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The Fall 2004 NYC Bone Seminar Series

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  • The Fall 2004 NYC Bone Seminar Series

    Dear colleagues and students:

    The Fall 2004 Bone Seminar Series kicks off Tuesday September 28 with
    a presentation by David T. Denhardt PhD of Rutgers University, who
    will speak on "Osteopontin, a Cytokine and Bone Matrix Protein,
    Augments Bone Remodeling, Metastasis, and Autoimmune Disease

    Details of all seminars appear below as well as on our website:

    The contents of the rest of this email is as follows:
    [1] Bone Seminar Series: General Information
    [2] September 28, 2004 Seminar: David T. Denhardt PhD
    [3] October 26, 2004 Seminar: Timothy G. Bromage PhD
    [4] November 16, 2004: Janet Rubin MD
    [5] December 7, 2004: Peter Bullough MD
    [6] "Pinch Hitter": Luis Cardoso Landa PhD
    [7] Questions and Feedback Contact


    [1] Bone Seminar Series: General Information

    The Bone Seminar Series focuses on bone research in general and the
    study of the mechanosensory system in bone in particular. The Series
    consists of eight seminars per academic year, four each in the Fall
    and Spring series.

    Program information for the Bone Seminars and the annual Bone Fluid
    Flow Workshop is regularly posted on our website:

    Comments on the website are welcome and may be addressed to Bill
    Green at or to me Steven Cowin PhD at

    Seminars are held in rooms on the ninth floor of the CUNY Graduate
    Center on Tuesdays from 7:00 to 8:30 PM. The CUNY Graduate Center is
    in the Altman Building at the corner of 34th Street and 5th Avenue,
    catty-corner from the Empire State Building. A social hour precedes
    each seminar starting at 5:45 PM with food (fruit plate, vegetable
    plate, cookies) and drinks (coffee and soft drinks). There is also a
    snack bar on the first floor. There are several subway lines nearby,
    and it is less than a ten-minute walk to either Grand Central Station
    or Penn Station. There is money to support parking for graduate
    students; apply to Steve Cowin (contact information at end of this


    [2] September 28, 2004 Seminar

    SPEAKER: David T. Denhardt PhD, Department of Cell Biology and
    Neuroscience, Rutgers University, Piscataway Campus

    TOPIC: Osteopontin, a Cytokine and Bone Matrix Protein, Augments Bone
    Remodeling, Metastasis, and Autoimmune Disease Progression

    PLACE AND TIME: Room 9204, CUNY Graduate Center, 7:00 PM

    ABSTRACT: Osteopontin (OPN) is a phosphorylated, glycosylated protein
    found not only extracellularly in all body fluids and in mineralized
    matrices but also intracellularly at the cytoskeletal/plasma membrane
    interface. The extracellular form is capable of engaging some
    half-dozen integrins and at least two CD44 variants. OPN signaling
    regulates gene expression (e.g., iNOS expression induced by
    endotoxin) and cell motility, stimulating a chemotactic response. It
    enhances the survival of cells exposed to various stresses by
    inhibiting apoptosis. OPN can stimulate tumor cell metastasis and the
    progression of autoimmune disease: Mice lacking OPN are less
    susceptible to arthritis induced by anti-type II collagen antibodies
    (Noda) and to experimental autoimmune encephalomyelitis induced by
    myelin oligodendrocyte glycoprotein peptides (Steinman, Cantor). They
    are also unable to remodel bone in response to various stresses
    (ovariectomy, hind-limb suspension), possibly in part because OPN is
    required for normal osteoclast function (Hruska, Noda, Sodek).

    RESEARCH INTERESTS of Dave Denhardt: His research interests currently
    focus on the systems physiology of OPN and TIMP-1 (tissue inhibitor
    of metalloproteinases-1). Both in different ways stimulate tumor cell
    metastasis and he would like to know why. With respect to OPN, he
    would like to understand how it functions in such apparently diverse
    processes as bone remodeling and autoimmune disease.


    [3] October 26, 2004 Seminar

    SPEAKER Timothy G. Bromage, PhD, Department of Biomaterials and
    Biomimetics, New York University College of Dentistry

    Confocal Circularly Polarized Light Microscopy of the Early Hominid Skeleton

    PLACE AND TIME: Room 9207, CUNY Graduate Center, 7:00 PM

    ABSTRACT: Skeletal microanatomy is typically investigated by some
    form of light microscopy on specially prepared samples, such as
    histological thin sections, or by scanning electron microscopy (SEM)
    of bulk specimens. However, unique African early hominid remains from
    Pliocene localities some 2-4 million years old are not readily
    available for histological sectioning, and bulk examination by SEM is
    restricted to first surfaces. A practical alternative is confocal
    scanning optical microscopy (CSOM). This permits "optical sectioning"
    upon and below the intact surfaces of opaque materials, which
    generates excellent reflection images and provides basic details of
    bone and tooth histological microanatomy equal to that produced by
    conventional research microscopes.

