非清髓性无关供者脐血移植与同胞供者骨髓移植治疗再生障碍性贫血的比较

目的 对非清髓性无关供者脐血移植与同胞供者骨髓移植治疗重型再生障碍性贫血(SAA)的临床效果进行评价和比较.方法 回顾性分析15例SAA患者进行非清髓性造血干细胞移植的临床资料,根据造血干细胞(HSC)来源的不同,将患者分为骨髓移植组(BMT组;6例)和脐血移植组(UCBT组;9例).对两组患者术后的外周血象、骨髓象、细胞嵌合体状态、移植物抗宿主病(GVHD)以及存活率等长期随访结果进行了统计学分析.结果 BMT组和UCBT组造血干细胞植入率分别为100%和66.7%,两组比较,差异有统计学意义(P＜0.05).UCBT组移植后大多数形成了供、受者型细胞混合嵌合体,BMT组大多数形成了供者型完全嵌合体.BMT组血象恢复正常的中位时间为25 d、UCBT组为120 d,BMT组骨髓象恢复正常的中位时间为25 d,UCBT组为150 d.BMT组慢性GVHD的表现以肝功能异常为主,而UCBT组则以皮疹为主.UCBT组术后早期感染率为33.3%,BMT组为16.7%.结论 非清髓性无关供者脐血移植和同胞供者骨髓移植均可成功治疗SAA;但与BMT比较,UCBT的造血功能恢复较慢、血型转变少而延迟、早期感染率较高、而慢性GVHD的程度却较轻.     

未成熟树突状细胞诱导大鼠免疫低反应性

目的观察供者来源的未成熟树突状细胞(imDCs)联合骨髓移植(BMT)对大鼠移植肾的保护作用,并探讨其机制.方法DA(RT1a)大鼠为供者,Lewis(RT11)大鼠为受者,Wistar大鼠为无关第三品系.将实验动物随机分为5组,每组8只,进行不同的预处理后进行肾移植.(1)阴性对照组受者不接受任何预处理;(2)imDCs诱导组受者术前7d经尾静脉注射经60Co照射(30 Gy)灭活的、供者来源的未成熟树突状细胞2×107/只;(3)BMT诱导组受者术前4 d经尾静脉注射供者来源的新鲜骨髓细胞2×108/只;(4)imDCs+BMT联合诱导组受者术前7 d经尾静脉注射经60Co照射(30 Gy)灭活的、供者来源的未成熟树突状细胞2×107/只,术前4 d经尾静脉注射供者来源的新鲜骨髓细胞2×108/只;(5)第三品系组预处理与imDCs+BMT联合诱导组相同,但供者肾脏来自Wistar大鼠.术后进行单向混合淋巴细胞反应(MLR);白细胞介素2(IL-2)逆转实验;体内细胞转移实验(DTH);流式细胞仪检测RT1a阳性细胞百分率.结果各组大鼠肾移植后平均存活时间分别为阴性对照组(7.12±1.25)d;imDCs诱导组(24.38±3.20)d;BMT诱导组(7.87±2.10)d;第三品系组(6.63±1.06)d;而imDCs+BMT联合诱导组延长到(80.75±16.88)d;后者与上述4组比较,差异均有统计学意义(P＜0.01).免疫耐受的大鼠脾细胞增殖程度(SI值,3.41)明显低于对照组(7.56),P＜0.01;转移耐受的Lewis大鼠(FI值,0.55)明显低于对照大鼠(0.93),P＜0.01;在免疫耐受的受者体内检测到RT1a阳性细胞.结论术前输注供者来源的未成熟树突状细胞联合骨髓移植,可成功诱导受者产生免疫耐受,显著延长肾移植大鼠的存活时间.可能机制为特异性T细胞克隆无能、T细胞的负向免疫调节以及嵌合体的形成.     

