Copyright © 1996 by the Biomedical Engineering Society
I'm honored to have the opportunity this year to try to help our Society continue to move ahead in this period of extraordinary excitement and promise for the field of biomedical engineering. I have no major philosophical statements to make in this, my first note to you, but would rather take this chance to familiarize you with the specifics of the aims the Board of Directors formulated at our last meeting in October 1996 for our various Committees for 1997. So, I will list below the 1997 Chairs for our Committees, along with the charges they are working on. The activities of our Society are, of course, intended to reflect your interests so I strongly encourage you to contact any of the Committee Chairs with additional suggestions for their areas or offers to help them in their tasks.
Our next Board of Directors meeting will be in April 1997, and I am looking forward to some reports of interim progress in these areas. I hope you will find that we are pursuing specific projects that you see as productive and important for our profession. And I welcome hearing from any of you regarding your personal thoughts about what else we could be trying to do. As is the case for most of us these days, you'll find me most efficiently via email at lauffen@mit.edu. I'll look forward to hearing from you!
Vince Turitto (Department of Biomedical Engineering, University of Memphis; vturitto@admin2.memphis.edu) -- Chair, Publications Board. The main charge to this Board this year is to arrange an improved publishing contract for our Society's flagship journal, Annals of Biomedical Engineering. We are seeking not only a continuation of the tremendous enhancement in quality that the Annals has accomplished over the past few years, but also increases in distribution to a wider readership and in financial returns to the Society.
Herb Voigt (Department of Biomedical Engineering, Boston University; hfv@enga.bu.edu) -- Chair, Program Committee. The main charge to this Committee this year is to come up with a more formalized way for the Society to help the local organizers of the BMES Annual Meetings to deal with issues in finances, logistics, programming, publicity, and industrial contacts in a manner that is systematic and consistent from year to year.
Cheng Dong(Department of Engineering Science & Mechanics, Pennsylvania State University; cxd23@.psu.edu) -- Chair, Membership Committee. The main charge to this Committee this year is to come up with at least one concrete strategy for translating the large student membership of the Society into sustained membership once the students graduate and move on into their professional careers, whether in industry or academia.
Mary Verstraete (Department of Biomedical Engineering, University of Akron; mary@brain.biomed.uakron.edu) -- Chair, Student Affairs Committee. The main charge to this Committee this year is, simply, to increase the number of BMES Student Chapters and the number of members in them.
Rick Waugh (Department of Biophysics, University of Rochester; rewaug@rbb1.biophysics.rochester.edu) -- Chair, Education & Public Affairs Committee. The main charge to this Committee this year is to develop a mechanism for more efficient communication of public issues relevant to Society members, especially via electronic avenues.
Art Johnson (Department of Agricultural Engineering, University of Maryland; aj16@umail.umd.edu) -- Chair, Affiliations Committee. The main charge to this Committee this year is to suggest specific steps that might be taken by BMES to help its members participate in activities of related professional societies -- and vice versa. Many intriguing possibilities can be envisioned in theory (joint memberships, joint meeting registrations, joint journal subscriptions, etc.) but which of these are desirable and practical may be more difficult to ascertain.
Giles Cokelet (Department of Biophysics, University of Rochester; cokelet@micro.biophysics.rochester.edu) -- Chair, Finance Committee. The main charge to this Committee this year is to articulate an accurate picture of the Society's financial flows, so that we can determine what areas are most appropriate to pursue in improving our financial stability (for example, meetings, memberships, journal?).
Knowles Overholser (Department of Biomedical Engineering, Vanderbilt University; overhoka@ctrvax.vanderbilt.edu) -- Chair, Constitution & Bylaws Committee. The most immediate prospective Constitution & Bylaws change is likely to come from activities of the Program Committee to formalize our meetings procedure.
Richard Normann (Department of Bioengineering, University of Utah; normann@m.cc.utah.edu) -- Chair, Awards Committee. This Committee has its usual charge of soliciting and selecting from nominations for the Society awards.
Jim Bassingthwaighte (Center for Bioengineering, University of Washington; jbb@nsr.bioeng.washington.edu) -- Editor, Annals of Biomedical Engineering and Jerry Collins (Department of Medicine, Vanderbilt University; jerry.collins@mcmail.vanderbilt.edu) -- Editor, BMES Newsletter. The Annals and Newsletter are the Society's two chief vehicles for communicating technical and professional information and ideas among its membership. As always, Jim and Jerry are charged with accomplishing this in the most attractive, influential, and cost-effective ways.
January 29, 1997 was marked by the passing of Loren Zech, Senior Member of the Biomedical Engineering Society. Loren was also a fellow of the American Federation for Clinical Research and of the American Heart Association, Council on Arteriosclerosis, and a member of IEEE, the American Institute of Nutrition, and the American Institute of Clinical Nutrition. His appointment for the last seven years of his life was as Clinical Investigator and Special Consultant, Office of the Director, National Heart, Lung, and Blood Institute, on detail to Laboratory of Mathematical Biology, Division Basic Sciences, National Cancer Institute. To most of his friends and colleagues, Loren was the continuing developer and enthusiastic proponent of SAAM, the compartmental analysis program developed in this laboratory earlier by his mentor, Mones Berman. A great number of scientists, I among them, were touched by this man's life and grieved by his death.
I met Loren in 1985 at the first conference on Mathematical Modeling in Experimental Nutrition at the University of Georgia. Many of the conference participants were just getting started in compartmental analysis of the metabolism of nutrients. To Loren, every novice modeler at that meeting was a friend to whom Loren became the mentor. I found later that dozens of scientists had been helped extensively by Loren. Some took sabbatical leave and spent the time working in Loren's laboratory. Many were guests in Loren's home for extended periods of time.
In 1989 I helped coordinate a conference on intermediary metabolism and modeling at which Loren was a featured speaker. Although his lecture to the group of 100 was informative, it was obvious that his preferred method of teaching was one-on-one, in front of a terminal. He was patient, encouraging, and as he talked with you his occasional tic of a wink led you to believe you were among his closest friends (which, upon further reflection, you realized was indeed the case).
In 1990, I became responsible for an area in the Exhibit Hall at the FASEB (later EB) spring meeting in conjunction with a Modeling in Nutrition seminar in which I was a participant. Loren began attending FASEB that year, spending the week in front of a computer in the area, demonstrating SAAM. In organizing the area, I invited Federally-sponsored modeling resources to demonstrate their software there. Loren brought SAAM from his laboratory and had a steady stream of visitors throughout the week. To each one, old friend or stranger, he was unfailingly polite, enthusiastic about the visitor's research, and helpful in defining and starting a modeling environment appropriate for that project. We continued to work together in the computing area each spring until 1996, when failing health prevented him.
