Radial alveolar count as a tool for the estimation of fetal age

Betz, P.; Nerlich, Andreas G.; Bussler, J.; Hausmann, Roland; Eisenmenger, Wolfgang

doi:10.1007/s004140050030

Cited by 23 publications

(9 citation statements)

References 8 publications

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“…The mean value for RAC is taken as a measure of lung maturation. They found an increase of the mean RAC in relation to gestational age, which has also been confirmed by other studies 61,62 . Askenazi and Perlman 19 used a modification of the method of Emery and Mithal, meaning that they counted the alveolar septi instead of alveoli (RAC alveolar septal count 2 1).…”

Section: Morphometric Radial Alveolar Countsupporting

confidence: 84%

The fetal lung 2: pulmonary hypoplasia

Laudy

Wladimiroff

2000

Ultrasound in Obstet & Gyne

140

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This review describes the pathogenesis of pulmonary hypoplasia and highlights its clinical, radiological and pathologic features, with emphasis on oligohydramniosrelated pulmonary hypoplasia. Since pulmonary hypoplasia may lead to severe respiratory distress immediately after birth and even to neonatal death, an accurate and patient-friendly prenatal test for early detection and distinction between lethal and non-lethal pulmonary hypoplasia is still highly desirable. An extended overview of the proposed methods for the prenatal prediction of pulmonary hypoplasia is presented.

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Section: Morphometric Radial Alveolar Countsupporting

confidence: 84%

The fetal lung 2: pulmonary hypoplasia

Laudy

Wladimiroff

2000

Ultrasound in Obstet & Gyne

140

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“…Reduced RAC and increased L m are potential indications of immaturity of the lung tissue at an age where the lung should have fully mature alveoli. 50,51 The magnitude of the observed changes is consistent with previously reported values from lung diseases, like BPD and chronic obstructive pulmonary disease, and animal models of disease. 52,53 Altered pressure-volume curves and increased compliance in Col6a1 À/À mice (Figure 3) support the finding of simplified parenchymal structure and obstructive lung disease, hallmark pathologic and functional findings in chronic and developmental lung diseases, including BPD.…”

Section: Discussionsupporting

confidence: 90%

Collagen VI Deficiency Results in Structural Abnormalities in the Mouse Lung

Mereness

Bhattacharya

Ren

et al. 2020

The American Journal of Pathology

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Collagen VI (COL6) is known for its role in a spectrum of congenital muscular dystrophies, which are often accompanied by respiratory dysfunction. However, little is known regarding the function of COL6 in the lung. We confirmed the presence of COL6 throughout the basement membrane region of mouse lung tissue. Lung structure and organization were studied in a previously described Col6a1 À/À mouse, which does not produce detectable COL6 in the lung. The Col6a1 À/À mouse displayed histopathologic alveolar and airway abnormalities. The airspaces of Col6a1 À/À lungs appeared simplified, with larger (29%; P < 0.01) and fewer (31%; P < 0.001) alveoli. These airspace abnormalities included reduced isolectin B4 þ alveolar capillaries and surfactant protein Cepositive alveolar epithelial type-II cells. Alterations in lung function consistent with these histopathologic changes were evident. Col6a1 À/À mice also displayed multiple airway changes, including increased branching (59%; P < 0.001), increased mucosal thickness (34%; P < 0.001), and increased epithelial cell density (13%; P < 0.001). Comprehensive transcriptome analysis revealed that the loss of COL6 is associated with reductions in integrin-paxillinephosphatidylinositol 3-kinase signaling in vivo. In vitro, COL6 promoted steady-state phosphorylated paxillin levels and reduced cell density (16% to 28%; P < 0.05) at confluence. Inhibition of phosphatidylinositol 3-kinase, or its downstream effectors, resulted in increased cell density to a level similar to that seen on matrices lacking COL6. (Am J Pathol 2020, 190: 426e441; https:// The extracellular matrix (ECM) is composed of the noncellular components of a tissue and provides multiple critical structural and signaling properties. Major components of the ECM include collagens, proteoglycans, glycoproteins, elastin, and fibronectin. Highly diverse organization of the ECM contributes a broad range of properties, including tissue stiffness and elasticity, to facilitate proper tissue and organ function. 1e3 In addition to structural properties, ECM can provide numerous signaling cues for events, including migration, proliferation, and differentiation, to direct development, healing, and homeostatic conditions. 4,5 This can be accomplished via direct interaction of cells with the matrix or by sequestration and release or presentation of growth factors by the matrix. Disruption of any of the functions of the ECM can be devastating to the tissue and is known to be involved in a multitude of diseases. 6The ECM is known to be critical in the development, organization, and maintenance of lung structure. During development and homeostasis, organization and presence of particular ECM components direct both cellular function and further remodeling and maturation of the matrix by the surrounding cells. This can be due to cell signaling initiated by interaction with matrix components or mechanotransduction, a process by which cells respond to the mechanical forces

