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Journal articles on the topic 'CEPCs'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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1

Tinelli, Francesca, Sara Nava, Francesco Arioli, et al. "Vascular Remodeling in Moyamoya Angiopathy: From Peripheral Blood Mononuclear Cells to Endothelial Cells." International Journal of Molecular Sciences 21, no. 16 (2020): 5763. http://dx.doi.org/10.3390/ijms21165763.

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The pathophysiological mechanisms of Moyamoya angiopathy (MA), which is a rare cerebrovascular condition characterized by recurrent ischemic/hemorrhagic strokes, are still largely unknown. An imbalance of vasculogenic/angiogenic mechanisms has been proposed as one possible disease aspect. Circulating endothelial progenitor cells (cEPCs) have been hypothesized to contribute to vascular remodeling of MA, but it remains unclear whether they might be considered a disease effect or have a role in disease pathogenesis. The aim of the present study was to provide a morphological, phenotypical, and functional characterization of the cEPCs from MA patients to uncover their role in the disease pathophysiology. cEPCs were identified from whole blood as CD45dimCD34+CD133+ mononuclear cells. Morphological, biochemical, and functional assays were performed to characterize cEPCs. A significant reduced level of cEPCs was found in blood samples collected from a homogeneous group of adult (mean age 46.86 ± 11.7; 86.36% females), Caucasian, non-operated MA patients with respect to healthy donors (HD; p = 0.032). Since no difference in cEPC characteristics and functionality was observed between MA patients and HD, a defective recruitment mechanism could be involved in the disease pathophysiology. Collectively, our results suggest that cEPC level more than endothelial progenitor cell (EPC) functionality seems to be a potential marker of MA. The validation of our results on a larger population and the correlation with clinical data as well as the use of more complex cellular model could help our understanding of EPC role in MA pathophysiology.
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2

Inčiūraitė, R., S. Juzėnas, R. Ramonaitė, and J. Skiecevičienė. "P036 MicroRNA composition of colon crypt-top and crypt-bottom epithelial cells in Ulcerative Colitis." Journal of Crohn's and Colitis 15, Supplement_1 (2021): S149. http://dx.doi.org/10.1093/ecco-jcc/jjab076.165.

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Abstract Background Ulcerative colitis (UC) is a chronic relapsing large intestine condition of inflammatory origin1. One of the most common features of UC is the injury of the intestinal barrier, which is composed primarily of colonic epithelial cells (CEpCs)2. The aim of this study was to identify UC-induced miRNA markers in CEpCs by determining the miRNA expression profile changes in crypt-top and crypt-bottom CEpC populations during active (aUC) and inactive (iUC) UC. Methods Crypt-top and crypt-bottom CEpCs were sorted from biopsies of healthy control (HC) individuals (n=19), patients with aUC (n=17) and iUC (n=15) using FACS technology. Total RNA was extracted, small RNA sequencing libraries were prepared and sequenced using Illumina platform. Sequencing data was processed with nextflow-core/smrnaseq pipeline. Differential expression, correlation, miRNA-target interactions, gene set enrichment analyses and data visualisation were performed using Rstudio software packages DESeq2, isomiRs, multimiR, SingleCellExperiment, clusterProfiler, ReactomePA, etc. The miRNAs with an adjusted p-value < 0.05, and absolute value of log2 fold change > 1 were considered to be significantly differentially expressed. Results 432 unique miRNAs were identified in samples. Changes of expression profile during aUC were identified in crypt-bottom CEpCs (compared to: (i) HC - 23 miRNAs, (ii) iUC - 22 miRNAs), as well as in crypt-top CEpCs (compared to: (i) HC - 28 miRNAs, (ii) iUC - 9 miRNAs). Also, 7 miRNAs were differentially expressed in crypt-bottom CEpCs and 3 miRNAs in crypt-top CEpCs during iUC compared to HC. 5 miRNAs were identified to be differentially expressed during aUC, 2 miRNAs - during iUC, and 11 miRNAs in HC when comparing expression profiles of crypt-bottom and crypt-bottom CEpCs. We also identified 16 and 14 miRNAs which expression in crypt-bottom and crypt-top CEpCs moderately (0.5<rho<0.7) correlated with Mayo score, respectively. Finally, the gene sets of pathways revealed the involvement of several miRNAs in biological processes and molecular functions associated with UC pathogenesis. Conclusion The changes of expression profiles of miRNAs revealed that crypt-top and crypt-bottom CEpCs respond to inflammation differently, the expression of these miRNAs reflects disease activity and modulates the processes of UC pathogenesis. References
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3

Gryszczyńska, Bogna, Magdalena Budzyń, Beata Begier-Krasińska, et al. "Association between Advanced Glycation End Products, Soluble RAGE Receptor, and Endothelium Dysfunction, Evaluated by Circulating Endothelial Cells and Endothelial Progenitor Cells in Patients with Mild and Resistant Hypertension." International Journal of Molecular Sciences 20, no. 16 (2019): 3942. http://dx.doi.org/10.3390/ijms20163942.

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The aim of the present study was to evaluate advanced glycation end products (AGEs) and soluble form of receptor RAGE (sRAGE) concentrations as well as the AGEs/sRAGE ratio in mild (MH) and resistant (RH) hypertensive patients in comparison with normotensive individuals. We also evaluated the association between AGEs, sRAGE as well as AGEs/sRAGE ratio and circulating endothelial cells (CECs) and circulating endothelial progenitor cells (CEPCs). The MH group consisted of 30 patients, whereas 30 patients were classified for the RH group. The control group (C) included 25 normotensive volunteers. AGEs and sRAGE were measured using enzyme-linked-immunosorbent assay (ELISA). The multicolor flow cytometry was used for analysis of CECs and CEPCs. Significantly higher levels of AGEs in RH cohort were observed as compared to C cohort. Furthermore, significantly lower sRAGE levels as well as a higher AGEs/sRAGE ratio were observed between MH and RH cohorts. Significant correlations were found in the MH cohort for sRAGE and CECs, and CEPCs. The elevation of AGEs levels suggests that oxidative modification of proteins occurs in hypertension pathogenesis. The decrease in sRAGE levels and elevation of the AGEs/sRAGE ratio in MH and RH groups may suggest that hypertensive patients are less protected against the side effects of AGEs as a consequence of an insufficient competitive role of sRAGE against the AGEs-RAGE axis. Finally, it may be concluded that the level of AGEs may be an independent predictor of the condition and function of the endothelium. Furthermore, sRAGE may be classified as a potential biomarker of inflammation and endothelium dysfunction.
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Religa, Piotr, Renhai Cao, Meit Bjorndahl, Zhongjun Zhou, Zhenping Zhu, and Yihai Cao. "Presence of bone marrow–derived circulating progenitor endothelial cells in the newly formed lymphatic vessels." Blood 106, no. 13 (2005): 4184–90. http://dx.doi.org/10.1182/blood-2005-01-0226.

