有氧运动协同骨髓干细胞动员对心肌梗死后心电图和血流动力学指标的影响

背景：心电图和血流动力学是评价心功能康复的有效指标,目前已经证实有氧运动或骨髓干细胞动员单一因素干预均可对心肌梗死动物心电图和血流动力学产生良好影响,而二者联合干预对心电图和血流动力学指标的影响尚未见文献报道。 目的：探讨有氧运动联合骨髓干细胞动员对缺血心脏心电图和血流动力学部分指标的影响。 方法：结扎大鼠左冠状动脉前降支制作急性心肌梗死模型,心肌梗死运动组和心肌梗死运动动员剂组大鼠于造模后1周在电动跑台进行有氧运动训练,每周训练5 d,持续8周。心肌梗死动员剂组和心肌梗死运动动员剂组大鼠在造模后3 h皮下注射生理盐水稀释的重组人粒细胞集落刺激因子10 μg/(kg•d),连续使用5 d。8周后检测心电图和血流动力学部分指标评价心功能。 结果与结论：心肌梗死大鼠左心室收缩压、左室内压最大上升速率和左室内压最大下降速率值均明显降低,左室舒张末压升高,提示心梗后心脏已发生心功能不全;心肌梗死运动组和心肌梗死动员剂组大鼠左心室收缩压、左室内压最大上升速率和左室内压最大下降速率值均有一定程度的升高,左室舒张末压有所下降,提示有氧运动和骨髓干细胞动员均能改善心梗大鼠心肌收缩和舒张功能;心肌梗死运动动员剂组大鼠心功能的各项评价指标更接近于正常对照组大鼠,说明有氧运动协同骨髓干细胞动员显著增强了大鼠心肌收缩性能,使心肌收缩/舒张功能都得到显著改善。     

姜黄素对骨髓间充质干细胞诱导肾移植免疫耐受的影响

背景：已有研究显示在大鼠肾移植时连续给予1×10⁷细胞浓度的骨髓间充质干细胞可诱导免疫耐受,但临床上尚未发现姜黄素对肾移植具有免疫调节作用。目的：在对肾移植后的大鼠给予骨髓间充质干细胞的基础上,同时给予不同剂量姜黄素,观察其免疫耐受的效果。方法：建立大鼠肾移植模型,随机分为4组：纯肾移植组,无治疗措施;骨髓间充质干细胞组：关腹前左骼静脉注射1×10⁷/kg骨髓间充质干细胞,第2天起尾静脉注射等量细胞,共10 d;骨髓间充质干细胞+低/高剂量姜黄素组：除给予骨髓间充质干细胞外,分别以2,10 mg/kg姜黄素溶液灌胃,共10 d。免疫组织化学染色法检测各组肾组织中转化生长因子β1的蛋白表达水平,酶联免疫吸附法检测血清中白细胞介素2,6水平。结果与结论：大鼠经肾移植后,纯肾移植组中肾小管上皮细胞以及间质细胞的转化生长因子β1蛋白表达、白细胞介素2,6水平均高于其他各组(P < 0.05)。与骨髓间充质干细胞组比较,骨髓间充质干细胞+低/高剂量姜黄素组的转化生长因子β1的蛋白表达降低(P < 0.05),血清白细胞介素2,6水平均低于骨髓间充质干细胞组(P < 0.05)。结果证实,大鼠肾移植时同时给予姜黄素与骨髓间充质干细胞注射,可有效地进行免疫调节,抑制性免疫排斥反应的发生,保护肾功能。 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

新生大鼠脊髓运动神经元的纯化培养与鉴定

背景：神经元是有丝分裂后的细胞,体外培养很难存活。脊髓运动神经元的分离、纯化和培养同时也是细胞培养的技术难点。 目的：建立新生大鼠脊髓运动神经元培养体系,并予以分类鉴定和测定其纯度。 方法：取新生大鼠脊髓腹侧组织分离成细胞悬液,经密度梯度离心及差速贴壁后纯化培养,采用免疫细胞化学双标染色法对培养盖片上的细胞予以鉴定、分类,结合Hoechst荧光染核,计数各细胞成分的含量。 结果与结论：细胞贴壁生长良好,神经元占85.8%,其中运动神经元达71.6%,星形胶质细胞占7.8%,NF200和胶质纤维酸性蛋白染色皆为阴性的细胞占6.4%。结果说明,取新生大鼠腹侧脊髓组织结合密度梯度离心及差速贴壁接种法可以培养出高纯度的脊髓运动神经元。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

