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Printable Handouts
Navigable Slide Index
- Introduction
- Morbidity and mortality of preterm birth
- Lipid trafficking from lipofibroblast to type II cell
- Tiktaalik
- Evolution of PTHrP receptors
- Phylogeny/ontogeny to homeostasis/repair
- Loss of homeostatic control within the alveoli
- Recrudescence of myofibroblasts in IPF
- Functional genomic homology: SB and lung
- PTHrP in the enriched unigenes
- PTHrP: necessary for normal lung development
- Stretch stimulates type II cell PTHrP expression
- Grobstein millipore experiment
- Functional homology between SB and lung
- Post-hatching development of swim bladder
- Rotating wall vessel bioreactor
- PTHrP is sensitive to gravitational force
- STS-58 “RATS in SPACE”
- PTHrP under gravitational force: results
- Cholesterol in the developing lung
- Tiktaalik and the transition to land
- The origins of life: chemiosmosis & homeostasis
- Cholesterol and the evolution of cells
- Evolution of multicellular forms
- Cholesterol and the unicellular phenotypes
- A cellular approach to evolution
- Lung structure and cell types
- Thinner wall of alveoli requires surfactant
- Lung physics 101
- Phanerozoic oxygen
- Oxygen/stretch and positive selection pressure
- Reducing lung biology to ‘first principles’
- Evolution of the lung - theorem
- Cell-cell signaling during lung morphogenesis
- Integration of lung, pituitary & adrenal physiology
- Phylogeny of surfactant lipid composition
- Phylogenetic parallelisms
- Lung PTHrP/R: blue print for terrestrial exaptations
- Homologies in skin and lung cell physiology
- Skin-brain homology
- Alveolus and glomerulus are homologous
- The example of Tiktaalik
Topics Covered
- Cortisol, lung surfactant and lung development
- Continuum from phylogeny and ontogeny to homeostasis and repair
- Functional genomic homology between SB and lung
- PTHrP and normal lung development
- PTHrP and gravity
- The origins of life: cellular evolution
- Oxygen/stretch and positive selection pressure
- Lung PTHrP/R as ‘blue print’ for other terrestrial exaptations
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Talk Citation
Torday, J.S. (2016, September 29). How to ‘deconvolute’ lung evolution - the evolutionary origins of pulmonary physiology [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/EWSF7710.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. John S. Torday has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
How to ‘deconvolute’ lung evolution - the evolutionary origins of pulmonary physiology
Published on September 29, 2016
25 min
Other Talks in the Series: Evolutionary Physiology
Transcript
Please wait while the transcript is being prepared...
0:00
My name is John Torday,
I'm a Professor of Evolutionary Medicine
at University of California, Los Angeles.
This is lecture 14
in the evolutionary physiology course,
the evolutionary origins
of pulmonary physiology.
0:15
In the late 1960s, it was discovered
that the hormone Cortisol
could accelerate lung development
in preterm lambs in the womb.
Primarily, stimulating lung surfactant
production by the alveolar type two cell,
thus eliminating surfactant deficiency,
a major cause of disease
or death in preterm infants.
This was a breakthrough
in the emerging discipline of neonatology
and is considered
one of the major discoveries
of 20th century biomedical research.
0:41
The fact that a simple molecule like cortisol
could have such a profound effect
on a complex process
such as lung development was the impetus
for the in-depth study
of its mechanism of action.
Fifty years later those studies culminated
in fundamental understanding
of how and why the mammalian lung evolved.
By focusing
on the cell-cell interactions involved
in regulating surfactant production,
that were necessary for the progressive
decrease in Alveolar diameter
to increase the surface area
to blood volume ratio.
The evolution of a lung is now understood.
Briefly, adipocyte
differentiation-related protein
shown as ADRP
actively facilitates the uptake,
storage and transfer of surfactant substrate
to the alveolar type II cell,
mediated by the effects of leptin
and PTHrP
or Parathyroid hormone-related protein.
The stretching of the alveolar wall
during breathing stimulates
these molecular signaling mechanisms,
maintaining homeostasis
within the alveolar space for oxygenation.
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