联合成骨细胞移植促进骨髓移植小鼠的造血功能重建

目的 探讨联合成骨细胞移植对骨髓移植小鼠造血功能重建的影响.方法 Balb/c小鼠60只,取其中18只制备移植用骨髓有核细胞和成骨细胞.将其余42只小鼠分为3组.单纯移植组:小鼠18只,仅进行骨髓移植(BMT);联合移植组:18只,进行BMT的同时每只小鼠输入成骨细胞2×106个;正常对照组:小鼠6只,不做任何处理,仅作为移植前的正常对照.移植组小鼠在全身照射(TBI)预处理后4 h经尾静脉注入骨髓细胞2×106个.移植后第7、14和21天,分别处死移植组小鼠6只,对小鼠的外周血细胞和骨髓单个核细胞(BMMNC)进行计数,采用流式细胞术测定BMMNC中CD34+细胞的百分比,使用HPIAS-1000高清晰度彩色病理图像系统测量骨髓造血组织面积,采用免疫组化染色法测定骨髓组织微血管密度(MVD).结果 移植后第7天,单纯移植组和联合移植组小鼠外周血细胞计数及BMMNC数均明显低于正常对照(P＜0.01).第21天时联合移植组小鼠白细胞、红细胞及BMMNC数明显恢复,血小板数已接近正常对照组;单纯移植组小鼠外周血细胞数和BMMNC数虽然有所恢复,但其恢复程度明显弱于联合移植组.移植后第7、14和21天,联合移植组外周血细胞计数及BMMNC数均明显高于同期单纯移植组(P＜0.01或P＜0.05).移植后第7、14、21天,单纯移植组和联合移植组小鼠骨髓造血组织面积、BMMNC中CD34+细胞百分比及骨髓组织MVD均明显低于正常对照组(P＜0.01),但联合移植组均高于同期单纯移植组(P＜0.01或P＜0.05).结论 联合成骨细胞移植能有效促进骨髓移植小鼠骨髓造血系统的重建.

Abstract：

Objective To explore the effects of cotransplantation with osteoblasts on hematopoietic reconstitution in mice after bone marrow transplantation (BMT). Methods The typical model of syngeneic BMT was established. 18 Balb/c mice were used to prepare the bone marrow nuclear cells and osteoblasts for BMT. The 42 Balb/c mice were randomly divided into 3 group:normal group (6 mice, without any treatment), the single BMT group ( 18 mice, given 2 × 106 bone marrow nuclear cells/each mouse) and the cotransplantation group of HSC with osteoblaats (18 mice,given 2 × 106 bone marrow nuclear cells and osteoblasts/each mouse). The following factors were measured on day 7, 14, 21 after BMT: peripheral blood cells, bone marrow mononuclear cells (BMMNC), the percentage of CD34+ cells in BMMNC (assayed by flow cytometry), the hematopoietic tissue changes (detected by HPIAS-1000 image analysis system) and micro vascular density (MVD) of bone marrow tissue (with immunohistochemistry). Results The levels of periphral WBC, RBC, PLT, BMMNC in the contransplantation group were higher than those in the single BMT group (P＜0. 01 or P＜0. 05). In the contransplantation group, the percentage of CD34+ cells in BMMNC, the hematopoietic tissue area and the MVD of bone marrow were also higher than the single BMT group on the 7th, 14th, 21st day after BMT(P＜0.01 or P＜0.05). Conclusion Cotransplantation with osteoblasts could significantly promote hematopoietic reconstruction in mice after BMT. Cotransplantation may represent a promising means of achieving higher engraftment rate after BMT.     

肥胖对吸入麻醉药作用的影响

目的 通过对标准体重患者及病理性肥胖患者接受不同时间手术和麻醉后苏醒时间及苏醒期表现的比较,探讨肥胖对吸入麻醉药作用的影响.方法 60例患者根据于术时间均分为短时间手术组(A组)和长时间手术组(B组),以体重指数(BMT)作为肥胖的判断标准,将每组患者分为标准体重患者(BMT≤25,A1组和B1组)和肥胖患者(30≤BMT≤40,A2组和B2组).采用异氟醚、芬太尼、丙泊酚、阿曲席铵行静吸复合全身麻醉,根据术中BIS监测及血流动力学变化调整用药,记录第一次自主呼吸恢复时问、出现不自主体动时间、言语指令睁眼时间、拔管时间以及患者出现躁动、恶心呕吐的情况.结果 B2组的肥胖患者术后自主呼吸恢复时间、出现不自主体动时间、言语指令睁眼时间以及拔管时间均明显长于A1、A2、B1组(P<0.01).结论 短时间手术肥胖对吸入麻醉药作用没有明显影响,对于长时间手术肥胖患者的苏醒时间明显延长.     

