+publisher:"Rutgers University" +contributor:("Fan, Huizhou")

Rutgers University

1. Cortese, Jillian Nicole, 1992-. Identification and characterization of Mycobacterium tuberculosis VapC50 toxin.

Degree: MS, Microbiology and Molecular Genetics, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/52140/

► Tuberculosis is a major health concern for a large portion of the world’s population, despite its reputation as an ancient disease. One of the main… (more)

▼ Tuberculosis is a major health concern for a large portion of the world’s population, despite its reputation as an ancient disease. One of the main concerns is the development of latent tuberculosis, where Mycobacterium tuberculosis remains dormant for months or years before being reactivated. Among all bacteria studied thus far, M. tuberculosis has the most toxin-antitoxin (TA) systems, with 88 discovered so far, 50 of which are VapBC systems. It is thought that these TA systems may aid the bacteria in establishing and/or maintaining M. tuberculosis cells in this nonreplicating persistent state characteristic of latent tuberculosis. TA systems have been shown to respond to various stressors that bacteria may encounter, including hypoxia, host immune responses, and nutrient starvation. VapBC, which is a type II TA system, is composed of an unstable antitoxin protein, VapB, that binds to the stable PIN domain-containing VapC toxin protein and blocks its activity. The goals of this M.S. research project were to isolate, characterize and identify the RNA target of one M. tuberculosis VapC toxin, VapC50. To this end, we first discovered that the annotated VapC50 gene was incorrect, and instead identified and cloned the correct VapC50 toxin. Expression of VapC50 in Escherichia coli resulted in growth inhibition, however, expression Mycobacterium smegmatis did not inhibit growth. Purification of recombinant VapC50 protein proved to be a difficult task and was only successful after the third trial, when the protein was expressed at 30C instead of 37C. Since most of the analysis of VapC toxins published highlight their tRNA cleaving ability, purified VapC50 was used to conduct a tRNA cleavage assay with all 45 tRNAs in M. tuberculosis. None of the 45 tRNAs were cleaved by VapC50, suggesting that this toxin may instead have a novel physiological role in this pathogen. Advisors/Committee Members: Boyd, Jeff (chair), Woychik, Nancy (internal member), Fan, Huizhou (internal member).

Subjects/Keywords: Mycobacterium tuberculosis

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APA (6^th Edition):

Cortese, Jillian Nicole, 1. (2017). Identification and characterization of Mycobacterium tuberculosis VapC50 toxin. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/52140/

Chicago Manual of Style (16^th Edition):

Cortese, Jillian Nicole, 1992-. “Identification and characterization of Mycobacterium tuberculosis VapC50 toxin.” 2017. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/52140/.

MLA Handbook (7^th Edition):

Cortese, Jillian Nicole, 1992-. “Identification and characterization of Mycobacterium tuberculosis VapC50 toxin.” 2017. Web. 17 Apr 2021.

Vancouver:

Cortese, Jillian Nicole 1. Identification and characterization of Mycobacterium tuberculosis VapC50 toxin. [Internet] [Masters thesis]. Rutgers University; 2017. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/52140/.

Council of Science Editors:

Cortese, Jillian Nicole 1. Identification and characterization of Mycobacterium tuberculosis VapC50 toxin. [Masters Thesis]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/52140/

Rutgers University

2. Russnak, Timothy, 1986-. Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency.

Degree: PhD, Microbiology and Molecular Genetics, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/56113/

►

HIV is a worldwide epidemic, remaining the ever-present specter among all matters regarding blood or other bodily fluids, such as sexual intercourse, healthcare, blood transfusions,… (more)

▼

HIV is a worldwide epidemic, remaining the ever-present specter among all matters regarding blood or other bodily fluids, such as sexual intercourse, healthcare, blood transfusions, or even surgery, particularly in resource-poor areas. While antiretroviral drug therapy is highly successful in suppressing the virus and preventing transmission, it cannot cure the infection due to latency – the ability of HIV to go into a silent state within cells; once drug therapy is stopped, reactivating latent virus will cause a surge of the viral load within days or weeks. Current drug therapies do not act on this latent reservoir, necessitating lifelong adherence to medication, which is both extremely costly and comes with negative side effects. The mainstay of research into HIV latency deals with teasing apart the mechanisms involved in establishing and maintaining latency, in the hopes of finding drug compounds which can efficiently reverse latency and thus purge the body of hidden HIV. In searching for cellular pathways involved in latency, our lab has employed a genome-wide negative-selection screen, which indicated that the ubiquitin-proteasome system plays a role in maintaining latency. This led us to discover that proteasome inhibitors act as bifunctional antagonists of HIV, both reversing the latent state and reducing infectivity of virions. We went on to identify the specific ubiquitin-proteasome pathway that is involved in maintaining latency. We then investigated the activity of a small-molecule inhibitor of one component of the ubiquitin-proteasome system, showing its ability to reactivate latent HIV in both a primary cell model and in cells taken from aviremic HIV+ patients. These results are a proof-of-concept that inhibition of a specific ubiquitin-proteasome pathway can allow for specific reversal of HIV latency.

Advisors/Committee Members: Gelinas, Celine (chair), Walworth, Nancy (internal member), Roth, Monica (internal member), Fan, Huizhou (outside member), School of Graduate Studies.

Subjects/Keywords: HIV infections – Treatment

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APA (6^th Edition):

Russnak, Timothy, 1. (2018). Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/56113/

Chicago Manual of Style (16^th Edition):

Russnak, Timothy, 1986-. “Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/56113/.

MLA Handbook (7^th Edition):

Russnak, Timothy, 1986-. “Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency.” 2018. Web. 17 Apr 2021.

Vancouver:

Russnak, Timothy 1. Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/56113/.

Council of Science Editors:

Russnak, Timothy 1. Investigating the ubiquitin-proteasome system for targeted reversal of HIV-1 latency. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/56113/

Rutgers University

3. Al-Asadi, Amer, 1980-. Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism.

Degree: PhD, Physiology and Integrative Biology, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/57463/

►

Alteration of glucose metabolism is a unique feature for a majority of cancers. Cancer cells exhibit aerobic glycolysis also known as the Warburg effect even… (more)

▼

Alteration of glucose metabolism is a unique feature for a majority of cancers. Cancer cells exhibit aerobic glycolysis also known as the Warburg effect even in the presence of oxygen. During this mode of glucose metabolism, a majority of pyruvate is converted to lactate rather than entering mitochondria for complete oxidation through oxidative phosphorylation. The functional importance of aerobic glycolysis to cancer cells is becoming clear. Basically, aerobic glycolysis prevents pyruvate from complete oxidation inside mitochondria. This shunts glycolytic intermediates to pathways for synthesis of NADPH and building blocks of macromolecules, which are required for cell growth and proliferation. Pyruvate entrance into mitochondria is enhanced via mitochondrial uncoupling, a process that permits proton influx through the mitochondrial inner membrane without generating ATP. Consequently, mitochondrial uncoupling stimulates “idle ” oxidation of acetyl-CoA, leading to complete oxidation of glucose. Thus, we hypothesize that safe mitochondrial uncouplers could be strong anticancer agents to inhibit the anabolic role of the Warburg effect. We utilized two approaches to address this hypothesis. First, we tested two mitochondrial uncoupler compounds, NEN (niclosamide ethanolamine) and oxyclozanide, on their metabolic effects and anti-cancer activities. We used metabolomics NMR to study the effect of mitochondrial uncoupling on glucose metabolism in colon cancer MC38 cells. We further examined the anti-cancer effect of NEN and oxyclozanide in cell models and hepatic metastasis of colon cancer in animal model. We found that mitochondrial uncoupling stimulates pyruvate influx to mitochondria and decreases various anabolic pathway activities. Moreover, mitochondrial uncouplers arrest cell cycle progression, inhibit cell proliferation and reduce clonogenicity. Furthermore, oral treatment with mitochondrial uncouplers diminishes hepatic metastasis of colon cancer cells transplanted intrasplenically in mice. Second, we tested MB1-47, a novel mitochondrial uncoupler with good pharmacokinetic and toxicological profiles, in preventing and treating pancreatic cancer. Our study demonstrated that MB1-47 is effective in inducing mitochondrial uncoupling in pancreatic cancer cells and inhibits the proliferation of multiple murine and human pancreatic cancer cell lines. In the tumor xenograft mouse models, oral MB1-47 treatment exhibits excellent activity in preventing tumor growth and metastasis. Our data support a unique approach for targeting cancer cell metabolism for cancer prevention and treatment and identified prototype compounds for this mechanism.

Advisors/Committee Members: Fondell, Joseph (chair), Fan, Huizhou (internal member), Jin, Shengkan (internal member), Banerjee, Debabrata (outside member), School of Graduate Studies.

Subjects/Keywords: Cancer cells; Pancreas – Cancer

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APA (6^th Edition):

Al-Asadi, Amer, 1. (2018). Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/57463/

Chicago Manual of Style (16^th Edition):

Al-Asadi, Amer, 1980-. “Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/57463/.

MLA Handbook (7^th Edition):

Al-Asadi, Amer, 1980-. “Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism.” 2018. Web. 17 Apr 2021.

Vancouver:

Al-Asadi, Amer 1. Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57463/.

Council of Science Editors:

Al-Asadi, Amer 1. Preventing and treating hepatic metastases of colon and pancreatic cancers by targeting cancer cell metabolism. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57463/

Rutgers University

4. Desai, Malhar, 1993-. Cellular and molecular studies of the human pathogen Chlamydia trachomatis.

Degree: MS, Physiology and Integrative Biology, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/57530/

► Chlamydia trachomatis is a gram-negative bacterium and human pathogen responsible for the most prevalent sexually transmitted infection in the world. Epidemiologic studies indicate that the… (more)

▼ Chlamydia trachomatis is a gram-negative bacterium and human pathogen responsible for the most prevalent sexually transmitted infection in the world. Epidemiologic studies indicate that the number of new C. trachomatis infections reported in the US likely approaches as much as 0.5 per a population of 100 every year. This, when paired with the fact that all current forms of treatment for C. trachomatis infections have unintended side effects including harm to gut and vaginal microbiota, has compelled many biologists to look to further research on C. trachomatis in hopes of developing new antichlamydial agents. In this thesis, I review several projects involving C. trachomatis that provide a framework for understanding both the growth and the developmental cycle of C. trachomatis. Through a mixture of in-depth proteomics, transcriptomics, and in vivo assays, I present five overall conclusions: (i) Lactobacilli-derived lactic acid, at concentrations that are physiological in the cervicovaginal lumen, can disrupt the outer membrane complex of and inactivate C. trachomatis; (ii) immunoprecipitation of chlamydial elementary bodies (EBs) using an antibody against a cell-surface protein of C. trachomatis is not an efficient method for purifying the bacterium; (iii) the growth of bacterial species that share significant sequence identity may not always be similar in media containing the same sera; (iv) the Chlamydia-specific transcription factor, GrgA, can stimulate transcription from promoters recognized by two different σ factors of C. trachomatis and has differential affinity for these two σ factors; (v) GrgA may associate with multiple subunits of the chlamydial RNA polymerase and, considering its role in transcription regulation and its specificity, may prove to be an excellent target for novel therapeutic agents against C. trachomatis. Advisors/Committee Members: Desai, Malhar, 1993- (author), Fondell, Joseph (chair), Fan, Huizhou (internal member), Millonig, James (internal member), Walworth, Nancy (internal member), School of Graduate Studies.

Subjects/Keywords: Chlamydia trachomatis

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APA (6^th Edition):

Desai, Malhar, 1. (2018). Cellular and molecular studies of the human pathogen Chlamydia trachomatis. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/57530/

Chicago Manual of Style (16^th Edition):

Desai, Malhar, 1993-. “Cellular and molecular studies of the human pathogen Chlamydia trachomatis.” 2018. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/57530/.

MLA Handbook (7^th Edition):

Desai, Malhar, 1993-. “Cellular and molecular studies of the human pathogen Chlamydia trachomatis.” 2018. Web. 17 Apr 2021.

Vancouver:

Desai, Malhar 1. Cellular and molecular studies of the human pathogen Chlamydia trachomatis. [Internet] [Masters thesis]. Rutgers University; 2018. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57530/.

Council of Science Editors:

Desai, Malhar 1. Cellular and molecular studies of the human pathogen Chlamydia trachomatis. [Masters Thesis]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57530/

Rutgers University

5. Ibironke, Olufunmilola, 1978-. Air pollution particulate matter effects on adaptive human antimycobacterial immunity.

Degree: PhD, Physiology and Integrative Biology, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/

►

Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies provide evidence that indoor (household) air pollution increases the… (more)

▼

Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies provide evidence that indoor (household) air pollution increases the risk of new infections with Mycobacterium tuberculosis (M.tb) and development of TB. The mechanisms by which exposure to ‘real-world’-derived urban ambient (outdoor) particulate matter (PM) adversely affects M.tb-specific human host T cell functions in vitro have not been studied. In this thesis research, we explored the effects of air pollution PM2.5 (≤2.5 µm, median aerodynamic diameter) collected in the Iztapalapa municipality of Mexico City on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). Upon in vitro exposure, PM2.5 was observed in clusters of free, non-membrane-bound particle agglomerates in the cytoplasm of the exposed cells. PM2.5 exposure did not alter the expression of activation marker CD54 on antigen presenting cells (APC), however, increased the expression of CD80 while decreasing the constitutively expressed CD86 on monocytes during M.tb infection. Exposure to PM2.5 of M.tb-infected PBMC led to an increase of intracellular growth of M.tb, indicating loss of M.tb growth controlling capacity of the cells that occurred independent of PM-induced changes to PBMC viability. Exposure of PBMC to PM2.5 also altered M.tb-specific T-cell immune responses by (1) decreasing the surface expression of early T cell activation markers CD69 and CD25 on T cells, (2) inhibiting the intracellular expression of both interferon-gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α), and (3) decreasing the expression of T-box transcription factor TBX21 (T-bet) known to directly regulate the expression of IFN-γ. In contrast, PM2.5 exposure increased the intracellular expression of the anti-inflammatory cytokine interleukin 10 (IL-10) and the phosphorylation of transcription factor STAT-3. The observed PM2.5-induced decrease in the expression of human pro-inflammatory M.tb-specific T cell cytokines, and the loss of intracellular M.tb growth control are associated with the increased expression of anti-inflammatory cytokine IL-10 and decreased expression of transcription factor T-bet. Together, the findings of this study suggest that the PM2.5-induced decrease of critical human host immune cell functions against M.tb represents the mechanistic correlate of epidemiological observations that outdoor air pollution exposure is associated with increases in the incidence of TB and with adversely modified TB treatment outcomes.

Advisors/Committee Members: Fan, Huizhou (chair), Langer, Jerome (internal member), Haimovich, Beatrice (internal member), Medina, Daniel (internal member), School of Graduate Studies.

Subjects/Keywords: Air – Pollution; Tuberculosis

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APA (6^th Edition):

Ibironke, Olufunmilola, 1. (2019). Air pollution particulate matter effects on adaptive human antimycobacterial immunity. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60169/

Chicago Manual of Style (16^th Edition):

Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.

MLA Handbook (7^th Edition):

Ibironke, Olufunmilola, 1978-. “Air pollution particulate matter effects on adaptive human antimycobacterial immunity.” 2019. Web. 17 Apr 2021.

Vancouver:

Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/.

Council of Science Editors:

Ibironke, Olufunmilola 1. Air pollution particulate matter effects on adaptive human antimycobacterial immunity. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60169/

Rutgers University

6. Lou, Liping, 1982-. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.

Degree: PhD, TRPM7, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

► The TRPM7 (Transient Receptor Potential Melastatin 7) ion channel is a unique member of the TRP channel family, possessing its own functional kinase domain at… (more)

▼ The TRPM7 (Transient Receptor Potential Melastatin 7) ion channel is a unique member of the TRP channel family, possessing its own functional kinase domain at its COOH-terminus. As a Mg2+-permeable ion channel, TRPM7 has frequently been linked to the regulation of magnesium reabsorption at both the cellular and whole-body level. Mg2+ plays a pivotal role in human health and disease, and therefore, its level in the body has to be tightly regulated via ion channels and transporters in the functional unit of the kidney, the nephron. TRPM6, the close homolog of TRPM7, has been identified to be the major player regulating Mg2+ reabsorption in the distal convoluted tubule of the nephron. A major gap in our knowledge of TRPM7 is whether the channel is involved in regulating magnesium homeostasis in the proximal tubule of the nephron, where TRPM7 is highly expressed. To gain insight into the function of TRPM7 in the proximal tubule, we generated two conditional strains of proximal tubule-specific trpm7 KO mice, using PEPCK-Cre and gGT-Cre mice. The Mg2+ status of the proximal tubule trpm7 knockout mice was assessed but we did not obtain any evidence that the Mg2+ homeostasis was disrupted in the animals, indicating TRPM7 does not play a major role in proximal tubule to regulate whole-body magnesium homeostasis. However, large cavities and reduced cortical layers in the kidney anatomy of some female gGT-Cre KO trpm7 mice were observed. TRPM7 has previously been implicated in the regulation of cell-cell adhesion, having recently been found to contribute to the intercellular junction formation in the bladder urothelium. We performed transmission electron microscopy (TEM) analysis of the tissue slides obtained from the cortex of the kidneys from gGT-Cre KO trpm7 mice and found that tubule epithelial cells from the trpm7 KO mice had more impaired intercellular junctions than that from the control mice. We next investigated the relationship between TRPM7 and cell-cell adhesion process, employing the proximal tubule epithelial cell line, opossum kidney (OK) cells, as a cellular model. Mass spectrometric analysis uncovered that TRPM7 interacted with a cell adhesion protein called plakoglobin. Using immunocytochemical assays, we discovered that TRPM7 co-localized with plakoglobin and another adherens junction protein called E-cadherin. Application of the TRPM7’s channel blocker NS8593 to OK cells reduced E-cadherin expression and localization to adherens junctions. Taken together, these data suggest that TRPM7 is involved in controlling cell-cell adhesion in proximal tubule epithelial cells. In this study, we also explored the mechanism(s) by which TRPM7’s cellular localization is regulated. Using biochemical and immunocytochemical approaches, we identified a regulatory site at the COOH-terminus of TRPM7, the channel’s PDZ-binding motif, through which the localization of TRPM7 in OK cells could be regulated. Deletion of the channel’s PDZ-binding motif shortened the retention time of the mutant TRPM7 (TRPM7ΔPDZ) at adherens… Advisors/Committee Members: Runnels, Loren W (chair), Ryazanov, Alexey G (internal member), Sesti, Federico (internal member), Fan, Huizhou (outside member), School of Graduate Studies.

Subjects/Keywords: Pharmacology, Cellular and Molecular; TRP channels

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APA (6^th Edition):

Lou, Liping, 1. (2019). Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

Chicago Manual of Style (16^th Edition):

Lou, Liping, 1982-. “Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60852/.

MLA Handbook (7^th Edition):

Lou, Liping, 1982-. “Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.” 2019. Web. 17 Apr 2021.

Vancouver:

Lou, Liping 1. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/.

Council of Science Editors:

Lou, Liping 1. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

Rutgers University

7. Nandankar, Nimisha, 1997-. Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice.

Degree: MS, Endocrinology, 2020, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64353/

► Kisspeptin (encoded by Kiss1), a neuropeptide critically involved in neuroendocrine regulation of reproduction, is primarily synthesized in two discrete hypothalamic nuclei: the anteroventral periventricular nucleus… (more)

▼ Kisspeptin (encoded by Kiss1), a neuropeptide critically involved in neuroendocrine regulation of reproduction, is primarily synthesized in two discrete hypothalamic nuclei: the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC). Current data indicates that AVPV Kiss1 is important for the pre-ovulatory luteinizing hormone (LH) surge unique to females as well as estrogen-induced positive feedback control of GnRH and LH. In contrast, ARC Kiss1 neurons, which largely co-express the neuropeptides NKB and dynorphin (collectively known as KNDy neurons), are thought to be the major regulators of pulsatile release of GnRH and LH, and mediate estrogen- induced negative feedback control of both GnRH and LH. Previous studies have not definitively separated the specific roles of Kiss1 in the AVPV versus KNDy-ARC neurons in the downstream control of GnRH and LH release. Therefore, we generated a Pdyn-Cre/Kiss1fl/fl (KO) mouse model to target Kiss1 in KNDy neurons to differentiate KNDy neuron-specific function from AVPV Kiss1 function in the maturation and maintenance of the reproductive axis. qRT-PCR data documented the loss of Kiss1 expression in the mediobasal hypothalamus (containing ARC) compared to controls, whereas Kiss1 in the preoptic area (containing AVPV) was similar in both KO and controls. Immunofluorescent staining for kisspeptin confirmed the loss of Kiss1 specifically in the ARC of KO mice. Although no changes in pubertal body weight gain or pubertal onset were observed in KO animals, KO females exhibited disrupted estrous cyclicity in adulthood. Interestingly, KO female mice had disrupted estrous cycles presenting with persistent diestrus and a small vaginal opening. We tested the hypothesis that ARC KNDy neurons are necessary for generating and maintaining episodic LH pulsatile release by serial collection of whole blood and measuring LH. KO female mice exhibited significantly fewer LH pulses in a 3-hour timespan compared to controls, suggesting that KNDy neurons were functionally compromised. These observations indicate the central role of KNDy neurons in the regulation of GnRH/LH pulsatility and estrous cyclicity. The functional effects of disrupted estrous cyclicity and slowed LH pulsatility observed in KO females result in arrested folliculogenesis and infertility. Future experiments will determine whether ARC Kiss1 deletion disrupts the KNDy- driven negative feedback response of LH to gonadectomy, as well as address potential sex differences in ARC Kiss1-mediated negative feedback control of LH release. Advisors/Committee Members: Radovick, Sally (chair), Fan, Huizhou (internal member), Babwah, Andy V (outside member), School of Graduate Studies.

Subjects/Keywords: Physiology and Integrative Biology

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APA (6^th Edition):

Nandankar, Nimisha, 1. (2020). Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64353/

Chicago Manual of Style (16^th Edition):

Nandankar, Nimisha, 1997-. “Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice.” 2020. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/64353/.

MLA Handbook (7^th Edition):

Nandankar, Nimisha, 1997-. “Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice.” 2020. Web. 17 Apr 2021.

Vancouver:

Nandankar, Nimisha 1. Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice. [Internet] [Masters thesis]. Rutgers University; 2020. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64353/.

Council of Science Editors:

Nandankar, Nimisha 1. Deletion of arcuate nucleus-specific Kiss1 disrupts estrous cyclicity and LH pulsatility in female mice. [Masters Thesis]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64353/

8. Royal, Remi, 1989-. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.

Degree: MS, Physiology and Integrative Biology, 2013, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828

► The Kv2.1 (KCNB1) channel is expressed in the cortex and hippocampus. Interaction between cysteine residues of the kv2.1 channel plays a role in the formation… (more)

Subjects/Keywords: Potassium channels; Potassium – Oxidation

10 more images…

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APA (6^th Edition):

Royal, Remi, 1. (2013). Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. (Masters Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828

Chicago Manual of Style (16^th Edition):

Royal, Remi, 1989-. “Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.” 2013. Masters Thesis, Rutgers University. Accessed April 17, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828.

MLA Handbook (7^th Edition):

Royal, Remi, 1989-. “Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.” 2013. Web. 17 Apr 2021.

Vancouver:

Royal, Remi 1. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. [Internet] [Masters thesis]. Rutgers University; 2013. [cited 2021 Apr 17]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828.

Council of Science Editors:

Royal, Remi 1. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. [Masters Thesis]. Rutgers University; 2013. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828

9. Mahdi, Amar Hekmat, 1977-. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.

Degree: PhD, Physiology and Integrative Biology, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/53735/

► Homologous recombination (HR) is the only error-free pathway for the repair of DNA double strand breaks (DSBs). BRCA1 and BRCA2, the two major breast cancer… (more)

▼ Homologous recombination (HR) is the only error-free pathway for the repair of DNA double strand breaks (DSBs). BRCA1 and BRCA2, the two major breast cancer suppressor proteins, play essential roles in HR-mediated repair of DSBs by promoting the recruitment of RAD51, the recombination enzyme, to DNA damage sites for the initiation of HR. PALB2 (partner and localizer of BRCA2) plays a key role in this pathway by acting as a chromatin adaptor for BRCA2 and a linker between BRCA1 and BRCA2. Like BRCA1 and BRCA2, PALB2 is a tumor suppressor gene itself. Germline, heterozygous mutations in the gene increase the risk of breast, ovarian and pancreatic cancers. However, its mechanism is not fully understood. To investigate the in vivo role of the PALB2-BRCA1 interaction, we previously generated a Palb2 knockin mouse strain that contains a mutation that disrupts BRCA1 binding. This mouse model also allows us to bypass the embryonic lethality of the Palb2 KO mice. In this study, we hypothesized that the direct communication between the two proteins is critical for proper DNA damage repair and response in vivo and for suppression of tumorigenesis. Indeed, both immunohistochemistry (IHC) and immunofluorescence (IF) demonstrated that different tissues of the Palb2 mutant mice have higher levels of endogenous DSBs (gamma H2AX foci) and slower DSB repair kinetics after ionizing radiation (IR). Yet, mutant cells were more resistant to cell death. When aged under normal conditions, mutant mice showed increased tumor incidence in multiple tissues, particularly in the liver. Upon challenging of these mutant mice with carcinogen administration or gamma irradiation, they showed accelerated tumor development as compared with wild-type (wt) mice. When crossed with Trp53 mutant mice, the compound mutant mice showed greatly accelerated development of tumors typically associated with mutations in p53, i.e. thymic lymphoma, osteosarcoma and soft tissue sarcoma, etc. Whole exome sequencing (WES) of the tumors arising from Palb2m/m;Trp53+/- mice revealed loss of the wt allele of Trp53 in the majority of tumors, with at least some tumors showing focal deletions of the wt gene, suggesting that disruption of BRCA1-PALB2/BRCA2 axis promotes regional genomic deletions that may lead to loss of other tumor suppressors such as p53. These results underscore the importance of the BRCA1-PALB2/BRCA2 pathway for tumor suppression and suggest a potentially novel mechanism for BRCA/PALB2-mediated tumor suppression, which is by preventing Trp53/TP53 loss of heterozygosity (LOH), which would allow for tumor development. Finally, we also found constitutively elevated levels of reactive oxygen species (ROS) and activation of NF-kB, a redox sensitive transcription factor, in tissues and cells from the mutant mice. Given its established pro-survival function, NF-kB activation could explain why cells in the mutant mice are resistant to apoptosis upon irradiation despite having increased and prolonged DNA damage. This finding also suggests that the NF-kB pathway… Advisors/Committee Members: Bunting, Samuel (chair), Fan, Huizhou (internal member), Xia, Bing (internal member), Chan, Chang (outside member).

Subjects/Keywords: Cancer – Prevention; Breast – Cancer

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APA (6^th Edition):

Mahdi, Amar Hekmat, 1. (2017). Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/53735/

Chicago Manual of Style (16^th Edition):

Mahdi, Amar Hekmat, 1977-. “Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.” 2017. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/53735/.

MLA Handbook (7^th Edition):

Mahdi, Amar Hekmat, 1977-. “Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.” 2017. Web. 17 Apr 2021.

Vancouver:

Mahdi, Amar Hekmat 1. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53735/.

Council of Science Editors:

Mahdi, Amar Hekmat 1. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53735/

Rutgers University

10. Al-Hraishawi, Haidar Khaioon, 1986-. Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels.

Degree: MS, Physiology and Integrative Biology, 2016, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/49903/

► This study is to compare primary hyperparathyroidism (PHPT) patients with different iPTH levels for serum calcium and other laboratory values. In this retrospective study, 212… (more)

▼ This study is to compare primary hyperparathyroidism (PHPT) patients with different iPTH levels for serum calcium and other laboratory values. In this retrospective study, 212 patients who presented at Robert Wood Johnson Hospital were assessed for metabolic and characteristic features of PHPT. Patients were divided into two groups according to their serum intact parathyroid hormone (iPTH) levels. Student t- tests were used to compare the two groups for differences in age, body mass index (BMI), adenoma weight, and laboratory test values which included serum calcium, iPTH, 25OHD, lipid panel, serum creatinine, ALP, and 24 hr. urinary calcium. Pearson`s correlation coefficient was used to assess the relationship. Of the 212 PHPT patients, 100 (17 males and 83 females) were classified as m-iPTH group (iPTH below 140 pg/ml), whereas 112 patients (25 males and 87 females) were classified as h-iPTH group (iPTH above 140 pg/ml). Higher-iPTH patients are younger than m-iPTH patients. No statistic significant differences in BMI, T-cholesterol and TG were found between the m-iPTH and h-iPTH groups. Higher- iPTH patients compared with m- iPTH, had slightly but significantly higher calcium, lower 25OHD, lower HDL, higher ALP, and very close to have higher adenoma weight. Additionally, we found iPTH was positive correlated with serum calcium, adenoma weight, and triglyceride (TG) levels, and negatively correlated with HDL and 25OHD. Intact PTH did not correlate with BMI and T- cholesterol levels. Furthermore, 24 hr. urinary calcium and serum ALP were positively associated with iPTH levels but not significantly (P = 0.08, P = 0.09) respectively. These correlations were independent of serum calcium and 25OHD levels except TG was dependent of reduced 25OHD, while serum ALP was dependent of calcium levels. These findings from our analysis consistent with previous studies suggesting iPTH levels correlated metabolic syndrome. Additionally, our results suggest that h- iPTH patients tend to be younger ones, with lower HDL, lower 25OHD, and higher ALP. While the underline mechanisms for these changes are unclear, we speculate that the elevated iPTH levels might decrease HDL directly or indirectly through increasing insulin resistance by weight gain, and increases ALP through PTH receptors on osteoblasts. This study supported our hypothesis that iPTH levels are an important factor to contribute in the management of PHPT patients. Intact PTH levels, lipid panel, 25OHD, ALP in addition to calcium levels might also need to be considered in the therapeutic decision for PHPT patients. Advisors/Committee Members: Fan, Huizhou (chair), Wang, Xiangbing (internal member), Haimovich, Beatrice (outside member).

Subjects/Keywords: Hyperparathyroidism

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

APA (6^th Edition):

Al-Hraishawi, Haidar Khaioon, 1. (2016). Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/49903/

Chicago Manual of Style (16^th Edition):

Al-Hraishawi, Haidar Khaioon, 1986-. “Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels.” 2016. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/49903/.

MLA Handbook (7^th Edition):

Al-Hraishawi, Haidar Khaioon, 1986-. “Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels.” 2016. Web. 17 Apr 2021.

Vancouver:

Al-Hraishawi, Haidar Khaioon 1. Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels. [Internet] [Masters thesis]. Rutgers University; 2016. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49903/.

Council of Science Editors:

Al-Hraishawi, Haidar Khaioon 1. Comparison of metabolic and characteristic features of primary hyperparathyroidism patients with different intact PTH levels. [Masters Thesis]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49903/

Rutgers University

11. Battaglia, Lauren, 1988-. Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency.

Degree: MA, Cell and Developmental Biology, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/41721/

► Chlamydia is the most common cause of sexually transmitted bacterial infection worldwide and it leads to severe complications for women who become infected. Following initial… (more)

▼ Chlamydia is the most common cause of sexually transmitted bacterial infection worldwide and it leads to severe complications for women who become infected. Following initial infection, the bacterial pathogen ascends from the lower genital tract to the upper genital tract leading to pelvic inflammation and scarring of inflamed tissue. The scarring can lead to ductal obstruction, causing retention of fluid in the upper genital tract and ovaries, termed hydrosalpinx. This inflammation due to Chlamydia infection can lead to infertility. Despite the commonality of the disease and its severe consequences, the molecular pathogenesis and mechanism of pelvic inflammation following Chlamydia infection has yet to be elucidated. We investigated the molecular pathogenesis and its relation to host autophagy here. The ATG5 gene is required for autophagy. Our lab has previously shown via mouse model that deletion of the ATG5 gene in myeloid cells results in a significant increase in upper genital tract inflammation following Chlamydia infection. To further investigate the role of autophagy in Chlamydia pathogenesis, mice with deleted ATG5 gene in epithelial cells were intravaginally infected with Chlamydia. The infection was monitored through weekly vaginal swabbing and calculation of Chlamydia bacterial titers from each swab. After Chlamydia infection cleared, the animals were sacrificed, upper genital tract pathology was observed and cytokine analysis was conducted on the vaginal swabs that were taken throughout the infection. The p62 autophagy protein acts as a scaffold to bring bacterial pathogen to autophagy machinery. In the current study, p62-deficient mice were obtained and infected with Chlamydia. Vaginal swabbing throughout Chlamydia infection allowed us to estimate bacterial titers and assay the host cytokine response to the infection, and finally the upper genital tracts of the animals were removed for observation. We found no significant difference in the pathology, bacterial clearance, or cytokine analysis between epithelial Atg5-deficient animals and wild type animals. This suggests that the Chlamydia bacteria may be employing mechanisms to evade or inhibit host autophagy in epithelial cells to promote its own survival. Additionally, there was no significant difference in the pathology, bacterial clearance, or cytokine analysis between the p62-deficient animals and wild type animals. Advisors/Committee Members: Fan, Huizhou (chair), Jacinto, Estela (internal member), Haimovich, Beatrice (outside member).

Subjects/Keywords: Chlamydia infections in animals; Chlamydia; Generative organs, Female – Diseases

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

APA (6^th Edition):

Battaglia, Lauren, 1. (2013). Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/41721/

Chicago Manual of Style (16^th Edition):

Battaglia, Lauren, 1988-. “Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency.” 2013. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/41721/.

MLA Handbook (7^th Edition):

Battaglia, Lauren, 1988-. “Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency.” 2013. Web. 17 Apr 2021.

Vancouver:

Battaglia, Lauren 1. Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency. [Internet] [Masters thesis]. Rutgers University; 2013. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41721/.

Council of Science Editors:

Battaglia, Lauren 1. Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency. [Masters Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41721/

Rutgers University

12. Hafiz, Ikram. The optimization of transformation efficiency in bacterium Chlamydia muridarum.

Degree: MS, Transformation, 2021, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/65382/

► Chlamydia trachomatis is an obligate intracellular microbe that is responsible for trachoma and chlamydia in much of the developing world, but is difficult to manipulate… (more)

Subjects/Keywords: Chlamydia muridarum; Physiology and Integrative Biology

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

APA (6^th Edition):

Hafiz, I. (2021). The optimization of transformation efficiency in bacterium Chlamydia muridarum. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/65382/

Chicago Manual of Style (16^th Edition):

Hafiz, Ikram. “The optimization of transformation efficiency in bacterium Chlamydia muridarum.” 2021. Masters Thesis, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/65382/.

MLA Handbook (7^th Edition):

Hafiz, Ikram. “The optimization of transformation efficiency in bacterium Chlamydia muridarum.” 2021. Web. 17 Apr 2021.

Vancouver:

Hafiz I. The optimization of transformation efficiency in bacterium Chlamydia muridarum. [Internet] [Masters thesis]. Rutgers University; 2021. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/65382/.

Council of Science Editors:

Hafiz I. The optimization of transformation efficiency in bacterium Chlamydia muridarum. [Masters Thesis]. Rutgers University; 2021. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/65382/

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