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Dr. Kwok has taught thousands of graduate, undergraduate, pre-med, pre-health, nursing, and athletic training students in a variety of subjects including Biology, Chemistry, Computer Science, Mathematics, Statistics and MCAT since 2001. He also worked in the industry as a Project Manager and a Principal Investigator for a medical device company, and as a Senior Biomedical Engineer for a Fortune 500 company.
Dr. Kwok currently teaches Biology, in particular, Developmental Biology and Anatomy & Physiology at Frostburg State University. He mentors undergraduate and honors students with pre-health concentrations. Dr. Kwok remains active with the biotech and biomedical industry and continues to develops projects in collaborations with the industry to support student research. His past and present projects include investigative research in the fields of biotechnology, biomedical devices, biodefense, stem cell biology, synthetic bone grafts, diabetic foot ulcer, HIV/AIDS, cancer vaccine, reproductive biology, developmental biology, liver physiology, septic shock, PLEX-ID, respiratory virus surveillance, new biomedical product development, entrepreneurship, intellectual property and innovation management. He has published articles in leading U.S. journals such as American Journal of Physiology and has presented in national and international conferences such as Experimental Biology in these fields.
Dr. Kwok received his three bachelor degrees with high honors and distinctions in Biology, Chemistry and Japanese at the University of Hawaii at Manoa (2000). He received his graduate degrees including a Master in Business Administration (MBA) in 2003 and a Ph.D. in Biology in 2008 at the University of North Carolina at Charlotte. He is a registered Patent Agent (PA) with the United States Patent and Trademark Office (USPTO) and affiliates with a patent lawfirm located in Charlotte, N.C. since 2009.
Current And Recent Courses Taught
Selected Projects Highlight
Hormonal Regulation of Peri-implantation Embryo and Uterus
As an endogenous smooth muscle relaxant and vasodilator, nitric oxide (NO) increases vascular permeability and uterine quiescence at the implantation site. NO is also important in regulating peri-implantation embryo development. Nitric oxide synthase (NOS) produces intracellular NO and three isoforms of NOS exists: endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS). The naming of these enzymes can sometimes be confusing, because most cells express all three isoforms of NOS. Inducible NOS produces a short-lived spike in NO at high concentration; whereas eNOS and nNOS produce low levels of NO for a sustainable period. Despite the beneficial effects at physiological level, NO produced at high concentration may react rapidly with superoxide (O2-) or possibly with hydrogen peroxide (H2O2) to cause oxidative damage. Superoxide dismutase (SOD) is one of several enzymes that can limit this detrimental effect of high levels of NO at the cellular level in the uterus. Hence, my research effort in Developmental Biology can be classified in two areas: hormonal regulation of NOS and SOD (1) in peri-implanatation embryo and (2) in the uterus of mouse and human. Quantitative reverse transcription-PCR analysis has indicated that blastocyst embryos isolated just before implantation in the uterus only express eNOS and nNOS; in contrast, two-cell, four-cell, and morula embryos express all three NOS isoforms. To investigate the hormonal regulation of NOS and SOD in the murine uterus, ovariectomized CD-1 mice were given daily subcutaneous injections of progesterone for four days and were given a 17β-estradiol injection on Day-4 to induce implantation. Results have demonstrated that 17β-estradiol up-regulates eNOS and nNOS (but not iNOS) and down-regulates SOD in the peri-implantation uterus. To further advance the study, endometrial tissues from women receiving hysterectomy for reasons other than endometrial disease were obtained to study the hormonal regulation in human. In situ hybridization has indicated that iNOS is only found in the stroma during the proliferative phase of the uterine cycle and expands to include the epithelial cells during the secretory phase and menses; in contrast, eNOS and nNOS are localized in both epithelial and stromal cells during the proliferative and secretory phases, but only eNOS is found in the stroma during menses. These studies have suggested that a well-coordinated spatiotemporal regulation of NOS and SOD enzymes by estrogen and progesterone in the control of NO production is essential for proper embryonic development and uterine implantation, and these scientific findings have been presented at national and international conferences.