骨髓移植并发非感染性肺综合征

骨髓移植(BMT)是将别人或自己的骨髓移植到体内，其本质是移植造血干细胞。由于干细胞有不断自我复制和分化为成熟血细胞(红、白细胞、巨核细胞)及免疫活性细胞的能力，故移植后可重建受者的骨髓造血和修复人体淋巴组织与单核细胞的免疫功能。BMT包括同卵挛生同胞间的移植(同基因，     

《临床外科杂志》对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。     

《临床外科杂志》对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(12)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。     

本刊对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。4.质子数(原子序数)标注在元素符号的左下角。例如:_(82)Pb,_(26)Fe。     

《临床外科杂志》对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。4.质子数(原子序数)标注在元素符号的左下角。例如:_(82)Pb,_(26)Fe。     

《临床外科杂志》对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用箩马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。4.质子数(原子序数)标注在元素符号的左下角。例如:~(82)Pb,_(26)Fe。     

本刊对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。4.质子数(原子序数)标注在元素符号的左下角。例如:_(82)Pb,_(26)Fe。5.离子价和表明阴、阳离子的符号"+"或"-"标注于元素符号的右上角,离子价数写在符号前。例如:正2价的镁离子,应写     

骨髓移植小鼠急性移植物抗宿主病早期弥漫性肺损伤中TH17细胞的作用

目的 探讨骨髓移植小鼠急性移植物抗宿主病(aGVHD)早期肺损伤中TH 17细胞的作用和机理.方法 Balb/c小鼠为受鼠,经致死量全身照射(TBI)后,输注C57BL/6小鼠来源的骨髓细胞和脾细胞,建立aGVHD模型.实验分为3组:TBI组小鼠仅接受TBI,异基因骨髓移植(BMT)组小鼠TBI后输注供者骨髓细胞和脾细胞,常山酮(HF)组小鼠TBI后输注骨髓细胞和脾细胞,并注射HF.动态观察小鼠GVHD的表现,并进行肺组织病理学、T淋巴细胞亚群及相关细胞因子的检测.结果 移植后小鼠出现典型GVHD的表现.移植后6d时HF组肺组织病理学评分为(2.00±0.35)分,BMT组为(0.67±0.07)分.BMT组TH 1细胞占CD4+T淋巴细胞的比例为(5.53±0.11)％,TH 17细胞占(1.04±0.34)％;HF组TH1细胞占(8.61±0.21)％,TH 17细胞占(0.49±0.07)％;组间比较,差异有统计学意义(P＜0.05).两组均未检测到TH2细胞.移植后6d,BMT组白细胞介素(IL)-17A为(2.81±0.19)pg/ml,γ干扰素(IFN-γ)为(42.97±0.23) pg/ml; HF组IL-17A＜0.8 pg/ml,IFN-γ为(9.89±0.51)pg/ml;组间比较,差异有统计学意义(P＜0.05).两组均未检测到IL-10.结论 在异基因造血干细胞移植早期阻断TH17细胞及其细胞因子的分泌,导致炎症因子分泌失衡,加重肺损伤.     

本刊对论文中化学元素与核素符号书写的要求

<正>根据国家标准GB 3100~3102-1993《量和单位》,本刊对论文中化学元素与核素符号的书写规定如下。1.化学元素符号使用罗马(正)体,首字母大写,在符号后不加圆点。2.核素的核子数(质量数)标注在元素符号的左上角。例如:~(14)N,~(60)Co,不写成"~(14)氮或N~(14),~(60)钴或Co~(60)。3.分子中核素的原子数标注在核素符号的右下角。例如:~(14)N_2。4.质子数(原子序数)标注在元素符号的左下角。例如:_(82)Pb,_(26)Fe。5.离子价和表明阴、阳离子的符号"+"或"-"标注于元素符号的右上角,离子价数写在符号前。例如:正2价的镁离子,应写     

