bluuebunny/crossref_metadata_2025_split huggingface dataset:
Investigating the Effects of Premedical Experiences on Medical Student Neuroanatomy Self‐Efficacy
Authors: Bergden Jessica , Immekus Jason , Brueckner‐Collins Jennifer 
Published: May 2022

One key issue in medical education is medical student fear of learning and applying neuroanatomy called neurophobia. In a previous study, we found a negative correlation between neurophobia and neuroanatomy self‐efficacy (one’s confidence in their ability to complete neuroanatomy tasks). Our findings suggest increasing neuroanatomy self‐efficacy may reduce one’s neurophobia. Additionally, the literature shows self‐efficacy improves academic achievement and clinical performance in medical school. It is unknown whether experiences before medical school may later influence medical student neuroanatomy self‐efficacy. This study aims to fill this literature gap by isolating which premedical experiences most significantly influence neuroanatomy self‐efficacy. We hypothesize medical students with premedical neuroanatomy‐specific experience will exhibit greater neuroanatomy self‐efficacy than students without this experience.Instrumentation to measure neuroanatomy self‐efficacy and categorize premedical experiences was developed and administered to medical students (n=233). Premedical experiences were categorized as: neuroscience (NSC), neuroanatomy (NAC), neuroscience and neuroanatomy (NSAC), cadaveric gross anatomy (GR), or anatomy and physiology (AP). An analysis of variance with a Tukey’s post‐hoc test was performed to isolate which premedical experience(s) showed significant differences in neuroanatomy self‐efficacy compared to students with no previous experience. All statistical tests were performed at the p=0.05 level. IRB approval was obtained.Data analysis showed indirect premedical neuroanatomy exposure as part of a premedical gross anatomy course (GR) resulted in greater neuroanatomy self‐efficacy (p=0.01, Cohen’s d= 0.50) compared to students with no previous experience. Interestingly, enrollment in a premedical molecular neuroscience (NSC) or neuroanatomy (NAC) course individually did not show an increase in neuroanatomy self‐efficacy. Only medical students with both premedical NSC and NAC experiences (NSAC) demonstrated higher neuroanatomy self‐efficacy than students with no premedical experience (p= 0.001, Cohen’s d= 0.52).Premedical exposure to neuroanatomy as part of a gross anatomy course (GR) or enrollment in both premedical neuroanatomy andneuroscience courses (NSAC) appears to be associated with higher neuroanatomy self‐efficacy in medical students. Considering the decline in neurologists, and fewer medical students choosing neurology, these findings support youth STEM initiatives to provide increased access to both neuroscience and neuroanatomy experiences along with cadaveric gross anatomy.
Cannabinoid Receptor‐Mediated Synaptic Signaling and Neural Plasticity in Central Olfactory Neurons
Authors: Heinbockel Thomas , Wang Ze‐Jun 
Published: May 2022

Our studies aim to understand integrative and computational mechanisms that allow main olfactory bulb neurons to respond to afferent input and synaptic or feedback signals. The endocannabinoid (eCB) signaling system has been functionally implicated in many brain regions but our understanding of the role of cannabinoid receptor type 1 (CB1R) in olfactory processing remains limited. Endocannabinoids are known to mediate retrograde signaling at synapses in several brain regions through a form of short‐term neural plasticity. Endocannabinoids are released from depolarized principal neurons and rapidly diffuse to presynaptic inhibitory interneurons to transiently reduce presynaptic firing and neurotransmitter (GABA) release (Depolarization‐Induced Suppression of Inhibition, DSI).We study the function of the endocannabinoid system in regulating neural activity at synapses in the main olfactory bulb, the first central relay station in the brain for the processing of olfactory information coming from the nose. Our experimental approach uses electrophysiological recording techniques, specifically whole cell patch‐clamp recordings. Previously, using anatomical approaches, we showed that CB1R is present in periglomerular processes of a GAD65‐positive population of interneurons but not in mitral cells, key output neurons. We detected eCBs in the mouse main olfactory bulb as well as the expression of CB1R and other genes associated with the cannabinoid signaling system.Output neurons such as mitral cells and tufted cells in the olfactory bulb are computational elements in brain circuits that integrate incoming signals with membrane properties to generate behaviorally relevant synaptic output. Our data support the notion that retrograde signaling is present in neural circuits involving mitral and tufted cells. Mitral and tufted cells release endocannabinoids and, through retrograde signaling, inhibit presynaptic interneurons such as periglomerular cells, which controls the GABA release of these presynaptic neurons. This, in turn, allows mitral and tufted cells to temporarily regulate their synaptic input and relieve them from synaptic inhibition. Endocannabinoids function as retrograde messengers to regulate neural signaling and mediate plasticity at olfactory bulb synapses with potential effects on olfactory threshold and behavior.
Estrogen‐mediated signaling mechanisms regulate voluntary running behavior in rats
Authors: Mathis Victoria , Points Lauren , Pope Brock , Lee Chia‐Ming , Li Yaru , Winter Lori , Clayton Sarah , Yuan Li‐Lian 
Published: May 2022

