Contents:
Neurology
Studies Widen 'Therapeutic Window,' Shed Light on Disease Targets
"Cancers are very different. That's exactly the model you should have for stroke. Stroke is not just one disease—it's actually a bunch of different diseases that may have some similar manifestations," says Schwamm, above left with colleagues Walter Koroshetz (center) and Guy Rordorf.
Stroke researchers at Massachusetts General Hospital report good news this month: the chances of preventing brain damage and enhancing recovery after a stroke may be greater than previously thought.
Until recently, doctors believed little could be done after 24 hours to limit the spread of tissue damage. In the November Stroke, Walter Koroshetz, Lee Schwamm, and colleagues announce a more generous estimate. Using imaging methods that reveal the state of brain tissue at various stages in 14 stroke patients, they found damage continued for an average of 32.7 hours. In one patient, damage progressed for 61 hours.
"What this means is that the window of opportunity for therapies designed to prevent the growth of stroke is much greater than we thought, maybe 24 to 48 hours," says Schwamm, assistant professor of neurology. The same imaging techniques can be used to diagnose the nature of a stroke and refine treatments.
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Like his fellow researchers, Ferdinando Buonanno (right) is using new technologies to not only assess but arrest the spread of damage in stroke patients. "Almost every way you devise to kill cells, growth factor can save them," says Seth Finklestein (left). He and his colleagues are using growth factors to limit the spread of stroke and enhance recovery.
MGH colleague Seth Finklestein, associate professor of neurology, delivered a similar message at the 28th annual meeting of the Society for Neuroscience, held this month in Los Angeles. By blocking a tiny artery on the right side of the brain of rats, he and his colleagues were able to create a stroke with a very specific behavioral consequence: an inability to place the left paw on a table. Finklestein reported that he and his colleagues were able to restore the lost paw function by injecting a growth factor into rats three days after a stroke. Their previous studies had shown function could be restored by giving growth factor 24 hours after a stroke.
"So we have extended the therapeutic window for recovery from stroke in a rat from 24 hours to 3 days at a minimum," says Finklestein, adding, "But rats are rats."
Schwamm agrees. "Ten to 15 years ago if you developed a drug that could reduce the size of a stroke in an animal model, that would be big news. Now, 30 to 40 compounds do that. It's not big news to prove it in a rat. You have to prove it in a person."
The bad news is that despite the horde of promising new compounds designed to prevent the spread of stroke, only one drug has passed clinical trials. One problem is that human strokes are much more complex and variable than those induced in lab animals. They have many causes--blood clots can form in the heart or in the brain, and they can occur in large or tiny vessels in many different regions.
"It's not just like tying up a blood vessel in a specific place and that's it," says Schwamm. "It's very dynamic--a clot may be expanding and contracting. Blood may be flowing in from neighboring collateral vessels to support the region in some patients but not in others."
All of these factors will affect how a patient responds to a particular therapy. "If you just say a stroke is a stroke, your chance of developing the right therapy goes right through the window. There's just not going to be a magic bullet that makes all strokes better," Schwamm says.
Similarly, many drugs fail clinical trials not because they do not work but because the researchers do not take into account who is most likely to benefit from them. "A lot of potentially good drugs have been put six feet under by a bad trial design," says Schwamm. "The key to stroke therapy and trials is to carefully pick your patients, ones that you think will benefit," says Finklestein.
The good news, once again, is that the imaging techniques used by Schwamm and his colleagues make it possible to do just that. By revealing the distribution and rate of blood flow and the amount of tissue already damaged, they can help doctors decide whether and how to treat a patient. "For example, if we see there's all this territory that is vulnerable and that might die if we don't do something, but on the picture of what's died already, there is almost nothing--those are the people we have a real chance to save," Schwamm says.
Still, few people make it to the hospital within the first day after a stroke--mostly because they do not know the signs of stroke. Koroshetz, associate professor of neurology, is currently heading a project to increase public awareness. Schwamm has designed a Web site that doctors and nurses at satellite clinics can use to identify and refer stroke patients who are eligible for new protective treatments.
Finklestein and Schwamm and his colleagues are currently working with pharmaceutical companies to test promising new drugs. "New molecular techniques are going to revolutionize stroke treatment as long as the pharmaceutical companies get smart and stay smart about the way they design clinical trials," Schwamm says.
