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Vanderbilt University
1.
Mukherjee, Sudeshna.
Timing of gestational arrest prior to miscarriage.
Degree: PhD, Epidemiology, 2014, Vanderbilt University
URL: http://hdl.handle.net/1803/14285 
► Risk of miscarriage (i.e. a pregnancy loss before 20 completed weeks of gestation) is known to differ by race but timing of loss is not…
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▼ Risk of miscarriage (i.e. a pregnancy loss before 20 completed weeks of gestation) is known to differ by race but timing of loss is not well established in the literature. The gap between biological pregnancy loss identified by ultrasound and clinical manifestation of that loss may bias effect estimates for early-pregnancy exposures associated with miscarriage. Right from the Start (RFTS) is a unique and diverse prospective pregnancy cohort that captures uniform early first-trimester ultrasound information and pregnancy-related behaviors from first-trimester interviews in order to study the distribution of this gap.
Nearly 13% of women in this cohort experienced a pregnancy loss (n=697), the majority of whom have ultrasound data available (73%, n=509). Ultrasounds were conducted between 40 and 95 days gestation from last menstrual period (LMP) for this cohort. Gestational arrest prior to miscarriage was observed in 38.7% of losses (n=197). The mean gap between LMP and estimated gestational age at arrested development (GAAD) was 19.3 ± 15.0 days (median GAAD gap was 19 days). The GAAD gap did not differ by race or pregnancy intention.
In order to determine if failing to account for this gap influences effect estimates we assessed exposures commonly associated with pregnancy loss. We compared models that estimated gestational age based on self-reported LMP and models that incorporated gestational age at time of arrested development (GAAD). We used bootstrap methods to determine the magnitude of bias for both models. Smoking during pregnancy was not modified by race and was not associated with miscarriage risk within this cohort for either current or former smokers compared to never smokers in either model. Stratified by race and adjusted for confounding, the protective effect of vitamin use on miscarriage risk was stronger among White women than Black women when using the LMP models (Whites aHR=0.34, 95% CI [0.21, 0.54]; Blacks aHR=0.53, 95% CI [0.33, 0.84]), while no substantial difference by race was observed with the GAAD models (Whites aHR=0.43, 95% CI [0.24, 0.76]; Blacks aHR=0.44, 95% CI [0.26, 0.74]).
Models that use self-reported LMP to estimate gestational age underestimate the true value of first-trimester smoking exposure on miscarriage risk by as much as 15% for current smokers and 5% of former smokers when compared to models that use GAAD (the bootstrap bias ratio between models for current smokers ratio=0.85, 95% CI [0.75, 0.94]; for former smokers ratio=0.95, 95% CI [0.92, 0.97]). When stratified by race, the bias was nearly 20% for both Whites and Blacks for miscarriage risk associated with early pregnancy vitamin exposure (Whites bias ratio= 0.79, 95% CI [0.62, 0.87]; Blacks bias ratio=1.19, 95% CI [1.13, 1.45]). These results suggest that early-pregnancy exposures associated with miscarriage risk are influenced by proper classification of gestational arrest prior to loss, and that the magnitude and direction of bias differs by race. By more accurately identifying which insults have occurred…
Advisors/Committee Members: Katherine E. Hartmann (committee member), Aaron M. Kipp (committee member), Pingsheng Wu (committee member), Digna R. Velez Edwards (Committee Chair).
Subjects/Keywords: reproductive epidemiology; misclassification and bias; miscarriage; gestational arrest
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APA (6th Edition):
Mukherjee, S. (2014). Timing of gestational arrest prior to miscarriage. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14285
Chicago Manual of Style (16th Edition):
Mukherjee, Sudeshna. “Timing of gestational arrest prior to miscarriage.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021.
http://hdl.handle.net/1803/14285.
MLA Handbook (7th Edition):
Mukherjee, Sudeshna. “Timing of gestational arrest prior to miscarriage.” 2014. Web. 03 Mar 2021.
Vancouver:
Mukherjee S. Timing of gestational arrest prior to miscarriage. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1803/14285.
