scholarly journals Automatic Synthesis of Anthropomorphic Pulmonary CT Phantoms

2015 ◽  
Author(s):  
Daniel Jimenez-Carretero ◽  
Raul San Jose Estepar ◽  
Mario Diaz Cacio ◽  
Maria J Ledesma-Carbayo
Keyword(s):  
Human Lung ◽  
Pulmonary Arteries ◽  
Structural Complexity ◽  
Automatic Synthesis ◽  
Good Correspondence ◽  
Pulmonary Vessel ◽  
Great Density ◽  
Quantitative Measurements ◽  
Growth Methods ◽  
Complete Framework

The great density and structural complexity of pulmonary vessels and airways impose limitations on the generation of accurate reference standards, which are critical in training and in the validation of image processing methods for features such as pulmonary vessel segmentation or artery-vein (AV) separations. The design of synthetic computed tomography (CT) images of the lung could overcome these difficulties by providing a database of pseudorealistic cases in a constrained and controlled scenario where each part of the image is differentiated unequivocally. This work demonstrates a complete framework to generate computational anthropomorphic CT phantoms of the human lung automatically. Starting from biological and image-based knowledge about the topology and relationships between structures, the system is able to generate synthetic pulmonary arteries, veins, and airways using iterative growth methods that can be merged into a final simulated lung with realistic features. Visual examination and quantitative measurements of intensity distributions, dispersion of structures and relationships between pulmonary air and blood flow systems show good correspondence between real and synthetic lungs.

scholarly journals Pulmonary Vessel Obstruction Does Not Correlate with Severity of Pulmonary Embolism

2019 ◽  
Vol 8 (5) ◽  
pp. 584 ◽  
Author(s):  
Marianne Lerche ◽  
Nikolaos Bailis ◽  
Mideia Akritidou ◽  
Hans Jonas Meyer ◽  
Alexey Surov
Keyword(s):  
Pulmonary Embolism ◽  
Statistical Significance ◽  
Pulmonary Arteries ◽  
Severity Index ◽  
Clinical Severity ◽  
Pulmonary Vessel ◽  
Wells Score ◽  
Clot Burden ◽  
Spearman’S Correlation ◽  
D Dimer

The aim of the present study was to analyze possible relationships between pulmonary vessel obstruction and clinically relevant parameters and scores in patients with pulmonary embolism (PE). Overall, 246 patients (48.8% women and 51.2% men) with a mean age of 64.0 ± 17.1 years were involved in the retrospective study. The following clinical scores were calculated in the patients: Wells score, Geneva score, and pulmonary embolism severity index (PESI) score. Levels of D-dimer (µg/mL), lactate, pH, troponin, and N-terminal natriuretic peptide (BNP, pg/mL) were acquired. Thrombotic obstruction of the pulmonary arteries was quantified according to Mastora score. The data collected were evaluated by means of descriptive statistics. Spearman’s correlation coefficient was used to analyze associations between the investigated parameters. P values < 0.05 were taken to indicate statistical significance. Mastora score correlated weakly with lactate level and tended to correlate with D-dimer and BNP levels. No other clinical or serological parameters correlated significantly with clot burden. Thrombotic obstruction of pulmonary vessels did not correlate with clinical severity of PE.

scholarly journals Pulmonary vessel casting in a rat model of monocrotaline-mediated pulmonary hypertension

2020 ◽  
Vol 10 (3) ◽  
pp. 204589402092212
Author(s):  
Zhongkai Zhu ◽  
Yifan Wang ◽  
Amy Long ◽  
Tianyu Feng ◽  
Maria Ocampo ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Rat Model ◽  
Vascular System ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Control Group ◽  
Wall Thickening ◽  
Arterial Remodeling ◽  
Pulmonary Vessel ◽  
Pulmonary Arterial