Loren was my alter ego. He and I graduated from electrical engineering programs in the same year. Later, we migrated to life science applications, he in medicine, I in biomedical engineering. We were each the father of three, and Loren was as solicitous of my children's progress as he was proud of his own. He soon became aware that my father was in poor health, and always after that, no matter how short the conversation, asked about him. Although we came from different religious backgrounds, his devoutness was a strength to me.
I will never forget taking him to an awards lecture and later a reception of the BMES at one FASEB meeting. "So this is where the systems physiologists have gone!" he exclaimed. Soon after, I was privileged to sponsor his application for Senior membership.
Loren's personal preferences were modest. At a meeting, a clean, inexpensive room and simple food would do. Once in Atlanta, as we were driving together Loren spotted a roadside vendor selling Vidalia onions. At his insistence, we stopped. I'm sure he had the only bag of onions on the Washington flight that evening.
As well as I felt I knew Loren and as much as I loved him, there are others who were closer and who will miss him perhaps more deeply than I. Here are comments from some of them.
From Peter Greif, his office partner for fifteen years: " It has been my honor to work with him ... over the past 15 years. During that time we shared many long conversations. Throughout my acquaintance with him, he has shown a tremendous commitment to science (his bibliography), his patients, his friends and his family. During the last one and a half years, Loren has been valiantly battling multiple myeloma. During his numerous hospitalizations and later at his funeral, I came to meet many wonderful people associated with this man. Through them I better appreciate the contributions he has made to their lives and the love that they feel towards him." Peter has established a WWW page at URL http://www.cpcug.org/user/greif/loren.html_honoring Loren. Some of the following comments can be found within that document.
From Waldo Fisher of the University of Florida, in eulogy: "(F)oremost, as I knew Loren, he was an explorer of physiology, yes, and a superb teacher. He had the ability to phrase questions so that the answers which were forthcoming were useful in furthering an understanding of a problem or the grasping of a concept. Surely my most vivid recollections are of the many hours we spent sitting in front of a computer while we extracted from a set of numbers the hidden truths they told. And, as our understanding of the workings of the system progressed, the complexities of the physiology became apparent. The tragedy of today is the short life of this man who had so much vitality and much more to contribute. My solace is to have had my life enriched by sharing his."
From Bob Phair, his co-worker and friend of twenty-five years, also in eulogy: "Nearly a quarter century ago, my mentor at the NIH, Mones Berman, was scheduled to interview Loren Zech for a position in the NCI's new Laboratory of Mathematical Biology. Mones, however, was not in Bethesda, and I, as a young staff fellow, was hurriedly recruited to conduct the interview. So that's how Loren and I first met. As we talked about mathematics and bio-medicine, it was as if each of us knew what the other would say before he said it. Perhaps it was because we both had degrees in electrical engineering, or perhaps it was our common desire to be at the NIH and work with the world's best mathematical modeler of human metabolic biology, but whatever it was, Loren and I, for 25 years, shared both the challenges and the mission of computational biology. For 25 years when I had what I thought was a really wonderful result, it was Loren who I wanted to tell first. I'd make the trip down from Johns Hopkins or I'd catch him at a national meeting. His eyes would light up and a special knowing grin would animate his face as he saw each realization of his own conviction that new and important biological information could be extracted from large and complex data sets. Loren Zech saw clearly the great power of computational biology to make sense of the complexities of human physiology and pathophysiology -- I'm deeply saddened that he will not be with us to see it become a mainstream tool - a critical tool for the emerging field of functional genomics.
"Students often ask what it takes to be a good modeler of biological systems. Loren and I once agreed that what it takes is two seemingly contradictory passions: a passionate desire to comprehend the 'big picture', and a coexisting passion for attending to details. Loren showed us that this is a wonderful paradigm for life, and for the practice of medicine as well as for science. No one saw the big picture better than Loren. Physicians often identify internists as those who best see the big picture, but Loren saw all of medicine as a subspecialty of engineering. He was, in all the best senses of the phrase, a human engineer. He knew the details of biomedical science and he cared about the details of our lives -- his colleagues' lives, his students' lives, his friends' lives, his patients' lives, and the lives of his family. I feel lucky to have known him, and blessed to have been his friend."
From Charles Schwartz, longtime associate, a third eulogy: "I first met Loren Zech in Mones Berman's office at the NIH in 1975. Loren had black hair everywhere, including lots on his head and a full beard. He wore wire rimmed glasses that were loosely taped together. He had recently come from San Francisco. Phyllis and I had lived in San Francisco two years previously, so I thought 'Oh No!' another brilliant fancy-free liberal from California. The brilliant part proved correct, but I got to know a hard working, focused and honest person who tried to convince me that his senator, Barry Goldwater, was becoming too liberal.
"Born in St. Claire, Michigan, Loren grew up in Arizona. He was always interested in both engineering and biologic sciences. However, in his 11th grade chemistry lab, sources say, he poured flammable chemicals down the drain. An explosion ensued causing significant damage to the new high school. He tended toward theoretical research ever since.
"After finishing medical training, Loren came to NIH to work with Mones Berman; Mones was by far the most influential person, outside the family, in Loren's life. Dr. Berman had profound influences, all positive, not only on Loren but on many others here today. After Mones' death, Loren in turn had a major influence on the careers of many scientists throughout the world. Loren was especially effective at nurturing the work of others; he helped us improve and understand our work; then he stepped aside and never took credit for himself. He was modest-to-a-fault, avoiding the limelight.
"I can say as a teacher and practitioner of medicine and more importantly as a mortal man, three things of which I am convinced and in which I take comfort: First, my friend's suffering is over. He is whole again in God's hands. Second, my friend's life did not stop when his heart stopped; life does change but does not end. Third, my friend leaves a wonderful legacy in his family who grieves at their loss but each of whom carries a lot of Loren with them. Bad things do happen to good people. Joy and sorrow are a part of life; as a physician, Loren knew that, AND he knew that death was not the opposite of life, but rather its companion.
"I've lost a dear friend. You have lost a son, husband, and father. Loren would want us to celebrate his life and spirit today and tomorrow, and forever. He wants us to join him in facing squarely whatever lies ahead. Death is a small thing in the large picture and anything that really matters goes on!"
