+publisher:"Texas A&M University" +contributor:("Johnson, Natalie M")

Texas A&M University

1. Wilson, Melinda R. Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study.

Degree: MS, Toxicology, 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/157798

► Integration and communication of diverse information into human health assessments is often challenging given the wide variety of data types and sources under consideration. In… (more)

Subjects/Keywords: read-across; glycol ether; data integration; data visualization; REACH; Toxicological Priority Index; ToxPi; Chemical-Biological Read-Across; CBRA; PCA

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APA (6^th Edition):

Wilson, M. R. (2016). Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157798

Chicago Manual of Style (16^th Edition):

Wilson, Melinda R. “Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study.” 2016. Masters Thesis, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/157798.

MLA Handbook (7^th Edition):

Wilson, Melinda R. “Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study.” 2016. Web. 23 Jan 2021.

Vancouver:

Wilson MR. Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study. [Internet] [Masters thesis]. Texas A&M University; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/157798.

Council of Science Editors:

Wilson MR. Data Integration and Visualization for Transparent Communication in Read-Across: a Glycol Ether Case Study. [Masters Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157798

Texas A&M University

2. Rychlik, Kristal Ann. Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response.

Degree: PhD, Toxicology, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/161638

► There is considerable evidence showing that exposure to particulate matter air pollution during important developmental windows, such as the prenatal period, can cause adverse respiratory… (more)

▼ There is considerable evidence showing that exposure to particulate matter air pollution during important developmental windows, such as the prenatal period, can cause adverse respiratory outcomes. Mechanisms underlying increased risks from in utero exposure are largely unknown. Since epigenetic modifications have been recognized as an important mediator of developmental reprogramming following environmental exposures in early life, the primary objective of this research was to establish a representative model of prenatal air pollution exposure to probe underlying mechanisms leading to adverse respiratory responses in offspring. The preliminary study (aim 1) established the proof-of-principle for differential air pollution-induced epigenetic changes across varying genetic background. Two strains (BALB/c and C57Bl/6 mice) were exposed to diesel exhaust particulate matter (DEPM), a major constituent of outdoor air pollution, throughout pregnancy. Following sacrifice at postnatal day 2, offspring global DNA methylation and hydroxymethylation was quantified in lung tissue. Results indicate differential methylation in BALB/c mice but not C57Bl/6. In aim 2, BALB/c and C57Bl/6 dams were exposed to a representative particulate air pollution mixture throughout gestation using a refined exposure model, and offspring response to allergen challenge was evaluated. After 4 weeks of chronic exposure to house dust mite allergen, offspring from both strains exposed to PM in utero demonstrated a reduced inflammatory response compared to filtered air controls. Airway hyperresponsiveness, a typical feature of asthma, was significantly different based on strain; however, air pollution exposure did not affect this response. In order to investigate the relevance of this model in an exposed human population, we conducted a pilot project (aim 3) evaluating exposure to particulate air pollution during pregnancy in a region in South Texas with a high incidence of childhood asthma. Results demonstrate low levels of air pollution exposure during pregnancy measured by personal sampling of fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs). Overall, findings from this work lay a foundation for further clarifying the mechanisms underlying childhood respiratory disease resulting from early life air pollution exposure. Advisors/Committee Members: Johnson, Natalie M (advisor), Porter, Weston (advisor), Criscitiello, Michael (committee member), Harvey, Roger B (committee member).

Subjects/Keywords: air pollution; atopy; asthma

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APA (6^th Edition):

Rychlik, K. A. (2017). Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/161638

Chicago Manual of Style (16^th Edition):

Rychlik, Kristal Ann. “Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response.” 2017. Doctoral Dissertation, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/161638.

MLA Handbook (7^th Edition):

Rychlik, Kristal Ann. “Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response.” 2017. Web. 23 Jan 2021.

Vancouver:

Rychlik KA. Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/161638.

Council of Science Editors:

Rychlik KA. Prenatal Exposure to Particulate Air Pollution and Effects on Postnatal Immune Response. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/161638

3. Cheng, Yating. The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands.

Degree: PhD, Toxicology, 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/159030

► LncRNAs are a group of non-coding RNAs containing >200 nucleotides and these RNAs have no significant protein coding potential. In the past 10-15 years the… (more)

▼ LncRNAs are a group of non-coding RNAs containing >200 nucleotides and these RNAs have no significant protein coding potential. In the past 10-15 years the role of lncRNAs in cancers have been demonstrated, however, their function in tumors and potential for drug targeting are not well defined. We studied two lncRNAs, HOXA transcript at the distal tip (HOTTIP) and metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in pancreatic cancer using the in vitro cell lines and in vivo xenograft or transgenic mouse models. Our results demonstrated that both lncRNAs are pro-oncogenic in the pancreatic cancer, supported by the observation that knockdown of HOTTIP and MALAT1 decreased cell proliferation, migration/invasion and increased apoptosis. HOTTIP might exhibit some pro-oncogenic functions, via the regulation of HOXA gene clusters in a cis-regulating manner. On the other hand, MALAT1 regulate responses of pancreatic cancer cells in part via polycomb repressive complex 2 (PRC2) dependent and independent pathways. Our transcriptomic results support the important but distinct roles of HOTTIP and MALAT1 in pancreatic cancer and we also show that MALAT1 expression can be targeted by small molecule drugs. In the second part of this dissertation, we studied several microbiota-derived aryl hydrocarbon receptor (AhR) ligands. The AhR is a ligand-activated transcription factor with an evolving role in the normal physiological development and diseases. Gut microbiota metabolites are important for mediating communication between gut microflora and the host. It has recently been shown that the gut microbiota produces several metabolites that are AhR ligands. Microbiota-derived tryptophan metabolites and 1,4-dihydroxy-2-napthoic acid (DHNA) and related compounds are reported to be AhR ligands as evidence by their induction of cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) and other AhR-responsive genes. We hypothesized the microbiota-derived AhR ligands are selective AhR modulators (sAhRMs) and their induction responses are compound, gene and cell context dependent. We have carried out extensive studies on tryptophan metabolites, DHNA and related compounds in both human and mouse colon cancer cell lines, and have observed that some of these compounds exhibited partial agonist/antagonist activities that are both gene and cell context specific. Advisors/Committee Members: Safe, Stephen H (advisor), Johnson, Natalie M (committee member), Phillips, Timothy D (committee member), Porter, Weston W (committee member), Tian, Yanan (committee member).

Subjects/Keywords: Long noncoding RNAs; Pancreatic cancer; Gut microbiota, AhR

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APA (6^th Edition):

Cheng, Y. (2016). The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/159030

Chicago Manual of Style (16^th Edition):

Cheng, Yating. “The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands.” 2016. Doctoral Dissertation, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/159030.

MLA Handbook (7^th Edition):

Cheng, Yating. “The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands.” 2016. Web. 23 Jan 2021.

Vancouver:

Cheng Y. The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands. [Internet] [Doctoral dissertation]. Texas A&M University; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/159030.

Council of Science Editors:

Cheng Y. The Role of Long Noncoding RNAs in Cancer and Microbiota-derived Aryl Hydrocarbon Receptor Ligands. [Doctoral Dissertation]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/159030

4. Pulczinski, Jairus Cyril. Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas.

Degree: MSPublic Health, Environmental Health, 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/157807

► Traffic-related air pollution (TRAP) contributes significantly to overall ambient air pollution, and exposure to TRAP has been implicated in the development of an array of… (more)

▼ Traffic-related air pollution (TRAP) contributes significantly to overall ambient air pollution, and exposure to TRAP has been implicated in the development of an array of disease states, including asthma, chronic obstructive pulmonary disease (COPD), and lung cancer. TRAP exposure in utero and in early childhood can induce heritable epigenetic alterations. Additionally, in utero and early life TRAP exposure is linked to cognitive impairment, reduced lung function, asthma susceptibility, small for gestational age, and preterm birth. Furthermore, the risk of negative health outcomes increases with small incremental increases in particulate matter (PM) concentrations. Currently, many epidemiologic studies examining air pollution exposure in general or during pregnancy use sophisticated modeling to map exposure, or active air monitors for brief (24 to 48 hours) exposure assessments and use these findings to extrapolate study populations exposure across a lifetime or the course of pregnancy. Furthermore, the EPA utilizes stationary monitors, with limited coverage, to measure air quality and identify regions that fail to meet Air Quality Index (AQI) Standards. This study was conducted to assess the effect of microenvironment on TRAP exposure among pregnant women, a susceptible population, in a region with high childhood asthma incidence, Hidalgo County, Texas. Women were equipped with active air monitors and GPS devices for three separate 24-hour time points to examine the role the microenvironment has on PM exposure as well as examine variation between participants and between sampling points. Participants’ exposure was found to be highly variable and average PM2.5 ranged from almost nonexistent, at 1.92µg/m³, to unhealthy, at 126.7µg/m³. Over 82% of participants experienced exposure outside of the “Good” range set by the EPA, and almost a quarter of participants experienced PM2.5 exposure considered “Unhealthy” by the EPA. These results are intriguing given that these participants reside in a region that regularly falls into the “Good” AQI category. Moreover, for this population, the home microenvironment was the dominant microenvironment experienced and the largest single contributor to overall PM2.5 exposure. This study speaks to the inherent variability associated with measuring PM in a population and the need for refined measures of exposure that capture microenvironment variation. Advisors/Committee Members: Johnson, Natalie M (advisor), McDonald, Thomas (committee member), Phillips, Timothy (committee member), Han, Daikwon (committee member).

Subjects/Keywords: PM2.5; microenvironment; South Texas; exposure assessment

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APA (6^th Edition):

Pulczinski, J. C. (2016). Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157807

Chicago Manual of Style (16^th Edition):

Pulczinski, Jairus Cyril. “Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas.” 2016. Masters Thesis, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/157807.

MLA Handbook (7^th Edition):

Pulczinski, Jairus Cyril. “Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas.” 2016. Web. 23 Jan 2021.

Vancouver:

Pulczinski JC. Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas. [Internet] [Masters thesis]. Texas A&M University; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/157807.

Council of Science Editors:

Pulczinski JC. Exposure to Traffic-Related Air Pollution among Pregnant Women in South Texas. [Masters Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157807

5. Skiles, William Mark. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.

Degree: PhD, Biomedical Sciences, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/173200

► In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how… (more)

▼ In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how environmental exposures influence the long-term health of an organism. Chemical pollutants, dietary deficiencies, embryonic stress and multiple other external factors have all demonstrated long-lasting effects upon development, metabolism, and health even after transient exposures. The mechanisms by which these exposures can impact development far beyond the period of exposure remain largely unknown. To gain better insight into the developmental origins of both birth defects and disease, we must better understand how environmental exposures alter development. In this work, we will examine the capacity of the environment to impact chromatin states, and then determine whether these changes are heritable; and are thus potentially causal in the development of disease. This is an important question due to the recent recognition that aberrant chromatin states can lead to pathological patterns of gene expression, a circumstance commonly referred to as “epimutations”. Dysregulation of gene expression patterns during development have been shown to cause a multitude of irregular phenotypes in offspring and lifelong disorders in mature organisms. This altered chromatin state, coined an epimutation by Dr. Emma Whitelaw, is important due to the mutation not being in the genetic code itself, but in the way DNA regulatory regions are packaged within the chromatin template, and thus accessed by the protein factors directing gene transcription. The body of work presented here will examine the ability of common environmental exposures to modulate chromatin structure. We will examine these changes over time in an effort to better understand the inheritance of epigenetic change. Secondly, we will measure whether environmentally induced alterations in chromatin structure within the germline persist, and are heritable. These questions are all relevant to better understanding the developmental origins of disease. Advisors/Committee Members: Golding, Michael C (advisor), Long, Charles R (advisor), Seabury, Christopher M (committee member), Johnson, Natalie M (committee member).

Subjects/Keywords: oxidative stress; assisted reproductive technologies; genomic imprinting; histone demethylase; TET; DNMT; DNA methylation; epigenetics; developmental programming; DOHAD; birth defect; epigenetics; preconception; sperm

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APA (6^th Edition):

Skiles, W. M. (2017). Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173200

Chicago Manual of Style (16^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Doctoral Dissertation, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/173200.

MLA Handbook (7^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Web. 23 Jan 2021.

Vancouver:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/173200.

Council of Science Editors:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/173200

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