Bioengineering Seminar Schedule
Fall 2002
Special Seminar
Monday, August 12, 12 Noon- 1pm, Room 210 Hallowell
Mitochondrial reactive oxygen species regulate proinflammatory responses in lung capillaries
Dr. Kaushik Parthasarathi
Post-Doctoral Research Scientist
Department of Physiology & Cellular Biophysics
Columbia University
St.Luke's-Roosevelt Hospital Center
New York, NY
Abstract
Cytokine-induced lung expression of the endothelial (EC) leukocyte receptor, P-selectin initiates leukocyte rolling. To elucidate the early EC signaling that induces the expression, we conducted real-time digital imaging studies in lung venular capillaries. We compared receptor- versus non-receptor-mediated effects, by infusing capillaries with respectively, tumor necrosis factor a (TNFa) and arachidonate. At concentrations adjusted to give equipotent increases in the cytosolic Ca2+ (Ca2+CYT), both agents increased reactive oxygen species (ROS) production and EC P-selectin expression. Blocking the Ca2+CYT increases abolished ROS production; blocking ROS production abrogated P-selectin expression. TNFa, but not arachidonate, released Ca2+ from endoplasmic stores and increased mitochondrial Ca2+. Further, Ca2+ depletion mitigated TNFa responses, but completely abolished arachidonate responses. These differences in Ca2+ mobilization by TNFa and arachidonate were reflected in spatial patterning in the capillary in that the TNFa effects were localized at branch-points, while the arachidonate effects were non-localized and extensive. Further, mitochondrial blockers inhibited the TNFa- but not the arachidonate-induced responses. These findings indicate that the different modes of Ca2+ mobilization determined the spatial patterning of the proinflammatory response in lung capillaries. Responses to TNFa revealed that EC mitochondria regulate the proinflammatory process by generating ROS that activate P-selectin expression.
Friday, August 30, 12:15- 1:15 pm, Room 210 Hallowell
Welcome to New Students and Overview of the Department of Bioengineering
Herbert Lipowsky
Professor and Head
Department of Bioengineering
Penn State University
Friday, September 6, 12:15- 1:15 pm, Room 210 Hallowell
Changes in Muscles Function Following Orthopedic Surgery
Stephen Piazza
Assistant Professor
Department of Kinesiology, Mechanical Engr., and Orthopedics & Rehab.
Penn State University
Abstract
Orthopedic surgeries often change the actions of muscles. These alterations may occur by design (e.g., in a tendon transfer) or as a consequence of a procedure performed for a different purpose (e.g., total joint replacement for osteoarthritis). This research is focused on characterizing such mechanical changes in order to refine surgical techniques, improve artificial joint and prosthesis designs, and permit more informed treatment decisions.
Friday, September 13, 12:05- 1:15 pm, Room 210 Hallowell
Design of Multifunctional Instruments for Minimally Invasive Surgery
Mary Frecker
Assistant Professor
Department of Mecanical Engineering
Penn State University
Abstract
In Minimally Invasive Surgery (e.g. laparoscopic, endoscopic) there is a need for instruments with improved dexterity and the ability to provide non-linear access. This research is focused on addressing this need by developing methods to design multifunctional instruments. Both traditional linkage mechanisms and compliant mechanisms are designed to serve as multifunctional end-effectors in MIS instruments. Compliant mechanisms are single-piece flexible structures that use elastic deformation to achieve motion. The feasibility of using piezoelectric materials as actuators in smart, compliant instruments is also assessed. The systematic design methods, as well as prototype fabrication and evaluation are discussed.
Friday, September 20, 12:15- 1:15 pm, Room 210 Hallowell
Nanoscale Bioengineering with Molecular Motors
William Hancock
Assistant Professor of Bioengineering
Penn State University
Friday, September 27, 12:15- 1:15 pm, Room 210 Hallowell
IgE Receptors and Rafts: A Model for Lipid and Protein Cooperation in Signaling
Erin Sheets
Assistant Professor
Department of Chemistry
Penn State University
Abstract
In the allergic response, crosslinking of IgE-IgE receptor complexes on mast cells by multivalent antigen initiates the signaling events that eventually lead to degranulation (the exocytotic release of histamine). Cholesterol-rich lipid domains, or "rafts", within the plasma membrane facilitate the phosphorylation of the IgE receptor by the Src family tyrosine kinase Lyn in the first biochemical step of this signaling cascade. The actin cytoskeleton then acts to downregulate signaling by separating the IgE receptors from rafts. By using fluorescence microscopy, we can follow the spatial and temporal dynamics of several molecules that participate in IgE receptor signaling and identify where pathways diverge and how responsive these pathway branches are to ongoing receptor crosslinking. Our laboratory will be developing new micro- and nanofabricated tools for answering fundamental questions in ligand-stimulated systems such as IgE receptor signaling.
