iPEnd T32 Postdoctoral Trainees

Current Trainees

 

Soma Banerjee, MBBS, PhD (2024-Present)
Advisors:
Manish Patankar, PhD | Obstetrics & Gynecology
Jon Levine, PhD | Neuroscience, Wisconsin National Primate Research Center
Aleks Stanic-Kostic, MD/PhD | Obstetrics & Gynecology

iPEnd T32 Research: We are exploring the rhesus macaques as a model for studying the pathogenesis of human endometriosis, based on the observation that endometriosis is a spontaneously occurring disease in rhesus macaques with incidence rates similar to humans (between 5-10%). Not only is anatomy of the reproductive tract in rhesus macaque analogous to humans, additionally, endometriosis in rhesus macaques is managed with progestins and GNRH agonists- the same agents that are also used for clinical management of endometriosis in women. For my postdoctoral research, I am conducting whole genomic and spatial transcriptomic studies that compare endometriosis tissues in rhesus macaques to banked human endometriosis samples, hypothesizing that the endometriosis that occurs spontaneously as well as through the knockdown of the hypothalamic ERα in rhesus is representative at the molecular level to endometriosis observed in women. If successful, we will have further evidence that rhesus serve as an excellent model to study the basic biology of this disease with the goal of developing novel tests for early diagnosis and treatment in reproductive age women. With this research, I bring current skills and expertise from PCOS studies to a new disease area, enhance my proficiency in the analysis of highly complex datasets, and gain experience working with non-human primates. My long-term research interests include all aspects of reproductive physiology including benign and malignant disorders of the female reproductive tract and maternal and fetal disorders of pregnancy, with a focus on discovering useful and effective insight on the pathophysiology and management of these conditions.

 

Gabriela de Faria Oliveira, PhD (2023-Present)
Advisors:
Anthony Auger, PhD | Psychology
Jon Levine, PhD | Neuroscience, Wisconsin National Primate Research Center
Walid Farhat, MD | Pediatrics

Linked In

iPEnd T32 Research: I am a researcher dedicated to advancing our understanding of the critical period of pubertal development and its associated sex differences — a research focus that aligns with the NICHD’s mission to ensure healthy development and well-being for all children, youth, and families. My work employs translational animal models, including rats and nonhuman primates, with a specialized focus on the common marmoset (Callithrix jacchus) — a species I have studied for over a decade. Recent findings from my research demonstrate that the puberty blocker leuprolide reduces anxiety-like behavior in a rodent model. Building on this foundation, my current work investigates the impact of the long-acting puberty blocker Lupron Depot on learning and anxiety-related behaviors in a nonhuman primate model. By leveraging the controlled environment of animal models, I aim to generate rigorous, translational evidence that addresses key limitations of human studies. Ultimately, my goal is to contribute to basic science while fostering a more informed, evidence-based, and unbiased understanding of the effects of puberty blockers, thereby supporting the health, development, and well-being of diverse populations.

 

Alysia Vang, PhD (2024-Present)
Advisors:
Laura Hernandez, PhD | Animal & Dairy Sciences
Joao Dorea, PhD | Animal & Dairy Sciences
Anne Eglash, MD | Family Medicine


iPEnd T32 Research:
Insufficient glandular tissue (IGT), or mammary hypoplasia, refers to breast tissue that contains insufficient glandular tissue to produce sufficient milk to support infant growth and development. Approximately, 5-15% of women are unable to produce sufficient milk due to IGT. The etiology of IGT is unclear and the condition can present differently in individuals. My PhD work involved the use of ultrasound imaging to quantify mammary gland development in dairy calves to predict lactation potential. My postdoctoral work aims to translate this work to quantify secretory tissue growth during gestation to predict lactation potential in humans with the goal that appropriate clinical care is received postpartum for both the parent and child.

 

Andrea Killian Wegrzynowicz, PhD (2024-Present)
Advisors:
Aleks Stanic-Kostic, MD/PhD | Obstetrics & Gynecology
Laura Cooney, MD | Obstetrics & Gynecology

Linked In

iPEnd T32 Research: My work broadly encompasses using single-cell and spatial transcriptomics to assess tissue-specific differences in reproductive pathologies. Primarily, I am focusing on polycystic ovarian syndrome, the most common endocrine condition in females of reproductive age. PCOS commonly contributes to infertility and is comorbid with obesity. Systemic inflammation is observed in PCOS, but it is not well established how this inflammation affects the ovaries specifically, and how it is related to or separate from obesity. I am investigating how inflammation in the ovary differs in PCOS and control patients, as well as how this inflammation contributes to fertility outcomes. Additionally, I am collaborating on investigations of placental abnormalities in Rhesus macaque and mouse models, to improve our understanding of placental structure and inflammation in conditions such as pre-eclampsia and pre-term birth.