One thing they may have to realize is that human clinical trials are all too human. "We don't always get them right--we may choose the wrong dose or regimen. But that does not mean the drug is not effective," Finklestein says. "For me this is not a one shot deal. This is a field we want to bring to fruition."
--Misia Landau
For further information, please visit the following Web sites:
General information on stroke
American Heart Association
The journal Stroke
On January 21, 1998, Ernst ter Haar left a note on his adviser's desk. "Tom, We have the structure of clathrin. You might want to stop by. Cheers, Ernst."
Before stopping by, Tom Kirchhausen, associate professor of cell biology and investigator at the Center for Blood Research, picked up a bottle of champagne to celebrate this identification of the crystal structure of part of a protein essential for sorting and shipping materials throughout cells.
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L to r: ter Haar, Kirchhausen, Musacchio and Harrison solved the structure of the globular foot of clathrin.
Howard Hughes investigator and professor of biological chemistry and molecular pharmacology Stephen Harrison, who collaborated on the research with Kirchhausen, says, "This structure and what we hope will follow gives us a first crack at a full dissection of the various components of the cell's sorting machinery."
The Anatomy of Clathrin
The piece of machinery the researchers dissected is a key portion of the protein clathrin, which has three identical legs that sprawl out from a central hub, each terminating in a globular foot. Kirchhausen and his colleagues, including Andrea Musacchio, a fellow in the Harvard-Armenise Center for Structural Biology and a member of Harrison's Children's Hospital lab, report the structure of the foot and part of the leg in the November 13 Cell.
The foot, known as the "terminal domain," is considered the most active portion of clathrin. It binds adapter proteins and other molecules that grab the cell membrane and pull it inwards to form vesicles. In this process, dozens of clathrin molecules assemble around the vesicle, their legs overlapping to form a spherical protein cage. In a cell, thousands of such assemblies form every minute with great specificity.
"There are so many subtleties when you look at coated vesicles. It's like a three-dimensional jigsaw puzzle," says Kirchhausen. "What is stunning is that one of those structures can get together with no errors."
Once the vesicle has formed, it can be transported throughout the cell, usually arriving at an endosome. Before depositing the membrane cargo, the clathrin cage breaks up, releasing the three- legged proteins to form another cage elsewhere.
Although they have a good description of the transport protein, researchers have yet to figure out what regulates and orchestrates the formation and dismantling of the cages as well as the molecular details of clathrin's interaction with the adapter proteins.
By deciphering clathrin's structure at an atomic level, researchers can start
to understand those mysteries (see sidebar p. 5). Kirchhausen and his colleagues
found that the terminal domain looks like a propeller with seven blades. The
configuration of the propeller, says Kirchhausen, is well suited to many different
specific
interactions, just what is required to sort through the mix of proteins found
at the cell membrane. Already they have found that a binding site for arrestin,
an adapter for certain G-proteincoupled receptors, lies between two of
the propeller blades.
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Clathrin is essential for sorting and transport within the cell. Tom Kirchhausen and his colleagues solved the crystal structure of the foot of clathrin, a protein involved in receptor-mediated endocytosis. The overall clathrin molecule consists of three legs radiating from a central hub. |
Kirchhausen says one new area of research would be to disable pieces of the molecule and to watch how it affects cell trafficking. This would reveal what proteins rely on clathrin for transport and where they bind.
The project reflects a divide-and-conquer approach to cell biology research, says Harrison. "Biological function can be effectively studied at a molecular level, and from there one can build back up to a real understanding rather than just a phenomenological description of the subcellular machinery."
The same strategy may be the one that crystallographers wind up using to solve the entire structure of clathrin, a tricky problem due to the molecule's spindly legs. Kirchhausen, who has been studying clathrin for nearly 20 years, sees the solution of the foot as a first step toward determining the structure of an entire coated vesicle.
