Modeling of photoplethysmography signal for quantitative analysis of endothelial cells during reactive hyperemia

2012 ◽  
Author(s):  
Farhad Shiri ◽  
Bahar Firoozabadi ◽  
Mohammad Said Saidi
Keyword(s):  
Endothelial Cells ◽  
Quantitative Analysis ◽  
Reactive Hyperemia

scholarly journals Quantitative Analysis of the KSHV Transcriptome Following Primary Infection of Blood and Lymphatic Endothelial Cells

Pathogens ◽  
2017 ◽  
Vol 6 (1) ◽  
pp. 11 ◽  
Author(s):  
A. Gregory Bruce ◽  
Serge Barcy ◽  
Terri DiMaio ◽  
Emilia Gan ◽  
H. Jacques Garrigues ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Quantitative Analysis ◽  
Primary Infection ◽  
Lymphatic Endothelial Cells

QUANTITATIVE ANALYSIS OF (PRO)RENIN RECEPTOR IN THE MEDIUM OF HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS, HUVEC

2011 ◽  
Vol 29 ◽  
pp. e94
Author(s):  
K. B. Biswas ◽  
A. H.M.N. Nabi ◽  
Y. Arai ◽  
T. Nakagawa ◽  
A. Ebihara ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Quantitative Analysis ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals STUDY OF VASCULAR ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE

2021 ◽  
pp. 81-89
Author(s):  
Maryna Stoikevych ◽  
Nataliia Nedzvetska ◽  
Nataliia Fedorova
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Endothelium ◽  
Bowel Disease ◽  
Reactive Hyperemia ◽  
Vascular Endothelial ◽  
Inflammatory Bowel

Abstract. Currently, inflammatory bowel disease (IBD) is the most complex and not fully resolved problem in modern gastroenterology. IBD, with its two main subtypes, Crohn's disease (CD) and ulcerative colitis (UC), is a complex multifactorial pathology caused by external and internal factors, including host genetics, the immune system, environmental factors, and the gut microbiome. The possible involvement of endothelial dysfunction is also discussed. There is evidence that in diseases characterized by chronic systemic inflammation, it affects the properties of the arteries and causes both endothelial dysfunction and changes in arterial stiffness. The aim is to study the functional state of the vascular endothelium in patients with inflammatory bowel diseases. Material and methods. A total of 69 patients with IBD aged 18 to 70 years (44.0 ± 1.4 years) were examined. All patients were divided into 2 groups depending on the nosology. 1st group consisted of 45 patients with UC, among them 23 women (51.1 %) and 22 men (48.9 %), 2nd group – 24 patients with HC, of which 14 women (58.3 %) and 10 men (41.7 %). To assess endothelial function, the method for determining endothelium-dependent vasodilation of the brachial artery (BA) in a test with reactive hyperemia was used to assess the change in BA diameter (dPA), a ATL PHILIPS HDI 5000 SONOS CT ultrasound machine with a 7.5 MHz linear transducer was used. The endothelial function index was calculated as the difference between dPA after decompression and the initial value, expressed as a percentage. The content of a soluble vascular cell adhesion molecule 1 (VCAM-1) was determined in blood serum by an enzyme immunoassay using a test system («Bender MedSystems GmbH», Austria) using an enzyme immunoassay analyzer «Stat Fax 303 Plus» («Awareness Technology Inc.», USA). The number of desquamated endothelial cells in the peripheral blood was determined by the method of J. Hladovec. Results. In the study of endothelium-dependent vasodilation (EDVD) PA in a test with reactive hyperemia, dysfunctions of the vascular endothelium were found in 75.4 % of the examined patients. Changes in vascular endothelial function were found in 82.3 % of patients with UC and 62.5 % with CC, mainly due to endothelial dysfunction (ED). Significant differences were found between the indicators of the average increase in dPA in the test with reactive hyperemia with decreased endothelial function (DEF) and normal endothelial function (NEF), as well as with DEF and ED in patients with severe UC. ED was observed 5.2 times more often than NEF (c2 = 56.8; p < 0.001) and 2.6 times more often than PFE (c2 = 31.5; p < 0.001). With moderate severity of the disease, DEF and ED occurred with the same frequency and 2.2 times higher than the number of patients with NEF (c2 = 11.3; p = 0.0008), changes in endothelium-dependent vasodilation were accompanied by a significant increase in the VCAM-1 level in serum of all IBD patients, but the highest expression of VCAM-1 was observed in UC. At the same time, the concentration of VCAM-1 was inversely correlated with endothelium-dependent vasodilation of BA (r = - 0.54, p < 0.01), which is confirmed by the quantitative characteristics of the level of VCAM-1 in various states of the endothelium. The study of the content of circulating desquamated endothelial cells in the peripheral blood made it possible to establish an increase in their number by 5 times with ED – up to (15.5 ± 4.8) × 104/L (p < 0.05), 2 times with DEF – up to (5.7 ± 0.3) × 104/L (p < 0.001) versus (3.1 ± 0.4) × 104/L in the control group. An inverse correlation was found between the number of desquamated endothelial cells and endothelium-dependent BA vasodilation (r = - 0.59, p < 0.01). Conclusions. The results of a comprehensive study of the functional state of the vascular endothelium indicate that the course of IBD is accompanied by a syndrome of endothelial dysfunction (with a predominance of DE), which is characterized by a decrease in endothelium-dependent vasodilation of BA, an increase in the level of VCAM-1 and the content of circulating desquamated endothelial cells in the blood. Keywords: inflammatory bowel disease, Crohn's disease, ulcerative colitis, endothelial dysfunction.

