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Dr. Pacifici serves on the Scientific and Medical Advisory Board of the MHE Research Foundation
Research authored by Dr. Pacifici
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List of Publications via PubMed
(NIH National Library of Medicine)
Research authored by Dr. Pacifici
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List of Publications via PubMed
(NIH National Library of Medicine)
| Dr. Pacifici's research |
Questions to the Scientific & Medical Advisory Board,
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Conditional Kif3a ablation causes abnormal hedgehog signaling topography, growth plate dysfunction, and
excessive bone and cartilage formation during mouse skeletogenesis
Full Text Publication ~ Development 2007 134: 2183-2193.
Eiki Koyama1,, Blanche Young1, Motohiko Nagayama1, Yoshihiro Shibukawa1,*, Motomi Enomoto-Iwamoto1, Masahiro
Iwamoto1, Yukiko Maeda2, Beate Lanske2, Buer Song3,, Rosa Serra3 and Maurizio Pacifici1,
1 Department of Orthopaedic Surgery, Thomas Jefferson University College of Medicine, Philadelphia, PA 19107, USA.
2 Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02138, USA.
3 Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
The motor protein Kif3a and primary cilia regulate important developmental processes, but their roles in skeletogenesis remain
ill-defined. Here we created mice deficient in Kif3a in cartilage and focused on the cranial base and synchondroses. Kif3a
deficiency caused cranial base growth retardation and dysmorphogenesis, which were evident in neonatal animals by anatomical
and micro-computed tomography (µCT) inspection. Kif3a deficiency also changed synchondrosis growth plate organization and
function, and the severity of these changes increased over time.
By postnatal day (P)7, mutant growth plates lacked typical zones of chondrocyte proliferation and hypertrophy, and were
instead composed of chondrocytes with an unusual phenotype characterized by strong collagen II (Col2a1) gene expression but
barely detectable expression of Indian hedgehog (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13) and osterix (Sp7).
Concurrently, unexpected developmental events occurred in perichondrial tissues, including excessive intramembranous
ossification all along the perichondrial border and the formation of ectopic cartilage masses.
Looking for possible culprits for these latter processes, we analyzed hedgehog signalling topography and intensity by
monitoring the expression of the hedgehog effectors Patched 1 and Gli1, and of the hedgehog-binding cell-surface component
syndecan 3. Compared with controls, hedgehog signaling was quite feeble within mutant growth plates as early as P0, but was
actually higher and was widespread all along mutant perichondrial tissues.
Lastly, we studied postnatal mice deficient in Ihh in cartilage; their cranial base defects only minimally resembled those in Kif3a-
deficient mice. In summary, Kif3a and primary cilia make unique contributions to cranial base development and synchondrosis
growth plate function.
Their deficiency causes abnormal topography of hedgehog signaling, growth plate dysfunction, and un-physiologic responses
and processes in perichondrial tissues, including ectopic cartilage formation and excessive intramembranous ossification.
Key words: Kif3a, Primary cilia, Cranial base synchondroses, Hedgehog signaling, Syndecans, Growth plate, Intramembranous
ossification, Ectopic cartilage, Exostoses, Mouse
Abstract 2005 MHE Conference
Syndecans: Cell Surface Modulators of Growth Plate Chondrocyte Behavior and Function
Maurizio Pacifici Department of Orthopaedic Surgery,
Thomas Jefferson University College of Medicine, Philadelphia, PA 19107
Syndecans are single-pass integral membrane components that serve as co-receptors for growth factors and cytokines and can
elicit signal transduction via their cytoplasmic tails. We will present studies from our group on syndecan biology and function in
the growth plates of developing long bones in chick and mouse embryos. Gain- and loss-of-function data indicate that
syndecan-3 has important roles in restricting mitotic activity to the proliferative zone of growth plate and may do so in close
cooperation and interaction with the signaling molecule Indian hedgehog (Ihh), and that syndecan-2 may participate in growth
plate-associated ossification. Biochemical and protein-modeling data suggest a dimeric/oligomeric configuration for syndecan-3
on the chondrocyte’s cell surface. Analyses of embryos mis-expressing syndecan-3 or lacking Ihh provide further clues on
syndecan-3/Ihh interdependence and interrelationships.
