Travel Outside Of The US Causing Increased Health Risks To Americans
More than 2,000 physicians and scientists from around the world
are convening at the 55th American Society of Tropical Medicine
and Hygiene annual meeting in Atlanta this week to discuss the latest
advances in prevention and treatment of global infectious disease
threats - with one of the key topics discussed being the diseases
travelers are bringing back to the United States upon returning
from vacation or business trips either abroad and/or to tropical
regions.
Presentations on this topic this week will include:
* Trends in Travel-Associated Dengue Among U.S. Residents -- Researchers
from the San Juan branch of the Centers for Disease Control and
Prevention (CDC) will discuss their findings of 1193 travelers from
49 states with suspected dengue infections. Persons infected by
Dengue often don't see the symptoms of fever, headaches, muscle
and joint pain for up to a week after being affected and have often
returned from their travels. If not treated, the disease can cause
severe bleeding and kidney and heart damage. This research addresses
countries that have a higher risk of dengue for travelers, preventive
methods for travelers and the U.S. states that have been most affected
by this disease during the past decade.
* Walking the Line: Emerging Infectious Diseases on the U.S./Mexico
Border -- Scientists from the CDC and the University of Texas School
of Public Health will address why the Texas/Mexico is becoming one
of the fasted growing hot spots for the spread of infectious diseases
with the border now having one of the highest incidences of tuberculosis
in the U.S. They will also discuss how the U.S./Mexico border is
seeing an increase in dengue fever cases, an infectious disease
transmitted by mosquitoes.
* Chikungunya virus in French Travelers - Approximately 808 cases
of this emerging disease -- which is similar to a West Nile virus
as it is passed to the blood through a mosquito bite -- have been
diagnosed in Europe by researchers from l'Hospital Nord de Marseille,
France and the CDC among travelers in mainland France, Germany,
Italy, Norway and Switzerland. Most recently, cases are being diagnosed
in the U.S. which lends concern that more travelers returning to
the U.S. from Europe, particularly France, may carry the virus and
increase its spread further in the U.S.
###
Contact: Ivette Morello
American Society of Tropical Medicine
and Hygiene
Detrusor Smooth Muscle Cells May Be Critical In Induction Of Bladder
Inflammation Pathophysiology
Main Category: Urology / Nephrology News
Article Date: 22 Feb 2006 - 6:00 PST
Bladder biopsies from patients with Painful Bladder Syndrome/Interstitial
Cystitis (PBS/IC) are characterized by an increased number of activated
bladder mast cells in the detrusor.
Bouchelouche and colleagues from Copenhagen isolated and cultured
human detrusor smooth muscle cells and assayed protein expression
and secretion of molecules that have been shown to be key in the
promotion of mast cell recruitment, proliferation, and maturation.
These include monocyte chemoattractant protein-1 (MCP-1), stem
cell factor (SCF), and interleukin 6 (IL-6).
The authors demonstrated that mast cell mediators IL-4, and IL-13
separately or in combination with IL-1_ and TNF-_ induce the expression
and secretion of MCP-1, IL-6 and SCF by cultured human detrusor
smooth muscle cells.
This finding may provide the explanation for the presence of mast
cells in detrusor smooth muscle layers with possible implications
for the pathophysiology of PBS/IC.
It is also interesting that during inflammation, human detrusor
smooth muscle cells can be forced to adopt a secretory, less contractile
phenotype. Thus, the detrusor smooth muscle cell itself may provide
an attractive target of the drug therapy of painful bladder syndrome.
By Philip M Hanno, MD, MPH
J. Urol., 175:760-765 (February), 2006
Link Here.
Bouchelouche K, Andresen L, Alvarez S, Nordling J, Nielsen OH, Bouchelouche
P
URO Today
The only urology website with original content written by global
urology opinion leaders actively engaged in clinical practice.
http://www.urotoday.com
Gene Therapy For Muscular Dystrophy Fixes Frail Muscle Cells In
Animal Model, Stanford Study Finds
Main Category: Muscular Dystrophy News
Article Date: 27 Dec 2005 - 15:00 PST
A new gene therapy technique that has shown promise in skin disease
and hemophilia might one day be useful for treating muscular dystrophy,
according to a new study by researchers at Stanford University School
of Medicine.
