Knowledge of the Brain Death Concept in Dominican Immigration Residents in Spain and Florida

The Latin American population has a double way of immigration, one toward the United States by proximity and another toward Spain by sociocultural affinity. This population increase is affecting organ donation and transplantation in receiving countries.

Uptake of iodine-123-α-methyl tyrosine by gliomas and non-neoplastic brain lesions

Using single-photon emission tomography (SPET), the radiopharmaceuticall,-3-iodine-123--methyl tyrosine (IMT) has been applied to the imaging of amino acid transport into brain tumours. It was the aim of this study to investigate whether IMT SPET is capable of differentiating between high-grade gliomas, low-grade gliomas and non-neoplastic brain lesions. To this end, IMT uptake was determined in 53 patients using the triple-headed SPET camera MULTISPECT 3. Twenty-eight of these subjects suffered from high-grade gliomas (WHO grade III or IV), 12 from low-grade gliomas (WHO grade II), and 13 from non-neoplastic brain lesions, including lesions after effective therapy of a glioma (five cases), infarctions (four cases), inflammatory lesions (three cases) and traumatic haematoma (one case). IMT uptake was significantly higher in high-grade gliomas than in low-grade gliomas and non-neoplastic lesions. IMT uptake by low-grade gliomas was not significantly different from that by non-neoplastic lesions. Diagnostic sensitivity and specificity were 71% and 83% for differentiating high-grade from low-grade gliomas, 82% and 100% for distinguishing high-grade gliomas from non-neoplastic lesions, and 50% and 100% for discriminating low-grade gliomas from non-neoplastic lesions. Analogously to positron emission tomography with radioactively labelled amino acids and fluorine-18 deoxyglucose, IMT SPET may aid in differentiating high-grade gliomas from histologically benign brain tumours and non-neoplastic brain lesions; it is of only limited value in differentiating between non-neoplastic lesions and histologically benign brain tumours.     

EGCG调控miR-133a/b-3p和TGF-β1/Smad3抗慢性阻塞性肺疾病的作用研究

目的:探讨表没食子儿茶素没食子酸酯(EGCG)对慢性阻塞性肺疾病(COPD)大鼠的保护作用和机制。方法:通过烟熏和脂多糖滴注建立大鼠COPD模型。每日灌胃给予100或200 mg/kg EGCG,4 w后观察肺部形态学改变。检测肺促炎细胞因子、MDA、GSH、SOD水平。免疫组化法评价纤维连接蛋白(fibronectin)和波形蛋白(vimentin)表达情况,Western blot检测TGF-β_1、p-Smad3表达水平,q PCR检测fibronectin、vimentin、TGF-β_1mRNA和微小RNA(miR)-133a/b-3p水平。结果:与正常对照组比较,模型组肺泡壁破损明显,肺组织促炎细胞因子、MDA及Smad3磷酸化水平显著升高,GSH、SOD、miR-133a/b-3p水平显著降低,fibronectin、vimentin、TGF-β_1蛋白表达显著升高。与模型组比较,EGCG能改善COPD大鼠的肺损伤,显著降低促炎细胞因子、MDA和Smad3的磷酸化水平,升高GSH、SOD、miR-133a/b-3p水平,并减少fibronectin、vimentin、TGF-β_1蛋白表达。结论:EGCG能改善COPD大鼠的肺损伤,其作用机制与调控肺TGF-β_1/Smad3和miR-133a/b-3p水平,抑制氧化应激和炎症有关。     