Despite the myriad social and health benefits of exercise, humans display heterogeneous levels of participation. Significant progress has been made in identifying molecular events, systems, and mechanisms that support exercise’s beneficial effects, but it is not clear yet what regulates exercise behavior itself or serves to maintain prolonged chronic exercise behavior.The human heterogeneity in voluntary exercise can be recapitulated in a rodent model of wheel running, a behavior with high rewarding properties. While rats given continuous access to running wheels all began with low running activity, a 3‐week training program dramatically increased running activity and uncovered a wide range of individual differences in running behavior. In addition, we have identified intriguing sex differences in this model. Compared to age‐matched males, female rats exhibited significantly higher levels of average daily running. When assessing individual female rats’ running behavior, we also observed a repetitive peak‐valley pattern of running activity, with peaks coinciding with the proestrus stage (highest estrogen level) in the rat estrous cycle. Bilateral ovariectomy (OVX) not only lowered their overall running activity, but also completely eliminated cyclical variations. Furthermore, low dose estrogen replacement via osmotic mini‐pumps in an OVX background restored running activity to pre‐OVX levels, and acute estradiol injections were able to replicate running peaks. Collectively, those results suggest estrogen exerts strong regulation of female running activity. By taking individual and sex differences into consideration in the experimental design, we anticipate our subsequent biochemical assays will identify signaling molecules and pathways involved in running activity that is driven by a surge of estradiol.
Effects of Physical Activity During Pregnancy on Maternal and Fetal Health Outcomes
Authors: Abuoqab Lema O. 
Published: May 2022

IntroductionPhysical activity during pregnancy and its effects on fetal fat accrual and lipids has not been deeply explored. The purpose of this study was to further investigate how fitness during pregnancy relates to neonatal adiposity.Methods30 mothers were surveyed using the Pregnancy Physical Activity Questionnaire (PPAQ) at early pregnancy (EP; 12‐16 weeks), and of these 27 completed the study at late pregnancy (LP; 34‐36 weeks). Mothers were analyzed by sedentary, light, moderate, and vigorous activities, involvement in caregiving, occupations, and exercise. Mothers’ body composition (% fat and fat free mass) assessed by air densitometry (BOD POD), and BMI, were tracked throughout pregnancy. Infant adiposity (% fat via air densitometry/PEA POD) was measured within 48 hours of birth. Umbilical venous (UV) lipid levels were measured in the clinical pathology lab by standard methodology. Associations between maternal physical activity and infant outcomes were analyzed using non‐parametric Spearman correlation.ResultsEP fitness scores were positively correlated with parity (P=0.0047). EP overall scores were positively correlated with higher first trimester maternal BMI (P=0.0205). EP fitness scores were negatively correlated with infant % fat free mass (P=0.0407), and showed no significant correlation with any other infant factors post birth. LP PPAQ scores were negatively correlated with infant % fat free mass (P=0.0180); and positively correlated to infant % fat (P=0.0230). LP fitness scores, unlike EP, were negatively correlated with UV LDL, non‐HDL, and cholesterol readings (P=0.0172, P=0.0347, and P=0.0087, respectively). Infants of mothers who decreased in fitness between EP and LP had trends of higher levels of UV HDL, LDL, and non‐LDL compared to infants of mothers who had increased fitness.ConclusionUnexpectedly, higher maternal fitness levels correlated with higher maternal BMI and infant adiposity, potentially due to skewness in the PPAQ towards questions involving household or caregiving activity. Indeed, higher fitness scores were associated with parity. As postpartum weight retention is a risk factor for obesity, this may also explain the positive correlation between fitness and infant adiposity, potentially mediated by high maternal BMI. As the change in maternal fitness from EP to LP is correlated with UV lipids, our findings suggest that modifications of maternal physical activity during pregnancy may impact lipid transfer in utero. Future studies should investigate the effect of maternal fitness on placental function.
MDH CURE Community Faculty Fellows: A new mentoring program supporting Biochemistry CUREs
Authors: Gentile Lisa , Provost Joseph , Bell Ellis , Springer Amy 
Published: May 2022