--Cassie Ferguson
Clathrin Linked to HIV Protein, Suggests Antiviral Strategy
Solving the structure of clathrinÕs foot hints at how HIV-1 manages to hijack the cell's control over the traffic of CD4 molecules and MHC class I antigens. In the November 5 Current Biology, Kirchhausen, Louis DeTulleo, a graduate student in virology, and their colleagues report on one way an HIV-1 protein called Nef regulates the selection of CD4 and its placement into clathrin vesicles. The new observations help clarify the link between clathrin and Nef, which is known as an important factor in the progression of HIV-1 in humans and SIV in monkeys. Nef has a polypeptide loop that hangs off an otherwise compact body. In the middle of the loop sits a pair of leucine residues, a motif known to direct some molecules into the clathrin pathway. When Kirchhausen's team altered NefÕs pair of leucines, they observed that the protein was no longer found in clathrin-coated structures. While this had no effect on the surface expression of MHC class I antigens, it turned out that it decreased the number of CD4 molecules on the surface of the cell. Kirchhausen says he has not yet dissected the interactions between Nef and CD4, but the new work suggests that Nef binds to the adapter proteins, which then fit between the clathrin molecules as they form a cage. Disrupting the interaction of Nef with adapters may be a useful antiviral strategy. "You prevent the insertion of Nef into clathrin coated pits, and you block the downregulation of CD4," says Kirchhausen.
Were Ludwig van Beethoven still around today, he would probably pick up the November Nature Genetics. In it, Harvard researchers announce they have found the gene underlying some balance disorders and a form of deafness whose symptoms resemble those that silenced the maestro's world. Like Beethoven, members of three unrelated families described in the paper began losing their hearing in their 20s and became deaf by midlife.
The paper is a collaborative effort among the laboratories of Cynthia Morton, the William Lambert Richardson professor of obstetrics, gynecology and reproductive biology and professor of pathology at HMS and Brigham and Women's Hospital; Joseph Nadol, the Walter Augustus Lecompte professor of otology and laryngology at HMS and the Massachusetts Eye and Ear Infirmary; Jonathan Seidman, Howard Hughes investigator and the Henrietta B. and Frederick H. Bugher Foundation professor of genetics at HMS; Christine Seidman, Howard Hughes investigator at BWH and professor of genetics at HMS; and other researchers.
A Field in the Making
The investigation, funded in part by NIH and the Howard Hughes Medical Institute, comes as the latest in a recent salvo of studies that are just beginning to open up the auditory sense to molecular biology. The present paper represents the ninth deafness gene identified so far, all in the past four years. Up to 3 percent of the population is estimated to have inherited some form of progressive deafness. Almost 40 percent of people over 60 have some hearing loss.
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Among the researchers who have found a gene linked to balance disorder and a form of deafness are Joseph Nadol (bottom left, holding a temporal bone, the part of the skull base containing the inner ear), Christine and Jonathan Seidman (bottom right), and (on top from l to r) research assistant Nahid Robertson, medical student Leonard Lu (who was working in the Seidman lab), and Cynthia Morton. |
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Deafness poses special challenges to the classical methods of medical genetics--linkage analysis and positional cloning. Scientists use them to tie chromosomal areas to diseases by analyzing how a disease trait is passed on in a family. As many as 200 genes are estimated to be involved in hearing and may contribute to hundreds of different kinds of disease. Moreover, 70 percent of hearing loss occurs without other clinical symptoms that could help physicians distinguish one kind from another. About 175 hearing disorders that do have additional symptoms are recognized clinically, but their genetic background is mostly unknown.
Many deaf people in the U.S. further confound gene sleuths by intermarrying. Often, two deaf people bear hearing children who learn sign language, grow up in the deaf community and marry within it, complicating its gene pool even more.
Morton took a different approach. With her coworkers, she established a subtractive cDNA library--a method aimed at identifying among all human genes only those that are active specifically in the tissue of interest. In this case, Morton created a set of about 700 genes likely to be involved in hearing since they are expressed in the developing human cochlea.
Her approach was meant to speed up linkage analysis, which often ties a disease to a chromosomal region that is too large to allow easy identification of the culprit gene within it. Morton's approach, she reasoned, would supply candidate genes with precise chromosomal "addresses."
The Gene–Disease Link
Her team first considered the new gene, COCH, such a candidate because
it is highly expressed only in the cochlea. COCH turned out to reside
in an area on chromosome 14 that researchers led by the Seidmans and Nadol at
MEEI had, in 1996, reported to house a gene for the deafness disorder DFNA9.
Then researchers led
by Jim Hudspeth, of Rockefeller University, found the chick homologue to the
human gene and looked to see exactly where it was expressed. Morton realized
that the chick version occurred in precisely those areas of the inner ear that
the MEEI researchers had reported to be histologically abnormal in patients
with DFNA9.
To clinch the case, the Harvard researchers then studied COCH in three families with DFNA9 and, indeed, found that all deaf family members had mutations in the gene.
