This image was lost some time after publication.

Harvard embargoes a press release on curing the blind, then sends a one-hour correction to the whole recipient list. Just wanted to give y'all a heads up so this news can break a whole hour earlier — after everyone sits on it for four days. The journo who passed this on explains why these embargoes happen:

I'm told that the deal on these embargoed releases is usually that the publicist gave some prestigious outlet an exclusive in return for the embargo. For example, your first Embargo Breaker, Congresspedia, had cut a deal with the WaPo (verified!) in exchange for embargoing the story until after the WaPo broke it. I'm fine with people making those deals, but doesn't that make it really stupid to turn around and send out the news as junk mail to strangers?

After the jump, the offending release.

> From: "Jamie Newton"
> Date: May 10, 2006 10:17:26 AM PDT
> To: (redacted)
> Subject: Embargo time correction (for Sunday)
> The embargo date for the release below should be 1 PM ET on Sunday,
> not 2 PM ET as originally listed (due to a miscommunication with
> the journal). Sorry for any inconvenience this may have caused. —
> Jamie
> ***
> A study to appear Sunday, May 11 in Nature Neuroscience (online
> edition) describes a naturally occurring, previously unrecognized
> growth factor that stimulates regeneration in injured optic nerves
> - raising the possibility of treating blindness due to optic-nerve
> damage and the hope of achieving similar regeneration in the spinal
> cord and brain. A press release is below; for links to additional
> resources, visit:
> Site1339/mainpageS1339P1sublevel206.html.
> A high-resolution image of the regenerating optic nerve is
> available.
> If I can be of help, just let me know.
> Sincerely,
> Jamie Newton
> Public Affairs
> Children's Hospital Boston
> (phone and e-mail redacted)
> Sunday, May 14, 2006, 1 pm ET
> CONTACT: Jamie Newton, Children's Hospital Boston
> (phone and e-mail redacted)
> Previously unknown molecule spurs regeneration in the optic nerve
> Researchers at Children's Hospital Boston have discovered a
> naturally occurring growth factor that stimulates regeneration of
> injured nerve fibers (axons) in the central nervous system. Under
> normal conditions, most axons in the mature central nervous system
> (which consists of the brain, spinal cord and eye) cannot regrow
> after injury. The previously unrecognized growth factor, called
> oncomodulin, is described in the May 14 online edition of Nature
> Neuroscience.
> Neuroscientists Yuqin Yin, MD, PhD, and Larry Benowitz, PhD, who
> are also on the faculty of Harvard Medical School, did their
> studies in the optic nerve, which connects nerve cells in the eye's
> retina to the brain's visual centers, and is often used as a model
> in studying axon regeneration.
> When oncomodulin was added to retinal nerve cells in a Petri dish,
> with known growth-promoting factors already present, axon growth
> nearly doubled. No other growth factor was as potent. In live rats
> with optic-nerve injury, oncomodulin released from tiny sustained-
> release capsules increased nerve regeneration 5- to 7-fold when
> given along with a drug that helps cells respond to oncomodulin.
> Yin, Benowitz and colleagues also showed that oncomodulin switches
> on a variety of genes associated with axon growth.
> Benowitz, the study's senior investigator, believes oncomodulin
> could someday prove useful in reversing optic-nerve damage caused
> by glaucoma, tumors or traumatic injury. In addition, the lab has
> shown that oncomodulin works on at least one other type of nerve
> cell, and now plans to test whether it also works on the types of
> brain cells that would be relevant to treating conditions like
> stroke and spinal cord injury.
> The current study builds on work Benowitz, Yin and colleagues
> published a few years ago. Studying the optic nerve, they found -
> quite by accident - that an injury to the eye activated axon
> growth: it caused an inflammatory reaction that stimulated immune
> cells known as macrophages to move into the eye.
> "To make this finding clinically useful, we wanted to understand
> what was triggering the growth, so we could achieve nerve
> regeneration without causing an injury," Benowitz says.
> Working in Benowitz's lab, Yin took a closer look and found that
> the macrophages secreted an essential but as-yet unidentified
> protein. Further studies revealed it to be oncomodulin, a little-
> known molecule first observed in association with cancer cells.
> "Out of the blue, we found a molecule that causes more nerve
> regeneration than anything else ever studied," Benowitz says. "We
> expect this to spur further research into what else oncomodulin is
> doing in the nervous system and elsewhere."
> For oncomodulin to work, it must be given along with an agent that
> raises cell levels of cyclic AMP, a "messenger" that initiates
> various cellular reactions. Increased cyclic AMP levels are needed
> to make the oncomodulin receptor available on the cell surface.
> A two-pronged approach
> Benowitz also notes that there is another side to the nerve-
> regeneration problem: overcoming agents that act as natural
> inhibitors of axon growth. These inhibitors are the subject of
> intense study by several labs, including that of Zhigang He, PhD,
> at Children's Hospital Boston.
> In a study published in 2004, Benowitz and postdoctoral fellow
> Dietmar Fischer, PhD, collaborated with He to combine both
> approaches - overcoming inhibition and activating the growth state
> (by injuring the lens of the eye) - and achieved dramatic optic-
> nerve regeneration. Now that Benowitz has isolated oncomodulin, he
> believes even greater regeneration is possible by combining it with
> agents that counteract growth inhibitors.
> "We're in the midst of an exciting era of research in nerve
> regeneration," Benowitz says. "There are a lot of promising leads
> in the area of blocking molecules that inhibit regeneration. But to
> get really strong regeneration, you also have to activate nerve
> cells' intrinsic growth state."
> The study was funded by the National Eye Institute (part of the
> National Institutes of Health), the Patterson Family Trust, the
> European Commission, and Boston Life Sciences, Inc. The
> oncomodulin technology has been licensed by Boston Life Sciences,
> Inc. (BLSI; Hopkinton, Mass.), which is testing recombinant
> oncomodulin for ocular indications in pre-clinical studies. BLSI
> has also licensed other axon regeneration technologies developed at
> Children's. For more information on BLSI's activities, contact
> Sharon Correia at (redacted).
> Children's Hospital Boston is home to the world's largest research
> enterprise based at a pediatric medical center, where its
> discoveries have benefited both children and adults since 1869.
> More than 500 scientists, including eight members of the National
> Academy of Sciences, nine members of the Institute of Medicine and
> 11 members of the Howard Hughes Medical Institute comprise
> Children's research community. Founded as a 20-bed hospital for
> children, Children's Hospital Boston today is a 347-bed
> comprehensive center for pediatric and adolescent health care
> grounded in the values of excellence in patient care and
> sensitivity to the complex needs and diversity of children and
> families. Children's also is the primary pediatric teaching
> affiliate of Harvard Medical School. For more information about the
> hospital and its research visit:
> research/.
> - ### -