|
The following are releases from Harvard University.
Article 1 (one)
McLean Study Identifies New Area of Brain Linked to Drug Addiction
FOR IMMEDIATE RELEASE:
October 11, 2005
Belmont, MA - Researchers at Harvard-affiliated McLean Hospital say they have identified an area of the
brain that appears to play a key role in why cocaine and other stimulants are so highly addictive, a finding that could ultimately
lead to new targeted treatments for addiction and other brain disorders.
"We found the region of the brain known as the cerebellar vermis, which is also involved in other psychiatric illnesses,
appears to play a role in drug addiction," said lead researcher Carl Anderson, PhD, of McLean Hospital's
Brain Imaging Center. The research appears in the Oct. 12 issue of the journal Neuropsychopharmacology.
"Scientists previously contended that the vermis had little involvement in addiction or other disorders involving dopamine.
This changes the perspective on how brain regions may interact during addiction. It introduces an entirely new player," Anderson
added. The study involved the review of previously published data on the vermis that had not been analyzed for its involvement
in addiction. The vermis, a worm-shaped brain area located in the cerebellum near the back of the head, affects people's ability
to concentrate.
In the original study conducted in 1998 by Luis Maas, MD, PhD, one of the authors of the new report, researchers used magnetic
resonance imaging (MRI) to scan the brains of 10 crack-cocaine abusers as they viewed a video of people lighting up a crack
pipe. When compared to a control group of non-users, the study found that the users-and not the comparison subjects-both reported
an increased desire for cocaine following this cue and had increased activity in several brain areas, including the anterior
cingulate cortex.
The new analysis conducted by McLean's Anderson and colleagues shows activation in the vermis in cocaine users while they
viewed the cocaine-use video. "The vermis appears more responsive to cocaine cues in people who abuse cocaine," said co-author
Marc J. Kaufman, PhD.
As part of the investigation, Anderson also reanalyzed data from an unrelated study collected by Alan J. Fischman, MD,
in collaboration with Bertha Madras, PhD, two authors of the new study. Their earlier analysis showed the distribution of
a drug that targets the dopamine transporter, the protein that seems to be blocked by such stimulants as cocaine, through
the use of positron emission tomography (PET). The new data show, in non-drug using subjects, that the vermis may contain
dopamine transporters and thus may be a target for cocaine and other stimulants, thereby increasing dopamine in the brain.
If the vermis plays a key role in the brain's dopamine system, as the new McLean Hospital findings suggest, this could
explain its role in addiction, as well as in other brain disorders, such as Parkinson's disease, which is characterized by
a shortage of dopamine, and ADHD.
The new findings "seem to support the conclusion that the vermis is a brain area involved in stimulant response," Anderson
said. "If this finding holds true, it could help change our understanding of addiction."
"One possibility is that the vermis acts as an "Achilles Heel" in sensitive individuals," he noted. "This information could
ultimately help us to develop addiction treatments by targeting the vermis therapeutically."
McLean Hospital, consistently ranked the nation's top psychiatric hospital by U.S News and World
Report, is an affiliate of Harvard Medical Schoool and Massachusetts
General Hospital and a member of Partners HealthCare.
Bacterium Proves Essential to Immune System Development.
Carbohydrate on bug's coat tips the system toward Cell-mediated response.
In the July 15, 2005 Cell, a team led by Dennis Kasper, the William Ellery Channing Professor of Medicine at Brigham
and Women's Hospital and professor of microbiology and molecular genetics at Harvard Medical School (HMS), and Sarkis Mazmanian,
HMS instructor in microbiology and molecular genetics, both at the Channing laboratory, reports that Bacteriodes fragilis
aids immune system development.
Mammals contain approximately a thousand species, and one trillion cells, of bacteria to every gram of intestinal contents.
The team studied germ-free mice and found that these mice have fewer CD4+ T cells in their immune system. When B. fragilis
colonized the mice, their CD4+ T cell levels were restored.
Another team in Kasper's lab previously announced that T cells could recognize certain bacterial carbohydrates as antigens.
Kasper and Mazmanian found that if the mice were colonized with a strain of B. fragilis that lacked the carbohydrate polysaccharide
A (PSA), the bacteria could no longer restore T cell levels in the mice.
The team found that PSA induces the Th1 subset of T cells. The immune system relies on a balance between these cell-mediated
responses and antibody-mediated, or Th2, responses. Kasper said that mice and humans raised in sterile environments have immune
systems skewed toward Th2 responses. If bacterial factors like PSA are necessary for development of the Th1 arm of the immune
system, it would reinforce that bacteria is essential for immune function.