Council of Science Editors:
Mukherjee S. Timing of gestational arrest prior to miscarriage. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14285
Vanderbilt University
2.
Michels, Kara Ann.
Uterine Fibroid Severity in Pregnancy.
Degree: PhD, Epidemiology, 2014, Vanderbilt University
URL: http://hdl.handle.net/1803/13832
► Uterine fibroids are benign tumors associated with an increased risk of irregular vaginal bleeding and abdominal pain. Disease severity can be described in the context…
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▼ Uterine fibroids are benign tumors associated with an increased risk of irregular vaginal bleeding and abdominal pain. Disease severity can be described in the context of total fibroid volume, number of tumors, and growth of tumors. Despite more than one-in-ten pregnant women being affected by fibroids, the influence of increasing disease severity on symptoms is not well described among this population. Data from a prospective pregnancy cohort (Right from the Start: A study of early pregnancy health, 2000-2012) were used to show that non-linear relationships between total fibroid volume and the risks for bleeding and pain in the first trimester exist—and that these relationships differ by maternal race. Increasing number of tumors increased risk of self-reported pain and pain with bleeding. Longitudinal models were used to identify maternal and fibroid characteristics associated with fibroid growth during pregnancy. As in previous studies, increases in disease severity (increases in total fibroid volume), were noted for many women at the beginning of pregnancy, regardless of race. Nulliparity and first trimester bleeding and pain were possible risk factors for growth in total volume and number of tumors—suggesting that experiencing symptoms may be indicative of fibroid formation or growth.
Advisors/Committee Members: Katherine E. Hartmann (committee member), Kristin R. Archer (committee member), Fei Ye (committee member), Digna R. Velez Edwards (Committee Chair).
Subjects/Keywords: leiomyoma; multilevel; obstetrics; polytomous logistic regression; southeast
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APA (6th Edition):
Michels, K. A. (2014). Uterine Fibroid Severity in Pregnancy. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13832
Chicago Manual of Style (16th Edition):
Michels, Kara Ann. “Uterine Fibroid Severity in Pregnancy.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021.
http://hdl.handle.net/1803/13832.
MLA Handbook (7th Edition):
Michels, Kara Ann. “Uterine Fibroid Severity in Pregnancy.” 2014. Web. 03 Mar 2021.
Vancouver:
Michels KA. Uterine Fibroid Severity in Pregnancy. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1803/13832.
Council of Science Editors:
Michels KA. Uterine Fibroid Severity in Pregnancy. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/13832
Vanderbilt University
3.
Giri, Ayush.
Modifiable and non-modifiable risk factors for pelvic organ prolapse.
Degree: PhD, Epidemiology, 2015, Vanderbilt University
URL: http://hdl.handle.net/1803/14413
► Pelvic organ prolapse (POP) is characterized by the descent of pelvic organs (uterus, bladder, and bowels) from their normal anatomical positions into the vaginal space…
(more)
▼ Pelvic organ prolapse (POP) is characterized by the descent of pelvic organs (uterus, bladder, and bowels) from their normal anatomical positions into the vaginal space due to defects in the pelvic floor support system. Obesity may influence POP but findings from studies are not always consistent. A systematic-review of the literature was undertaken here and a meta-analysis was conducted to evidence that being over-weight and obese increased odds of having POP, compared with women with normal-weight. Literature suggests POP is heritable, and is likely influenced by a host of predisposing and modifiable factors; however this notion of interaction has not been formally assessed. Considering childbirth is the strongest risk factor and obesity, the most-practicably modifiable risk factor for POP, analyses were undertaken to identify whether single nucleotide polymorphisms (SNPs) in/around 96 candidate genes modify the associations between parity and POP and body mass index (BMI) and POP in European American, African American and Hispanic women from the Women’s Health Initiative Hormone Therapy (WHI-HT) trial. Although signals were not statistically significant considering multiple-comparisons, SNPs from several potential gene regions were noted to interact with BMI (<i>COL11A1</i>, <i>CADM2</i>, <i>ELN</i>, <i>ACTN3</i>, <i>NRXN3</i>, <i>FTO</i>, and <i>TMEM160</i>) and with parity (<i>CADM2</i>, <i>ETV5</i>, and <i>ITPR2</i>) to influence POP. Epidemiologic evidence also suggests racial disparity in POP prevalence; however, whether continental genetic ancestry plays a part has not been examined. An admixture mapping study of POP was undertaken in African American women from the WHI-HT. One chromosomal region (15:q262) showed a statistically significant inverse association with European ancestry, while another (1:q42.1-42.3) showed a suggestive positive association with European ancestry in relation to POP. This work demonstrates the multifactorial etiology of POP and the need to further investigate the mechanisms of how these factors interrelate to manifest POP.
