WWW.NATURE.COM/NATURE
This press release is copyright Nature.
PLEASE CITE NATURE AND OUR WEBSITE www.nature.com/nature AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO http://www.nature.com/nature
Human Genetics: Interpreting our past from genomic information
Humans are keenly interested in their origins, and we now have more DNA information than ever to help us to reconstruct our genetic history. Two papers in this week’s Nature delve into the rapidly expanding databank to produce new nuggets of information.
Carlos Bustamante and colleagues combine large data sets for the American population to reveal that — for their sample at least — European–American populations have more potentially damaging mutations per variable DNA site than African–American populations. Given the large amount of data used, their discovery settles a debate about the number of these damaging mutations in human populations, and supports the idea that European–Americans as a whole, and not just specific isolated groups, went through a more recent population ‘bottleneck’ than did African–Americans.
Andrew Singleton, Noah Rosenberg and colleagues characterize more than 500,000 DNA markers in the human genome, using 485 volunteers from the Human Genome Diversity Project. They describe the extent of variations across 29 different populations, from Africa, through Europe and the Middle East, through central to South-East Asia, to Oceania and the Americas. Their data resolution is nearly two orders of magnitude greater than previous assessments of human populations and includes both single base changes and changes in larger chunks called copy-number variants. Comparison of these two types of genetic variation enables an increasingly accurate assessment of the complete structure of the human family tree.
CONTACT
Carlos Bustamante (Cornell University, Ithaca, NY, USA)
Tel: +1 607 255 1640; E-mail: [email protected]
Andrew Singleton (National Institute on Aging, Bethesda, MD, USA)
Tel: +1 301 451 6079; E-mail: [email protected]
Noah Rosenberg (University of Michigan, Ann Arbor, MI, USA)
Tel: +1 734 615 9556; E-mail: [email protected]
**********************************************************
PRESS RELEASE FROM NATURE BIOTECHNOLOGY
http://www.nature.com/naturebiotechnology
This press release is copyrighted to Nature Biotechnology.
Renewable cell therapy for diabetes inches closer
DOI: 10.1038/nbt1393
Researchers have converted human embryonic stem (ES) cells into cells that release insulin in response to glucose and alleviate a diabetes-like condition in mice. With further research and development, this approach, reported online in Nature Biotechnology, could lead to a renewable source of cells for the treatment of diabetes.
Type 1 diabetes and some forms of type 2 diabetes involve the loss of pancreatic ‘beta’ cells, which regulate blood glucose (sugar) levels by releasing insulin. In previous work, Emmanuel Baetge and colleagues described a method for driving human ES cells part of the way along the developmental path of the pancreas to becoming beta cells. The resulting cells could not carry out the key function of mature beta cells, which is to release insulin in response to glucose.
In their new study, Baetge’s team shows that if immature pancreatic cells derived from human ES cells are transplanted into mice, in 1–3 months they will develop into glucose-responsive, insulin-secreting cells. These in vivo–matured cells are able to regulate the blood glucose levels of mice whose own beta cells have been destroyed by a chemical treatment—an animal model that mimics some forms of diabetes. The blood glucose control achieved is of similar effectiveness to that obtained by transplanted human islets.
The principle of treating diabetes by transplantation of pancreatic beta cells (within islets) has been demonstrated using the so-called Edmonton protocol. Thus far, this therapy has relied on cells from donor pancreases. Because the supply of such cells is very limited, there is great interest in developing alternative sources of beta cells, including cells derived from human ES cells.
Author contact:
Emmanuel Baetge (Novocell Inc, San Diego, CA, USA)
Tel: +1 858 455 3555; E-mail: [email protected]
For media inquiries relating to editorial content/policy for Nature Biotechnology, please contact the journal directly:
Nature Biotechnology, San Francisco
Kathy Ascheim
Tel: +1 415 403 9022; E-mail: [email protected]
***************************************************************
PRESS RELEASE FROM NEUROPSYCHOPHARMACOLOGY
http://www.nature.com/npp/
This press release is copyrighted to the journal Neuropsychopharmacology.
PLEASE CITE neuropsychopharmacology AND THE neuropsychopharmacology WEBSITE AS THE SOURCE OF THE FOLLOWING ITEM. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO www.nature.com/npp/
Treatment-resistant depression might be in the genes
Variation in the gene coding for the potassium channel TREK1 may explain why some patients with depression do not respond to commonly prescribed antidepressants. If confirmed, this finding, reported online this week in the journal Neuropsychopharmacology, could lead to better ways of identifying and treating patients unlikely to benefit from conventional drug regimens.
Roy Perlis and colleagues studied the genes of patients who did not respond to an initial trial of selective serotonin reuptake inhibitors (SSRIs). Of these patients, they found that those with a common variation in the gene for TREK1, often failed to respond to one or two subsequent treatments. SSRIs are known to inhibit TREK1 and mice lacking this channel are resistant to depression. These results suggest TREK1 could regulate one’s response to antidepressants.
While further research is necessary to determine how these variations interfere with treatment, this study is one of the first to examine the genetic underpinnings of treatment resistant depression, a prevalent and costly disease with a poor prognosis.
Author contact:
Roy Perlis (Massachusetts General Hospital, Boston, MA, USA)
Tel: +1 617 726 7426; E-mail: [email protected]
Editorial contact:
Diane Drexler (Neuropsychopharmacology, Nashville, TN, USA)
Tel: +1 615 324 2371; E-mail: [email protected]
PRESS CONTACTS
For media inquiries relating to embargo policy for the Journal Neuropsychopharmacology:
Katherine Anderson (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]
For media inquiries relating to the American College of Neuropsychopharmacology:
Tel: +1 615 324 2360; E-mail: [email protected]
**************************************************************
PRESS CONTACTS…
For North America and Canada
Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]
For Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]
For the UK/Europe/other countries not listed above
Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]
Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]
About Nature Publishing Group
Nature Publishing Group (NPG) is a division of Macmillan Publishers Ltd, dedicated to serving the academic, professional scientific and medical communities. NPG's flagship title, Nature, was first published in 1869. Other publications include Nature research journals, Nature Reviews, Nature Clinical Practice and a range of prestigious academic journals including society-owned publications. NPG also provides news content through Nature News and scientific career information through Naturejobs.
NPG is a global company with headquarters in London and offices in New York, San Francisco, Washington DC, Boston, Tokyo, Paris, Munich, Hong Kong, Melbourne, Delhi, Mexico City and Basingstoke. For more information, please go to www.nature.com
