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A potential role of TLR2 in xenograft rejection of porcine iliac endothelial cells: An in vitro study.

Porcine vascular endothelial cells are a major participant in xenograft rejection. The Toll-like receptor 2 (TLR2) pathway plays an important role in both innate and adaptive immunity. The specific role of TLR2 in the response to a xenograft has not been reported. Whether the TLR2 pathway in pig vascular endothelial cells is involved in acute rejection needs to be investigated, and the mechanism is explored.

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Efficient Generation of an Fah/Rag2 Dual-Gene Knockout Porcine Cell Line Using CRISPR/Cas9 and Adenovirus.

The shortage of human hepatocytes continues to be a significant limitation for the widespread application of hepatocyte transplantation and bioartificial liver (BAL) support therapy. Recombinant activation gene 2 (Rag2) and fumarylacetoacetate hydrolase (Fah)-deficient mice could be highly repopulated with human hepatocytes. However, Fah/Rag2-deficient mice can only produce up to 1 × 10 human hepatocytes per mouse. We hypothesized that 2-10 × 10 human hepatocytes can be produced per Fah/Rag2-deficient pig, which is an adequate supply for hepatocyte transplantation and BAL therapy. In a novel approach, we used stably transfected Cas9 cells and single-guide RNA adenoviruses containing fluorescent reporters to enrich porcine cells with Fah/Rag2 dual gene mutations. This resulted in the construction of Fah/Rag2 double knockout porcine iliac artery endothelial cells, which were subsequently used for generating Fah/Rag2-deficient pigs.

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Differential replication efficiencies between Japanese encephalitis virus genotype I and III in avian cultured cells and young domestic ducklings.

Japanese encephalitis virus (JEV) genotype dominance has shifted to genotype I (GI) from genotype III (GIII) in China as demonstrated by molecular epidemiological surveillance. In this study, we performed a serological survey in JEV-non-vaccinated pigs to confirm JEV genotype shift at the sero-epidemiological level. The average ratio of GI/GIII infection was 1.87, suggesting co-circulation of GI and GIII infections with GI infection being more prevalent in pigs in China. To gain an insight into the reasons for this JEV genotype shift, the replication kinetics of seven recently-isolated JEV isolates including three GI strains and four GIII strains were compared in mosquito C6/36 cells, chicken fibroblast cells (DF-1) and porcine iliac artery endothelial cells (PIEC). We observed that GI strains replicated more efficiently than GIII strains in DF-1 and PIEC cells, particularly in DF-1 cells with titers reaching 22.9-225.3 fold higher than GIII strains. This shows an enhanced replication efficiency of GI viruses in avian cells. To examine this enhanced replication efficiency in vivo, young domestic ducklings were used as the animal model and inoculated with GI and GIII strains at day 2 post-hatching. We observed that GI-inoculated ducklings developed higher viremia titers and displayed a comparatively longer viremic duration than GIII-inoculated ducklings. These results conform to the hypothesis of an enhanced replication efficiency for GI viruses in birds. There are 36 amino acid differences between GI and GIII viruses, some of which may be responsible for the enhanced replication efficiency of GI viruses in birds. Based on these findings, we speculated that the enhanced replication of GI viruses in birds would have resulted in higher exposure and therefore infection in mosquitoes, which could result in an increased transmission efficiency of GI viruses in the birds-mosquitoes-birds enzootic transmission cycle, thereby contributing to JEV genotype shift.

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Pulsatility Index as a Novel Parameter for Perfusion in Mouse Model of Hindlimb Ischemia.

In clinical settings, the pulsatility index (PI) has become a widely used tool for monitoring obstetrics or other vascular diseases. It is based on the maximum Doppler shift waveform derived from ultrasonography. However, it remains unclear whether the PI levels are correctly predicted from the perfusion in mouse model of hindlimb ischemia.

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[ENDOTHELIAL DYSFUNCTION AND MICROSCIRCULATION FEATURES IN PATIENTS WITH HIGH RISK OF DEVELOPMENT OF REPERFUSION SYNDROME IN CONDITIONS OF RECONSTRUCTION ARTERIAL OPERATIONS].

