+publisher:"Rutgers University" +contributor:("Sarkar, Dipak")

Rutgers University

1. Al-Yasari, Ali Mosa Rashid, 1981-. Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.

Degree: PhD, Endocrinology and Animal Biosciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/

► Recently, it was reported in our laboratory that binge-like alcohol drinking for three weeks prior to conception by female rats produces poor birth outcome and… (more)

▼ Recently, it was reported in our laboratory that binge-like alcohol drinking for three weeks prior to conception by female rats produces poor birth outcome and defects in the offspring’s body stress response. These effects occur even after alcohol abstinence prior to conception, during pregnancy and postnatal care. Offspring born after preconception alcohol exposures (PCAE) show abnormalities in expression of the stress regulatory gene Pro-opiomelanocortin (Pomc) in the hypothalamus, resulting in higher stress hormone responses to a stress challenge and increased anxiety-like behavior. Since stress is often connected with increased body risk for metabolic diseases and since POMC-expressing neurons are known to control glucose homeostasis, I hypothesized that PCAE disrupts POMC neuronal function to increase susceptibility to developing hyperglycemia in animals. To test this hypothesis, I determined if PCAE had the ability to alter glucose homeostasis and increase the susceptibility to develop high fat diet (HFD)-streptozotocin (STZ)-induced diabetes in the offspring. The aims of my study were to determine the effects of PCAE on pancreatic, hepatic, and hypothalamic POMC/BEP neuronal abnormalities, and how the BEP replacement ameliorates these effects. In this study, 21 female adult Sprague Dawley rats were divided body weight-matched and randomly into three groups; the control group receiving rat chow and water ad libitum (AD; N=7), the alcohol-fed group (AF; N=7) receiving a liquid diet containing ethanol (6.7%), or the calorie-matched pair-fed (PF; N=7) group receiving an isocaloric liquid control diet. After 30 days of feeding, all rats were given normal chow ad libitum for three weeks; the estrus cycle was monitored and bred them with normal adult males to produce offspring. The pups were weaned at the age of postnatal day (PND) 25 and were randomly selected one animal from each litter to have three body weight-matched different groups (AD, PF, and AF, N=7). At the age of two months, offspring of AF exposed animals showed significantly higher fasting blood glucose and leptin and lower insulin and glucagon levels as compared with AD and PF offspring. Oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) data showed higher blood glucose and lower insulin production in AF in comparison with AD and PF offspring. Further, glucose-stimulated insulin secretion (GSIS) results demonstrated that AF group showed lowest insulin secretion as a response to an oral glucose solution in comparison with AD and PF groups. To evaluate the mechanistic link between PCAE effects on pancreatic homeostasis, I measured inflammatory markers such as; COX-2, IFN-γ, IL-6, and CD3 in whole (endocrine & exocrine) pancreatic tissue, insulin and glucagon in pancreatic islets by immunohistochemistry (IHC). Compared to AD and PF control groups, offspring from AF animals displayed higher levels of inflammatory markers accompanied with low pancreatic insulin and high glucagon expression, indicating the metabolic… Advisors/Committee Members: Sarkar, Dipak K (chair), Bello, Nicholas T (internal member), Anthony, Tracy G (internal member), Haimovich, Beatrice (outside member), School of Graduate Studies.

Subjects/Keywords: Diabetes; Alcoholism

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APA (6^th Edition):

Al-Yasari, Ali Mosa Rashid, 1. (2017). Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55304/

Chicago Manual of Style (16^th Edition):

Al-Yasari, Ali Mosa Rashid, 1981-. “Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/55304/.

MLA Handbook (7^th Edition):

Al-Yasari, Ali Mosa Rashid, 1981-. “Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?.” 2017. Web. 18 Jan 2021.

Vancouver:

Al-Yasari, Ali Mosa Rashid 1. Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/.

