Lecture 16

Question 1

What is Barth syndrome?

Answer 1

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Question 2

Where is the mutation in Barth syndrome? What is the specific mutation?

Answer 2

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Question 3

What does *12 mean?

Answer 3

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Question 4

What is the mitochondrial function? How does it do this?

Answer 4

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Question 5

What is the electron transfer chain?

Answer 5

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Question 6

How does Barth syndrome affect the function of mitochondria? What is the consequence of this?

Answer 6

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Question 7

What do you do when you have a disease, but know little about the phenotype?

Answer 7

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Question 8

What needs to be checked with IPSC cells?

Answer 8

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Question 9

What cells were the Barth syndrome patient cells differentiated into? Why?

Answer 9

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Question 10

How were they differentiated into cardiomyocytes? What factors were used? How was it checked?

Answer 10

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Question 11

How did these IPSC cardiomyocytes be checked to confirm that it was Barth syndrome cells?

Answer 11

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Question 12

What showed that there was a reduced mitochondrial function is BTH-CM?

Answer 12

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Question 13

What were the different interventions which they tried on the BTH-CM? What was the outcome of the best treatment option?

Answer 13

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Question 14

What is linoleic acid?

Answer 14

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Question 15

How does linoleic acid affect basal oxygen consumption in BTH-CM?

Answer 15

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Question 16

What do mitochondria specifically do in cardiomyocyte cells? What was found to be the problem in Barth syndrome cells?

Answer 16

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Question 17

What is a consequence of this?

Answer 17

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Question 18

How did Linoleic acid affect the sarcomeric organisation and contractile strength?

Answer 18

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Question 19

What about acquired disease? What is it? Why is it harder to be modelled?

Answer 19

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Question 20

What are examples of acquired disease?

Answer 20

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Question 21

What are the properties of the airway wall of an asthmatic?

Answer 21

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Question 22

What are the clinical symptoms of asthma?

Answer 22

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Question 23

What are the current therapeutic strategies for asthma? What is the problem currently with this?

Answer 23

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Question 24

How to model asthma on a chip?

Answer 24

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Question 25

How was the bronchial chip designed?

Answer 25

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Question 26

What was used to stimulate the contraction of the bronchi?

Answer 26

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Question 27

How to model the increased constricted state in asthma on a chip?

Answer 27

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Question 28

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?

Answer 28

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Question 29

What does this mean?

Answer 29

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Question 30

How were interventions tested on the asthma chip? What was the process? What was the outcome?

Answer 30

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Question 31

How do β-agonists work?

Answer 31

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Question 32

What affects the contractile strength smooth muscle?

Answer 32

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Question 33

What is Rho-A? What does it do? What are the levels like in the asthmatic chip?

Answer 33

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Question 34

What are the manners in which to relax muscle?

Answer 34

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Question 35

Will Rho-A inhibitors promote relaxation of smooth muscle?

Answer 35

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Question 36

Could the combined effect of ISO and Rho-A promote greater relaxation?

Answer 36

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Question 37

What are the issues and challenges of organs on chips and diseases on chips?

Answer 37

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