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Bone marrow (BM)-derived circulating endothelial precursor cells (CEPCs) have been reported to incorporate into newly formed blood vessels under physiologic and pathologic conditions. However, it is unknown if CEPCs contribute to lymphangiogenesis. Here we show that in a corneal lymphangiogenesis model of irradiated mice reconstituted with enhanced green fluorescent protein (EGFP)-positive donor bone marrow cells, CEPCs are present in the newly formed lymphatic vessels. Depletion of bone marrow cells by irradiation remarkably suppressed lymphangiogenesis in corneas implanted with fibroblast growth factor-2 (FGF-2). Further, transplantation of isolated EGFP-positive/vascular endothelial growth factor receptor-3-positive (EGFP+/VEGFR-3+) or EGFP+/VEGFR-2+ cell populations resulted in incorporation of EGFP+ cells into the newly formed lymphatic vessels. EGFP+/CEPCs were also present in peritumoral lymphatic vessels of a fibrosarcoma. These data suggest that BM-derived CEPCs may play a role in “lymphvasculogenesis.”
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5

Rafat, Neysan, Grietje Ch Beck, Jutta Schulte, Jochen Tuettenberg, and Peter Vajkoczy. "Circulating endothelial progenitor cells in malignant gliomas." Journal of Neurosurgery 112, no. 1 (2010): 43–49. http://dx.doi.org/10.3171/2009.5.jns081074.

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Object Recent experimental work suggests that circulating endothelial progenitor cells (cEPCs) are recruited to the angiogenic vascular system of malignant gliomas. Consequently, the level of cEPCs has been proposed as a novel biomarker for the diagnosis and monitoring of these lesions. The aim of the present study was to examine the level of cEPCs and the level of EPC mobilizing mediators in the blood of patients with malignant gliomas. The authors were also interested in whether a correlation could be observed between the level of cEPCs and the extent of glioma angiogenesis determined by conventional methods. Methods Peripheral blood mononuclear cells from the whole blood of 12 patients with malignant gliomas (all glioblastomas multiforme [GBMs]), 10 with metastases to the brain, and 10 healthy volunteers were isolated using Ficoll density gradient centrifugation. The number of cEPCs was quantified by fluorescence-activated cell sorting analysis using antibodies against CD34, CD133, and VEGFR-2. Serum concentrations of VEGF and granulocyte-macrophage colony-stimulating factor (GM-CSF) were determined using the enzyme-linked immunosorbent assay. Histological analysis of tumor blood vessel density was performed by CD34 immunohistochemical staining. Results The number of cEPCs was significantly higher in patients with GBMs than in those with metastases (p < 0.04) or in the healthy volunteers (p < 0.004). The serum VEGF concentrations in patients with GBMs and metastases were significantly higher than in the healthy volunteers (p < 0.0001). Similar findings were observed for concentrations of GM-CSF. In addition, the patients in the GBM group with higher levels of cEPCs had significantly higher tumor blood vessel densities (1.71 ± 1.17% of total area) compared with patients who had low levels of cEPCs (0.62 ± 0.28% of total area; p < 0.02). Conclusions Endothelial progenitor cells are increasingly mobilized in patients with malignant gliomas, and their levels correlate with tumor angiogenic activity. Therefore, the authors' results suggest that cEPCs may have the potential to serve as a novel biomarker for the identification of patients who would benefit from antiangiogenic therapy for GBM.
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Asadian, Simin, Vahid Siavashi, Masoumeh Jabarpour, et al. "Circulating endothelial progenitor cells in pregnant women with premature rupture of membranes: potential association with placental disorders." Reproduction, Fertility and Development 30, no. 12 (2018): 1689. http://dx.doi.org/10.1071/rd17523.

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The frequency of preterm labour has risen over the last few years. Plasma oestrogen concentrations differ between patients who deliver before term and those who deliver at term. Oestrogen can influence the kinetics of circulating endothelial progenitor cells (cEPCs). Here, we attempted to identify the potential association of cEPCs with the incidence of complications typical of prematurity. The study groups consisted of 60 pregnant women with premature rupture of membranes (PROM; less than 37 weeks) and 50 term pregnant women (more than 38 weeks). cEPCs were isolated from term pregnant women and pregnant women with PROM and then migratory, proliferative, tubulogenic and functional properties of these cells along with serum secretion of important EPC chemotactic cytokines were analysed. In addition, the effect of 17β-oestradiol on biological features of cEPCs harvested from pregnant women was investigated. Our results showed that an increased concentration of oestrogen in women with PROM was associated with increased numbers of cEPCs, with these cells having increased oestrogen receptor α expression together with augmented proliferative, migratory and colony-formation properties. 17β-oestradiol induced proliferation, migration and angiogenic secretory activity of cEPCs from pregnant women. Overall, circulation mobilisation of EPCs in pregnant women may be associated with placental disorders.
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7

Chen, Ji, Shuzhen Chen, Yusen Chen, et al. "Circulating endothelial progenitor cells and cellular membrane microparticles in db/db diabetic mouse: possible implications in cerebral ischemic damage." American Journal of Physiology-Endocrinology and Metabolism 301, no. 1 (2011): E62—E71. http://dx.doi.org/10.1152/ajpendo.00026.2011.

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For determining the implications of circulating endothelial progenitor cells (cEPCs) and cellular membrane microparticles (MPs) in diabetic stroke, levels of EPCs, EPC-MPs, and endothelium-derived MPs (EMPs) and their correlations with blood glucose concentration, cerebral microvascular density (cMVD), and ischemic damage were investigated in type 2 diabetic db/db and db/+ (wild-type control) mice. Therapeutic efficacy of EPC infusion (preincubated with MPs) was also explored. Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) surgery. Ischemic damage and cMVD were determined using histological analyses. The levels of cEPCs and MPs were determined using flow cytometric analyses. EPC generation and functions were evaluated by in vitro cell cultures. Results showed the following. 1) In db/db mice, the basal level of cEPCs was less and cMVDs were lower, but the levels of circulating EPC-MPs and EMPs were more; 2) MCAO induced a larger infarct volume and less of an increase in cEPCs in db/db mice; 3) the level of cEPCs correlated with blood glucose concentration (negatively), cMVD (positively), and ischemic damage (negatively), but the levels of EPC-MPs and EMPs correlated inversely with those parameters; 4) EPCs were reduced and dysfunctional in db/db mice, and preincubation with db/db MPs impaired EPC functions; and 5) infusion of EPCs preincubated with db/+ MPs increased the level of cEPCs and reduced ischemic damage, and these beneficial effects were reduced or lost in EPCs preincubated with db/db MPs. These data suggest that reduced cEPCs, impaired EPC generation/function, and increased production of MPs might be the mechanisms responsible for increased ischemic damage seen in db/db mice.
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8

Sun, J., W. Zheng, Y. Zhang, and Z. Gu. "AB0639 EXOSOMES DERIVED FROM ENDOTHELIAL CELLS PREVENT OSTEOBLAST APOPTOSIS IN STEROID-INDUCED OSTEONECROSIS OF THE FEMORAL HEAD RAT MODEL VIA THE PI3K/AKT/Bcl-2 SIGNAL PATHWAY." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1353.2–1353. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3088.