Council of Science Editors:

Al-Yasari, Ali Mosa Rashid 1. Does preconception alcohol abuse make the offspring vulnerable to developing type II diabetes?. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55304/

Rutgers University

2. Jabbar, Shaima, 1978-. Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary.

Degree: PhD, Animal Sciences, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/55511/

►

Alcohol exposure during gestation increases susceptibility to the development of pituitary tumors in response to estrogen in rat offspring. While the mechanism underlie this effect… (more)

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Alcohol exposure during gestation increases susceptibility to the development of pituitary tumors in response to estrogen in rat offspring. While the mechanism underlie this effect is not fully understood, serum estradiol (E2) and pituitary aromatase mRNA expression are increased in fetal alcohol exposed (FAE) offspring, which suggests a role for the estrogen axis. To test our hypothesis, pregnant Fischer 344 rats were fed between gestational days 7 and 21 with a liquid diet containing alcohol (AF), pair-fed with isocaloric liquid diet (PF), or fed rat chow (AD). At 60 days of age, animals were ovariectomized and received a subcutaneous estradiol implant. Rats were sacrificed at various times point after estradiol implantation. At the time of sacrifice, pituitaries of these animals were inspected for tumor growth. Estradiol treatment time-dependently increased pituitary weight in AF group as compared to AD and PF groups. After 120 days of estradiol treatment, inspection of the pituitary revealed that most tumors in the AF group were hemorrhagic and showed expansion to the surrounding tissue. Pituitary tumors from FAE offspring showed strong nuclear p53 and Ki67 expression. Significantly higher mRNA levels of hemorrhage-associated genes and proteins (PTTG, FGF4 and MMP-9) and multipotency genes and proteins (SOX2, Oct4 and CD133) were also observed in pituitary tumor tissues from AF group as compared with PF and AD groups. To test whether FAE enhances the population of cancer stem cells (CSCs) in the pituitary in response to estradiol, pituitaries were collected, and plated in ultra-low plates to promote pituisphere formation. The growing spheres were enzymatically dissociated to permit serial passaging. Assessment of a panel of genes related to multipotency (OCT4, NANOG, KLF4, SOX2, CD133, CD44, nestin and CD34) indicated that mRNA and protein expression of most of these genes was significantly higher in pituitary cells derived from spheres of AF animals as compared to AD. Pituitary cells derived from spheres of AF animals showed higher cell proliferation, migration and colony formation rates as compared to the control group. The pituitary cells derived from AF spheres were able to grow in immunodeficient mice. These data suggest that alcohol feeding enhances pituitary tumor development, and may program the pituitary to express pluripotent and growth promoting molecules under the estrogenic influence to induce aggressive pituitary tumor.

Advisors/Committee Members: Sarkar, Dipak (chair), Belden, William (internal member), Cohick, Wendie (internal member), Reuhl, Kenneth (outside member), Verzi, Michael (outside member), School of Graduate Studies.

Subjects/Keywords: Fetal alcohol spectrum disorders; Pituitary gland

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APA (6^th Edition):

Jabbar, Shaima, 1. (2017). Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55511/

Chicago Manual of Style (16^th Edition):

Jabbar, Shaima, 1978-. “Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary.” 2017. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/55511/.

MLA Handbook (7^th Edition):

Jabbar, Shaima, 1978-. “Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary.” 2017. Web. 18 Jan 2021.

Vancouver:

Jabbar, Shaima 1. Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55511/.

Council of Science Editors:

Jabbar, Shaima 1. Fetal alcohol exposure increases susceptibility to tumorigenesis in the pituitary. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55511/

Rutgers University

3. Cabrera, Miguel Alexander. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.

Degree: PhD, Endocrinology and Animal Biosciences, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

►

Fetal alcohol exposure has many detrimental effects on the developing brain and can cause fetal alcohol spectrum disorders (FASDs). Many FASDs patients show lifelong stress… (more)

