Melissa Louise Knothe Tate

Prof. Dr. Melissa Louise Knothe Tate


Research Focus & Metrics

Academic Career Length

37Years (1990-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 July 2003 in The International Journal of Biochemistry & Cell Biology
Verified
Journal Article
Closed access
MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate
JAJosée R Adamson
Josée R Adamson
ATAndrea E Tami
Andrea E Tami
TBThomas W Bauer
Thomas W Bauer

1 October 2003 in Journal of Biomechanics
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Journal Article
Closed access
MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate

27 January 2015 in Journal of Microscopy
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Journal Article
Open access
PDF file
AEA.L. Eberle
A.L. Eberle
SMS. Mikula
S. Mikula
RSR. Schalek
R. Schalek
JLJ.W. Lichtman
J.W. Lichtman
MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate
DZD. Zeidler
D. Zeidler
Summary: Electron–electron interactions and detector bandwidth limit the maximal imaging speed of single‐beam scanning electron microscopes. We use multiple electron beams in a single column and detect secondary electrons in parallel to increase the imaging speed by close to two orders of magnitude and demonstrate imaging for a variety of samples ranging from biological brain tissue to semiconductor wafers.

1 February 1998 in Bone
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Journal Article
Closed access
MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate
PNP. Niederer
P. Niederer
UKU. Knothe
U. Knothe

9 July 2012 in Journal of Orthopaedic Research
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Journal Article
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CCCéline Colnot
Céline Colnot
XZXinping Zhang
Xinping Zhang
MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate
While century old clinical reports document the periosteum's remarkable regenerative capacity, only in the past decade have scientists undertaken mechanistic investigations of its regenerative potential. At a Workshop at the 2012 Annual Meeting of Orthopaedic Research Society, we reviewed the molecular, cellular, and tissue scale approaches to elucidate the mechanisms underlying the periosteum's regenerative potential as well as translational therapies engineering solutions inspired by its remarkable regenerative capacity. The entire population of osteoblasts within periosteum, and at endosteal and trabecular bone surfaces within the bone marrow, derives from the embryonic perichondrium. Periosteal cells contribute more to cartilage and bone formation within the callus during fracture healing than do cells of the bone marrow or endosteum, which do not migrate out of the marrow compartment. Furthermore, a current healing paradigm regards the activation, expansion, and differentiation of periosteal stem/progenitor cells as an essential step in building a template for subsequent neovascularization, bone formation, and remodeling. The periosteum comprises a complex, composite structure, providing a niche for pluripotent cells and a repository for molecular factors that modulate cell behavior. The periosteum's advanced, “smart” material properties change depending on the mechanical, chemical, and biological state of the tissue. Understanding periosteum development, progenitor cell‐driven initiation of periosteum's endogenous tissue building capacity, and the complex structure–function relationships of periosteum as an advanced material are important for harnessing and engineering ersatz materials to mimic the periosteum's remarkable regenerative capacity. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1869–1878, 2012

15 September 2000 in Journal of Experimental Biology
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Journal Article
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MTMelissa Louise Knothe Tate
Melissa Louise Knothe Tate
RSR. Steck
R. Steck
MFM. R. Forwood
M. R. Forwood
PNP. Niederer
P. Niederer
Load-induced extravascular fluid flow has been postulated to play a role in mechanotransduction of physiological loads at the cellular level. Furthermore, the displaced fluid serves as a carrier for metabolites, nutrients, mineral precursors and osteotropic agents important for cellular activity. We hypothesise that load-induced fluid flow enhances the transport of these key substances, thus helping to regulate cellular activity associated with processes of functional adaptation and remodelling. To test this hypothesis, molecular tracer methods developed previously by our group were applied in vivo to observe and quantify the effects of load-induced fluid flow under four-point-bending loads. Preterminal tracer transport studies were carried out on 24 skeletally mature Sprague Dawley rats. Mechanical loading enhanced the transport of both small-and larger-molecular-mass tracers within the bony tissue of the tibial mid-diaphysis. Mechanical loading showed a highly significant effect on the number of periosteocytic spaces exhibiting tracer within the cross section of each bone. For all loading rates studied, the concentration of Procion Red tracer was consistently higher in the tibia subjected to pure bending loads than in the unloaded, contralateral tibia. Furthermore, the enhancement of transport was highly site-specific. In bones subjected to pure bending loads, a greater number of periosteocytic spaces exhibited the presence of tracer in the tension band of the cross section than in the compression band; this may reflect the higher strains induced in the tension band compared with the compression band within the mid-diaphysis of the rat tibia. Regardless of loading mode, the mean difference between the loaded side and the unloaded contralateral control side decreased with increasing loading frequency. Whether this reflects the length of exposure to the tracer or specific frequency effects cannot be determined by this set of experiments. These in vivo experimental results corroborate those of previous ex vivo and in vitro studies. Strain-related differences in tracer distribution provide support for the hypothesis that load-induced fluid flow plays a regulatory role in processes associated with functional adaptation.