Advisors/Committee Members: Katherine E. Hartmann (committee member), Digna R. Velez Edwards (committee member), Melinda C. Aldrich (committee member), Bingshan Li (committee member), Todd L. Edwards (Committee Chair).
Subjects/Keywords: Epidemiology of POP; Admixture mapping; Gene-environment interactions; Obesity and pelvic organ prolapse; Pelvic organ prolapse (POP); Women's Health
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APA (6th Edition):
Giri, A. (2015). Modifiable and non-modifiable risk factors for pelvic organ prolapse. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14413
Chicago Manual of Style (16th Edition):
Giri, Ayush. “Modifiable and non-modifiable risk factors for pelvic organ prolapse.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021.
http://hdl.handle.net/1803/14413.
MLA Handbook (7th Edition):
Giri, Ayush. “Modifiable and non-modifiable risk factors for pelvic organ prolapse.” 2015. Web. 03 Mar 2021.
Vancouver:
Giri A. Modifiable and non-modifiable risk factors for pelvic organ prolapse. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1803/14413.
Council of Science Editors:
Giri A. Modifiable and non-modifiable risk factors for pelvic organ prolapse. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/14413
Vanderbilt University
4.
Oliver, Kendra Helen.
Novel implications of lost serotonin transporter function on platelet biology.
Degree: PhD, Pharmacology, 2016, Vanderbilt University
URL: http://hdl.handle.net/1803/13914
► Reduced platelet aggregation and a mild bleeding phenotype has been observed in patients chronically taking selective serotonin reuptake inhibitors (SSRIs) that block the serotonin transporter…
(more)
▼ Reduced platelet aggregation and a mild bleeding phenotype has been observed in patients chronically taking selective serotonin reuptake inhibitors (SSRIs) that block the serotonin transporter (SERT). Here, I explore this relationship between platelet activation, specifically αIIbβ3 activation, and the loss of SERT function. First, using a pharmacological approach, we investigate the role of acute loss of SERT function on platelet αIIbβ3 activation. We find that acute treatment with SSRIs does not alter αIIbβ3 activation but reduced αIIbβ3-mediated platelet spreading. Next, two models of sustained loss of SERT function were used to investigate platelet αIIbβ3 activation; the SERT knockout mouse (SERT-/-) mice and mice treated with citalopram for 6-days. Both models replicate the mild bleeding phenotypes noted in human patients taking SSRIs. Following transfusion of wild-type platelets into SERT-/- mice, SERT-/- bleeding times were reduced to WT levels suggesting defects in platelet function. We examined αIIbβ3 activation (JON/A binding) and granule exocytosis with P-selectin surface expression (CD62p binding) following ADP stimulation and found reduced ADP-mediated αIIbβ3 activation in SERT-/- platelets. Acute treatment of platelets with SSRIs (paroxetine and citalopram) to prevent serotonin uptake during activation did not alter ADP-mediated αIIbβ3 activation. However, 5HT2AR antagonists significantly reduced ADP-mediated αIIbβ3 activation. These findings suggest that serotonin synergizes with ADP through 5HT2AR activation, but not acute SERT uptake. Furthermore, SERT-/- platelets displayed reduced serotonin enhanced ADP-mediated αIIbβ3 activation, likely due to reduced 5HT2AR cell surface levels. This again suggests acute function of SERT does not alter ADP-mediated αIIbβ3 activation but that sustained loss of SERT function alters surface expression of 5HT2AR and ultimately reduces ADP-mediated αIIbβ3 activation. Lastly, I discuss the hypercoaguability phenotype of the β3 integrin mutation, which models the human PIA2 polymorphism. This mutation leads to a primed αIIbβ3 integrin characterized by increased baseline Src-signaling. The hypercoaguability phenotype can be rescued with the Src inhibitor SKI606 but, interestingly, is also hyperserotonergic. We find that blockage of the SERT transporter with 6-day citalopram treatment is also able to rescue the KI thrombin clotting time. These findings further establish a connection between serotonergic regulation and αIIbβ3 activation in platelet function. This body of work expands the current knowledge of serotonin in platelet biology and supports a more physiologically based understanding of the effects of SSRIs on platelet function.