The next big question--How does COCH cause hearing loss?--is still
unanswered. The gene is new and its protein unknown. But the scientists
are following one important clue. All the detected mutations lie in a region
of COCH that is homologous to the gene for Factor C, a protein found
in the horseshoe crab Limulus polyphemus. This well-studied protein
is known to bind lipopolysaccharide, which in itself reveals
nothing about hearing loss. Yet, speculates Morton, maybe the COCH protein normally
binds some fat- or sugar-containing molecule. COCH mutations might impede
this binding and lead, over time, to the buildup of material that could choke
off the sensory cells and the tips of the auditory nerve, a suggestion MEEI
scientists found evidence for in previous research.
Interpreting histopathology results in deafness, however, can be ambiguous, Morton says. Since deaf people live normal life spans, their postmortem tissue typically shows an 80-year-old cochlea that may not have functioned for 50 years or more, making it impossible to tell whether abnormalities arose before or after the onset of hearing loss. The COCH gene for the first time gives researchers a genetic and biochemical handle on testing the notion.
To facilitate other investigations, Morton is distributing her cDNA library to interested scientists and has put infor-mation about its genes on a Web site: www.bwh.partners.org/pathology.
--Gabrielle Strobel
For many years researchers have known that cells rely on the proto-oncogene Ras for multiple tasks. Overactive Ras protein causes tumors. In the Drosophila eye, cells need Ras to form properly, and few cells seem to survive without Ras. But separating out Ras's various roles in survival, differentiation, and proliferation has been difficult.
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| Researchers can turn on the hid gene, causing massive cell death in the eye of the fruit fly (left). Expressing an activated form of Ras prevents hid from doing its damage (right). |
An article in the Oct. 28 Cell helps illuminate how cells choose between life and death. Using the fruit fly's versatile genetics, Kristin White, assistant professor of dermatology, and Phani Kurada, research fellow in dermatology, both at HMS and MGH, found that turning on Ras inhibited the activity of genes known to trigger cell death in the eye, embryo, and midline glia. The researchers show that activating Ras decreased the mRNA for one of the apoptotic genes called hid, suggesting Ras plays a role in hid's transcriptional regulation.
In addition, White and Kurada found that genes interacting with Ras
in cell differentiation also
influenced cell death. Genes downstream of Ras affected the cells' ability
to survive, suggesting the
same pathway keeps cells alive
and helps them differentiate properly. Drosophila's EGF receptor, or
DER, also protected cells from dying. DER's involvement makes sense because
cells often require growth factors such as EGF or NGF to inhibit apoptosis.
So the availability of growth factors regulates how many cells will live, White
says.
An article in the Oct. 26 Archives of Internal Medicine concludes that doctors often prescribe the most familiar, rather than the most effective medications, when treating a common heart disorder.
Randy Stafford, professor of medicine at HMS and MGH, and his colleagues looked at drugs used in treating atrial fibrillation, a condition caused by abnormal electrical impulses in the heart. The researchers showed that for two categories of drugs, doctors tend to prescribe older medications. For instance, in treating the excessively high and often uncomfortable heart rate resulting from atrial fibrillation, doctors relied more on digoxin, rather than the newer and more efficacious calcium channel and beta blockers. Stafford says doctors also underutilize the newer members of another class of drugs, sinus rhythm medications. These drugs work to completely correct the abnormal communication between the heart's upper and lower chambers in atrial fibrillation. Although considered a riskier approach, Stafford says, doctors should recognize the improved treatment offered by the sinus rhythm drugs, and more patients should receive these medications.
"The bottom line is that physicians seem to be more traditional than one might hope. We need to look into different ways of getting out the information on drug treatment," Stafford says.
Researchers have found that a mutant zebrafish has defects similar to those found in people with a rare blood disease. The fish represents not only the first animal model for the disease, but also the first zebrafish model for any human disorder.
Leonard Zon, associate professor of pediatrics at HMS and Children's Hospital; Alison Brownlie, a graduate student at HMS and Children's; and their colleagues report in the November Nature Genetics that defects in the zebrafish mutant sauternes--named after a white wine because of its pale red blood cells--stem from alterations in an enzyme critical for making the iron compound heme. People with the blood disorder congenital sideroblastic anemia have mutations in the same enzyme, linking the fish defect to the human disease. Without heme, neither fish nor humans can generate enough hemoglobin.