缺血后处理局灶性脑缺血再灌注模型大鼠相关通路以及白细胞介素8的表达

背景：缺血后处理能够激发内源性保护作用,抑制缺血再灌注后的炎症反应,但具体机制目前尚不明确。目的：观察缺血后处理对局灶性脑缺血再灌注大鼠Toll样受体4-核因子κB信号转导通路以及白细胞介素8表达的影响,进一步阐述缺血后处理的神经保护机制。方法：将110只大鼠随机分为假手术组10只、模型组和缺血后处理组各50只,将大鼠按照Zea-Longa法建立局灶性脑缺血再灌注模型,再进行缺血后处理,即大脑中动脉闭塞2 h后进行3个循环的再灌注15 s/缺血15 s,设模型组和假手术组作对照。对各组进行神经行为学评分,TTC染色测定脑梗死体积,免疫组织化学法检测脑组织Toll样受体4、核因子кB和白细胞介素8蛋白表达,原位杂交法检测其mRNA表达。结果与结论：模型组、缺血后处理组大鼠都出现神经行为学缺失及缺血侧大脑半球梗死。再灌注6,12,24,48,72 h,与模型组相比,缺血后处理组大鼠神经行为学评分显著改善(P < 0.05)、脑梗死体积明显减少(P < 0.05)。模型组和缺血后处理组Toll样受体4、核因子кB、白细胞介素8蛋白和mRNA表达于再灌注6 h时已升高,24 h达峰值。再灌注6,12,24,48,72 h,与模型组各对应时间点亚组比较,缺血后处理组上述各因子表达均显著降低(P < 0.05)。结果证实,缺血后处理可抑制缺血再灌注引起的炎症反应,通过抑制Toll样受体4-核因子κB信号转导通路和下调白细胞介素8的表达,以此发挥神经保护作用。  中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

Shikonin protects chondrocytes from interleukin-1beta-induced apoptosis by regulating PI3K/Akt signaling pathway

Chondrocyte apoptosis is mostly responsible for the development and progression of osteoarthritis. IL-1β is generally served as an agent that induces chondrocyte apoptosis. Shikonin exerts its anti-inflammatory effect on cartilage protection in vivo. We aimed to explore the protective effect of shikonin on interleukin-1beta (IL-1β)-induced chondrocyte apoptosis and the potential molecular mechanisms. Chondrocytes were isolated from the joints of newborn Sprague-Dawley rats. The MTT assay and LDH cell death assay were used to determine the cell viability and chondrocyte apoptosis was detected by Annexin-V/PI staining and nucleosomal degradation. The contents of phosphorylated-PI3K (p-PI3k), phosphorylated-Akt (p-Akt), Bcl-2, Bax, and cytochrome c were detected by Western blotting. A quantitative colorimetric assay was used to detect the caspase-3 activity. Our results showed that pretreatment with shikonin (4 μM) inhibited cytotoxicity and apoptosis induced by IL-1β (10 ng/ml) in chondrocytes. Shikonin pretreatment also decreased the activity of IL-1β that decreased Bcl-2 expression and levels of p-PI3K and p-Akt, and increased Bax expression, cytochrome c release, and caspase-3 activation. It also reversed the activity of IL-1β that promoted the synthesis of matrix metalloproteinase-13 and inhibited the expression of tissue inhibitor of metalloproteinase-1 expression, with the net effect of suppressing extracellular matrix degradation. These data suggested that shikonin may protect chondrocytes from apoptosis induced by IL-1β through the PI3K/Akt signaling pathway, by deactivating caspase-3.     

Dysplastic changes in erythroid precursors as a manifestation of lead poisoning: report of a case and review of literature

Dysplastic changes in erythroid precursors occur not only in patients with hematologic diseases, but also those with other diseases. Here, we report on a patient that presented with dysplastic changes in erythroid precursors due to lead poisoning from the intake of Chinese folk remedies.     

PD-L1 blockade improves immune dysfunction of spleen dendritic cells and T-cells in zymosan-induced multiple organs dysfunction syndromes

This research is to investigate the role of tolerant spleen dendritic cells (DC) in multiple organs dysfunction syndromes (MODS) at late stage. Tolerant DC and MODS were induced by intraperotineal injection of zymosan. The immunity of DC was determined by examining interleukin (IL)-10, IL-12, IL-2, major histocompatibility complex (MHC), CD86, programmed death (PD-1), programmed death ligand 1 (PD-L1), paired immunoglobulin-like receptor B (PIR-B) or T-cell proliferation in serum, spleen homogenate, DC culture or DC/T-cell co-culture. The PD-L1/PD-1 pathway was blocked using PD-L1 antibody. The IL-12p70 in serum, spleen homogenate and DC culture supernatant were decreased at 5 d and 12 d after zymosan injection while the IL-12p40 and IL-10 were increased. The expression of MHC, cluster of differentiation 86 (CD86), PD-1 and PD-L1 in spleen DCs were increased at early stage after zymosan injection. At 5 d and 12 d, the expression of MHC and CD86 was reduced while the expression of PD-1, PD-L1 and PIR-B was increased, accompanied with decreased proliferation of T-cell and decrease of IL-2 in spleen and serum. Application of PD-L1 antibody improved the above changes. At late stage of MODS mice induced by zymosan, the expression of co-stimulators and inhibitors in spleen DCs was imbalanced to form tolerant DCs which reduced the activation of T-cells. PD-L1 antibody improved the immune tolerance of DCs through intervening PD-1/PD-L1 pathway, and attenuated the inhibition of T-cell activities by tolerant DCs and the immune inhibition.     