The data and the conclusions reached provide insights into mechanisms fine-tuning chondrocyte proliferation and function and
ossification events in the developing and growing skeleton and into how abnormalities in these fundamental mechanisms may
subtend human congenital pathologies, including osteochondromas in hereditary multiple exostoses syndrome.
excessive bone and cartilage formation during mouse skeletogenesis
Full Text Publication ~ Development 2007 134: 2183-2193.
Eiki Koyama1,, Blanche Young1, Motohiko Nagayama1, Yoshihiro Shibukawa1,*, Motomi Enomoto-Iwamoto1, Masahiro
Iwamoto1, Yukiko Maeda2, Beate Lanske2, Buer Song3,, Rosa Serra3 and Maurizio Pacifici1,
1 Department of Orthopaedic Surgery, Thomas Jefferson University College of Medicine, Philadelphia, PA 19107, USA.
2 Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02138, USA.
3 Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
The motor protein Kif3a and primary cilia regulate important developmental processes, but their roles in skeletogenesis remain
ill-defined. Here we created mice deficient in Kif3a in cartilage and focused on the cranial base and synchondroses. Kif3a
deficiency caused cranial base growth retardation and dysmorphogenesis, which were evident in neonatal animals by anatomical
and micro-computed tomography (µCT) inspection. Kif3a deficiency also changed synchondrosis growth plate organization and
function, and the severity of these changes increased over time.
By postnatal day (P)7, mutant growth plates lacked typical zones of chondrocyte proliferation and hypertrophy, and were
instead composed of chondrocytes with an unusual phenotype characterized by strong collagen II (Col2a1) gene expression but
barely detectable expression of Indian hedgehog (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13) and osterix (Sp7).
Concurrently, unexpected developmental events occurred in perichondrial tissues, including excessive intramembranous
ossification all along the perichondrial border and the formation of ectopic cartilage masses.
Looking for possible culprits for these latter processes, we analyzed hedgehog signalling topography and intensity by
monitoring the expression of the hedgehog effectors Patched 1 and Gli1, and of the hedgehog-binding cell-surface component
syndecan 3. Compared with controls, hedgehog signaling was quite feeble within mutant growth plates as early as P0, but was
actually higher and was widespread all along mutant perichondrial tissues.
Lastly, we studied postnatal mice deficient in Ihh in cartilage; their cranial base defects only minimally resembled those in Kif3a-
deficient mice. In summary, Kif3a and primary cilia make unique contributions to cranial base development and synchondrosis
growth plate function.
Their deficiency causes abnormal topography of hedgehog signaling, growth plate dysfunction, and un-physiologic responses
and processes in perichondrial tissues, including ectopic cartilage formation and excessive intramembranous ossification.
Key words: Kif3a, Primary cilia, Cranial base synchondroses, Hedgehog signaling, Syndecans, Growth plate, Intramembranous
ossification, Ectopic cartilage, Exostoses, Mouse
Abstract 2005 MHE Conference
Syndecans: Cell Surface Modulators of Growth Plate Chondrocyte Behavior and Function
Maurizio Pacifici Department of Orthopaedic Surgery,
Thomas Jefferson University College of Medicine, Philadelphia, PA 19107
Syndecans are single-pass integral membrane components that serve as co-receptors for growth factors and cytokines and can
elicit signal transduction via their cytoplasmic tails. We will present studies from our group on syndecan biology and function in
the growth plates of developing long bones in chick and mouse embryos. Gain- and loss-of-function data indicate that
syndecan-3 has important roles in restricting mitotic activity to the proliferative zone of growth plate and may do so in close
cooperation and interaction with the signaling molecule Indian hedgehog (Ihh), and that syndecan-2 may participate in growth
plate-associated ossification. Biochemical and protein-modeling data suggest a dimeric/oligomeric configuration for syndecan-3
on the chondrocyte’s cell surface. Analyses of embryos mis-expressing syndecan-3 or lacking Ihh provide further clues on
syndecan-3/Ihh interdependence and interrelationships.
The data and the conclusions reached provide insights into mechanisms fine-tuning chondrocyte proliferation and function and
ossification events in the developing and growing skeleton and into how abnormalities in these fundamental mechanisms may
subtend human congenital pathologies, including osteochondromas in hereditary multiple exostoses syndrome.