Zon says studying the mutant fish could give insight into congenital sideroblastic anemia and the biochemical processes affected by a lack of heme. Already, researchers have shown that red blood cells do not differentiate properly in sauternes mutants. Over the course of red blood cell development, the nucleus, which typically condenses, remains enlarged. An embryonic globin gene initiates its expression late, and a transcription factor usually downregulated during the later stages of development, stays around. The studies suggest a feedback mechanism requiring heme synthesis for normal red blood cell development.
--Briefs above by Judy Silber
Thousands of American babies are born with HIV despite the existence of therapies that markedly reduce the chances of infection. Many of these babies could be born infection-free if prenatal HIV testing became a routine part of prenatal care, according to an Institute of Medicine (IOM) report issued in October by a panel chaired by Marie McCormick, the Sumner and Esther Feldberg professor of maternal and child health at the School of Public Health and director of the Harvard Center for Children's Health.
One of the biggest strides in the battle against HIV was the finding in 1994 that giving the antiretroviral drug zidovudine (ZDV, formerly AZT) to pregnant HIV-positive women could reduce by about two thirds the chance that a child would be infected. This led to the creation of federal guidelines advising caregivers to encourage expectant mothers to be tested for HIV. As a result, the number of new pediatric AIDS cases declined by about 43 percent between 1992 and '96.
But many barriers, such as a lack of time, inhibit caregivers from counseling and testing every expectant mother, the panel of researchers found.
In their report, McCormick and her colleagues advise that the HIV test be included in the battery of tests that all women routinely undergo in the early stages of pregnancy. Women would be told that they will be tested and given the option to refuse. The report, "Reducing the Odds: Preventing Prenatal Transmission of HIV in the United States," was issued to Congress in the hope that the recommendations will be incorporated into physician's guidelines or legislation.
No one questions that there is a severe shortage of organs for transplantation. Nearly 60,000 Americans are waiting for organ transplants, and ten or more die every day because an organ does not become available in time. Many people believe the answer lies in increasing public awareness of the need for organs. But an article in the November American Journal of Public Health points to a bigger problem--the donation community has little idea how well or poorly it is doing in collecting available organs, says principal author Cindy Christiansen, assistant professor of ambulatory care and prevention at HMS and Harvard Pilgrim Health Care.
The current standards for organ procurement organization (OPO) effectiveness rely on a donors-per-million-population measure, assuming uniformity across the U.S. But such an assumption has never been systematically tested.
This study, conducted by HMS, HSPH, the Partnership for Organ Donation, and other organizations recognizes that OPO regions are defined by the hospitals they contain. Readily available information about hospital characteristics in a region can be used to generate valid estimates of organ donor potential for that region.
Using the results from medical-records reviews to test a range of predictor variables, the authors show that it is possible to generate accurate estimates of donor potential in a geographic region based on five key hospital variables: number of deaths, number of staffed beds, Medicare case-mix index, medical school affiliation, and trauma center designation.
"A major application of this model is to provide a realistic baseline against which OPOs and policymakers can assess donation performance and target areas for improvement. Given the size of the gap between current performance and estimated potential, even a conservative estimate can be highly useful to OPOs in setting goals," Christiansen says.
Researchers can turn on the hid gene, causing massive cell death in the eye of the fruit fly (top). Expressing an activated form of Ras prevents hid from doing its damage (bottom).
Dolin Started as HMS Dean for Clinical Programs in October
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Raphael Dolin intends to be involved in activities at the affiliated hospitals. |
Focus: You have returned to a familiar community: you earned your degrees at Harvard and did a residency and fellowship at affiliated institutions in Boston. What in particular drove your interest in becoming the dean for clinical programs at Harvard Medical School?
Dolin: This is a very exciting opportunity--a chance to take part in the leadership team that Drs. Martin and Kasper are putting together to implement their vision of increased collaboration and interaction among members of the Harvard medical community. My family and I are looking forward to taking advantage of everything the city and the area have to offer.
You will be leading a new clinical trials initiative at HMS-affiliated hospitals. What aspects of your experience will be most valuable in this effort?
Being a department chair at the University of Rochester gave me an appreciation for the various components of a medical center, namely the missions of education, research, and clinical care, and for the interaction of those components. That interaction is both a challenge and an enormous opportunity for synergy. It's exciting to be at the center of efforts to facilitate those interactions. Our modern medical and public health problems are so complex that we really need to take advantage of the interplay of these elements to make significant progress.
