+publisher:"Cornell University" +contributor:("Coonrod, Scott A.")

1. Kartha, Nithya. CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE.

Degree: PhD, Genetics and Development, 2017, Cornell University

URL: http://hdl.handle.net/1813/56907

► The American Cancer Society estimates that in the year 2017, approximately 40,000 women will die from breast cancer. The vast majority of these breast cancer… (more)

▼ The American Cancer Society estimates that in the year 2017, approximately 40,000 women will die from breast cancer. The vast majority of these breast cancer cases (80-85%) are sporadic in nature, developing spontaneously within the lifetime of a woman. While there is a significant amount of knowledge regarding the genetic drivers of hereditary breast cancers, there is very little known about the genes responsible for driving sporadic breast cancers, largely in part due to the dearth of appropriate mouse models of this disease. The C3H-MCM4Chaos3(Chaos3) mouse model bears a single endogenous mutation in a gene encoding a component of the MCM2-7 replication helicase, which our lab has previously shown results in a state of chronic replication stress and downstream genomic instability, leading to a strain-specific phenotype of female mice developing spontaneous mammary adenocarcinomas. In my graduate research work, I have utilized this powerful and unique mouse model to determine the genetic drivers of these sporadic mammary tumors (MTs), based on relevance to human breast cancer data available publicly. My analyses of recurrent genomic alterations present in these Chaos3 MTs revealed that the majority of them (>80%) contained heterozygous deletions of a gene encoding the chromatin remodeling component Arid1a. Importantly, ARID1A is also frequently deleted (monoallelically) in a significant subset of human breast cancers (between 30-50%, depending on the specific study cited), based on data from The Cancer Genome Atlas (TCGA). I have characterized the pathways being altered upon overexpression of Arid1a in Chaos3 MT cells, and have identified potential direct transcriptional targets of Arid1a regulation using this in vitro system. I have further shown that the heterozygous loss of Arid1a is a critical maintenance factor for MT growth in this model, and that endogenous induction of Arid1a expression to wild-type levels is sufficient to significantly slow down MT cell proliferation in vitro. This is suggestive of a haploinsufficient role for Arid1a tumor suppression, in a manner similar to TP53, and offers an intriguing therapeutic opportunity of inducing the remaining ARID1A allele to potentially reduce MT growth in the subset of human breast cancers that retain an intact copy of this powerful tumor suppressor gene. Advisors/Committee Members: Schimenti, John C. (chair), Coonrod, Scott A. (committee member), Weiss, Robert S. (committee member).

Subjects/Keywords: Genetics; Breast cancer; Molecular biology; Arid1a; Chromatin remodelers; Mouse model; SWI/SNF; Biochemistry

…Shen2, Carolyn Maskin1, Marsha Wallace3 and John C. Schimenti1 Affiliations: 1 Cornell… …University, College of Veterinary Medicine, Dept. of Biomedical Sciences, Ithaca, NY 14853, USA 2…

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APA (6^th Edition):

Kartha, N. (2017). CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/56907

Chicago Manual of Style (16^th Edition):

Kartha, Nithya. “CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE.” 2017. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/56907.

MLA Handbook (7^th Edition):

Kartha, Nithya. “CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE.” 2017. Web. 04 Mar 2021.

Vancouver:

Kartha N. CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/56907.

Council of Science Editors:

Kartha N. CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/56907

Cornell University

2. Goldstein, Orly. Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36147

► As of October 2013, around 285 million people are visually impaired worldwide. For an important subset of these, this visual impairment is genetic. That is,… (more)

▼ As of October 2013, around 285 million people are visually impaired worldwide. For an important subset of these, this visual impairment is genetic. That is, they have inherited mutant genes that prevent sight by affecting an element critical for vision. Understanding the genetic basis of these diseases offers insight into the mechanisms involved in photoreceptor development, function, and maintenance as well as significant potential for therapies addressed at cure or prevention. In recent decades, understanding of the cellular and molecular mechanisms of vision has expanded dramatically. In particular, many genes have been discovered that are vital for normal function of the retina, the delicate, multilayered, light-sensitive layer at the back of the eye that connects by the optic nerve to the brain. Retinitis pigmentosa (RP) is a subgroup of inherited eye diseases causing retinal degeneration. In the U.S.A alone, an estimated 100,000 people have inherited RP, either as an autosomal dominant, autosomal recessive, or X-linked disease. Among these, about 50% of cases of autosomal recessive RP cannot be explained by so far identified genes, and for many of the known genes, their role in vision is unclear. The dog also suffers from inherited eye diseases. The canine disease homolog of RP is referred to as Progressive Retinal Atrophy (PRA). Because of the unique population structure and genetic differences within and among the various breeds of dogs, this animal model offers a remarkable tool for discovering genetic mechanisms in vision and serves as a therapeutic model for potential gene therapy. In the present work, we have investigated nine different canine diseases (OSD, erd, prcd, cd, crd1, crd2, crd3, Basenji PRA, and Italian Greyhound PRA), characterized them, discovered the genes responsible for their phenotype, and determined the broad spectrum of breeds affected by them. These studies utilized classical genetic methods such as linkage and candidate gene approaches, and were expanded to employ Linkage Disequilibrium and Association Studies. We discovered two novel genes, PRCD and STK38L, both of which cause PRA in dogs, but had not previously been recognized as involved in vision or visual disorders, and thereby identified novel pathways critical for vision, as well as genes potentially responsible for human RP. We also identified novel mutations in six known genes (COL9A2, COL9A3, ADAM9, PDE6B, IQCB1, and SAG) that cause five different diseases, and thereby established new animal models for potential gene therapy in their human counterparts. We identified the exact deletion points of the cd disease in a broad spectrum of breeds affected by this disease, showing that they are all inherited Identical By Descent (IBD). We discovered the potential involvement of a microRNA in retinal degeneration in the Italian greyhound PRA, the first such evidence in a large animal model, and the first suggestion that retinal degeneration can be caused by alteration in gene expression regulated by microRNA. We developed screening… Advisors/Committee Members: Acland, Gregory Maurice (chair), Meyers-Wallen, Vicki N (committee member), Schimenti, John C. (committee member), Coonrod, Scott A. (committee member).

Subjects/Keywords: Retinal degeneration; Genetic mutation; Canine PRA

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APA (6^th Edition):

Goldstein, O. (2014). Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36147

Chicago Manual of Style (16^th Edition):

Goldstein, Orly. “Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36147.

MLA Handbook (7^th Edition):

Goldstein, Orly. “Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population.” 2014. Web. 04 Mar 2021.

Vancouver:

Goldstein O. Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36147.

Council of Science Editors:

Goldstein O. Insight Into Sight: Deciphering The Heterogeneity Of Hereditary Retinal Degeneration In The Canine Population. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36147

Cornell University

3. Kim, Boram. The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes.

Degree: PhD, Veterinary Medicine, 2013, Cornell University

URL: http://hdl.handle.net/1813/33817

► Ca2+ oscillation is hallmark of mammalian fertilization that is thought to mediate egg activation process, and dramatic targeting of the endoplasmic reticulum (ER) to the… (more)

▼ Ca2+ oscillation is hallmark of mammalian fertilization that is thought to mediate egg activation process, and dramatic targeting of the endoplasmic reticulum (ER) to the microvillar subcortex, is known to provide calcium pools for subsequent activation and embryo development. While the mechanisms by which Ca2+ oscillation govern later embryonic development are poorly understood, emerging evidences indicate the critical role of Ca2+ oscillation in embryonic development, for example, by regulating recruitment of maternal mRNAs. Mater (Nlrp5) and Padi6 are oocyte-and early embryo-restricted maternal effect genes that are required for embryonic development beyond the 2-cell stage. Interestingly, PADI6 localizes to, and is required for the formation of oocyte-specific structure termed cytoplasmic lattices (CPLs). Based on similarity between MATER and PADI6, we hypothesized that MATER is also required for CPL formation. Indeed, ultrastructural analysis of Matertm/tm oocytes show ~90% reduced volume of CPLs and immuno-EM demonstrates the localization of MATER to CPLs, indicating MATER as a component of CPLs. Interestingly, Tubulin was also identified as a CPL component and that Tubulin interacts with PADI6. Given that Tubulin drives organelle movement, the role of Tubulin-PADI6-CPLs in organelle distribution during oocyte maturation was demonstrated. Given above observations, we further hypothesized that Mater plays a role in ER distribution and function, Ca2+ homeostasis in oocytes. We first investigated ER distribution by microinjecting DiI into oocytes and found that, as opposed to WT oocytes, the ER in metaphase-II Matertm/tm oocytes failed to concentrate around the spindle and cortical clusters were reduced. As cortical clusters are thought to be important for Ca2+ oscillation, then we tested if the pattern of Ca2+ oscillation is altered in Matertm/tm oocytes after in vitro fertilization. Intriguingly, Matertm/tm oocytes show altered Ca2+ oscillation pattern, lower amplitude and higher frequency. Then we demonstrated the reduced amount of intracellular Ca2+ stores in Matertm/tm oocytes, in part, contribute to such phenotype. Finally, the localization of IP3R-I, an essential player in releasing Ca2+ from ER, was altered in supporting of ER distribution. Taken together, this observation support the hypothesis that MATER is required for CPL formation and is involved in ER distribution and Ca2+ homeostasis in oocytes. Advisors/Committee Members: Coonrod, Scott A. (chair), Schimenti, John C. (committee member), Parrish, Colin Ross (committee member), Clark, Theodore G. (committee member).

Subjects/Keywords: MATER; cytoplasmic lattice; calcium homeostasis

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APA (6^th Edition):

Kim, B. (2013). The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/33817

Chicago Manual of Style (16^th Edition):

Kim, Boram. “The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes.” 2013. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/33817.

MLA Handbook (7^th Edition):

Kim, Boram. “The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes.” 2013. Web. 04 Mar 2021.

Vancouver:

Kim B. The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes. [Internet] [Doctoral dissertation]. Cornell University; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/33817.

Council of Science Editors:

Kim B. The Role Of Mater In Cytoplasmic Lattice Formation, Endoplasmic Reticulum Distribution, And Calcium Homeostasis In Mouse Oocytes. [Doctoral Dissertation]. Cornell University; 2013. Available from: http://hdl.handle.net/1813/33817

4. Murphy, Patrick. Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods.

Degree: PhD, Genetics, 2013, Cornell University

URL: http://hdl.handle.net/1813/33788

Subjects/Keywords: Epigenetics; Cancer; Single Molecule Nanofluidics

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APA (6^th Edition):

Murphy, P. (2013). Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/33788

Chicago Manual of Style (16^th Edition):

Murphy, Patrick. “Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods.” 2013. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/33788.

MLA Handbook (7^th Edition):

Murphy, Patrick. “Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods.” 2013. Web. 04 Mar 2021.

Vancouver:

Murphy P. Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods. [Internet] [Doctoral dissertation]. Cornell University; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/33788.

Council of Science Editors:

Murphy P. Mechanisms Of Epigenetic Regulation Characterized Using Novel Single Molecule And Traditional Methods. [Doctoral Dissertation]. Cornell University; 2013. Available from: http://hdl.handle.net/1813/33788

Cornell University

5. Mohan, Swapna. Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis.

Degree: PhD, Physiology, 2014, Cornell University

URL: http://hdl.handle.net/1813/36175

► Gametogenesis is one of the most important biological processes in the life of an organism because it results in the production of gametes, haploid cells… (more)

▼ Gametogenesis is one of the most important biological processes in the life of an organism because it results in the production of gametes, haploid cells that pass on the organism's genetic material to its offspring. However, it a very complicated, intricate process that demands a very high level of regulation. This regulation is to ensure error free meiotic and post-meiotic divisions resulting in a haploid gamete. Errors during the meiotic process can result in defective embryos or fetal demise. Among mammals, humans exhibit a very high rate of gamete defects (~25%) leading to high rates of early embryo loss. Stage-specific cell signaling cascades such as the MAPK pathway regulate meiosis and germ-cell development. In addition to this, MAPKs specifically ERKs, are thought to be involved in cellular division, cytoskeletal reorganization and segregation of genetic material. So far pharmacological approaches have been used to study the action of ERKs in oocytes in vitro using inhibitors of the ERK pathway. However, these are not truly reflective of the physiological environment of the ovary. Hence, in order to better understand the mechanism of action of ERKs on oocyte division, I have generated an Erk2 conditional deletion system driven by an oocyte specific Cre on an Erk1 null background. I hypothesized that deregulation of the MAPK pathway in oocytes will produce drastic changes in the cytokinesis and in chromosome segregation. Mutant females were found to be infertile, with gross chromosome misalignment on metaphase spindles in oocytes, and severe early embryonic loss. This phenotype was accompanied by loss of phosphorylation of several downstream targets such as MSK1 and histone H3. Several possible new targets have also been identified in this study by comparing phosphrylation profiles of oocytes from various genotypes. Our results demonstrate that ERK activity specifically within the oocyte is essential for meiotic resumption and for normal pre-implantation development. Advisors/Committee Members: Cohen, Paula (chair), Johnson, Patricia A (committee member), Coonrod, Scott A. (committee member), Southard, Teresa L (committee member), Roberson, Mark Stephen (committee member).

Subjects/Keywords: ERK; Oocyte; Meiosis

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APA (6^th Edition):

Mohan, S. (2014). Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36175

Chicago Manual of Style (16^th Edition):

Mohan, Swapna. “Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36175.

MLA Handbook (7^th Edition):

Mohan, Swapna. “Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis.” 2014. Web. 04 Mar 2021.

Vancouver:

Mohan S. Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36175.

Council of Science Editors:

Mohan S. Investigating The Role Of The Mapk Proteins Erk1 And Erk2 On Mammalian Gametogenesis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36175

Cornell University

6. Mohanan Nair Padmini, Sunish. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36176

► Numerous recent studies have shown that epigenetic modifications play a significant role in cancer pathogenesis. The PADs are a family of epigenetic enzymes that catalyze… (more)

▼ Numerous recent studies have shown that epigenetic modifications play a significant role in cancer pathogenesis. The PADs are a family of epigenetic enzymes that catalyze citrullination, a reaction by which PADs convert peptidyl-arginine to neutral citrulline, leading to the disruption of protein-protein interactions. Our lab has found that PAD2 has a critical role in breast cancer progression. The goal of this thesis research was to further elucidate the role of PAD2 in epithelial carcinogenesis using PAD2 overexpression tumor cell lines and a MMTV-FLAG-hPAD2 transgenic mouse model. We also aimed to evaluate how PAD2 may play a direct role in regulating chronic inflammation via macrophage extracellular chromatin trap release ("ETosis"). Interestingly, we found that 40% of the MMTV-FLAG-hPAD2 overexpressing transgenic mice developed proliferative skin lesions after five months of age. The tumors expressed the transgenic form of FLAG-hPAD2 and showed increased expression for inflammatory cytokines such as IL6 and IL8. As the next step we conducted a two-stage chemical carcinogenesis study to further evaluate the predilection of MMTV-FLAG-hPAD2 mice to develop more invasive skin tumors and compare the histopathology of these tumors with the WT tumors. We found that a higher percentage of MMTV-FLAG-hPAD2 mice developed skin papillomas and the transgenic tumors were more invasive. Furthermore, hPAD2 expression levels were highly positively correlated with chemokine levels and negatively correlated with the cell adhesion markers suggesting the role of PAD2 in assisting epithelial-mesenchymal transition. We had previously shown that PAD4 isozyme in neutrophils is involved in chromatin decondensation and extracellular chromatin trap release. In this thesis research we provide evidence on how PAD2 is involved in macrophage extracellular trap (MET) release. Using in vitro macrophage culture models, we found that PAD2 is critical in functional MET release and that METs contain high levels of histone H4 citrulline 3 (H4Cit3) modification. Using human tongue SCC tissue, we show that CD68+ macrophage associated ETs exist in tumor tissue and are highly positive for citrullinated histones. Additionally, we show that PAD2-rich macrophages associated with chronic subclinical inflammation in adipose tissue also release METs suggesting the significant role of PAD2 in chronic inflammation via MET release. Collectively, these studies provide strong experimental evidence establishing PAD2 as a potential oncogene, a therapeutic target for immunomodulation and a regulator of obesity and tumor associated inflammation. Advisors/Committee Members: Coonrod, Scott A. (chair), August, Avery (committee member), Fischbach, Claudia (committee member), Weiss, Robert S. (committee member).

Subjects/Keywords: Peptidylarginine deiminase 2 (PAD2); Cancer progression; Extracellular chromatin traps (ETosis)

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APA (6^th Edition):

Mohanan Nair Padmini, S. (2014). Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36176

Chicago Manual of Style (16^th Edition):

Mohanan Nair Padmini, Sunish. “Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36176.

MLA Handbook (7^th Edition):

Mohanan Nair Padmini, Sunish. “Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.” 2014. Web. 04 Mar 2021.

Vancouver:

Mohanan Nair Padmini S. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36176.

Council of Science Editors:

Mohanan Nair Padmini S. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36176

Cornell University

7. Meng, Hsien-Wei. Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36083

► SELEX, the process of selecting aptamers, is often hampered by the difficulty of preparing target molecules in their native forms and by a lack of… (more)

Subjects/Keywords: Aptamer; Cell-SELEX; Yeast Surface Display

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Meng, H. (2014). Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36083

Chicago Manual of Style (16^th Edition):

Meng, Hsien-Wei. “Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36083.

MLA Handbook (7^th Edition):

Meng, Hsien-Wei. “Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display.” 2014. Web. 04 Mar 2021.

Vancouver:

Meng H. Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36083.

Council of Science Editors:

Meng H. Development Of Dna Aptamers By Cell-Selex Using Yeast Cell Surface Display. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36083

Cornell University

8. Lin, Changyou. Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense.

Degree: PhD, Immunology, 2014, Cornell University

URL: http://hdl.handle.net/1813/36062

► Cytolethal distending toxin (CDT) of C. jejuni, a leading cause of intestinal illness worldwide, and H. hepaticus, a laboratory mice pathogen causes cell cycle arrest… (more)

▼ Cytolethal distending toxin (CDT) of C. jejuni, a leading cause of intestinal illness worldwide, and H. hepaticus, a laboratory mice pathogen causes cell cycle arrest and induces apoptosis in eukaryotic cells. In the present studies, the interactions of CDT with host innate defense mechanisms were investigated within the context of intestinal infection. The acute stage of intestinal infection by C. jejuni is characterized by massive transepithelial migration of activated PMNs into the intestinal lumen. Recently, neutrophil extracellular traps (NETs) have emerged as an important innate host defense mechanism against bacterial pathogens. We hypothesize that CDT nuclease mediates resistance against extracellular killing in NETs. First, NETs were discovered to capture C. jejuni in non-human primates with acute campylobacteriosis. The lack of direct induction of NETs formation in vitro by C. jejuni indicates NETs formation in C. jejuni infection might be indirectly mediated by components present within the intestinal microenvironment. Although C. jejuni were efficiently captured within NETs, they themselves did not induce NET fromation. However, once captured, C. jejuni survived within NETs, and CDT did not play a role in escape of C. jejuni from NETs. Taken together, the data suggest that within the context of the intestinal tract, NETs likely provide innate defense by a mechanism of bacterial exclusion and disposal by intestinal peristalsis. Given that CDT-induced intoxication of epithelial cells leads to a DDR, we hypothesized that CDT-intoxicated intestinal epithelial cells display a senescenceassociated secretory phenotype (SASP). Following treatment of human intestinal epithelial cells with sub-lethal doses of CDT from either C. jejuni or H. hepaticus or C. jejuni whole cell lysates, we observed persistent DDR including cell growth arrest and upregulation of [gamma]-H2AX, accumulation of intracytoplasmic beta-galactosidase, and expression of pro-inflammatory cytokines IL-6 and IL-24 and CXCL-8 chemokine characteristic of SASP. In sum, the data reveal that activation of senescence pathways is a novel and potentially important downstream mechanism of CDT-induced genotoxicity that might contribute to host innate defense during intestinal infection by bacterial pathogens. Advisors/Committee Members: Duhamel, Gerald E. (chair), Coonrod, Scott A. (committee member), Denkers, Eric Young (committee member).

Subjects/Keywords: Cytolethal Distending Toxin; Neutrophil Extracellular Trap; Cellular senescence

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APA (6^th Edition):

Lin, C. (2014). Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36062

Chicago Manual of Style (16^th Edition):

Lin, Changyou. “Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36062.

MLA Handbook (7^th Edition):

Lin, Changyou. “Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense.” 2014. Web. 04 Mar 2021.

Vancouver:

Lin C. Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36062.

Council of Science Editors:

Lin C. Interaction Between Cytolethal Distending Toxin Produced By Campylobacter Jejuni And Helicobacter Hepaticus And Host Innate Immune Defense. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36062

9. Rinaldi, Vera Da Silva Garcia. Genetically dissecting the meiotic checkpoint active during prophase I in female mice.

Degree: PhD, Comparative Biomedical Sciences, 2017, Cornell University

URL: http://hdl.handle.net/1813/56716

► Females have a non-renewable number of gametes at birth. These oocytes are extremely sensitive to environmental factors that generate DNA damage. Oocyte death due to… (more)

▼ Females have a non-renewable number of gametes at birth. These oocytes are extremely sensitive to environmental factors that generate DNA damage. Oocyte death due to DNA damage can result in infertility and ovarian failure. In contrast to postnatal oocytes, at earlier stages of gametogenesis these cells withstand hundreds of developmentally programmed DNA breaks (DSBs). During the first meiotic division these DSBs promote synapsis (homologous chromosomes pairing), and recombination, which are both essential for sexual reproduction and environmental fitness. However, DSB repair and synapsis need to occur in a timely manner, or the quality of the gametes becomes compromised. The mechanisms that guarantee oocyte quality were hypothesized to operate through two independent pathways: one that surveys DNA integrity, and the other synapsis. However, I present experimental evidence that oocytes defective for either DNA repair or synapsis are eliminated by the same DNA damage response. Furthermore, through the detailed analysis of DNA repair dynamics, I provide evidence that the protein HORMAD2, which localizes to unsynapsed chromosomes, regulates DSB-repair. I hypothesize that HORMAD2 interferes with repair by preventing broken DNA from using the sister chromatid as a repair template. This “block to sister-chromatid repair” (BSCR) assures that the homologous chromosome is the substrate of choice. Whereas BSCR guarantees homologous recombination, it also prevents unsynapsed chromosomes from fixing DSBs. Thus, failure to synapse will result in persistent DSBs. Since DNA damage causes oocyte death postnatally, unsynapsed chromosome will trigger the DNA damage checkpoint. Through the understanding of this checkpoint, I was able to test if the transient inhibition of the DNA damage checkpoint protein (CHK2) prevents oocyte death. My finding that oocyte death was prevented, and fertility was preserved, provides evidence that chemically protecting oocyte from DNA damaging agents is a viable clinical approach. This result will hopefully translate into a treatment to delay ovarian failure. Taken together these results have implications on our current understanding of the prophase I checkpoint. TEACHING AS RESEARCH My interest in improving teaching strategies led me to research the qualitative outcome of using a novel teaching tool during the laboratory section of a histology course. I tested an interactive response system (IRS) as formative assessment tool. I found that IRS results in a positive experience, however my study was not able to detect quantitative difference on students’ grades was detected. Advisors/Committee Members: Schimenti, John C. (chair), Coonrod, Scott A. (committee member), Alani, Eric E. (committee member), Cohen, Paula (committee member).

Subjects/Keywords: teaching; Developmental biology; meiosis; Biology; Genetics; reproduction; DNA-damage checkpoint; fertility; gametogenesis

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APA (6^th Edition):

Rinaldi, V. D. S. G. (2017). Genetically dissecting the meiotic checkpoint active during prophase I in female mice. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/56716

Chicago Manual of Style (16^th Edition):

Rinaldi, Vera Da Silva Garcia. “Genetically dissecting the meiotic checkpoint active during prophase I in female mice.” 2017. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/56716.

MLA Handbook (7^th Edition):

Rinaldi, Vera Da Silva Garcia. “Genetically dissecting the meiotic checkpoint active during prophase I in female mice.” 2017. Web. 04 Mar 2021.

Vancouver:

Rinaldi VDSG. Genetically dissecting the meiotic checkpoint active during prophase I in female mice. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/56716.

Council of Science Editors:

Rinaldi VDSG. Genetically dissecting the meiotic checkpoint active during prophase I in female mice. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/56716

Cornell University

10. Ren, Yi. The Hedgehog Signaling Pathway In The Mouse Ovary.

Degree: PhD, Animal Science, 2012, Cornell University

URL: http://hdl.handle.net/1813/29526

► The hedgehog (HH) signaling pathway plays critical roles in the Drosophila ovary. Previous studies have provided basic information on the pattern of expression of genes… (more)

▼ The hedgehog (HH) signaling pathway plays critical roles in the Drosophila ovary. Previous studies have provided basic information on the pattern of expression of genes within the HH signaling pathway in the mouse ovary and on potential effects of HH signaling on cultured ovarian cells. An in vivo approach with transgenic mice is necessary to determine the function of HH signaling. The studies in this dissertation used the Amhr2cre/+SmoM2 transgenic mouse line to investigate phenotypes associated with over-activation of hedgehog signaling in the ovary. Results of these studies determined that HH signaling can influence ovarian follicle development. Female Amhr2cre/+SmoM2 mice are infertile. Although mutant mice had developmental defects in the Mullerian duct, the primary cause of infertility was the failure of ovulation based on the fact that oocytes were trapped in the follicles of superovulated mice. No difference in HH signaling activity was detected between controls and mutants around the time of ovulation. Cumulus expansion was suboptimal but could not explain the complete loss of fertility in the mutants. Luteinization occurred and generated normal levels of progesterone in plasma, although there was a delay in corpus luteum (CL) formation. The major phenotype in the ovaries of mutant mice was reduced mRNA levels of genes typical of smooth muscle in the thecal-interstitial compartment and reduced expression of smooth muscle actin (SMA) associated with blood vessels in the theca, indicating that the thecal vasculature failed to mature. Failure of vascular maturation was most likely the leading cause of anovulation in Amhr2cre/+SmoM2 mutant mice. Vascular maturation failed to occur in the ovaries of mutant mice beginning at the primary stage of follicle development. The SmoM2-yellow fluorescent protein (YFP) fusion gene was expressed in the neonatal ovaries of mutant mice and HH signaling activity was elevated in mutants compared to controls around the time of birth. The vascular network in the cortex of ovaries on days 2 and 4 was of higher density in mutant mice compared to controls. Microarray analyses identified elevated mRNA levels of genes involved in vascular development, particularly genes involved in the formation of vascular networks and in the interaction between endothelial and vascular mesenchymal cells. HH signaling was over-active around the time of birth and may have altered development of the thecal vasculature, possibly leading to the lack of vascular maturation in follicles throughout life. Around the time of birth, levels of mRNA for genes involved in steroid production were elevated in the ovaries of mutant mice compared to controls. Some of these genes are normally expressed in the fetal adrenal gland, such as Cyp17a, Cyp21a, Cyp11b and Shh. Immunohistochemistry of CYP17A, CYP21A and SHH confirmed the expression of these genes in the ovaries of mutant mice but not controls, indicating the presence of adrenal-like cells in the ovaries of mutant mice around the time of birth. This is possibly… Advisors/Committee Members: Quirk, Susan Mary (chair), Coonrod, Scott A. (committee member), Schimenti, John C. (committee member), Wolfner, Mariana Federica (committee member).

Subjects/Keywords: hedgehog signaling; ovary; development

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ren, Y. (2012). The Hedgehog Signaling Pathway In The Mouse Ovary. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/29526

Chicago Manual of Style (16^th Edition):

Ren, Yi. “The Hedgehog Signaling Pathway In The Mouse Ovary.” 2012. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/29526.

MLA Handbook (7^th Edition):

Ren, Yi. “The Hedgehog Signaling Pathway In The Mouse Ovary.” 2012. Web. 04 Mar 2021.

Vancouver:

Ren Y. The Hedgehog Signaling Pathway In The Mouse Ovary. [Internet] [Doctoral dissertation]. Cornell University; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/29526.

Council of Science Editors:

Ren Y. The Hedgehog Signaling Pathway In The Mouse Ovary. [Doctoral Dissertation]. Cornell University; 2012. Available from: http://hdl.handle.net/1813/29526

Cornell University

11. Ledet, Melissa McDowell. The Mammary Gland in Health and Disease.

Degree: PhD, Biomedical and Biological Sciences, 2019, Cornell University

URL: http://hdl.handle.net/1813/67458

► The mammary gland is a conserved, defining feature among mammals; however, there is much variation between species in both healthy functions, such as lactation, and… (more)

▼ The mammary gland is a conserved, defining feature among mammals; however, there is much variation between species in both healthy functions, such as lactation, and diseases, such as mammary cancer and mastitis. Species such as the cow, for example, are expert lactators, while lactation insufficiency remains a problem for many women. Mammary cancer is common in species such as humans, dogs and cats, but is rare in other species such as horses, cows and pigs. The majority of this work focuses on mammary stem/progenitor (MaSC) cells as these are the cells thought to drive lactation and to be at least partly responsible for mammary cancer development. These cells have been successfully isolated and characterized in mice, humans, and cows; however, these methods use species-specific antibodies and thus cannot be broadly applied across species. We first describe a novel method for isolating and characterizing MaSC from many different species in an antibody-independent manner. We then describe two projects that use this method for a comparative species approach to define possible underlying mechanisms behind mammary cancer resistance. In the second project we discovered that the secretome of equine MaSC kills a subset of human breast cancer cells, establishing the potential therapeutic effects of the MaSC secretome. With this in mind, we focused on the other primary disease of the mammary gland: mastitis, an inflammatory disease most commonly caused by bacterial infections. We found that the secretome of bovine MaSC repairs epithelial and endothelial cell damage and contains antimicrobial peptides, making it a good option for complementary mastitis therapy. In our final project, we once again demonstrate the advantages of using a comparative species approach to identify potential treatments for canine and feline mammary cancer, modeled after what has previously been described for breast cancer in humans. Collectively, this work denotes two potential mechanisms for cancer resistance in domestic species and highlights the potential therapeutic benefits of the MaSC secretome. Advisors/Committee Members: Van de Walle, Gerlinde (chair), Weiss, Robert S. (committee member), Coonrod, Scott A. (committee member), Kurpios, Natasza (committee member).

Subjects/Keywords: Cellular biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ledet, M. M. (2019). The Mammary Gland in Health and Disease. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/67458

Chicago Manual of Style (16^th Edition):

Ledet, Melissa McDowell. “The Mammary Gland in Health and Disease.” 2019. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/67458.

MLA Handbook (7^th Edition):

Ledet, Melissa McDowell. “The Mammary Gland in Health and Disease.” 2019. Web. 04 Mar 2021.

Vancouver:

Ledet MM. The Mammary Gland in Health and Disease. [Internet] [Doctoral dissertation]. Cornell University; 2019. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/67458.

Council of Science Editors:

Ledet MM. The Mammary Gland in Health and Disease. [Doctoral Dissertation]. Cornell University; 2019. Available from: http://hdl.handle.net/1813/67458

Cornell University

12. McElwee, John. Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36093

► Breast cancer is the most frequently diagnosed cancer in women, with over 1 million new cases in the world each year. Recently, in addition to… (more)

▼ Breast cancer is the most frequently diagnosed cancer in women, with over 1 million new cases in the world each year. Recently, in addition to genetic mutations, numerous studies have found that epigenetics plays a direct role in the etiology of breast cancer. The PADIs are a family of epigenetic enzymes that catalyze citrullination, with previous work in our lab showing that PADIs can convert both protein and histone arginine to citrulline, leading to the disruption of protein-protein interactions, as well as direct transcriptional downregulation. Previous research has suggested a potential oncogenic role for PADI2 in breast cancer, though no formal analysis existed. The studies herein investigate the potential role of PADI2 as a novel oncogene and therapeutic target in the treatment of breast cancer in vitro and in vivo. First, using an in vitro model of breast cancer progression (MCF10AT), we show that PADI2 is upregulated upon the malignant transformation of cells, especially in MCF10DCIS cells, which recapitulate the highly invasive comedo-like ductal carcinoma in situ (DCIS) tumors seen in humans. Secondly, using RNA-seq, we show that PADI2 is highly correlated with HER2/ERBB2 overexpression across 57 breast cancer cell lines. We concluded this study by validating the use of our first-generation PADI inhibitor, Cl-amidine, as a therapeutic agent for the treatment of breast cancer both in vitro and in vivo. Following this, we further investigated the functional relationship between PADI2 and HER2 expression. Interestingly, PADI2 appears to function both upstream and downstream of HER2, potentially indicating a role in an oncogenic positivefeedback loop with HER2. Previous evidence from our lab established that PADI2 functions as an ER co-activator via the citrullination of histone H3 arginine 26 (H3R26) at ER-target gene promoters. We show here that PADI2 can bind to the HER2 promoter and downstream ERE; thus, suggesting that the epigenetic regulation of HER2 gene expression by PADI2 occurs via similar mechanisms to ER-target genes. Moreover, we were able to validate our highly potent next-generation PADI inhibitor, BB-Cl-amidine, in the treatment of breast cancer cells in vitro. Lastly, using a mouse model of PADI2 overexpression (MMTV-FLAGPADI2), we found that 20% of mice developed skin lesions after five months. These tumors express high levels of transgenic human PADI2 and display markers of increased inflammation and invasiveness-EMT. Furthermore, a subset of these tumors showed via histopathological analysis to have undergone malignant progression to highly invasive squamous cell carcinomas. Collectively, these studies provide functional and mechanistic evidence establishing PADI2 as a potential novel oncogene and target for cancer therapy. Advisors/Committee Members: Coonrod, Scott A. (chair), Soloway, Paul (committee member), Schimenti, John C. (committee member), Lin, David M. (committee member).

Subjects/Keywords: Peptidylarginine deiminase; Cl-amidine; PADI2

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

McElwee, J. (2014). Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36093

Chicago Manual of Style (16^th Edition):

McElwee, John. “Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36093.

MLA Handbook (7^th Edition):

McElwee, John. “Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target.” 2014. Web. 04 Mar 2021.

Vancouver:

McElwee J. Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36093.

Council of Science Editors:

McElwee J. Identification Of Peptidylarginine Deiminase-2 (Padi2) As A Potential Oncogene And Therapeutic Target. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36093

Cornell University

13. Lu, Yen-Chun. COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING.

Degree: PhD, Biological and Environmental Engineering, 2018, Cornell University

URL: http://hdl.handle.net/1813/64956

► Three-dimensional (3D) cell culture has been broadly used to mimic the in-vivo microenvironment. Compared with traditional methods for 3D culture in which cells are embedded… (more)

▼ Three-dimensional (3D) cell culture has been broadly used to mimic the in-vivo microenvironment. Compared with traditional methods for 3D culture in which cells are embedded within a bulk extracellular matrix, compartmentalized hydrogel microcapsules, such as those with a core-shell structure, provide better mass transfer due to higher surface-to-volume ratio. In addition, such capsules can be fabricated by a multi-fluidic electrostatic co-spraying technique at a high production rate (> 10,000 capsules/min) with nearly monodisperse spherical shape and tunable size, and they can be cultured in suspension for scalable biomanufacturing applications. In this dissertation, I first proved the feasibility of producing complex microcapsules by using the electrostatic co-spraying technique. Then, I demonstrated the applications of core-shell decoupled microcapsules in large-scale production of microtissues, for example, tumoroids, hepatocyte/stromal aggregates, and small intestinal organoids, all of which could be used for applications such as drug screening and disease modeling. Lastly and most importantly, I used the core-shell microcapsules to study the effect of physical confinement on mammary tumorigenesis. It has been known that physical microenvironment, including matrix stiffness, plays an important role in cancer initiation and progression. In this work, I discovered that confinement – a new physical parameter unlike stiffness - can also induce malignant transformation in mammary epithelial cells. I found that MCF10A cells, a benign mammary cell line that forms growth-arrested polarized acini in Matrigel, transforms into cancer-like cells within the same Matrigel material following confinement in alginate shell hydrogel microcapsules. The confined cells exhibited a range of tumor-like behaviors, including uncontrolled cellular growth and invasion. Additionally, 4-6 weeks after transplantation into the mammary fad pads of immunocompromised mice, the confined cells formed large palpable masses that exhibited histological features similar to that of carcinomas. Taken together, my findings not only suggest confinement as a previously unrecognized mechanism for malignancy induction in mammary epithelial cells but also provide a new, microcapsule-based, high throughput platform in therapeutic development for breast cancer. Advisors/Committee Members: Ma, Minglin (chair), Fischbach, Claudia (committee member), Coonrod, Scott A. (committee member).

Subjects/Keywords: Chemical engineering; Biophysics; Breast cancer; Biomedical engineering; 3D Cell Culture; cell encapsulation; biomanufacturing; hydrogel

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lu, Y. (2018). COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/64956

Chicago Manual of Style (16^th Edition):

Lu, Yen-Chun. “COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING.” 2018. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/64956.

MLA Handbook (7^th Edition):

Lu, Yen-Chun. “COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING.” 2018. Web. 04 Mar 2021.

Vancouver:

Lu Y. COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/64956.

Council of Science Editors:

Lu Y. COMPARTMENTALIZED HYDROGEL MICROCAPSULES AND THEIR APPLICATIONS IN MICROTISSUE ENGINEERING. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64956

Open Access Theses and Dissertations