Too Legit To Quit?

How long can a newly minted PhD last without having a first author paper to his name?

Evidently, about 3 months...

Robey TE, Murry CE. Absence of regeneration in the MRL/MpJ mouse heart following infarction or cryoinjury. Cardiovasc Pathol. 2008;17:6– 13.

The text is available with subscription here. Email me or post a comment if you would like a .pdf.

This is the lead article in the first issue of the 2008 volume of Cardiovascular Pathology. Who says you can't publish negative results? If you recall, there was a bit of a splash earlier this decade about a funny mouse that could (amazingly!) regenerate its heart after injury. To catch up about how this over-hyped story has played out in the last 7 years, read this nice review.

It took a year for this to go to press after it was accepted, hence the lag between earning the PhD and being published. There are more on the way, hopefully including a pair I polished up for submission last Friday. But none will receive the fanfare I afforded this one. There is just something special about the first time.

As far as the post's title, what's up with PhD students slaving in the lab for years and then deciding not to pursue a career in academic science after all? I don't know. Check back with me in a couple of years.

Damage Control...

Today's Science Daily reported a study by a Boston research group (Mark Keating's) that has identified a drug delivery technique using a drug called periostin that could rebuild heart tissue without stem cells. This drug causes heart cells to re-enter the cell division cycle 100 times more than normal 12 weeks after a mouse was given a heart attack. In any other tissue, this abundant increase in division would cause a tumor. But since heart cells hardly ever divide, what they saw was an increase from 0.01% to 1.0% when the marker for cell division (BrdU for my biologist readers) was given for 6 days. Just as a way of reference, that much BrdU given to an animal would cause almost 50% of the intestine to be positive.

These drastic increases in cell division are what is needed in order to harness any latent ability in the heart for cell division. While this group did find that heart function improved after treatment with their drug patch, it is unclear to me whether this is due to the effects of cell division or other effects of the drug, namely different scar properties.

The original document (needing institutional subscription) is here.