Part of the clinical dean's job is to manage the connections between the School and the faculty, the faculty and its affiliated institutions, and among the institutions themselves. What do you see as the biggest obstacles to this, and how do you envision your role in helping to overcome them?
The single biggest obstacle has to do with the sheer size of the Harvard medical community: its clinical facilities, the size of its faculty, the number of residents and other trainees. To promote additional collaboration among these elements is logistically a challenge. At the same time, the breadth and depth of opportunities here is an enormous strength. The approach must be grounded in open, two-way, frequent communications among the various segments of the Harvard medical community. I don't think there's any shortcut. We need to invest time and respect the process. There's no substitute for being where the clinical action is, at the hospitals, and I hope to be involved as much as I can in activities there.
As an AIDS researcher, what do you see as the most promising developments in that field? Will you urge an expanded role for the Harvard medical community in AIDS clinical trials?
There are some particularly promising approaches that utilize host-immune responses to combat HIV infection in combination with more potent antiretroviral drugs. Important insights are being gained from work within the Harvard community, both immunologic insights and basic science that has elucidated critical features of HIV's structure and replication. Putting all these together is a complicated task that will require the best minds in basic science, clinical research, and public health. I think Harvard has as great a breadth and depth of talent in these areas as any place in the world. The Harvard medical community is already one of the leaders in AIDS clinical trials, so we're starting with a very strong base. My own clinical research on AIDS vaccines is something I hope to expand here, and discussions with collaborators have already begun.
--Tom Reynolds
Faculty Council
At the October meeting of the Faculty Council, the dean announced that Nancy Oriol, assistant professor of anesthesia at Beth Israel Deaconess, had been reelected as vice chairperson of the Faculty Council and chairperson of the Docket Committee, for the fourth consecutive year.
The council voted to award three Doctor of Medicine degrees, twelve Master of Medical Sciences degrees, and two Doctor of Medical Sciences in Oral Biology degrees in November to students who had recently completed all requirements.
Linda Wilcox, ombudsperson for HMS, reported that during AY97-98, 528 individuals contacted the Ombuds Office (up from 497 the previous year) on issues including sexual harassment, job situations, discrimination, and generic abuse. Since its creation in 1991, over 3,000 people have contacted the office. As in the past, career management issues were the most frequently cited. Issues related to sexual harassment remained constant while those of discrimination rose. Of calls to the office, 35.5 percent were from men and 64.5 from women. There was an increase in the number of contacts regarding intellectual property issues, such as proprietorship of work, authorship, conflict of interest, professional misconduct, misrepresentation of data, protocol errors, and plagiarism. This represents a 70 percent increase (from 10 to 17 cases) over the previous year.
Wilcox suggested supervisors could help alleviate problems before they occur by becoming familiar with effective management skills. She suggested supervisory training might include the best practices for hiring, managing, and firing; exposure to institutional policies, procedures, and laws on sexual harassment and discrimination; and the institution's standards on supervision.
Community members can obtain information about the Ombuds Office and the issues it handles through its Web site at www.med.harvard.edu/ombuds.
HST's Mission
Joseph Bonventre, professor of medicine at HMS and MGH and master of the HarvardMIT Division of Health Sciences and Technology, gave an update of activities at HST. He said its mission is to develop and conduct educational and research programs across disciplines at MIT, Harvard, and the teaching hospitals, using science and engineering to solve problems in biology and medicine. HST students are trained for research and leadership roles in medicine, biomedical sciences, and biomedical engineering. Research programs include integration of molecular, cell, and tissue biology with quantitative physiology; biomedical engineering and biological physics; imaging sciences and technology; biological and medical informatics; and clinical therapeutic discovery, delivery, and assessment.
Bonventre said that approximately 320 students are currently enrolled. HST programs include Medical Engineering and Medical Physics; the Speech and Hearing Sciences Doctoral Program; the Radiological Joint Program; Medical Informatics; Medical Sciences; and Clinical Investigator Training. Bonventre stressed the need to work on financial underpinnings to increase the number of core faculty within HST and to endow the research assistant program.
Enhancing the Status of Women
The council approved a request by the Joint Committee on the Status of Women to revise its bylaws and mission statement. The revisions reflect the naming of two cochairs. Jacqueline Wolf, associate professor of medicine at BWH, currently represents the faculty and Vonda Shannon, program and special projects coordinator in Biological and Biomedical Sciences at HMS represents HMS staff.