Pulmonary hypertension is a chronic vascular disease characterized by pulmonary vasoconstriction and pulmonary arterial remodeling. Pulmonary arterial remodeling is mainly due to small pulmonary arterial wall thickening and lumen occlusion. Previous studies have described intravascular changes in lung sections using histopathology, but few were able to obtain a fine detailed image of the pulmonary vascular system. In this study, we used Microfil compounds to cast the pulmonary arteries in a rat model of monocrotaline-induced pulmonary hypertension. High-quality images that enabled quantification of distal pulmonary arterial branching based on the number of vessel bifurcations/junctions were demonstrated in this model. The branch and junction counts of distal pulmonary arteries significantly decreased in the monocrotaline group compared to the control group, and this effect was inversely proportional to the mean pulmonary artery pressure observed in each group. The patterns of pulmonary vasculature and the methods for pulmonary vessel casting are presented to provide a basis for future studies of pulmonary arterial remodeling due to pulmonary hypertension and other lung diseases that involve the remodeling of vasculature.

Expression of VEGF and its receptors Flt-1 and Flk-1/KDR is altered in lambs with increased pulmonary blood flow and pulmonary hypertension

2003 ◽  
Vol 285 (1) ◽  
pp. L222-L231 ◽  
Author(s):  
Eugenia Mata-Greenwood ◽  
Barbara Meyrick ◽  
Scott J. Soifer ◽  
Jeffrey R. Fineman ◽  
Stephen M. Black
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Immunohistochemical Analysis ◽  
Muscle Layer ◽  
Pulmonary Epithelium ◽  
Pulmonary Vessel ◽  
Smooth Muscle Layer ◽  
Vegf Signaling

Utilizing in utero aortopulmonary vascular graft placement, we developed a lamb model of congenital heart disease and increased pulmonary blood flow. We showed previously that these lambs have increased pulmonary vessel number at 4 wk of age. To determine whether this was associated with alterations in VEGF signaling, we investigated vascular changes in expression of VEGF and its receptors, Flt-1 and KDR/Flk-1, in the lungs of shunted and age-matched control lambs during the first 8 wk of life. Western blot analysis demonstrated that VEGF, Flt-1, and KDR/Flk-1 expression was higher in shunted lambs. VEGF and Flt-1 expression was increased at 4 and 8 wk of age ( P <0.05). However, KDR/Flk-1 expression was higher in shunted lambs only at 1 and 4 wk of age ( P <0.05). Immunohistochemical analysis demonstrated that, in control and shunted lambs, VEGF localized to the smooth muscle layer of vessels and airways and to the pulmonary epithelium while increased VEGF expression was localized to the smooth muscle layer of thickened media in remodeled vessels in shunted lambs. VEGF receptors were localized exclusively in the endothelium of pulmonary vessels. Flt-1 was increased in the endothelium of small pulmonary arteries in shunted animals at 4 and 8 wk of age, whereas KDR/Flk-1 was increased in small pulmonary arteries at 1 and 4 wk of age. Our data suggest that increased pulmonary blood flow upregulates expression of VEGF and its receptors, and this may be important in development of the vascular remodeling in shunted lambs.

scholarly journals Gene expression profile of angiogenic factors in pulmonary arteries in COPD: relationship with vascular remodeling

2016 ◽  
Vol 310 (7) ◽  
pp. L583-L592 ◽  
Author(s):  
Jéssica García-Lucio ◽  
Gemma Argemi ◽  
Olga Tura-Ceide ◽  
Marta Diez ◽  
Tanja Paul ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Remodeling ◽  
Univariate Analysis ◽  
Pulmonary Arteries ◽  
Smooth Muscle Cell Proliferation ◽  
Pulmonary Vessel