肾小管肝型脂肪酸结合蛋白对小鼠IgA肾病的肾脏保护作用

Objective To investigate the renoprotection of tubular L-FABP in murine IgA nephropathy (IgAN） induced by bone marrow transplantation(BMT). Methods IgAN models were reconstituted by BMT from IgAN-prone mice into mice (Tg) transgenically tubular overexpressing human L-FABP (hL-FABP) and wild type (WT) mice. These recipients were sacrificed at 6 and 12 weeks after BMT and their kidneys were collected. The expressions of hL-FABP, fibronectin (FN) and monocyte chemoattractant protein-1(MCP-1) mRNA were detected by real-time PCR. hL-FABP, FN, type Ⅳ collagen (Col Ⅳ), hemeoxygenase-1(HO-1) and 4-hydroxy-2-nonenal (4-HNE) modified proteins were detected by Western blotting. The distribution of hL-FABP and FN protein in kidney was detected by immunohistochemistry. The level of serum IgA, urinary albumin and urinary hL-FABP was detected by ELISA. Results (1) IgAN was reconstituted in both Tg and WT mice by BMT: mesangial IgA deposition and up-regulation of serum IgA. The levels were not significantly different between two groups (Tg-ddY and WT-ddY). (2) hL-FABP was expressed in proximal tubular cells of normal Tg mice. The mRNA (1.62±0.32 vs 0.46±0.09, P<0.01) and protein expression (1.74±0.76 vs 1.14±0.31, P<0.01) of hL-FABP was up-regulated in Tg-ddY kidney and urinary hL-FABP level (?滋g/g creatinine) was significantly increased (59.87±26.75 vs 31.01±14.86, P<0.05) at the 6th week after BMT. (3) WT-ddY mice showed a significantly higher urinary albumin level (mg/L) (828±656 vs 82±22, P<0.01), severer mesangial matrix expansion (P<0.01),more glomerular FN and Col Ⅳ deposition at the 12th week. (4) Up-regulation of renal hL-FABP was associated with significant suppression of renal HO-1 expression (P<0.05), accumulation of 4-HNE modified proteins (P<0.05) and MCP-1 mRNA expression (P<0.01) in Tg-ddY mice. Conclusion Tubular L-FABP may lessen the progression of glomerular damage at early stages of IgAN by reducing oxidative stress and inflammatory mediators.     

Granulocyte-colony stimulating factor enhanced the recruitment of bone marrow cells into the heart

Objective: We traced and evaluated bone marrow-derived cells after granulocyte-colony stimulating factor (G-CSF) treatment in the doxorubicin-induced cardiomyopathic heart in the time course. Methods: C57BL/6 male mice received doxorubicin (15 mg/kg, i.p.). At 1 week after administration of doxorubicin, the mice were irradiated (900 cGy) followed by transplantation of bone marrow cells (BMT) derived from transgenic mice expressing green fluorescent protein (GFP) (1×10⁶) via a tail vein (BMT). G-group (n=22) received G-CSF (50 μg/kg/day×8 days, s.c.) after BMT, while C-group (n=17) received saline. At 4 and 7 weeks after BMT, heart sections were fixed to evaluate bone marrow-derived GFP cells (BMD-GFP) with immunostaining for Troponin I (TnI), atrial-natriuretic peptide (ANP), connexin 43, von Willebrand factor, and Ki67. Result: There were migrated BMD-GFP in the whole heart of all animals. In the time course, migrated BMD-GFP increased in G-group. At 7 weeks the number of migrated BMD-GFP in G-group (56.2±15.6/HPF) was larger than that in C-group (18.9±10.7/HPF) (p<0.05). TnI- and connexin 43-positive BMD-GFP were spindle-shaped. Von Willebrand factor-positive BMD-GFP showed thinner-shape. ANP- and Ki67-positive BMD-GFP showed oval-shape. The numbers of these positive cells derived from BMD-GFP, not different between the 2 groups, did not change from 4 to 7 weeks. Conclusion: The migration of BMD-GFP into the heart increased from 4 to 7 weeks after BMT by G-CSF. However, cardiomyocytes and endothelial cells originating from BMD-GFP were very few and neither increased nor changed in their shapes and numbers in the short term.     