The Malate Dehydrogenase Cures Community Faculty Fellows (MCC‐FF) Program is part of an NSF RCN sponsored program focused on expanding and sustaining community among faculty teaching a course in the course undergraduate research experience (CURE) format using malate dehydrogenase (MDH). All faculty interested in adopting an MDH CURE are welcomed to become part of this supportive national group working together to provide research opportunities to their students within the context of the labs they teach. In addition, each faculty fellow will be part of a regional hub of local faculty teaching MDH CUREs. These regional hubs will host workshops, office hours, and expertise in MDH CUREs. Opportunities to teach well developed MDH CUREs or to design new MDH CUREs exist, as do opportunities to collaborate on particular MDH labs with faculty at different institutions.Starting in Summer 2022, we will be forming the first of four, two‐year MCC‐FF cohorts providing individually mentored training. The program will provide two years of individually mentored experience to the faculty members who want to teach labs in a CURE format using MDH. During the first summer they will participate in virtual and hands‐on professional development (a one day virtual workshop, a 2 day hands‐on workshop, and a flexibly scheduled week long period of time where faculty fellows have access to their mentors as they adapt techniques/protocols to their home institutions). In the second year, these faculty fellows will teach their first MCC CURE course and develop mentorship skills help mentor subsequent cohorts of faculty fellows. Up to nine faculty per cohort will be selected for additional financial support including funds to purchase minor equipment/instrumentation. The selection of these faculty will give preference to faculty from under‐resourced institutions and/or those who work with large populations of students from backgrounds traditionally underrepresented in higher education. Faculty fellows will be selected from different types of institutions (community colleges, MSIs, PUIs, regional comprehensives, research intensives), teaching different types of courses (introductory, advanced, interdisciplinary, remote/online), at different places in their careers (new faculty members, experienced faculty members interested in changing pedagogical approaches). For faculty who teach with a postdoctoral fellow, graduate TA, or UG TA, these students will also be affiliated with the cohort and have access to training/support. Expectations of cohort membership are that faculty will be working to get an MDH CURE up and running as part of their teaching load within 2 years, will be an active part of their local network, and in the future will become a mentor to new faculty fellows.
FXR1 Decreases Blood Pressure by Regulating Vascular Contractility
Authors: St. Paul Amanda , Preston Kyle , Corbett Cali , Leigh Tani , Kelemen Sheri , Okune Rachael , Eguchi Satoru , Haines Dale , Autieri Michael 
Published: May 2022

