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Prelabor rupture of the membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Lami Yeo, Francesca Gotsch, Eleazar Soto, Sonia S. Hassan, Juan Pedro Kusanovic, Ray Bahado-Singh
The reliability of lung maturity tests from amniotic fluid collected vaginally has been challenged (198,199). This section reviews the correlation between the L/S ratio and PG results in amniotic fluid obtained by amniocentesis and from the vaginal pool. Shaver and associates compared the phospholipid profile of paired amniotic fluid samples in 28 patients with preterm PROM (192). No significant difference was found in the concentrations of PG, phosphatidylinositol, phosphatidylethanolamine, and phosphatidylserine in amniotic fluid obtained by the two sampling methods. The L/S ratio was higher in fluid collected transvaginally than in fluid collected transabdomin-ally, but this difference did not reach statistical significance. The only phospholipid clearly increased by vaginal contamination was lysolecithin.
Mechanistic Aspects of Neurodegeneration in Alzheimer’s Disease and the Role of Phytochemicals as Restorative Agents
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Anindita Kundu, Vivekananda Mandal, Sujata Wangkheirakpam, Subhash C. Mandal
The internalization and subsequent endosomal trafficking of proteins and membranes along the endocytic pathway is a fundamental cellular process. This was shown to be subject to extensive regulation by phosphoinositides (PIs), phosphorylated derivatives of the minor membrane phospholipid, phosphatidylinositol. The most abundant PI, phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2], serves as an indicator of plasma membrane identity and, combined with cargo proteins, is instrumental in the initiation of clathrin-coated pit (CCP) formation.
Acute Alveolar Injury: Experimental Models
Published in Joan Gil, Models of Lung Disease, 2020
Surface tension might be increased in the lung during injury by reduction in the quantity of surfactant, by intrinsic abnormality of surfactant or by changes induced by components of edema fluid. During acute nitrosourethane injury both profound reductions in the quantity and intrinsic abnormality of the remaining surfactant occur. Changes in quantities of major surfactant phospholipids in alveolar lavage after injury are shown in Table 2 (Liau et al., 1984). Exhaustive lavage was carried out with large volumes of normal saline (10 ml/g normal lung weight) to assure quantitative recovery of phospholipids possibly sequestered in reversibly closed alveoli. Disaturated phosphatidylcholine (DSPC), the major surface active phospholipid decreases to between 20 and 35% of control levels (depending on the dose of nitrosurethane) at peak injury (6-8 days) and returns to about 80% of control levels late in recovery (15-20 days). Total phospholipids, phosphatidylcholine (PC), and phosphatidylethanolamine follow the same pattern but the changes are somewhat smaller. Phosphatidylglycerol (PG) decreases strikingly to about 20% of control at peak injury but, in contrast to PC and DSPC, it remains at this low level during recovery. The quantity of phosphatidylinositol is significantly higher during late recovery (days 15-20) than in controls or at peak injury.
Effect of inflammation on cytochrome P450-mediated arachidonic acid metabolism and the consequences on cardiac hypertrophy
Published in Drug Metabolism Reviews, 2023
Mohammed A. W. ElKhatib, Fadumo Ahmed Isse, Ayman O. S. El-Kadi
In cardiomyocytes, it has been demonstrated that 15-HETE enhances the sensitivity of β-adrenergic response induced by isoproterenol and thus has been suggested to be involved in HF through triggering cardiac fibrosis (Wallukat et al. 1994; Levick et al. 2007; Kayama et al. 2009; Zhang L et al. 2014). It has been demonstrated that norepinephrine evoked its hypertrophic effects by stimulating the production of 15-HETE and 12-HETE (Parmentier et al. 2001). From a mechanistic point of view, 15-HETE is significantly deposited into the cellular pool of phosphatidylinositol. The phosphatidylinositol containing 15-HETE is converted into diacylglycerol substituted with 15-HETE. This particular diacylglycerol could modulate PKC (Wallukat et al. 1994). 15-HETE triggered adventitial fibrosis and phenotypic changes in fibroblasts dependent on TGF-β1 cascade (Zhang L et al. 2014). This is in agreement with a previous study with baicalein, an inhibitor of 12/15-LOX, which ameliorated cardiac fibrosis observed in spontaneously hypertensive rats (Kong et al. 2011). Additionally, wogonin and baicalein, which are 12/15-LOX inhibitors, have been documented to reduce collagen deposition following Ang II treatment (Kong et al. 2010).
Clinical development of an anti-GPC-1 antibody for the treatment of cancer
Published in Expert Opinion on Biological Therapy, 2022
Saikat Ghosh, Pie Huda, Nicholas Fletcher, Douglas Campbell, Kristofer J. Thurecht, Bradley Walsh
Proteoglycans are composed of glycosylated proteins with covalently attached glycosaminoglycan (GAG) chains [1]. In 1990, David et al. reported their seminal investigation of a novel membrane-associated proteoglycan present in human lung fibroblasts [2]. The cDNA of the proteoglycan was cloned and sequenced by the research group and the core protein was found to contain short hydrophobic amino acid sequences at its C-terminus without a proper cytoplasmic domain. Both these features were reminiscent of membrane-bound phosphatidylinositol-anchored proteins. At the time, the process of phospholipid anchoring through an enzyme-catalyzed transamidation reaction was known as glypiation. This led to proposal of the name ‘Glypican’ by David et al. for the newly discovered ‘glypiated proteoglycan.’
Lithium – past, present, future
Published in International Journal of Psychiatry in Clinical Practice, 2020
It has been generally accepted that the most important biochemical mechanisms of lithium action are connected with intracellular signalling, especially, the phosphatidylinositol (PI) system, and with the inhibition by lithium of the glycogen synthase kinase-3beta (GSK-3β) (Brown and Tracy 2013). Lithium inhibits inositol monophosphatase-1 which ameliorates inositol depletion-related mitochondrial dysfunction. Changes in PI signalling measured as a spread of growth cones were postulated to make a common effect of the first generation mood stabilisers (lithium, valproate and carbamazepine) (Williams et al. 2004). Lithium also influences the adenylyl cyclases which convert ATP into cyclic adenosine monophosphate (cAMP), an element of this system being the cAMP response element-binding protein (CREB), the regulator of gene expression. Lithium inhibits another component of intracellular signalling such as protein kinase C (PKC). This mechanism of lithium is shared with another mood-stabilizing drug, valproate, and made a basis to introduce PKC inhibitor, tamoxifen, to the treatment of mania (Palacios et al. 2019).