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Candida and parasitic infection: Helminths, trichomoniasis, lice, scabies, and malaria
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Candida are dimorphic organisms with blastospore and mycelial forms. The blastospore form (budding yeast) is associated with transmission and colonization, and is the form found in the bloodstream in systemic infection. Germinated yeast with mycelia and pseudohyphae is the tissue-invasive form that causes symptomatic disease. The Candida life cycle is one of rapid budding, maturation, and degeneration. Budding occurs as a new cell outgrowth from the mother blastospore. Following mitosis, a septum partitions the two cells and budding resumes in each cell. Mycelium formation begins as a cylindrical outgrowth from the cell wall. Septa are laid down behind the apical tip as the hyphae shoot lengthens. Blastospores are then produced just behind the newly created septa. Pseudohyphae are a morphologic derivative between budding and hyphal growth that is found in all Candida species (8).
Introduction to virus structure, classification, replication, and hosts
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Philippe Simon, Kevin M. Coombs
Many enveloped viruses exit the cell through a process termed budding, in which the virus “buds” from the cell, acquiring its envelope at the same time. Budding may or may not damage the cell, and in some cases, the cell subsequently recovers from viral infection. In some cases, budding at the outer membrane is restricted to a particular surface of the cell; it can occur at either the apical (top) surface (e.g., orthomyxoviruses and paramyxoviruses) or at the basal (bottom) surface (e.g., rhabdoviruses and some retroviruses).
A Complicated Pulmonary Cystic Echinococcosis in Pregnancy
Published in Wickii T. Vigneswaran, Thoracic Surgery, 2019
Yulia N. Matveeva, Kalpaj R. Parekh
E. multilocularis cause lesions composed of numerous irregular cysts of various sizes, without clear demarcation from surrounding tissues. The cysts are composed of a thin, laminated layer with minimal or no germinative layer. The reproduction occurs by lateral budding. The lack of limiting membrane and exogenous budding allows infiltration and destruction of adjacent tissues similar to malignant processes. Central necrosis and irregular calcifications are present in 70% of cases as a result of host defense mechanisms.
A classification based on tumor budding and immune score for patients with hepatocellular carcinoma
Published in OncoImmunology, 2020
Li Wei, Zhang Delin, Yuan Kefei, Wu Hong, Huang Jiwei, Zhang Yange
Tumor budding, first introduced in colorectal tumors, was defined as the presence of single tumor cell or small groups of up to four tumor cells at the intratumoral area or invasive front.7–11 In colorectal cancer, the Union of International Cancer Control classified tumor budding as an “additional prognostic indicator”.12 In addition to colorectal cancers, tumor budding is also a novel prognostic indicator independent of tumor stage and tumor grade in diverse types of tumor including esophageal, gastric, bladder, lung and pancreatic tumors.11,13-19 However, the prognostic value of tumor budding in HCC remains unknown. Tumor budding is thought to be a reflection of epithelial–mesenchymal transition (EMT) process and it is featured by two malignant characteristics, cellular discohesion, and active invasion.20,21 In addition, tumor budding phenotype showed constitutive activation of the WNT signaling pathway, and the downstream molecule β-catenin was deemed as integral components of EMT process.22
Glycosylation of extracellular vesicles: current knowledge, tools and clinical perspectives
Published in Journal of Extracellular Vesicles, 2018
Charles Williams, Felix Royo, Oier Aizpurua-Olaizola, Raquel Pazos, Geert-Jan Boons, Niels-Christian Reichardt, Juan M. Falcon-Perez
Intercellular communication is essential to the correct functioning of multicellular organisms. Aside from chemical endocrine systems and protein growth factors, this is also achieved through the secretion and uptake of extracellular vesicles (EVs) – submicron particles consisting of a lipid bilayer with a cargo of functional proteins, RNA molecules and metabolites. The term EV comprises a taxonomy of vesicle designations, each classified mainly by their mode of biogenesis [1,2]. While apoptotic bodies are formed during programmed cell death, microvesicles and exosomes are produced by cells in normal and stressful conditions. Respectively, these latter classes originate either by directly budding from the cell membrane or through an endosomal pathway. Vesicle classification based on particle size alone is problematic as the diameters of the different vesicles types are on a continuous, overlapping scale. Although described as early as 1946 [3], EVs were often dismissed as degradation products or cellular debris and not identified as vehicles for the horizontal transfer of biomolecules until recently [4]. Early work included ultrastructural studies of subcellular compartments that defined the biogenetic pathways for these particles [5,6] and the 1996 discovery that exosomes can stimulate T-cells through antigen presentation resulted in a broad increase of interest in EV research [7]. This increase in research activity was further cemented by the 2006 finding that EVs contain RNA cargoes [8,9]. The field now enjoys an exponential growth in the number of publications [10] and EVs have now been isolated from an ever-expanding array of biofluids and cell types [1].
Extracellular vesicles derived from cancer-associated fibroblasts induce the migration and invasion of oral squamous cell carcinoma
Published in Journal of Extracellular Vesicles, 2019
Mauricio Rocha Dourado, Johanna Korvala, Pirjo Åström, Carine Ervolino De Oliveira, Nilva K. Cervigne, Luciana Souto Mofatto, Debora Campanella Bastos, Ana Camila Pereira Messetti, Edgard Graner, Adriana Franco Paes Leme, Ricardo D. Coletta, Tuula Salo
In summary, our results show that CAF-EV promotes migration and budding pattern of invasion in OSCC cells. The budding formation may represent the initial steps of the local tumour invasion and could be related to the further development of distant metastases. CAF-EV-treated tumour cells revealed a modified gene expression associated with metabolic pathways and up-regulation of genes associated with tumour invasion such as ROCK2, FLOT1, and FAM129B. These results suggest an active transference of EV cargo from the surrounding stroma to the tumour, and the detailed molecular mechanisms by which this process develops needs to be further investigated.