News Release

JCI table of contents: Nov. 23, 2009

Peer-Reviewed Publication

JCI Journals

EDITOR'S PICK: Gene implicated in stress-induced high blood pressure

Do stressful situations make your blood pressure rise? If so, your phosducin gene could be to blame according to a team of researchers, at the University of Freiburg, Germany, and the Medical College of Wisconsin, Milwaukee, that has identified a role for the protein generated by the phosducin gene in modulating blood pressure in response to stress in both mice and humans.

The team, led by Lutz Hein and Ulrich Broeckel, generated mice lacking phosducin and found that they had increased baseline blood pressure when compared with normal mice and that they showed enhanced increases in blood pressure in response to post-operative stress. Analysis in humans indicated that a number of phosducin gene variants were associated with certain stress-dependent blood pressure responses. Further, one gene variant in particular was associated with elevated baseline blood pressure. These data led the authors to suggest that phosducin might be a good target for drugs designed to alleviate stress-induced high blood pressure. In an accompanying commentary, however, Guido Grassi, at Clinica Medica, Italy, notes that further studies are needed before the therapeutic implications of these data can really be determined.

TITLE: Phosducin influences sympathetic activity and prevents stress-induced hypertension in humans and mice

AUTHOR CONTACT:
Lutz Hein
University of Freiburg, Freiburg, Germany.
Phone: 49-761-2035314; Fax: 49-761-2035318; E-mail: lutz.hein@pharmakol.uni-freiburg.de.

Ulrich Broeckel
Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Phone: (414) 955-2369; Fax: (414) 456-6516; E-mail: broeckel@mcw.edu.

View this article at: http://www.jci.org/articles/view/38433?key=ch6PLgvm06ENhpLnhy41

ACCOMPANYING COMMENTARY
TITLE: Phosducin – a candidate gene for stress-dependent hypertension

AUTHOR CONTACT:
Guido Grassi
Clinica Medica, Monza, Milan, Italy.
Phone: 39-039-233-357; Fax: 39-039-322-274; Email: guido.grassi@unimib.it.

View this article at: http://www.jci.org/articles/view/41508?key=JtWzBvLn9C3r9GYN8BN8


EDITOR'S PICK: Lessons for HIV learned from monkey control of SIV infection

SIV is a virus related to HIV that can infect monkeys. In some strains of monkey (which are known as natural hosts) SIV does not cause disease, whereas it does in others (which are known as susceptible hosts). It is hoped that understanding why SIV does not cause disease in natural hosts will provide insight into how to control HIV infection of humans. Two independent research teams, one led by Michaela C. Müller-Trutwin, and the other led by Guido Silvestri, Ashley Haase, and David Kelvin, have now determined that SIV induces vigorous activation of the immune system, in particular upregulation of genes stimulated by immune molecules known as IFNs, in both natural and susceptible hosts, but strikingly, the responses are later brought under control only in the former. In an accompanying commentary, Nina Bhardwaj and Olivier Manches, at New York University Langone Medical Center, New York, discuss how the lessons learned from these studies might impact HIV vaccine design and therapy.

TITLE: Global genomic analysis reveals rapid control of a robust innate response in SIV-infected sooty mangabeys

AUTHOR CONTACT:
Guido Silvestri
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-5363; Fax: (215) 573-5369; E-mail: gsilvest@mail.med.upenn.edu.

Ashley T. Haase,
University of Minnesota, Minneapolis, Minnesota, USA.
Phone: (612) 624-4442; Fax: (612) 626-0623; E-mail: haase001@umn.edu.

David J. Kelvin
University Health Network, Toronto, Ontario, Canada.
Phone: (416) 581-7605; Fax: (416) 581-7606; E-mail: dkelvin@uhnresearch.ca.

View this article at: http://www.jci.org/articles/view/40115?key=oNmMSIkn4H9JdUJ72v6a

ACCOMPANYING ARTICLE
TITLE: Nonpathogenic SIV infection of African green monkeys induces a strong but rapidly controlled type I IFN response

AUTHOR CONTACT:
Michaela C. Müller-Trutwin
Institut Pasteur, Paris, France.
Phone: 33-1-40-61-39-69; Fax: 33-1-45-68-89-57; E-mail: michaela.muller-trutwin@pasteur.fr.

View this article at: http://www.jci.org/articles/view/40093?key=8rqR89T5BZYeJ7KuHW55

ACCOMPANYING COMMENTARY
TITLE: Resolution of immune activation defines nonpathogenic SIV infection

AUTHOR CONTACT:
Nina Bhardwaj
The New York University Langone Medical Center, New York, New York, USA.
Phone: (212) 263-5814; Fax: (212) 263-6729; Email: Nina.Bhardwaj@med.nyu.edu.

View this article at: http://www.jci.org/articles/view/41509?key=YH73bnLajqEZK6CETk0O


HEMATOLOGY: Double trouble: the protein GSK-3 controls self-renewal and commitment of blood stem cells

TITLE: Pivotal role for glycogen synthase kinase-3 in hematopoietic stem cell homeostasis in mice

AUTHOR CONTACT:
Peter S. Klein
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-2179; Fax: (215) 573-4320; E-mail: pklein@mail.med.upenn.edu.

View this article at: http://www.jci.org/articles/view/40572?key=JnYgR1FfQ3JoB2G24T0j

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