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Fetal and neonatal medicine
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
4.17. Which of the following statements is/are correct for the newborn?More than 90% of surfactant phosphatidylcholine (PC) is recycled.There is very little catabolism of exogenously adminstered PC.Exogenously administered PC is recycled like endogenously produced PC.Surfactant protein A is essential for surfactant biophysical properties.Surfactant proteins Β and C enhance the spread of phospholipids at the air-liquid interface of alveoli.
Mechanical Properties of the Lungs
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Phospholipids are present in abundance in surfactant; the charged choline ends are polar and hydrophilic and lie within the fluid lining the alveolus, while the hydrophobic fatty acid chains project into the alveolar gas. Some 90% of surfactant is lipid, with most being phospholipid, but some is cholesterol. The main lipid content is dipalmitoyl phosphatidyl choline, with significant amounts of phosphatidyl glycerol. Proteins which comprise 2%–8% of surfactant include surfactant protein (SP)-A, SP-B, SP-C and SP-D. SP-A is a large glycoprotein which regulates the turnover of surfactant and interacts with the other components of surfactants to lower surface tension.
Asphyxia-triggered Inflammatory Reaction Patterns of the Lung
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Ewgenija Gutjahr, Burkhard Madea
Suffocation, causing an interruption of the air flow and various processes of counter-regulation, is associated with strong forced breathing and an over-excitement of the autonomic nervous system by mechanical asphyxia [40], requiring an alveolar surface integrity. In human lungs, the pulmonary surfactant protein A (SP-A), produced by type II alveolar cells, serves as a film on the surface of the alveoli to reduce the tension and to facilitate their unfolding during breathing. Consequently, its secretion is increased under hypoxic conditions, causing a respiratory deficiency syndrome in case of its deficiency. The usefulness of SP-A as a practical diagnostic marker of fatal mechanical asphyxia in forensic autopsy cases was investigated by Zhu et al. [40]. In their study, they proved a significantly increased intensity of SP-A staining in the intra-alveolar space, accompanied by many massive aggregates in approximately 60 per cent of 27 asphyxia cases, findings not observed in the control group of 16 cases of poisoning and peracute deaths [40]. Cecchi et al. [8] confirmed the same tendency for the formation of massive intra-alveolar precipitates of SP-A in 32.4 per cent of cases of mechanical asphyxia (grade III) compared to 18.4 per cent of control cases (grade I).
A study of pneumoproteins in crystalline silica exposed rock drillers
Published in Inhalation Toxicology, 2022
Dag G. Ellingsen, Bente Ulvestad, May Britt Lund, Nils Petter Skaugset, Liv Ingunn Bjoner Sikkeland
Pneumoproteins are regarded as markers of lung injury and inflammation. Surfactant protein (SP) A (SP-A) and SP-D are mainly synthesized in alveolar type II cells (AT II) and catabolized by alveolar macrophages (AMs) and AT II (Ikegami 2006; Han and Mallampalli 2015). SP-A and SP-D have a multitude of functions, e.g. the ability to recognize and bind pathogens, attach the opsonized pathogens to phagocytic cells, and to reduce inflammation through a number of cellular receptors (Sorensen 2018; Watson et al. 2019). SP-D has also important roles in maintaining pulmonary surfactant, as shown by increased alveolar and tissue phosphatidylcholine and increased number of foamy macrophages in SP-D deficient mice (Botas et al. 1998; Korfhagen et al. 1998). One important role of SP-A in the homeostasis of surfactant is to promote surfactant uptake by pneumocytes (Nathan et al. 2016; Olmeda et al. 2017). Club cell protein 16 (CC-16) is synthesized in CCs present throughout the respiratory tract with the highest density in the respiratory bronchioles. Anti-inflammatory properties of CC-16 have been shown in mice (Laucho-Contreras et al. 2016).
Bioinspired polymer nanoparticles omit biophysical interactions with natural lung surfactant
Published in Nanotoxicology, 2019
Moritz Beck-Broichsitter, Adam Bohr
A direct interaction of the plain PLA nanoparticles with essential components of lung surfactant (Hu et al. 2013, 2017), such as hydrophobic surfactant proteins (Raesch et al. 2015; Kumar et al. 2016; Whitwell et al. 2016) (no relevant depletion of the PL content and/or conversion of LSA to less surface active SSA was detected) provoked the observed dysfunction of the lung surfactant preparation. A decline of the “free” surfactant proteins B and C content caused a distinct architecture of the lung surfactant “machinery” at the air/liquid interface having less favorable biomechanical properties (Beck-Broichsitter et al. 2014b), with surfactant protein C showing slightly higher adsorption tendency toward the plain PLA nanoparticles (Figure 1(B)). Consequently, γads and γmin values of up to ∼30 and >10mN/m, respectively, were registered for LSA in the presence of plain PLA nanoparticles. Such drastic shifts in composition and biophysical function of lung surfactants are usually only seen for severe airway diseases (Zuo et al. 2008; Griese 1999).
Genetic Testing Is Messier in Practice than in Theory: Lessons from Neonatology
Published in The American Journal of Bioethics, 2022
Katharine Press Callahan, Chris Feudtner
Let’s make these issue more concrete. Consider a neonate with congenital diaphragmatic hernia, an anomaly with high associated mortality and morbidity. Suppose that this patient is sicker than most patients with the same anomaly, prompting physicians to order whole genome sequencing. Testing reveals an uncertain but possibly pathogenic variant in a gene encoding a surfactant protein, and other mutations in this gene are known to cause respiratory distress of varying severity. Is this patient’s genetic mutation the reason his illness is more severe than other patients with the same anomaly? Should the finding of uncertain meaning change acute medical management, or influence the decision about whether the patient is a candidate for extracorporeal membrane oxygenation?