No announcement yet.

Revised Spring 2003 NYC Bone Seminar schedule

This topic is closed.
  • Filter
  • Time
  • Show
Clear All
new posts

  • Revised Spring 2003 NYC Bone Seminar schedule

    To Bone Researchers in the NYC area:
    The NYC Mineralized Tissue Seminar will now have its first
    spring seminar on Thursday night March 20th. The Seminar schedule for
    February 27th, and canceled due to the snow threat, has been
    rescheduled for June 5th. Abstracts for each of the spring seminars
    are given below.


    The Bone Seminar Series has as its focus the mechanosensory system in
    bone. The series sponsors eight seminars a year beginning in
    September and continuing until April or May. The seminar program is
    regularly posted on, a website dedicated to research
    on the mechanosensory system in bone.



    The first three seminar series will be held in Room C201 (on the
    concourse level, below the ground floor) at the CUNY Graduate Center
    on Thursdays from 7 to 8:30 PM. The fourth seminar on June 5th will
    be held in Room 9204. 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. There will be some socializing before
    the seminar in the seminar room from 5:45 PM. Also, from 5:45 PM
    until 7 PM there will be food (fruit plate, vegetable plate, cookies)
    and drink (coffee and soft drinks) available in the seminar room.
    There is also a Graduate Center snack bar on the first floor; besides
    the usual snacks and drinks the 365 Express also carries beer and
    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 the bottom).


    MARCH 20th, 2003 in room C201 at the CUNY Graduate Center at 7 PM.

    Speaker: NICOLA C. PARTRIDGE, Ph.D., Professor and Chairman,
    Department of Physiology & Biophysics, UMDNJ-Robert Wood Johnson
    Medical School, Piscataway, NJ 08854.


    Abstract: Parathyroid hormone (PTH) plays a central role in
    regulation of calcium metabolism but also appears to have a role as
    an anabolic hormone for bone. The hormone has multiple actions,
    including many direct changes in the functions of the osteoblast. To
    date, all of its skeletal effects appear to be mediated by binding to
    a single receptor on osteoblasts. In this process, PTH causes a
    change in osteoblastic gene expression and function. Apart from
    producing osteoclast-activating factors such as RANKL and interleukin
    -6 (IL-6) in response to PTH, the osteoblast appears to also have a
    direct role in matrix degradation in response to this hormone. For
    instance, PTH induces collagenase-3 gene transcription in
    osteoblastic cells through a cAMP-dependent pathway requiring de novo
    protein synthesis. Thus, this is a secondary effect that involves the
    induction and activation of specific transcription factors acting on
    this gene. We identified the PTH-response elements as being the
    activator protein-1 (AP-1) and the core binding factor a1 (Cbfa1)
    binding sites in the collagenase-3 promoter. We have demonstrated a
    PTH-dependent cooperative interaction between the sites and the
    proteins binding to them. By gel shift analysis, we have shown
    enhanced binding of c-Fos and c-Jun proteins at the AP-1 site upon
    treatment with PTH but no significant change in the level of Cbfa1
    binding to its site. Supporting our earlier work, the PKA pathway was
    shown to be the only pathway regulating the collagenase-3 promoter as
    a mediator of PTH action. The importance of this pathway was
    demonstrated by the fact that PTH stimulates the transactivation of
    activation domain-3 in Cbfa1 through its PKA site. PTH regulates both
    transcription factors through this pathway, either by increasing
    their expression or altering their phosphorylation. Our hypothesis of
    the functions of these proteins is that they interact physically in a
    nucleosomal structure, recruiting other proteins such as
    co-activators, modifiers of the nucleosome and the general
    transcription factors. If there is time, I will talk about some of
    our new work on PTH regulation of novel genes in osteoblasts.

    parathyroid hormone (PTH) induces the transcription of collagenase-3
    in osteoblastic cells. This involves the protein kinase A pathway
    and induction of activator protein-1 transcription factors as well as
    phosphorylation of another transcription factor, core binding factor
    a1. Thus, PTH regulates both transcription factors through this
    pathway, either by increasing their expression or altering their
    phosphorylation. Our hypothesis of the functions of these proteins is
    that they interact physically in a nucleosomal structure, recruiting
    other proteins such as co-activators, modifiers of the nucleosome and
    the general transcription factors. In another project, we are
    investigating the signal transduction pathways whereby PTH induces
    anabolic effects on bone and determining novel genes regulated by
    this hormone. In two other projects we have shown that extracellular
    concentrations of collagenase-3 are regulated by the existence of a
    specific receptor that binds the enzyme. Subsequent internalization
    and degradation of collagenase-3 require transfer to the endocytotic
    receptor, the low-density lipoprotein receptor-related protein. We
    have recently purified and identified the specific receptor as a
    170-kDa protein. We are now further characterizing the collagenase-3
    removal process in osteoblasts, fibroblasts as well as chondrocytes
    from patients with osteoarthritis. The latter work could lead to new
    treatments for this disease.