The JCSW's goals and objectives include providing a forum to enable women at HMS and HSDM to advance professionally, to network, and to build collegial relationships. Wolf mentioned many of the year's accomplishments including career development seminars and community service efforts; ESL tutoring; and the JCSW Thanksgiving food, clothing, and toiletries drive for Rosie's Place that provided 125 bags and boxes of donated goods. This year's drive is under way throughout the Quad.
Both cochairs spoke of the importance of the interface between staff and faculty on the JCSW. The JCSW also sponsored successful Black History Month and leadership events and organized the first Dean's Awards for the Support and Advancement of Women Faculty. This year's faculty recipients were Tom Delbanco, Suzanne Fletcher, and Ann Klibanski. Two additional administrator awards were presented to Joan Reede and Eleanor Shore.
The council also recommended the use of the Harvard name for a new center: the Harvard Skin Disease Research Center. The request will be sent to HU's Office of the Provost for final approval. Thomas Kupper, the center's director, and T.B. Fitzpatrick, professor of dermatology, said that the center--in existence since 1994 and one of six NIH-funded centers of this type in the country--is a multidisciplinary, multi-institutional effort to study diseases of the skin through work in areas such as transgenic models, morphology, and cell analysis and cell cultures.
Its mission is to recruit biomedical scientists who work in areas related to skin and to focus on questions relevant to the pathophysiological process in skin. In addition to the core facilities already in existence, new cores are planned in genomic analysis and leukocyte migration. Kupper stressed that the strong input from many hospitals and from other non-HMS departments within HU makes the center worthy of the Harvard name.
Finally, Oriol and Shore discussed feedback about communication between the Faculty Council and members of the faculty. At the September meeting, in a discussion of the impact of the council, Oriol noted that in the past three years, the council had heard 68 different issues on which members contributed 38 votes or advisories to the dean.
Faculty Council 1998-99
| Joseph Martin, Chairperson, Dean of the Faculty of Medicine | joseph_martin@hms.harvard.edu | HMS | |
| Nancy Oriol, Vice-Chairperson of the Faculty Council and Chairperson of the Faculty Council Docket Committee | noriol@bidmc.harvard.edu BID | ||
| R. Bruce Donoff, Dean, HSDM, ex officio | bruce _donoff@hms.harvard.edu | HSDM | |
| Dennis Kasper, Executive Dean for Academic Programs, ex officio |
dennis_kasper@hms.harvard.edu | HMS | |
| Eleanor Shore, Dean for Faculty Affairs, HMS, ex officio | eleanor_shore@hms.harvard.edu | HMS | |
| * | Paul Cleary, | cleary@hcp.med.harvard.edu | HMS |
| Patricia Come, | pcome@bics.bwh.harvard.edu | HPHC | |
| David DeMaso, | demaso@a1.tch.harvard.edu | CH | |
| *Patricia Donahoe, |
donahoe.patricia@mgh.harvard.edu | MGH | |
| Susan Ettner, | ettner@hcp.med.harvard.edu | HMS | |
| Leslie Shu Tung Fang, | lesfang@msn.com | MGH | |
| Rashi Fein, | rfein@hms.harvard.edu | HMS | |
| Ernesto Gonzalez, | gonzalez.ernesto@mgh.harvard.edu | MGH | |
| Donna Greenberg, | dgreenberg@partners.org | MGH | |
| Jerome Groopman, | jgroopman@west.bidmc.harvard.edu | BID | |
| Harley Haynes, | hahaynes@bics.bwh.harvard.edu | BWH | |
| Linda Heffner, | ljheffner@bics.bwh.harvard.edu | BWH | |
| Julie Ingelfinger, | ingelfinger@helix.mgh.harvard.edu | MGH | |
| Shukri Khuri, | khuri@med.va.gov | WRVA | |
| Herbert Kressel, | hkressel@mercury.bih.harvard.edu | HMS | |
| Catherine Lee, | clee@hms.harvard.edu | HMS | |
| * | Craig Lillehei, | lillehei@.tch.harvard.edu | CH |
| Theresa McLoud, | tmcloud@partners.org | MGH | |
| Barbara McNeil, | mcneil@hcp.med.harvard.edu | HMS/BWH | |
| Robert Moellering, | rmoellering@bidmc.harvard.edu | BID | |
| Carol Nadelson, | cnadelso@hms.harvard.edu | BWH | |
| Lynn Peterson, | lpeterson@bics.bwh.harvard.edu | HMS | |
| Orah Platt, | platt@a1.tch.harvard.edu | CH | |
| * | David Potter, | david_potter@hms.harvard.edu | HMS |