Article 2B(Two B)
Size of brain structure could signal vulnerability
to anxiety disorders
Area appears smaller in those that continue to react to images
associated with discomfort
BOSTON - July 11, 2005 - The size of a particular structure in the brain
may be associated with the ability to recover emotionally from traumatic events. A new study by researchers from Massachusetts
General Hospital (MGH) finds that an area called the ventromedial prefrontal cortex is thicker in volunteers who appear better
able to modify their anxious response to memories of discomfort. The report will appear in the Proceedings of the National
Academy of Science and has received early online release on the PNAS website.
"We've always wondered why
some people who are exposed to traumatic experiences go on to develop anxiety disorders like post-traumatic stress disorder
and others do not," says Mohammed Milad, PhD, a research fellow in the MGH Department of Psychiatry, the study's lead author.
"We think this study provides some potential answers."
In the classical model of conditioned fear, individuals respond
with physical and emotional distress to situations that bring back memories of traumatic events. Such responses are normal
and usually diminish over time, as those situations are repeated without unpleasant occurrences. But some people continue
to respond with what can be overwhelming fear and may develop post-traumatic stress disorder (PTSD).
For example,
it would not be unusual for a soldier who experienced a traumatic battlefield situation to become distressed when hearing
noises that bring back those memories, such as the sound of a helicopter. Most commonly, repeated exposure to such sounds
without additional trauma reduces or extinguishes the fearful response - a phenomenon called "extinction memory." But some
individuals continue to experience anxiety, along with other symptoms characteristic of PTSD, when hearing the sounds.
Prior
studies in animals have suggested that the ventromedial prefrontal cortex (vmPFC) - an area on the lower surface of the brain
- may be involved in extinction memory. The vmPFC may help to quell potential fears by inhibiting the activity of the amygdala,
an area known to be involved with fear. The current study was designed to see if the structure of the vmPFC is related to
the ability to modify response to an unpleasant memory.
Over a period of two days, 14 volunteer study participants
viewed a series of digital photos of two different rooms. Each room contained a lamp that was turned on - sometimes with a
red light, sometimes a blue light. On the first day, participants viewed the photos several times, and then viewed them again
with a mild electric shock - described as annoying but not painful - delivered to their hands right after a lamp with a blue
light appeared. They then viewed a series of the photos with no shocks administered.
On the second day, measurements
of skin conductance were taken while the volunteers once again viewed the photos with both colors of lights displayed but
no shocks given. A measurement of anxiety level, skin conductance is determined by the amount of perspiration on the palm
of the hand. After that part of the experiment, the volunteers had structural magnetic resonance (MR) images taken of their
entire brains.
The MR studies showed that those participants who appeared to have less anxiety response upon viewing
the blue lights the second day, as measured by skin conductance, also had a thicker vmPFC. "That was the only area of the
brain that correlated with extinction memory," says Milad. "So, these results suggest that a bigger vmPFC may be protective
against anxiety disorders or that a smaller one may be a predisposing factor. But exactly how that might work we just don't
know."
Scott Rauch, MD, the senior author of the paper and director of the Psychiatric Neuroscience Research Division
in MGH Psychiatry, notes that future research could look at genetic or environmental factors that may underlie these differences
in brain structure and also investigate whether vmPFC size predicts the success of exposure-based therapies for anxiety disorders.
Another factor to study would be whether vmPFC measurement should be used to screen those likely to be exposed to traumatic
situations or to develop preventive strategies. Rauch is an associate professor of Psychiatry at Harvard Medical School.
The
report's co-authors are Roger Pitman, MD, of MGH Psychiatry; Brian Quinn and Bruce Fischl, PhD, of MGH Radiology, and Scott
Orr, PhD, of the VA Medical Center in Manchester, N.H. The study was supported by grants from the National Institute of Mental
Health and the MGH Tosteson Fellowship.
Massachusetts General Hospital, established in 1811, is the original and largest
teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States,
with an annual research budget of more than $450 million and major research centers in AIDS, cardiovascular research, cancer,
cutaneous biology, medical imaging, neurodegenerative disorders, transplantation biology and photomedicine. In 1994, MGH and
Brigham and Women's Hospital joined to form Partners HealthCare System, an integrated health care delivery system comprising
the two academic medical centers, specialty and community hospitals, a network of physician groups, and nonacute and home
health services.
