Venous ulceration represents the most prevalent form of difficult-to-heal wounds and these problematic wounds require a significant amount of healthcare resources for their treatment. In order to develop effective treatment regimens a clearer understanding of the underlying pathological processes that lead to skin breakdown is required. However, to date, most of these studies have tended to focus on describing the pathology of already-established ulcers. By bringing together relevant aspects of diverse disciplines such as inflammation, cardiovascular, and connective tissue biology, we aim to provide an insight into how circulatory abnormalities that are caused by the underlying disease etiology can induce local tissue inflammation resulting in tissue breakdown. Initially this results in internal tissue damage but if the underlying disease is not treated, the internal tissue damage can worsen and lead to open ulceration. This article discusses the cause-and-effect relationships between chronic venous insufficiency and venous ulceration, focusing particularly on the biological processes that lead from the underlying disease condition to overt ulceration. Available evidence also suggests that formation of pressure, diabetic foot and arterial ulcers, and ulcers as results of blood disorders, is also likely to share some of the same biological processes as venous ulcers.
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http://dx.doi.org/10.1111/j.1524-475X.2007.00250.x | DOI Listing |
Stem Cells Dev
January 2025
Department of Clinical Pharmacy and Pharmacy Practices, Faculty of Pharmacy, University Malaya, Kuala Lumpur, Malaysia.
Hypertension, commonly known as high blood pressure, is a significant health issue that increases the risk of cardiovascular diseases, stroke, and renal failure. This condition broadly encompasses both primary and secondary forms. Despite extensive research, the underlying mechanisms of systemic arterial hypertension-particularly primary hypertension, which has no identifiable cause and is affected by genetic and lifestyle agents-remain complex and not fully understood.
View Article and Find Full Text PDFCurr Cardiol Rep
January 2025
Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY, 10029, USA.
Purpose Of The Review: This review aims to discuss the process of cardiomyocyte maturation, with a focus on the underlying molecular mechanisms required to form a fully functional heart. We examine both long-standing concepts associated with cardiac maturation and recent developments, and the overall complexity of molecularly integrating all the processes that lead to a mature heart.
Recent Findings: Cardiac maturation, defined here as the sequential changes that occurring before the heart reaches full maturity, has been a subject of investigation for decades.
J Clin Microbiol
January 2025
Department of Internal Medicine, Section of Infectious Diseases, Erasmus University Medical Center, Rotterdam, the Netherlands.
An accurate diagnosis of invasive aspergillosis (IA) in patients with underlying hematological malignancies relies heavily on galactomannan detection. In this study, we compared the VirCLIA chemiluminescence immunoassay (CLIA) with the frequently used Platelia enzyme-linked immunosorbent assay (ELISA) on serum from hematology patients with suspected IA. Patients were categorized according to EORTC/MSGERC 2020 definitions into proven/probable IA and possible/no IA.
View Article and Find Full Text PDFmBio
January 2025
Department of Infectious Diseases and Immunology, Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Aichi, Japan.
The human cellular cytidine deaminases APOBEC3s (A3s) inhibit virion infectivity factor (Vif)-deficient HIV-1 replication. However, virus-encoded Vifs abolish this defense system by specifically recruiting A3s to an E3 ubiquitin ligase complex to induce their degradation. The highly conserved Vif PPLP motif is critical for the Vif-mediated antagonism of A3s and is believed to be important for Vif multimerization.
View Article and Find Full Text PDFJ Virol
January 2025
Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, Jilin, China.
Unlabelled: Respiratory syncytial virus (RSV) infections continue to plague infants, young children, and older individuals worldwide. Since there is no specific treatment for RSV, characterizing the interactions between RSV and host factors remains crucial for the eventual development of robust therapeutic interventions. In our previous study, guanylate binding protein 5 (GBP5) was shown to promote excessive RSV-small hydrophobic (RSV-SH) protein secretion by microvesicles and inhibited viral replication.
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