Regulation of Hepatic Microcirculation in Septic Shock and Endotoxemia
The clinical significance of studying hepatic microcirculation in septic shock and endotoxemia is related to multiple organ failures (MOFs). MOF is the major cause of death in intensive care units (ICUs). Among the many organs that progressively fail during MOFs, the organ that first fails is usually the liver. As a result, my research interest has focused on the signaling and molecular pathways that regulate blood flow in the hepatic sinusoids of the liver. My research studies have demonstrated that endotoxin increases portal resistance to reduce hepatic blood perfusion by limiting nitric oxide (NO) production from liver sinusoidal endothelial cells (LSECs) at least through the regulation of two distinct signaling cascades: Caveolin-1 (Cav-1) and Rho-kinase. The first studied signaling mechanism involves Cav-1, which binds to endothelial NOS (eNOS) in membrane caveolae to inhibit eNOS activity. Western blots and immunoprecipitation experiments have shown that endotoxin upregulates Cav-1 expression and increases eNOS/Cav-1 association to inhibit endothelin-1 (ET-1)-mediated eNOS activation. When Cav-1 is disrupted pharmacologically with methyl-β-cyclodextrin or is completely knocked out using a genetic model, ET-1-mediated NO production is restored even in the presence of endotoxin. The second studied pathway involves Rho-kinase that also binds to eNOS to inhibit its activity, but the exact mechanism of this inhibition was not well understood. It has been established in the literature that actin monomers bind and stimulate eNOS activity; my research data has indicated that Rho-kinase mediates the effect of endotoxin in the inhibition of ET-1-mediated eNOS activation by inhibiting actin depolymerization. These studies have suggested that Cav-1 and Rho-kinase mediate the effects of endotoxin in the inhibition of ET-1-mediated eNOS activation in the LSECs to hinder liver microcirculation, and these research data have been presented in seven scientific conferences and led to three first-authored articles in peer-reviewed journals.
Bone Physiology & Stem Cell Biology
Osteogenic Differentiation of Stem Cells on Orthopedic Devices for Spinal Fusion
In the United States, it has been estimated that more than 500,000 bone grafting procedures are performed annually, with about half of these procedures related to spinal fusion. These numbers easily exceed the number of available musculoskeletal donors. This discrepancy in the supply and demand of bone allografts has stimulated the development and sales of bone graft substitutes in the U.S. The successful performance of bone grafts and their substitutes depends on their ability to facilitate new bone formation through the biological processes of osteoconduction, osteoinduction, and osteogenesis. The use of osteoinductive proteins, such as bone morphogenetic proteins (BMPs), stimulates bone formation by targeting and activating undifferentiated stem cells and connective tissue cells. Similarly, mitogenic growth factors target and accelerate the osteogenic activity of previously differentiated cells. Although these advances have improved clinical outcomes, their applications have been limited by the requirement for a superior tissue scaffold or delivery carrier. My research group has engineered a self-assembled bioscaffold carrier (E-Matrix) composed of denatured collagen and dextran which has been shown to be an effective carrier for recombinant human BMP-2 (rhBMP-2) in a rat spinal fusion model. Our latest bone graft, TrioMatrix™, contains this collagen-based osteoconductive bioscaffold (E-Matrix), an osteoconductive nano-scale hydroxyapatite (nanOss™ HA), and osteoinductive demineralized bone matrix (DBM). Osteogenic cells such as mesenchymal stem cells (MSCs), aminotic stem cells (ASCs), embryonic stem cells (ESCs) or induced pluripotent stem cells (iPSCs) can then be added to TrioMatrix to provide a bone-graft substitute that has all of the necessary components for bone formation: osteoconduction, osteoinduction, and osteogenesis. In a study that has been presented at the TERMIS 2010 conference, I have investigated the in vitro effects of the components of TrioMatrix on bone cell functioning by measuring alkaline phosphatase (ALP) activity of fibroblasts, endothelial cells, osteoblasts, and MSCs. My research data has shown that ALP activity was appropriately increased in either human MSCs or SAOS-2 osteosacroma cells incubate with TrioMatrix or its individual components for spinal fusion. In addition, there was no inappropriate increase in ALP activity in either fibroblasts (CCD-1112Sk) or endothelial (HUVEC) cells when incubated with either complete TrioMatrix or its individual components that may cause ectopic bone formation following implantation.
