China 
Africa 
Explore chapters and articles related to this topic
Biological Responses of Mobile Phone Frequency Exposure
Published in Jitendra Behari, Radio Frequency and Microwave Effects on Biological Tissues, 2019
The tight junctions, which seal the endothelial cells together, limit paracellular leakage of molecules. A bilayered basal membrane supports the ablumenal side of the endothelial cells. The glial astrocytes, surrounding the surface of the basal membrane cells, are important for the maintenance, functional regulation, and repair of the BBB. The protrusions of the astrocytes, called end feet, cover the basal membrane on the outer endothelial surface and thus form a second barrier to hydrophilic molecules and connect the endothelium to the neurons. About 25% ablumenal membrane of the capillary surface is covered by pericytes (Frank et al. 1987), which are a type of macrophages. Seemingly, they are in the position to significantly contribute to the central nervous system (CNS) and immune mechanisms (Thomas 1999). Also, perivascular structures such as astrocytes and pericytes as well as a bilayered basal membrane help maintain the BBB (Salford et al. 2007).
Conducting and Conjugated Polymers for Biosensing Applications
Published in John R. Reynolds, Barry C. Thompson, Terje A. Skotheim, Conjugated Polymers, 2019
C. Pitsalidis, A.M. Pappa, C.M. Moysidou, D. Iandolo, R.M. Owens
In the case of electrically inactive (non-electrogenic) cells, electronic measurements can be used to estimate surface coverage and cell viability as well as their differentiation. This technique is based on the electrical impedance spectroscopy developed by Giaever and Keese.166 This technique has also been adapted to evaluate the integrity of a specific type of tissue (composed of certain epithelial and endothelial cell types) that in vivo serve as physical barriers by tightly controlling ionic flux. Ion transport in between cells (paracellular ion flux) is regulated by protein structures known as tight junctions, the state of their functionality providing information about barrier tissue and indicative of certain disease states. Thus, by measuring the electrical resistance (transepithelial/endothelial resistance) of a specific cell layer upon its treatment with specific drugs/toxins, one can derive knowledge on the effect of the applied compounds on the investigated barrier tissues. Interestingly, these kinds of measurements have significant advantages over traditional assays, such as a lactate dehydrogenase assay used to evaluate toxicity, thanks to improved temporal resolution, dynamic measurements and enhanced sensitivity.
Centralized Endothelial Mechanobiology, Endothelial Dysfunction, and Atherosclerosis
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Ian Chandler Harding, Eno Essien Ebong
Cell-to-cell junctions are prime examples of decentralized mechanotransduction structures. They contain a variety of multiprotein complexes that are used to maintain contact between neighboring cells and to support physiological functions such as paracellular permeability and cell-to-cell communication. The major complexes at cell-to-cell junctions are adherens junctions, tight junctions, and gap junctions. Adherens junctions are protein complexes that create extracellular bridges between neighboring cells, initiate and stabilize cell-to-cell contact, and affect cellular processes such as intracellular signaling and transcriptional regulation [153]. Adherens junctions are formed by the transmembrane protein vascular endothelial cadherin (VE-cadherin) (Figure 7.4), which is then attached to the actin cytoskeleton through a series of catenin family proteins [154]. Another cell-to-cell junction, tight junctions, help regulate paracellular permeability. They are mainly composed of two transmembrane proteins, occludins and claudins, which are similarly linked to the actin cytoskeleton by linker proteins, mainly the zonula occludens (ZO) proteins 1, 2, and 3 (ZO-1, ZO-2, and ZO-3) [153]. Lastly, gap junctions are intercellular channels created by proteins called connexins [155]. These proteins allow for the diffusion of ions and small molecules, thereby allowing cellular communication [155]. Additionally, the aforementioned junctions and proteins are accompanied by other junctional proteins such as platelet endothelial cell adhesion molecule-1 (PECAM-1), which can both bridge ECs and serve as an anchor for circulating platelets and blood cells.