Article
3(Three)
Chimpanzee genome effort shines light on human evolution
Broad Institute, Washington University lead decoding effort
By Alvin Powell
Harvard News Office
An international research consortium has unraveled the chimpanzee genetic code, finding that humans and chimps
share 96 percent of their genetic blueprint in an advance that has already begun to shed light on what makes humans "human."
The research effort, led by scientists at the Broad Institute of MIT and Harvard, the Washington University
School of Medicine in St. Louis, and the University of Washington, Seattle, focused on the chimpanzee in hopes that genetic
comparisons with humanity's closest relative will lead to answers to both practical questions - such as the causes of human
disease - and to more fundamental questions on human biology.
In addition to their obvious physical differences, humans and chimpanzees have different responses to Alzheimer's
disease, malaria, and HIV/AIDS, for example.
"We're focusing on the differences as a way to shed light on ourselves," said Eric Lander, Broad Institute
director and professor of systems biology at Harvard Medical School, who led the project along with Richard Wilson of the
Washington University School of Medicine in St. Louis and Robert Waterston of the University of Washington, Seattle. "This
is a case where evolutionary analysis is a direct handmaiden to biomedicine."
Among the 3 billion base pairs in the DNA of both humans and chimpanzees, researchers found differences in
40 million sites. It is in those sites where the differences between the two species lie.
"Just what makes us human? Now, in a sense, we can answer that question," said Tarjei Mikkelsen of the Broad
Institute and the research paper's lead author. "We now have a nearly complete catalog of all genetic differences between
humans and chimps and there's about 40 million of them. And any human-specific trait that's encoded in our DNA is caused by
one or more of those 40 million changes."
The research, published in the Sept. 1 issue of the journal Nature, puts the chimpanzee with humans, mice,
and rats as the only mammals whose DNA has been decoded and published in a major scientific journal.
When measured by changes in their genetic codes, humans and chimpanzees are about 10 times more different
than are individual humans from each other. By comparison, human and mouse DNA have about 60 times more differences than do
human and chimpanzee DNA.
The research was conducted by the Chimpanzee Sequencing and Analysis Consortium, which involved 67 researchers
in the United States, Israel, Italy, Germany, and Spain. The sequencing and assembly of the chimpanzee genome was done at
the Broad Institute and at the Washington University School of Medicine in St. Louis.
In addition to the Broad Institute, which is a collaboration of Harvard and the Massachusetts Institute of
Technology, the effort involved researchers from Harvard Medical School and the Faculty of Arts and Sciences.
The work, funded by the National Institutes of Health's National Human Genome Research Institute, cost between
$20 million and $30 million. It was released at a news conference in Washington, D.C., on Wednesday (Aug. 31). The DNA used
in the project came from a chimp at the Yerkes National Primate Research Center in Atlanta named Clint, who died last year
from heart failure.
Reading the code
An organism's genetic code is contained in long, complex molecules called DNA located in the nucleus of every
cell. DNA is a ladderlike structure made up of joined pairs of just four kinds of subunits called bases. The sequence of these
bases - which vary from human to human and from chimpanzee to human - contain an organism's genetic information.
It is through changes in the sequence of bases in an organism's DNA - by adding, subtracting, or substituting
- that evolution occurs and it is through that process that humans and chimpanzees came to differ.
Scientists believe that humans and chimpanzees diverged from a common ancestor about 6 million years ago.
Since that time, both species have continued to evolve, acquiring traits that make them different from both that ancestor
and from each other.
Though completing the chimpanzee genome is an achievement in itself, it is the ability to now compare chimpanzee
and human DNA side-by-side that has researchers excited.
The differences between the two genetic codes include 35 million sites where DNA base pairs differ and another
5 million sites where a portion of the genetic code - up to thousands of base pairs - has been inserted or deleted.
The comparison is already bearing fruit, revealing areas of rapid change and highlighting areas to target
for future research.
Researchers found that the most rapidly changing genes in humans, chimpanzees, and other mammals include those
involving reproduction, the sense of smell, and the immune response that protects creatures from infection and disease.
In addition, they found that the genes changing unusually quickly in humans and chimpanzees, compared with
other mammals, include those involved in sound perception, nerve signal transmission, and production of sperm.
Among the genes that appear to be evolving more rapidly in humans than in chimpanzees are those called transcription
factors. These genes are known to control other genes, including one thought to be involved in the appearance of speech in
humans.
