bluuebunny/crossref_metadata_2025_split huggingface dataset:
Training Students on Effective Small Group Dynamics Impacts Student Behavior and Learning Outcomes
Authors: Singh Atul K. 
Published: April 2020

PURPOSESchools have invested significantly in training faculty to become proficient in developing and facilitating student small group learning. However, small group approach continues to receive mixed reviews, and assessing effectiveness of this type of learning experimence is challenging. An important factor that may be overlooked is lack of student training in this methodology. The aim of this study was to determine if training students on effective small group dynamics would result in changes in student behavior and attitude as well as improved outcomes.METHODSIRB approval was obtained to engage students in three activities: 1) training session focused on effective small group dynamics; 2) audiotape recording of small group interactions during two learning sessions prior to training (Pre), and two sessions following training (Post); and 3) survey of student attitudes and perceptions. Training involved a one‐hour session focused on the students’ responsibility for success in small group, nature of high performing individuals in group work, self‐identification of group participant type (initiator, over participant, blocker, deserter, etc.), patterns of effective communication in assent and dissent, sharing roles within the group, setting guidelines and best practices for the group, and reflection and assessment of group effectiveness. For the recorded small group sessions, three trained evaluators independently used an original rubric to assess each recorded session. Rubrics scored various items including participation, role playing, time on task, identification of learning objectives, and patterns of effective communication. Rubric scores were averaged for each session both pre and post training. Additionally, a 15‐question, Likert scale survey was developed to assess student attitudes. This survey was administered three times to each student: 1) prior to participation in any small group activity; 2) following the two Pre small group sessions, and immediately prior to training; and 3) immediately after recording the Post small group sessions. Survey items gathered student perceptions related to preparation, peer interactions, and general effectiveness of the activity.RESULTSPreliminary analysis of audio recordings suggest that following training, students participated more often and more equally. Students also encouraged and requested information from peers more frequently. However, although students were instructed to vary roles and focus on stated objectives, little change was noted in these areas when comparing Pre to Post sessions. Student survey responses also revealed that general enjoyment increased, students felt more empowered to contribute, and were able to avoid tangential discussions more effectively following training.CONCLUSIONThis study indicates that training students on effective small group dynamics influences behaviors and perceptions that impact student enjoyment and learning success.Support or Funding InformationNo funding to report
The Role of Pyruvate Kinase Isoform M1/2 in Colorectal Cancer
Authors: Park Bohye , Kim Ji Yeon , Crumbley Christopher , Wirthwein Kaci , Riffey Olivia , Beaird Jacob , Smith Mary , Donohoe Dallas 
Published: April 2020

Colorectal cancer cell (CRC) increases the utilization of glucose and decreases the oxidation of butyrate, which is a primary energy source for non‐cancerous colonocytes. Butyrate is a short‐chain fatty acid that is a bacterial‐derived fiber fermentation product. It takes years for the colorectal adenoma to manifest as it progresses toward invasive carcinoma. Within this timeframe, the adenoma must acquire key genomic and metabolic modifications that promote tumor growth and progression. Understanding the metabolic shift mechanisms away from butyrate oxidation to glycolysis in the CRC is significant. The overexpression of the pyruvate kinase isoform M2 (PKM2) is observed in biopsies of colorectal cancer patients, which is a hallmark of cancer. Pyruvate kinase is a metabolic enzyme that catalyzes the last step in glycolysis, which converts phosphoenolpyruvate to pyruvate generating ATP. PKM1 is generally expressed in adult differentiated tissues, such as normal non‐cancerous colonic tissue, where it promotes oxidative metabolism. In contrast, PKM2 is expressed in proliferating cells, including colorectal cancer cells, where it enhances aerobic glycolysis. However, the function of PKM2 in colorectal cancer tumorigenesis remains controversial. Our preliminary studies suggest that PKM2 drives colorectal metabolism away from butyrate and toward glucose utilization. A stable knockdown of PKM2 in colorectal cancer cells increased the oxidation of butyrate. The major hypothesis for this project is that through enhancing glucose utilization and suppressing butyrate, utilization PKM2 promotes colorectal tumor progression. Here, we demonstrate that, when expressed rather than PKM2, the PKM1 increases butyrate oxidation in cancerous colonocytes.Support or Funding InformationUSDA R011770176
Amplification of Love bugs (Plecia nearctica) Fungal Community DNA using the ITS86F and ITS4 primers
Authors: Grant Caylin Marie , Stamper Fre’Keliah Breana , Haggins Danielle Keyandra , Sakura-Lemessy Adia Issa , Okafor Uzoma 
Published: April 2020

Plecia nearctica better known as love bugs or honeymoon flies are species of march fly that originated from parts of Central America and the Southern eastern United States. This research is aimed at investigating the selectivity of using the ITS86F and ITS4R, in amplifying fungi community on lovebugs and sex differentiation (male or female). Libraries will be constructed from PCR‐amplified fragments, sequenced and compared against sequences deposited in GenBank. The results will show the specific selectivity of the following fungal: Ascomycetes, Basidiomyces and Zygomycetes. Amplified products generated by the ITS86F and ITS4, which will be aligned with a range of fungi species. This will be the first reported use and assessment of the ITS86F and ITS4, primers in amplifying fungal community from love bugs.Support or Funding InformationAlbany State University STEM Center for Undergraduate Research
Structure of the E6/E6AP/p53 Complex in Human Papillomavirus
Authors: Fassler Amy , Bhat Tara , Rens Davis , Chojnacki Kennan , Neil Uma 
Published: April 2020