Pulmonary vessel remodeling in chronic obstructive pulmonary disease (COPD) involves changes in smooth muscle cell proliferation, which are highly dependent on the coordinated interaction of angiogenic-related growth factors. The purpose of the study was to investigate, in isolated pulmonary arteries (PA) from patients with COPD, the gene expression of 46 genes known to be modulators of the angiogenic process and/or involved in smooth muscle cell proliferation and to relate it to vascular remodeling. PA segments were isolated from 29 patients and classified into tertiles, according to intimal thickness. After RNA extraction, the gene expression was assessed by RT-PCR using TaqMan low-density arrays. The univariate analysis only showed upregulation of angiopoietin-2 ( ANGPT-2) in remodeled PA ( P < 0.05). The immunohistochemical expression of ANGPT-2 correlated with intimal enlargement ( r = 0.42, P < 0.05). However, a combination of 10 factors in a multivariate discriminant analysis model explained up to 96% of the classification of the arteries. A network analysis of 46 genes showed major decentralization. In this network, the metalloproteinase-2 ( MMP-2) was shown to be the bridge between intimal enlargement and fibrogenic factors. In COPD patients, plasma levels of ANGPT-2 were higher in current smokers or those with pulmonary hypertension. We conclude that an imbalance in ANGPT-2, combined with related factors such as VEGF, β-catenin, and MMP-2, may partially explain the structural derangements of the arterial wall. MMP-2 may act as a bridge channeling actions from the main fibrogenic factors.

Effect of long-term high-altitude hypoxia on fetal pulmonary vascular contractility

2008 ◽  
Vol 104 (6) ◽  
pp. 1786-1792 ◽  
Author(s):  
Qin Xue ◽  
Charles A. Ducsay ◽  
Lawrence D. Longo ◽  
Lubo Zhang
Keyword(s):  
High Altitude ◽  
Pulmonary Arteries ◽  
Common Mechanism ◽  
Maximal Response ◽  
Pulmonary Vessel ◽  
Altitude Hypoxia ◽  
Protein Levels ◽  
High Altitude Hypoxia ◽  
Increased Risk

Hypoxia in the fetus and/or newborn is associated with an increased risk of pulmonary hypertension. The present study tested the hypothesis that long-term high-altitude hypoxemia differentially regulates contractility of fetal pulmonary arteries (PA) and veins (PV) mediated by differences in endothelial NO synthase (eNOS). PA and PV were isolated from near-term fetuses of pregnant ewes maintained at sea level (300 m) or high altitude of 3,801 m for 110 days (arterial Po2 of 60 Torr). Hypoxia had no effect on the medial wall thickness of pulmonary vessels and did not alter KCl-induced contractions. In PA, hypoxia significantly increased norepinephrine (NE)-induced contractions, which were not affected by eNOS inhibitor NG-nitro-l-arginine (l-NNA). In PV, hypoxia had no effect on NE-induced contractions in the absence of l-NNA. l-NNA significantly increased NE-induced contractions in both control and hypoxic PV. In the presence of l-NNA, NE-induced contractions of PV were significantly decreased in hypoxic lambs compared with normoxic animals. Acetylcholine caused relaxations of PV but not PA, and hypoxia significantly decreased both pD2 and the maximal response of acetylcholine-induced relaxation in PV. Additionally, hypoxia significantly decreased the maximal response of sodium nitroprusside-induced relaxations of both PA and PV. eNOS was detected in the endothelium of both PA and PV, and eNOS protein levels were significantly higher in PV than in PA in normoxic lambs. Hypoxia had no significant effect on eNOS levels in either PA or PV. The results demonstrate heterogeneity of fetal pulmonary arteries and veins in response to long-term high-altitude hypoxia and suggest a likely common mechanism downstream of NO in fetal pulmonary vessel response to chronic hypoxia in utero.

scholarly journals Nonlinear control of transcription through enhancer-promoter interactions

2021 ◽  
Author(s):  
Jessica Zuin ◽  
Gregory Roth ◽  
Yinxiu Zhan ◽  
Julie Cramard ◽  
Josef Redolfi ◽  
...  
Keyword(s):  
Chromosome Structure ◽  
Temporal Dynamics ◽  
Three Dimensional ◽  
Structural Complexity ◽  
Genomic Region ◽  
Quantitative Measurements ◽  
Topologically Associating Domains ◽  
Transcriptional Effect ◽  
Target Promoters