The consortium found a small number of genes that have undergone dramatic change, with more than 50 genes
in humans missing from chimpanzees, including three key genes involved in inflammation. The absence of those genes in chimpanzees
may explain the known differences between chimpanzees and humans in their inflammatory and immune response. In addition, six
regions of the human genome appear to have been acquired relatively recently, over the last 250,000 years, and to contain
changes so advantageous that they rapidly spread through the population. These areas are prime targets for future research.
"The most concrete result of this work is that we now have this complete catalog - nearly complete catalog
- of human-chimp differences," Mikkelsen said. "Both our laboratory and many other laboratories around the world are sifting
through these ... to find the relevant, important changes."
Article 4 (four)
Urine Test Tracks Deadly Birthmarks
Also used to detect cancers
By William J. Cromie
Harvard News Office
A simple urine test holds
promise for detecting both life-threatening birthmarks and the presence of cancer. Out-of-control growth of both is tied to
proteins that reveal themselves in urine.
Although not yet approved by the Food and Drug Administration, results from such tests are already being used to
guide treatment of children with disfiguring birthmarks and adults with cancer. Urine tests, now given to all people as part
of every physical, might someday provide doctors with valuable information difficult to obtain by other means.
"Many birthmarks, caused by abnormal growth of blood or lymphatic vessels, go away without treatment," notes Marsha
Moses, associate professor of surgery at Harvard Medical School and Children's Hospital Boston. "But some grow frightfully
big before they start to regress - big enough to kill a child. Also, some birthmarks grow unseen, inside the body. We can
look at the urine of these children and predict the extent and activity of the abnormalities. Such a capability gives physicians
data they can use to treat these patients more effectively."
The same is true for cancer. Last year, Moses and her colleagues announced discovery of ADAM 12, a protein found
in the urine of breast cancer patients. Increasing amounts of this protein in urine signal that the cancer is getting worse.
In both birthmarks and cancer tumors, treatments that decrease levels of these compounds mean patients are getting
better.
"The beauty of testing for urinary markers, especially in younger patients, is that it's not invasive," Moses points
out. "These diseases expose sick kids to so much invasive poking and prodding that any information physicians can get without
this is a good thing."
Moses' lab boasts one of, if not the, world's largest bank of urine samples of cancer patients. But Moses urges
people to hold their urine. "We receive unsolicited samples from all over the country," she says, "But we can't do anything
with them because our tests have not yet been approved for general use."
A test is tested
The urinary markers are known as matrix metalloproteinases, thankfully shortened to MMPs. In 1998, Moses and colleagues
published a report showing that growth of blood vessels requires MMPs (see May 7, 1998, Gazette). She noted that the more
MMPs found in cancer patients' urine, the more vessels were being attracted to their tumors, and the bigger and faster those
tumors grow. At present, 30 to 40 different drugs are under development to treat tumors by blocking such growth.
In the medical business, blood-vessel growth is known as "angiogenesis," and its anti-drugs are called angiogenesis
inhibitors. One of them, Avastin, has been approved for treatment of colon cancer in 28 countries including the United States.
It is also being tested on patients with cancers of the kidney, breast, and ovaries.
Jennifer Marler, a former research fellow at Children's Hospital Boston, pointed out that growth of birthmarks,
like blood-vessel tumors, responds to treatment with anti-angiogenesis drugs. She suggested to Moses that urine samples might
provide a new way to help determine which troubling birthmarks will respond to these drugs.
Moses and Marler put together a research team that included Steven Fishman, a surgeon at Children's Hospital with
extensive experience in treating disfiguring and life-threatening birthmarks. The group, including members of Children's vaunted
Vascular Anomalies Program, tested the urine of 217 children with such birthmarks and compared it with that of 74 healthy
kids of the same age. In the July issue of the medical journal Pediatrics, the team reports that more than half of patients
with blood-vessel tumors showed high levels of MMPs. In addition, 41 percent of those with vascular malformations - twisted,
tangled wads of blood vessels that grow uncontrollably - had abnormally high levels of the proteins.
This study suggests that angiogenesis also plays a key role in the growth of vascular malfunctions. It opens the
door for treating them, as well as the tumors, with angiogenesis-blocking drugs.
Fishman and his colleagues then successfully treated two young children in the study with drugs and surgery. Afterward,
MMPs could no longer be detected in their urine.