From Blossom Patterson, an associate at NIH: "Loren set me on my career track, as I suspect he did for many. What started out as one of many projects for me -- the design and analysis of a small selenium pharmacokinetics study -- ended up being a major focus of my work. Without his efforts, help, and encouragement, I suspect there would never have been a selenite or a selenomethionine model. He spent vast amounts of time patiently teaching me about building models and showing me how to use SAAM. He delighted in the interplay between what was known about the physiology of Se metabolism and the implications of the developing model. He never lost sight of what he considered one of the most important aspects of modeling -- generating new hypotheses to be tested. Loren was an exceedingly generous person, never wanting to take the credit that was truly his.
"One of Loren's favorite stories, which I expect you've heard about, was that he was told in medical school that he was independent beyond utility to himself -- what I liked best about his telling that story was that he took such pleasure in it. Loren embodied, and thoroughly enjoyed, independence. He was independent in his thoughts, direction, and actions. In my opinion, his exceptional success as a scientist was due, in large measure, to this attitude toward his work. He used to say that NIH was the perfect environment for him, as he was free to pursue his interests and set his own agenda and direction. His immense accomplishments show how right he was in his assessment. His life has enriched not only the scientific community, but also the lives and work of those fortunate enough to have worked with him."
From Janet Novotny, USDA: "I feel very fortunate to have had the opportunity to know and work with Loren Zech. Loren was a wonderful person in so many ways. My first meeting with Loren is an example of his great generosity with his time. I had downloaded the SAAM program from the FTP site and was trying to build a model. The SAAM commands were foggy to me, so I decided to phone Drs. Greif and Zech for some advice. Loren answered the phone and despite his busy schedule, he invited me to visit him with my data at NIH that very afternoon. We spent several hours pouring over the data and re-structuring the model. From that point on I had the regular pleasure of working with Loren on modeling problems. He was a very generous and kind man, a bright and thorough scientist, and a wonderful friend. I was very fortunate to have known Loren and I will miss him very dearly."
From Carol Marzetta: "I have known Loren for about 14 years. As a graduate student at Bowman Gray School of Medicine back in the early 1980's, Loren generously offered to teach me multi-compartmental modelling using SAAM as a part of my studies on lipoprotein metabolism in nonhuman primates. On two separate occasions during my graduate work, Lori (Loren's wife) housed me, fed me and cared for me, while Loren mentored and taught me kinetic modeling. He shared with me his knowledge during the day and his family at night. It was the perfect blend of professional education and personal compassion. Loren was on my Ph.D. defense committee and was a major contributor and supporter of my education. He and I published 2 papers together based on my graduate work. In the 12 years since I graduated, Loren and I have stayed in touch and he has continued to stay interested in my career and life, offering me help in any way he could. I have lost not only a mentor and great educator, but a friend as well. There are many things that can be said about Loren's contribution to the scientific field, but I suspect he has made an equally strong impact on the personal lives of many of us as well. For me, my loss goes far beyond the education he so patiently taught me. I have lost a friend and colleague that I truly loved and I will miss him dearly."
From Oscar Linares, Geriatric Services, UMMC: "My recollections are many, but what stands out is that Loren taught me a different way of thinking along quantitative lines, and he provided me with a tool to express my thoughts -- SAAM. He told me that to be a good biomodeler you no longer had to be good at doing long calculations by hand as an essential skill and he showed me how I could get SAAM to do them instead. I have many fond memories of Loren but my favorite are those of him telling me tales from the heroic age of hand calculation."
"I will miss my friend forever!"
From Steve Coburn, for himself and Doug Townsend, colleagues in Fort Wayne, IN: "Our first encounter with Loren immediately revealed his talent and his unique personality. We were initiating studies of the kinetics of vitamin B-6 metabolism. Someone told us about the SAAM program and suggested that we contact Loren. I telephoned him and said that I had heard that he could supply SAAM. He confirmed that he could. I asked how much it would cost. He said it was free, but we would never figure out how to use it from the instruction manual. If we could come to Washington, he would explain it to us. When did we want to come? He offered to work with us at any time, including weekends. All this in five minutes of conversation with a person he had never met before. I said that before I could set a date, I wanted to check the schedule of Doug Townsend, a mathematician who was working with me. Loren immediately responded that SAAM was deliberately designed to eliminate the need for a mathematician.
"Doug and I arranged to meet with Loren on July 3, 1985 on our way home from the first conference on Mathematical Modeling in Experimental Nutrition in Athens, Georgia. He spent the entire day with us. As supper time approached he offered to continue working with us on the July 4 holiday. We ended up working until 9 or 10 p.m. on July 3 to avoid imposing any more on his holiday. That experience was a typical example of Loren's willingness to do whatever was necessary to assist his colleagues. SAAM is a unique tool. Through SAAM Loren's contributions will continue to assist life scientists for many years to come. We benefitted greatly from our contacts with Loren. He will be missed by all of us."
A final eulogy, from Ray Boston, longtime associate of Loren on the SAAM project: "Whenever a friend passes away I believe that a part of us also passes away. The love, care, and commitment that we have grown to depend on from that friendship passes away. We are left with a void, a sense of emptiness, and an apparently unfillable space within us that was our friend. Loren has left each of us with this void, but I know that through our memories of the love and care that he so willingly gave us, this void will prove to be a power within ... we will be far richer for having had our Loren ... What is a friend? Is a friend someone we know will always be there for us? Is a friend someone whose counsel is always positive but cutting to the core of a problem? Is a friend someone whose heart is open, whose mind is available, and whose commitment is unswerving? Because, to me this was Loren. A man who knew no boundaries of help, a man who was always there.... When I had my heart surgery just a couple of months after arriving in this country 5 years ago, who do you imagine was liaising with medical professionals to ensure that I got the best treatment? Who do you think was on his way to be by my side as I underwent the procedure? Who do you think was ready to greet me as I was wheeled out of the operating theater? Throughout the time I have known Loren he was always ready with his love, care, advice, and time.... It was evident to me from the very first time that I met Loren that he was an intensely committed family man ... indeed within a week of meeting him I was invited to the Zech home to meet with Loren's pride and joy ... his family. This was a warm, welcoming, and close family with whom one could instantly establish rapport. Loren's love for his wife, Lori, and his pride in his children were without equal. He was determined to provide well for them all and his desire to see that the children had the most appropriate opportunities to develop their interests, was insatiable.... Testimony that Loren was a pillar amongst scientists comes from the group assembled here this morning paying their respects. Clinicians, mathematicians, epidemiologists, statisticians, scientists, agricultural scientists, pharmacologists, environmental scientists have all been assisted by, guided by, and instructed by Loren. Loren's patience and care in describing new problem perspectives has shed light on the way his associates and followers look at problems.
