Links for downloading references are:
Here are the questions for the Nov 24, 2008 class.
1. Suggest at least one age-related pathology that may be caused by changes in the potential of stem cells to differentiate and replace lost cells.
2. In what ways might stem cells grow old?
3. What role(s) might DNA damage play in stem cell aging?
4. What problems need to be solved before considering stem cell therapy for a specific age-related pathology?
Here are the questions for Nov 17. Sorry for posting them late. I just realized it when I started to browse through the papers for tomorrow's class.
1. What are the goals of the NIA's Intervention Testing Program (ITP)? What was a major criticism of the early results obtained, and published, by the ITP investigators?
2. Why was it important for Bodnar et al. to demonstrate that cells with increased levels of transgenically-generated telomerase catalytic subunit had a normal karyotype?
3. What are sirtuins, and what proteins do they act on?
4. In the study by Baur et al., which changes summarized in Table 1 are most likely to contribute to extended life span in resveratrol-fed animals?
Here are the links for the references that will be discussed on Nov 17.
These are the questions for November 10, 2008
1. What was the major conclusion from the McCay paper?
2. Why did Miller use genetically heterogeneous mice for his experiments on predictors of longevity? What was his main conclusion?
3. What is a biomarker of aging? Why are biomarkers of aging highly sought?
4. What are the goals of the NIA's Intervention Testing Program (ITP)? What was a major criticism of the early results obtained, and published, by the ITP investigators?
5. What is autophagy? Why might it be beneficial?
6. What effect might rapamycin have on life span in mice?
References to review follow.
Warner 2004
(This one was on the end of last weeks questions to add for this week).
Hanson2004
Here are the links:
Time, damage and ageing : what really matters? Rejuvenation Res. 10:373-375 is not accessible through library, We should ask Warner to send us this paper.
Here are the questions that Huber prepared for November 3. Would someone be willing to send Edgar the links to directly access reading materials?
1. Suggest an explanation for why SOD-deficient mice are viable, but fibroblasts taken from such mice are not when grown in air.
2. What is the significance of increased levels of plasma alanine aminotransferase activity in mice exposed to diaquat?
3. How do Han et al. explain the changes in gene expression patterns observed in diquat-treated mice?
4. Would you predict that GPx1-deficient mice would be short-lived? What about SOD2-deficient mice?
5. Should we consider the 'free radical theory of aging' disproved by evidence that oxidative damage and tumor incidence in mice can increase significantly without affecting life span?
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Please add Hansen et al., 2008 to the reading list for November 10. I have listed 6 articles in all, but I hope you will read all of these more for their 'flavor' rather than for the details.
Here you can download at least two of the three articles that will be discussed on October 20.
This paper requires windows XP, internet explorer, or mozilla.
Giogio 2005
Additional questions for Oct 13, 2008. Please refer to questions posted one week earlier.
6. How does the cell prevent oxidative damage to proteins?
7. How does the cell repair oxidized proteins?
8. What special role do methionine side chains play in protein oxidative damage?
9. Why might unscheduled DNA repair be relevant to life span?
Here you can download at least two of the three articles that will be discussed on October 13.
You may be able to obtain Harman 1956 if you have a subscription for Science/AAAS or you request a free subscription. The link is
Questions for October 6 - Control of cell proliferation: aging, cancer and p53.
1. Dr. Hayflick's paper in Experimental Cell Research was rejected for publication many times before it was finally accepted for publication. Why was this?
2. Why did Seshadri and Campisi conclude in their 1990 paper that repression of c-fos transcription was the only good candidate in their experiments for being causative in irreversible growth arrest in human fibroblasts?
3. Why do eukaryotic chromosomes shorten each time a cell divides?
4. Why are senescent cells 'good citizens', but 'bad neighbors'?
5. p53 promotes apoptosis, but inhibits cell proliferation. How could you explain the observations that a particular p53 mutant mouse develops aging phenotypes prematurely, but is resistant to spontaneous tumor formation, considering that mutations in p53 are found in many human tumors, and that cancer is a very common cause of death in mice?
(Huber will update the syllabus for weeks 6 - 15 this coming weekend).
Here you may access material to be discussed on Oct 6, 2008
The questions for Week 4 (Sept 29, 2008) are:
1. The level of many hormones, including growth hormone, decrease with age. What do you think of the general strategy of doing growth hormone replacement in older humans to rejuvenate them?
2. Would you generally recommend growth hormone therapy for people born as dwarfs, midgets, etc?.
Here you may access literature to be discussed on Sep 29, 2008
The questions for Week 3 (Sept 22, 2008) are:
1. Other than lifespan extension, what common feature ties together the observations about mutations in age-1 and daf-2, and the inhibition of mTOR?
2. What explanations are there for the pleiotrophic effects of age-1 mutations?
3. What scientific progress occurred after the paper published by Freidman and Johnson in 1987, that facilitated the paper published by Morris et al. in1996?
4. What role does the protein product of daf-16 play in understanding the paper by Kenyon et al.
5. How does any of the above relate to the nutritional status of an organism?
Here you may access literature to be discussed on Sep 22, 2008