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STANFORD-UCSF MERGER ENDS
Stanford and UC San Francisco have
agreed to an amicable separation of their two clinical operations
and expect to bring their merged enterprise to an official close
in the spring. The leadership of the two academic medical centers
had envisioned the two-year-old enterprise, known as UCSF Stanford
Health Care, as an opportunity to help steer their institutions
through a period of crisis in health care.
* But
the merged operation encountered financial and organizational obstacles
that, in the final analysis, seemed
insurmountable. On Oct. 28, 1999, Stanford President Gerhard Casper
wrote a letter to UC President Richard Atkinson, requesting a formal
separation. "With great anguish, I have concluded that, in our efforts
to find bold solutions to the problems of academic medical centers,
we have taken on too much. We have failed to achieve a new common
UCSF Stanford Health Care culture that would provide the whole-hearted
support needed," Casper wrote.
The University of California Regents
sanctioned the move on November 18. The two universities now are
taking the legal and regulatory steps to disengage their operations
and are gradually decentralizing key functions. The goal is to complete
the dissolution by March 2000.
University officials recognized from
the start of the merger in November 1997 that they were breaking
new ground, as the enterprise meshed a public and private university.
They viewed it as a way to help both medical centers through a period
of mounting financial pressures, including staggering Medicare cuts
mandated by the federal Balanced Budget Act of 1997 and declining
reimbursements from managed care companies. By combining operations,
the two partners expected to enhance their position in the marketplace
by sharing resources in contracting, purchasing, marketing, information
technology and other services, and by creating an integrated faculty
that would be second to none.
"We and UCSF entered into this venture
with the very best of intentions -- to position our medical centers
in the best possible way," says Eugene Bauer, MD, dean of Stanford
School of Medicine and Stanford's vice president for medical affairs.
But the financial pressures proved
to be daunting. By the second year, UCSF Stanford lost ground to
further Medicare cutbacks, rising costs for drugs and supplies and
higher merger transaction costs than anticipated. It finished the
1998-1999 fiscal year with an $86 million loss, of which $66 million
was related to operations losses at the UCSF/Mount Zion Medical
Center in San Francisco.
Moreover, the faculties at the two
institutions never integrated in the way initially envisioned by
the merger. In the end, faculty members remained loyal to their
home institutions. "If there was a failure to be ascribed, it's
that UCSF Stanford Health Care didn't present a ve hicle
to which the UCSF and Stanford faculties could transfer their loyalties,"
Bauer says.
Given the venture's faltering ability
to meet its goals, Presidents Casper and Atkinson asked on August
3, 1998, for a reassessment of the structure of the merged organization.
That review involved intense discussions, jointly and separately,
between the leadership and faculty at both sites.
In the end, the conclusion was that
"our unitary management structure has not given us the flexibility
and resources that we needed for managing the north and south sites
effectively," Casper said in his letter.
Despite the merger's dismantling, the
two partners have agreed to continue to collaborate on information
technology and home health care. They are also exploring the prospect
of maintaining an integrated children's service -- an area in which
joint faculty efforts proved successful.
In addition, the many academic collaborations
fostered by the merger will continue, Bauer says. He says he expects
no disruption to patient care or to the school's research and teaching
activities as a result of the separation.
"Both Stanford and UCSF are strong
and remain deeply committed to education, to our research enterprise
and to the health care community we serve," Bauer says. "This will
not affect the commitments our institutions have -- not one iota."
Bauer says he is now "guardedly optimistic"
about Stanford's financial future. Stanford and Packard hospitals
together are now projected to have an operating profit of $15 million
in the current fiscal year, which began in September, he says. Stanford
will renew its focus on growing programs, such as those in general
surgery, gastroenterology and bone marrow transplantation and must
continue to keep its expenses down in order to ensure continued
success, he says. -- RR
WHY THE OTHER
LANE ISN'T ALWAYS AS
FAST AS IT SEEMS
Creeping along in traffic, you can't help but think
the world is passing you by. First one car rolls past, then another,
then another -- and your lane scarcely advances. Look, even that
rusty Volkswagen bus is getting ahead.
Fuming at the tortoise holding up your lane, you
barge into the next lane at the first gap in traffic.
