用后,3组疗效比较：对照组和抱膝滚腰组相比,差异无统计学意义（P〉0．05）;结合组与对照组、抱膝滚腰锻炼组相比,差异有统计学意义（均P〈0．01）。3组治疗后的VAS评分与ODI指数与治疗前相比,差异均有统计学意义（均P〈0．01）;治疗后结合组的VAS疼痛评分与ODI指数与其他两组相比,差异有统计学意义（均P〈0．01）。随访期间,后两组患者平均每月的腰痛指数与对照组相比差异有统计学意义（均P〈0．01）。结论：抱膝滚腰锻炼操作简单、无花费,是腰椎退行性骨关节病疗效比较好的防治方法。     

Increased RANK ligand in bone marrow of orchiectomized rats and prevention of their bone loss by the RANK ligand inhibitor osteoprotegerin

Orchiectomized (ORX) rats were used to examine the extent to which their increased bone resorption and decreased bone density might relate to increases in RANKL, an essential cytokine for bone resorption.Serum testosterone declined by > 95% in ORX rats 1 and 2 weeks after surgery (p < 0.05 versus sham controls), with no observed changes in serum RANKL. In contrast, RANKL in bone marrow plasma and bone marrow cell extracts was significantly increased (by  100%) 1 and 2 weeks after ORX. Regression analyses of ORX and sham controls revealed a significant inverse correlation between testosterone and RANKL levels measured in marrow cell extracts (R = − 0.58), while marrow plasma RANKL correlated positively with marrow plasma TRACP-5b, an osteoclast marker (R = 0.63). The effects of RANKL inhibition were then studied by treating ORX rats for 6 weeks with OPG-Fc (10 mg/kg, twice/week SC) or with PBS, beginning immediately after surgery. Sham controls were treated with PBS. Vehicle-treated ORX rats showed significant deficits in BMD of the femur/tibia and lower trabecular bone volume in the distal femur (p < 0.05 versus sham). OPG-Fc treatment of ORX rats increased femur/tibia BMD and trabecular bone volume to levels that significantly exceeded values for ORX or sham controls. OPG-Fc reduced trabecular osteoclast surfaces in ORX rats by 99%, and OPG-Fc also prevented ORX-related increases in endocortical eroded surface and ORX-related reductions in periosteal bone formation rate. Micro-CT of lumbar vertebrae from OPG-Fc-treated ORX rats demonstrated significantly greater cortical and trabecular bone volume and density versus ORX-vehicle controls. In summary, ORX rats exhibited increased RANKL protein in bone marrow plasma and in bone marrow cells, with no changes in serum RANKL. Data from regression analyses were consistent with a potential role for testosterone in suppressing RANKL production in bone marrow, and also suggested that soluble RANKL in bone marrow might promote bone resorption. RANKL inhibition prevented ORX-related deficits in trabecular BMD, trabecular architecture, and periosteal bone formation while increasing cortical and trabecular bone volume and density. These results support the investigation of RANKL inhibition as a strategy for preventing bone loss associated with androgen ablation or deficiency.     

The effects of homocysteine and MTHFR genotype on hip bone loss and fracture risk in elderly women

Summary  Few studies have evaluated the effects of homocysteine and methylenetetrahydrofolate reductase (MTHFR) genotype on age-related bone loss. In our 5-year cohort study with 1,213 women aged 70–85 years, high homocysteine is associated with greater hip bone loss but not fracture risk. The effect of MTHFR genotype on bone density and fracture is weak. Introduction  Previous studies on the effects of homocysteine and MTHFR genotype on bone mineral density (BMD) and osteoporotic fracture risk have shown inconsistent results. Few studies have evaluated their effects on age-related bone loss. We evaluated the effects of homocysteine and MTHFR genotype variation on hip BMD and fracture risk over 5 years in a cohort of 1,213 community-dwelling women aged 70–85 years. Methods  Nutritional intake and prevalent fracture status were assessed at baseline, plasma homocysteine was measured at year 1, and hip dual-energy X-ray absorptiometry (DXA) BMD was measured at years 1 and 5. Clinical incident osteoporotic fractures confirmed by radiographic report were collected throughout the study and the MTHFR gene C677T and A1298C polymorphisms genotyped. Data were analyzed using analysis of covariance and Cox proportional hazard regression. Results  The highest tertile of homocysteine was associated with a greater hip BMD loss over 4 years (−2.8%) compared to the middle (−1.6%) and lowest tertiles (−1.2%) (P < 0.001). This effect remained after adjustment for covariates. There was no effect of homocysteine on fracture prevalence or incidence. MTHFR gene variation was only weakly related to one of the bone outcome measures. Conclusion  In this study population, high homocysteine is associated with greater hip bone loss but not fracture risk.