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Cystic Fibrosis and Pancreatic Disease
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Elissa M. Downs, Jillian K. Mai, Sarah Jane Schwarzenberg
CF is an autosomal recessive, genetic multi-system disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR gene produces protein that functions as a channel across the membrane of cells that produce bodily secretions such as mucus, sweat, saliva, and digestive enzymes. Since this channel transports chloride ions into and out of cells, it controls the flow of water and hence the amount of liquid in these bodily secretions. Mutations in the gene lead to defective proteins that prevent the flow of chloride and of water producing abnormally thick mucus. These mutations are classified by the part of the protein pathway that is defective (see Table 19.1) and lead to varying phenotypes of disease. These are responsible for the prominent pulmonary and gastrointestinal manifestations. The most common mutation is F508del that leads to an abnormally folded CFTR protein.
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Chloride: In human physiology, chloride ions help in the maintenance of regulating fluid balance, blood volume, electrolyte homeostasis, intracellular and extracellular fluid homeostasis, blood pressure, preservation of electrical neutrality, and pH of body fluids in a human body.125–127 The chloride ion is an important biomarker for a vast range of clinical conditions and, as a routine practice, is analytically determined in the sweat, urine, feces, and blood. Following intake of edible salt from diverse food sources, a human body gets chloride, which is absorbed in the intestine, while the excess amount gets excreted in the urine.125–128 However, excessive chloride levels indicate serious metabolic disorders, including metabolic acidosis or alkalosis, and a disruption in chloride channel expression and function, leading to multiple diseases and disorders in diverse organs.126–128
Release of Nickel Ion from the Metal and Its Alloys as Cause of Nickel Allergy
Published in Jurij J. Hostýnek, Howard I. Maibach, Nickel and the Skin, 2019
Jurij J. Hostýnek, Katherine E. Reagan, Howard I. Maibach
Definition and thereby reconstitution of human sweat in absolute terms is not feasible because of variability in its composition and pH. Gender differences are marked, and fluctuations occur due to environmental as well as subjective, endocrine factors. Most striking are changes in composition due to the rate of sweat secretion. Sodium and chloride content, one decisive factor in the corrosivity of sweat, is low under quiescent conditions due to the reabsorption (conservation) mechanism before sweat reaches the ostium of the sweat duct (Cage and Dobson, 1965). Sodium ion level can be as low as 1.7 meq/1 and chloride ion 2.8 meq/1 (Grice et al., 1975). As sweating rate increases, that control mechanism is overwhelmed and the salt concentration can rise, approximating or even exceeding that in plasma (Guyton, 1991).
Emerging strategies in nanotechnology to treat respiratory tract infections: realizing current trends for future clinical perspectives
Published in Drug Delivery, 2022
Minhua Chen, Zhangxuan Shou, Xue Jin, Yingjun Chen
Cystic fibrosis (CF) is a fatal chronic pulmonary infection that occurs due to a defect in transmembrane protein which is known as cystic fibrosis transmembrane conductance regulator (CFTR) which regulates chloride ion secretion (Winstanley et al., 2016). The chloride ion imbalance decreased the volume of surface liquid in the airways, mucus dehydration, and lessens mucus clearance which eventually leads to the secretion and accumulation of viscous mucus in the airways and causes bronchial obstruction (Ong et al., 2019). In the early stages of the disease, S. aureus and H. influenzae are found in abundance whereas, in the advance stages P. aeruginosa, Burkholderia cenocepacia, Stenotrophomonas maltophilia, and Achromobacter xylosoxidans are found profusely (Klinger-Strobel et al., 2015). P. aeruginosa infection is mostly accountable for most of the premature deceases of CF patients (De Boeck, 2020). Thus, inhibiting chronic colonization caused by P. aeruginosa is the key aim for the early treatment of CF. The lungs of CF patients even after receiving antibiotic regimens and aerosolization of tobramycin are persistently colonized by P. aeruginosa (Moreau-Marquis et al., 2008). To improve the chloride ion transport functions, CFTR modulators, i.e. ivacaftor, lumacaftor, and tezecaftor have been used. However, refinement in toxicity, specificity, and adverse effects is required to expand the use and effectiveness of these medicines (Robinson et al., 2018).
Study of FA12 peptide-modified PEGylated liposomal doxorubicin (PLD) as an effective ligand to target Muc1 in mice bearing C26 colon carcinoma: in silico, in vitro, and in vivo study
Published in Expert Opinion on Drug Delivery, 2022
Atefeh Biabangard, Ahmad Asoodeh, Mahmoud Reza Jaafari, Mohammad Mashreghi
The best docking complexes regarding binding energy among all peptides were selected for further MD simulations. Simulations were performed using the GROMACS 5.1.1 package [29] with the GROMOS96 43a1 force field. First of all, the peptide-protein complex was embedded into a cubic box of TIP3P water, which extended to a10 Å between the protein and the box edge. The chloride ion (Cl−) was added to neutralize the system. The particle mesh Ewald (PME) method [30] and SHAKE algorithm [31] were used during the simulation. In all directions, periodic boundary conditions were applied. Initially, the system was subjected to energy minimization using the steepest descent technique, which was set to a maximum of 1000 kJ/(mol∙nm). After 50,000 steps minimization, the system was equilibrated during 100 ps under a constant volume ensemble (NVT) with a position restraint on all water oxygen. The time step for the simulation was set to 2 fs. Afterward, constant pressure simulations (NPT) were run for 1 ns and maintained at 300 K and a pressure of 1 bar. Finally, the productive MD simulations (without positional constraints) of 100 ns were performed on the whole system (T = 300 K and P = 1 bar). All covalent bonds to hydrogen atoms were constrained using the default linear constraint solver (LINCS) algorithm [32].
Ketamine, at low dose, decrease behavioural alterations in epileptic diseases induced by pilocarpine in mice
Published in International Journal of Neuroscience, 2020
Fatma Tannich, Kamel Barhoumi, Ahmed Rejeb, Mohamed Aouichri, Ouajdi Souilem
Histological observations revealed the presence of neuronal degeneration especially in cortical layers and the CA3 region of the hippocampus in epileptic animals and massive gliosis observed especially in the cortex. These histological findings are similar to those revealed by Curia and Russo [22,23]. In our study, differences in staining intensity are due to the presence of oedema, especially, in the sub-area of the granular layer in the (DG) [5]. Against, the neuronal damage is not found in any of the animals treated with ketamine. Toxicity induced by the glutamate, during epilepsy, may be due to excessive and uncontrolled influx Ca2+ into the cell. This calcium influx, leads to mitochondrial alterations leading to apoptosis and inducing cell damage [24]. In addition, depolarization leads to the blockade of sodium channels and thus to a further increase of sodium influx. The ionic balance is restored by a passive influx of chloride ions. Thus, hyperosmolarity leads to cell lysis by important water influx into the cell. During neuronal degeneration, glial cells proliferate and migrate to lesion sites and contribute to the amplification of cellular damage by releasing of neurotoxic molecules and pro-inflammatory cytokines [25]. It appears, from this histological study, that administration of ketamine limited brain oedema in the hippocampus and different cortical layers. Loss and De Oliveira [15] demonstrated that the blockade of NMDA receptors by ketamine prevents metabolic events leading to induced neuronal death during SE in all brain regions.