 

Alumni

 

Marcela Ambrogi, DVM, MS, PhD (2022-2024)
Advisors:
Chad Vezina, PhD | Comparative Biosciences
Jenna Racine, MD | Obstetrics & Gynecology

Current position: Postdoctoral Researcher, Urology, UW-Madison

iPEnd T32 Research: Urinary tract infection (UTI) is the most common bacterial infection in pregnancy, with an estimated incidence of approximately 20% (Yan et al. 2018). About two-thirds of women with a UTI during pregnancy take antibiotics, and antibiotic resistance is a growing concern (Johnson et al. 2021). We have identified a novel innate response to UTI driven by a rare population of urethral epithelial cells that synthesize and secrete serotonin. We developed and optimized a mouse model of ascending UTI by instilling uropathogenic E. coli UTI89 into the urethra. Using this model, we collected exciting preliminary evidence that bacteria stimulate serotonin secretion from the urethra, causing it to activate a serotonin receptor on urethral pacemaking cells and initiate smooth muscle contraction, thereby expelling bacteria from the urinary tract. As the translational component of this study, we also propose to use Electronic Health records data for deliveries from the PeriBank database to look for consistent data showing manipulation of the serotonergic system in pregnancy can reduce UTI and associated complications.

 

Beth Lett, PhD (2022-2024)
Advisors:
Irene Ong, PhD | Obstetrics & Gynecology and Biomedical Informatics
Aleks Stanic-Kostic, MD/PhD | Obstetrics & Gynecology

Current position: Postdoctoral Researcher, OBGYN, UW-Madison

iPEnd T32 Research: I am an early career interdisciplinary scientist working with bioinformatics and applied multi-omics research for human health and precision medicine. My PhD work involved genetics underlying different reproductive events in cattle that present as a negative to the dairy industry but potentially beneficial to beef production. In these projects, I conducted data cleaning and curation, GWAS analysis, short and long-read alignments, structural variant, InDel, and SNP detection, and molecular validation. For the postdoctoral work I have transitioned into a different realm of omics work in transcriptomics of both single-cell and spatial and from animals to human health to utilize discoveries made in computational biology to inform choices and health outcomes in clinical settings. My current project is working with preeclampsia and trying to understand the architectural differences between healthy and diseased tissue samples and identification of biomarkers for earlier detection.

 

Jessica Vazquez, PhD (2021-2023)
Advisors:
Aleksandar K. Stanic, MD/PhD | Obstetrics & Gynecology
Thaddeus (Ted) Golos, PhD | Comparative Biosciences
Jenny Gumperz, PhD | Medical Microbiology & Immunology

Current position: Scientist I, OBGYN, UW-Madison | Linked In

iPEnd T32 Research: Recent studies have highlighted the link between fetal and early life exposures and the development of non-communicable diseases, such as cardiovascular disease and metabolic syndrome. My project aims at understanding how sterile inflammation at the maternal-fetal interface impacts the development of the fetal immune system. Developing a deeper understanding of the effects of maternal inflammation on fetal immune development will provide opportunities for the development of targeted therapeutics either in utero or once offspring are born. This project has also allowed me to develop expertise in the use of the non-human primate as a model for human disease.

 

Luca Clemente, PhD (2021-2023)
Advisors:
Derek Boeldt, PhD | Obstetrics & Gynecology
Manish Patankar, PhD | Obstetrics & Gynecology

Current position: Postdoctoral Researcher, OBGYN, UW-Madison

iPEnd T32 Research: Preeclampsia is associated with increased expression of pro-inflammatory cytokines and loss of the vasodilatory and barrier functions of the vascular endothelium. Our prior experiments have found that incubation of human umbilical vein endothelial cell (HUVEC) monolayers with TNFα or IL-1β degrades barrier function over a 20-hr period. We hypothesize that the loss of barrier function correlates with EC shifting into a “nonprofessional” immunomodulatory phenotype. In vivo, these cytokine-altered EC may induce immune cell recruitment and activation at the endothelial surface, contributing to a highly inflammatory microenvironment. Recent experiments we have conducted have found that cytokine exposure does indeed lead to increased EC expression of immunomodulatory proteins associated with immune cell recruitment and activation, likely contributing to PE-related vascular inflammation. Furthermore, the heterogeneity of protein expression patterns within treatment groups raises the possibility that subpopulations of HUVEC may be primed for unique functional relationships with immune cells. These data support the hypothesis that specific cytokine-driven EC-immune cell interactions may play a role in the pro-inflammatory vascular microenvironment and drive PE-related endothelial dysfunction. The identification of key immunomodulatory molecules may provide clinicians with specific drug targets that can be pharmacologically inhibited, thereby preventing the inflammatory cascade observed in some types of preeclampsia.