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Steve Cowin
08-24-2003, 01:27 AM
To Bone Researchers in the NYC area:
The NYC Mineralized Tissue Seminar will now have its first
fall seminar on Thursday night September 4th. Abstracts for each of
the fall seminars are given below.

THE FALL 2003 BONE SEMINAR SERIES

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. There are four seminars
in the fall and four in the spring of each year. The seminar program
is regularly posted on www.bonenet.net, a website dedicated to
research on the mechanosensory system in bone.

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THE FALL 2003 BONE SEMINAR PROGRAM

The seminar series will be held at the CUNY Graduate Center on
Thursdays from 7 to 8:30 PM. The first and last fall seminars will be
held in Room 9205 on the ninth floor while the two seminars in
between the first and the last will be in Room C205 (on the concourse
level, below the ground floor). 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 wine.
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).

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SEPTEMBER 4th, 2003 in room 9205 at the CUNY Graduate Center at 7 PM.

Speaker: ROBERT J. MAJESKA, PhD, Research Associate Professor,
Department of Orthopaedics, Mount Sinai School of Medicine, New York,
NY, 10029.

Title: THE VASCULATURE IN FRACTURE HEALING

Abstract: Proper vascular function is universally acknowledged to be
essential for fracture healing; however, the precise role played by
the blood vessels during the healing process remains poorly
understood. Angiogenesis inhibitors that selectively target cells of
the vascular system are potentially useful tools to manipulate the
development of blood vessels with minimal direct effects on the
tissues in which they reside. Utilizing this experimental approach,
we and others have shown that angiogenesis inhibitors can impair
fracture healing in animal models. Studies from our laboratory have
shown that the angiogenesis inhibitor TNP-470 dramatically inhibited
fracture healing in rats, suppressing both intramembranous and
endochondral pathways of bone formation. The initial phase of healing
appeared to be most sensitive to inhibition. Impairment of fracture
healing was associated with reduced vascularization and altered gene
expression in developing callus tissue. More recent in vitro studies
showed that high concentrations of of angiogenesis inhibitor reduced
growth of cells derived from bone and bone marrow, but did not impair
responsiveness to BMP, supporting the concept that the failure to
heal fractures properly was a result of impaired blood vessel
development. Current studies are aimed at identifying crucial early
events in healing that are affected by angiogenesis inhibitors, and
determining whether fracture healing inhibition is reversible.

RESEARCH INTERESTS OF BOB MAJESKA: Research interests center on the
cell biology of skeletal tissues, with emphasis on the cells that
form bone and cartilage (i.e. the osteoblast and chondrocyte
lineages). A combination of in vitro and in vivo studies are used to
understand the regulation of bone cell activities by a variety of
stimuli including hormones, growth factors and the extracellular
matrix. In recent years, these studies have largely focused on bone
and cartilage formation during fracture healing.

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OCTOBER 15th, 2003 in room C205 at the CUNY Graduate Center at 7 PM.

Speaker: MICHAEL P. WHYTE, M.D. Division of Bone and Mineral
Diseases, Washington University School of Medicine; and Center for
Metabolic Bone Disease and Molecular Research, Shriners Hospitals for
Children; St. Louis, Missouri.

Title: WHEN OSTEOCLASTS RUN AMOK:
HERITABLE DISORDERS OF
THE RANKL/OPG/RANK/NF-kB SIGNALING PATHWAY

Abstract: Soon after the discovery and characterization of the
receptor activator of nuclear factor-kB (RANK) and the decoy receptor
osteoprotegerin (OPG) and their ligand RANKL among the tumor necrosis
factor (TNF) superfamily, the important RANKL/OPG/RANK/NF-kB
signaling pathway became understood for osteoclast formation and
action. Subsequently, the genetic basis of several rare metabolic
bone diseases confirmed the major role these proteins play in human
skeletal homeostasis.

Familial expansile osteolysis (FEO), early-onset Paget bone disease
in Japan (PBD2), and expansile skeletal hyperphosphatasia (ESH) are
all inherited as autosomal dominant traits. Each condition is caused
by a tandem duplication of different length in exon 1 of the
TNFRSF11A gene encoding RANK. Trapping of RANK within osteoclasts
because its signal peptide sequence is elongated seems to activate
the NF-kB pathway leading to these systemic skeletal disorders
featuring accelerated bone turnover. Deafness during infancy or
early childhood together with the onset of lytic skeletal lesions
that expand bone and can mimic Paget bone disease (PBD) characterize
the pediatric and young adult manifestations of FEO and ESH,
respectively. In fact, patients with FEO and ESH respond well to
bisphosphonate therapy. Reports of additional cases or families with
ESH, FEO, and PBD2 will be essential to know if there is greater
phenotypic overlap among these disorders that differ merely by the
insertion of 5, 6, or 9 amino acids, respectively, in the signal
peptide of RANK.

