Birth Defects Research Part A: Clinical and Molecular Teratology

Cover image for Vol. 100 Issue 6

Edited By: Michel Vekemans

Impact Factor: 3.146

ISI Journal Citation Reports © Ranking: 2012: 17/41 (Developmental Biology); 24/85 (Toxicology)

Online ISSN: 1542-0760

Associated Title(s): Birth Defects Research Part B: Developmental and Reproductive Toxicology, Birth Defects Research Part C: Embryo Today: Reviews

Featured

  • Paracrine cellular and extracellular matrix interactions with mesenchymal progenitors during pulmonary alveolar septation

    Paracrine cellular and extracellular matrix interactions with mesenchymal progenitors during pulmonary alveolar septation

    Alveolar cellular interactions during septal formation. A schematic diagram of developing alveolar sacs showing the predominant cell-types and peptide-growth factors and extracellular matrix molecules, which are most relevant to this review. The prenatal saccule transitions to the alveolar duct at birth and subdivides into alveoli through secondary septal elongation. The alveolar duct-alveolar junction is subjected to greater mechanical tension than the basilar portions of the alveoli and is more richly endowed with elastic fibers. Paracrine interactions between interstitial fibroblasts and lipid interstitial fibroblasts, pericytes and capillary endothelium, and between lipid interstitial cells and alveolar type 2 cells (AT2) are shown with red double arrow heads. Budding septa progressively elongate as interstitial fibroblasts are repositioned and remodel the extracellular matrix through peptide growth factors such as transforming growth factor-β (TGFβ). AT1, alveolar type 1 cell; AT2, alveolar type 2 cell; VEGF, vascular endothelial growth factor; PDGF-A, platelet derived growth factor-A, TGFβ transforming growth factor-β. Several peptide growth factors which are discussed in the review are shown interacting with target cells. Red double-headed arrow shows paracrine cellular interactions.

  • Assessment of inhibited alveolar-capillary membrane structural development and function in bronchopulmonary dysplasia

    Assessment of inhibited alveolar‐capillary membrane structural development and function in bronchopulmonary dysplasia

    Determination of alveolar volume and the carbon monoxide diffusing capacity by single breath hold. A: Inhalation of test gas containing a mixture of nondiffusible helium (closed circles) and highly diffusible carbon monoxide (open circles). B: During the single breath hold near total lung capacity, the test gas is rapidly diluted in the alveolar gas. Nonabsorbable helium remains within the alveolus, and its fractional dilution measured at exhalation determines the alveolar volume (VA). C,D: The rate of carbon monoxide uptake is determined by diffusion across the alveolar membrane (DM, C), as well as diffusion into the available pulmonary capillary volume and the reaction with hemoglobin (θ·Vc, D).

  • Bronchopulmonary dysplasia: Clinical perspective

    Bronchopulmonary dysplasia: Clinical perspective

    Original BPD with areas of hyperinflation and emphysema with adjacent dense areas of atelectasis.

  • Developmental determinants and changing patterns of respiratory outcomes after preterm birth

    Developmental determinants and changing patterns of respiratory outcomes after preterm birth

    Histological presentation of new BPD. (A,B) Histology of a patient with fatal new BPD, demonstrating increased distal airspaces with decreased septation and reduced alveolarization (A); as well as pulmonary vascular wall thickness is present in small arteries (arrow in (B)), suggestive of pulmonary hypertension. (C,D) Confocal images of postnatal day 7 mouse lungs exposed to either room air (C) or 85% O2 hyperoxia (D) from birth onward. Note that the hyperoxic lung exhibits reduced alveolarization, exemplifying the alterations in distal airspace that mimics new BPD, a chronic lung disease characterized by impaired gas exchange commonly found in extremely premature infants exposed to mechanical ventilation and oxygen supplementation. Nuclei are stained with DAPI (blue) and green signal is extracellular matrix autofluorescence.

  • Vascular mediators in chronic lung disease of infancy: Role of endothelial monocyte activating polypeptide II (EMAP II)

    Vascular mediators in chronic lung disease of infancy: Role of endothelial monocyte activating polypeptide II (EMAP II)

    EMAP II's antiangiogenic and pro-inflammatory properties may contribute to the pathologic processes associated with bronchopulmonary dysplasia.

  • Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia

    Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia

    Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD). The three major postnatal factors act on the immature lung initiating an inflammatory cascade involving specific cells and cytokines. Local/systemic sepsis is most prominent among the three to cause inflammation, followed by hyperoxia and invasive ventilation (as noted by the thickness of the arrows). These, in turn, instigate effects promoting cell death, cell cycle arrest, and abnormal production of growth factors, matrix proteins, and vascular factors. Mediators that have been consistently reported to have the above noted effects have been listed in the figure. The net result is impaired alveolarization and dysregulated vascularization culminating in the pulmonary phenotype of BPD. Ang-2: Angiopoietin 2. For additional abbreviations and details, please see text.

  • Nuclear factor-kappa-B signaling in lung development and disease: One pathway, numerous functions

    Nuclear factor‐kappa‐B signaling in lung development and disease: One pathway, numerous functions

    Pathways Leading to Activation of NFκB. A: In the canonical pathway of activation, the IKK kinase complex, consisting of kinases IKKα and IKKβ, and the regulatory subunit IKKγ, phosphorylate IκBα on serines 32 and 36. This results in the rapid ubiquitination and degradation of IκBα, which unmasks nuclear localization sequences present on the NFκB subunits, resulting in the rapid translocation of active NFκB complexes into the nucleus, where they bind to κB binding sites in the promoters of target genes and promote gene expression or repression. B: In the noncanonical pathway, IKKα is activated by the NFκB-inducing kinase (NIK), resulting in the processing of p100 to p52, and the nuclear translocation of RelBp52 dimers, which bind to unique κB elements. C: IKK-independent atypical activation of NFκB (observed in response to hypoxia/reoxygenation, or H2O2 stimulation) can occur by means of tyrosine kinase-mediated phosphorylation of IκBα on tyrosine 42, and subsequent dissociation or degradation of IκBα.

  • Paracrine cellular and extracellular matrix interactions with mesenchymal progenitors during pulmonary alveolar septation
  • Assessment of inhibited alveolar‐capillary membrane structural development and function in bronchopulmonary dysplasia
  • Bronchopulmonary dysplasia: Clinical perspective
  • Developmental determinants and changing patterns of respiratory outcomes after preterm birth
  • Vascular mediators in chronic lung disease of infancy: Role of endothelial monocyte activating polypeptide II (EMAP II)
  • Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia
  • Nuclear factor‐kappa‐B signaling in lung development and disease: One pathway, numerous functions

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Birth Defects Research Distinguished Scholar Awards

Birth Defects Research Distinguished Scholar AwardsCongratulations to Dr. Bengt Källen, the winner of the Birth Defects Research Distinguished Scholar Award for his paper in Birth Defects Research: Part A: In vitro fertilization (IVF) in Sweden: Risk for congenital malformations after different IVF methods. Details of the Award can be read here.

The Teratology Society 54th Annual Meeting

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