Lecture 16 Flashcards
What is Barth syndrome?
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Where is the mutation in Barth syndrome? What is the specific mutation?
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What does *12 mean?
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What is the mitochondrial function? How does it do this?
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What is the electron transfer chain?
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How does Barth syndrome affect the function of mitochondria? What is the consequence of this?
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What do you do when you have a disease, but know little about the phenotype?
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What needs to be checked with IPSC cells?
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What cells were the Barth syndrome patient cells differentiated into? Why?
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How were they differentiated into cardiomyocytes? What factors were used? How was it checked?
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How did these IPSC cardiomyocytes be checked to confirm that it was Barth syndrome cells?
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What showed that there was a reduced mitochondrial function is BTH-CM?
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What were the different interventions which they tried on the BTH-CM? What was the outcome of the best treatment option?
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What is linoleic acid?
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How does linoleic acid affect basal oxygen consumption in BTH-CM?
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What do mitochondria specifically do in cardiomyocyte cells? What was found to be the problem in Barth syndrome cells?
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What is a consequence of this?
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How did Linoleic acid affect the sarcomeric organisation and contractile strength?
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What about acquired disease? What is it? Why is it harder to be modelled?
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What are examples of acquired disease?
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What are the properties of the airway wall of an asthmatic?
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What are the clinical symptoms of asthma?
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What are the current therapeutic strategies for asthma? What is the problem currently with this?
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How to model asthma on a chip?
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How was the bronchial chip designed?
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What was used to stimulate the contraction of the bronchi?
sadadasd
How to model the increased constricted state in asthma on a chip?
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What happened to the bronchial cells when exposed to IL-13? What was the response on contraction? What happened physically to the cells?
What does this mean?
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What does this mean?
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How were interventions tested on the asthma chip? What was the process? What was the outcome?
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How do β-agonists work?
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What affects the contractile strength smooth muscle?
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What is Rho-A? What does it do? What are the levels like in the asthmatic chip?
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What are the manners in which to relax muscle?
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Will Rho-A inhibitors promote relaxation of smooth muscle?
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Could the combined effect of ISO and Rho-A promote greater relaxation?
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What are the issues and challenges of organs on chips and diseases on chips?
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