AbstractChromosome structure in mammals is thought to regulate transcription by modulating the three-dimensional interactions between enhancers and promoters, notably through CTCF-mediated interactions and topologically associating domains (TADs)1–4. However, how chromosome interactions are actually translated into transcriptional outputs remains unclear. To address this question we use a novel assay to position an enhancer at a large number of densely spaced chromosomal locations relative to a fixed promoter, and measure promoter output and interactions within a genomic region with minimal regulatory and structural complexity. Quantitative analysis of hundreds of cell lines reveal that the transcriptional effect of an enhancer depends on its contact probabilities with the promoter through a non-linear relationship. Mathematical modeling and validation against experimental data further provide evidence that nonlinearity arises from transient enhancer-promoter interactions being memorized into longer-lived promoter states in individual cells, thus uncoupling the temporal dynamics of interactions from those of transcription. This uncovers a potential mechanism for how enhancers control transcription across large genomic distances despite rarely meeting their target promoters, and for how TAD boundaries can block distal enhancers. We finally show that enhancer strength additionally determines not only absolute transcription levels, but also the sensitivity of a promoter to CTCF-mediated functional insulation. Our unbiased, systematic and quantitative measurements establish general principles for the context-dependent role of chromosome structure in long-range transcriptional regulation.

scholarly journals Human immunodeficiency virus transgenic rats exhibit pulmonary hypertension

2011 ◽  
Vol 301 (3) ◽  
pp. L315-L326 ◽  
Author(s):  
Amie K. Lund ◽  
JoAnn Lucero ◽  
Lindsay Herbert ◽  
Yushi Liu ◽  
Jay S. Naik
Keyword(s):  
Human Immunodeficiency Virus ◽  
Pulmonary Arteries ◽  
Systolic Pressure ◽  
Male Rats ◽  
Control Male ◽  
Pulmonary Vessel ◽  
Altered Expression ◽  
Fischer 344 ◽  
Immunodeficiency Virus ◽  
The Right

Human immunodeficiency virus (HIV)-associated pulmonary arterial hypertension (PAH) is a serious noninfectious disease involving an aberrant increase in pressure in the blood vessels of the lung, which leads to right ventricular (RV) heart failure and can eventually result in death. A lack of viable animal models of HIV-PAH has limited the identification of signaling pathways involved in HIV-mediated onset and progression of PAH. To determine whether the HIV-1 transgenic (HIV Tg) rat displays pathophysiological end points associated with PAH, we evaluated peak RV systolic pressure (RVSP), RV hypertrophy, pulmonary vessel remodeling, and alterations in gene expression by real-time PCR and microarray. RVSP was measured by RV catheterization via the right jugular vein in 3- and 9-mo-old HIV Tg and age-matched Fischer 344 (control) male rats while under 2% isoflurane anesthesia. RVSP was elevated in the HIV Tg rats (34.2 ± 2.5 mmHg) compared with the F344 controls (21.2 ± 2.5 mmHg), with more significant elevations in the 9-mo-old HIV Tg rats (42.5 ± 3.7 mmHg). We observed significant increases in RV wall thickness in HIV Tg rats compared with controls, both histologically and by echocardiograph measurement. HIV Tg rats also show increased thickening of the pulmonary artery and remodeling of small pulmonary arteries, as well as altered expression of gene pathways associated with PAH. These data represent the first analysis of PAH in HIV Tg rats and suggest that this model will be useful for investigating pathways and identifying potential therapies for HIV-PAH.