    APRIL 10th, 2003 in room C201 at the CUNY Graduate Center at 7 PM.

    Speaker: HELEN H. LU, PhD, Department of Biomedical Engineering,
    Columbia University in the City of New York.


    Abstract: Optimal treatment modalities in orthopedics are needed to
    meet the demands of an aging yet still active population. Due to
    limitations associated with existing biological and synthetic grafts,
    tissue engineering has emerged as an alternative approach in
    orthopedic repair and regeneration. An area of recent interest is
    the design of interfaces to facilitate the integration of bone with
    tissues such as muscle, cartilage, ligaments, and tendon. The nature
    of the tissue-tissue interface is important in the fixation of
    existing implants to bone, and in the integration of a variety of
    tissues formed in vitro using tissue engineering approaches.
    Development of a bone-soft tissue interface is a highly complex
    problem, involving the engineering of both soft and hard tissue, as
    well as the interfacial region. This talk will first describe our
    research efforts in bone tissue engineering utilizing a composite
    scaffold of biodegradable polymers and bioactive ceramics seeded with
    bone-forming cells, as well as the use of bone morphogenetic proteins
    in promoting mineralization by varied cell sources. Next, results
    from our work in tissue engineering of the anterior cruciate ligament
    using a three-dimensional, porous, biodegradable, and braided
    construct will be presented. The design, in vitro and in vivo
    characterizations, and optimization of both soft and hard tissue
    engineering constructs will be discussed. Finally, current efforts
    in the integration of soft and hard tissues will be described, and
    new research directions will be proposed.
    RESEARCH INTERESTS OF HELEN LU: Dr. Lu's research focuses on the
    regeneration of a functional interface between bone and
    ligaments/tendons, as well as the interface connecting bone and
    cartilage. Providing a mechanically functional interface between the
    biomaterial and bone tissue, and between bone and soft tissue will
    significantly improve the long-term stability of the implant. Dr.
    Lu's research group at the Biomaterials and Interface Tissue
    Engineering Laboratory at Columbia University are developing in vitro
    culturing systems to mimic the formation of the interface between
    bone and soft tissue (cartilage and ligament) in vivo. These systems
    are used to examine the effect of co-culturing on the growth and
    differentiation of osteoblasts, chondrocytes and ligament
    fibroblasts. Results from these studies are being utilized to design
    3-D, tissue engineered scaffold systems that can be applied in the
    treatment of osteoarthritis and anterior cruciate ligament injuries.


    MAY 8th, 2003 in room C201 at the CUNY Graduate Center at 7 PM.

    Speaker: STEPHEN C. COWIN, PhD. Distinguished Professor of Biomedical
    and Mechanical Engineering, Director of the New York Center for
    Biomedical Engineering, The City College of New York


    Abstract: The structural adaptations of living require a cell-based
    mechanosensing system with a sensor cell that perceives the
    mechanical deformation of the mineralized matrix in which the cell
    resides, a cell-based mechanosensing system not unlike that in the
    ear. One of the most perplexing features of this mechanosensory
    system in bone is the very low strain level that a whole bone
    experiences in vivo compared to that needed to produce a response in
    cells. The amplitudes of the in vivo strains generally fall in the
    range 0.04 to 0.3 percent for animal locomotion and seldom exceed 0.1
    percent. These strains are nearly two orders of magnitude less than
    those needed (1% to 10%) to elicit biochemical signals necessary for
    communication of the sensing cells with the cells that deposit and
    resorb bone tissue. There is a paradox in the bone mechanosensing
    system in that the strains that activate the bone cells are at least
    an order of magnitude larger than the strains to which the whole bone
    organ is subjected. A hierarchical model ranging over length scales
    that differ by 9 orders of magnitude, from the subcellular level to
    the whole bone level, is used to resolve this paradox. Using this
    extended model, it is possible to explain how the fluid flow around a
    bone cell process can lead to strains on the cell process structure
    that are two orders of magnitude greater than the ambient strains in
    the mineralized matrix in which the cell resides. This bone
    mechanosensory system has many features in common with the auditory

    RESEARCH INTERESTS OF STEVE COWIN: His principal research interest is
    the mechanics of materials, particularly in determining the influence
    of microstructure on the gross mechanical behavior of granular,
    composite, and biological materials. He concentrated on bone
    mechanics for many years and has been interested in tissue building
    process in skeletal tissues in recent years.