Abnormal Increase in a Distinct Subset of Nestin-Expressing Cells in the Bone Marrow of Myelodysplastic Syndromes

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 3887-3887
Author(s):  
Luan Cao-Sy ◽  
Naoshi Obara ◽  
Tatsuhiro Sakamoto ◽  
Takayasu Kato ◽  
Hidekazu Nishikii ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Quantitative Analysis ◽  
Myelodysplastic Syndromes ◽  
Hematopoietic Stem ◽  
Distinct Subset ◽  
Hsc Niche ◽  
Normal Human ◽  
Vascular Structures ◽  
Intimal Layer

Abstract Background: Nestin-expressing cells (NeC) have been characterized to consist of hematopoietic stem cell (HSC) niche in the mouse bone marrow (BM). Decreases of BM NeC have been reported in myeloproliferative neoplasms (MPN) in humans and in the mouse model of MPN. These lines of information further emphasize the importance of the NeC for the maintenance of normal hematopiesis. Nevertheless, NeC appear to be heterogenous; nestin is reported to be expressed in multiple types of BM stromal cells distinct from each other, with regard to the anatomical localization and the cell-surface antigen expression pattern. One type is reported to be localized adjacent to sinusoids and another type surrounding arterioles. A subset of endothelial cells also appears to be a candidate of NeC in the BM. It is thus critical to define the identities of distinct subsets of BM NeC. Furthermore, each subset of NeC needs to be studied in the human BM from normal subjects and those with BM diseases to understand pathophysiologic significance of NeC in patients. Myelodysplastic syndromes (MDS) are a clonal disease characterized by ineffective hematopoiesis and an increased risk of transformation into acute myeloid leukemia. In this disease, anormalities of BM microenvironment have been repeatedly reported; however, consensus in detail has not been reached. Purpose: To define the identities of distinct subsets of NeC in the BM from normal human subjects and to explore their abnormalities in MDS. Methods:Formalin-fixed paraffin-embedded BM biopsy samples from lymphoma patients without BM involvement (designated normal) and from MDS patients were immunostained with antibodies against six markers: nestin, CD34, laminin, α-smooth muscle actin (αSMA), glial fibrillary acidic protein (GFAP), and neurofilament heavy chain (NFH). Immunohistochemistry (IHC) and immunofluorescence (IF) staining were performed. The microscopic analysis of IHC-stained samples involved 10 randomly selected fields of view at 400× magnification, where the numbers of NeC and CD34-positive spindle-shaped cells were counted for quantitative analysis, as well as the association of these two types of cells was evaluated. IF samples were analyzed by a confocal laser scanning microscope using 10 randomly selected fields of view at 63× magnification. Then, nestin-, GFAP-, and NFH-stained areas were measured using the confocal LAS AF software for quantitative analysis. Results:NeC were found at multiple locations in distinct contexts in the normal human BM. A majority of NeC were present in association with the arterior/arteriolar structures. These artery/arteriole-associated NeC were distributed at each of the three layers; the intimal layer inside the laminine-stained basement membrane, the tunica media epressing αSMA, and the adventitial layer outside the αSMA-stained structure. The NeC located at the intimal layer expressed the highest level of nestin. The NeC were present in a close proximity with the CD34-expressing endothelial cells, although whether the endothelial cells co-expressed nestin and CD34 was unclear. The NeC at the other layers showed relatively lower levels of nestin expression. We identified NeC which did not associate with the vascular structures, albeit at a low frequency and with weak nestin staining in the normal human BM. In MDS BM, there was a significant increase in the NeC that were unassociated with the vascular structures. A portion of these increased NeC co-expressed GFAP. These cells potentially represented Schwann cells, because some of them surrounded the NFH-stained structure. Consistent with this, GFAP- and NFH-stained areas were increases in the MDS BM, together with the nestin-stained areas when measured by the confocal LAS AF software. Discussion: Multiple subsets of NeC were identified in the normal human BM as well as in the MDS BM. It is yet elusive whether each subset of NeC has a HSC niche function. In MDS BM, there was an increase in a distinct subset of NeC. The origin of these cells was elusive, but the Shwann cells normally present along with the arterial/arteriolar structures could be a candidate, because in the normal BM, a portion of GFAP-expressing cells along with the vascular structures expressed nestin. It should be elucidated whether the increased sympathetic nervous structure is involved in the pathophysiology of MDS. Disclosures Obara: Alexion Pharmaceuticals: Honoraria, Research Funding.