In the study, scheduled to be published online in the Proceedings
of the National Academy of Sciences the week of Jan. 2, the researchers
used gene therapy to introduce a healthy copy of the gene dystrophin
into mice with a condition that mimics muscular dystrophy. The dystrophin
gene is mutated and as a result produces a defective protein in
the roughly 20,000 people in the United States with the most common
form of the disease.
Using gene therapy to treat muscular dystrophy isn't a new idea.
Thomas Rando, MD, PhD, associate professor of neurology and neurological
sciences, said that researchers have tried several different techniques
with variable success. One hurdle is getting genes into muscle cells
all over the body. Another is convincing those cells to permanently
produce the therapeutic protein made by those genes.
The gene therapy technique Rando and postdoctoral fellow Carmen
Bertoni, PhD, used was developed by Michele Calos, PhD, associate
professor of genetics. One of the main advantages of this method
is that it could potentially provide a long-term fix for a variety
of genetic diseases, including muscular dystrophy.
In muscular dystrophy, the muscle cells break down and are slowly
replaced by fat. Eventually people with the disease are confined
to a wheelchair and usually die in their 20s. There is currently
no effective treatment for the disease, which explains why gene
therapy remains a hope despite the significant hurdles.
Rando said the PNAS paper highlights an additional requirement
for any gene therapy to be successful: the introduced gene must
produce healthy dystrophin protein in large quantities in order
to repair the entire muscle cell. Previous muscular dystrophy gene
therapy studies did not look at whether the introduced dystrophin
spread along the entire length of the muscle cell, which can be
many millimeters long in mice or inches long in humans.
In the upcoming paper Bertoni used a standard gene therapy method
to introduce two genes - dystrophin and a gene that makes a glowing
protein - into mice with a mouse version of muscular dystrophy.
She found that in mice producing insufficient dystrophin, she could
see the glowing protein slowly leak out of the cell. This leakiness
is a sign that the cell is not healed. In contrast, when she used
Calos' gene therapy technique to introduce the genes, the muscle
cell contained high levels of dystrophin distributed along the length
of the cell and the glowing protein stayed within the cell, suggesting
that the abundant dystrophin repaired the ailing muscle.
"If you have a single cell that's a foot long and you only
correct a few inches, you've done very little," Rando said,
"Whereas if you correct it from end to end, you truly cure
the disease in that cell."
Both Rando and Calos point out that the road to a gene therapy
cure for muscular dystrophy is still a long one. However, Calos
is confident that her technique will be a part of the journey towards
a cure for the disease and for other diseases such as hemophilia
and the skin disease, epidermolysis bullosa. Early trials using
her approach have looked promising in animal models of both of these
diseases.
"I think our approach has a lot of potential to overcome issues
that have slowed the field of gene therapy," Calos said.
Calos said her approach has two advantages: one is that in her
method the gene gets inserted directly into the cell's own DNA,
which is why the correction is permanent. In some other methods
the gene stays outside the DNA and slowly breaks down. The second
advantage is that her method doesn't rely on a virus to disperse
the DNA and therefore avoids some of the issues, including cancer
and an immune reaction, that have turned up in viral gene therapy
trials. Instead this approach uses naked DNA that travels through
the bloodstream to cells of the body.
For his part, Rando said that no matter how well gene therapy works
in an isolated muscle, researchers still must figure out how to
get that gene to muscles throughout the body. Despite the remaining
hurdles, both Rando and Calos said that their study is a step towards
eventually treating muscular dystrophy and other diseases using
gene therapy.
Other researchers who contributed to this work include research
assistants Sohail Jarrahian and Yining Li, postdoctoral scholar
Thurman Wheeler, MD, and graduate student Eric Olivares, PhD. The
project was supported by grants from the Muscular Dystrophy Association.
Stanford University Medical Center integrates research, medical
education and patient care at its three institutions - Stanford
University School of Medicine, Stanford Hospital & Clinics and
Lucile Packard Children's Hospital at Stanford. For more information,
please visit the Web site of the medical center's Office of Communication
& Public Affairs at mednews.stanford.edu.
Amy Adams
amyadams@stanford.edu
Stanford University Medical Center
stanford.edu/MedCenter/MedSchool
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