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2009 Conference abstract
Mechanisms of Exostosis Formation in Mouse Models of HME
Maurizio Pacifici1 and Jeffrey D. Esko2
1Department of Orthopaedic Surgery, Thomas Jefferson University, School of Medicine, Philadelphia, PA. 2Department of Cellular
and Molecular Medicine, University of California, San Diego, La Jolla, CA.
The mechanisms by which exostoses form along the growth plates of long bones and other skeletal elements remain largely
unclear. Since the majority of HME patients carry loss-of-function mutations in Ext1 or Ext2, other groups previously created
heterozygous null Ext1 (Ext1+/-) mice that were expected to display traits of HME patients. Surprisingly, the mutant mice did
not completely mimic the human phenotype. Exostosis-like masses were observed in 10-20% of the mice only, and the ectopic
masses were rather small and atypical in organization and were limited to the ribs. Based on immunohistochemical evidence that
human exostoses contain far less heparan sulfate (HS) than would be expected of a heterozygous Ext mutation (about 50% of
control levels), we reasoned that mice producing lower amounts of HS chains may be able to mimic the human condition more
closely. Thus, we created and examined double heterozygous Ext1+/-/ Ext2+/- mice. Indeed, the double hets mice did display
stereotypic exostoses along their long bones that were characterized by a distal cartilaginous cap followed by a pseudo growth
plate and were oriented at a 90 degree angle with respect to the long axis of the long bones. We even observed
osteochondromas masses at other locations. The data strongly indicate that exostosis formation and organization are
intimately sensitive to, and dependent on, HS production and/or content and that frequency of exostosis formation can be
increased by progressive decreases in Ext expression. At the Conference, we will present data from an additional mouse model
of HME and data from mesenchymal cell cultures that provide important insights into the mechanisms of exostosis induction and
formation.
Mechanisms of Exostosis Formation in Mouse Models of HME
Maurizio Pacifici1 and Jeffrey D. Esko2
1Department of Orthopaedic Surgery, Thomas Jefferson University, School of Medicine, Philadelphia, PA. 2Department of Cellular
and Molecular Medicine, University of California, San Diego, La Jolla, CA.
The mechanisms by which exostoses form along the growth plates of long bones and other skeletal elements remain largely
unclear. Since the majority of HME patients carry loss-of-function mutations in Ext1 or Ext2, other groups previously created
heterozygous null Ext1 (Ext1+/-) mice that were expected to display traits of HME patients. Surprisingly, the mutant mice did
not completely mimic the human phenotype. Exostosis-like masses were observed in 10-20% of the mice only, and the ectopic
masses were rather small and atypical in organization and were limited to the ribs. Based on immunohistochemical evidence that
human exostoses contain far less heparan sulfate (HS) than would be expected of a heterozygous Ext mutation (about 50% of
control levels), we reasoned that mice producing lower amounts of HS chains may be able to mimic the human condition more
closely. Thus, we created and examined double heterozygous Ext1+/-/ Ext2+/- mice. Indeed, the double hets mice did display
stereotypic exostoses along their long bones that were characterized by a distal cartilaginous cap followed by a pseudo growth
plate and were oriented at a 90 degree angle with respect to the long axis of the long bones. We even observed
osteochondromas masses at other locations. The data strongly indicate that exostosis formation and organization are
intimately sensitive to, and dependent on, HS production and/or content and that frequency of exostosis formation can be
increased by progressive decreases in Ext expression. At the Conference, we will present data from an additional mouse model
of HME and data from mesenchymal cell cultures that provide important insights into the mechanisms of exostosis induction and
formation.
Nov 3, 2009 Jefferson researchers receive $3.9 million in Challenge grants
EurekAlert (press release) - Washington,DC,USA
Maurizio Pacifici, Ph.D., director of Orthopedic Research, will receive $1 million over two years to study Hereditary Multiple
Exostosis Syndrome (HME)
EurekAlert (press release) - Washington,DC,USA
Maurizio Pacifici, Ph.D., director of Orthopedic Research, will receive $1 million over two years to study Hereditary Multiple
Exostosis Syndrome (HME)
| Jeff Esko, Ph.D, Hundson Freeze, PhD, Maurizio Pacifici, Ph.D. |
| Photo's taken during the Third International MHE Research Conference |
| ||||||||||
Dr. Pacifici has relocated his lab from Thomas Jefferson University, and is now the Director of the Translational
Research Program in Pediatric OrthopaedicsThe Children's Hospital of Philadelphia.
