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The diagnosis and management of preterm labor with intact membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Tinnakorn Chaiworapongsa, Francesca Gotsch, Lami Yeo, Ichchha Madan, Sonia S. Hassan
Amniotic fluid can also be tested for fetal lung maturity. This can be done with the standard tests, including the lecithin/sphingomyelin (L/S) ratio, phosphatidylglycerol, TDx-FLM surfactant albumin ratio, and lamellar body count. In the presence of lung maturity, heroic measures with aggressive tocolysis should be considered carefully.
The Use of Tracers in Transport Studies
Published in Joan Gil, Models of Lung Disease, 2020
Maya Simionescu, Nicolae Ghinea
Type II epithelial cells are bona fide secretory cells that produce and actively secrete surfactant components by exocytosis into the air space. Lamellar body membrane fuses with the apical cell plasmalemma and upon fission the lamellae are extruded extracellularly. To maintain the balance in the distribution of membranes among the the participants in the exocytotic process, an almost comparable amount of membrane must be internalized from the cell surface.
The Role of Biological Lipids in Skin Conditioning
Published in Randy Schueller, Perry Romanowski, Conditioning Agents for Hair and Skin, 2020
Since its earliest descriptions (reviewed in Ref. 7), hypotheses have abounded about the function of the epidermal lamellar body. These ellipsoidal organelles, measuring about 'A X '/a appear initially in the first supra basal cell layer, the stratum spinosum, and continue to accumulate in the stratum granulosum, accounting for about 10% of the volume of the granular cell cytosol. In the outer granular layer, lamellar bodies move to the lateral and apical surfaces, where they are poised to undergo rapid exocytosis (8,9). The lamellar body contains parallel membrane stacks enclosed by a limiting trilaminar membrane. Whereas each lamella appears to be a "disk" in cross sections, with a major electron-dense band separated by electron-lucent material divided centrally by a minor electron-dense band, recent studies have shown instead that lamellar body contents comprise a single membrane structure folded in an accordion-like fashion.
Regulation of the autophagy plays an important role in acute kidney injury induced acute lung injury
Published in Renal Failure, 2022
Ruolin Wang, Siheng Shen, Luyong Jian, Shuhua Liu, Qi Yuan, Huahui Guo, Jiasheng Huang, Penghui Chen, Renfa Huang
According to previous studies, the autophagosome can be identified by the limiting membrane that is partially visible as two bilayers separated by a narrow electron-lucent cleft. The observations from TEM detection revealed that the autophagosomes are formed in the cells of the tissues of both renal and lung after IRI, accompanied by serious pathological changes in renal tissues. The nucleus was deformed and the epithelial cells had fallen off. However, the lipid droplets and vacuoles were occasionally observed in the cells. The pathological changes in the lung tissues were more serious, with the necrosis and deformation of the nucleus, large cell gaps, and lamellar body vacuoles. Furthermore, compared to that of rats from the IRI group, more autophagosomes were observed in the IRI rats treated with RA, while almost no autophagosomes were observed in the rats from the sham group. Additionally, compared to that of the rats from the IRI group, the rats of the 3-MA group showed significantly decreased amount of the autophagosomes, while tissue lesions were dramatically serious. The results showed the same trend at all time points (Figure 1).
Continuous positive airway pressure affects mitochondrial function and exhaled PGC1-α levels in obstructive sleep apnea
Published in Experimental Lung Research, 2021
Ching-Chi Lin, Wei-Ji Chen, Yi-Kun Sun, Chung-Hsin Chiu, Mei-Wei Lin, I-Shiang Tzeng
Lacedonia et al. showed that the Mt/N DNA ratio is higher in subjects with OSA than in control subjects. Oxygen metabolites are higher in subjects with OSA and positively correlate with the ratio of Mt/N DNA.27 Ultrastructural changes characterized by mitochondrial swelling, lamellar body degeneration, and remodeling around the perivascular and peri-bronchial space were observed in the lungs of a canine model of OSA.28 Mice used as a model of chronic intermittent hypoxia display increased expression of voltage-dependent anion channels, impaired hearing ability, and decreased abundance and abnormal morphology of hair-cell mitochondria. The mRNA levels of PGC1-α are also higher in mice with chronic intermittent hypoxia.13 In this study, the Mt/N DNA ratio and protein levels of PGC1-α in the EBC of subjects with OSA before CPAP treatment were higher than those in controls and were restored after CPAP treatment. Our results indicate that before CPAP, OSA has mitochondrial dysfunction in the upper respiratory tract. Effective CPAP treatment can restore mitochondrial function and the protein levels of PGC1-α in the EBC in the upper respiratory tract.
Advances in understanding of Netherton syndrome and therapeutic implications
Published in Expert Opinion on Orphan Drugs, 2020
Evgeniya Petrova, Alain Hovnanian
At the structural level, KLKs hyperactivity causes premature desquamation by cleavage of corneodesmosin and the corneodesmosomal cadherins Desmoglein 1 (DSG1) and Desmocollin 1 (DSC1) [37,53–55], proteolytic processing of pro-Filaggrin [56] and degradation of Filaggrin [27,28]. Furthermore, cleavage of DSG3 and DSG4 by KLK14 contributes to hair abnormalities and alopecia [48]. KLKs regulate stratum corneum lipid permeability barrier, hence transepidermal water loss, by proteolytic degradation of the lipid-processing enzymes β-Glucocerebrosidase and Acid sphingomyelinase [57,58]. Furthermore, by activating PAR-2 receptor, KLKs downregulate lamellar body secretion by corneocytes [59]. This correlates with observations of altered intercellular lipid composition and altered expression of lipid-processing enzymes as well as abnormal lipid organization in the stratum corneum of NS patients [60,61]. Epidermal Elastase 2 is also involved in the induction of lipid abnormalities as transgenic ELA2 mice lack lipid lamellae in the extracellular space of the cornified layer [43]. Altered lamellar body secretion in Netherton syndrome leads to absent or irregular lipid inter-corneocyte lamellae [62] Figures 3.