Role of Inflammation and Ischemia after Implantation of Xenogeneic Pulmonary Valve Conduits: Histological Evaluation after 6 to 12 Months in Sheep

2003 ◽  
Vol 26 (5) ◽  
pp. 411-420 ◽  
Author(s):  
M.H. Wilhelmi ◽  
P. Rebe ◽  
R. Leyh ◽  
M. Wilhelmi ◽  
A. Haverich ◽  
...  
Keyword(s):  
Heart Valve ◽  
Pulmonary Arteries ◽  
Histological Evaluation ◽  
Pulmonary Vessel ◽  
Inflammatory Reactions ◽  
Endothelial Surface ◽  
Degenerative Alterations ◽  
Valve Prostheses ◽  
Post Implantation

Objective Commercially available biological heart valve prostheses undergo degenerative changes, which finally lead to complete destruction. Here we evaluate the role of inflammation and ischemia after implantation of xenogeneic heart valve conduits (XPC) generated by novel concepts of tissue engineering. Methods Acellularized (a-)XPC and autologus re-seeded (s-)XPC were implanted into sheep. Samples were taken as follows: after acellularization (n=2), after re-seeding (n=2), 6 months (seeded/non-seeded: n=3/5), 9 months (n=2/5), and 12 months (n=3/2) post implantation. Five native porcine conduits served as control. Using histological methods, samples were evaluated for pathological changes and existence/density of microvessels. Results Prior to implantation a-XPC were completely free of cells. Six months after implantation, leaflets and pulmonary arteries of s-XPC and a-XPC showed good endothelial surface coverage. Microvessel density within the myocardial cuffs and pulmonary vessel walls were comparable to control in all grafts. However, 6, 9 and 12 months after implantation pathological severe microvessel ingrowth, calcification and cellular infiltrations were observed on a-XPC and s-XPC valves, whereas myocardial cuffs and XPC-artery walls showed only mild degenerative alterations. Conclusions Inflammatory reactions play a pivotal role in the degeneration of a-XPC and s-XPC. Thus, since ischemia seems to have little or no influence on this process, inflammation inductive factors should be the center of interest.

scholarly journals Sex-dependent change in the reactivity of isolated pulmonary arteries of gonadectomized rats under the intermittent hypoxia of different degree

2021 ◽  
Vol 20 (3) ◽  
pp. 77-83
Author(s):  
N. V. Pankova ◽  
M. M. Artemieva ◽  
N. A. Medvedeva
Keyword(s):  
Pulmonary Arteries ◽  
Female Rats ◽  
No Donor ◽  
Pulmonary Vessel ◽  
Male And Female ◽  
Pulmonary Vessels ◽  
Constant Flow Rate ◽  
Dilatory Response ◽  
Male And Female Rats ◽  
Dependent Change

Introduction. Pulmonary vasoconstriction is one of factors of hypoxic pulmonary hypertension (HPH). The progression of this disease depends on the degree of hypoxiа and seх. The aim of this study was to investigate the reactivity of isolated pulmonary vessels of male and female rats with HPH to vasoactive factors. Materials and methods. The experiments were on male and female of Wistar rats 190–200 g, which were gonadectomized. All animals were divided into 4 groups. One group of males and female rats was kept in a vivarium (21 % О2 ). To simulate HPH, other rats were exposed to hypobaric hypoxia for 10 hours a day at an oxygen content in the inhaled air equal to 13 % (pP O2 103.7 mmHg) or 10 % (pP O2 78,2 mmHg), or 8 % (pP O2 63,5 mmHg) as compared to its content at 21 % (pP О2 159 mmHg). After that, a third-order pulmonary vessel was perfused at a constant flow rate with vasoconstrictors and vasodilators. The reaction was recorded by the change in perfusion pressure. Results. In females with HРН 10 %O2 , constricting response to serotonin were greater than in males. In normotensive males, the dilatory response to sodium nitroprusside (NP) was less than in female. Exposure to hypoxia induced an increase in NP responses. Conclusion. Increased reactivity of pulmonary vessels to serotonin is a factor of pathogenesis of HPH in females, in contrast to males. Increased reactivity to NO donor in males exposed to hypoxia сan be used for a pharmacological target for HPH.

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