Functional and anatomical recovery of endothelium after denudation of coronary artery

1988 ◽  
Vol 254 (6) ◽  
pp. H1081-H1090 ◽  
Author(s):  
Y. Hayashi ◽  
H. Tomoike ◽  
K. Nagasawa ◽  
A. Yamada ◽  
H. Nishijima ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Reactive Hyperemia ◽  
Balloon Catheter ◽  
Experimental Period ◽  
Conscious State ◽  
Percent Recovery ◽  
Electromagnetic Flow Probe ◽  
Coronary Dilation

Endothelium-related coronary dilation after balloon denudation was compared with the extent of luminal lining of the regenerated endothelial cells. Under conditions of asepsis, a pair of 10-MHz piezoelectric crystals, an electromagnetic flow probe, and a cuff occluder were placed on the left circumflex coronary artery. Seven to 10 days after this instrumentation, the dogs were anesthetized and the endothelium was removed with the use of a balloon catheter. Immediately after balloon denudation, coronary dilations following reactive hyperemia (reactive dilation) and acetylcholine 3 micrograms/kg iv were reduced to 19 +/- 5 (P less than 0.01) and 10 +/- 4% (P less than 0.01) of control, respectively. In 2, 5, and 7–10 days after denudation, reactive dilation in the conscious dogs was 24 +/- 7 (n = 16), 71 +/- 10 (n = 11), and 75 +/- 9% (n = 5) of control, respectively. Acetylcholine-induced coronary dilation in conscious state was 52 +/- 12 (n = 9), 116 +/- 17 (n = 7), and 94 +/- 24% (n = 2) of control in 2, 5, and 7-10 days after denudation, respectively. There was a positive linear relation between the extent of reactive dilation and acetylcholine-induced dilation from 2 to 10 days after denudation (r = 0.734). The amount of reactive hyperemia, nitroglycerin-induced coronary dilation, and ergonovine-induced coronary constriction remained constant during the experimental period. The area covered by the endothelial cells at the denuded site was 8 +/- 3 (n = 5), 18 +/- 9 (n = 6), 64 +/- 9 (n = 6), and 81 +/- 11% (n = 3) of the denuded area in 0, 2, 5, and 7-10 days after denudation, respectively, which linearly related to the percent recovery of reactive dilation (r = 0.912). Thus reactive dilation or acetylcholine-induced coronary dilation depended on the presence of endothelium, irrespective of the shape or alignment of the regenerated tissues. These findings may be clinically relevant because anatomical integrity of the endothelium might be assessed in vivo by reactive dilation or acetylcholine-induced coronary dilation.

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