骨髓移植诱导临床心脏移植后供者特异性免疫耐受方案的探讨

目的 探讨骨髓移植诱导临床心脏移植后供者特异性免疫耐受的可行性.方法 采取供心的同时采用改良"灌流法"获取供者的骨髓350 ml,经过滤及离心处理后,加入细胞冷冻保护液共80ml,分装于低温冻存袋,经程序降温,置于-80℃冰箱中保存.在常规原位心脏移植术后40 d,取冻存骨髓快速复温,穿刺受者双侧髂后上嵴,立即行骨髓腔内骨髓细胞输注(IBM-BMT),共输注单核细胞1.2×107/kg,CD34+细胞2.38×105/kg.骨髓输注前3 d行预处理,包括应用氟达拉滨、抗胸腺细胞球蛋白及全身淋巴结照射.骨髓移植后静脉应用他克莫司(Tac),维持血Tac浓度谷值在10～20μg/L;3周后改为口服Tac+吗替麦考酚酯(MMF);6周后改为环孢素A及MMF.分别于心脏移植后2、4、8和12周采集受者外周血,分别于术后4、8和12周采集受者的骨髓,应用短串联重复序列-聚合酶链反应法检测供者嵌合体.心脏移植后每周行心肌内心电图检查,每月行心肌活检1次.术后3个月,取受者及第三者外周血单核细胞,行混合淋巴细胞反应(MLR).结果心脏移植后1、2及3个月时受者的外周血及髂骨内骨髓细胞中供者来源的细胞比例分别为26.3%、19.1%、4.8%和46.3%、24.4%、7.6%.IBM-BMT后心肌内心电图监测显示心肌阻抗及R波波幅无明显变化.术后3个月行心内膜心肌活检,未见排斥反应征象.术后3个月时行超声心动图检查,提示心脏舒张、收缩功能良好.MLR提示受者对供者特异性刺激呈现低反应性,而对第三者仍保持良好的免疫活性(P＜0.01).结论 采取分期骨髓移植免疫耐受诱导方案可安全、有效地建立嵌合体,成功诱导心脏移植后供者特异性免疫耐受,但远期效果有待进一步研究.

Abstract：

Objective To investigate a new strategy of bone marrow transplantation (BMT) for donor-specific tolerance induction after heart transplantation. Methods Donor bone marrow cells (BMCs)were harvested simultaneously with donor cardiac graft using modified perfusion method (PM) ,then stored in a -80 ℃ refrigerator after filtration and centrifugation. Whole BMCs (IBM-BMT) (monocytes 1.2 ×107/kg,CD34+ cells 2.38× 105/kg) in host iliac bones were injected into the bone marrow cavity 40 days after heart transplantation. Preconditoning regimens that consisted of fludarabine, antithymoctye globin and total lymphoid irradiation were performed 3 days before BMT. Tacrolimus (Tac) was administrated intravenously after BMT or orally in conjunction with mycophenolate mofetil (MMF) 3 weeks later.Cyclosporine and MMF were orally administrated 6 weeks later. Donor chimerism was detected using short tandem repeats-polymerase chain reaction in monocytes from peripheral blood at the 2nd,4th, 8th or 12th week after BMT or BMCs at the 4th, 8th or 12th week after BMT. Intramyocardium electrocardiography examination or endomyocardial biopsy was performed weekly or monthly respectively. Mixed lymphocyte reactions (MLR) were performed 3 months after BMT. Results Donor chimerism in monocytes in peripheral blood or BMCs in iliac bones measured at the 1 st,2nd and 3rd month after BMT was 26.3%, 19.1%,4.8% ,and 46.3%, 24.4%, 7.6%, respectively. After 3-month follow-up, there was no rejection confirmed by endomyocardial biopsy or intramyocardium electrocardiography. Echocardiography revealed that the diastolic and systolic function of the cardiac graft was maintained well 3 months after BMT. MLR revealed donor-specific hyporesponsiveness while immunocompetence was preserved to third-party antigens. Conclusion These findings indicate that the two-stage BMT strategy is a safe and feasible method for the induction of donor-specific tolerance via stable mixed chimerism and needs to be further confirmed after a long-term observation.     

