The rat race of getting funded

In this creative writing piece, Dr. Thiel explores an alternate approach for the grant review process, ultimately concluding that the current pipeline is not inappropriately rigorous

Thomas Gellhaus, MD

Dr. Thomas Gellhaus, the recently appointed Division Director for General Obstetrics and Gynecology, brings to the Department a wealth of clinical experience and passions for teaching, advocacy, and providing care to patients in the developing world

Marygrace Elson, MD, MME

Marygrace Elson, MD, MME, joins us as guest editor for this issue of Proceedings in Obstetrics and Gynecology, which is focused on topics related to education. Dr. Elson is the Vice-Chair for Education, Residency Program Director, and Clinical Professor, Dr. William C. Keettel Chair of Obstetrics and Gynecology in the Department of Obstetrics and Gynecology at the University of Iowa

Stephen K. Hunter, MD, PhD

Stephen Hunter is a Professor and Division Director of Maternal-Fetal Medicine in the Department of Obstetrics and Gynecology at the University of Iowa. He’s an outstanding clinician, is the Associate Director of the Iowa Statewide Perinatal Care Program, and maintains a high-quality research program

Mark K. Santillan, MD

Dr. Mark Santillan, MD, brings a great deal of energy to his position as Assistant Professor in the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Iowa. As an active physician in the high-risk obstetrics clinic, researcher into the causes of preeclampsia, and Clinical Research Director for the Maternal Fetal Tissue Bank, that level of energy is a must

Michael J. Goodheart, MD

Dr. Michael Goodheart is an Assistant Professor of Obstetrics and Gynecology in the Division of Gynecologic Oncology at the University of Iowa. In addition to clinical duties, Dr. Goodheart does research the focus of which is unraveling the role of the Wnt pathway in endometrial cancer

An exploratory study of the variables impacting preterm birth rates in New Mexico

BACKGROUND: Preterm birth (PTB) is a substantial health problem that accounts for significant infant morbidity and mortality and poses an economic burden to both individuals and the state of residence. The goal of this study was to identify maternal risk factors for PTB in New Mexico, a poor state with a unique ethnic background, in order to identify populations at increased risk that would benefit from intervention. METHODS: This was a cross-sectional retrospective exploratory analysis of 377,770 singleton live births in the state of New Mexico from 1991-2005. Gestational age of less than 37 weeks was defined as PTB. The Kotelchuck Index was used as a measure for level of prenatal care described as inadequate, intermediate, adequate, and intensive. RESULTS: Of the live births analyzed, 28,036 of these were preterm (7.4%). Overall the PTB rate rose at a rate of 0.18% per year from 1991-2005. Among patients with medical risk factors, the absence of prenatal care was associated with higher odds for PTB as compared to adequate prenatal care. Other risk factors were unmarried status, education less than high school, tobacco/alcohol use, black, Asian, and white Hispanic ethnicity, and the presence of one or more medical risk factors. Statistically significant protective factors for PTB were age 25-29, education surpassing high school, and Native American race. CONCLUSIONS: This study identified several factors that correlate with increased PTB in New Mexico, in particular ethnicity and level of prenatal care. The finding that Native American patients have a lower PTB rate compared to other groups, even though this group is traditionally one of low socioeconomic status in New Mexico, signifies that other factors yet to be identified affect PTB

A predictive model for serous epithelial ovarian cancer chemo-response using clinical characteristics

One of the prognostic factors most highly associated with ovarian cancer survival is response to initial chemotherapy. Current prediction models of chemo-response built with comprehensive molecular datasets, like The Cancer Genome Atlas (TCGA), could be improved by including clinical and outcomes data designed to study response to treatment. The objective of this study was to create a prediction model of ovarian cancer chemo-response using clinical-pathological features, and to compare its performance with a similar TCGA clinical model

Tocotrienol Affects Oxidative Stress, Cholesterol Homeostasis and the Amyloidogenic Pathway in Neuroblastoma Cells: Consequences for Alzheimer’s Disease

One of the characteristics of Alzheimer´s disease (AD) is an increased amyloid load and an enhanced level of reactive oxidative species (ROS). Vitamin E has known beneficial neuroprotective effects, and previously, some studies suggested that vitamin E is associated with a reduced risk of AD due to its antioxidative properties. However, epidemiological studies and nutritional approaches of vitamin E treatment are controversial. Here, we investigate the effect of α-tocotrienol, which belongs to the group of vitamin E, on AD-relevant processes in neuronal cell lines. In line with the literature, α-tocotrienol reduced the ROS level in SH-SY5Y cells. In the presence of tocotrienols, cholesterol and cholesterol esters, which have been shown to be risk factors in AD, were decreased. Besides the unambiguous positive effects of tocotrienol, amyloid-β (Aβ) levels were increased accompanied by an increase in the activity of enzymes responsible for Aβ production. Proteins and gene expression of the secretases and their components remained unchanged, whereas tocotrienol accelerates enzyme activity in cell-free assays. Besides enhanced Aβ production, tocotrienols inhibited Aβ degradation in neuro 2a (N2a)-cells. Our results might help to understand the controversial findings of vitamin E studies and demonstrate that besides the known positive neuroprotective properties, tocotrienols also have negative characteristics with respect to AD

Vitamin D and Its Analogues Decrease Amyloid-β (Aβ) Formation and Increase Aβ-Degradation

Alzheimer’s disease (AD) is characterized by extracellular plaques in the brain, mainly consisting of amyloid-β (Aβ), as derived from sequential cleavage of the amyloid precursor protein. Epidemiological studies suggest a tight link between hypovitaminosis of the secosteroid vitamin D and AD. Besides decreased vitamin D level in AD patients, an effect of vitamin D on Aβ-homeostasis is discussed. However, the exact underlying mechanisms remain to be elucidated and nothing is known about the potential effect of vitamin D analogues. Here we systematically investigate the effect of vitamin D and therapeutically used analogues (maxacalcitol, calcipotriol, alfacalcidol, paricalcitol, doxercalciferol) on AD-relevant mechanisms. D2 and D3 analogues decreased Aβ-production and increased Aβ-degradation in neuroblastoma cells or vitamin D deficient mouse brains. Effects were mediated by affecting the Aβ-producing enzymes BACE1 and γ-secretase. A reduced secretase activity was accompanied by a decreased BACE1 protein level and nicastrin expression, an essential component of the γ-secretase. Vitamin D and analogues decreased β-secretase activity, not only in mouse brains with mild vitamin D hypovitaminosis, but also in non-deficient mouse brains. Our results further strengthen the link between AD and vitamin D, suggesting that supplementation of vitamin D or vitamin D analogues might have beneficial effects in AD prevention