    This is all very well, but African early hominid repositories do not
    have available CSOM technologies, requiring that we bring such an
    instrument to the fossils. This has prompted development of the first
    portable CSOM, the prototype of which has recently been taken to
    Ethiopia, Kenya, and South Africa for its first glimpse of the hard
    tissue microanatomy of Australopithecus, Paranthropus, and early Homo
    species. CSOM imaging of the dentition is demonstrating
    species-specific variations of enamel structure related to functional
    and life history adaptations. Further, because the portable CSOM is
    configured to generate reflected circularly polarized light images,
    we are able to study and analyze preferential collagen fiber
    orientations in bone tissue and thus skeletal function in our fossil

    RESEARCH INTERESTS of Tim Bromage: Comparative hard tissue biology
    and microanatomy in relation to functional, life history, and
    environmental reconstruction; human evolution; development of
    practical solutions to technical problems of mineralized tissue
    specimen preparation and imaging.


    [4] November 16, 2004 Seminar

    SPEAKER: Janet Rubin MD, Professor of Medicine, Division of
    Endocrinology and Metabolism, Emory University School of Medicine and
    the Atlanta Veterans Affairs Medical Center, Atlanta, GA

    TOPIC: Turning Mechanical Signals into Biological Effects

    PLACE AND TIME: Room 9205, CUNY Graduate Center, 7:00 PM

    ABSTRACT: Biophysical input generated during normal physiologic
    loading is a major determinant of bone mass and morphology. Our
    laboratory's interest is in how bone cells sense and transduce
    signals generated during loading and how this cellular response leads
    to skeletal adaptation to its mechanical environment. We have shown
    that substrate strain regulates gene expression in bone stromal
    cells, decreasing expression of RANKL and increasing expression of
    eNOS/nitric oxide. These changes generate a local environment that is
    inhibitory for osteoclast recruitment. The ability of mechanical
    strain to induce this functional response requires activation of the
    ERK1/2 MAP-kinase pathway. The proximal signaling cascade leading to
    ERK1/2 activation is stunningly specific, and suggests that the
    putative mechanotransducer occupies a discrete membrane location. Our
    most recent work suggests that the mechanical signal arises from
    events occurring within a lipid raft. Distal to ERK1/2 activation, we
    will also consider possible mechanisms by which strain may inhibit
    RANKL gene transcription through altering chromatin interactions with
    the RANKL promoter. By defining the mechanisms involved in strain
    regulation of osteoclast formation we hope to generate new paradigms
    for understanding how cells convert mechanical information into
    biological effects.

    RESEARCH INTERESTS of Janet Rubin: Mechanical and hormonal control of
    bone remodeling, gene therapy systems, tumor metastases in bone.


    [5] December 7, 2004 Seminar

    SPEAKER: Peter Bullough MD, Director of Laboratory Medicine, Hospital
    for Special Surgery, New York, NY; Professor of Pathology, Cornell
    Medical School, New York, NY

    TOPIC: Bone and Subchondral Bone Involvement in the Etiology of Arthritis

    PLACE AND TIME: Room 9204, CUNY Graduate Center, 7:00 PM

    ABSTRACT: Focal degenerative changes occur in some joints very early
    in life. These changes in the articular cartilage appear to occur on
    the unloaded, rather than loaded, areas of the joint. Just as unused
    bone and unused muscle atrophy, so may unused cartilage. If these
    unloaded structures were never subjected to mechanical stress,
    degeneration at these sites perhaps would not be important. However,
    bones, including their articular ends, are in a constant state of
    change through the process of remodeling, which continues throughout
    life. Joint surfaces are not, in general, spherical, and therefore
    must be incongruent during most of their arc of movement. In the
    young person, this incongruity maintains physiologic loading and
    joint nutrition. Studies have shown age-related changes in the
    remodeling process that lead to increasing joint congruity in old
    age. These age-related increases in congruity may result in a
    redistribution of load in the joint such that there is an increased
    stress on formerly unloaded atrophic cartilage. Arthritis always
    results in a change in joint shape. It is suggested that a change in
    shape caused by a disturbance in the remodeling process may itself be
    an important contributing cause of osteoarthritis.

    RESEARCH INTERESTS of Peter Bullough: "I have had a long-time
    interest in the question 'Why do people get arthritis?' The study
    material has been the joints resected in joint replacement, which
    account for around 30% of all orthopaedic procedures where I work."