Congratulations, you may have fallen victim to an
illusion. While our brains excel at many things, monitoring the
relative speed of traffic is not one of them, according to Robert
Tibshirani, PhD, professor of health research and policy and of
statistics. In a paper published in the September 2, 1999, issue
of Nature, Tibshirani and Donald Redelmeier, from the University
of Toronto, showed that drivers often overestimate the average speed
of an adjacent lane of traffic. Drivers' impressions are so
skewed that most would opt to change lanes even when their own lane
was going faster, on average.
Why are we so easily misled? We could get an accurate
reading of our relative speed simply by counting the number of cars
we pass and that pass us, Tibshirani says. But instead, our minds
rely on a subjective and clearly fallible impression of our progress.
Using a computer simulation of two lanes of traffic
moving at the same average speed, Tibshirani and Redelmeier discovered
what they think is the basis for this misperception. When traffic
becomes dense, we spend more time being passed than passing other
cars.
To understand how this difference creates an illusion,
imagine you are driving on a congested, two-lane highway. Although
the two lanes are traveling at the same average speed, at any moment
one lane may be going faster or slower than the other. Say you are
in the lane that is temporarily faster. Because cars tend to bunch
together when they slow down, you will quickly pass a cluster of
cars, which you don't bother to count. Then when your lane slows,
a line of cars starts to pass you -- but they are the same cars
you just overtook. Moreover, because the passing cars have now spread
out, they will take longer to pass you, and it seems like more cars
are going by.
Simple competitveness may also propel lane-hopping,
says Tibshirani. Moving slowly while car after car speeds past feels
like defeat to many drivers. Magnifying this feeling, our attention
tends to be directed forward and to the side during driving, and
cars we overtake quickly disappear from our field of vision -- and
consequently from our awareness. Cars that have passed us, though,
usually remain in sight -- becoming persistent reminders that we
are lagging.
Still, Tibshirani doesn't argue against all lane
changes. The perception that the next lane is moving faster is sometimes
right. Also, his work leaves open the possibility that drivers can
gain time by darting aggressively from lane to lane.
Tibshirani argues for a conservative approach. "You
are often better off staying where you are, in terms of safety and
in terms of speed," he says. -- ML
BONE CEMENT EASES SPINE PAIN
By injecting liquid bone cement directly
into the cracks of a broken vertebra, interventional neuroradiologists
at Stanford are able to strengthen the fractured bone and provide
permanent pain relief to people suffering from excruciating spinal
fractures. Many patients for whom traditional methods have proved
ineffective have experienced a dramatic improvement within 24 hours
of the new treatment, researchers say.
"It's kind of like getting a cavity
filled when you go to the dentist," says Huy M. Do, MD, of the minimally
invasive procedure known as percutaneous vertebroplasty. But the
pain associated with a fractured vertebra makes a toothache seem
trivial.
According to Do, an assistant professor
of radiology at Stanford, about 750,000 new vertebral fractures
occur each year in the United States, and about 115,000 of them
result in hospitalization. The traditional treatment methods of
bed rest, pain medication and back bracing are frequently insufficient
at relieving the often debilitating pain.
* In percutaneous
vertebroplasty, Do and his colleagues insert a needle into the spine
to reach the fracture site. They
then inject a bone cement called
polymethylmethacrylate (PMMA). In its initial liquid form, PMMA
fills any cavities or spaces within the damaged bone. After an hour
or two, the liquid hardens into a body-friendly cement.
"Tests have shown that it has strength
and stress-resistance that is stronger than bone," says Do. This
super-strong compound is able to shore
up fragile bone and support broken vertebrae.
PMMA has been used as a bone replacement
for many years in the United States, but it requires open surgery.
Percutaneous vertebroplasty has the advantage of being a minimally
invasive procedure. According to Do, a typical treatment is performed
under conscious sedation and local anesthetic on an outpatient basis,
making the improvements all the more dramatic. Some patients who
have difficulty standing due to the pain of fractured vertebrae
are able to walk out of the hospital the same day after vertebroplasty,
and almost all experience significant or complete pain relief within
24 hours, he says.