Friday, October 4, 12:15 - 1:15 pm, Room 210 Hallowell
Surface Modification of Shape Memory Alloys by Ion Implantation
Wendy Crone
Assistant Professor
Department of Mechanical Engeering
University of Wisconsin
Abstract
The combination of shape memory effect, pseudoelasticity, and good biocompatibility makes near-equiatomic NiTi alloy an important material for medical device applications. The alloy has been used in orthodontic dental arch wires and medical guide wires for diagnostic and therapeutic catheters for many years. More recently, NiTi has been used in endovascular stents to provide a self-expanding mechanical superstructure that can be implanted in a vessel with minimally-invasive methods. Our research explores the use of Plasma Source Ion Implantation (PSII) as a surface modification technique for creating a functionally graded surface on NiTi to improve characteristics important for employing this material in medical devices. Our experimental results showed that a functionally graded surface, composed of an amorphous surface, a transition layer, and a precipitate accommodation layer, is formed by the ion implantation processing. This produced an increase in surface hardness, as well as improved wear and corrosion resistance of NiTi, while maintaining good biocompatibility. We have demonstrated enhanced fretting wear characteristics and we have explored the influence of such factors as surface hardness, surface finish, lubrication, and pseudoelasticity on this alloy's wear resistance. We have also demonstrated that surface modification of NiTi with PSII fortifies the passivation layer, which is important to corrosion resistance, and produces a higher Ti:Ni ratio leaving fewer free Ni+2 ions on the surface. Additionally, we have shown that protein adsorption, cell adhesion, and cell spreading are not negatively impacted by the PSII surface modification.
Friday, October 11, 12:15 - 1:15 pm, Room 210 Hallowell
Construction and Destruction of Microtubules
Dave Odde
Department of Biomedical Engineering
University of Minnesota
Minneapolis, Minnesota
Abstract
Microtubules are linear filaments of the cytoskeleton that serve as tracks for molecular motor-based transport in axons and for segregation of chromosomes in mitosis, and generally serve to organize the intracellular environment. Understanding what dictates the construction and destruction of microtubules is important in the seemingly diverse medical problems of cancer and restenosis after stent placement, both of which can be treated with the microtubule assembly-promoting drug taxol (paclitaxel). The seminar will review our recent work on 1) katanin, an ATPase that forms a microtubule severing complex, and 2) microtubule dynamics in dividing cells. The latter topic will also illustrate a new approach we have developed, called model-convolution, for comparing mathematical models to molecular behaviors observed by fluorescence microscopy.
Friday, October 18, 12:15- 1:15 pm, Room 210 Hallowell
Intracellular Endothelial Cell Mechanics Induced by Shear Stress
Brian P. Helmke
Assistant Professor
Department of Biomedical Engineering
University of Virginia
Charlottesville, VA
Abstract
Endothelial dysfunction associated with atherogenesis occurs in regions of the arterial tree with complex geometry
and shear stress distribution. Mechanisms by which endothelial cells sense the hemodynamic environment and transduce
changes into functional adaptation remain poorly characterized. However, intermediate filament deformation induced
by onset of shear stress
suggests that the cytoskeleton provides a pathway for redistribution of intracellular force to sites where signal
transduction occurs. Spatial localization of shear-induced actin ruffling suggests mechanical sensing among adjacent
cells, and stress fiber displacement and bending indicates altered interactions with focal adhesion complexes.
Thus, the regulation of intracellular mechanics in response to extracellular forces may regulate the initiation
and integration of multiple mechanochemical signaling
networks critical to endothelial function.
