Background: In vascular pathology the endothelial lesions easily reflect on blood cells, inducing a reactive state. In the present study the eventual presence of activation signals in leukocytes and platelets was tested.
Methods: Fifty-eight subjects with major vascular pathology and 14 with lower limbs venous insufficiency were studied, together with a control group of 25 normal subjects. Elastase PMN, superoxide ion, leukocytes and subpopulation count, platelet factor 3, clot retraction, heparin in neutralizing activity (HNA plasmatic and intraplatelet), platelet count and volume were tested.
Results: As regards leukocytes, it was observed a significative increase of elastase PMN and monocytes number for both the studied pathologies, of superoxide ion and leukocyte number only for major vascular pathology; for platelets, an inhibition of functionality, revealed by clot retraction test for arterious and venous pathologies and by HNA test only for the venous one.
Conclusions: As regards the leukocyte activation, elastase PMN is particularly responsive to the endothelial lesion both in arterious and in venous districts, while superoxide ion appears to increase in presence of a marked alteration. The level of monocytes is indicative of an inflammatory condition and of leukocytes of an atherosclerotic inflammatory process. As for platelets, the test clot retraction is specifically sensible to the endothelial abnormality in both the arterious and venous pathologies with addition of an abnormal HNA test only in venous insufficiency. This platelet dysfunction is probably due to endothelial release of vasoactive and heparin amplifying substances.
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PLoS One
January 2025
School of Chemical Engineering, National Technical University of Athens, Zografou, Athens, Greece.
The aim of this study is to demonstrate the enhanced efficiency of combined therapeutic strategies for the treatment of growing tumors, based on computational experiments of a continuous-level modeling framework. In particular, the tumor growth is simulated within a host tissue and treated as a multiphase fluid, with each cellular species considered as a distinct fluid phase. Our model integrates the impact of chemical species on tumor dynamics, and we model -through reaction-diffusion equations- the spatio-temporal evolution of oxygen, vascular endothelial growth factor (VEGF) and chemotherapeutic agents.
View Article and Find Full Text PDFStem Cells
January 2025
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX13QX, UK.
The large majority of Alzheimer's disease (AD) cases are sporadic with unknown genetic causes. In contrast, only a small percentage of AD cases are familial, with known genetic causes. Paradoxically, there are only few validated mouse models of sporadic AD but many of familial AD.
View Article and Find Full Text PDFAnn Surg Oncol
January 2025
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Background: Tumor microvasculature is an important component of the tumor microenvironment (TME), and it has been reported that tumor microvasculature induces TME to become immunosuppressive via vascular endothelial growth factor. However, the significance of this in adenocarcinoma with epidermal growth factor receptor (EGFR) common mutations has not been fully investigated.
Methods: We analyzed 262 patients with adenocarcinoma harboring EGFR common mutations who underwent surgery at Kyushu University Hospital between 2006 and 2021.
ACS Nano
January 2025
Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410013, China.
Atherosclerosis (AS) is a prevalent inflammatory vascular disease characterized by plaque formation, primarily composed of foam cells laden with lipids. Despite lipid-lowering therapies, effective plaque clearance remains challenging due to the overexpression of the CD47 molecule on apoptotic foam cells, inhibiting macrophage-mediated cellular efferocytosis and plaque resolution. Moreover, AS lesions are often associated with severe inflammation and oxidative stress, exacerbating disease progression.
View Article and Find Full Text PDFJCI Insight
January 2025
Division of Nephrology, The University of Alabama at Birmingham, Birmingham, United States of America.
Disrupted feeding and fasting cycles as well as chronic high fat diet (HFD)-induced obesity are associated with cardiovascular disease risk factors. We designed studies that determined whether two weeks of time-restricted feeding (TRF) intervention in mice fed a chronic HFD would reduce cardiovascular disease risk factors. Mice were fed a normal diet (ND; 10% fat) ad libitum or HFD (45% fat) for 18 weeks ad libitum to establish diet-induced obesity.
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