Do's arrival at Stanford in July 1999
from the University of Virginia marked the first time Stanford began
to perform vertebroplasty. Since July, 15 patients have undergone
the bone-strengthening procedure at Stanford, and all 15 have experienced
complete pain relief. Studies at the University of Virginia with
a larger number of patients indicate an overall success rate of
80 percent.
* Despite the dramatic
effects of vertebroplasty, it is offered at only a few institutions
across the country. "A lot of
people don't know about this yet," says Do. "I think the key is
to get the word out to patients because until now, the only treatment
option available was rest and pain medication."
In the face of such gradual and uncertain
improvement, vertebroplasty may seem like a godsend to many sufferers.
Most of the patients treated at Stanford are elderly women with
osteoporosis. Their weak bones are particularly susceptible to fracture,
and once bedridden by an injury, it is difficult for them to regain
their strength and mobility. Vertebroplasty can also repair spines
weakened by metastatic cancer, chronic steroid usage or other types
of bone disease.
For more information, contact Do at
650-723-6767 or huymdo@stanford.edu. -- KC
FAMILY MEDICINE FITS HER JUST
RIGHT
For fourth-year medical student Sarah Morgan, medical
school has been about far more than attending lectures and brooding
over textbooks. Even the most cursory look at her lengthy list of
extracurricular activities reveals that she has been an active participant
in her own education. Morgan came to Stanford medical school with
a strong interest in primary care -- and while here, she has jumped
into a variety of activities that have allowed her to put her classroom
knowledge into practice.
So, perhaps it should be no surprise that Morgan's
efforts have won her a Pisacano scholarship for student leaders
in the specialty of family medicine.
Morgan's scholarship, given by the Nicholas J. Pisacano,
MD, Memorial Foundation, will provide nearly $50,000 during her
last two years of medical school and three years of residency. The
foundation, which awarded five such scholarships this year, grants
them annually to students who demonstrate strong commitment to family
practice and who "show demonstrable leadership skills, superior
academic achievement, strong communication skills, identifiable
character and integrity and a noteworthy level of community service."
This description fits Morgan like a latex exam glove.
Last year, Morgan served as the clinic manager at
the Arbor Free Clinic. The clinic is staffed by Stanford medical
students and faculty who volunteer their time to provide free health
care to the homeless and others in need.
Morgan served as president of the Stanford Family
Medicine Interest Group and Stanford Women in Medicine and also
as the regional coordinator for Medical Students for Choice.
In addition, Morgan co-organized an obstetrics/pediatrics
class that matches students with pregnant women and assisted with
a Stanford Center for Biomedical Ethics project investigating decision-making
processes involved in the treatment of women with AIDS from diverse
ethnic backgrounds.
Morgan says she hasn't decided where she wants to
do her residency, but she plans to eventually return to her home
in Vermont, where she'd like to join a group practice in a semi-rural
setting.
"That's kind of what brought me to medicine," she
says. "I guess I'm just a generalist at heart. Family practice is
the best fit for me." GM
STUDY EXPLORES MYSTERIOUS BRAIN DEPOSITS
LINKED TO HUNTINGTON'S DISEASE
One subtle sign of Huntington's disease
is the accumulation of globs of a puzzling material within brain
cells. The stuff amasses surreptitiously during the emergence of
the inherited condition's outward manifestations -- disabling movement
disorders, behavioral disturbances and dementia.
Stanford researchers now have new information
about how these destructive cellular deposits form. They believe
an enzyme is responsible for the sticky mess in the brain; and they
have documented, for the first time, the activity of the enzyme
in diseased brain tissue. Understanding how and why these abnormal
aggregates collect inside brain cells is a necessary step toward
finding a way to prevent or cure the disease, which strikes one
in 10,000 people.
The theory of an enzyme culprit was
first proposed in 1993. One year later an alternative theory was
advanced and two conflicting scientific camps have existed ever
since.
* One thing the
scientists agree on is that a faulty version of the huntingtin protein
plays a major role in the disease.
In the huntingtin protein of most people, the subunit glutamine
is repeated 36 times. But in the mutated protein found in people
with the disease, the subunit is repeated more than 36 times, leading
to an extended protein tail. In each generation of victims the subunit
iteration increases. The more repeats, the longer the tail and the
more quickly the disease strikes, until eventually sufferers die
before passing their devastating inheritance to their offspring.
