Psych Central

JCI table of contents April 1, 2005

03/11/05

EDITORS' PICK:

Birthing a new model of aspirin therapy in preeclampsia

Preeclampsia is a hypertensive disorder that occurs during pregnancy and can be detrimental to the health of the developing fetus and the mother. Low-dose aspirin therapy has been used to treat preeclampsia, but this strategy is controversial some researchers believe that it prevents preeclampsia while others find it increases related complications.

In a study appearing online on March 17, in advance of the April 1 print edition of the Journal of Clinical Investigation, Colin Funk and colleagues from the University of Pennsylvania describe a new mouse model that mimics the effects of low dose aspirin to explore how such therapy would impact blood clotting and reproductive functions.

The mice generated have reduced levels of prostaglandin H synthase 1 (PGHS1), a platelet protein that contributes to the heart-healthy effects of aspirin therapy. The authors find that these mice had the expected decreased platelet aggregation, inhibition of thrombosis, and impaired inflammatory responses typically seen with aspirin therapy. However, the uterine and ovarian environments were altered only slightly and allowed for normal induction of labor, normal litter size and similar development of offspring.

This new mouse model will have significant value in studying the role of low dose aspirin in several pathological conditions, such as preeclampsia, thrombosis and inflammation. The results suggest that low-dose aspirin treatment may prevent preeclampsia without compromising reproductive function.

TITLE: Differential impact of prostaglandin H synthase 1 knockdown on platelets and parturition

AUTHOR CONTACT:
Colin D. Funk
Queen's University, Kingston, Ontario, Canada
Phone: 613-533-3242; Fax: 613-533-6880; E-mail: funkc@post.queensu.ca

View the PDF of this article at: https://www.the-jci.org/press/23683.pdf
From 5:00PM USA EST Thursday March 17, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml

Oncology

Cholesterol adrift on a lipid raft affects cancer progression

Lipid rafts are small regions in the membranes of cells that contain high levels of cholesterol. In a study appearing online on March 17, in advance of the April 1 print edition of the Journal of Clinical Investigation, Michael Freeman and colleagues from Harvard Medical School examine whether the cholesterol content of lipid rafts plays a role in prostate cancer. The authors show that depletion of cholesterol by a cholesterol- lowering drug (simvastatin) induces death of prostate cancer cells. Elevating cholesterol content had the opposite effect, promoting tumor growth and decreasing death of the cancerous cells. Thus, the cholesterol content of lipid rafts in cell membranes may mediate tumor survival and may be a potential target involved in tumor progression.

TITLE: Cholesterol targeting alters lipid raft composition and cell survival in prostate cancer cells and xenografts

AUTHOR CONTACT:
Michael Freeman
Children's Hospital Boston, Boston, Massachusetts, United States
Phone: 617-355-6054; Fax: 617-730-0238; E-mail: michael.freeman@childrens.harvard.edu

View the PDF of this article at: https://www.the-jci.org/press/19935.pdf
From 5:00PM USA EST Thursday March 17, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml

Physiology

Liver disease faces a new menace

Liver damage after organ transplantation or hemorrhagic shock is due to a type of injury known as ischemia/reperfusion, occurring when blood flow is temporarily stopped and, upon restoration, leads to massive inflammation and death of liver cells. Studies have shown that a protein called NF kappa B plays a role in this type of injury, but its precise function is unclear. In a study appearing online on March 17, in advance of the April 1 print edition of the Journal of Clinical Investigation, Christian Trautwein and colleagues from Hannover Medical School interfere with NF kappa B function in liver cells to examine its role in liver injury. The researchers found that inhibiting NF kappa B protects against liver injury by decreasing expression of inflammatory proteins and may be a therapeutic target in liver disease.

TITLE: Deletion of IKK2 in hepatocytes does not sensitize these cells to TNF-induced apoptosis, but protects from ischemia/reperfusion-injury

AUTHOR CONTACT:
Christian Trautwein
Hannover Medical School, Hannover, Germany
Phone: 49-511-532-6620; Fax: 49-511-532-5692; E-mail: Trautwein.Christian@mh-hannover.de

View the PDF of this article at: https://www.the-jci.org/press/23493.pdf
From 5:00PM USA EST Thursday March 17, 2005 a PDF of this article will be available at:
http://www.jci.org/papbyrecent.shtml

Immunology

Thymic recovery restores T cells

New immune T cells mature in the thymus throughout life, but the aging thymus works less effectively and this is especially problematic in people who are immunocompromised. In a study appearing online on March 17, in advance of the April 1 print edition of the Journal of Clinical Investigation, Frances Hakim and colleagues from the National Institutes of Health examine the mechanism underlying this age-related alteration in thymic function. The researchers studied thymic size in adults with breast cancer who were recovering from chemotherapy. They demonstrate that the thymus can continue to grow for over a year after chemotherapy. This is not because the adult thymus is simply being filled back up with T cell precursors, but instead it is actually undergoing a long period of structural regrowth with new T cell generation. This is the first time that the immunocompromised adult thymus has been shown to be able to restore circulating T cell populations to normal levels and has implications for recovery from disease, infection, and chemotherapy.

TITLE: Age-dependent incidence, timecourse, and consequences of thymic renewal in adults

AUTHOR CONTACT:
Frances T. Hakim
National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States
Phone: 301-402-3627; Fax: 301-402-8690; E-mail: fhakim@helix.nih.gov

View the PDF of this article at: https://www.the-jci.org/press/22492.pdf
From 5:00PM USA EST Thursday March 17, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml

Source: Eurekalert & others

Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
    Published on PsychCentral.com. All rights reserved.

 

 

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