Recipient hypertonic saline infusion prevents cardiac allograft dysfunction

Objective

Hypertonic saline (HTS) has potent immune and vascular effects. We assessed recipient pretreatment with HTS on allograft function in a porcine model of heart transplantation and hypothesized that HTS infusion would limit endothelial and left ventricular (LV) dysfunction following transplantation.

The relationships among monocyte subsets,miRNAs and inflammatory cytokines in patients with acute myocardial infarction

Background

Acute myocardial infarction (AMI) causes irreversible myocardial damage and release of inflammatory mediators, including cytokines, chemokines and miRNAs. We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI.

Extracellular vesicles transmitted miR-31-5p promotes sorafenib resistance by targeting MLH1 in renal cell carcinoma

Sorafenib provides survival benefits in patients with advanced renal cell carcinoma (RCC), but its use is hampered by acquired drug resistance. It is important to fully clarify the molecular mechanisms of sorafenib resistance, which can help to avoid, delay or reverse drug resistance. Extracellular vesicles (EVs) can mediate intercellular communication by delivering effector molecules between cells. Here, we studied whether EVs are involved in sorafenib resistance of RCC and its possible molecular mechanisms. Using differential centrifugation, EVs were isolated from established sorafenib-resistant RCC cells (786-0 and ACHN), and EVs derived from sorafenib-resistant cells were uptaken by sensitive parental RCC cells and thus promoted drug resistance. Elevated exogenous miR-31-5p within EVs effectively downregulated MutL homolog 1 (MLH1) expression and thus promoted sorafenib resistance in vitro. Mice experiments also confirmed that miR-31-5p could mediate drug sensitivity in vivo. In addition, low expression of MLH1 was observed in sorafenib-resistant RCC cells and upregulation of MLH1 expression restored the sensitivity of resistant cell lines to sorafenib. Finally, miR-31-5p level in circulating EVs of RCC patients with progressive disease (PD) during sorafenib therapy was higher when compared to that in the pretherapy status. In conclusion, EVs shuttled miR-31-5p can transfer resistance information from sorafenib-resistant cells to sensitive cells by directly targeting MLH1, and thus magnify the drug resistance information to the whole tumor. Furthermore, miR-31-5p and MLH1 could be promising predictive biomarkers and therapeutic targets to prevent sorafenib resistance.     

Ex vivo identification of atherosclerotic plaque calcification by a 31P solid-state magnetic resonance imaging technique.

Calcified tissue is a common component of atherosclerotic plaques, and occurs most often in mature plaques. The process of calcification is a poorly understood risk factor that may contribute to a plaque's vulnerability to sudden rupture. In this study a solid-state imaging sequence, termed single-point imaging (SPI), was used to observe calcification directly in ex vivo atherosclerotic plaques. Standards were used to validate the ability of (31)P SPI to detect and differentiate calcification from crystalline cholesterol, phospholipids, and other plaque components. After suitable experimental parameters were found, human carotid specimens obtained by endarterectomy were imaged ex vivo by (31)P solid-state imaging and standard (1)H methods. In contrast to (1)H imaging methods, (31)P imaging detected only the calcification in the plaque.     

不同输血方式对肺鳞癌患者围术期TNF—α和IL—lO的影响

[目的]探讨同种输血和自体输血对肺鳞癌患者围术期肿瘤坏死因子-α(TNF-α)和白细胞介素—10(IL—10)的影响和相互关系。[方法]2001年1月至2003年1月对31例肺鳞癌患者行肺癌根治术，将其分为两组，同种输血组(A组)17例，自体输血组14例(B组)。测定两组围术期血清中TNF-α和IL—10的浓度。[结果]A组输血后d1与输血前相比血清中TNF-α、IL-10浓度增高，以IL—10变化尤为明显，输血后d5TNF-α降低并接近输血前的水平，明显低于B组，IL—10仍明显高于输血前的水平。B组中不同时问IL—10无显著变化，TNF-α于ds明显高于输血前。[结论]肺鳞癌患者围术期同种输血后血清中TNF-α降低与IL—10升高有关，IL—10升高可能是同种输血后免疫抑制的重要原因。自体输血可减轻或去除这一作用。     

慢性乙型肝炎中可溶性白细胞介素2受体与其它血清学指标的关系

目的 :探讨血清可溶性白细胞介素 2受体 (sIL 2R)在慢性乙型病毒性肝炎 (慢乙肝 )中的发病机制及sIL 2R与肝纤维化指标、肝功能的相关关系。方法 :对 312例肝活检病人按组织病理学炎症和纤维化程度进行分级分期 ,同时检测了病人血清sIL 2R、肝功能及肝纤维化相关指标。结果 :血清sIL 2R均值较对照组明显增高 (P <0 .0 1) ,增幅随着肝脏病理炎症和纤维化程度的加重而逐渐加大 ,各组间比较差异有显著性 (P <0 .0 5或P <0 .0 1)。sIL 2R与血清白蛋白 (A)呈显著负相关 ,与血清脯氨酸肽酶 (PLD)、Ⅳ型胶原 (CⅣ )、层粘连蛋白 (LN)、透明质酸 (HA)、Ⅲ型前胶原氨基端肽 (PⅢNP)、肝功指标中的TB、DB、G、ALT、AST、AKP、γ GT呈显著正相关 (P <0 .0 5或P <0 .0 1)。结论 :慢乙肝病人血清sIL 2R水平与A呈显著负相关 ,与PLD、CⅣ、LN、HA、PⅢNP呈显著正相关 ;sIL 2R的血清水平能反映肝脏组织学病变的程度 ,可作为判断肝组织炎症和纤维化程度的参考指标。     

Immunoregulatory Factor Released From a Cell Line Derived From Human Decidual Tissue

ABSTRACT: The culture supernatant of the TTK-1 cell line, established from human decidual tissue, was found to contain a factor that strongly suppressed the mixed lymphocyte reaction (MLR). The mechanism of the MLR-suppressive activity as well as the biochemical characterization of this factor was analyzed. The TTK-1 supernatant suppressed the MLR much more strongly than the culture supernatants of the three other malignant cell lines examined. The molecular weight of this factor was estimated to be between 43 kilodaltons (kd) and 67 kd by gel filtration chromatography. The TTK-1 supernatant also suppressed the proliferation of the interleukin 2 (IL-2)-dependent T cell lines, but did not suppress that of the IL-2-independent T cell lines, suggesting that the TTK-1 supernatant inhibited the action of IL-2 and subsequently suppressed the MLR. The fact that the TTK-1 cell line originated from human decidual tissue might imply the important role of this factor in immunological fetomaternal balance.     

~(99)Tc-MDP对类风湿性关节炎患者外周血单核细胞产生细胞因子的影响

目的 :探讨“云克”(99Tc MDP)治疗类风湿性关节炎 (RA)的免疫机制。方法 :采用ELISA双抗体夹心法 ,观察“云克”体外对RA患者外周血单核细胞 (PBMC)产生白介素 1(IL 1)和可溶性白介素 2受体 (sIL 2R)的影响。结果 :“云克”有抑制RA患者IL 1的分泌及细菌脂多糖 (LPS)的促分泌作用 ,并对可溶性白介素 2受体的自发分泌及植物血素 (PHA)诱导分泌均有抑制作用。结论 :“云克”对RA的治疗机制可能与其降低IL 1和sIL 2R的作用有关