    JUNE 5th, 2003 in room 9204 at the CUNY Graduate Center at 7 PM.

    Speaker: MITCHELL B. SCHAFFLER, Ph.D., Professor of Orthopaedics,
    Cell Biology and Anatomy & Director of Orthopaedic Research,
    Department of Orthopaedics, The Mount Sinai School of Medicine and
    Co-Director, New York Center for Biomedical Engineering, City College
    of New York


    Abstract: Skeletal tissues maintain a balance between mechanical wear
    and tear (i.e. fatigue) damage and intrinsic, matrix-level repair.
    Imbalance in this damage-repair homeostasis, either because of
    excessively rapid damage accumulation or because of ineffective,
    inadequate or inappropriate biological responses to chronic injury,
    leads to pathology and, ultimately, mechanical failure of skeletal
    elements. These processes are implicated in a wide range of
    conditions, including overuse injuries, tissue fragility in aging,
    tendon and ligament failures and degenerative joint disease.
    A major function of Haversian (osteonal) remodeling is to
    remove and replace regions of compact bone that accumulate
    microdamage due to fatigue. However, little is known about the
    damage or remodeling responses that occur at the levels of fatigue
    expected to result from normal wear and tear. In particular, how
    bone-remodeling units "target" microscopically damaged areas of bone
    is unknown. Our recent studies of remodeling-repair of microdamage
    find that intracortical resorption effectively removes both
    linear-type microcracks and diffuse matrix damage. Alterations of
    osteocyte and canalicular integrity are observed in microdamaged
    areas. Resorption spaces were also seen within areas of cortex in
    which no bone matrix damage occurred, but alterations of osteocyte
    and canalicular integrity were evident. Recent studies indicate that
    these alterations of osteocyte integrity correspond to osteocyte
    apoptosis, or programmed cell death. Thus, osteocyte death or damage
    may provide a key stimulus for this signaling or targeting the
    remodeling process in bone.

    RESEARCH INTERESTS OF MITCH SCHAFFLER: Major research efforts in bone
    biomechanics and tissue physiology, with emphasis on understanding
    mechanical wear and tear (fatigue) processes in skeletal tissues, and
    the cellular/molecular mechanisms used in the detection and repair of
    connective tissue matrix injury. Related areas of interest extend to
    aging and skeletal fragility, including osteoporosis, and the healing
    and regeneration of bone.



    The Interinstitutional Steering Committee (ISC) will make decisions
    concerning the seminar series, including the selection of speakers.
    Interesting, high quality seminar speakers are sought. Seminar
    attendees are asked to help in the identification of investigators
    with new results relative to the bone research, questions of current
    interest and distinguished bone researchers visiting New York City
    who might be persuaded to present a seminar. Presentations by
    advanced graduate students and post-docs are encouraged.
    The members of the Interinstitutional Steering Committee (ISC) are
    Adele Boskey (Head of the Mineralized Tissue Section at the Hospital
    for Special Surgery and Professor of Biochemistry at the Weill
    Medical College of Cornell University), Timothy Bromage (Director of
    the Hard Tissue Research Unit and Professor of Anthropology at Hunter
    College of CUNY), Stephen C. Cowin (Director of the New York Center
    for Biomedical Engineering (NYCBE) and Professor of Biomedical and
    Mechanical Engineering at the City College of the City University of
    New York (CUNY)), Susannah P. Fritton (Director of the Tissue
    Mechanics Laboratory, New York Center for Biomedical Engineering and
    Associate Professor of Biomedical Engineering at the City College of
    CUNY), X. Edward Guo (Director of the Bone Bioengineering Laboratory
    and Assistant Professor of Bioengineering at Columbia University),
    Clinton T. Rubin (Professor and Chair of the Department of Biomedical
    Engineering, and Director of the Center for Advanced Technology in
    Medical Biotechnology at SUNY Stony Brook) and Mitchell B. Schaffler
    (Director of Orthopaedic Research and Professor of Orthopedics, Cell
    Biology and Anatomy at the Mount Sinai School of Medicine). Each of
    these people represents a community consisting of senior bone
    research people, graduate students and, in most cases, undergraduate


    Stephen C. Cowin
    Director, New York Center for Biomedical Engineering
    School of Engineering
    The City College
    138th Street and Convent Avenue
    New York, NY 10031-9198, U. S. A.

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

    To unsubscribe send SIGNOFF BIOMCH-L to
    For information and archives: