Good morning! Hope this morning's newsletter finds you well. The walk staff has just returned a fun and rewarding few days at the American Heart Association Scientific Sessions in Orlando.   

Now, it's 6:15 am and I'm sitting at my computer, reflecting back on the many inspirational people we met in Florida. These new friends come from all over the world; Emory, Harvard, Duke, Oxford, and many other locales.  

A Grand Walk with a Doc Welcome to you all!!  

Our new Ivy League reader friends, here in the Publishing Studio Wing of Walk with a Doc Land we are very serious and studious.     

Having just having finished this morning's print editions of The New York Times, Columbus Dispatch, The Economist, New England Journal of Medicine, and Popular Science, I'm content. I'm filled with a warm radiance ("That doesn't make sense") knowing that all our new friends are receiving their first Walk with a Doc newsletter today.

As this is your first edition, we would like to walk you through a typical newsletter. In these communications, you will find a very high level of discussion that you have grown accustomed to at your prestigious institutions. Not unlike yourselves, our newsletter subscribers are borderline genius; recent testing has put them in the uppermost percentile of the world's population.   

In our emails, we often intially the mood with some humor. For example, today we will share this:

So in Orlando, we were leaving the Molecular Genetic presentation by Lawrence Triplett MD PhD on N-acetylcysteine and its' role in deregulation of 6'7' tyrosine diphosphodiesterase allele on the ras-knockout oncogene. After 90 minutes of this phenomenal intellectual discourse, I turned to Brian, our assistant regional director of Walk with a Doc's Translational Science Institute and say,

"That was incredible! I had figured that among CYP2C19*2 heterozygotes there would be a platelet-reactivity index of 46.9, turns out that is only the noncarriers!"

Brian then turns to me, smiles and says,

"Well then, we better not give you 75 mg of prasugrel next time you decide to enroll in the pharmacogenomic clopidogrel arm of the TIMI trial!"

You know, funny stuff like that.

But we realize, it can't all be a stab at humor. We have to give our readers some meat. Something that will improve the quantity and QUALITY of their lives and their friend's lives. This week's medical news is a perfect example:

Many small mammals survive the winter by hibernating, entering long periods of cold torpor that are interspersed with brief periods of arousal back to euthermia. This cycling is accompanied by wide changes in oxygen consumption, perfusion of tissues and ATP turnover, and the arousal period in particular is challenging because of oxidative stress associated with the huge increase in oxygen consumption needed to support thermogenesis by brown adipose tissue and skeletal muscle. Well-developed antioxidant defences are needed. The present study analyses responses of the redox-sensitive transcription factor, NF-κB, in skeletal muscle over six points on the torpor-arousal cycle to gain insight into its regulation and role during hibernation. Immunoblotting was used to analyse NF-κB p50 and p65 subunit levels, nuclear versus cytoplasmic localization and DNA-binding activity as well as levels and phosphorylation state of the IκBα inhibitor and the kinase IKK that phosphorylates IκBα to trigger its dissociation from NF-κB. The data were generally consistent with an activation of NF-κB during the entrance into torpor with responses including an auto-up-regulation of p50 subunits seen during early torpor and elevated IκBα protein during arousal. Protein levels of two downstream antioxidant targets showed differential regulation, Mn-superoxide dismutase (MnSOD) rising during early torpor versus heme oxygenase 1 (HO-1) increasing during early arousal. The mRNA transcript levels of p50, p65, HO-1 and MnSOD also showed differential expression over the torpor-arousal cycle. The results suggest that antioxidant defences are up-regulated at specific phases of the torpor-arousal cycle and that NF-κB mediates such protective responses.