JCI table of contents May 1, 2005
New vaccine means bye-bye to bacteria in the lung
Pseudomonas aeruginosa is a bacterium that can cause respiratory tract infections, which can be life threatening in patients who have cystic fibrosis. It is therefore important to develop a vaccine against this pathogen. Appearing online on 1 April 2005 in advance of print publication of the May issue of The Journal of Clinical Investigation, Ronald Crystal and colleagues from Cornell University use a novel strategy to create a genetic vaccine against P. aeruginosa.
The researchers use a modified adenovirus vector vaccine expressing a region of the outer membrane of P. aeruginosa, called OprF, which had previously been recognized as a promising vaccine candidate. This region of the bacteria was expressed in the capsid area of the vector. Immunization of mice with this vaccine induced antibody production and protected the mice from exposure to a deadly dose of the bacteria. Importantly, the mice could be repeatedly given the vaccine and the immune response against P. aeruginosa was boosted. Usually, adenovirus vectors do not allow for repeated infection.
These results may be useful in the development of vaccines against bacterial pathogens. The findings that a vaccine against Pseudomonas aeruginosa is therapeutic in mice offers promise for patients with cystic fibrosis or other disorders that prevent them from effectively fighting off respiratory tract infections.
TITLE: Protection against pulmonary P. aeruginosa infection following immunization with a replication-deficient adenovirus
Ronald G. Crystal
Weill Medical College of Cornell University, New York, NY USA
Phone: (212) 746-2258; Fax: (212) 746-8383; E-mail: firstname.lastname@example.org
View the PDF of this article at: https://www.the-jci.org/article.php?id=23135
How fat-blasting drugs really work
The incidence of type 2 diabetes (T2D) is increasing around the world. It is associated with mortality due to cardiovascular disease because people with T2D have high plasma levels of VLDL (the "bad" cholesterol) and other lipids. A drug called Pioglitazone (Pio), which activates a protein called PPAR gamma, can treat some aspects of T2D but it is not clear exactly how this drug works. In a study appearing online on 1 April 2005 in advance of print publication of the May issue of The Journal of Clinical Investigation, Henry Ginsberg and colleagues from Columbia University examine how Pio can lower plasma lipid levels and raise HDL (the "good" cholesterol) levels in people with T2D.
The researchers uncover unexpected effects of Pio on lipid metabolism in the liver. Patients treated with Pio had reduced plasma triglyceride levels and decreased VLDL in the circulation. But the patients did not show any change in liver secretion of VLDL or another lipid, apoB. Thus, the reduced VLDL was associated with increased efficiency of triglyceride clearance and fat breakdown from plasma.
These results offer new insights into the complex mechanisms whereby PPAR gamma activators affect lipid metabolism. This work is of interest to clinical diabetologists, physiologists studying lipid metabolism, and individuals working in the field of PPAR gamma receptors.
TITLE: Effects of the PPAR gamma agonist pioglitazone on lipoprotein metabolism in patients with type 2 diabetes mellitus
Henry N. Ginsberg
Columbia University, New York, NY USA
Phone: (212) 305-9562; Fax: (212) 305-3213; E-mail: email@example.com
View the PDF of this article at: https://www.the-jci.org/article.php?id=23219
TNFR2, not TNFR1, the real culprit in glomerulonephritis
Progressive glomerulonephritis is a disease that can cause kidney failure. TNF alpha is a protein that has been shown to cause inflammation and suppress the immune system, and it plays a functionally important role in the development of glomerulonephritis. TNF can bind to two different receptors -– TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2). In a study appearing online on 1 April 2005 in advance of print publication of the May issue of The Journal of Clinical Investigation, Tanya Mayadas and colleagues from Harvard University demonstrate that TNFR2 on kidney cells is the receptor that promotes the tissue injury seen in glomerulonephritis. These data suggest that blockade of TNFR2 may be a promising strategy in the treatment of glomerulonephritis.
TITLE: Renal cell–expressed TNF receptor 2, not receptor 1, is essential for the development of glomerulonephritis
Tanya N. Mayadas
Harvard Medical School, Boston, MA USA
Phone: (617) 525-4336; Fax: (617) 525-4333; E-mail: firstname.lastname@example.org
View the PDF of this article at: https://www.the-jci.org/article.php?id=23348
A new relationship between synaptopodin and alpha actinin
Synaptopodin is a protein found in the kidney in the brain where it binds to actin and regulates the shape and motility of cells in these areas. In a study appearing online on 1 April 2005 in advance of print publication of the May issue of The Journal of Clinical Investigation, Peter Mundel and colleagues from Mt. Sinai School of Medicine examine mice lacking synaptopodin to better understand its function in vivo. The authors show that synaptopodin cooperates with alpha-actinin, a protein similar to actin, to regulate actin filament formation and the cellular skeleton organization in neurons and kidney cells. A better understanding of synaptopodin in the kidney may aid in elucidating new therapeutic targets for focal segmental glomerulosclerosis, a kidney disease caused by mutations in the alpha-actinin gene. Understanding the regulation of alpha-actinin in the brain by synaptopodin may help scientists understand diseases involving impaired synaptic plasticity, like Alzheimer disease.
TITLE: Synaptopodin regulates the actin bundling activity of alpha-actinin in an isoform specific manner
Mt. Sinai School of Medicine, New York, NY USA
Phone: (212) 659-9332; Fax: (212) 849-2643; E-mail: email@example.com
View the PDF of this article at: https://www.the-jci.org/article.php?id=23371
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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