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Dermal filler complications and management
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The complement system is comprised of approximately thirty proteins which are synthesised by the liver and are permanently in circulation in blood plasma. When complement proteins are triggered by microbial antigens, a cascade of events is initiated with the intention of destroying pathogens through phagocytosis, cytolysis and inflammation. Phagocytosis is triggered via a process called opsonisation, where opsonin proteins are used to mark infected or dying cells to be phagocytosed. Cytolysis occurs through the formation of the membrane attack complex (MAC) which effectively punches a hole within the plasma membrane of bacteria, causing them to rupture due to an inflow of extracellular fluid. Finally, inflammation is stimulated by the binding of complement proteins to mast cells to encourage them to secrete histamine which increases blood vessel permeability to allow cells of the immune system to extravasate and reach the target area.
Celiac disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
In the normal human small intestine, three major lineages of IELs participate in the defense of the mucosal surface. The most prominent IEL is the cytolytic CD8αβ+CD4− T-cell receptor (TCR) αβ population (IE-CTLs); CD4+ TCRαβ+ and TCRγδ+ populations are also present. The IE-CTLs in humans simultaneously encompass characteristics of conventional adaptive T cells (expression of heterodimeric CD8αβ coreceptor and antigen-driven variable T-cell receptors) and innate T cells (expression of natural killer receptors recognizing inducible nonclassical major histocompatibility complex [MHC] class I molecules). Interestingly, unlike in the peripheral blood and the liver, human IELs selectively express natural killer (NK) receptors of the C-type lectin family. The most represented natural killer receptors are NKRP1-A, receptors of the CD94/NKG2 family, and the NKG2D receptor. Under physiologic conditions, IELs express high levels of inhibitory CD94/NKG2A receptors and low levels of activating NKG2D receptors. As IELs are effector cells, they can exert TCR-mediated cytolysis ex vivo. However, the level of cytolysis is low in the absence of additional stimuli. Furthermore, the IELs cannot kill NK cell targets.
Effector Mechanisms for Macrophage-Induced Cytostasis and Cytolysis of Tumor Cells
Published in Gloria H. Heppner, Amy M. Fulton, Macrophages and Cancer, 2019
Carleton C. Stewart, Anita P. Stevenson, John Hibbs
In the previous section we discussed the kinetics of cytolysis. Prior to cell death, however, activated macrophages induce tumor cell cytostasis. In addition, some tumor cell phenotypes may not progress to cytolysis after developing cytostasis.36 A major question, which has eluded an answer, is whether cytostasis is concomitant with, independent of, or a prerequisite for cell death. Current dogma also holds that macrophages kill neoplastic and transformed cells but spare normal cells. In a review of the literature, we were unable to find any reports on whether macrophages caused cytostasis in normal cells. Accordingly, we designed experiments to determine if macrophages inhibit the progression through the cell cycle of normal fibroblasts even though they do not kill them.49
Mass spectrometry-based clinical proteomics – a revival
Published in Expert Review of Proteomics, 2021
Inconsistency between findings from different labs seems to obstruct the validation of biomarker leads via MS-based proteomics [4]. Proteins come in many forms and abundances, and reside in distinct locations. Surface proteins, for example, are valuable for diagnosis as they can mark specific cells. However, these proteins are often firmly embedded in hydrophobic bilayers and can be troublesome to identify by MS-based proteomics [5]. For patient comfort, diagnostic tests are ideally performed on liquid biopsies, containing functional proteins, vesicles and cytolysis proteins. Diagnostic proteins are often hidden in the bulk of high-abundant, functional proteins, evading identification when not enriched. Protocols optimized for detecting (sub)sets of proteins systematically exclude large sets of proteins presuming they are of little importance to the phenotype, thus possibly creating a biomarker blind spot. Further, such protocols often transfer poorly to other labs and multiple entry points exist for variability to sneak in, during either sample preparation, data acquisition or data analysis [6].
Contributions of caspase-8 and -9 to liver injury from CYP2E1-produced metabolites of halogenated hydrocarbons
Published in Xenobiotica, 2018
Yoshio Ijiri, Ryuji Kato, Maiko Sadamatsu, Mina Takano, Yuki Yasuda, Fumiaki Tanaka, Chiyo Oishi, Hideki Imano, Yoshikatsu Okada, Kazuhiko Tanaka, Tetsuya Hayashi
Liver histological findings reported in Figure 1(C) were examined under light microscopy by HE staining at 6, 12 and 24 h after treatment. The liver tissues obtained from the control rats appeared normal (Figure 1C, Control). No major abnormalities were found in the liver tissues 6, 9 and 12 h after CCl4 administration (data not shown). However, centrilobular hepatocyte necrosis was observed 24 h after CCl4 administration (Figure 1C, CCl4). Many cells exhibited enucleation and nuclear fragmentation, and became crescent-shaped. Cytolysis and cellular degeneration were also observed in CCl4-induced liver injury. No infiltration of inflammatory cells such as lymphocytes was observed 24 h after CCl4 administration. In the halothane 1 ml/kg group, whole liver injury was observed, while the 2 ml/kg group exhibited extensive hepatocyte necrosis (Figure 1C, Halothane). No pathological changes were observed in the sevoflurane (1, 2 and 4 ml/kg) groups (Figure 1C, Sevoflurane).
Methotrexate enhances oxidative stress, apoptosis, and ultrastructural alterations in the placenta of rat
Published in Ultrastructural Pathology, 2022
Amany Mohamed Shalaby, Khalid Mohammed Mohammed Albakoush, Mohamed Ali Alabiad, Mohammed Alorini, Fatima A. Jaber, Mahmoud Ramadan Elkholy, Shereen Elsayed Tawfeek
Cystic degeneration of glycogen cells in the MTX-exposed placenta detected in our study was distinguished by aberrant preservation of large amounts of cytoplasmic vacuolation of glycogen cells. Eosinophilic fibrinous material was found in these vacuoles. The degraded cells underwent cytolysis and then coalesced into a series of giant cysts filled with a homogenous acidophilic mass, many leftover glycogen clusters, erythrocytes, macrophages, and cell debris. These degraded cells did not regress. Although in normal development, the majority of glycogen cells vanish at the completion of pregnancy.2 In animal studies, many substances cause the cystic degeneration of glycogen cells, such as 6-mercaptopurine14 and streptozotocin.21