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Background:Osteonecrosis of the femoral head (ONFH) is a common disease caused by many trauma factors and un-trauma factors. Among those un-trauma factors, steroid-induced osteonecrosis of the femoral head (SNFH) accounted for a large proportion and mainly concentrated in young people. SNFH has been reported as an irreversible disease and associated with the damage of blood vessels and the loss balance of bone homeostasis. Circulating endothelial progenitor cells (CEPCs), one part of circulating endothelial cells (CECs), are immature precursor cells with proliferative potential. The damage of vascular endothelial cells in SNFH has been confirmed by many studies, but the changes of CECs and CEPCs in the peripheral blood of patients with SNFH have not been studied yet.Objectives:The objective of the study is to explore the number of CECs and CEPCs in SNFH patients and normal people and then investigate whether EC-secreted exosomes (EC-exos) could prevent the progression of SNFH in rat model and its mechanism of action.Methods:We collect peripheral blood of 3 SNFH patients and 3 heathy people and detected the levels of CECs and CEPCs by Flow cytometer. TEM, NTA and western blot was used to characterize the isolated EC-exos. Annexin V-FITC/PI double staining with flow cytometric analysis and western blot were used to evaluate MC3T3-E1 cells apoptosis. CCK-8, scratching experiment and transwell were used to evaluate MC3T3-E1 cells viability and migration ability. Micro-CT and morphological staining were used to evaluate the progress of SNFH in rat model.Results:Firstly, we found that the number of CECs and CEPCs in the peripheral blood was decreased in SNFH patients than normal people. Then our results indicated that EC-exos could improve the migration, viability and prevent apoptosis of osteoblasts under dexamethasone by activating the PI3K/AKT/Bcl-2 signal pathway in vitro. Finally, our Micro-CT and morphological staining results in SNFH rat model revealed that EC-exos prevented the progression of SNFH.Conclusion:EC-exos could enhance the cell viability and migration ability of osteoblasts under dexamethasone and play an anti-apoptosis role against steroids-induced osteoblast apoptosis by activating the PI3K/AKT/Bcl-2 signal pathway. EC-exos prevented the progression of SNFH in rat model.References:[1]Zalavras CG, Lieberman JR. Osteonecrosis of the femoral head: evaluation and treatment. J Am Acad Orthop Surg. 2014;22(7):455-64.[2]Microsurgery Department of the Orthopedics Branch of the Chinese Medical Doctor A, Group from the O, Bone Defect Branch of the Chinese Association of R, Reconstructive S, Microsurgery, Reconstructive Surgery Group of the Orthopedics Branch of the Chinese Medical A. Chinese Guideline for the Diagnosis and Treatment of Osteonecrosis of the Femoral Head in Adults. Orthop Surg. 2017;9(1):3-12.[3]Mont MA, Jones LC, Hungerford DS. Nontraumatic osteonecrosis of the femoral head: ten years later. J Bone Joint Surg Am. 2006;88(5):1117-32.[4]Yuan HF, Zhang J, Guo CA, Yan ZQ. Clinical outcomes of osteonecrosis of the femoral head after autologous bone marrow stem cell implantation: a meta-analysis of seven case-control studies. Clinics (Sao Paulo). 2016;71(2):110-3.[5]Houdek MT, Wyles CC, Packard BD, Terzic A, Behfar A, Sierra RJ. Decreased Osteogenic Activity of Mesenchymal Stem Cells in Patients With Corticosteroid-Induced Osteonecrosis of the Femoral Head. J Arthroplasty. 2016;31(4):893-8.Disclosure of Interests:None declared.
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Ray, Sabina L., David J. Coulson, Megan Li Yuen Yeoh, et al. "The Role of miR-342 in Vascular Health. Study in Subclinical Cardiovascular Disease in Mononuclear Cells, Plasma, Inflammatory Cytokines and PANX2." International Journal of Molecular Sciences 21, no. 19 (2020): 7217. http://dx.doi.org/10.3390/ijms21197217.

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Cardiovascular disease (CVD) correlates with inflammation and a reduction in circulating endothelial progenitor cells (cEPCs). Recently, CVD was shown to be the main cause of mortality in individuals with type 1 diabetes (T1DM). In animals, miR-342 was shown to exert an anti-inflammatory effect in CVD. Hypothesis: miR-342-3p/-5p are downregulated in subclinical CVD (T1DM), whereas inflammatory cytokines are upregulated. We studied miR -342 -3p/5p in plasma/peripheral blood mononuclear cells (PBMCs) in 29 T1DM and 20 controls (HC). Vascular health was measured by fibronectin adhesion assay (FAA), cEPCs (CD45dimCD34+133+ cells) and by assessing inflammation and tissue inhibition of metalloproteases (TIMP-1). In T1DM IL-7, IL-8, TNFα and VEGF-C were increased in plasma. MiR-342-3p/-5p were downregulated in PBMCs in T1DM, but not in plasma. PANX2, chemokine receptors CXCR1/2 mRNAs, were increased in PBMCs in T1DM. MiR-342-3p was negatively correlated with TIMP-1, IL-6, IL-8, TNF-α, HbA1c and CXCR2, whilst miR-342-5p was negatively correlated with TIMP-1, IL-6, IL-8 and HbA1c. There was a positive correlation among miR-342-3p, FAA and cEPCs, and between miR-342-5p and cEPCs. ROC curve analyses showed significant downregulation of miR-342-3p/-5p at HbA1c > 46.45 mmol/mol, indicating their potential as biomarkers for subclinical CVD. Our findings validated animal studies and confirmed the proangiogenic properties of miR-342-3p/-5p. MiR-342-3p/-5p-based intervention or monitoring may prove to be beneficial in managing CVD.
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Pan, Qunwen, Jieyi Zheng, Donghui Du, et al. "MicroRNA-126 Priming Enhances Functions of Endothelial Progenitor Cells under Physiological and Hypoxic Conditions and Their Therapeutic Efficacy in Cerebral Ischemic Damage." Stem Cells International 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/2912347.