Scientists do not know what the huntingtin
protein does, but they do know that the glutamine tail is key to
the formation of the deposits. They just can't agree on how.
Supporters of the enzyme theory maintain
that the enzyme transglutaminase molds neighboring mutated huntingtin
proteins into large disorganized clumps that form the deposits.
Others believe that the glutamine tails on neighboring mutated proteins
spontaneously clasp together like teeth on a zipper.
Stanford neurology professor Lawrence
Steinman, MD, and his colleagues have uncovered new evidence that
supports the enzyme argument and casts doubt on the zipper theory.
They reported their findings in the June 22, 1999, issue of the
Proceedings of the National Academy of Sciences.
* In their study,
Steinman, graduate student Marcela Karpuj and postdoc Hideki Garren,
MD, PhD, studied brain tissue from people who had died from Huntington's
disease and compared it with samples from people who had died of
unrelated causes. Karpuj measured
transglutaminase activity in brain tissue from Huntington's disease
patients at the site where the aggregates occurred in the brain
nuclei. She found that transglutaminase activity was much greater
in samples taken from Huntington's disease victims than in those
from corresponding regions of normal brains.
When the aggregates were examined microscopically,
they showed the optical properties of clumps formed with the help
of transglutaminase, not the features of zippered aggregates.
According to Steinman, the new findings
may eventually lead to novel therapies for Huntington's disease
and other neurologic diseases characterized by long stretches of
glutamine residues. "It opens the very real possibility of attempting
to treat diseases mediated by proteins with polyglutamine domains,
by inhibiting transglutaminase in the brain," says Steinman. --
KW
STUDENTS LAUNCH MEDICAL REVIEW
Stanford medical students have created a law review-style
publication devoted to medicine -- the first of its kind in the
world, they say.
* The
Stanford Medical Review, which debuted this fall,
is run completely by medical students -- though the editors hope
to involve business and law students in future issues. The publication
is the brainchild of medical students Ronald W. Yeh and Pooya Fazeli,
who began working on the project in September 1997.
Fazeli says he had mused about starting such a review
for years. When he shared the idea with classmate Yeh, the project
took off.
"I was struck that law schools have journals to teach
students about journalism -- and that medical students would benefit
from the same kind of experience," Fazeli says. "It would prepare
us to have a voice in the national discussion of health care issues
when we graduate," he says.
Fazeli and Yeh gathered an editorial team and published
the first issue with funds from Stanford Medical Alumni Association,
the Stanford Medical Student Association and some members of the
editorial staff. They hope to publish twice a year.
* The
first issue of the magazine, focusing on the interaction of society
and medicine, includes articles by writers both
inside and outside of the Stanford community.
For information about contributing to the review,
contact Fazeli, fazeli@leland.stanford.edu. To subscribe, contact
Mai-Sie Chan, maisie@leland.stanford.edu. -- ED
LEARNING ABOUT THINKING
If you were standing in a crowded courtyard searching
for a friend wearing a red hat, how would you spot her?
According to William Newsome, PhD, professor of
neurobiology and a Howard Hughes Medical Institute investigator,
in this scenario, your brain would first screen out everything else
your eyes see and focus only on red things. From this more limited
group, you would then make your selection.
Newsome and graduate student Gregory Horwitz have
found a new group of brain cells that assist in this form of decision
making.
* Their findings,
which were reported in the May 14, 1999, issue
of Science, are based on their work with monkeys. But instead
of finding a red hat in a sea of people, the monkeys view a swarm
of roving dots on a video screen and decide whether the dots are
moving up or down. By measuring the electrical activity of individual
neurons in the monkey's brain during the exercise, the researchers
have been able to determine which cells are active at each step
of the decision-making process.
The exercise is a simple task for a human or a monkey
when all of the dots are moving in the same direction. But the challenge
grows when the dots are no longer in unison. If the number of dots
progressing in the same direction drops as low as 10 percent, making
the correct judgment becomes almost impossible.
