scholarly journals Quantitative splenic embolization possible: application of 8Spheres conformal microspheres in partial splenic embolization (PSE)

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Haohao Lu ◽  
Chuansheng Zheng ◽  
Bin Liang ◽  
Bin Xiong

Abstract Background To investigate the safety and efficacy of 8Spheres in partial splenic embolization. To explore the possibility of accurate control of splenic embolic volume by quantifying the number of microspheres used during PSE. Method The data of 179 patients who underwent PSE were collected. The patients were divided into two groups: 300–500 um microsphere group (N = 83) and 500–700 um microsphere group (N = 96). The spleen volume before PSE, infarct volume and infarct rate of the spleen after PSE, changes in peripheral blood cells after PSE, postoperative adverse events and incidence of infection were compared between the two groups. Results 300–500 um group vs 500–700 um group: postoperative spleen volume (cm3): 753.82 ± 325.41 vs 568.65 ± 298.16 (P = 0.008); spleen embolization volume (cm3): 525.93 ± 118.29 vs 630.26 ± 109.71 (P = 0.014); spleen embolization rate: 41.1 ± 12.3% vs 52.4 ± 10.1% (P = 0.021). Leukocytes and platelets were significantly increased after PSE in both groups; leukocyte, 1 month: 4.13 ± 0.91 vs 5.08 ± 1.16 (P = 0.026); 3 months: 4.08 ± 1.25 vs 4.83 ± 0.98 (P = 0.022); platelet, 1 month: 125.6 ± 20.3 vs 138.7 ± 18.4 (P = 0.019); 3 months: 121.8 ± 16.9 vs 134.3 ± 20.1 (P = 0.017). Incidence of abdominal pain after PSE, 72 (86.7%) vs 69 (71.9%), P = 0.027. The incidence of other adverse events and infections after PSE was not statistically different. Conclusion PSE with 8Spheres is safe and effective. The use of 500–700 um microsphere for PSE can make the increase of peripheral blood cells more stable. Each vial of 8Spheres corresponds to a certain volume of splenic embolization, so it is possible to achieve quantitative embolization in PSE.

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Lei Zuo ◽  
Jian Xie ◽  
Yun Liu ◽  
Shuo Leng ◽  
Zhijun Zhang ◽  
...  

Abstract Background Inflammation is integral to the pathophysiology of ischemic stroke and a prime target for the development of new stroke therapies. The aim of the present study is to seek out the regulatory mechanism of circCDC14A in neuroinflammatory injury in tMCAO mice. Methods The expression level of circCDC14A in peri-infarct cortex and plasma of mice were detected by qPCR. The localization of circCDC14A in peripheral blood cells and peri-infarct cortex of tMCAO mice were explored by in situ hybridization and immunofluorescence colocalization staining. Lentivirus were microinjected into lateral ventricular of brain or injected into tail vein to interfere with the expression of circCDC14A, thus their effects on behavior, morphology, and molecular biology of tMCAO mice were analyzed. Results The expression of circCDC14A in plasma and peri-infarct cortex of tMCAO mice significantly increased, and circCDC14A was mainly localized in neutrophils peripherally while in astrocytes in peri-infarct cortex centrally. Tail vein injection of lentivirus to interfere with the expression of circCDC14A significantly reduced the infarct volume (P < 0.01) at 72 h after reperfusion and density of activated astrocytes in peri-infarct cortex at 3 days, 5 days and 7 days after tMCAO modeling (all P < 0.0001). Moreover, mNSS (P < 0.0001) and survival rate (P < 0.001) were significantly improved within 7 days in si-circCDC14A group compared to circCon group. Additionally, morphology analysis showed the volume and surface area of each activated astrocytes significantly decreased (P < 0.0001). Quantification analysis measured the percentage of N2 phenotype among infiltrated neutrophils in brain sections and found N2 ratio was significantly higher in si-circCDC14A group compared to circCon group (P < 0.001). Conclusion Knocking down the expression of circCDC14A in peripheral blood cells relieved astrocytes activation in peri-infarct cortex, thereby relieved brain damage in the acute phase of ischemic stroke.


1987 ◽  
Vol 58 (03) ◽  
pp. 936-942 ◽  
Author(s):  
Lindsey A Miles ◽  
Edward F Plow

SummaryGlu-plasminogen binds to platelets; the monocytoid line, U937, and the human fetal fibroblast line, GM1380 bind both plasminogen and its activator, urokinase. This study assesses the interaction of these fibrinolytic proteins with circulating human blood cells. Plasminogen bound minimally to red cells but bound saturably and reversibly to monocytes, granulocytes and lymphocytes with apparent Kd values of 0.9-1.4 μM. The interactions were of high capacity with 1.6 to 49 × 105 sites/cell and involved the lysine binding sites of plasminogen. Both T cells and non-rosetting lymphocytes and two B cell lines saturably bound plasminogen. Urokinase bound saturably to gianulocytes, monocytes, non-rosetting lymphocytes and a B cell line, but minimally to T cells, platelets and red cells. Therefore, plasminogen binding sites of high capacity, of similar affinities, and with common recognition specificities are expressed by many peripheral blood cells. Urokinase receptors are also widely distributed, but less so than plasminogen binding sites. The binding ol plasminogen and/ or urokinase to these cells may lead to generation of cell- associated proteolytic activity which contributes to a variety of cellular functions.


2020 ◽  
Vol 11 ◽  
Author(s):  
Miguel A. Andrade-Navarro ◽  
Katja Mühlenberg ◽  
Eike J. Spruth ◽  
Nancy Mah ◽  
Adrián González-López ◽  
...  

Huntington's disease (HD) is an autosomal dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the Huntingtin gene. As disease-modifying therapies for HD are being developed, peripheral blood cells may be used to indicate disease progression and to monitor treatment response. In order to investigate whether gene expression changes can be found in the blood of individuals with HD that distinguish them from healthy controls, we performed transcriptome analysis by next-generation sequencing (RNA-seq). We detected a gene expression signature consistent with dysregulation of immune-related functions and inflammatory response in peripheral blood from HD cases vs. controls, including induction of the interferon response genes, IFITM3, IFI6 and IRF7. Our results suggest that it is possible to detect gene expression changes in blood samples from individuals with HD, which may reflect the immune pathology associated with the disease.


2001 ◽  
Vol 344 (3) ◽  
pp. 175-181 ◽  
Author(s):  
William I. Bensinger ◽  
Paul J. Martin ◽  
Barry Storer ◽  
Reginald Clift ◽  
Steven J. Forman ◽  
...  

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