Friday, October 25, 12:15 - 1:15 pm, 210 Hallowell
NO SEMINAR
Friday, November 1, 12:15 - 1:15 pm, 210 Hallowell
Orthopaedic Implants: From theoretical design and mechanical testing to in vitro and in situ
mechanotransduction
Marnie Saunders
Assistant Professor
Department of Orthopedics
Hershey Medical Center
Hershey, PA
Abstract
Although implants have been developed for many reasons including correction for pathologic joints, edentulous jaws, and fracture, one area where implant design has yet to prove successful is in the design of an implant for direct skeletal attachment (DSA). The development of such a system would enable an artificial limb to be directly attached to an amputee's residual limb. Our initial work in this area comprised numerical design of an implant utilizing finite element analysis (FEA) and adaptive bone remodeling theories (ABRT) to numerically approximate long-term changes in the bone as a result of implant introduction. Mechanical testing and a clinical trial were conducted in assessment of our system. Failure of the system occurred 12 weeks post-operatively and was attributed to the cellular actions at the bone/implant interface. We have shifted directions of our research focus to address the cellular interactions using in vitro mechanotransduction models. In these experiments, bone cells are subjected to mechanical loading and markers of activity are quantified in an attempt to understand how mechanical loading affects bone cell activity. Although these systems are widely used, they are particularly appropriate for isolating the cells and studying the effects of a particular variable, such as a hormone, on cellular activity and they are not conducive to the study of bone/implant interactions. To rectify this, we are currently developing in situ mechanotransduction models that incorporate multiple cell types (osteoblasts, osteoclasts and osteocytes) on a native bone wafer substrate incorporating the in vivo milieu. These systems we believe are more amenable to studying the load-induced bone cell activity that occurs in diseases such as osteoporosis, osteopetrosis and implant- and metastatic-induced osteolysis. Understanding that implant design and long-term function must address both the macroscopic (structural) and microscopic (cellular) levels will help to develop implants, such as the DSA system, that maintain structural stability and function while promoting healthy bone at the bone/implant interface.
Friday, November 8, 12:15 - 1:15 pm, 210 Hallowell
The Little Engine That Couldn't: The Role of Myosin in Left Ventricular Dysfunction
William Guilford
Assistant Professor
Department of Biomedical Engineering
University of Virginia
Charlottesville, VA
Abstract
Following myocardial infarction, the ability of the heart to contract is significantly reduced, even in regions
that did not experience a reduction in blood flow. This causes a disproportionate number of fatalities due to heart
failure in the first two days following MI. The molecular basis of left ventricular dysfunction in the "remote
zone" has been extensively debated. Recent evidence from our lab suggests that the cause of this dysfunction
is attack by reactive nitrogen species on myosin, the molecular
motor that causes muscle contraction. We will outline these new data, their implications to clinical care, and
the role of molecular mechanics in determining progression of this and other disease processes.
Friday, November 15, 12:15 - 1:15 pm, 210 Hallowell
Micromechanics of Soft Materials and the Applications of Optical Tweezers for Cellular Biomechanics
Daniel Ou-Yang
Department of Physics and Bioengineering
Lehigh University
Abstract
Mechanical properties and molecular structure of a material are often intimately related. For soft materials, such as gels, polymer solutions, dense emulsions or foams, it is not easy to gain insight of the local structures of the system from bulk mechanical properties because of the systems are spatial nonhomogeneous. For living systems, such as cells and tissues, the relationship between the mechanical property and their structures is even more complex because the interplay between the two; mechanical forces can stimulate biological responses and causes structural reorganization. There has been significant effort in the studies of micromechanics in the soft materials and methodologies developed by these efforts seem applicable to living systems. The presentation attempts to give an overview of these efforts including the research at my laboratory.
Friday, November 22, 12:15 - 1:15 pm, 210 Hallowell
Molecular Profiling and Tissue Heterogeneity
Aydin Tozeren
Professor and Director
Program in Integrated Bioinformatics
School of Biomedical Engineering, Science & Health Systems
Drexel University
Abstract
Recent research with high throughput biological tools indicate that large-scale molecular profiling when integrated with histology and other medical data has the potential for accurate sub classification of cancer type and stage. In fact, molecular profiling of tumor tissue through microarray and proteomic technologies have opened a new, promising era in the cancer diagnosis and therapy. Tissue heterogeneity is one of the important challenges concerning the large-scale molecular profiling of solid tissue. Heterogeneity in the tumor structure is a consequence of the variation in the gene expression profiles of the cells within the tumor. Such variation may induce directionality in structural patterns in the growth of lymph and capillary blood vessels. Nano- and micro-engineering technologies such as microfluidics and statistical methods need to be utilized to develop computer-driven quantitative methods of sample selection such that the tissue samples used are representative of the metastatic properties of whole tumors.