TM208-羟丙基-β-环糊精包合物的制备及其在大鼠体内的药动学研究

目的:4-甲基哌嗪-1-二硫代甲酸-(3-氰基-3,3-二苯基)丙酯盐酸盐(TM208)是我院合成的新抗肿瘤化合物,极难溶于水。本实验的研究目的是研制TM208-羟丙基-β-环糊精(HP-β-CD)包合物,并研究其在大鼠体内的药动学。方法:以共沉淀法制备TM208-HP-β-CD包合物,比较原药与包合物的紫外吸收光谱,X-射线衍射图谱,差示扫描量热图谱的变化;两组SD大鼠分别单剂量口服TM208混悬剂和TM208-HP-β-CD包合物,用HPLC法测定血药浓度;应用3P87药动学程序计算药动学参数。结果:TM208与TM208 HP-β-CD包合物紫外光谱一致; TM208经包合后晶体衍射峰消失;差示扫描量热法测定结果显示形成包合物后一种新物相峰出现;TM208在形成包合物后溶解度增大了700倍;大鼠单剂量给予TM208混悬剂和TM208-HP-β-CD包合物后,TM208的主要药动学参数C_(max)分别为(1．31±0．22)和(2．84±1．23)μg·mL~(-1),T_(max)分别为(10．2±4．18)和(3．31±0．541)h。AUC_(0～4(?)h)分别为(42．5±11．5)和(67．7±20．I)μg·mL~(-1)·h。统计分析结果显示,包合后TM208达峰时间显著缩短,峰浓度显著提高,相对生物利用度为159．3％。结论:TM208制备成HP-β-CD包合物后,在水中溶解度极显著增加,体内吸收速度与程度显著提高。     

Paeonol protects rat vascular endothelial cells from ox-LDL-induced injury in vitro via downregulating microRNA-21 expression and TNF-α release

Aim： Paeonol （2＇-hydroxy-4＇-methoxyacetophenone） from Cortex moutan root is a potential therapeutic agent for atherosclerosis. This study sought to investigate the mechanisms underlying anti-inflammatory effects of paeonol in rat vascular endothelial cells （VECs） in vitro.
Methods： VECs were isolated from rat thoracic aortas. The cells were pretreated with paeonol for 24 h, and then stimulated with ox-LDL for another 24 h. The expression of microRNA-21 （miR-21） and PTEN in VECs was analyzed using qRT-PCR. The expression of PTEN protein was detected by Western blotting. TNF-α release by VECs was measured by ELISA.

Results： Ox-LDL treatment inhibited VEC growth in dose- and time-dependent manners （the value of IC50 was about 20 mg/L at 24 h）. Furthermore, ox-LDL （20 mg/L） significantly increased miR-21 expression and inhibited the expression of PTEN, one of downstream target genes of miR-21 in VECs. In addition, ox-LDL （20 mg/L） significantly increased the release of TNF-α from VECs. Pretreatment with paeonol increased the survival rate of ox-LDL-treated VECs in dose- and time-dependent manners. Moreover, paeonol （120 μmol/L） prevented ox-LDL-induced increases in miR-21 expression and TNF-α release, and ox-LDL-induced inhibition in PTEN expression. A dual-luciferase reporter assay showed that miR-21 bound directly to PTEN＇s 3＇-UTR, thus inhibiting PTEN expression. In ox-LDL treated VECs, transfection with a miR-21 mimic significantly increased miR-21 expression and inhibited PTEN expression, and attenuated the protective effects of paeonol pretreatment, whereas transfection with an miR-21 inhibitor significantly decreased miR-21 expression and increased PTEN expression, thus enhanced the protective effects of paeonol pretreatment.

Conclusion： miR-21 is an important target of paeonol for its protective effects against ox-LDL-induced VEC injury, which may play critical roles in development of atherosclerosis.     