Dipsticks for diseases
Fishman's team evaluates and/or treats more than 1,000 patients a year from all over the world. He has begun giving
11 young patients an anti-angiogenesis drug that has been approved for treating adults with cancer. Nine of the children have
not responded to, or cannot be given, other available treatments. Two others received the drug under compassionate-use rules,
which means that surgeons have decided nothing else will help them.
These tests will mainly determine whether the anti-MMP drugs are safe. If results are positive, longer trials with
large numbers of children will follow. Urine mining is also being tested by Moses on a number of different cancers, including
very aggressive brain cancers known as glioblastomas.
Moses is pleased with what has been demonstrated about the potential of urine testing so far. But she knows that
a lot more research needs to be done before children with threatening birthmarks will be tested by their doctors on a routine
basis.
And Moses loves to think about what she calls "the big global picture." Besides MMPs associated with birthmarks
and breast cancer, others have been identified for detecting and monitoring prostate and ovarian cancer. She sees these as
part of urine "dipstick" checks that could be part of annual physicals some day. Compounds (antibodies) on dipsticks, which
detect various disease markers, will be quickly analyzed. "The results will not only help physicians find cancers, but predict
when they will spread, or come back again after treatment," she says. "And all from just a few drops of urine."
Article (5) five.
A new type of hybrid cell created at Harvard University could eventually solve the mystery of how embryonic stem cells
develop into specialized adult cells, and provide genetically tailored treatments for many human diseases. What's more, the
technique holds out the possibility of doing this without creating or destroying human embryos. The researchers fused adult
skin cells with embryonic stem cells in such a way that the genes of the embryonic cells reset the genetic clock of the adult
cells, turning them back to their embryonic form.
Kevin Eggan and his colleagues have succeeded in transforming adult skin cells into cells that behave very much like
embryonic stem cells, opening the door for new treatments of juvenile diabetes, Parkinson's and other diseases. Such adult-cum-embryo
cells, taken from people with juvenile diabetes, Parkinson's, Alzheimer's, and other genetic diseases, could reveal how such
diseases develop and provide novel treatment for them. For example, normal cells might be made to replace abnormal ones that
cause juvenile diabetes and Alzheimer's disease.
It should be possible to coax these newly created embryonic cells "into replacement cells and even organs," says biologist
Chad Cowan who participated in the experiments. "But it would definitely not be possible to clone the person from which the
adult cell came." These potentials are not just around the corner. "We feel this is an important achievement," notes Cowan.
"We're very excited about it. But we have many technical hurdles to overcome before we're ready for the showroom floor, before
we can wheel out the prototype model." Although the fusion method is more efficient and it satisfies many ethical concerns,
he continues, "the achievement does not mean ongoing research using embryonic stem cells should be stopped or even slowed.
Our technique may complement that of using these embryonic stem cells — even replace it some day — but that day
is a long way off."
Cowan is the lead author of a report of the research published in the August 26 issue of Science. The other authors are
Kevin Eggan, Douglas Melton, and Jocelyn Atienza of the Harvard Stem Cell Institute. Overcoming the hurdles:
The next step is to puzzle out how an embryonic cell can turn back, or reprogram, the genes of an adult cell. That could take
10 years, Cowan guesses. "But is will eventually happen, and it will mean scratching at some of biology's fundamental questions
in the process," he says. However, this long-term scratching at the fundamentals does not have to delay the use of hybrid
cells for helping patients. The quickest way to new treatments, the researchers believe, is finding a way to remove the embryonic
DNA. "That's the primary hurdle in the foot race to find treatments for patients, " Eggan states. The hybrid cells contain
two sets of DNA, or genes, one from the reprogrammed adult cell and one from the embryonic "starter" cell. To track disease
development, experimenters need to excise the latter. That done, they can determine how the adult cells differentiate into
diseased cells and tissues. "This seems like the simplest and fastest approach," Cowan comments, "but my experience in biology
is that the simplest things sometimes turn out to be the most difficult." This is why none of the researchers will venture
a guess on when it could happen, and why they advise against any slowdown in research that requires embryos to be created
or destroyed.