Aim - to study the state of the microcirculatory bed and the endothelial system in patients at risk of developing reperfusion syndrome and suggest methods for their correction. The work included 29 patients with obliterating diseases of the abdominal aorta and lower limb arteries with a high risk of developing reperfusion complications. Two groups of patients were identified. Group I - 8 patients, preoperative preparation include the generally accepted approaches. Group II - 21 patients whose preoperative preparation included, in addition to preparations for improving rheological blood conditions, prolonged epidural anesthesia, intravenous injection of hydroxyethylstarches, korvetin and alprostadil. In patients of both groups, a study was made of the state of the level of endothelial dysfunction, changes in capillary blood flow and arterio-venular blood shunting. Revascularization of the lower limbs in patients with a high risk of developing reperfusion complications leads to a deepening of endothelial dysfunction. The latter is characterized by a 2.3-fold increase (p<0.001) in the early postoperative period of circulating endothelial cells in the blood, by 2.5 times (p <0.001) endothelin-1, while a 1.3-fold decrease (p<0,05) P-selectin and in 1,7 times (p<0,05) E-selectin. The depth of the lesion of the endothelial system is indicated by a decrease of 29.9 % (p<0.001) in the level of NO. Deepening of endothelial dysfunction after reconstructive-reconstructive surgery is reflected in violations of the function of the microcirculatory bed. It is characterized by a 1.9-fold decrease (p<0.001) of skin perfusion, 2.0 times (p<0.001) in the erythrocyte concentration index and a 14% decrease (p<0.05) in capillary blood flow. This is facilitated by an increase of 14% (p<0.05) in skin perfusion pressure and an increase of 16% (p<0.05) in the resistance index of the microcirculatory bed, which leads to a decrease in tissue oxygenation to a level 3.38±0.14 mm.hg.

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Exenatide modulates tumor-endothelial cell interactions in human ovarian cancer cells.

Diabetes and cancer are prevalent diseases whose incidence is increasing globally. Diabetic women have a moderate risk increase in ovarian cancer, suggested to be due to an interaction between these two disorders. Furthermore, patients manifesting both diseases have associated worse prognosis, reduced survival and shorter relapse-free survival. According to current recommendations, incretin drugs such as Exenatide, a synthetic analog of Exendin-4, and Liraglutide are used as therapy for the type 2 diabetes (T2D). We studied the effects of GLP-1 and Exendin-4 on migration, apoptosis and metalloproteinase production in two human ovarian cancer cells (SKOV-3 and CAOV-3). Exendin-4 inhibited migration and promoted apoptosis through caspase 3/7 activation. Exendin-4 also modulated the expression of key metalloproteinases (MMP-2 and MMP-9) and their inhibitors (TIMP-1 and TIMP-2). Vascular endothelial cells, which contribute to the formation and progression of metastasis, were also analyzed. TNF-α-stimulated endothelial cells from iliac artery after Exendin-4 treatment showed reduced production of adhesion molecules (ICAM-1 and VCAM-1). Additionally, incretin treatment inhibited activation of apoptosis in TNF-α-stimulated endothelial cells. In the same experiment, MMPs (MMP-1 and MMP-9), which are relevant for tumor development, were also reduced. Our study demonstrated that incretin drugs may reduce cancer cell proliferation and dissemination potential, hence limiting the risk of metastasis in epithelial ovarian cancer.

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Characterization of roles of SpaA in Erysipelothrix rhusiopathiae adhesion to porcine endothelial cells.

Erysipelothrix rhusiopathiae is the causative agent of animal erysipelas and human erysipeloid. The major protective antigen SpaA was suggested to play important roles in E. rhusiopathiae adhesion to host cells, but there is no specific study on SpaA pathogenic roles in adhesion. In this study we characterized direct and indirect roles of SpaA in E. rhusiopathiae adhesion to porcine endothelial cells. Recombinant E. rhusiopathiae SpaA (rSpaA) successfully binded to porcine iliac arterial endothelial cells. rSpaA protein pre-incubating endothelial cells or rSpaA antiserum pre-incubating E. rhusiopathiae significantly decreased E. rhusiopathiae adhesion to endothelial cells. rSpaA successfully binded host plasminogen and fibronectin, and rSpaA antiserum significantly decreased plasminogen-recruitment activity but not fibronectin-recruitment activity of E. rhusiopathiae. In conclusion, SpaA acts as adhesin in E. rhusiopathiae adhesion to host cells, and SpaA binding activity to host plasminogen highly likely play roles in this adhesion.

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Reduction of In-Stent Restenosis by Cholesteryl Ester Transfer Protein Inhibition.

Angioplasty and stent implantation, the most common treatment for atherosclerotic lesions, have a significant failure rate because of restenosis. This study asks whether increasing plasma high-density lipoprotein (HDL) levels by inhibiting cholesteryl ester transfer protein activity with the anacetrapib analog, des-fluoro-anacetrapib, prevents stent-induced neointimal hyperplasia.

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Amniotic fluid stem cells ameliorate bladder dysfunction induced by chronic bladder ischemia in rat.

This study investigated the protective effect of human amniotic fluid-derived stem cells (hAFSCs) against bladder overactivity in rat model of atherosclerosis-induced chronic bladder ischemia.

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Augmentation of Muscle Blood Flow by Ultrasound Cavitation Is Mediated by ATP and Purinergic Signaling.

Augmentation of tissue blood flow by therapeutic ultrasound is thought to rely on convective shear. Microbubble contrast agents that undergo ultrasound-mediated cavitation markedly amplify these effects. We hypothesized that purinergic signaling is responsible for shear-dependent increases in muscle perfusion during therapeutic cavitation.

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