"The usual measures of scientific success relate to counts of papers, grants, and graduate students ... and Loren had his good share of all these. But where Loren stood alone was in capacity to inspire enthusiasm and commitment to his ideas in those whom he assisted. Loren was the penultimate one-on-one instructor and his efforts and goals will forever live on in those he taught.
"Let me close this perspective with a dichotomy ... Loren always thought of himself as a modeler. Maybe so ... but to me and I hope to you ... Loren was the model. The model friend, the model family man, the model scientist. So in losing Loren we inherit a void but if we reflect on what Loren has been to us, what he gave us, and how much richer we are for having him we can more easily fill that void. Loren's love and care for us will help all of us to endure our loss."
I copied the likeness of Loren from his WWW page to my computer desktop. I do not anticipate removing it. As I close my eyes I can hear that deep, gruff voice and see that conspiratorial wink encouraging me, urging me to follow...
A number of Student Travel Awards will be available to help defray travel costs of undergraduate and graduate students who attend the BMES Fall Meeting in San Diego.
Five graduate student awards will be presented to graduate students judged by a review committee consisting of BMES members on the basis of their scientific merit, originality and quality of the written presentation.
To apply for the awards, students must submit four copies of an extended abstract by June 2, 1997, in addition to the short abstract form. Extended abstracts must be limited to three pages, including illustrations and references, and must be typed single-spaced (10 or 12 point font size) and printed on 8.5x11 inch white paper with one-inch margins on all sides. The title of the report should appear on the top of the first page, followed by the author name(s), affiliation(s), and complete mailing address. Skip one line before the text. A letter of support is required from the student's scientific advisor or department chair certifying the originality of the student's effort. Each award consists of a certificate and a stipend in the amount of $300, which will be presented at the BMES Business Meeting on Saturday, October 4, 1997.
Undergraduate students may compete for one of five Whitaker Foundation Senior Student Bioengineering Design Awards. These awards are for bioengineering designs submitted by an individual student or a team of students. Students must have senior standing at the time of submission. Conceptual designs as well as complete prototypes may be submitted. Five awards consisting of a certificate and a check in the amount of $200 each will be presented at the meeting. Designs will be judged by a panel of BMES members on the basis of originality, significance, thoroughness of design analysis and performance evaluation. Multiple applications from single institutions are permitted. Each submission must be accompanied by a written statement from the department/division chairperson, or from the course director/instructor, confirming the major contribution(s) by the student(s) to the design. The design submissions must adhere to the following guidelines.
Submit by June 2, 1997, four copies of a two-to-three-page design description. Design descriptions must be single-spaced (font size 10 or 12 point) printed on 8.5x11 inch white paper, with one-inch margins on all sides. The title of the design description should appear at the top of the first page, followed by the student name(s), affiliation(s), and complete mailing address. Skip one line before typing the text of the design description. Each design description should include the following sections: Summary, Introduction, Design Objective, Description, Analysis and Performance Evaluation, Discussion, and References. Reasonable deviations from these section guidelines are permitted to accommodate individual projects. The winners, or a representative, are expected to present their work in a special session at the meeting.
Conceived by the Arizona State University BMES chapter in 1992 to promote student participation in the Annual Fall Meeting, the Fleetest Feet Award is given to the chapter that is represented at the meeting by the most students having traveled the most miles. A 10% bonus in mileage is granted to chapters that drive to the meeting instead of flying.
For further information and entry forms contact: Rita M. Schaffer, bmes@netcom.com
The Whitaker Young Investigator Award is offered each year by the Biomedical Engineering Society to stimulate research careers in biomedical engineering. The $1000 award and plaque are presented at the BMES Annual Fall Meeting to a young investigator whose originality and ingenuity in a published work were recognized by the Awards Committee.
The awardee is expected to be present to accept the award at the Biomedical Engineering Society Annual Fall Meeting. Travel expenses of up to $1000 will be reimbursed by the Society.
Conditions:
1. The award is in recognition of a high level of originality and ingenuity in a scientific work in biomedical engineering. The awardee must be within five years of receiving his or her highest degree.
2. Applications must include the candidate's curriculum vitae and confidential letters by two recognized authorities in the field of the work, neither of whom is associated with the institution at which the work was completed nor a co-author on the paper, attesting to the significance of the investigation described in the manuscript.
3. Because selection of the awardee will largely be based on the review of a published paper describing original work, if the candidate is not the sole author of the manuscript, she/he must be the first author and the manuscript must be accompanied by a letter from the co-authors attesting to the leading role of the applicant in carrying out the work.
4. Manuscripts must have been published, or accepted for publication, in a peer-reviewed journal after January 1, 1996.
Submit 4 copies of manuscripts, curriculum vitae, and the letters described above by July 1, 1997 to:
Richard A. Normann, Ph.D.
Chairman, BMES Awards Committee
Department of Bioengineering
506 Biomedical Polymers Research Building
University of Utah
Salt Lake City, UT 84112
(801) 581-7645
Keywords: asthma, epithelium, airway, mechanics, finite element analysis, remodeling, computational model
Introduction
Biomedical engineering, and biomechanics in particular, will have an increasingly important role to play as the need grows to apply the discoveries of molecular biology to large-scale biological systems. Molecular biologists lack the training to bridge the gap between events at the molecular scale and the function of an entire organ or organism. Engineers, on the other hand, are trained specifically in the skills of modeling complex systems that often function over a wide range of length or time scales. It seems logical therefore that biomedical engineers, familiar with the traditional engineering approach and knowledgeable in molecular biology, will make increasingly significant contributions to physiology and medicine.
One example can be found in the context of small airway mechanics and its role in pulmonary disease. Researchers have long been intrigued by the changes that occur in a human airway in diseases such as asthma, chronic obstructive pulmonary disease (COPD) and emphysema, and have recently begun to model these phenomena in an attempt to understand the pathological process better. Through these studies, the need to integrate effectively models of whole-organ behavior such as normal and labored breathing with investigations of small airway mechanics has become obvious due to the dominant role mechanics plays in airflow obstruction. Model studies focus on the determination of deformations and stress distributions within the airway wall resulting from forces acting either internally (i.e., due to smooth muscle activation) or externally (due to parenchymal tethering, differences in gas pressure, or surface tension). These studies, in turn, must be further related to investigations into the biological processes that determine airway wall mechanical properties and cause them to change as a result of disease-related remodeling.