IntroductionHypertension is a major risk factor for cardiovascular disease and stroke. Optimally treated hypertensive patients still have a 50% greater cardiovascular risk than untreated normotensive subjects. Despite current medication, half a million deaths in the United States include hypertension as a primary contributing cause in 2018 presenting a need for additional targets. Vascular smooth muscle cells (VSMCs) are the fulcrum of vascular disease, particularly hypertension. VSMCs play a critical role in vascular contractility and the regulation of blood pressure. Fragile X‐related protein (FXR1) is a muscle‐enhanced RNA binding protein and we previously found siRNA knock down of FXR1 increases inflammatory mRNA stability. Overexpression of FXR1 decreases inflammatory mRNA stability in VSMC. Little is known concerning FXR1 protein binding partners and its role in vascular disease. The specific aim of this study is to test the hypothesis that FXR1 regulates vascular contractility by RNA stability and protein interactions.ResultsWe generated a novel, VSMC‐specific FXR1 conditional knock out mouse (FXR1VSMC/VSMC) in order to establish an in vivo role of FXR1 in vascular disease. Preliminary data indicates that these mice show decreased diastolic (P < 0.05) blood pressure at baseline compared to controls. Gene ontology of RNA immuno‐precipitation sequencing analysis in human VSMCs identified that FXR1 binds to mRNA that participate in VSMC contractility and regulation of blood pressure‐ related pathways. Although considered an RNA stability protein, mass‐spectrometry identified that FXR1 interacts with proteins related to contractile processes such as cell migration, adhesion and stress fiber formation. FXR1 depletion in human VSMCs decreases mRNA abundance of contractile machinery. Future studies will determine the effect of FXR1 depletion on mRNA stability of these transcripts. Additionally, siRNA knock down of FXR1 decreased VSMC adhesion, migration and collagen gel contraction corroborating in vivo observations.ConclusionThese data are the first to suggest FXR1 regulates blood pressure and vascular contractility potentially by two mechanisms: mRNA stability and functional activity by protein‐protein interactions. The findings support FXR1 activity may represent a target for therapeutic invention to regulate blood pressure.
The miR‐200family regulates the epithelial stem cell niche during craniofacial and dental development
Authors: Amendt Brad A. , Leonard Riley J. , Su Dan , Eliason Steven L. 
Published: May 2022

Introduction & objective‐The murine lower incisor ectodermal organ contains a single epithelial stem cell niche that provides epithelial progenitor cells to the continuously growing rodent incisor. Calvaria sutures also contain stem cells that are regulated by specific factors. We have discovered that the microRNA (miR) ‐200 family is required for stem cell differentiation through targeting stem cell factors. We asked if the miR‐200 family regulated specific stem cell niches during development.Materials & methods‐ Our group used the plasmid‐based miR inhibitor system (PMIS) to knock down specific miR‐200 family members in mice and study their role during developmental processes. Our system inhibits one miR within a cluster to understand the role of that miR, which cannot be accomplished using gene targeting methods.Results‐We inhibited the miR‐200 family in developing murine embryos using new technology, resulting in an expanded epithelial stem cell niche and lack of cell differentiation. Inhibition of individual miRs within the miR‐200 cluster resulted in differential developmental and cell morphology defects. miR‐200 inhibition increased the expression of dental epithelial stem cell markers, expanded the stem cell niche and decreased progenitor cell differentiation. RNA‐seq. identified miR‐200 regulatory pathways involved in cell differentiation and compartmentalization of the stem cell niche. The miR‐200 family regulates signaling pathways required for cell differentiation and cell cycle progression. New miR‐200targets demonstrate gene networks and pathways controlling cell differentiation and maintenance of the stem cell niche.Conclusion‐This is the first report demonstrating how the miR‐200 family is required for in vivo progenitor cell proliferation and differentiation.Significance/implication‐This new approach has identified several new scientific advancements in stem cell niche biology. 1) miR‐200 family members are required for in vivo epithelial stem cell differentiation and stem cell niche maintenance; 2) The miR‐200 family regulates genes required for generating the different dental epithelial cell lineages; 3) miR‐200expression may be a common mechanism for defining the boundaries of adult epithelial stem cell niches; 4) By inhibiting the miRs that become active when a progenitor cell becomes fated to differentiate, the in vivo cell differentiation programs are determined assuming their terminal fates; 5) Dental epithelial stem cells and suture stem cells are regulated by members of the miR‐200 family to yield the differentiated progeny and determine cell fate.
Arterial Demonstration Device Illustrates Core Physiological Concepts
Authors: Sweeney Terrence E. 
Published: May 2022