Advisors/Committee Members: Heidi E. Hamm, Ph.D. (committee member), Ana M.D. Carneiro, Ph.D. (committee member), Digna R. Velez Edwards Ph.D., M.S. (committee member), Vsevolod Gurevich, Ph.D. (committee member), Jonathan Schoenecker, M.D., Ph.D. (Committee Chair).
Subjects/Keywords: platelet; SERT; serotonin; 5HT2AR
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APA ·
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APA (6th Edition):
Oliver, K. H. (2016). Novel implications of lost serotonin transporter function on platelet biology. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13914
Chicago Manual of Style (16th Edition):
Oliver, Kendra Helen. “Novel implications of lost serotonin transporter function on platelet biology.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021.
http://hdl.handle.net/1803/13914.
MLA Handbook (7th Edition):
Oliver, Kendra Helen. “Novel implications of lost serotonin transporter function on platelet biology.” 2016. Web. 03 Mar 2021.
Vancouver:
Oliver KH. Novel implications of lost serotonin transporter function on platelet biology. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1803/13914.
Council of Science Editors:
Oliver KH. Novel implications of lost serotonin transporter function on platelet biology. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/13914
Vanderbilt University
5.
Bray, Michael Joseph.
Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics.
Degree: PhD, Human Genetics, 2018, Vanderbilt University
URL: http://hdl.handle.net/1803/10965
► Uterine fibroids, benign tumors of the uterus, are the most common female pelvic tumor. Fibroids are highly heterogeneous, with some women developing a single small…
(more)
▼ Uterine fibroids, benign tumors of the uterus, are the most common female pelvic tumor. Fibroids are highly heterogeneous, with some women developing a single small fibroid while other women develop multiple and/or large fibroids. In addition, racial disparities in fibroid size and number support that fibroid characteristics have a genetic component. For example, African American (AA) women have more numerous and larger fibroids than European American (EA) women. Furthermore, AAs are two times more likely than EAs to receive surgical treatments for fibroids such as a hysterectomy. Unfortunately, most research on fibroids to date has not evaluated risk factors for specific fibroid characteristics. The purpose of this thesis is to provide a deeper understanding on both epidemiology and genetic risk factors of fibroid characteristics, fibroid number (single vs. multiple), volume of largest fibroid, and largest dimension of all fibroid measurements. After identifying epidemiologic risk factors for fibroid characteristics, this study identified several novel genetic loci associating with either fibroid size or number by methods of genome-wide association studies (GWAS) and admixture mapping studies. Lastly, this study estimated heritability of fibroids and fibroid size.
Advisors/Committee Members: Bingshan Li (committee member), Melissa F. Wellons (committee member), Todd L. Edwards (committee member), Nancy J. Cox (committee member), Digna R. Velez Edwards (committee member), David C. Samuels (Committee Chair).
Subjects/Keywords: admixture mapping study; genome-wide association study; uterine fibroids
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APA ·
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APA (6th Edition):
Bray, M. J. (2018). Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10965
Chicago Manual of Style (16th Edition):
Bray, Michael Joseph. “Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021.
http://hdl.handle.net/1803/10965.
MLA Handbook (7th Edition):
Bray, Michael Joseph. “Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics.” 2018. Web. 03 Mar 2021.
Vancouver:
Bray MJ. Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1803/10965.
Council of Science Editors:
Bray MJ. Evaluating Epidemiologic and Genetic Risk Factors for Uterine Fibroid Characteristics. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/10965
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