Oral Bacteria in The Development of Ventilator-Associated Pneumonia
Ventilator-associated pneumonia (VAP) is an ICU-acquired infection that is closely related to nasal or endotracheal intubations and mechanical ventilator support. Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae are usually predominant during the early onset VAP within the first 4 days of intubations; whereas Pseudomonas aeroginosa, Acinetobacter and Enterobacter species often predominate in the late onset VAP after 4 days of intubations. Although a variety of immunological defense mechanism normally protects the lower respiratory tract from the microflora of the upper aerodigestive tract, bacterial pneumonia is among the most common infections in hospital patients and is the leading cause of death among nosocomial infections. My research goal was to identify and to correlate the VAP-associated pathogens retrieved from the oral cavity with those from the lungs of patients at the time of diagnosis of VAP. At the onset of suspected VAP infection, tongue bacterial samples were acquired by wiping a sterile swab across both sides of the mid-dorsum region of the tongue, and bronchoalveolar lavage (BAL) was taken by one of the trauma surgeons by flushing and collecting sterile, non-bacteriostatic saline using an endoscope. To isolate the pathogens from the oral cavity, the swabs were rotated at room temperature for one to two hours before centrifugation. As for the BAL samples, the specimens were diluted and centrifuged to collect the bacteria pellets. Because many oral bacteria are uncultivated due to inadequate molecular methodology in the field as well as inappropriate choice of selective and non-selective media, more sensitive and reliable methods using PCR and DNA sequencing of the 16S ribosomal DNA (rDNA) were necessary for this study. After the bacterial DNAs were isolated (QIAamp DNA Mini Kit) and amplified with 9F forward and 1541R reverse primers, the amplicons were purified (QIAquick Gel Extraction Kit) and cloned into Escherichia coli (TOPO TA Cloning Kit). The transformed E. coli were spread on ampicillin plates, and colonies were selected for DNA sequencing (ABI 3100 DNA sequencer using a Big Dye terminator cycle sequencing ready reaction kit) in order to construct a 16S rDNA library. The 16S rDNA sequences of the inserts were compared to the known sequences in the public GenBank by BLAST and to the 76,000 sequences in the Ribosomal Data Project. This research study has indicated that there is an association of oral bacteria with the development of VAP.
Genetic Mutation of HIV-1 in Patients Before And After Seroconversion
Human immunodeficiency virus type 1 (HIV-1) evolves greatly within the human host due to the high error rate and the lack of proofreading ability of the viral reverse transcriptase; therefore, isolation of the virus within a host is often composed of a mixture of highly related but distinct viral genomes (i.e. quasispecies). Quasispecies diversity may increase over time; with the progression of the disease, the frequency of isolating HIV-1 that can induce cell-to-cell fusion in vitro to form multinucleated giant cells (or syncytia) increases. In the early onset of the infection, the transmitted non-syncytium-inducing (NSI) viruses have a low replication rate within the host. NSI viruses have high affinity for macrophages (i.e. M-tropic) and bind to CCR5 chemokine receptor to initiate cell invasion. With progression to AIDS, syncytium-inducing (SI) viruses emerge and replicate at a much higher rate than NSI viruses. SI viruses are associated with the rapid depletion of CD4+ T-cells (i.e. T-tropic) and bind to CXCR4 (a chemoattractant receptor for stromal cell-derived factor-1) for cell entry. In my research study, I have investigated the patterns of virus selection and adaptive changes of HIV-1 following primary infection. Replication-competent quasispecies were derived from viruses isolated from recipients (three homosexual men and one patient infected by needle stick injury) before and after seroconversion and from the presumed donors. Phenotypic analysis of the biological clones has been made to evaluate syncytial formation. Genetic analysis using PCR and RT-PCR to amplify the V3 regions of env, p17 region of gag, and pol gene sequences followed by phylogenetic analysis has also been performed. Results have indicated that the viral population after transmission is relatively homogeneous and is most commonly composed of the M-tropic or CCR5 phenotype, despite the presence of T-tropic or CXCR4 viruses in the donors. In instances in which a transmitted virus was found to have a T-tropic/CXCR4 phenotype, it was replaced by an M-tropic/CCR5 variant after seroconversion. The precise mechanism determining how such clones are selected remains unknown.