| * | Joan Reede, | jreede@hms.harvard.edu | HMS |
| Martin Samuels, | masamuels@bics.bwh.harvard.edu | BWH | |
| Isaac Schiff, | ischiff@partners.org | MGH | |
| Brian Seed, | seed@opal.mgh.harvad.edu | MGH | |
| Edward Seldin, | seldin.edward@mgh.harvard.edu | MGH | |
| Pamela Silver, | pamela-silver@dfci.harvard.edu | DFCI | |
| Timothy Springer, | springer@sprsgi.med.harvard.edu | HMS | |
| Charles Stiles, | charles_stiles@dfci.harvard.edu | DFCI | |
| * | Nancy Tarbell, | tarbell.nancy@mgh.harvard.edu | MGH |
| Christopher T. Walsh, | walsh@walsh.med.harvard.edu | HMS | |
| * | Marshall Wolf, | mawolf@bics.bwh.harvard.edu | BWH |
| * | Beverly Woo, | bwoo@bics.bwh.harvard.edu | BWH |
* Docket Committee members are indicated by an asterisk. Members of the faculty are encouraged to contact any of them, or any Faculty Council member, to comment on future agenda items or to share issues or concerns that might benefit from Faculty Council consideration.
Agenda for November 18 Faculty Council Meeting:
Request for Use of Harvard Medical School Name HMS Center for Palliative CareÑSusan
Block, Andrew Billings
Review and Recommendation from Committee on Medical EducationÑDaniel Federman
Committee to Assess the Effectiveness of Preclinical Curriculum in Providing
Basic Science Foundation for Core Clinical RotationsÑDaniel Podolsky
Committee to Assess Possible Improvements in Preparation of Students for Clinical
ClerkshipsÑMarshall Wolf
Committee on Professional Development at HMSÑGeorge Thibault
Report on Use of Harvard Medical School Name HMS Center of Excellence in WomenÕs
HealthÑ Eleanor Shore
Agenda for December 16 Faculty Council Meeting:
Report and Recommendations from Faculty CouncilÕs Subcommittee on Community
ServiceÑNancy Oriol Report and Recommendations from Service Learning Town MeetingÑ
Thomas Inui, Laurence Ronan
Explain why you think this person should receive this award. I frowned in frustration at the blank page. I knew that my adviser, Cathy Lee (or C. Lee as those in my lab call her), should win the BBS Mentoring Award, but capturing on paper the qualities that make her a good mentor proved challenging. As I struggled to write the nomination, many questions came to mind. What makes a mentor good or bad? Why does bad mentoring continue? What are the costs and rewards of being a good mentor?
Looking for answers, I turned to a guide from the National Academy Press called Adviser, Teacher, Role Model, Friend. It read: "A good mentor seeks to help a student optimize an educational experience, to assist the student's socialization into a disciplinary culture, and to help the student find suitable employment." But how do good mentors incorporate these goals in their day-to-day interactions with students?
Tailoring Mentorship
In many ways, deciding which behaviors characterize good or bad mentoring is a matter of personal taste. The amount of time and guidance that advisers offer to students, personalities and styles of mentoring, and advisers' expectations of students are all factors that vary depending on the individual. In turn, every student has his or her own unique needs and will value different characteristics in a mentor. Often the success of the mentorship depends on how well the expectations of the adviser and student match.
I am fortunate to have an adviser who surpasses all of my expectations. As a role model, she is a fair, cooperative, and enthusiastic researcher and mentor. Her door is always open, and she strives to be available to all of her students as much as possible. Although we meet often to discuss my results and future experiments, C. Lee urges me to think independently and come up with my own ideas. She encourages me to take courses, go to seminars, and attend meetings to help broaden my scientific knowledge. Aware of my interest in pursuing a non-academic career, she allows me to participate in activities that may help me make the transition into a new field. At the same time, she quietly yet persistently reminds me of my responsibilities and goals, emphasizing my strengths and abilities. I always feel that her focus is on helping me build self-confidence and achieve my obje