    [6] "Pinch Hitter"

    In the Fall 2004 Bone Seminar series we will be experimenting with
    the use of a pinch hitter. If, for any reason, the designated speaker
    cannot speak on a particular evening, the pinch hitter will
    substitute if s/he does not have a previous commitment. The
    designated pinch hitter will fulfill that role for only one seminar
    series. If the pinch hitter does not speak in the series for which
    s/he is designated, s/he will have a regularly scheduled seminar in
    the following series. Thus the pinch hitter for the Fall 2004 series,
    Luis Cardoso Landa, if he is not called upon to fill in on September
    28, October 26, November 16, or December 7, will present a Spring
    2005 Seminar.

    SPEAKER: Luis Cardoso Landa PhD, Postdoctoral Research Fellow,
    Department of Orthopaedics, Mount Sinai School of Medicine, New York,

    TOPIC: On the Ultrasonic Characterization of Anisotropic Cancellous
    Bone: An In Vitro Experimental and Theoretical Study Based on a
    Modified Biot's Theory

    ABSTRACT: Currently, the approach most widely used to examine bone
    loss is bone densitometry, which measures bone mass density by x-ray
    absorptiometry. Recently bone ultrasound attenuation (BUA) has seen
    wider clinical use. However, osteoporosis is not only characterized
    by a decreased bone mass density, but also by changes in the
    microstructure. These mass/density-based approaches cannot show the
    microarchitectural aspects of cancellous bone that are key to fully
    describing bone's mechanical integrity.

    In the material sciences field, ultrasonic wave propagation is a
    widely used nondestructive test to estimate the anisotropic
    mechanical properties of a media in an accurate manner. An acoustic
    wave is a mechanical disturbance reflecting the elasticity of the
    material where it is propagated. In a poroelastic media, wave
    velocity is affected by the mass quantity and the spatial
    distribution of the solid and fluid constituting the composite. If
    the porous media exhibit different mechanical properties for
    different directions of the space (mechanical anisotropy), it will
    accordingly exhibit different ultrasonic velocities (acoustic
    anisotropy); see figure at

    Nevertheless, a complex relationship exists between acoustic and
    mechanical properties in cancellous bone. The intimate processes
    determining the ultrasonic wave propagation phenomena in porous media
    are not only the consequence of elastic phenomenon, but also reflect
    inertial and viscous effects due to the interaction between the solid
    and fluid phases, which are frequency-dependent.

    Recently, an experimental and theoretical study to understand
    ultrasonic wave propagation on anisotropic cancellous bone was
    developed. In the experimental studies, human and bovine cancellous
    bones from different skeletal sites, exhibiting a large variability
    in porosity and microstructure, were evaluated in multiple
    directions. The porosity (and correlatively the bone mass density)
    was found to be a low predictor of the velocities and the mechanical
    properties of cancellous bone. As the variability in measured wave
    velocities was hypothesized related to the microstructure of bone, a
    novel architectural-density-based model of wave propagation was
    developed based on the Biot's theory. This model describes the
    velocity of waves as a function of porosity, structural parameters,
    tissue properties, and frequency of propagated ultrasonic waves.

    The predictability of the measured velocities and mechanical
    properties for the different orthogonal directions of the samples
    analyzed as a function of density and microstructure was highly
    improved, when compared to the density-based approach. Better
    estimation of bone mechanical properties is expected to result in
    enhanced discrimination of osteoporotic and nonosteoporotic bone.
    This approach provides the potential to use ultrasound measurements
    in bone to examine tissue architecture in addition to bone mass.

    RESEARCH INTERESTS of Luis Cardosa: The bone mechanotransduction
    processes regulated by osteocytes and the assessment of bone
    mechanical properties through different experimental, mathematical,
    and computational approaches.


    [7] Questions and Feedback Contact

    Stephen C. Cowin PhD
    New York Center for Biomedical Engineering
    Departments of Biomedical and Mechanical Engineering
    School of Engineering
    The City College of New York
    138th Street and Convent Avenue
    New York, NY 10031-9198, USA

    (212) 799-7970 (Office at Home)
    (212) 650-5208 (Office at Work)

    (212) 799-7970 (Office at Home)



    For bone research information, visit .
    Stephen C. Cowin
    2166 Broadway
    Apartment 12D
    New York, NY 10024

    Phone (212) 799-7970 (Office at Home)
    Fax (212) 799-7970 (Office at Home)
    Phone (212) 650-5208 (Work)
    Fax (212) 650-6727 (Work)
    Email or

    Stephen C. Cowin
    New York Center for Biomedical Engineering
    Departments of Biomedical and Mechanical Engineering
    The City College
    138th Street and Convent Avenue
    New York, NY 10031-9198, U. S. A.
    For information about the New York Center for Biomedical
    Engineering visit

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