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“…In addition, RAC has been reported to correlate well with gestational age (14). In the present study, we used lung-to-body weight ratio to diagnose pulmonary hypoplasia, and found that regardless of pulmonary hypoplasia, there was a strong correlation between RAC and gestational age.…”

Section: Discussionsupporting

confidence: 52%

Expression of Intrapulmonary Surfactant Apoprotein-A in Autopsied Lungs: Comparative Study of Cases with or without Pulmonary Hypoplasia

et al. 2000

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To investigate the functional maturity of the lungs of infants with pulmonary hypoplasia, we measured the expression of surfactant apoprotein-A (SP-A) in the autopsied lungs. Autopsied lungs were taken from 16 infants who died at birth or soon after. A lung-to-body weight ratio of less than 1.2% was defined as pulmonary hypoplasia. Eight infants were classified as belonging to the normal group, and eight as belonging to the pulmonary hypoplasia group. Many of the pulmonary hypoplasia group were complicated not only by pulmonary hypoplasia, but also by amniotic fluid volume abnormalities or an anatomical malformation. We measured the expression of SP-A immunologically using murine anti-human SP-A MAb in the autopsied lung tissue, and subjected the tissue to SP-A staining by the direct staining method. The expression of SP-A was assessed as one of four grades: Ϫ, Ϯ, 1ϩ, 2ϩ. The staining intensity of SP-A was high at 1ϩ or stronger in five infants of the normal group. SP-A expression was significantly reduced, however, in all infants of the pulmonary hypoplasia group except for one infant with normal amniotic fluid volume and relatively mild pulmonary hypoplasia. There was a significant negative correlation between the staining intensity of SP-A and two factors: pulmonary hypoplasia and abnormal amniotic fluid volume (p ϭ 0.039 and p ϭ 0.0063, respectively). In the present study, we demonstrated that SP-A expression was significantly reduced in infants with pulmonary hypoplasia. We speculate that the functional maturity of the lungs of infants with pulmonary hypoplasia is also suppressed. The alveolar lining is composed of type I and type II epithelial cells. Human pulmonary surfactants are lipid-protein complexes (lipoproteins) synthesized in type II cells. These surfactants are secreted into the alveolar space in order to cover the surface of alveoli and thus reduce alveolar surface tension. The functional expression of pulmonary surfactants requires specific proteins (apoproteins). To date, four types of surfactant apoproteins (SP) have been identified: SP-A, SP-B, SP-C, and SP-D. Of these, SP-A is the most prevalent form of SP (1). SP-A is a hydrophilic glycoprotein with a molecular weight of approximately 28 -36 kD, and the level of SP-A in the amniotic fluid, gastric juice, and respiratory aspirate is a useful indicator of the functional maturity of fetal and neonatal lung tissue (2, 3).In the present study, to assess the functional maturity of the lungs of infants with pulmonary hypoplasia, we measured the expression of SP-A immunohistologically using murine antihuman SP-A MAb in the autopsied lungs of infants who died at birth or soon after. METHODS Subjects.Autopsied lungs were taken from 16 infants at some point during a 21-y period between November 1976 and February 1998. Of the 16 infants, 14 came from the Division of Neonatal Intensive Care or the Department of Gynecology and Obstetrics at our hospital. These subjects had died at birth or within 5 d of birth. The remaining two infants came from the Neo...

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Radial alveolar count as a tool for the estimation of fetal age

Cited by 23 publications

References 8 publications

The fetal lung 2: pulmonary hypoplasia

The fetal lung 2: pulmonary hypoplasia

Collagen VI Deficiency Results in Structural Abnormalities in the Mouse Lung

Expression of Intrapulmonary Surfactant Apoprotein-A in Autopsied Lungs: Comparative Study of Cases with or without Pulmonary Hypoplasia

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