We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Talk outline
- What are the conventional risk factors for CHD
- The multifactorial nature of CAD
- Gene:environment interaction and risk of CAD
- Identifying gene:environment interaction
- The basis for gene:environment interactions
- Measurement of genetic and environmental factors
- What is gene environment interaction
- How to test for gene:environment interaction (1)
- How to test for gene:environment interaction (2)
- Prospective vs. case:control studies
- Candidate gene approach
- Examples of the candidate gene approach
- Northwick park heart study II
- APOE, smoking and CHD risk
- Role of ApoE and LPL in fat metabolism
- CHD risk by APOE genotype and smoking
- Can we replicate these results in another study?
- APOE E4 effect in smokers and non smokers
- APOE smoking and CHD risk mechanisms
- LPL: smoking interaction and CHD risk
- What is lipoprotein lipase and what does it do?
- Lipoprotein lipase function 1: hydrolysis
- Lipoprotein lipase function 2: bridging
- Common LPL variants
- Why are raised triglycerides a risk factor?
- LPL - a good candidate gene
- D9N, N291S: TG levels and risk of heart disease
- LPL:smoking interaction on HD risk
- Survival plot for LPL-D9N and smoking, NPHSII
- The mechanism for the LPL-D9N effect on risk
- The LPL-D9 and LPL-N9 bridging function test (1)
- The LPL-D9 and LPL-N9 bridging function test (2)
- Can we visualise the binding at 4 degrees?
- Mechanisms for LPL-N9:smoking interaction
- Nature and nurture
- Genome wide association scans
- Illumina and Affymetix CHIPs
- Results from the GWASs for CHD
- SNPSs that have been identified from GWAS
- Back to where we started
- Conclusion
Topics Covered
- Conventional CVHD risk factors
- Multifactorial nature of CVD
- Gene-environment interaction and how to test for it
- Candidate gene approach to CVD genetics vs. genome-wide scans
- Examples of the candidate gene approach and gene-environment interaction, APOE and smoking interaction, LPL and smoking
- Mechanisms for these effects
- Novel genes identified by genome-wide scans for CHD and lipid traits
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Talmud, P. (2008, November 24). Genetics of cardiovascular disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 5, 2024, from https://doi.org/10.69645/MBQC1651.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Philippa Talmud has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.