In this paper, I will outline the path of investigation that leads from macroscopic flow modeling down to events at the molecular level that alter the mechanics of small airways. These are inextricably linked, and I will attempt to demonstrate how investigations at the various scales greatly enhance our understanding of the disease process.
The Importance of Airway Mechanics in Pulmonary Airflow
The mechanical stiffness of the airway wall is a critical factor in determining respiratory flow rates as well as other aspects of respiratory function. In healthy individuals, the pressures generated during a cough or a forced expiration to initiate expiratory flow also cause partial airway collapse. This is beneficial in a cough because it increases velocities and shear stresses, thereby augmenting clearance. Airway compliance also leads to flow limitation in which the maximal flow at a given lung volume becomes independent of the level of respiratory effort exerted by the subject when the flow speed reaches the speed of wave propagation at some location along the airway tree (1, 2, 3). In healthy lungs, flow limitation occurs at flow rates never encountered during normal breathing, nor even at rates associated with heavy exercise. In obstructive diseases such as asthma, COPD and emphysema, however, flow limitation can occur at flow rates in the range of those necessary to maintain normal gas exchange. Flow limitation results from either an increase in the resistance of the peripheral airways, enhanced in the presence of airway smooth muscle constriction, or a decrease in effective airway stiffness with a consequent reduction in the tethering forces exerted by the lung parenchyma surrounding the airway.
Fluid dynamic models have provided an important tool in better understanding the relationship between respiratory airflow and airway mechanics. Using available morphometric data on the size and branching characteristics of the pulmonary tree (see Table 1) in combination with a fluid dynamic analysis, the pressure-flow relationship (the relationship between pressure generated by the respiratory muscles and expiratory flow rate) of the healthy lung during normal breathing has been predicted (4, 5), as has the flow-volume curve (illustrating the relationship between maximal expiratory flow rate and lung volume) for forced expiration (6). More recently, morphometric data describing the changes in airway wall thickness associated with asthma or COPD (7) have been introduced into these models to elucidate the mechanism and sites of increased flow resistance, including the effects of smooth muscle constriction (2, 8). Incorporation of these data into the model emphasizes the essential role of airway wall thickness in the enhanced airwa y narrowing seen in asthma or COPD. In the case of forced expiration, models reproduce reasonably well two features characteristic of disease, the reduction in peak flow and the increase in minimal or residual volume. Thus, several of the key factors linking airway pathology to altered function have been tentatively established.
Models of forced breathing rely on an accurate description of airway compliance. In the large airways, this is based on experimental data, in either excised human lungs (10) or intact dog lungs (11), that are cast in the form of a relationship between cross-sectional area and transmural pressure. While there are differences between these two approaches and certain deficiencies in the models (e.g., viscoelastic effects are ignored), the mechanical properties of the large airways are reasonably well characterized by this means. It is in the characterization of the small airways, those primarily responsible for the changes seen in disease, where our understanding is most deficient.
Focusing on how the constriction of small airways is treated in these models, we find that wall mechanics have been carefully avoided, because of the lack of empirical or theoretical knowledge of their mechanical behavior. The models avoid mechanics by specifying the amount of smooth muscle shortening, independent of wall elasticity or the external forces acting on the airway. Furthermore, it is assumed that the degree of shortening is the same for asthmatic and normal airways despite significant differences in wall thickness and composition between the two types. Assumptions such as these are necessary, given our current lack of an appropriate structural model to treat small airway narrowing in a more realistic manner and the experimental data to use in such a model. The present approach, however, leaves considerable uncertainty regarding the connection between the primary pathology of obstructive disease, which leads to remodeling of all layers in the airway wall, and the whole-organ manifestations of it. Despite the obvious importance of the structural characteristics of airways to pulmonary disease, it is fair to say that the fundamental link between the underlying airway pathology and the breathing deficit it produces remains poorly understood (12). To address these deficiencies, attention has recently been turned to airway structure in an attempt to model airway deformation and collapse more precisely in health and disease.
The Mechanics of Small Airways
Changes in lumenal area associated either with changes in transmural pressure or with muscular constriction are governed by the balance of forces in the airway wall. Following Okazawa et al. (13), we partition the wall of a pulmonary airway into the three primary layers shown in Figure 1: the regions inside the smooth muscle, those outside the smooth muscle, and the smooth muscle layer itself. When viewed from a structural perspective, the inner region of the airway wall is dominated by the dense collagen matrix of the lamina propria, located just outside the epithelium and basement membrane. Outside the lamina propria is the submucosa, a region of disordered connective tissue containing a significant amount of proteoglycan which is likely to be relatively compliant compared to the lamina propria. These represent the main structural elements of the airway wall which experience compression when smooth muscle is activated and constricts. Outside the smooth muscle is the adventitia which, while normally quite thin, can swell to several times its normal thickness in cases of pulmonary edema and airway inflammation. On its outer surface, the airway is embedded in, and structurally tethered to, the lung parenchyma. The alveolar septae that comprise the parenchyma attach to the adventitia and exert an outward acting force, helping to stabilize the airway and prevent collapse. This results from a combination of tissue-borne forces and surface tension forces acting at the gas-liquid interface within the alveoli. The final contribution to the overall force balance of the airway is due to the liquid layer that lines the inner lumenal boundary. Due to interfacial tension at the gas-liquid interface, a negative pressure that exerts an inward-acting force on the airway wall exists in the liquid layer.
The mechanical events associated with airway narrowing are complex and involve all of the components just mentioned. Prior to smooth muscle constriction, a balance exists between the parenchymal tethering forces (both elastic and surface film) pulling outward, the surface tension forces associated with the airway lining liquid pulling inward, and the mechanical strength (stiffness) of the airway wall which carries the load associated with the difference between the two. Stresses due to parenchymal tethering are roughly equal to the pressure in the pleural space, a value between 0.1 and 0.5 kPa relative to atmospheric pressure at functional residual capacity. The negative normal stress acting on the inside wall is somewhat smaller (<0.1 kpa if surface tension is estimated to be ~25 dyne/cm and the lumenal radius of a small airway to be about 250 µm). taken together, in the absence of contractile stimulation, the airway is subjected to a net positive transmural pressure. the external forces are opposed by stresses acting within the various layers of the airway wall.