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Endothelial progenitor cells (EPCs) have shown the potential for treating ischemic stroke (IS), while microRNA-126 (miR-126) is reported to have beneficial effects on endothelial function and angiogenesis. In this study, we investigated the effects of miR-126 overexpression on EPCs and explore the efficacy of miR-126-primed EPCs (EPCmiR-126) in treating IS. The effects of miR-126 overexpression on EPC proliferation, migratory, tube formation capacity, reactive oxygen species (ROS) production, and nitric oxide (NO) generation were determined. In in vivo study, the effects of EPCmiR-126 on the cerebral blood flow (CBF), neurological deficit score (NDS), infarct volume, cerebral microvascular density (cMVD), and angiogenesis were determined. Moreover, the levels of circulating EPCs (cEPCs) and their contained miR-126 were measured. We found (1) miR-126 overexpression promoted the proliferation, migration, and tube formation abilities of EPCs; decreased ROS; and increased NO production of EPCs via activation of PI3K/Akt/eNOS pathway; (2) EPCmiR-126 was more effective than EPCs in attenuating infarct volume and NDS and enhancing cMVD, CBF, and angiogenesis; and (3) infusion of EPCmiR-126 increased the number and the level of miR-126 in cEPCs. Our data indicate that miR-126 overexpression enhanced the function of EPCs in vitro and in vivo.
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Ahmed, Fahad, Sherin Bakhashab, Inda Bastaman, Rachel Crossland, Michael Glanville, and Jolanta Weaver. "Anti-Angiogenic miR-222, miR-195, and miR-21a Plasma Levels in T1DM Are Improved by Metformin Therapy, Thus Elucidating Its Cardioprotective Effect: The MERIT Study." International Journal of Molecular Sciences 19, no. 10 (2018): 3242. http://dx.doi.org/10.3390/ijms19103242.

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Type 1 diabetes (T1DM) is associated with increased cardiovascular disease (CVD) and reduced life expectancy. We thus hypothesized that anti-angiogenic miRs are increased in T1DM, and the cardioprotective effect of metformin is mediated via reducing those miRs. In an open label, case-controlled study, 23 T1DM patients without CVD were treated with metformin for eight weeks (TG), matched with nine T1DM patients on standard treatment (SG) and 23 controls (CG). Plasma miR-222, miR-195, miR-21a and miR-126 were assayed by real-time RT-qPCR. The results were correlated with: endothelial function (RHI), circulating endothelial progenitor cells (cEPCs) (vascular repair marker, CD45dimCD34+VEGFR2+ cells) and circulating endothelial cells (cECs) (vascular injury marker, CD45dimCD34+CD133-CD144+ cells). miR-222, miR-195 and miR-21a were higher in T1DM than CG; p = 0.009, p < 0.0001, p = 0.0001, respectively. There was an inverse correlation between logmiR-222 and logRHI (p < 0.05) and a direct correlation between logmiR-222 and logCD34+ (p < 0.05) in TG. Metformin reduced miR-222, miR-195 and miR-21a levels in TG; p = 0.007, p = 0.002 p = 0.0012, respectively. miRs remained unchanged in SG. miR-126 was similar in all groups. There was a positive association between changes in logmiR-222 and logcECs after metformin in TG (p < 0.05). Anti-angiogenic miRs are increased in T1DM. Metformin has cardioprotective effects through downregulating miR-222, miR-195 and miR-21a, beyond improving glycemic control.
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12

Wojas, S., S. Clemens, J. Hennig, et al. "Overexpression of phytochelatin synthase in tobacco: distinctive effects of AtPCS1 and CePCS genes on plant response to cadmium." Journal of Experimental Botany 59, no. 8 (2008): 2205–19. http://dx.doi.org/10.1093/jxb/ern092.

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13

Wojas, Sylwia, Stephan Clemens, Aleksandra SkŁodowska, and Danuta Maria Antosiewicz. "Arsenic response of AtPCS1- and CePCS-expressing plants – Effects of external As(V) concentration on As-accumulation pattern and NPT metabolism." Journal of Plant Physiology 167, no. 3 (2010): 169–75. http://dx.doi.org/10.1016/j.jplph.2009.07.017.

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14

Ambroziak, Łukasz. "The CEECs in global value chains: The role of Germany." Acta Oeconomica 68, no. 1 (2018): 1–29. http://dx.doi.org/10.1556/032.2018.68.1.1.

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This paper aims to present the role of Germany in the global value chains (GVCs) of 10 Central and Eastern European countries (CEECs) in 1995–2011. GVCs, being a result of the fragmentation of production processes, have changed the nature of economic globalisation. The study covers five Central European countries (CECs) (the Czech Republic, Hungary, Poland, Slovakia and Slovenia), the three Baltic States (Estonia, Lithuania and Latvia) as well as Bulgaria and Romania. Germany is chosen because it is the main trading partner of the majority of the CEECs. The illustration of the position of Germany in GVCs of the CEECs is based on trade statistics in value added terms. The research results show that Germany has become an engine of increasing integration of the CECs in the GVCs. The role of Germany as a supplier of inputs to the CECs’ exports (backward linkages) is larger than its role as an exporter of value added originating from the CECs (forward linkages).
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Cortelezzi, Agostino, Nicola Stefano Fracchiolla, Michela Cortiana, et al. "Pathogenetic Role of Mature and Progenitor Endothelial Cells in Pre-Eclampsia." Blood 108, no. 11 (2006): 3946. http://dx.doi.org/10.1182/blood.v108.11.3946.3946.

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Abstract Pre-eclampsia (PE) is a pregnancy-associated disorder of unknown cause. The pathological changes associated with PE (edema, proteinuria, coagulopathy, and renal and hepatic abnormalities) suggest a systemic maternal vascular dysfunction. PE is also associated with placental development defects and fetal growth restriction. The generation of vessels is divided into angiogenesis (the sprouting of capillaries from pre-existing vessels) and vasculogenesis, the development of blood vessels from in situ differentiating endothelial cells (ECs), which has been considered as occurring only in the prenatal period. However, circulating endothelial precursors (CEPs) are also present in the peripheral blood (PB) of adults and, in the case of pregnant women, may play important roles in vascularising the uterine endometrium at the time of embryo implantation and placentation. Furthermore, it has been found that the number of mature circulating endothelial cells (CECs) is increased in the PB of patients affected by cancer, sickle cell anemia, myocardial infarction or infections, but they have not been extensively studied in PE patients. Inorder to test the hypothesis that CEPs may be involved in the pathogenesis of PE and that CECs may represent a marker of the severity of ongoing vascular damage, we used flow cytometry to quantify the number of CEPs and CECs in 17 PE patients and 13 healthy pregnant women of similar gestational age. Immunocytofluorimetric assays showed that resting CECs were negative for CD45 but positive for P1H12 and CD31, whereas CEPs were positive for CD133 and CD34. Our 13 healthy controls had a mean number of 20.8 CECs/ml (range 9.22–77.11) and 1.05 CEPs/ml (range 0.07–3.43); the corresponding numbers in 27 samples from the 17 PE cases were 25.46/ml (range 1.65–126.34) and 0.42/ml (range 0–15.45). The PE cases had significantly fewer CEPs than the controls (p <0.05, Mann-Whitney test). Among the PE cases, we compared the samples collected during severe (16 samples) and mild PE (11 samples): the severe PE group showed significantly more CECs than the mild PE group (29.03/ml [range 1.65–120.78] vs 13.58/ml [range 7.67–126.34; p <0.02, Mann-Whitney test) but not CEPs (0.51/ml [range 0–15.45] vs 0.23/ml [range 0–1.41]). In conclusion, there is a reduction in CEPs during PE that may be consistent with an impaired response to vascular damage. As CEPs seem to play a crucial role in the vasculogenesis of the placental bed during pregnancy, this finding is consistent with the fetal growth restriction and placental maturation defects observed during pregnancy. Furthermore, the women with severe PE had more CECs (a marker of ongoing endothelial damage) than those with mild PE. Our findings are consistent with the hypothesis that PE is characterised by a systemic maternal vascular dysfunction, with reduced repair potential (fewer CEPs), and the increased number of CECs in the peripheral blood of women with severe PE correlates with disease severity. Further longitudinal studies are needed to verify their prognostic role.
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Hoeg, Rasmus T., Dean A. Jobe, Krista E. Asp, et al. "Circulating Endothelial Cells and Circulating Endothelial Progenitor Cells in Polycythemia Vera." Blood 108, no. 11 (2006): 4900. http://dx.doi.org/10.1182/blood.v108.11.4900.4900.

