georgeskohler

Argh, I wish we could just conserve our resources better! Oh well...

maybe what you are saying is not so far-fetched...I mean people do get genetic counseling about possible disease risk for offspring should a couple decide to have kids, right? But can you "breed out" diseases? Also, there are genetic factors that likely contribute to disease that interact in ways we don't understand/cannot predict, but maybe it will work I don't know.

Can someone explain what the main differences are in functions of cytotoxic T cells versus natural killer cells (...and are there also "natural killer T cells")? Is it right that NK cells recognize virally infected cells by reduced MHC I expression because the infecting agent takes over host machinery so the host makes less proteins? And do cytotoxic T cells kill cells presenting viral peptides in MHC I? I am confused...also do they both kill by releasing cytotoxic granules into the infected cell, or what is the mechanism?

It's a really complicated topic. Cells receive signals from other cells around them which tell them to proliferate or not to. One example of this is a growth factor produced by one cell can bind to a molecule on the surface of another cell, which tells that cell to proliferate. Cells have to replicate their DNA prior to dividing and the telomeres on chromosomes get shorter with each division. This is partially prevented by the telomerase enzyme, but ultimately normal cells will enter into a senescent state and won't continue to proliferate. One mechanism cancer cells get around this is by expressing more telomerase and inactivating proteins such as p53 whose normal function is to prevent uncontrolled proliferation. So, I think if you tried to reactivate telomerase, you could run into problems.

my thinking is on the one hand, most cells lose telomerase expression and telomeres can get so short with each cell division that eventually the cells cannot transmit the genetic material to daughter cells. hmm, what happens if you reactivate telomerase--cancer cells do this...

did you design the plasmid correctly? does expression of the protein have some deleterious effect?

good point, I guess both why medium with limited nutrients which basically starves the yeast causes that from a mechanistic standpoint and the potential adaptive significance (maybe spores are hardy and can survive the lack of nutrients and then enter into normal growth phase when nutrients are available again...) I know yeast can exist and be propagated in haploid or diploid form in culture.

in terms of dedifferentiating cells, we have turned adult somatic cells to induced pluripotent stem cells, and can differentiate these cells to many different cell types. Also, I think there is some value in showing we can synthesize a known chromosome--maybe down the road it will contribute to our understanding of chromatin structure...

oh yeah, agrobacterium...that's the one that forms that makes trees look all funky?

There was a whole issue of Science dedicated to the idea of capturing and storing CO2 that is emitted when we burn fossil fuels. Is our best option to pursue this strategy while continuing research on alternative energy sources? I understand the need for this I guess, but even if we can minimize leakage from underground storage, etc. to me this just highlights the need to really directly address our entropy crisis once and for all...what do you all think?

I wish I could form a pili and transfer chromosomes to bacteria and see what happens. I think homologous recombination is cool...like mitotic recombination is relatively rare, right? I guess there is recombinational repair. And meiotic recombination can generate cool combinations of alleles for the next generation.

Under starvation conditions (medium lacking nitrogen source) yeast will undergo meiosis to produce haploid spores. Why?

so the innate immune response is all that matters?

I agree.... well, germ cells have only one set of chromosomes, but yeah. It's also cool that small regulatory RNAs regulate gene expression and....other stuff. And then there are cells without nuclei like platelets, and Schwann cells which wrap around axons and that's cool....but I guess irrelevant...what would be a relevant response?

how about mitochondria in humans? okay, so that does not help, sorry!

oh wow, I did not see the Genetic Information Non-discrimination Act before...

animals provide important in vivo models. cannot just test drugs with cancer cell lines...well, i guess you can, but usually that is not too compelling on its own. Not that animal models dont have their own problems. Sometimes LD50 in mice does not always translate to drug cytotoxicity in humans and genetic differences among individuals accounting for differences in how a drug is metabolized compound this problem.

I'm sorry if this has been discussed in another thread: I was inspired by a lecture by the great Dr. Robert Weinberg (available online) to ask, given that science has advanced to the point that it is feasible to obtain the genetic profile for any given individual, what will be the most appropriate way to handle an individual's genetic information in the near future. For example, does an employer have the right to know if a job candidate has a particular genetic mutation which in some way might affect his/her ability to perform the job required of them (for instance, a mutation associated with increased susceptibility for a particular cancer)?

Going back to the question about targeting cancer cells--as written in previous posts here, in many cancers, the cancer cells express a certain protein (for example EGFR) to much higher levels than normal cells. A lot of research related to targeting tumor cells selectively has focused on monoclonal antibodies--such an antibody might bind specifically to EGFR, reducing the expression of the receptor/preventing it from dimerizing/preventing it from binding growth factor. I think the question about causes of cancer is also interesting. Viruses can also cause cancer, like HPV causes cervical cancer, and there is a vaccine for that. Yes, it is true that some people are more susceptible to cancer than others. In some cases there is a very clear genetic component--for example, it is more likely that someone who inherits a mutated copy of the Rb gene from one parent will acquire a mutation in the other gene, leading to retinoblastoma, than it is that someone who inherits two normal copies will acquire two mutations and end up with this condition. Of course diet and lifestyle are also important, and there is a clear correlation between trends in smoking and lung cancer incidence, and between the advent of refridgeration and the occurrence of gastric cancer. But an individual's genetic makeup will play a large role in determining whether one can smoke for 40 years and not get lung cancer. About the question of why can't we tell cells to kill bad cells, that's interesting. One of the main jobs of natural killer cells and cytotoxic T cells is to kill cells that are infected with viruses or bacteria; they can also kill tumor cells but tumor cells can evade being detected as well.

Does the set of MHC alleles an individual possesses significantly affect one's ability to combat certain diseases? Is it feasible to transplant cells (maybe reprogrammed cells...) into an individual before the recipient's immune system has developed (pre-thymic education, etc.) and in that way introduce different MHC alleles or other traits which might be beneficial without the risk of them being rejected by the immune system? Also, I think there have been studies indicating that MHC allelic diversity might influence mate choice. Specifically, one might choose for a mate someone with MHC alleles different from their own. What do others think?

History includes the study of past events, including scientific progress. But also, science investigates earth's history, evolution, etc. hmm...

also the CDC website is not bad...

what about antibodies against LPS? will there be some adaptive immune response?