Friday, November 29, 12:15 - 1:15 pm, 210 Hallowell
NO SEMINAR - THANKSGIVING BREAK
Friday, December 6, 10:00 - 11:00 pm, 129 A-B-C HUB
The Junctional Strand-Fiber Matrix Model of Capillary Permeability---Further Evaluations Based on New Modelling,Confocal Imaging, Ultrastructural, Cell -Cell Adhesion and Permeability Studies
Fitz-Roy Curry
Professor of Human Physiology
University of California, Davis
Abstract
We have proposed a new hypothesis and conceptual model to explain, at the cellular microstructural level, the local Starling forces which regulate the fluid balance between blood and tissue ( Hu et al, American Journal of Physiology: 279, H1724. 2000). The key concepts are: (1) the surface glycocalyx serves as the primary molecular filter for plasma proteins, and as a result the oncotic forces in the Starling Balance for transvascular water flows are developed across this barrier, and (2), the junctional strands with their orifice like breaks direct transvascular water flows through localized regions and thereby shield the lumenal side of the junction strand such that tissue proteins have difficulty diffusing upstream into this protected region. I will review recent experiments to test this hypothesis in both frog and rat microvessels, and the extension of similar concepts in fenestrated microvessels I will also review new experimental data on both the structure of the endothelial surface glycocalyx and the balance of adhesion and contractile mechanisms regulating increased water and solute flow through breaks in inter-endothelial cell junctions. The same matrix parameters which describe these transport functions are also likely to regulate other important microvascular functions including red cell and leukocyte hydrodynamics and recovery from injury.
Thursday, December 12, 2:30 - 3:30 pm, 210 Hallowell
Student Presentations - 15 minute presentations:
Effects of Simultaneous Wall Shear Stress and Circumferential Strain
on the Expression of Certain Endothelial Cell Junctional Proteins
by Danielle Berardi
Abstract
The stress phase angle (SPA) is the temporal phase angle between wall shear stress (WSS) due to flowing blood
and circumferential strain (CS) resulting from pressure fluctuations within the vasculature. SPA varies greatly
in the circulation and affects the endothelium. This study investigates the effects of SPA on the relative expression
of tight junction proteins occludin and zonula occludens-1 (ZO-1) and adherens junction protein vascular endothelial
cadherin (VE-cadherin) and their role in altering endothelial permeability. A specially designed multi-tube shear
induction apparatus with independent pressure settings allows for the control of SPA and thus the forces imparted
on bovine aortic endothelial cells (BAECs) cultured on elastic tubes. Two conditions examined are with a SPA of
0° and 180°, atheroprotective and atherogenic states, respectively, with a sinusoidal shear stress waveform
with a mean component of 10 dyn/cm2 and an amplitude of 10 dyn/cm2 (10 + 10 dyn/cm2 WSS) and 8% CS with a mean
pressure of 70 mmHg. Upon the completion of the experiments, protein is extracted from the cells and assayed by
Western blot analysis to determine the relative expression of occludin, ZO-1, and VE-cadherin. Experiments involving
pulsatile shear for 5 hours show a higher expression of all three proteins for the 0° SPA case when compared
to steady shear and static and pressurized controls, suggesting that the junctions are intact for this condition.
Meanwhile, the expression of all three proteins for the 180° SPA case is significantly lower than the 0°
SPA case while being at about the same level as the steady shear and control conditions, indicating that the junctions
may be less intact than those at 0° SPA. Therefore, these protein expression results appear to follow the hypothesis
that 0° SPA is atheroprotective and 180° SPA is atherogenic and that this protein expression may influence
the endothelial permeability.
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The Effect of Pulsatile Flow and Circumferential Strain
on Cox-2 and eNOS Endothelial Cell Gene Expression
by Michael Dancu
Abstract
Endothelial cell gene expression of eNOS and cox-2 under pulsatile flow and circumferential strain
Endothelial cells (EC) in vivo are subject to simultaneous wall shear stress (WSS) and circumferential strain (CS)
that are both oscillatory and act approximately in perpendicular directions. Wave reflections in the circulation
and the inertial effects of blood flow cause a temporal phase difference, stress phase angle (SPA), between WSS
and CS. The phase difference between WSS and CS creates a complex and time varying mechanical force pattern on
the EC monolayer that can be characterized by the SPA. The SPA varies significantly throughout the circulation
and is most negative in disease prone locations(i.e. outer wall of bifurcation and coronary arteries). Several
groups have studied the individual effects of WSS and strain and a few others have examined the simultaneous effects
of WSS and CS at SPA=0degrees. The effects of simultaneous WSS and CS on EC gene expression at physiologic SPA
have not been assessed. The endothelium acts as a mechanotransducer and sensor in the regulation of blood vessel
diameter in response to blood flow. It is known that WSS effects vasoactive agents such as nitric oxide, prostacyclin(PGI2),
and endothelin - 1(ET-1) and strain effects ET-1. Gene expression of eNOS, ET-1, COX-2 under various normal (0degrees
SPA) and pathologic (-180degreesSPA) SPA was assessed with QRT-PCR (quantitative reverse transcription polymerase
chain reaction). The QRT-PCR results show an inverse relation in vasoconstrictive vs. vasodilatory gene expression
as anticipated. 0 degrees SPA shows a pro-vasodilatory condition where eNOS gene expression increases and ET-1&COX-2
expression decreases. -180degrees SPA shows the opposite pro-vasoconstrictive trend that can be associated with
pro-atherogenic.