尿富含半胱氨酸蛋白61在对比剂肾病中的早期诊断价值

目的探讨尿富含半胱氨酸蛋白61(cysteine-rich protein 61,CYR61)在对比剂肾病(contrast-induced nephropathy,CIN)早期诊断中的价值。方法于2017年1月至2018年8月在徐州医科大学附属淮安医院招募择期拟行经皮冠状动脉介入术的患者。采集患者一般临床资料、血生化、血常规、血凝常规。留取患者术前及术后2 h、4 h、8 h尿标本,采用ELISA法检测尿CYR61水平。统计分析时根据术前估算肾小球滤过率(eGFR)将患者分为eGFR≥60 mL·min~(-1)·(1.73 m~2)~(-1)(n=197)和eGFR60 mL·min~(-1)·(1.73 m~2)~(-1)(n=50)两组,两组中再按患者是否发生CIN分为CIN组与非CIN组,分别进行亚组分析,并绘制受试者工作曲线(ROC)评价尿CYR61在CIN早期诊断中的价值。结果在eGFR≥60 mL·min~(-1)·(1.73 m~2)~(-1)组与eGFR60 mL·min~(-1)·(1.73 m~2)~(-1)组中,发生CIN的患者的尿CYR61水平均在术后4 h达到高峰,此后尿CYR61水平出现下降。将术后4 h尿CYR61用于诊断CIN的发生,分别绘制ROC曲线,结果表明,eGFR≥60 mL·min~(-1)·(1.73 m~2)~(-1)患者采用术后4 h尿CYR61诊断CIN的最佳临界值为293.67 ng/L,灵敏度与特异度分别为90.91%、83.33%,AUC为0.88(95%CI 0.82～0.92);eGFR60 mL·min~(-1)·(1.73 m~2)~(-1)患者采用术后4 h尿CYR61诊断CIN的最佳临界值为266.23 ng/L,灵敏度与特异度分别为100.00%、78.79%,AUC为0.89(95%CI 0.77～0.96)。结论在eGFR≥60 mL·min~(-1)·(1.73 m~2)~(-1)患者和eGFR60 mL·min~(-1)·(1.73 m~2)~(-1)患者中,术后4 h尿CYR61水平可作为CIN的早期诊断指标。     

胸外科手术患者PACU滞留时间延长的多因素分析

目的分析胸外科手术后患者麻醉后监护室(PACU)滞留时间延长(120min)的影响因素。方法回顾性分析495例胸外科手术患者的麻醉复苏记录单,按Logistic回归分析的要求进行量化或赋值,先行单因素回归,筛选有显著差异的各个因素再做多因素非条件回归分析。结果单因素回归分析:年龄60岁(OR=2.411,95%CI 1.592~3.742),ASA分级每增加1级(OR=1.833,95%CI 1.209~2.780),尿量20ml/h(OR=0.173,95%CI 0.065~0.458),术中心血管活性药物使用(OR=1.613,95%CI 1.198~2.173)对患者PACU滞留时间有明显影响。多因素回归分析:年龄60岁(OR=2.322,95%CI 1.448~3.722),术中心血管活性药物使用(OR=1.441,95%CI 1.050~1.976),尿量≤20ml/h(OR=0.139,95%CI 0.049~0.396)为PACU滞留时间延长的独立危险因素。结论胸外科手术患者PACU滞留时间延长的相关因素有年龄60岁、尿量≤20ml/h、术中使用血管活性药物、ASA分级增加。     

125I粒子照射与60Co放射治疗对肺腺癌细胞的生物学效应

目的探讨~(125)I粒子和~(60)Co照射两种不同照射方式对肺腺癌细胞生物学效应的影响。方法对肺腺癌细胞株A549、H1299及人正常肺上皮细胞BEAS-2B分别行~(125)I粒子和~(60)Co照射。~(125)I粒子组和~(60)Co照射组的照射剂量分别为2、4、6、8Gy,将不进行照射的细胞设定为对照组。分别检测细胞存活分数、细胞周期、细胞凋亡率及凋亡相关蛋白的表达水平。结果与对照组相比,~(125)I粒子组和~(60)Co照射组的细胞存活分数明显降低。在照射剂量为4、6、8Gy时,A549细胞表达较明显的G1期阻滞,H1299和BEAS-2B表达较明显的G2/M期阻滞。同时在照射剂量为4、6、8Gy时,两种照射方式均能导致肺腺癌细胞凋亡率明显升高。在照射剂量为4、8Gy时,两种照射方式都能显著上调Bax、Cleaved-caspase-3和Cleaved-PARP蛋白的表达并下调Bcl-2蛋白的表达。与~(60)Co照射组相比,~(125)I粒子组的A549、H1299细胞有更低的细胞存活分数、更明显的细胞周期阻滞效应及更高的细胞凋亡率,且对凋亡相关蛋白的调节效应更明显。对于BEAS-2B细胞株,细胞凋亡率和凋亡相关蛋白的表达基本未发生改变。结论 ~(125)I粒子照射和~(60)Co照射均有抑制肺腺癌细胞增殖、促进凋亡的作用,~(125)I粒子照射作用更明显。A549细胞较H1299细胞对放射治疗敏感性高。Bcl-2/Bax蛋白比的失衡和Caspase-3、PARP蛋白的激活在~(125)I粒子照射抑制肿瘤细胞增殖的效应中可能发挥重要的作用。     