We have created a hand‐held, interactive arterial demonstration device that simplifies the teaching of several core physiological concepts. The device consists of low breaking point one‐way spirometer valve coupled serially to a flow‐through latex balloon that is fitted distally with a flow restrictor. The spirometer valve models the aortic valve; the latex balloon models the elastic arteries; the restrictor valve models the peripheral resistance. The user blows vigorously and intermittently into the proximal end of the device, modeling the ventricle's stroke volume. Initially designed to clarify the role of elastic arteries in cardiovascular function, it became evident that the arterial demonstration device could be employed to explain and demonstrate a number of physiological principles, including the distinct structure and functions of arteries and veins, the pathophysiological impact of aortic valve dysfunction (using device versions that incorporate dysfunctional valves), and the Law of LaPlace. Further, the device can be used to demonstrate several core physiological concepts, including causality; flow down gradients; energy acquisition, transformation and use; and mass balance in elastic structures1. This extends the device's utility beyond cardiovascular principles, a foundational idea behind the pedagogical approach of incorporating Core Concepts of Physiology2 in physiological instruction. Several such approaches are described.1 Modell, H., Adv. Physiol. Educ. 23: 101‐107, 2000.2 Michaels, J et al. The core concepts of physiology: A new paradigm for teaching physiology.DOI 10.1007/978‐1‐4939‐6909‐8, Springer, 2017.
Treatment of Multidrug‐Resistant Bacterial Infections Using Quantum Dots
Authors: McCollum Colleen , Bertram John , Nagpal Prashant , Chatterjee Anushree 
Published: May 2022

Multidrug‐resistant (MDR) bacterial infections remain a major threat to public health, despite strides made in antibiotic development in the past century. The rise of MDR infections has demonstrated the dire need for new treatment strategies against infectious disease. MDR bacteria are predicted to cause ten million deaths annually worldwide by 2050, more than all cancers combined, unless significant strides are made in treatment options. While pharmaceutical companies devote years to develop a single drug for a single ailment, bacteria are quick to adapt, and MDR bacterial strains appear within only a couple years of the release of a new antibiotic. Our antibiotic discovery pipelines must accommodate the necessary shift away from traditional small molecule therapies toward more adaptive drugs.Here, we investigate new ways of combating MDR bacteria and apply those methods in vivo to optimize them for clinical use. We present a novel method for the treatment of infections caused by MDR bacteria: antibiotic photoactivated semiconductor nanoparticles called quantum dots (QDs). Photoactivated QDs kill bacteria by producing superoxide, which targets iron clusters in bacterial cells, and additionally have been shown to potentiate the activity of antibiotics against resistant bacteria. We have previously shown that this specific generation of superoxide allows for killing of bacterial cells without causing toxicity to surrounding mammalian cells in vitro. Indium phosphide (InP) QDs injected subcutaneously into mice caused no measured toxicity, measured through body weight, organ histology, and inflammation and oxidative stress markers in serum, to the host animal after six consecutive days of treatment. InP QDs are activated by near‐infrared (NIR) light, which was provided to the injection site using high‐intensity LEDs. We then used InP QDs to treat subcutaneous abscesses of MDR clinical isolate Escherichia coli in mice. As NIR light has high transmittance through skin and tissue, QDs injected under the skin were sufficiently activated for bacterial killing. We observed decreased bacterial count by QD dosages of 2 and 4 μM compared to PBS treatment. A 6000‐fold drop in abscess bacterial viability was observed in mice treated with 4 μM QDs compared to PBS control.This novel approach to treatment of infectious disease could provide necessary alternatives to small‐molecule drugs. The QDs offer a new method of using superoxide to kill bacteria, including bacteria that have developed resistance to small‐molecule drugs. Our QDs could revolutionize last‐resort treatments of burn and wound infections, with the potential to be expanded to other infection types.