When smooth muscle begins to contract, it pulls inward on outer layers of the airway wall and compresses inner layers. If the tissues inside the smooth muscle were in circumferential and radial tension to begin with, constriction of the smooth muscle would first tend to relieve that tension; once relieved (i.e., brought to a zero-stress state), further constriction would induce a compressive load on the inside layers. At this point, further shortening of the smooth muscle would be resisted by radial stresses (outward directed) acting on its outer and inner surfaces. Depending on the extent to which adventitial thickening has de-coupled the airway wall from the parenchyma, the bulk of this stress would be borne by compressive stresses inside the smooth muscle. These compressive loads could lead to mechanical instability and buckling. As shown later, the mode of buckling or collapse is determined essentially by two factors: the thickness of the lamina propria and the ratio of elastic moduli between the lamina propria and the submucosa, just as in the case of a layered composite or "sandwich panel" (14). Once the collapse pattern is established, airway narrowing proceeds by a progressive increase in the amplitude of the folds, producing a pattern often likened to a "rosette".
There is some evidence, anecdotal at this time, to suggest that the collapse mode of normal constricted airways differs from that in asthmatics. In normals, the number of folds tends to be greater and folds penetrate less far into the airway lumen when constricted (Figure 2, left) than in a typical asthmatic airway (right). This folding pattern could be one of the factors contributing to hyper-responsiveness (an exaggerated response to a broncho-constrictive agent) in a chronically inflamed airway. In one hypothesized scenario, shortening of the smooth muscle buckles the epithelium and airway resistance increases as the mucosal folds protrude into the airway lumen. As epithelial borders on these folds impinge on one another, the system stiffens, and this stiffening impedes further lumenal narrowing. Because impingement occurs later (or not at all) in an airway with fewer folds, the asthmatic airway will tend to collapse further and therefore exhibit greater airway obstruction.
Mucosal folding as a consequence of smooth muscle shortening has been the focus of several recent studies. The potential importance of folding pattern as a contributing factor to hyper-responsiveness in chronically inflamed airways was first pointed out by Lambert (15). Subsequent studies have sought to identify the factors that influence the folding pattern (16). In these studies the airway wall tissue between the smooth muscle and airway lumen is assumed to be comprised of two sub-layers: a thick but compliant outer layer (the submucosa) and a thin but relatively stiff inner layer (the lamina propria / basement membrane / epithelium). This model is based on the observations that epithelial circumference remains constant during airway constriction (17) and that the lamina propria with its high collagen content is likely to be relatively inextensible. These simulations focused on the determinants of the folding pattern, in particular, the mechanical factors which cause the large amplitude mucosal folding with relatively few circumferential folds characteristic of constricted asthmatic airways as opposed to the smaller and more numerous folds seen in normals. Results (Figure 3) indicate that the thickness of the stiff inner layer (lamina propria) and, to a lesser degree, the relative stiffness between the outer (submucosal) and inner layers, are the primary determinants of mucosal folding pattern. On the other hand, submucosal thickness has almost no influence on the buckling pattern.
Aside from predicting the folding pattern, these simulations hold the potential to predict airway narrowing as a function of transmural pressure; this is essential if airway mechanics are to be integrated with the models for pulmonary flow. The model predictions are shown in dimensionless form in Figure 4. To cast these results in dimensional terms requires knowledge of the compressive modulus for the inner wall tissue. Such measurements have not yet been made in normal airways, nor in airways with chronic inflammation. Preliminary tensile measurements (18) suggest a modulus of about 1 kPa which, if applicable to the submucosa, would indicate that a 0.7 kPa stress must be applied at the inner boundary of smooth muscle to produce a 50% reduction in lumenal cross-sectional area. This performance is well within the capabilities of smooth muscle (19) and suggests that airway wall compliance is an important component in the overall airway force balance. But more experiments are needed before one can specify the mechanical properties of the different layers as required by this model.
Airway Wall Remodeling
To advance this line of research, a better appreciation is needed of the changes attributable to the disease process that occur in the airway wall. For example, it is known that in asthma the airway wall remodels; all layers of the wall thicken (7) (see e.g., Table 1) and its structural characteristics are altered, as reflected, for example, by an increase in the amount of collagen found in the subepithelial layer (20). This effect might well be mediated by fibroblasts, cells that are known to produce collagens I and III, located in the submucosa. That epithelial cells can influence fibroblast proliferation has already been shown (21). The associated structural changes are unknown. To the extent that these changes make the airway more rigid, they would appear to be a desired response to hypersensitive airway smooth muscle. Contrary to that belief, more recent studies have shown that rigidity can lead to an altered buckling or folding pattern in the epithelium that could potentially augment airway obstruction rather than alleviate it (16). The question then becomes: What factors contribute to airway wall remodeling, and how might it be prevented?
These questions regarding the cause of airway wall remodeling have led to the hypothesis that, as observed in other tissues, airway epithelial cells or fibroblasts might respond to the unusual levels of physical stress associated with repeated smooth muscle constriction by initiating an inflammatory response and increasing the rate at which they produce certain constituents of the extracellular matrix, specifically, collagen, fibronectin and proteoglycan. Such an increase would account for the thickening described above. The levels of stress predicted by the computer modeling and shown on a stress map in Figure 5 are, in fact, far in excess of those known to elicit a variety of biological responses from arterial endothelial cells (22). While beneficial in other situations, this response could actually increase the degree of airway obstruction produced by a given level of smooth muscle activation and thereby aggravate the disease. To test these ideas will require experiments in which airway epithelial cells and/or fibroblasts, grown in culture, are subjected to stresses of the type generated by smooth muscle constriction. Using the methods of molecular biology, it should be possible to identify changes in cytokine gene expression responsible for the increased amounts of matrix material. Numerous candidates exist, as discussed in several recent reviews (23, 24). Several cytokines elicit a fibrotic response, such as those in the TGFB (transforming growth factor) family and PDGF (platelet-derived growth factor), both of which are produced by the airway epithelium. Others such as bFGF (basic fibroblast growth factor) act as mitogenic factors for the fibroblasts. Still others are proinflammatory including members of the interleukin family and TNFa (tumor necrosis factor). The endogenous peptide endothelin-1 (ET-1) is also synthesized in the epithelium and may play a role in smooth muscle hyperplasia and hypersecretion of mucus, two other features common to asthma. Identification of the essential biochemical agents and the mechanisms by which their synthesis is stimulated would provide a better understanding of airway wall remodeling, and potentially lead to methods of controlling or even reversing it. In turn, this new appreciation of small airway mechanics, and the molecular constituents that influence it, can be introduced to our large scale models of organ function to understand better the relationships between molecular and macroscopic events.