联合内皮祖细胞移植对小鼠骨髓移植预处理中肝脏内皮损伤的修复作用

目的 研究联合内皮祖细胞(EPC)移植对小鼠骨髓移植预处理中肝脏内皮损伤的修复作用.方法 将C57BL/6小鼠分为4组,每组10只.(1)正常对照组:小鼠不做任何处理,仅作为正常对照;(2)单纯照射组:单次给予全身照射(TBI)预处理,不进行骨髓移植;(3)单纯移植组:给予单纯照射组相同的TBI预处理,TBI后4 h内经小鼠尾静脉输注C57BL/6小鼠骨髓单个核细胞5×106/只;(4)联合移植组,小鼠的处理方式与单纯移植组相同,仅在骨髓移植的同时经尾静脉输注C57BL/6小鼠EPC 5×105/只.TBI后第2、4、7、14、21天,检测各组小鼠肝脏重量的变化情况,并于TBI后第4、7、14、21天对各组小鼠肝脏进行组织病理学检查.结果 单纯照射组、单纯移植组和联合移植组小鼠肝脏重量均于TBI后第2天开始明显增加,于第14天达到高峰,峰值分别为正常对照组的(1.65±0.15)倍(P＜0.05)、(1.61±0.06)倍(P＜0.05)和(1.11±0.4(0)倍(P＜0.05);以后均呈下降趋势,第21天时单纯照射组和单纯移植组肝脏重量仍明显高于正常对照组(P＜0.05),但联合移植组小鼠肝脏重量已完全恢复正常.组织病理学检查显示,单纯照射组小鼠肝窦内皮损伤明显,肝细胞水肿及严重的炎症细胞浸润,第7天时肝细胞水肿、坏死较前明显加重,几乎无存活的肝血窦内皮细胞;第14天时单纯移植组小鼠肝窦内皮损伤较前有所减轻,但到第21天时仍未恢复正常;联合移植组小鼠第7天时肝窦内皮及肝细胞水肿、坏死程度均较轻,到第14天时已基本恢复正常.结论 造血干细胞移植前的预处理会造成受者肝脏内皮损伤,且此损伤持续存在;移植时联合输注EPC能修复肝窦内皮的损伤.

Abstract：

Objective To study the repair function of united endothelial progenitor cells (EPC)transplantation on injured liver endothelium by bone marrow transplantation (BMT) conditioning.Methods C57BL/6 mice were divided into four groups randomly: normal control group, without any treatment; irradiation alone group, administered a total body irradiation(TBI) pretreatment, without BMT; (3) BMT alone group: C57BL/6 mice were infused with bone marrow mononuclearcells (MNC) 5 × 106/only through caudal vein not more than 4 h after the same TBI pretreatment as the irradiation alone group; united transplantation group: receiving the same way as the BMT alone group, but C57BL/6 mice were infused with EPC 5 × 105/only at the same time. Two, 4, 7, 14, and 21 days after the TBI, the changes of the liver weight were observed regularly. The histopathological examination of liver was done at the 4th, 7th, 14th, and 21st day after the TBI. Results In irradiation alone group, BMT alone group and united transplantation group the liver weight began to increase significantly on the day 2 and peaked at 14th day after the TBI, and the peaks were respectively (1.65±0. 15) times (P＜0. 05), (1.61 ±0.06) times (P＜0.05), and (1.11 ±0.40)times (P＜0. 05) of those in normal control group. At the day 14, the liver weight in irradiation alone group, BMT alone group and united transplantation group began to decrease, and on the day 21 the liver weight in united transplantation group had been completely restored to normal level, however the liver weight in irradiation alone group and BMT alone group were still significantly heavier than that in normal control group (P＜0. 05). Liver histopathological examination revealed that there were obvious sinusoidal endothelial cells (SEC) injury, hepatocyte edema and severe inflammatory cell infiltration in irradiation alone group, and on the day 7 the hepatocyte edema and necrosis were significantly worse than before, and almost no alive SEC were found. On the day 14 the injury of SEC in BMT alone group was lighter than before, but on the day 21 the injury had not returned to normal. On the day 7 the injury of SEC, hepatocyte edema and necrosis were alleviated in united transplantation group as compared with irradiation alone group and BMT alone group, and on the day 14 the injury had returned to normal basically. Conclusion The transplantation conditioning could damage recipient liver endothelium and the injury would persist, and united EPC infusion could repair the injured SEC following BMT.