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The New Techniques to Eliminate the Zero Velocity Bias of the Near Wall
Particle Imaging Velocimetry (PIV)
by Pramote Hochareon
Abstract
In most of the fluid mechanic experiments, including Artificial Heart Research, the instantaneous velocity field
with high special resolution is of important for further fluid dynamic analyses. Recently developed, PIV provides
the instantaneously quantitative flow field, by tracking particles displacement, dX, in the fluid between
finite time difference, dT, within finite fluid sub-volume. To obtain the wall shear stress, which is our
interest, the velocity closest to the wall must be obtained. However, the wall reflection potentially deceives
the cross correlation as the stationary particles, resulting in zero velocity bias. We have developed the technique
to zero mask non-fluid domain to eliminate the bias. The effect of the presence of the wall was investigated based
upon the variation of displacement magnitude, wall intensity, wall thickness, and background intensity. The first
two variables yield significant effect on cross correlation, while the last two do not. The result showed dramatic
improvement for the averaged velocity magnitude, 4 times of the conventional method. Further more, because of low
particle image density at the wall vicinity, the noise background occasionally survived the validation criteria
and gave near zero velocity magnitude, the residual zero bias. With the zero masking, the spectrum of valid velocity
vectors became distinguished from the residual zero bias. Histogram data filtering was implemented to recognize
the residual bias and truncate the bias, resulting in only legitimate data to be averaged. The filtering method
improved the velocity magnitude 7 times from the conventional method.
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Controlling the Direction of Microtubule Movements Using Microlithography
by Samira Moorjani
Abstract
Kinesin is a mechanochemical protein capable of utilizing the energy from adenosine triphosphate (ATP) and producing mechanical work. This enables the motor protein to move along microtubules. This is the basis of development of kinesin - powered machinery. The force produced during this interaction can be use to drive other micro and nano devices. Motility assays can be performed in vitro, employing a reverse geometry such that microtubules move along kinesin motors. The problem in extracting this force lies in the random directions of kinesin-driven microtubules. The net force produced is zero or almost negligible and hence cannot be utilized. The solution lies in controlling the direction of this movement. In an attempt to do this, microlithographically patterned channels were constructed on glass. The photoresist employed was SU-8. SU-8 is a high aspect ratio resist which produces vertical sidewalls. Using this method, 93% of microtubules that hit the interface between glass and photoresist were aligned. Depending upon the incident angle with which the microtubule hit the interface, the probability of alignment was calculated. These values ranged from 0.85 to 1 in the angular range from 0 to 90o. Furthermore, 86% of the microtubules moved parallel to the interface after the collision. Also, fluorescently labeled motors were used in motility assays to study binding on SU-8. It was found that equal or more number of motors were bound on SU-8 than on glass.
Friday, December 13, 12:15 - 1:15 pm, 210 Hallowell
Student Presentations- 15 minute presentations by:
The Role of the Glycocalyx in Leukocyte-Endothelium Interactions
by Aaron Mulivor
Abstract
The goal of this research is to identify the function of the endothelial cell glycocalyx during leukocyte adhesion.
The adhesion of leukocytes is a main component of inflammation, which can occur as a result of numerous types of
injuries or medical ailments such as stroke, bacterial infection and arthritis. Understanding the relationship
between the endothelial cell glycocalyx and leukocyte adhesion may elucidate a mechanism to control the inflammatory
response. The glycocalyx is a layer of macromolecules, approximately 50-500nm in thickness that coats the surface
of most known cell types. The most common glycosaminoglycan component of the glycocalyx is Heparan Sulfate (HS),
which is typically attached to a transmembrane protein called Sydencan-1. This research focused on the relationship
between HS and the ability of WBC to adhere to the EC. The results thus far indicate that during an fMLP induced
inflammatory response, when there is an increase in WBC adhesion to the EC, there is an almost 50% drop in the
amount of HS on the EC. This drop in HS can be mediated to almost negligible amounts by blocking the ability of
G-proteins to function by using Pertussis Toxin. This data suggests a correlation between G-protein signaling and
the ability of the EC to maintain the glycocalyx layer.