The Harvard group obtained the starter cells by growing embryos from excess fertilized cells acquired from fertilization
clinics with the owners' permission. Using such materials, Douglas Melton, the Thomas Dudley Cabot Professor of the Natural
Sciences in the Faculty of Arts and Sciences and co-director of the Harvard Stem Cell Institute, has created at least 17 new
lines of embryonic stem cells using private funds (see March 4, 2004 Gazette). These are not part of the cell lines eligible
for federal funding. The new work on hybrids was done using stem cells made by Melton, then some of the experiments were repeated
with a federally approved line of cells. The adult cells came from foreskin and pelvic areas. When all the problems are solved,
the Harvard team sees a new source of stem cells produced without the need to create or destroy embryos that some people insist
are "alive." "We will never satisfy all of the ethical objections to using embryonic stems cells," Cowan admits, "but we believe
that the majority of people will find this technique morally acceptable. "
Article (6) six
A new look at anaemia
A cure in fish could work in humans
By William J. Cromie
Harvard News Office
Scientists have discovered a new pathway by
which animals make hemoglobin, the red molecule vital for delivery of oxygen throughout the body. That knowledge has led to
curing anemia in fish. Humans could be next.
Leonard Zon and his colleagues at the Harvard Medical School were trying to find out how this amazing molecule forms by
studying zebrafish, small piscians whose transparent bodies allow their inner workings to be easily seen while they are alive.
The effort centered on a mutated strain of fish known as "shiraz." The researchers name their mutants after red or white wines,
depending on whether red or white blood cells are involved. The shiraz fish lacks hemoglobin, the molecule that binds with
oxygen in the cells of all red-blooded animals. Other mutants have names such as "Chianti" and "chardonnay."
The zebrafish is so important to researchers that its genome has been sequenced along with that of humans. Zon and his
team used this information to find and clone the gene that makes shiraz so pale. The gene has a less fun name, glutaredoxin
5, or grx5 for short.
More scientific detective work revealed that yeast has its own version of the same gene. That's strange because yeast doesn't
have blood, so it doesn't need hemoglobin. But yeast does need iron and its grx5 gene is involved in manipulating iron in
this fungus, best known for making beer and wine.
Zon and his team then made a mutant zebrafish with a doctored rendering of the yeast gene. "That rescued the fish," Zon
declares. "It could now make hemoglobin. Without hemoglobin, zerbrafish embryos lacking grx5 can absorb oxygen from water
through their skin. But eventually they die, most likely from their anemia."
Yeast, fish, and us
The big discovery here is that two biological functions, once thought to be entirely separate, act together to produce
hemoglobin, a substance without which creatures like humans become anemic. "It's nice to know about this pathway," Zon comments.
"It raises the possibility of developing a drug that might mimic the function of the grx5 gene. In yeast, there may be other
genes that suppress this defect and can be turned off. We have evidence that such suppressors exist in mice and humans. We
are working on these things now."
Several different types of anemia plague humans, but the most common form stems from a reduced level of hemoglobin. This
shortage, in turn, comes from a deficiency of iron, an essential ingredient of the red molecule. Similarities in the way yeast,
fish, and humans handle iron tie the whole thing together.
About five years ago, Zon and some colleagues discovered a gene, called ferroportin or iron transporter, which is responsible
for carrying iron from other parts of a cell to where hemoglobin is made. When you eat beef or spinach, this gene sees to
it that iron is moved from your intestines to the rest of your body. It also, Zon found, moves iron through the placenta from
a mother to her fetus. Zebrafish embryos get their iron in the same way. Thus, he says, "300 million years of evolution have
preserved the biochemical process by which moms deliver iron to their babies."
Zon's research also revealed that humans with mutated transporters have iron metabolism problems. "This was the first time
that a fish mutant was found to be associated with a human disease," he notes.
The newest discovery of how zebrafish combine iron transport with hemoglobin production is reported in the August 18 issue
of Nature. Lead author of the report is Rebecca Wingert, who was a graduate student when she, Zon, and their co-workers did
the research at Children's Hospital Boston and Dana-Farber Cancer Institute, teaching hospitals associated with Harvard Medical
School.
"We see patients that look like zebrafish mutants in that they both have trouble making hemoglobin in the same way," Zon
points out. "What we want to do next is to see if they have the mutated shiraz gene, grx5. After that, our hope is to find
ways to provide the missing parts that will keep this type of anemia from happening."
His laboratory also works on other diseases that can be traced to faulty iron transport. One such problem produces iron
overload rather than iron deficiency. Then there is anemia paired with ataxia, which causes certain brain cells to die, resulting
in impaired balance and walking, as well as problems with limb and eye movements and with speech.
Zon will do such studies in zebrafish. then apply what he learns to humans. "This small, transparent fish," he says, "turns
out to be a powerful tool for learning about many things that affect you and me."
|