miR-155联合超声对分化型甲状腺癌淋巴结转移的诊断价值分析

目的探讨微小RNA-155(miR-155)联合超声对分化型甲状腺癌淋巴结转移的诊断价值。方法选取接受治疗的分化型甲状腺癌患者112例作为甲状腺癌组,另选取同期收治的结节性甲状腺肿患者30例作为良性对照组。采用实时荧光定量PCR(qPCR)检测2组患者血清及组织中miR-155的相对表达量,分析分化型甲状腺癌患者血清及组织中miR-155的表达与临床病理参数的关系。采用受试者工作特征(ROC)曲线分析术前超声以及血清miR-155对分化型甲状腺癌淋巴结转移的诊断价值。结果甲状腺癌组的血清及组织中miR-155的相对表达量均明显高于良性对照组(P<0.01),有淋巴结转移、肿瘤直径>2 cm、TNM分期Ⅲ+Ⅳ期的患者血清及组织中miR-155的相对表达量分别高于无淋巴结转移、肿瘤直径≤2 cm、TNM分期Ⅰ+Ⅱ期的患者(均P<0.05)。ROC结果显示,超声以及血清miR-155对分化型甲状腺癌淋巴结转移均有一定的诊断价值,曲线下面积分别为:0.839(95%CI:0.760～0.919)、0.837(95%CI:0.763～0.912),但漏诊率和误诊率均超过10%。...     

Adenovirus-IL-10 relieves chronic rejection after mouse heart transplantation by inhibiting miR-155 and activating SOCS5

Objective: Chronic rejection remains the main factor that influence long-term survival of patients after heart transplantation. Interleukin-10 (IL-10) play critical role in macrophages-mediated transplant immune responses. We investigated the mechanism of IL-10 in macrophage related chronic rejection after mouse heart transplantation.Methods: Mouse heart transplant chronic rejection model was established to evaluate pathological changes in the allograft. Myocardial interstitial fibrosis, apoptosis, and inflammatory factor levels were detected in ad-IL-10-treated mice. The positive iNOS⁺ and Arg-1⁺ expressions, macrophage subset changes, and the proportion of regulatory T-cells (Tregs) and TIGIT⁺ Tregs were quantified by flow. In in vitro experiments, ad-IL-10 was transfected into macrophages followed by detection of apoptosis, phagocytosis, and CD163, CD16/32, and CD206 expression. The expression and relationships between IL-10, miR-155, and SOCS5 were also detected and verified. A rescue experiment was performed to evaluate macrophage function through the combined treatment of ad-IL-10 and overexpression of miR-155.Results: Significantly decreased IL-10 expression in chronic rejection during mouse heart transplantation was observed. Ad-IL-10-treated mice showed decreased pathological injury, perivascular fibrosis, apoptosis, inflammation, and iNOS⁺ and CD16/32⁺ expression, and increased Treg/TIGIT⁺ Treg cell, Arg-1⁺ and CD206⁺ cell proportion. Ad-IL-10-treated macrophages in vitro showed reduced apoptosis, improved phagocytosis, and M2 polarization. Mechanically, IL-10 negatively regulated miR-155 to activate SOCS5. Overexpression of miR-155 reversed IL-10 mediated-positive regulation of macrophage function.Conclusion: IL-10 downregulated miR-155 and activated SOCS5, thereby promoting macrophage M2 polarization to relieve chronic rejection after heart transplantation.     

微小RNA-29a通过沉默信息调节因子2相关酶类1基因调控肝细胞脂肪变性的机制

目的 探讨人肝细胞株L02脂肪变性时微小RNA-29a(miR-29a)的表达变化及其靶向沉默信息调节因子2相关酶类1(silent mating type information regulation 2 homolog-1,Sirt1)调节脂肪肝细胞脂肪沉积的机制.方法 采用油酸和棕榈酸混合物诱导建立非酒精性脂肪肝...     

miR-145通过调控MMP-2、MMP-9的表达对卵巢癌细胞调亡、增殖、迁移的影响

目的 研究微小RNA-145(miR-145)通过调控基质金属蛋白酶(MMP)-2、MMP-9的表达对卵巢癌细胞调亡、增殖、迁移的影响.方法 将卵巢癌细胞株随机分为3组,其中对照组为单纯卵巢癌细胞株,不做其他处理,进行正常培养;miR-145组为含miR-145质粒的慢病毒转染的卵巢癌细胞株;NC组为含NC质粒的慢病毒...