Integrating from Molecular to Whole-Organ Phenomena
Although studies of the type just described examining the molecular consequences of chronic airway inflammation are just getting underway, we can already anticipate how they will help us in our understanding of macroscopically-observable phenomena and, in turn, the entire spectrum of related pathologies. The over-reaching goal of this work is to understand the disease process, beginning with the smooth muscle-induced stresses and their potential link to biological remodeling that produce the observed changes in airway wall thickness and composition. These changes in turn alter the structural characteristics of the wall, and ultimately compromise the patient's ability to breathe, as reflected in standard pulmonary function tests. To achieve this goal, we need the tools of molecular biology to explore the nature of, and stimulus for, changes in tissue microstructure as well as the tools of engineering to integrate this new understanding into increasingly realistic models of organ function.
Acknowledgments
The author is indebted to J. Drazen, D. Elad, C. Hrousis, B. Ressler, A. Shapiro, J. Shin, and B. Wiggs for their numerous contributions to this work. In addition, the continuing support of the NHLBI (HL33009) and the Freeman Foundation is gratefully acknowledged.
References
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8. Wiggs, B.R. et al. Am. Rev. Respir. Dis. 145: 1251-1258, 1992.
9. Weibel, E.R. Morphometry of the Human Lung, Academic Press, 1963.
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12. Kamm R.D. and J.M. Drazen. Am. Rev. Respirat. Dis. 145: 11249-, 1992.
13. Okazawa, M. et al. In: Airways and Vascular Remodelling, Academic Press, 1994.
14. Allen, H.G. Analysis and Design of Structural Sandwich Panels, Pergamon Press, Toronto, 1969.
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21. Nakamura, Y. et al. Am. J. Physiol. 269 (Lung Cell. Mol. Physiol. 13): L377-387, 1995.
22. Davies, P.F. and S.C. Tripathi. Circ. Res. 72: 239-, 1993.
23. Raeburn, D. and S.E. Webber. Eur. Respir. J. 7: 2226-2233, 1994.
24. Roberts, C.R. Chest 107(3): 111S, 1995.
You are cordially invited to attend the 1997 Annual Fall Meeting of the Biomedical Engineering Society hosted by the Department of Bioengineering at the University of California, San Diego. The Fall Meetings of BMES have become an important focus for exchange and discussion of modern developments and evolving frontiers in biomedical engineering. A broad scientific program will be offered together with a pleasant social program and ample time for discussions and interchange of ideas.
The theme of the meeting is New Horizons and Innovations in Biomedical Engineering. Frontiers such as molecular bioengineering, cellular bioengineering, growth and transgene technology, will be interwoven with traditional programs in orthopaedic and cardiovascular bioengineering, cardiopulmonary bioengineering, neural engineering, medical image analysis, rehabilitation bioengineering and orthopaedic bioengineering, as well as biomedical engineering and society and industry. In addition to the scientific program, the social program will include a dinner at the world famous Sea World and a private Shamu Whale Show for the members of the conference.
The deadline for the receipt of the abstracts is June 2, 1997. No late entry will be considered. Symposia speakers must submit their abstracts at the same deadline. Abstracts will be published in a special issue of the Annals of Biomedical Engineering.
For further information, suggestions or requests regarding the scientific program, please contact Dr. John Frangos (frangos@ucsd.edu) or members of the Scientific Program Committee.
Tours to various attractions in San Diego are offered by Enjoy California Enterprises (619) 681-0500. For more information regarding specific tours, contact (619) 224-1234. The concierge at the Hyatt Islandia Hotel will assist with recommendations and tour information.
The differential between non-member and member registration fees will be credited towards the first year of membership in BMES for 1998, following completion of a BMES membership application form at the meeting. Full refunds of the registration fees will be provided until July 31, 1997; after this date the registration fees, minus 50%, will be refunded until September 1, 1997. No refunds will be provided after September 1, 1997. The registration fee includes the welcome reception, coffee breaks and lunches.
Tickets for the Evening at Sea World on October 4, 1997 (including banquet and private Shamu show) for all registrants, as well as accompanying persons, are as follows: $50 before June 2, $55 before July 31, and $60 on-site. Payment by credit card or personal check (in U.S. dollars) will be accepted. Visit the meeting's Web site at http://bmes97.ucsd.edu to register electronically.
At the meeting, registration desks will be set up in the Hyatt Islandia Hotel. Registration desk hours are as follows:
Thursday, 10/2 1:00 p.m. - 9:00 p.m.
Friday, 10/3 7:00 a.m. - 4:00 p.m.
Saturday, 10/4 7:00 a.m. - 4:00 p.m.
Sunday, 10/5 7:30 a.m. - 11:00 a.m.
Information about special events can be obtained at the registration desks. A conference badge is required for access to meeting rooms.
The Whitaker Young Investigator Award is given in recognition of a high level of originality and ingenuity in a scientific work in bioengineering. The award is open for competition for postdoctoral fellows up to five years after completion of their degree.
Meritorious Achievement Awards are given annually to the BMES student chapters judged to have outstanding activities and achievements.
Conceived by the Arizona State University BMES chapter in 1992 to promote student participation in the Annual Fall Meeting, the Fleetest Feet Award is given to the chapter that is represented at the meeting by the most students having traveled the most miles. A 10% bonus in mileage is granted to chapters that drive to the meeting instead of flying.
For further information on the student chapter and Young Investigator Award competitions contact: Rita M. Schaffer, Executive Director, Biomedical Engineering Society, P.O. Box 2399, Culver City, CA 90231, Tel: (310) 618-9322, Fax: (310) 618-1333, E-mail: bmes@netcom.com
The 1997 BMES Annual Meeting in San Diego, set for October 2-5, promises to continue our Society's trend of ever more vibrant and influential technical and professional activity in bioengineering. The local Organizing Committee led by Shu Chien, along with the national Program Committee headed by Herb Voigt, are doing a superb job with the sessions and publicity. We are looking forward to a rewarding time together with you there.
A very unfortunate circumstance has, however, only recently come to our attention. That is, the first day of the meeting coincides with Rosh Hashanah, one of the holy days of the Jewish faith. This, of course, will prevent many prospective participants from attending the early part of the meeting, and perhaps make it problematic for them to attend at all. On behalf of the Board of Directors, I extend a deep and sincere apology for our negligence in noting this conflict when the meeting was scheduled two years ago. We will certainly be more vigilant in scheduling future meetings, to our best ability.
