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3. A brief history of evolutionary biology
- Prof. Neil Blackstone
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4. Major transitions in the history of life
- Prof. Neil Blackstone
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5. On the origins of life
- Dr. William B. Miller Jr.
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6. The origin of eukaryotes
- Prof. Neil Blackstone
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7. Trichoplax and the origin of animal complexity
- Prof. Bernd Schierwater
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8. On the value of comparative physiology
- Prof. Karen L. Sweazea
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11. How to ‘deconvolute’ lung evolution - evolutionary lessons from cell culture
- Prof. John S. Torday
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12. Using lung evolution as a cipher for physiology - pathophysiology
- Prof. John S. Torday
-
13. The unicellular origins of complex physiology
- Prof. John S. Torday
-
14. Pleiotropy - cellular-molecular evolution in action
- Prof. John S. Torday
Printable Handouts
Navigable Slide Index
- Introduction
- Mechanism for neutral lipid trafficking
- Bronchopulmonary dysplasia: an atavistic disease
- PPARg agonist effects
- De Duve hypothesis
- Disease prevention
- Healthcare costs for the top 5 chronic diseases
- Future health and longevity prediction
- A (r)evolutionary approach to medicine
- The evolutionary cell-cell communication approach
- Physiologic evolution
- Evolution of PTHrP receptors
- Homology between swim bladder & lung
- PTHrP among genes for swim bladder development
- Post-hatching development of swim bladder
- Importance of a cellular approach to evolution
- Grobstein millipore experiment
- Lung tissue complexity
- Unicellular organisms evolution
- Phanerozoic oxygen
- Developments due to oxygen changes
- Lung Physics 101
- Mechanism of lung evolution
- The underlying metabolic drive for land adaptation
- Oxygen/stretch and positive selection pressure
- PTHrP: necessary for normal lung development
- PPARg treatment
- Phylogenetic parallelisms (lung, heart, kidney)
- Homologies between skin and lung cell physiology
- Alveolus and glomerulus homology
- Lung-brain homology
- Cholesterol gene deletion
- b-adrenergic receptor
- Predictive model
Topics Covered
- Neutral Lipid Trafficking
- Bronchopulmonary Dysplasia (BPD) as failed cell-cell interactions
- PPARγ prevention of BPD
- de Duve Hypothesis
- Preventive Medicine
- PTHrP, Glucocorticoid and βAdrenergic Receptor gene duplications
- Oxygen effects on cell-cell interactions
- Phylogeny of lung, kidney, heart
- Skin-lung homology
- Lung-kidney homology
- Lung-brain homology
- Predictive Model
Talk Citation
Torday, J.S. (2016, March 31). Using lung evolution as a cipher for physiology - pathophysiology [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 12, 2024, from https://doi.org/10.69645/YCQH1307.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.
A selection of talks on Clinical Practice
Transcript
Please wait while the transcript is being prepared...
0:00
JOHN S. TORDAY:
My name is John Torday.
I'm a professor of evolutionary
medicine at UCLA.
This is lecture 15 in
the evolutionary physiology lecture
series entitled, "Using
Lung Evolution as a Cipher
for Physiology and Pathophysiology."
0:18
The premise of the evolutionary
approach to physiology
and pathophysiology alike is that
the unicellular interrelationships
that mediate structure
and function are part
of the history of
cell-cell communications
that coincide with
ontogeny and phylogeny.
From this perspective,
the lung is the best understood
complex physiologic
mechanism, so it will
be used as a cipher to understand
physiology and pathophysiology
as a continuum, rather than
as the dogmatic associations
and correlations of conventional
descriptive physiology
and the dichotomous
perspective on disease
as the absence of
health, which still
prevails in the era of genomics,
proteomics, metabolomics, etc.
Shown in this schematic is
the role of the lipofibroblast
in homeostatic regulation
of lung surfactant,
mediating the recruitment
of neutral lipid substrate
from the microcirculation for
the on-demand production of surfactant,
preventing alveolar collapse
due to elevated surface
tension on expansion of
the lung for gas exchange.
Damage by a wide variety
of agents, ranging
from pressure, or
barotrauma, to oxygen,
or oxotrauma, infection,
and prematurity,
all funneling through
the mechanism of lipfibroblast injury
in which loss of cell-cell
communication with the alveolar
type II cell causes
transdifferentiation of
the lipofibroblast to a myofibroblast.
A myofibroblast is the final
common pathway for all chronic lung
diseases, including
Brocopulmonary Dysplasia, or BPD,
a chronic lung disease
caused by lung immaturity.