Compound heterozygous loss of Ext1 and Ext2 is sufficient for formation of multiple exostoses in mouse ribs and
long bones.
Zak BM, Schuksz M, Koyama E, Mundy C, Wells DE, Yamaguchi Y, Pacifici M, Esko JD.
Bone. 2011 May 1;48(5):979-87. Epub 2011 Feb 15.
To read Click Here
Abstract
Multiple Hereditary Exostoses (MHE) syndrome is caused by haploinsufficiency in Golgi-associated heparan sulfate polymerases
EXT1 or EXT2 and is characterized by formation of exostoses next to growing long bones and other skeletal elements. Recent
mouse studies have indicated that formation of stereotypic exostoses requires a complete loss of Ext expression, suggesting
that a similar local loss of EXT function may underlie exostosis formation in patients. To further test this possibility and gain
greater insights into pathogenic mechanisms, we created heterozygous Ext1(+/-) and compound Ext1(+/-)/Ext2(+/-) mice.
Like Ext2(+/-) mice described previously (Stickens et al. Development 132:5055), Ext1(+/-) mice displayed rib-associated
exostosis-like outgrowths only. However, compound heterozygous mice had nearly twice as many outgrowths and, more
importantly, displayed stereotypic growth plate-like exostoses along their long bones. Ext1(+/-)Ext2(+/-) exostoses contained
very low levels of immuno-detectable heparan sulfate, and Ext1(+/-)Ext2(+/-) chondrocytes, endothelial cells and fibroblasts in
vitro produced shortened heparan sulfate chains compared to controls and responded less vigorously to exogenous factors
such as FGF-18. We also found that rib outgrowths formed in Ext1(f/+)Col2Cre and Ext1(f/+)Dermo1Cre mice, suggesting
that ectopic skeletal tissue can be induced by conditional Ext ablation in local chondrogenic and/or perichondrial cells. The study
indicates that formation of stereotypic exostoses requires a significant, but not complete, loss of Ext expression and that
exostosis incidence and phenotype are intimately sensitive to, and inversely related to, Ext expression. The data also indicate
that the nature and organization of ectopic tissue may be influenced by site-specific anatomical cues and mechanisms.
Research Program in Pediatric OrthopaedicsThe Children's Hospital of Philadelphia.
Compound heterozygous loss of Ext1 and Ext2 is sufficient for formation of multiple exostoses in mouse ribs and
long bones.
Zak BM, Schuksz M, Koyama E, Mundy C, Wells DE, Yamaguchi Y, Pacifici M, Esko JD.
Bone. 2011 May 1;48(5):979-87. Epub 2011 Feb 15.
To read Click Here
Abstract
Multiple Hereditary Exostoses (MHE) syndrome is caused by haploinsufficiency in Golgi-associated heparan sulfate polymerases
EXT1 or EXT2 and is characterized by formation of exostoses next to growing long bones and other skeletal elements. Recent
mouse studies have indicated that formation of stereotypic exostoses requires a complete loss of Ext expression, suggesting
that a similar local loss of EXT function may underlie exostosis formation in patients. To further test this possibility and gain
greater insights into pathogenic mechanisms, we created heterozygous Ext1(+/-) and compound Ext1(+/-)/Ext2(+/-) mice.
Like Ext2(+/-) mice described previously (Stickens et al. Development 132:5055), Ext1(+/-) mice displayed rib-associated
exostosis-like outgrowths only. However, compound heterozygous mice had nearly twice as many outgrowths and, more
importantly, displayed stereotypic growth plate-like exostoses along their long bones. Ext1(+/-)Ext2(+/-) exostoses contained
very low levels of immuno-detectable heparan sulfate, and Ext1(+/-)Ext2(+/-) chondrocytes, endothelial cells and fibroblasts in
vitro produced shortened heparan sulfate chains compared to controls and responded less vigorously to exogenous factors
such as FGF-18. We also found that rib outgrowths formed in Ext1(f/+)Col2Cre and Ext1(f/+)Dermo1Cre mice, suggesting
that ectopic skeletal tissue can be induced by conditional Ext ablation in local chondrogenic and/or perichondrial cells. The study
indicates that formation of stereotypic exostoses requires a significant, but not complete, loss of Ext expression and that
exostosis incidence and phenotype are intimately sensitive to, and inversely related to, Ext expression. The data also indicate
that the nature and organization of ectopic tissue may be influenced by site-specific anatomical cues and mechanisms.
