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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.
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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.
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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.