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[Ca2+]I-Independent Signaling Mechanism in Tumor Cell-Induced
Endothelial Junction Disassembly
by Hsin Hsin Peng
Abstract:
Although the involvement of endothelial [Ca2+]i in leukocyte-endothelial cell interaction has been extensively studied, a potential involvement of endothelial [Ca2+]i in tumor cell-initiated signaling events leading to dissociation of endothelial cell junctional integrity remains unclear. In this study, we monitored the [Ca2+]i in human umbilical vein endothelial cells and bovine aortic endothelial cells following contacts with human melanoma cells. We show that a transient rise in endothelial [Ca2+]i was elicited specifically by tumor cells, and this response utilized classical PLC / IP3 pathways that release Ca2+ from the endoplasmic reticulum. Moreover, tumor contact-induced dissociation of VE-cadherins between neighboring endothelial cells was evident from tyrosine-phosphorylation of VE-cadherin and immunological staining. Most importantly, we show that endothelial cells do not require [Ca2+]i for the dissociation of VE-cadherin junctions in response to melanoma cell contact. These findings indicate a clear divergence from the classical leukocyte-endothelial signaling mechanism and suggest an important difference in endothelial signaling pathways recruited by tumor cells in breaching the vasculature.
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PMN-assisted Melanoma Cell Adhesion to the Endothelium:
Experimental Results and Mathematical Model
by Margaret J. Slattery
Abstract:
Metastasis is the primary cause of cancer related deaths, over 500,000 annually in the United States. Tumor
cell adhesion and motility are factors that directly determine the extent of tumor progression. We have characterized
a novel microenvironment that promotes tumor cell adhesion that may lead to an increase in metastatic efficiency.
Melanoma cells do not express the appropriate adhesion molecules for attaching to the endothelium. We hypothesize
that melanoma tumor cells, specifically C8161 cells, can influence neutrophil (PMNs) activity to improve their
own adhesion. Increased Interleukin-8 production and Mac1 expression by PMNs was detected when they were co-cultured
with C8161 melanoma cells. When human PMNs were present in the tumor cell suspension, C8161 migration increased
by 85% over C8161 under the 4dyn/cm2 flow condition. Utilizing PMNs as an adhesive bridge to the endothelium, melanoma
cells may improve their adhesion and thus improve their trans-endothelial migration efficiency. A mathematical
model previously put forth by Hellum et al. (Biophys.J. 50:479, 1986) has been modified to reproduce the experimental
conditions of flow-migration and parallel plate assays. Changes to the model account for different adhesion kinetics
of the PMN-melanoma system and wall effects in shear-induced aggregation. Parameters of particular interest are
heterotypic collision frequency (Nc) and resultant adhesion frequency (Nca). Variables that influence these parameters
include shear stress, shear rate and cell density. These model parameters will be compared in the future with experimentally
obtained values.
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Design of a High Frequency Annular Array for Medical Imaging
by Kevin Snook
Abstract
As the operational frequencies of medical ultrasound devices increase, new applications in many medical disciplines
are emerging. Single element devices of up to 100 MHz in frequency have been used in both ophthalmology and dermatology;
however, though these devices have superior spatial resolution at their focus, the focus is on the order of tens
or hundreds of microns. To increase the depth of view, the devices are scanned axially as well as laterally, which
greatly increases the risk for patient injury, particularly in ocular imaging.
Annular arrays provide a means to electronically focus at different depths, thus eliminating the need for mechanical
movement along the axis. However, current technology has been limited to designs below 20 MHz, which do not produce
an adequate resolution. A 50 MHz, 6-element annular array has been developed for ocular imaging using construction
methods adapted from high frequency single element design and micromachining technology. One-dimensional and finite
element modeling were used to optimize the design of the array. Using an 8 micron wire phantom, the axial and lateral
resolutions were determined to be between 50-95 microns and 100-300 microns respectively, throughout a depth of
10-18 mm. The preliminary images of an eye in vitro are also shown.
For additional information, contact Ms. Doretta Garvey, Dept of Bioengineering, Tel: 814.865.1407 or E-Mail: bioe@psu.edu