Dr. Maurizio Pacifici, was contacted by our foundation in 2005, we sparked his interest and he attended the Second
International MHE Research Conference. During this conference he realized he could apply his extensive knowledge to the better
understanding and furthering the goal of discovering a cure for Multiple Hereditary Exostoses. Dr. Pacifici played a key role on
the advisory committee for the 2009 Third International MHE Research Conference at this conference he unveiled a new MHE
mouse model. This MHE mouse model is now being used to understand how Exostoses (tumors) develop in MHE patients and
being used in the development of the key factors necessary for the discovery and testing of possible treatments for MHE. Dr.
Pacifici became Chairman of the MHE Research Foundations 18 member Scientific and Medical Advisory Board in 2010 and is Co-
Organizer of the Fourth International MHE Research Conference along with Sarah Ziegler to be held Nov 1-4, 2012. In 2010 to
expand his research became Director of the Translational Research Program in Pediatric Orthopaedics at THE CHILDREN’S
HOSPITAL OF PHILADLEPHIA (CHOP). In May of this year Dr. Pacifici co-authored a research publication in the world renowned
Journal BONE. These finding were so impressive the cover was dedicated entirely to this. “Compound heterozygous loss of
Ext1 and Ext2 is sufficient for formation of multiple exostoses in mouse ribs and long bones”
Dr. Pacifici is a world leader in biomedical research; his work focuses on mechanisms controlling skeletal development and
growth in fetal and postnatal life. Emphasis is on identification of molecular regulators acting at the nuclear level that direct
commitment, determination and differentiation of progenitor skeletal cells. The aim is to target those regulators in gene- and
drug-based therapies to repair and reconstruct skeletal tissues affected by pathologies, in congenital skeletal defects. Emphasis
is also on signaling diffusible factors that normally act within developing skeletal elements to coordinate growth and
morphogenesis. When these factors escape skeletal tissues and diffuse into adjacent non-skeletal tissues due to failure of
restraining topographical mechanisms, they can trigger pathologies, including Multiple Hereditary Exostoses and heterotopic
ossification. Experimental therapies are being tested to restore normal factor-restraining mechanisms and block or reverse
those pathologies.
Dr. Pacifici received his Ph.D. in Developmental Biology from the University of Rome in 1974. He received a European Molecular
Biology Fellowship at the end of which he was appointed Assistant Professor at the University of Rome School of Medicine and
in 1999 to the present had been an external examiner of Ph.D. thesis for this University. He then joined the faculty at the
University of Pennsylvania first in the School of Medicine and subsequently in the School of Dental Medicine 1997 and was
appointed Professor. He joined the faculty of Thomas Jefferson University in 2004 as Professor and Director in the Department
of Orthopaedic Surgery until the relocation of his lab over to CHOP. He is a member of Skeletal Biology Development and
Disease Study Section at the National Institutes of Health, his research has been funded continuously by the National Institutes
of Health for over 25 years. Dr. Pacifici has published over 150 peer reviewed Research Journal publications, 18 editorials and
book chapters and has given numerous invited lectures around the world many of these lectures on MHE that have been so
desperately needed to educate professionals and bring awareness to our cause. He has served and continues to serve on many
Research Societies Advisory Boards including The Orthopaedic Research Society, The American Society for Matrix Biology, and
Journal Editorial Boards including Matrix Biology, Cell Communication and Signaling and is a member of the Orthopaedic
Research Advisory Board for the Shriners Hospitals for Children.
Dr. Pacifici is married to Dr. Robin Wagner-Pacifici who is the Chairperson in the Department of Sociology at The New School in
NYC. They have three children: Adriano is a second year law school student, Laura is working as a paralegal in a Washington
DC firm, and Stefano is a second year college student at Tufts University. When not working, Dr. Pacifici enjoys playing tennis,
working-out, reading and having a great meal!
International MHE Research Conference. During this conference he realized he could apply his extensive knowledge to the better
understanding and furthering the goal of discovering a cure for Multiple Hereditary Exostoses. Dr. Pacifici played a key role on
the advisory committee for the 2009 Third International MHE Research Conference at this conference he unveiled a new MHE
mouse model. This MHE mouse model is now being used to understand how Exostoses (tumors) develop in MHE patients and
being used in the development of the key factors necessary for the discovery and testing of possible treatments for MHE. Dr.