Increased expression of 78 kD glucose-regulated protein promotes cardiomyocyte apoptosis in a rat model of liver cirrhosis

Aims: This study was to investigate the role and underlying mechanism of 78 kD glucose-regulated protein (GRP78) in cardiomyocyte apoptosis in a rat model of liver cirrhosis. Methods: A rat model of liver cirrhosis was established with multiple pathogenic factors. A total of 42 male SD rats were randomly divided into the liver cirrhosis group and control group. Cardiac structure analysis was performed to assess alterations in cardiac structure. Cardiomyocytes apoptosis was detected by TdT-mediated dUTP nick end labeling method. Expression of GRP78, CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, nuclear factor kappa-light-chain-enhancer of activated B cells p65 subunit (NF-κB p65) and B cell lymphoma-2 (Bcl-2) was detected by immunohistochemical staining. Results: The ratios of left ventricular wall thickness to heart weight and heart weight to body weight were significantly increased with the progression of liver cirrhosis (P < 0.05). Apoptosis index of cardiomyocytes was significantly increased with the progression of liver cirrhosis (P < 0.05). The expression levels of GRP78, CHOP and caspase-12 were significantly increased in the progression of liver cirrhosis (P < 0.05). The expression levels of NF-κB p65 and Bcl-2 were highest in the 4-wk liver cirrhosis, and they were decreased in the 6-wk and 8-wk in the progression of liver cirrhosis. GRP78 expression levels were positively correlated with apoptosis index, CHOP and caspase-12 expression levels (P < 0.05). CHOP expression levels were negatively correlated with NF-κB p65 and Bcl-2 expression levels (P < 0.05). Conclusion: Increased expression of GRP78 promotes cardiomyocyte apoptosis in rats with cirrhotic cardiomyopathy.     

种植体结构改变对种植体-骨界面皮质骨区应力影响的三维有限元分析

背景：种植体-骨界面的生物力学效应是骨吸收重要的影响因素之一。模仿天然牙周膜的新结构种植体或可改善其界面应力的分布情况。 目的：探讨不同的咬合负载条件下,改变传统种植体内部结构对种植体-骨界面皮质骨区应力分布、峰值的影响,为新结构种植体的优化设计及临床应用提供理论依据。 方法：用Pro/ENGINEER软件建立新结构的种植体(模型A)与无螺纹的传统柱状种植体(模型B)的数字模型,采用Ansys软件分析在相同骨质及相同受力环境下种植体-骨界面皮质骨区应力峰值、应力带分布的变化规律。 结果与结论：垂直加载时,模型A在不同受力大小时应力峰值均较模型B降低17.54%;45°加载时,模型A应力峰值较模型B降低(2.59%),模型B的高应力区向颊侧集中趋势明显。咀嚼模拟加载时,模型A的应力峰值均较模型B低,其差值在施力方向与种植体轴向夹角(β)等于12°时最大(0.353 2 MPa),在β > 12°后逐渐减小;并且模型A在促进骨组织生长最适应力峰值、维持骨组织健康应力峰值两个量化指标中,均比模型B适用角度范围大(A：0°-28°,0°-58°;B：0°-24°,0°-56°)。提示优化设计种植体结构的改变可改善种植体-骨界面皮质骨区的应力分布,降低应力峰值,可在更大范围内降低骨皮质吸收的风险。 中国组织工程研究杂志出版内容重点：生物材料;骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性;组织工程     

SOD2基因多态性与突发性耳聋的遗传易感性研究

目的：探讨人线粒体超氧化物歧化酶2(mitochondrial superoxide dismutase 2, SOD2)基因多态性与云南地区突发性耳聋(idiopathic sensorineural hearing loss, SSNHL)患者遗传易感性的关系。方法采用病例-对照研究,选取78例(男35,女43)突发性耳聋患者和与之性别、年龄相匹配的85例(男39,女46)对照群体,对 SOD2基因的3个标签 SNP 位点(rs5746136、 rs2842960、 rs4880)进行基因分型,统计并分析了基因频率和基因型频率分布与突发性耳聋的遗传易感性的关系。结果在 rs5746136位点(OR ＝2.136,95％ CI ＝1.147~3.978, P ＝0.016)上的 A/ G 基因型可能是中国突发性耳聋患者的危险基因型,而 rs2842960和 rs4880则和中国突发性耳聋患者无相关性;结论 SOD2基因多态位点 rs5746136 A/ G 基因型可能增加突发性耳聋患者的风险,可以作为预测 SSNHL 患者发病危险及早期防治的的遗传标记。