Wednesday, May 30, 2012
Anyone that knows me knows that I have been called a bit of a coffee snob, as I like to roast my own beans at home...so I don't really need another reason to drink coffee - however I thought that I would mention the findings of this just-published study in New England Journal of Medicine, ominously titled "Association of Coffee Drinking with Total and Cause-Specific Mortality". I held my breath as I read that the study, carried out by the Epidemiology group at the National Institutes of Health, followed the health outcomes of nearly 230,000 men and 170,000 women aged 50-71 years of age. Those are some big numbers - over the period of the study, some 13 years, nearly 50,000 participants passed away. After adjusting for age, coffee drinkers were more likely to die! **stifle inward scream**. However, it turns out however, that coffee drinkers actually also include many more smokers than non-coffee drinkers - so after separating out the smokers, coffee drinkers actually have a significantly reduced risk of dying from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections, but not for deaths due to cancer. I know you want to know *how* much coffee had an effect - interestingly it was different for men and women - for men, the effect was evident at less than a cup a day, and maxed at 1 cup thru more than 6. For women, 2-3 cups produced an average 13% reduction in mortality, with protection maxing out at more than 6 cups per day (average 15% reduction). Apparently, it didn't matter if you drank mostly caffeinated, or decaf either -- but what I wonder is if there was also any relationship with use of sweetener (sugar or artificial) in the coffee. Anyhow, studies like this do still have limitations - people with existing cancer, heart disease or who had had a stroke at baseline were excluded, and coffee intake was reported once, at baseline. Nevertheless, I'm liking this data - if you have access to NEJM, you can read the paper, by Neal Freedman et al. here --
Tuesday, May 22, 2012
From the Hanson lab, this paper published today in PLoS ONE describes a study carried out with meticulous attention to detail and proper use of controls while analyzing ME/CFS patient samples for murine-leukemia related viruses. Although novel MLV-like GAG sequences were isolated and sequenced from the patient samples (as opposed to controls collected from the same sites) Lee et al. concludes that it is not possible to determine the origin of these sequences, although the samples were not contaminated with mouse DNA at a detectable level. First, bravo! to the Hanson group for being able to get anything published that might go against the current dogma regarding MLV-like viruses in human samples published -- I guarantee you that there are people with similar data whom don't want to torture themselves by attempting to publish. The fact is, that it seems somehow MLV-like nucleic acids somehow end up in patient samples quite a bit, albeit at exceedingly low levels. Theoretically, even if there was an MLV-type infection in a human, it would be rapidly eliminated (unless of course we don't know everything about the immune system yet). I wonder if it is possible that such viruses could hide somewhere in the body, not replicating much - perhaps killing host cells occasionally resulting in a release of (potentially degraded) viral nucleic acid that is ultimately detected in the blood stream. I haven't analyzed these sequences yet compared to those we have detected in tissue samples from BPH patients, but seeing as our sequences were recently published on the USPTO website, someone else will probably try that. The link to the Hanson paper is here --
Thursday, May 17, 2012
OK so for those fellow scientists out there that might read this blog, this is depressing - but we need to think about it now...it is more than likely that due to a failure of congress to agree on the budget, sequestration will kick in in January 2013. That means if you are lucky enough to have NIH funding, then you will likely suffer a cut of 7.3% of your yearly budget (as prices for everything we use in the lab increase) -- in addition, that will be on top of the already 17% cut from your budget (or more or less, depending on which part of NIH funds you) -- so how do you do the same for less and less each year? In my lab, we already started making most of our own kits, which takes extra time and has its own risks -- potentially diminishing productivity - but can save a lot of money -- we were able to cut about 20% of overall consumable costs this way, but now we are at the bare bones level - so if this cut comes in, the logical choice is to cut salaries - and that means jobs. We are not unique, this is going to affect everyone who is NIH funded, or funded by any other part of government. Furthermore, Dr. Collins, who is the NIH Director, testified to congress that if the "Budget Control Act" is implemented, then thousands of less grants will be able to be funded. That's more jobs gone. But this isn't just about jobs either, its about moving forward with research on cancer treatment and prevention- and every other disease - it's about making sure there is a reason for young people who are interested in science feel that there is a future career in scientific research - What can you do if you care about NIH funded research? Click on the link below, it will lead you to the American Association for Cancer Research website and from there you can contact your members in congress to let them know, they need to do whatever it takes to prevent forced sequestration - and pass a fair budget now! Contact Congress now!
Tuesday, May 15, 2012
Can there possibly be too much of a good thing? Supplements such as folic acid can be vital if your diet is deficient in folate (as most people's diets were prior to the mandated fortification of the US), especially if you are planning to have a child...and in the case of folate deficiency, it is clear that DNA is likely to become damaged, potentially causing tumors- but if it is so important to have enough, can having too much also be a problem? Read all about it at JNCI -
Thursday, May 10, 2012
everything from the genome to the metabolome...if you can think it, there is probably a database for it - the journal Nucleic Acids Research has kindly put together a list of these sites -- access it here --
Monday, May 7, 2012
In this recent manuscript from JP Issa's group, DNA methylation of a CMV promoter driving GFP was examined - histone deacetylase inhibitors were able to reactivate the promoter, leading to GFP expression; however the promoter remained methylated. The inhibitors were effective for approximately two weeks, after which time the promoter became silent once again. Treatment with inhibitors of DNA methylation however, were able to induce permanent activation of the gene. These findings suggest that if this scenario is relevant to other promoters, it will be necessary to target DNA methylation when designing novel treatments as HDAC inhibitors are only able to temporarily "reset" chromatin. click here to read it for yourself.
Wednesday, May 2, 2012
May 4, 2012
West Wing Auditorium, Shadyside Hospital, 5230 Centre Ave (NOTE LOCATION)
1:00 Dr. Tony Schwacha, Department of Biological Sciences, University of Pittsburgh
“The Mcm2-7 helicase couples DNA replication to checkpoint control and sister chromatid cohesion”
1:30 Shweta Nayak, Oesterreich Lab, Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Magee Womens Research Institute
“Epigenetic regulation of histone variants—role in endocrine resistant breast cancer?”
2:00 Dr. J. Richard Chaillet, Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Magee Womens Research Institute
“DNA demethylation in plants and animals”
2:30 Refreshment break
3:00 Dr. Yoel Sadovsky, Department of OBGYN and Reproductive Sciences, Magee Womens Research Institute
“Unprecedented functions of placental microRNAs”
3:30 Dr. Joe Martens, Department of Biological Sciences, University of Pittsburgh
“Identification of a new set of molecular tools to study transcription-dependent chromatin dynamics”
4:00 Dr. Vasily Studitsky, Professor, Department of Pharmacology, UMDNJ-Robert Wood Johnson Medical School, Rutgers University
“Mechanisms and regulation of transcription in chromatin”
After the final talk we will adjourn to the Church Brew Works, 3525 Liberty Avenue in Bloomfield, for further discussions.
Please email firstname.lastname@example.org to be included on the PCC email list.
Funding generously provided by Abcam and the University of Pittsburgh