Microplastics and human health: Integrating pharmacokinetics
Published in Critical Reviews in Environmental Science and Technology, 2023
The main routes of exposure to microplastics for humans consist of ingestion, inhalation, and dermal contact. The digestive system is important in the digestion and absorption of nutrients and electrolytes, which occur mainly in the small intestine. The small intestine may also play an important role in the absorption of microplastics (Figure 1). Contact of microplastics with the intestinal mucosa is dependent on their ability to cross the intestinal mucus, facilitated through a formation of a corona of organic matter or intestinal contents (Powell et al., 2007) or due to small particle sizes (Szentkuti, 1997). After crossing the intestinal mucus, particles come in contact with the intestinal epithelium, being internalized by the following mechanisms: (i) transcytosis, the uptake and transport of smaller particles by enterocytes; (ii) internalization by M cells (e.g. micropinocytosis, phagocytosis, and receptor-mediated endocytosis) or other cells in the intestinal mucosa adjacent to Peyer’s patches; (iii) paracellular transport, through gaps between cells dependent on concentration gradients and particle sizes, increasing when tight junction integrity is compromised; (iv) persorption through gaps in the villi during cell turnover (desquamation zones), openings of tight junctions during the migration of macrophages, or damage to the epithelium (e.g. erosion and ulceration), for larger particles (e.g. 7–70 µm); (v) uptake by migratory phagocytes (e.g. intestinal macrophages and dendritic cells) directly from the intestinal lumen (Delon et al., 2022).
Biopolymeric nanocarrier: an auspicious system for oral delivery of insulin
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Suchitra Kumari Panigrahy, Awanish Kumar
The translocation mechanism of nanocarriers in the intestinal epithelium involves either paracellular or transcellular transport.a) Paracellular pathway: It is the preferred route for the transport of hydrophilic drugs. However tight junction between the epithelial cells restricts or blocks the passage of macromolecules or particles larger than 1 nm [5]. Therefore, as is widely recognized, polymeric NPs cannot diffuse through the intestinal barrier via the paracellular route. So to enhance paracellular transport of nanocarriers, tight junctions opened reversibly by using permeation enhancers such as cationic (Chitosan and its derivatives) and anionic (polyacrylic acid and its derivatives) polymers or calcium chelators [82]. The cationic and anionic polymers disassemble tight junctions whereas calcium chelators disrupt adherence and tight junctions by activating protein kinase C [71]. But it still limits the transport of nanoparticles larger than 20 nm into the bloodstream [96].b) Transcellular pathway: Nanocarriers can be taken up by enterocytes or M cells of Peyer’s patches in this pathway by overcoming pre-systemic hepatic metabolism leading to increased drug bioavailability. Due to their larger size nanocarriers cannot diffuse through cells by passive diffusion. So the active transcellular transport begins with an endocytic process that occurs at the apical cell membrane; then the particles are transported through the cells and release at their basolateral pole [13].
Toxicological and pharmacokinetic properties of sucralose-6-acetate and its parent sucralose: in vitro screening assays
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Susan S. Schiffman, Elizabeth H. Scholl, Terrence S. Furey, H. Troy Nagle
The assessment of transepithelial electrical resistance (TEER) and permeability in human transverse colon epithelium in the current in vitro study found that sucralose-6-acetate and sucralose both disrupt gastrointestinal epithelial tight junctions and mucosal barrier function at mM concentrations in the absence of bacteria. A significant collapse of TEER occurred after a single 24-hr exposure to 40 mM sucralose which is only 6.7-fold greater than the concentration of sucralose currently approved by the European Union (2004) for use in a single syrup-type food supplement at 2400 mg/kg (6 mM). Integrity of the intestinal epithelial barrier is dependent upon tight junctions, the specialized complexes which connect adjacent cells and provide a physical and functional barrier that limits or regulates passive diffusion of ions, solutes, macromolecules, and cells from the lumen through the paracellular space. Sucralose-6-acetate and sucralose reduced the transepithelial resistance and enabled ions and macromolecules to pass from the apical (luminal) to the basolateral side of intestinal epithelium through the paracellular pathways. Enhanced intestinal permeability (leaky gut) that enables passage of microorganisms and metabolites into the body plays a major role in IBD (Lee 2015; Welcker et al. 2004), chronic liver disease (Mohandas and Vairappan 2017), as well as pathogenesis of colorectal cancer (Sánchez-Alcoholado et al. 2020). Further, elevated intestinal permeability in conjunction with repeated ingestion and retention of colonic contents over days may increase intraluminal concentration, absorption, and systemic exposure to sucralose and sucralose-6-acetate resulting long-term in bioaccumulation and toxicity.