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Fetal alcohol exposure has many detrimental effects on the developing brain and can cause fetal alcohol spectrum disorders (FASDs). Many FASDs patients show lifelong stress response abnormalities, demonstrated by an augmented response to stress hormones such as adrenocorticotropin and corticosterone (Lee et al., 2000), which are likely driven by alterations the hypothalamic-pituitary-adrenal (HPA) axis function (Zhang et al., 2005). Using a rat animal model, we have shown that postnatal ethanol exposure reduces the number and function of stress regulatory β-endorphin producing neurons in the hypothalamus, inducing a hyper-stress response (Sarkar et al., 2007; Logan et al., 2015). Microglia are one of the innate immune cells in the CNS and can be categorized as activated or ramified. Activated microglia are associated with an increase in proinflammatory responses and phagocytosis while ramified microglia are associated with maintaining homeostasis through dynamic communication, remodeling of neuronal synapses, and surveying the environment (Bell-Temin et al., 2013). How β-endorphin neurons communicate with microglia to maintain normal homeostasis has yet to be addressed. β-endorphin can also bind to both mu- and delta-opioid receptors and may serve as a form of communication between β-endorphin neurons and microglia. Exosomes are small vesicles (30-150 nm) that play an important role in local and distant communication between cells. They carry unique cargo (proteins, mRNA, miRNA, and other non-coding RNAs) from the cells they originate from that can affect the recipient cell’s homeostasis and induce apoptosis. Additionally, complement proteins, generally known for their role to opsonize foreign pathogens and support phagocytosis of dying cells may also play a role in ethanol-induced β-endorphin neuronal cell death. Here I demonstrate that ethanol-induced apoptosis of β-endorphin neurons is caused by activation of microglia to release proinflammatory cytokines, pro-apoptotic exosomes, and C1q. Furthermore, mu-opioid receptors activation is critical to ethanol-induced activation of microglia to induce apoptosis of β-endorphin neurons and antagonism of mu-opioid receptors attenuated the ethanol effect. Delta-opioid receptors antagonism did not have an effect on ethanol-induced β-endorphin neuronal cell death.

Advisors/Committee Members: Sarkar, Dipak K (chair), Roepke, Troy A (internal member), Bello, Nicholas T (internal member), Wu, Longjun (outside member), School of Graduate Studies.

Subjects/Keywords: Fetal alcohol spectrum disorders

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APA (6^th Edition):

Cabrera, M. A. (2018). Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

Chicago Manual of Style (16^th Edition):

Cabrera, Miguel Alexander. “Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.” 2018. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/58931/.

MLA Handbook (7^th Edition):

Cabrera, Miguel Alexander. “Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation.” 2018. Web. 18 Jan 2021.

Vancouver:

Cabrera MA. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/.

Council of Science Editors:

Cabrera MA. Fetal alcohol exposure induces neurotoxic effects on β-endorphin neurons through microglial activation. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/58931/

Rutgers University

4. Polanco, Tiffany, 1982-. Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis.

Degree: PhD, Animal Sciences, 2011, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000061439

►

Altered fetal programming as a result of a suboptimal in utero environment can increase disease susceptibility in adulthood. Alcohol exposure in utero increases mammary cancer… (more)

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Altered fetal programming as a result of a suboptimal in utero environment can increase disease susceptibility in adulthood. Alcohol exposure in utero increases mammary cancer risk in rodents. Mammary development affects breast cancer risk, as a denser, hyperproliferative gland increases mammary cancer risk. Therefore we hypothesized that alcohol exposure in utero increases the action of the IGF-I/E2 system leading to hyperproliferative mammary glands and ultimately increased cancer susceptibility. We first established a model where fetal alcohol leads to increased mammary tumor susceptibility. Pregnant rats were fed a liquid diet containing ethanol (alcohol-fed), a control isocaloric liquid diet, or rat chow ad libitum. Alcohol-fed dams were acclimated to increasing concentrations of ethanol (2.2% and 4.4%), then fed 6.7% ethanol from day 7 to 21 of gestation. To investigate tumorigenesis, N-nitroso-N-methlyurea (NMU) was administered to induce tumor formation at postnatal day 50. Rats were palpated for iii tumors weekly and euthanized at 23 weeks post-NMU injection, or in a second study at 16 weeks post-injection. At 16 weeks post-injection, tumor multiplicity was greater and tumor latency was decreased in the alcohol-fed group compared to controls. At 23 weeks post-NMU injection alcohol-fed animals developed more malignant tumors and more estrogen receptor-α negative tumors with less IGF binding protein-5 expression relative to controls, indicative of poor prognosis breast cancer in women. To determine if mammary development is altered by in utero alcohol exposure, a study was conducted in which animals were euthanized prepubertally and postpubertally. Mammary glands from alcohol-fed animals showed increased proliferation and aromatase expression prior to and immediately after puberty. Mammary and hepatic IGF-I mRNA levels were also higher in alcohol-fed animals. In a separate study it was determined that alcohol-fed animals also have higher circulation E2 than controls. Together, these data indicate that alcohol exposure in utero increases susceptibility to mammary tumorigenesis, and leads to a tumor phenotype indicative of poor prognosis breast cancer. These changes may be related to enhanced early mammary development via the IGF/E2 systems. Therefore, women born to mothers who drank alcohol during pregnancy may represent a high risk group for aggressive breast cancer.