Pacifici became Chairman of the MHE Research Foundations 18 member Scientific and Medical Advisory Board in 2010 and is Co-
Organizer of the Fourth International MHE Research Conference along with Sarah Ziegler to be held Nov 1-4, 2012. In 2010 to
expand his research became Director of the Translational Research Program in Pediatric Orthopaedics at THE CHILDREN’S
HOSPITAL OF PHILADLEPHIA (CHOP). In May of this year Dr. Pacifici co-authored a research publication in the world renowned
Journal BONE. These finding were so impressive the cover was dedicated entirely to this. “Compound heterozygous loss of
Ext1 and Ext2 is sufficient for formation of multiple exostoses in mouse ribs and long bones”
Dr. Pacifici is a world leader in biomedical research; his work focuses on mechanisms controlling skeletal development and
growth in fetal and postnatal life. Emphasis is on identification of molecular regulators acting at the nuclear level that direct
commitment, determination and differentiation of progenitor skeletal cells. The aim is to target those regulators in gene- and
drug-based therapies to repair and reconstruct skeletal tissues affected by pathologies, in congenital skeletal defects. Emphasis
is also on signaling diffusible factors that normally act within developing skeletal elements to coordinate growth and
morphogenesis. When these factors escape skeletal tissues and diffuse into adjacent non-skeletal tissues due to failure of
restraining topographical mechanisms, they can trigger pathologies, including Multiple Hereditary Exostoses and heterotopic
ossification. Experimental therapies are being tested to restore normal factor-restraining mechanisms and block or reverse
those pathologies.
Dr. Pacifici received his Ph.D. in Developmental Biology from the University of Rome in 1974. He received a European Molecular
Biology Fellowship at the end of which he was appointed Assistant Professor at the University of Rome School of Medicine and
in 1999 to the present had been an external examiner of Ph.D. thesis for this University. He then joined the faculty at the
University of Pennsylvania first in the School of Medicine and subsequently in the School of Dental Medicine 1997 and was
appointed Professor. He joined the faculty of Thomas Jefferson University in 2004 as Professor and Director in the Department
of Orthopaedic Surgery until the relocation of his lab over to CHOP. He is a member of Skeletal Biology Development and
Disease Study Section at the National Institutes of Health, his research has been funded continuously by the National Institutes
of Health for over 25 years. Dr. Pacifici has published over 150 peer reviewed Research Journal publications, 18 editorials and
book chapters and has given numerous invited lectures around the world many of these lectures on MHE that have been so
desperately needed to educate professionals and bring awareness to our cause. He has served and continues to serve on many
Research Societies Advisory Boards including The Orthopaedic Research Society, The American Society for Matrix Biology, and
Journal Editorial Boards including Matrix Biology, Cell Communication and Signaling and is a member of the Orthopaedic
Research Advisory Board for the Shriners Hospitals for Children.
Dr. Pacifici is married to Dr. Robin Wagner-Pacifici who is the Chairperson in the Department of Sociology at The New School in
NYC. They have three children: Adriano is a second year law school student, Laura is working as a paralegal in a Washington
DC firm, and Stefano is a second year college student at Tufts University. When not working, Dr. Pacifici enjoys playing tennis,
working-out, reading and having a great meal!
|
| Maurizio Pacifici, Ph.D. Director of the Translational Research Program in Pediatric Orthopaedics at The Children's Hospital of Philadelphia Has been awarded the 2011 MHE Research Foundation "The Humanitarian Scientific Achievement Award" He will also be presented the following awards by members of the U. S. Congress ~ N. Y. State Senate The Borough of Brooklyn, City of New York. CITATIONS PROCLAMATIONS CERTIFICATES OF RECOGNITION These awards will be presented during the FUNTASIA Research Banquet to be held Sunday Sept, 25,2011 TO READ MORE ABOUT THIS EVENT OR TO ATTEND CLICK HERE |
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Click here to verify.# HON Conduct 282463 and is the patient support link on the US Government Genetics Home Reference (http://ghr.nlm.nih.gov)
website, also linked for Patient Information on The Diseases Database a cross-referenced index of human disease, as well as the
Intute: health & life sciences a free online service providing access to the very best Web resources for education and research located in the UK
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