Juvenile Paget disease (JPD), also called "idiopathic
hyperphosphatasia," is caused by autosomal recessive inheritance of
deletion or deactivating mutations in TNFRSF11B - the gene which
encodes OPG. OPG gene deletion can lead to high circulating levels
of RANKL and exuberant RANK effect causes this generalized skeletal
disorder also featuring accelerated bone turnover manifesting during
infancy or early childhood with deafness, skeletal deformity, and
recurrent fracture which can be lethal by early adult life
unless there is antiresorptive therapy.

RESEARCH INTERESTS OF MICHAEL P. WHYTE: Heritable disorders of bone
and mineral metabolism.

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NOVEMBER 6th, 2003 in room C205 at the CUNY Graduate Center at 7 PM.

Speaker: E. DIANNE REKOW, DDS, PhD, Director of Translational
Research, NYU College of Dentistry, Division of Biological Science,
Medicine, and Surgery, New York, NY 10010

Title: EFFECTS OF SCAFFOLD MICRO ARCHITECTURE
FEATURES ON BONE FORMATION

Abstract: Scaffold features at all length scales affect bone
formation within the scaffold. At the nano-scale, surface chemistry
plays an important role, especially related to biocompatibility. On
the other end of the spectrum, the macro design of implants can
create form and, in the short term, contribute to restoration of
strength for function. In the middle length scales, surface texture
(the microstructure) has been shown to be particularly important in
the success of dental endosseous implants. Our investigations
indicate that other micro architecture (mesoscale in the ten to
hundreds of micrometer length) also plays an important role. This
presentation will describe differences in bone response in large
trephine defects (in skeletally mature New Zealand white rabbits)
filled with scaffolds fabricated from different materials with
prescribed micro architectures created using solid-free-form
fabrication technologies. Scaffold micro architecture did not alter
the rate of bone development but did substantially alter the patterns
of bone that develops. Identical micro architecture in scaffolds
fabricated from different materials elicits different bone response.
Some material and micro architecture combinations created multiple
sites of seemingly independent bone islands scattered throughout the
scaffolds. Unexpectedly bone ingrowth was shown (and confirmed with
a second set of experiments) to develop in materials with pore sizes
nearly an order of magnitude smaller than expected. This suggests
that by appropriately tailoring material and micro architecture
combinations, time to fill a scaffold could be accelerated.

RESEARCH INTERESTS OF DIANNE REKOW: Dr. Rekow's interest in tissue
engineering focuses on bone response to scaffold features, especially
in length scales of 1-100 micrometers. The interaction between
features including pore size, connectivity, and density as well as
surface texture and microporosity of the supporting walls within the
scaffold has not yet been elucidated and offers some interesting
challenges in defining efficient and cost-effective studies. While
the results apply to all bone repair, as an orthodontist and
biomedical engineer, her concern is primarily motivated by restoring
form and function in the craniofacial complex. The research group
includes collaborations with investigators from New York University
and the University of Medicine and Dentistry of New Jersey.

DECEMBER 10th, 2003 in room 9205 at the CUNY Graduate Center at 7 PM.

Speaker: TIMOTHY M. WRIGHT PhD, Senior Member, Research Division,
Hospital for Special Surgery, Professor of Applied Biomechanics,
Dept. of Orthopaedic Surgery, Weill Medical College of Cornell
University

Title: BIOMECHANICAL CHALLENGES IN JOINT RECONSTRUCTION

Abstract: Total joint arthroplasty is among the most successful and
cost effective surgical procedures and remains the best treatment for
long-term pain relief and restoration of function for patients
suffering with diseased or damaged joints. Nonetheless, the desire
by both patients and surgeons to treat joint problems at earlier
stages than might be indicated for conventional joint replacement has
spurred increased interest in the development of a much broader
spectrum of possible solutions from more functional implant designs
to interpositional spacers to synthetic plugs to autografts and
finally to engineered tissues. In many respects, the biomechanical
problems involved in all these solutions are the same - transferring
large loads across the joints into the remaining healthy skeleton. At
the same time, the ability to manipulate existing bone tissue through
mechanical and biological influences and to control the development
of engineered tissues through similar approaches raises exciting
possibilities for joint reconstruction. Important first steps are to
determine how significantly mechanical influences can alter bone
tissue and what mechanical factors are key in controlling the
alteration. Our research group has begun this examination by applying
controlled loads to both cancellous and cortical bone in animal
models. Such platforms provide effective tools for pursuing research
questions in this vital area.

RESEARCH INTERESTS OF TIMOTHY WRIGHT: Dr. Wright's research is
focused on performance of bone-implant systems, with an emphasis on
the influence of design and material properties on wear behavior of
total joint replacements, and on the relation between composition,
structure, and function in bone tissue.

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ORGANIZATION OF THE SEMINAR SERIES

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 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
students.

PLEASE DIRECT YOUR QUESTIONS AND FEEDBACK TO

Stephen C. Cowin
New York Center for Biomedical Engineering
Departments of Biomedical and Mechanical 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)
Email ,


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