Advisors/Committee Members: Polanco, Tiffany, 1982- (author), Cohick, Wendie S (chair), Sarkar, Dipak (internal member), Katz, Larry (internal member), Thomas, Paul (outside member).

Subjects/Keywords: Children of prenatal alcohol abuse; Breast – Cancer – Etiology; Alcohol – Physiological effect

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

APA (6^th Edition):

Polanco, Tiffany, 1. (2011). Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis. (Doctoral Dissertation). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000061439

Chicago Manual of Style (16^th Edition):

Polanco, Tiffany, 1982-. “Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis.” 2011. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000061439.

MLA Handbook (7^th Edition):

Polanco, Tiffany, 1982-. “Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis.” 2011. Web. 18 Jan 2021.

Vancouver:

Polanco, Tiffany 1. Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis. [Internet] [Doctoral dissertation]. Rutgers University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000061439.

Council of Science Editors:

Polanco, Tiffany 1. Effect of fetal alcohol on mammary carcinogenesis: the role of the estrogen/IGF axis. [Doctoral Dissertation]. Rutgers University; 2011. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000061439

Rutgers University

5. Zhu, Qiaoqiao, 1991-. Crosstalk between long non-coding RNAs and circadian chromatin.

Degree: PhD, Circadian rhythms, 2020, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/

►

The circadian rhythm is governed by transcriptional negative feedback facilitated by oscillating histone modifications and chromatin remodeling. The circadian rhythm is entrained by external zeitgebers… (more)

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The circadian rhythm is governed by transcriptional negative feedback facilitated by oscillating histone modifications and chromatin remodeling. The circadian rhythm is entrained by external zeitgebers (light and temperature) and are conserved in Neurospora, Drosophila, zebrafish, and mammals. The clock gene frequency in Neurospora and Period2 in vertebrates have natural antisense transcripts (NATs) whose function is not understood. In this dissertation I examined the connection among the circadian clock, non-coding RNAs and heterochromatin formation on both on the genome-wide and locus-specific level using a multi-organism approach. I performed a genome-wide study, using RNA-seq and ChIP-seq to understand the role of H3 lysine 4 methyltransferase (KMT2/SET-1) and histone H3 lysine 9 methyltransferase (KMT1/DIM-5) in Neurospora to understand the role of 2 seemingly opposing modifications. Integrated analysis of RNA-seq and ChIP-seq showed crosstalk and redistributions between histone H3 lysine 4 tri-methylation (H3K4me3) and histone H3 lysine 9 tri-methylation (H3K9me3). I also examined how perturbing the expression of a diurnal lncRNA affected downstream heterochromatin formation at the telomeres. The core circadian clock controls rhythms in TERRA, a long noncoding RNA that originates from telomeres and my research shows alcohol disrupts the diurnal rhythm in TERRA and heterochromatin at the telomere, which in theory makes telomeres more susceptible to DNA damage. I also examined the Per2 NAT, Per2AS and found the diurnal rhythm in Per2AS is dependent on BMAL1. Using the ChIRP-MS, I identified Per2AS-interacting proteins. Specifically, I found hnRNP M interacts with Per2AS and hnRNP M is required to maintain the normal amplitude and period of Per2. Furthermore, I demonstrate that hnRNP M is necessary for H3K9me3 and H3K27me3 at Per2. These findings support a model where Per2AS may serve as scaffold for hnRNP M and other associated proteins that assist in heterochromatin formation at Per2. Collectively, this dissertation furthers our understanding of the circadian clock, non-coding RNAs, and circadian regulated facultative heterochromatin formation.

Advisors/Committee Members: Belden, William J. (chair), Anthony, Tracy G (internal member), Sarkar, Dipak (internal member), Lee, KiBum (outside member), School of Graduate Studies.

Subjects/Keywords: Ribonucleases; Endocrinology and Animal Biosciences

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APA (6^th Edition):

Zhu, Qiaoqiao, 1. (2020). Crosstalk between long non-coding RNAs and circadian chromatin. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64311/

Chicago Manual of Style (16^th Edition):

Zhu, Qiaoqiao, 1991-. “Crosstalk between long non-coding RNAs and circadian chromatin.” 2020. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/64311/.