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Abstract Background: Angiogenesis and thrombosis, two conditions associated with perturbation of the vascular endothelium and increased CECs, are frequently observed in PV. We performed this study to quantify and characterize CECs in patients with PV and to determine whether CEC profile is associated with thrombotic complications. We also quantified CEPs in a subgroup of patients. Methods: We used flow cytometry to prospectively analyze CECs and CEPs in the whole blood of healthy patients (n=20) and patients with PV (n=30; 13 treated with hydroxyurea, 12 undergoing phlebotomy alone, and 5 never treated). CECs (CD45−/CD31+/CD146+) were quantified and characterized to determine their apoptotic (annexin stain) or activation (CD106+) states. Cells with CD45−/CD31+/CD133+/VEGF-R2+ immunophenotype were considered CEPs. Results: CEC levels in PV patients were higher compared to healthy controls (median 53 cells/mL [range, 11–392] vs 18.5 cells/mL [range, 4–66]; P< .0001). However, the proportions of apoptotic (17.3% [range, 0–87.5] vs 25.9% [range, 0–57.1]; P= .87) and activated (0.7% [range, 0–28.6] vs 0% [range, 0–57.1]; P= .14) CECs were similar between the two groups. In PV patients with high levels (≥2 SD above control mean or ≥53 cells/mL) of CECs (n=14), 5 (36%) developed thromboses. Four (25%) of 16 PV patients with CEC levels similar to healthy controls developed thromboses. The rates of thrombosis between the groups were not statistically different (P= .69). In addition, CEC count, activation, and apoptosis were similar between the hydroxyurea-treated group and the group not treated with hydroxyurea. We detected low numbers of CEPs in PV patients (n=25) that were similar to controls (4 cells/mL [range, 0–100] vs 8 cells/mL [range, 0–60]; P= .34). Conclusions: CECs, but not CEPs, are significantly increased in PV patients. However, there appears to be no association between CEC number, activation or apoptotic state and the development of thromboses. In addition, hydroxyurea therapy does not appear to effect endothelial cells.
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Biguzzi, Eugenia, Patrizia Mancuso, Franca Franchi, et al. "Circulating endothelial cells (CECs) and progenitors (CEPs) in severe haemophiliacs with different clinical phenotype." British Journal of Haematology 144, no. 5 (2009): 803–5. http://dx.doi.org/10.1111/j.1365-2141.2008.07519.x.

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18

Locatelli, M. A., G. Curigliano, L. Fumagalli, et al. "Bevacizumab and oral chemotherapy for patients with lymphangitic breast cancer: A phase II randomized study of bevacizumab with sequential versus concurrent oral vinorelbine plus capecitabine." Journal of Clinical Oncology 27, no. 15_suppl (2009): 1031. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.1031.

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1031 Background: Antiangiogenic agents are most likely to be effective in patients (pts) with an extensive cutaneous neo-angiogenic trait of disease. There is a compelling need to monitor the biological activity of such agents and identify markers of efficacy. Methods: We evaluated the activity and biological effects of bevacizumab (B) (15 mg/kg, iv q 3 weeks) in a phase II randomized trial in pts with locally advanced breast cancer (BC) with lymphangitic spread to the chest wall. Primary aim was to assess activity and toxicity of B administered alone followed by sequential oral vinorelbine (V) plus capecitabine (C) (arm A) or with concurrent V plus C (arm B). Secondary aim was to evaluate predictive role of circulating progenitor cells (CECs) and progenitor endothelial cells (CEPs) as surrogate markers of antiangiogenic activity. We collected blood samples of all pts at baseline, at day 12, 42, and at progression. Results: Planned accrual was of 43 pts of whom 23 were enrolled (9 pts in arm A; 14 pts in arm B). Median age was 51 years (range 35–68). Most of the pts had a “triple negative” phenotype [19/23 (82%)]. 10/23 pts (43%) received ≥ 2 previous lines of chemotherapy. 19 pts (82 %) are evaluable for response and all 23 pts are evaluable for toxicity. We observed 5 PR (45%) and 6 SD (55%) in arm B. In arm A, while on B alone, 6 (75%) of the pts had PD and 2 (25%) had a short term SD. Adding VC to B 2 PR (25%), 3 SD (37.5%), and 3 PD (37.5%) were observed. Toxicity profile was typical for use of B (hypertension). The absolute mean number of CECs was 158/ml (range 45–461) (n = 23) at baseline, 116/ml at +12 (range 47–275), and 194/ml at +42 (range 36–891). Mean absolute value of CEPs was 270 (range 28–1060) at baseline, 245/ml at D+12 (range 14–981), and 143/ml (range 5–610) at D+42. The fraction of apoptotic/necrotic CECs was 54±19% at baseline, 64±21 at+12, and 52±18 at+42. Conclusions: Preliminary data showed that B alone is not an effective treatment in pts with lymphangitic spread of BC to the chest wall. Additional data on CECs and CEPs are needed to clarify their potential usefulness as a surrogate markers of antiangiogenic activity of B-based regimen. No significant financial relationships to disclose.
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Szmytkowski, Czesław. "CEPAS 2002." Radiation Physics and Chemistry 68, no. 1-2 (2003): 1. http://dx.doi.org/10.1016/s0969-806x(03)00215-9.

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Brown-Glaberman, Ursa Abigail, Jennifer M. Specht, Maria Iannone, Brenda F. Kurland, Robert B. Livingston, and Alison Stopeck. "Circulating biomarkers in patients receiving neoadjuvant chemotherapy combined with sunitinib for locally advanced breast cancer." Journal of Clinical Oncology 31, no. 15_suppl (2013): 1089. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.1089.

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1089 Background: Biomarkers to guide the use of antiangiogenic therapy are lacking. Circulating endothelial cells (CECs) and their progenitor cells (CEPs) are increased in cancer patients. VCAM is an endothelial protein increased in response to VEGF stimulation, while CAIX is elevated in states of hypoxia; both correlate with tumor aggressiveness. Methods: We examined these circulating biomarkers in a phase II neoadjuvant trial in 63 patients (pts) with locally advanced HER2 negative breast cancer treated with 12 weeks (wks) of paclitaxel (T) plus sunitinib (S) followed by 15 wks of daily oral cyclophosphamide and weekly doxorubicin plus daily G-CSF (AC+G-CSF). Toxicity and clinical outcomes are reported as a separate abstract. Blood was collected at baseline, wk 12 and pre-surgery. For this analysis, responders were defined as patients with a pathologic complete response (pCR) and/or MDACC CPS+EG score ≤ 2 (a validated score combining clinical and pathologic results for predicting survival in the neoadjuvant setting). Plasma VCAM and CAIX levels were measured by ELISA using commercially available validated kits and CEC/CEPs by flow cytometry in our laboratory as previously published. Results: 28 (44%) pts were responders. CECs decreased significantly in response to T+S (p = 0.04) but not further with AC+G-CSF. No significant changes were seen in CEPs. VCAM and CAIX levels increased in pts with baseline levels below the median in response to T+S (VCAM p = 0.0003, CAIX p = 0.009). ER negative tumors had higher levels of plasma VCAM and CAIX at baseline compared to ER positive tumors (VCAM p = 0.01, CAIX p = 0.1). Lower baseline levels of VCAM and CAIX were associated with both response and pCR. VCAM and CAIX levels were correlated at baseline (r = 0.4, p = 0.01). Conclusions: CEC, VCAM, and CAIX levels significantly changed after treatment with T + S. Higher baseline levels of VCAM and CAIX were associated with ER negative tumors and lower response rates. Our results suggest that elevated baseline VCAM and CAIX levels are associated with more aggressive biology, and may correspond to less (not more) favorable outcome with the addition of a targeted antiangiogenic agent. Clinical trial information: NCT00513695.
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Shin, S., H. Jeung, J. Ahn, et al. "Mobilized circulating endothelial progenitor cells after the first cycle of chemotherapy with prophylactic G-CSF can be used as a predictive biomarker and patient selection marker for anti-angiogenesis combination treatment." Journal of Clinical Oncology 25, no. 18_suppl (2007): 4638. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.4638.

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4638 Background: We investigated whether the level of circulating endothelial progenitor cells (CEPs) and endothelial cells (CECs) could be used as surrogate predictors of clinical outcome in patients receiving taxotere-based chemotherapy for advanced gastric cancer. Methods: Peripheral blood mononuclear cells were obtained in 49 gastric cancer patients who received taxotere combined with 5-FU and leucovorine (FLT regimen) after chemotherapy and prophylactic G-CSF treatment. To categorize the endothelial cells, immunofluorescent staining for specific endothelial cell markers (CD34, vWF, P1H12, CD31) was used. The changes of CEPs and CECs and their clinical significance on the response prediction and prognosis were analyzed. Results: After the first cycle of chemotherapy, the numbers of CD34+/vWF+, CD34+, vWF+, P1H12+ and CD31+ cells of 49 patients were 19.5 (2.7% of PBMCs), 20.1 (2.7%), 30.0 (4.8%), 12.9 (2.7%) and 214.3 (26.5%) cells/ml, respectively. The number of CD34+/vWF+ and CD34+ cells after the first and second cycle of chemotherapy were found to be higher in non-responders than responders (the first cycle: P=.012 and P=.008, the second cycle: P=.027 and P=.013, respectively). Moreover, the level of CD31+ cells after the second cycle of chemotherapy were significantly decreased compared with the first cycle in the patients who showed response (P=.026). In non-responders, however, the level of CD34+ cells was significantly increased after the second cycle of chemotherapy (P=.034). The level of CD34+ cells significantly related to the median time to progression (TTP) (6.1 and 4.0 months in CD34low and CD34high, respectively, cutoff level: 5.8, P=.046). Conclusion: CD34+/vWF+ and CD34+ cells can be used as a biomarker for prediction and prognosis in taxotere-based chemotherapy. CEP after the first cycle of chemotherapy can be a selection marker for addition of anti-angiogenic treatment after chemotherapy. No significant financial relationships to disclose.
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Naveira, Raquel. "Habitado, Junco, Cepas." Comunicação & Educação, no. 22 (December 30, 2001): 106. http://dx.doi.org/10.11606/issn.2316-9125.v0i22p106-107.

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23

Nole, F., E. Munzone, F. Bertolini, et al. "Circulating endothelial cells (CECs), progenitors (CEPs), and circulating tumor cells (CTCs) for prediction of response in patients with advanced breast cancer (ABC) receiving metronomic oral vinorelbine (oV): Preliminary results." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14572-e14572. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14572.

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e14572 Background: Metronomic administration of chemotherapy given once or more per week with no extended gaps was shown to be effectively anti-angiogenic, causing growth arrest or apoptosis of endothelial cells in tumor neo-vessels. Preclinical and clinical studies indicate that ultra-low concentrations of various microtubule inhibitors inhibit proliferation or migration of endothelial cells. We investigated in a phase II study the activity of metronomic administration of oV in ABC, kinetics and response prediction of CECs, CEPs, CTCs and of other biomarkers of angiogenesis (soluble VEGF, VEGFr2, TSP1, bFGF). CT perfusion scans were also performed. Methods: From February 2008, 47 pts with ABC received oV (50 mg/die TTW). Currently 20 pts are evaluable for both activity and biomarker assessment. Baseline levels of biomarkers of angiogenesis were correlated with clinical response. Results: Shown in Table . Conclusions: We found that the baseline value of apoptotic cells (expressed as % of total cells) was significantly correlated with outcome. The baseline total, viable, and apoptotic CEC count and CTCs might provide an indirect measure for angiogenic turnover and an indicator of better response to anti-angiogenic therapy, supporting the use of metronomic treatments in patients expressing high levels of baseline CECs. Updated results will be presented together with correlation with perfusion CT scan and levels of CTCs. [Table: see text] No significant financial relationships to disclose.
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Glade Bender, J. L., P. C. Adamson, S. Baruchel, et al. "A phase I study of bevacizumab in children with refractory solid tumors: A Children’s Oncology Group study." Journal of Clinical Oncology 24, no. 18_suppl (2006): 9017. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.9017.

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9017 Background: Bevacizumab is a humanized monoclonal antibody targeting the vascular endothelial growth factor (VEGF-A) that has demonstrated significant growth inhibition in several pre-clinical models of pediatric solid tumors. However, the agent has never been tested in pediatric patients. Methods: A phase I dose escalation study in children with refractory solid tumors was conducted to define the dose limiting toxicities (DLTs), and to determine the pharmacokinetics (PK) and recommended phase II dose of bevacizumab administered by IV infusion every 2 weeks in 28-day cycles. Cohorts were enrolled at dose levels of 5, 10, and 15 mg/kg; the final dose level was expanded to include at least 3 children <6 years of age. Serial blood samples were collected for PK, plasma VEGF concentration, and circulating mature and progenitor endothelial cells (CECs/CEPs). Results: 20 patients (10 male), median age 13 yrs (range 1–21), were enrolled at dose levels 5 (n=3), 10 (n=3), and 15 (n=14) mg/kg. 18 patients were fully evaluable for toxicity (one withdrew consent prior to treatment and the second was removed for rapid disease progression). A total of 67 cycles were administered with a median of 3 per patient (range 1–16). Treatment was well tolerated and no DLTs were observed. Only one grade 3 toxicity, lymphopenia, was attributed to drug. Non-dose limiting, grade 1–2 toxicities included infusional reaction (n=3), rash (n=3), mucositis (n=2), and proteinuria (n=3). There was no hypertension, hemorrhage or thrombosis reported. There were no partial or complete responses; 3 pts with Ewings and 2 pts with soft tissue sarcoma had disease stabilization for > 3 months. The serum exposure to bevacizumab as measured by AUC appeared to increase in proportion to dose. The median clearance of bevacizumab was 4.1 ml/day/kg (range 3.2–15.9), and the median T1/2 was 11.8 days (range 3.9–14.6). In some patients, a rapid rate of rise in plasma VEGF, increase in mature CECs or decrease in CEPs was observed. Conclusion: Bevacizumab at doses up to 15mg/kg every two weeks is well tolerated in children with solid tumors. No significant financial relationships to disclose.
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25

Meng, Cai, Jingru Zhang, Xiaoping Li, et al. "CEPC Linac design." International Journal of Modern Physics A 34, no. 13n14 (2019): 1940005. http://dx.doi.org/10.1142/s0217751x19400050.

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The Circular Electron–Positron Collider (CEPC) is a 100-km ring [Formula: see text] collider for a Higgs factory. The injector of CEPC is composed of Linac and Booster. The Linac is a normal conducting S-band Linac with a frequency of 2860 MHz; it provides electron and positron beams at an energy of up to 10 GeV with 100 Hz repetition frequency of 100 Hz. The Linac design and dynamic simulation results are discussed in detail in this paper, including electron bunching system, positron source, electron bypass transport line, damping ring and main Linacs.
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26

Distelzweig, Peter, and Karen Zwier. "Introduction to the CEPOS Discussion." American Catholic Philosophical Quarterly 92, no. 1 (2018): 107–21. http://dx.doi.org/10.5840/acpq2018921139.

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27

Lass, Amir. "The need for more CEPHS." Fertility and Sterility 73, no. 2 (2000): 418. http://dx.doi.org/10.1016/s0015-0282(99)00516-6.

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28

Brandileone, M. C. C., R. C. Zanella, M. L. C. Tondella, L. Gheesling, V. S. D. Vieira, and G. M. Carlone. "Febre purpúrica brasileira, virulência em modelo animal do Haemophilus Aegyptius (H. influenzae biogrupo aegyptius)." Revista do Instituto de Medicina Tropical de São Paulo 35, no. 3 (1993): 259–69. http://dx.doi.org/10.1590/s0036-46651993000300007.

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Febre Purpúrica Brasileira (FPB) é causada por cepas invasoras de Haemophilus aegyptius (H. influenzae biogrupo aegyptius, Hae). Estas cepas invasoras foram diferenciadas de cepas de Hae associadas apenas a conjuntivites (cepas não invasoras) através de marcadores moleculares específicos. Modelo de ratos recém nascidos depletados de complemento foi aplicado ao estudo de cepas de Hae, associadas e não associadas a FPB, com o objetivo de se caracterizar seus potenciais de virulência. Com dose infectante de 10(5) células, as cepas invasoras causaram bacteriemia em 80-100% dos ratos inoculados,.e a magnitude da bacteriemia variou de 10(2,5±0,49) a > 10(4,69) ufc/ml de sangue. Usando a mesma dose infectante as cepas controles não causaram bacteriemia frequente (0 a 50%) e a magnitude variou de 0 a 10(3,69±0,53) ufc/ml de sangue. As doses infectantes capazes de causar bacteriemia em 50% dos ratos inoculados (DB50%) para as cepas invasoras de Hae variaram de < 10³ a 10(4,2) bactérias, enquanto que para as cepas não invasoras, as DB50% variaram de 10(6,2) a > 10(7,3) bactérias. Imunização passiva com antissoros produzidos com cepas invasoras demonstrou que os ratos foram protegidos das bacteriemias causadas pelas cepas homólogas, mas não da infecção causada pela cepa heteróloga. Comparando a bacteriemia causada pelas cepas de Hae com a bacteriemia causada pelo H. influenzae b, cepa Eagan (Hib), foi demonstrado o maior potencial de invasibilidade de Hib. Este modelo animal demonstrou ser útil para esclarecer o maior potencial de virulência das cepas invasoras de Hae.
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29

Hinchliff, Sue. "CEPs: your professional currency." Nursing Standard 8, no. 17 (1994): 20–21. http://dx.doi.org/10.7748/ns.8.17.20.s44.

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30

Geng, Huiping. "Pretzel scheme for CEPC." International Journal of Modern Physics A 31, no. 33 (2016): 1644013. http://dx.doi.org/10.1142/s0217751x16440139.

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CEPC was proposed as an electron and positron collider ring with a circumference of 50–100 km to study the Higgs boson. Since the proposal was made, the lattice design for CEPC has been carried out and a preliminary conceptual design report has been written at the end of 2014. In this paper, we will describe the principles of pretzel scheme design, which is one of most important issues in CEPC lattice design. Then, we will show the modification of the lattice based on the lattice design shown in the Pre-CDR. The latest pretzel orbit design result will also be shown. The issues remained to be solved in the present design will be discussed and a brief summary will be given at the end.
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Bian, Tianjian, Jie Gao, Chuang Zhang, et al. "CEPC booster design study." International Journal of Modern Physics A 32, no. 34 (2017): 1746009. http://dx.doi.org/10.1142/s0217751x17460095.

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In September 2012, Chinese scientists proposed a Circular Electron Positron Collider (CEPC) in China at 240 GeV center-of-mass energy for Higgs studies. The booster provides 120 GeV electron and positron beams to the CEPC collider for top-up injection at 0.1 Hz. The design of the full energy booster ring of the CEPC is a challenge. The ejected beam energy is 120 GeV and the injected beam energy is 6 GeV. In this paper we describe two alternative schemes, the wiggler bend scheme and the normal bend scheme. For the wiggler bend scheme, we propose to operate the booster ring as a large wiggler at low energy and as a normal ring at high energy to avoid the problem of very low dipole magnet fields. For the normal bend scheme, we implement the orbit correction to correct the earth field.
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Liou, Ying-Jay, Mu-Hong Chen, Ju-Wei Hsu, Kai-Lin Huang, Po-Hsun Huang, and Ya-Mei Bai. "Associations between increased circulating endothelial progenitor cell levels and anxiety/depressive severity, cognitive deficit and function disability among patients with major depressive disorder." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-97853-9.

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AbstractThe association of major depressive disorder (MDD) with cardiovascular diseases (CVDs) through endothelial dysfunction is bidirectional. Circulating endothelial progenitor cells (cEPCs), essential for endothelial repair and function, are associated with risks of various CVDs. Here, the relationship of cEPC counts with MDD and the related clinical presentations were investigated in 50 patients with MDD and 46 healthy controls. In patients with MDD, a battery of clinical domains was analysed: depressed mood with Hamilton Depression Rating Scale (HAMD) and Montgomery–Åsberg Depression Rating Scale (MADRS), anxiety with Hamilton Anxiety Rating Scale (HAMA), cognitive dysfunction and deficit with Digit Symbol Substitution Test (DSST) and Perceived Deficits Questionnaire-Depression (PDQ-D), somatic symptoms with Depressive and Somatic Symptom Scale (DSSS), quality of life with 12-Item Short Form Health Survey (SF-12) and functional disability with Sheehan Disability Scale (SDS). Immature and mature cEPC counts were measured through flow cytometry. Increased mature and immature cEPC counts were significantly associated with higher anxiety after controlling the confounding effect of systolic blood pressure, and potentially associated with more severe depressive symptoms, worse cognitive performance and increased cognitive deficit, higher social disability, and worse mental health outcomes. Thus, cEPCs might have pleiotropic effects on MDD-associated symptoms and psychosocial outcomes.
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33

Fernández, S., P. Castro, P. Molina, et al. "Circulating endothelial cells (CECS) and circulating endothelial progenitor cells (CEPCS) in septic and non-infectious systemic inflammatory response syndrome." Intensive Care Medicine Experimental 3, S1 (2015). http://dx.doi.org/10.1186/2197-425x-3-s1-a307.

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34

Sun, Chao, Weiren Lan, Bin Li, et al. "Glucose regulates tissue-specific chondro-osteogenic differentiation of human cartilage endplate stem cells via O-GlcNAcylation of Sox9 and Runx2." Stem Cell Research & Therapy 10, no. 1 (2019). http://dx.doi.org/10.1186/s13287-019-1440-5.

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Abstract Background The degenerative disc disease (DDD) is a major cause of low back pain. The physiological low-glucose microenvironment of the cartilage endplate (CEP) is disrupted in DDD. Glucose influences protein O-GlcNAcylation via the hexosamine biosynthetic pathway (HBP), which is the key to stem cell fate. Thiamet-G is an inhibitor of O-GlcNAcase for accumulating O-GlcNAcylated proteins while 6-diazo-5-oxo-l-norleucine (DON) inhibits HBP. Mechanisms of DDD are incompletely understood but include CEP degeneration and calcification. We aimed to identify the molecular mechanisms of glucose in CEP calcification in DDD. Methods We assessed normal and degenerated CEP tissues from patients, and the effects of chondrogenesis and osteogenesis of the CEP were determined by western blot and immunohistochemical staining. Cartilage endplate stem cells (CESCs) were induced with low-, normal-, and high-glucose medium for 21 days, and chondrogenic and osteogenic differentiations were measured by Q-PCR, western blot, and immunohistochemical staining. CESCs were induced with low-glucose and high-glucose medium with or without Thiamet-G or DON for 21 days, and chondrogenic and osteogenic differentiations were measured by Q-PCR, western blot, and immunohistochemical staining. Sox9 and Runx2 O-GlcNAcylation were measured by immunofluorescence. The effects of O-GlcNAcylation on the downstream genes of Sox9 and Runx2 were determined by Q-PCR and western blot. Results Degenerated CEPs from DDD patients lost chondrogenesis, acquired osteogenesis, and had higher protein O-GlcNAcylation level compared to normal CEPs from LVF patients. CESC chondrogenic differentiation gradually decreased while osteogenic differentiation gradually increased from low- to high-glucose differentiation medium. Furthermore, Thiamet-G promoted CESC osteogenic differentiation and inhibited chondrogenic differentiation in low-glucose differentiation medium; however, DON acted opposite role in high-glucose differentiation medium. Interestingly, we found that Sox9 and Runx2 were O-GlcNAcylated in differentiated CESCs. Finally, O-GlcNAcylation of Sox9 and Runx2 decreased chondrogenesis and increased osteogenesis in CESCs. Conclusions Our findings demonstrate the effect of glucose concentration on regulating the chondrogenic and osteogenic differentiation potential of CESCs and provide insight into the mechanism of how glucose concentration regulates Sox9 and Runx2 O-GlcNAcylation to affect the differentiation of CESCs, which may represent a target for CEP degeneration therapy.
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35

"CEPES PUBLICATIONS." Higher Education in Europe 11, no. 3 (1986): 115–16. http://dx.doi.org/10.1080/0379772860110319.

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"CEPES PUBLICATIONS." Higher Education in Europe 11, no. 1 (1986): 149. http://dx.doi.org/10.1080/0379772860110118.

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"CEPES PUBLICATIONS." Higher Education in Europe 11, no. 2 (1986): 113. http://dx.doi.org/10.1080/0379772860110217.

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"CEPES PUBLICATIONS." Higher Education in Europe 15, no. 3 (1990): 89–90. http://dx.doi.org/10.1080/0379772900150315.

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"CEPES PUBLICATIONS." Higher Education in Europe 17, no. 1 (1992): 170. http://dx.doi.org/10.1080/0379772920170114.

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"CEPES PUBLICATIONS." Higher Education in Europe 18, no. 1 (1993): 114–15. http://dx.doi.org/10.1080/0379772930180116.

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"CEPES NEWS:." Higher Education in Europe 19, no. 3 (1994): 94–105. http://dx.doi.org/10.1080/0379772940190315.

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"CEPES PUBLICATIONS." Higher Education in Europe 12, no. 1 (1987): 127–28. http://dx.doi.org/10.1080/0379772870120119.

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"CEPES PUBLICATIONS." Higher Education in Europe 22, no. 3 (1997): 431–32. http://dx.doi.org/10.1080/0379772970220313.

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"CEPES PUBLICATIONS." Higher Education in Europe 24, no. 1 (1999): 165–66. http://dx.doi.org/10.1080/0379772990240117.

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"CEPES PUBLICATIONS." Higher Education in Europe 24, no. 3 (1999): 465–66. http://dx.doi.org/10.1080/0379772990240315.

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"CEPES PUBLICATIONS." Higher Education in Europe 12, no. 2 (1987): 107–8. http://dx.doi.org/10.1080/0379772870120214.

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"CEPES PUBLICATIONS." Higher Education in Europe 12, no. 3 (1987): 107–8. http://dx.doi.org/10.1080/0379772870120318.

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48

"CEPES PUBLICATIONS." Higher Education in Europe 12, no. 4 (1987): 127–28. http://dx.doi.org/10.1080/0379772870120420.

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"CEPES PUBLICATIONS." Higher Education in Europe 13, no. 1-2 (1988): 183–84. http://dx.doi.org/10.1080/0379772880130126.

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"CEPES PUBLICATIONS." Higher Education in Europe 13, no. 3 (1988): 111–12. http://dx.doi.org/10.1080/0379772880130315.

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