Although it is impossible to make any substantial changes in the meeting dates at this late time, the local Organizing Committee has agreed to extend every effort to accommodate needs of individuals who would still like to attend the meeting despite conflict with observance of their religious faith. If abstracts for oral or poster presentation are submitted with a statement of date restrictions, the Committee will try to arrange the appropriate sessions to make participation feasible, to the extent possible. Regrettably we of course cannot guarantee that all conflicts will be resolved, but we hope that some help can be provided.
Please do not hesitate to contact me if you have any ideas about how the Society might additionally remedy this problem. We are grateful for forgiveness and forbearance from all of you to whom our mistake has given distress.
Douglas A. Lauffenburger
1997 October 2-5 BMES Annual Fall Meeting, San Diego, CA
1998 October 10-12 BMES Annual Fall Meeting, Cleveland,OH
1999 October 14-16 BMES Annual Fall Meeting(with EMBS) Atlanta, GA
2000 BMES Annual Fall Meeting, Seatle, WA
Faculty Positions in Mechanical Engineering/Biomechanics
The Engineering Department of Trinity College invites applications to fill a 5-year, full-time, continuing contract position in Mechanical Engineering with a research and graduate teaching interest in Biomechanics at the Assistant Professor level, to begin in fall 1997. This candidate will be expected to teach undergraduate and graduate courses, and to conduct a successful research program in biomechanics. These responsibilities will be shared between the Trinity Engineering program and the recently established Biomedical Engineering Alliance for central Connecticut (BEACON). Research interests in all aspects of biomechanics are welcome.
Trinity College, located in Hartford, Connecticut, is a highly selective liberal arts institution with an enrollment of 1800 undergraduates. Trinity is unique in supporting an ABET accredited Engineering department within its liberal arts environment for over a century. Bioengineering research and teaching collaboration in the greater Hartford are a has been significantly strengthened by a new $1 million Whitaker grant for development of BEACON. This consortium includes Trinity College, the University of Connecticut, the University of Connecticut Health Center, the University of Hartford, and area medical centers.
Candidates must have an earned doctorate in Biomedical or Mechanical Engineering. Interested applicants should send a CV, a statement of teaching and research objectives and the names and addresses of three references to: Dr. Joseph L. Palladino, Department of Engineering, 333 MCEC, Trinity College, 300 Summit St., Hartford, CT 06106 (joseph.palladino@mail.trincoll.edu). Applications will be reviewed starting April 1 and will continue until the position is filled. Trinity College is an Equal Opportunity/Affirmative Action employer.
Rensselaer Biomedical Engineering Department
Faculty Position
The Department of Biomedical Engineering at Rensselaer Polytechnic Institute invites applications for a tenure track faculty position at the rank of assistant professor. The successful applicant must have a Ph.D. or equivalent degree, and will be expected to conduct research, supervise graduate students, and teach courses in his/her specialty are a as well as in Rensselaer's undergraduate engineering curriculum. Candidates should have a strong background and research expertise in the development and application of computational methods and computer simulation in conjunction with orthopedic or dental biomechanics, cardiovascular biomechanics, cellular mechanics, or tissue mechanics. The position is available as early as Summer 1997. A complete resume and three professional references should be sent by June 15, 1997 to: John B. Brunski, Ph.D., Chair, Search Committee, Biomedical Engineering Department, Jonsson Engineering Center, Room 7049, Rensselaer Polytechnic Institute, 110 8th Street, Troy, NY 12180-3590, Phone: (518)276-6963, Fax: (518)276-3035, Email: brunsj@rpi.edu.
Rensselaer is an equal opportunity/affirmative action employer. Women and minority applicants are especially encouraged.
Faculty Position in Medical Informatics
University of North Carolina at Chapel Hill
Department of Biomedical Engineering and Medicine
The University of North Carolina at Chapel Hill is seeking a faculty member in the Division of Medical Computing and Informatics in the Department of Biomedical Engineering with a joint appointment in the Department of Medicine. The position is Tenure Track at the level of Assistant Professor, with 50% protected time for the first three years of the appointment.
The individual should have substantial expertise in Medical Informatics. Clinical activities will be performed through the Department of Medicine. The University has a National Library of Medicine fellowship training program in Medical Informatics, and the faculty member will be expected to assist in fellow training and mentoring. The faculty member will be expected to develop an active investigative program in Medical Informatics. Applicants should have an M.D., and be Board certified or eligible in Internal Medicine.
Areas of special interest at the University include: development of clinical information systems; medical information retrieval and management; telemedicine; decision-support systems; the training of health professionals in medical computing and information management.
Applicants should send their curriculum vitae to: John Loonsk, M.D., Co-Chair, Faculty Search Committee, The University of North Carolina at Chapel Hill, The School of Medicine, Department of Biomedical Engineering, Room 152 MacNider, Chapel Hill, NC 27599-7575.
The University of North Carolina at Chapel Hill is an Equal Opportunity/Affirmative Action Employer. Minorities and women are encouraged to identify themselves voluntarily.
Faculty Position in Instrumentation, Microelectronics, and Telemedicine
University of North Carolina at Chapel Hill
Department of Biomedical Engineering
The Department of Biomedical Engineering at the University of North Carolina is inviting applications for a faculty position at the research assistant\research associate professor level. The successful applicant is expected to: 1) have demonstrated ability to work with a broad range of healthcare professionals to develop a funded research program related to telemedicine/telehealth applications, 2) have credentials for teaching at the graduate level in one or more of the following areas: telecommunications/networking, microelectronics, and bioinstrumentation, and 3) work closely with existing faculty in the departments Instrumentation/Microelectronics/Telemedicine and Medical Informatics tracks. Applicants should have a Ph.D. degree in Biomedical Engineering, Electrical Engineering, or a closely related field. Applicants should submit a letter of application, a curriculum vitae, a list of three professional references, and an email address by (at least 30 days after first ad appearance) to: Henry Hsiao, Ph.D., Chair, Faculty Search Committee, Department of Biomedical Engineering, The School of Medicine, The University of North Carolina at Chapel Hill, CB# 7575, 152 MacNider, Chapel Hill, NC 27599-7575. The University of North Carolina at Chapel Hill is an Equal Opportunity/Affirmative Action employer. Minorities and women are encouraged to identify themselves voluntarily.
Address questions, comments, and corrections to:
Pin Lu
pinlu@cc.memphis.edu
Rita Schaffer
bmes@netcom.com
Last Updated: June 22, 1998