MLA Handbook (7^th Edition):

Zhu, Qiaoqiao, 1991-. “Crosstalk between long non-coding RNAs and circadian chromatin.” 2020. Web. 18 Jan 2021.

Vancouver:

Zhu, Qiaoqiao 1. Crosstalk between long non-coding RNAs and circadian chromatin. [Internet] [Doctoral dissertation]. Rutgers University; 2020. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/.

Council of Science Editors:

Zhu, Qiaoqiao 1. Crosstalk between long non-coding RNAs and circadian chromatin. [Doctoral Dissertation]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64311/

Rutgers University

6. Ramos, Brigette, 1993-. The effect of alcohol on genetically modified exosome deposition in the hypothalamus.

Degree: MS, Exosome, 2020, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/64354/

► Fetal Alcohol Syndrome (FAS) is a condition, particularly found in children, characterized by damage to the central nervous system as a result of alcohol exposure… (more)

▼ Fetal Alcohol Syndrome (FAS) is a condition, particularly found in children, characterized by damage to the central nervous system as a result of alcohol exposure during a woman’s pregnancy (Wilhoit et al., 2017). Areas of the brain that are affected include the hippocampus, basal ganglia, cerebellum, and hypothalamus. Once exposed to alcohol, the production of Beta-endorphins (βEP), a neuronal peptide involved in inhibiting stress in the hypothalamic arcuate nucleus, is reduced (Sprouse-Blum et al., 2010). On the other hand, there are cells, such as microglia, that can be stimulated during alcohol exposure. Microglia perform several essential functions in the brain, such as a role in neuroinflammation, regulation of brain development, and work as CNS macrophages (Colonna et al., 2017). Microglia are also capable of releasing exosomes, small membrane vesicles involved in neuronal communication and immune functions, including adaptive and innate immune responses (Fruhbeis et al., 2012). Using a rat animal model, our overall objective revolved around how exosomes, derived from genetically modified microglial cells, could be introduced through the periphery to influence βEP and glial interaction in the brain, and whether transportation of these exosomes could be altered by alcohol administration. We observed that the exosomes successfully passed through the blood-brain barrier (BBB) and were able to deposit into the hypothalamic arcuate nucleus. There was an increase in exosome deposition and a reduction in βEP neurons in alcohol treated rats, in comparison to the control or non-treated animal models. However, the exosomes displayed an inability to colocalize within the βEP neurons in both alcohol and non-treated animals. Therefore, we found that genetically modified exosomes can bypass the BBB and travel into the brain to localize into the hypothalamic arcuate area, more so through alcohol administration, and affect glial and βEP communication. Further research in observing where the exosomes are colocalizing is essential in finding what other roles the exosomes are involved in. Advisors/Committee Members: Sarkar, Dipak (chair), Mckinnon, Randall (internal member), Alder, Janet (internal member), D'rcangelo, Gabriella (internal member), School of Graduate Studies.

Subjects/Keywords: Fetal alcohol spectrum disorders; Physiology and Integrative Biology

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APA (6^th Edition):

Ramos, Brigette, 1. (2020). The effect of alcohol on genetically modified exosome deposition in the hypothalamus. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/64354/

Chicago Manual of Style (16^th Edition):

Ramos, Brigette, 1993-. “The effect of alcohol on genetically modified exosome deposition in the hypothalamus.” 2020. Masters Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/64354/.

MLA Handbook (7^th Edition):

Ramos, Brigette, 1993-. “The effect of alcohol on genetically modified exosome deposition in the hypothalamus.” 2020. Web. 18 Jan 2021.

Vancouver:

Ramos, Brigette 1. The effect of alcohol on genetically modified exosome deposition in the hypothalamus. [Internet] [Masters thesis]. Rutgers University; 2020. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64354/.

Council of Science Editors:

Ramos, Brigette 1. The effect of alcohol on genetically modified exosome deposition in the hypothalamus. [Masters Thesis]. Rutgers University; 2020. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/64354/

7. Agapito, Maria. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.

Degree: Neuroscience, 2013, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

Subjects/Keywords: Proopiomelanocortin; Fetus – Metabolism; Fetal alcohol syndrome

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APA (6^th Edition):

Agapito, M. (2013). The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. (Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Agapito, Maria. “The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.” 2013. Thesis, Rutgers University. Accessed January 18, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Agapito, Maria. “The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons.” 2013. Web. 18 Jan 2021.