* The researchers
have found that as the difficulty of the task increases, the activity
of the decision-making neurons decreases. "The
neurons are firing differently depending on the confidence the animal
has in its decision," says Newsome.
The monkey is only given a two-second glimpse at
the dots out of the corner of his eye before he must make a decision
on their direction. To communicate his decision, he looks toward
target points at the top and bottom of the computer screen. A glance
up or down indicates the dots are moving across the screen accordingly.
The researchers found that neurons in a region of
the brain called the superior colliculus -- known to be responsible
for some motor functions -- were activated when the moving dots
appeared on the screen and remained active until the monkey moved
his gaze and indicated his decision. The activity of these individual
neurons remained high during the brief delay between the time the
dots disappeared and the time the monkey received the cue to make
a decision.
This delay matters because it lets researchers discern
which neurons are activated merely by the retina's registration
of the motion: The activity of these neurons ceases as soon as the
moving dots disappear. But Newsome and his team believe that the
neurons that continue firing until the monkey is allowed to make
his selection are involved in the decision-making process. The decrease
in activity of these neurons as the task becomes more difficult
provides further evidence that the researchers have found some of
the cells responsible for cognition and high-level thought processes.
-- KW
IMPLANTS GET EYE IN SHAPE, CORRECT
NEARSIGHTEDNESS
Not so long ago, if you were nearsighted you had
only three choices: glasses, contacts or squinting at a blurry world.
Then came surgical techniques that reshape the cornea -- the clear,
curved window at the front of the eye -- to improve how it focuses
light.
Now, a Stanford ophthalmologist is offering a surgical
alternative that corrects vision without cutting or removing tissue
from the central part of the cornea, through which most light enters
the eye.
The technique involves inserting semicircular plastic
implants into the edge of the cornea, leaving the central region
undisturbed. By flattening the cornea, the implants can bring clear
vision to people who have mild to moderate nearsightedness, says
Edward E. Manche, MD, assistant professor of ophthalmology and director
of cornea and refractive surgery at Stanford.
Manche was one of the first eye surgeons in the United
States trained to perform this quick, outpatient procedure, which
was approved by the federal Food and Drug Administration earlier
this summer.
"Your eyes are too long" sounds like a childhood
taunt, but it's actually the basis for nearsightedness. Because
of this elongation, light rays from distant objects focus somewhere
in the interior of the eye, instead of on the light-sensitive retina
at the back of the eye. As a result, these objects appear blurry.
* For nearsighted
patients, the defect often lies in a cornea that bulges out too
far. The implants, each thinner than a dime,
work by pulling down the edge of the cornea, drawing the entire
cornea back and shrinking the bulge. Clearer vision results because
the focal point of the eye also moves back, and a crisp image reaches
the retina.
The procedure is fast and painless. Manche first
numbs the patient's eyes with anesthetic drops, then slips each
implant through a slit at the cornea's edge. A pair of implants
goes into each eye, pos itioned on opposite
sides of the cornea. Treating both eyes requires about 30 minutes,
Manche says, after which patients immediately begin to notice improved
vision.
In nationwide trials, within a year nearly 97 percent
of treated patients achieved 20/40 vision, the legal limit to drive.
About 75 percent of the patients attained at least 20/20 vision,
and 54 percent saw even sharper at 20/15, Manche says.
Unlike laser surgery, where the surgeon uses a laser
to thin the central part of the cornea, no tissue is removed and
the implants can be taken out if the patient is dissatisfied with
the results, Manche says.
* The new procedure
has another advantage over laser surgery. Because
the implants are placed in the margin of the cornea, the central
zone is not disturbed. This ensures that this vital part of the
eye will not scar or turn cloudy, both of which can lead to blurring
of vision.
For the recipient, the implants aren't any more noticeable
than contact lenses, though most patients have fluctuating visual
acuity for a week or two, Manche says. Other possible side effects
include seeing haloes and glare at night.
The new procedure works only on patients with mild
to moderate nearsightedness -- from -1 to -3 diopters on their eyeglasses
prescription -- and those with very mild astigmatism of no more
than -1 diopter. For more information, contact program coordinator
Leslie Lyssenko at 650-498-7020. -- ML
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