Selected Recent Publications
2013 Wenjuan Xu, Kevin Madison, Michael Flinn, Willson Kwok. Applying Virtualization Technology in Security Education. 4th World Conference on Learning, Teaching and Educational Leadership.
2010 Willson Kwok and Mark G. Clemens. Targeted mutation of caveolin-1 (Cav-1) alleviates the effect of endotoxin in the inhibition of endothelin-1 (ET-1)-mediated eNOS activation in the liver. Shock 33(4): p 392-398.
2009 Willson Kwok, Sang-Ho Lee, Catherine Culberson, Katarzyna Korneszczuk and Mark G. Clemens. Caveolin-1 mediates endotoxin inhibition of endothelin-1-induced endothelial nitric oxide synthase activity in liver sinusoidal endothelial cells. American Journal of Physiology - Gastrointestinal and Liver Physiology 297: G930-G939.
Selected Recent Presentations
2013 Willson Kwok. Engineering of a stem stell and nanotechnology based bone graft substitute. 3rd World Congress on Cell Science & Stem Cell Research, Baltimore, MD, USA, November 20 to 22, 2013.
2010 Willson Kwok, Francis Lamberti, Billy Lloyd, Adam MacMillan, Edward Ahn and Ronald Hill. A novel collagen-based carrier for spinal fusion. TERMIS-North America 2010, Orlando, FL, USA, December 5 to 8, 2010.
2009 Willson Kwok and Mark G. Clemens. A novel signaling pathway mediates the molecular effect of LPS in inhibition of eNOS activation involving cofilin and VASP. Experimental Biology 2009, New Orleans, LA, USA, April 18 to 22, 2009.
2008 Willson Kwok and Mark G. Clemens. Actin modulates the LPS-inhibited ET-1 activation of eNOS in hepatic sinusoidal endothelial cells. The Liver Meeting 2008, San Francisco, CA, USA, October 31 to November 4, 2008.
2008 Willson Kwok. Research and commercialization of a novel compound for prevention of septic shock and improvement of blood flow. Charlotte Biotechnology Conference, Charlotte, NC, USA, October 28, 2008.
2008 Willson Kwok and Mark G. Clemens. Genetic manipulation of caveolin-1 mimics the effect of LPS in the regulation of endothelin-1-mediated endothelial nitric oxide synthase activation in hepatic sinusoidal endothelial cells. 31st Annual Conference on Shock, Cologne, Germany, June 28 to July 2, 2008.
2008 Willson Kwok, Sang-Ho Lee, Katarzyna Korneszczuk, Cathy Culberson, David L. Gray and Mark G. Clemens. LPS inhibits endothelin-1 (ET-1)-mediated endothelial nitric oxide synthase activation through the RhoA/Rho-kinase pathway in hepatic sinusoidal endothelial cells. Experimental Biology 2008, San Diego, CA, USA, April 5 to 9, 2008.
2007 Willson Kwok and Mark G. Clemens. Caveolin-1 modulates eNOS activity in hepatic sinusoidal endothelial cells. Nanotechnology in Biology and Medicine, Charlotte, NC, USA, November 5, 2007.
2007 Willson Kwok, Sang-Ho Lee, Anahita A. Lasboo, Cathy Culberson, and Mark G. Clemens. Caveolin-1 modulates phosphorylation of eNOS in hepatic sinusoidal endothelial cells. The 8th Annual World Congress of Microcirculation, Milwaukee, WI, USA, August 15 to 19, 2007.
2006 Willson Kwok, Nury Steuerwald, Yvette Huet-Hudson. The Expression and Spatiotemporal Localization of Nitric Oxide Synthase and Superoxide Dismutase Isoforms during the Menstrual Cycle in the Human Uterus. Society of the Study of Reproduction 29th Annual Meeting, Omaha, NE, July 21 to August 1, 2006.
2005 Willson Kwok, Nury Steuerwald, Yvette Huet-Hudson. Estrogen Regulation of NOS Isoforms in the Mouse Periimplantation Uterus. Society of the Study of Reproduction 28th Annual Meeting, Montreal, Canada, July 24 to 27, 2005.
Selected Awards & Honors
Selected Professional Memberships
Last Updated on 07-24-2014 at 06:58:58 AM