Vancouver:

Agapito M. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 18]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Agapito M. The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons. [Thesis]. Rutgers University; 2013. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

8. Bekdash, Rola Aldana, 1971-. Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene.

Degree: Neuroscience, 2012, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063984

Subjects/Keywords: Fetal alcohol syndrome; Fetus—Development; Gene expression

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APA (6^th Edition):

Bekdash, Rola Aldana, 1. (2012). Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene. (Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063984

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bekdash, Rola Aldana, 1971-. “Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene.” 2012. Thesis, Rutgers University. Accessed January 18, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063984.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bekdash, Rola Aldana, 1971-. “Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene.” 2012. Web. 18 Jan 2021.

Vancouver:

Bekdash, Rola Aldana 1. Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene. [Internet] [Thesis]. Rutgers University; 2012. [cited 2021 Jan 18]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063984.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bekdash, Rola Aldana 1. Epigenetic effects of fetal alcohol exposure on hypothalamic proopiomelanocortin gene. [Thesis]. Rutgers University; 2012. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063984

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rutgers University

9. Maeng, Lisa Y., 1983-. The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress.

Degree: Psychology, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/41858/

Subjects/Keywords: Stress management for women; Women – Psychology; Women – Health and hygiene; Stress (Psychology) – Sex differences

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APA (6^th Edition):

Maeng, Lisa Y., 1. (2013). The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/41858/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Maeng, Lisa Y., 1983-. “The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress.” 2013. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/41858/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Maeng, Lisa Y., 1983-. “The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress.” 2013. Web. 18 Jan 2021.

Vancouver:

Maeng, Lisa Y. 1. The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41858/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Maeng, Lisa Y. 1. The stressed female brain: dissociating the prelimbic and infralimbic regions of the medial prefrontal cortex in the suppression of learning after acute stress. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41858/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rutgers University

10. Franklin, Tina Carla, 1985-. The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model.

Degree: Cell and Developmental Biology, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/41769/

Subjects/Keywords: Fetal alcohol syndrome; Microglia; Stress (Physiology) – Endocrine aspects

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

APA (6^th Edition):

Franklin, Tina Carla, 1. (2013). The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/41769/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Franklin, Tina Carla, 1985-. “The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model.” 2013. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/41769/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Franklin, Tina Carla, 1985-. “The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model.” 2013. Web. 18 Jan 2021.

Vancouver:

Franklin, Tina Carla 1. The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41769/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Franklin, Tina Carla 1. The immediate and long term effects of microglial cell activation on stress response in fetal alcohol exposure model. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41769/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rutgers University

11. Zhang, Changqing, 1984-. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.

Degree: Animal Sciences, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

Subjects/Keywords: Endorphins; Rats – Effect of stress on; Alcohol – Physiological effect; Cancer – Etiology; Cancer in animals

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❌

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

APA (6^th Edition):

Zhang, Changqing, 1. (2013). Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhang, Changqing, 1984-. “Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.” 2013. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/42092/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhang, Changqing, 1984-. “Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats.” 2013. Web. 18 Jan 2021.

Vancouver:

Zhang, Changqing 1. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhang, Changqing 1. Role of beta-endorphin in control of stress and cancer progression in fetal alcohol exposed rats. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/42092/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rutgers University

12. Spiegler, Elizabeth Kuhn, 1986-. The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development.

Degree: Nutritional Sciences, 2014, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/44219/

Subjects/Keywords: Beta carotene; Vitamin A deficiency; Vitamin A in human nutrition; Embryology, Human

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❌

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

APA (6^th Edition):

Spiegler, Elizabeth Kuhn, 1. (2014). The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/44219/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Spiegler, Elizabeth Kuhn, 1986-. “The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development.” 2014. Thesis, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/44219/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Spiegler, Elizabeth Kuhn, 1986-. “The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development.” 2014. Web. 18 Jan 2021.

Vancouver:

Spiegler, Elizabeth Kuhn 1. The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development. [Internet] [Thesis]. Rutgers University; 2014. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/44219/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Spiegler, Elizabeth Kuhn 1. The role of beta-carotene and its cleavage enzymes during vitamin A deficiency and mammalian embryonic development. [Thesis]. Rutgers University; 2014. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/44219/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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Open Access Theses and Dissertations