Human Papillomavirus (HPV) is the most common sexually transmitted pathogen in humans and the primary cause of cervical cancer. The tumor suppressor p53, in its normal state, regulates cell growth and survival through mechanisms including DNA repair and apoptosis. The E6 oncoprotein directly inhibits p53s function by attaching itself to a ubiquitin ligase, E6AP, which in turn forms a complex with p53. E6 and E6AP form a heterodimer by binding at a leucine‐rich docking site, known as the LxxLL motif. The heterodimer then forms a binding pocket with p53, which is the cause of the inactivation of p53 function. Researchers are attempting to identify potential binding pocket function in the complex in order to form a protein inhibition mechanism that can block further proliferation of cervical cancer. Understanding the interactions of the E6/E6AP/p53 complex is leading to the development of unique antiviral and chemotherapeutic agents for cervical cancer. The Marshfield High School MSOE Center for BioMolecular Modellng for SMART Team used 3D modelling and printing technology to examine the structure‐function relationships of the E6/E6AP/p53 complex.Support or Funding InformationMarshfield Clinic LaboratoriesMSOE Center for BioMolecular ModelingMarshfield Area Community Foundation
Blood Pressure, Vascular Reactivity, and SOD Expression/Activity in Mas1 Receptor Knockout Rats in the Dahl Salt‐Sensitive Genetic Background
Authors: Zheleznova Nadya N. , Terashvili Maia , Bullis Jack , Stumpf Megan , Nguyen Linh , Geurts Aron , Lombard Julian H. 
Published: April 2020

Dahl salt‐sensitive (SS) rats are the most widely used rodent genetic model of human salt‐sensitive hypertension. Earlier studies have established the importance of impaired regulation of the renin gene in contributing to endothelial dysfunction in SS rats and the protective effect of low dose angiotensin II (ANG II) infusion in restoring endothelial function via the ANG II type1 receptor (AT1R) in the SS genetic background. Activation of the Mas1 receptor (Mas1R) for angiotensin (1‐7) [ANG (1‐7)] generally opposes ANG II‐mediated effects of AT1R activation. In Sprague‐Dawley rats fed high salt diet, binding of ANG (1‐7) to the Mas1R can activate NRF2 defenses and restore impaired endothelial function. The goal of the present study was to provide initial phenotyping of a Mas1R knockout (Mas1R KO) rat in the Dahl SS genetic background. Mas1R KO rats and wild type (WT) controls (12–15 weeks old) were maintained on a low salt (LS; 0.4% NaCl) or switched to a high salt (HS; 4% NaCl) diet for 3 days or 10 days. Arterial pressure measured via telemetry was similar in Mas1R KO rats (121±7 mmHg, n=3) and WT rats fed LS diet (124 mmHg, n=2) and increased in WT (138 mmHg, n=2) and Mas1R KO rats (132±5 mmHg, n=3) fed HS diet for 10 days. In rats fed LS diet, Mas1R KO eliminated vasodilator responses to ANG (1‐7) and AVE0991 (Mas receptor agonist) in middle cerebral arteries (MCA) and mesenteric resistance arteries (MRA) and reduced acetylcholine (ACh) reactivity in MCA. Because superoxide dismutase (SOD) enzymes contribute to antioxidant defense by catalyzing the dismutation of superoxide radicals and help to prevent diseases related to oxidative stress and endothelial dysfunction, we measured superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2) activity in the liver of WT and Mas1R KO rats after 3 days of HS diet. High salt diet increased SOD1 activity (WT‐LS 1.04±0.16 U/ml vs WT‐HS 1.65±0.12 U/ml) and SOD2 activity (WT‐LS 0.76±0.03 U/ml vs WT‐HS 1.06±0.11 U/ml) in WT rats, but not in Mas1R KO rats. SOD1 and SOD2 mRNA expression (evaluated via RT‐PCR) tended to increase in WT rats fed HS diet vs. LS diet (1.3 – 1.8 fold change, p > 0.05). SOD1 mRNA expression was significantly higher in HS‐fed Mas1R KO rats vs. Mas1R KO rats fed LS diet (2.8 fold change, p = 0.01) and SOD2 mRNA tended to increase as well (1.7 fold change; p = 0.1). SOD1 and SOD2 protein expression measured by Western blot analysis was similar in WT and Mas1R KO rats fed either LS or HS diet. The present study using the Mas1 receptor knockout in the Dahl SS rat genetic background suggests that Mas1R activation by its agonists (AVE 0991) and ANG (1‐7) improves endothelial function and may provide novel therapeutic strategies for the treatment of low‐renin salt‐sensitive hypertension.Support or Funding InformationNIH #HL‐128242 and NIH #R21‐OD024781
Rapid Accumulation of Triacylglycerol in the Liver is a Component of the Acute Exercise Response and May Serve a Protective Role Against Lipotoxicity
Authors: Henderson Gregory C. , Tuazon Marc A. 
Published: April 2020

We have previously shown that the content of triacylglycerol (TAG) in the liver transiently increases after a single bout of exercise in untrained mice, and this phenomenon has been observed in human subjects as well. This discovery depicted a new phenomenon in the metabolic exercise response. Here we propose the term “lipogenic flexibility” to describe this ability to rapidly alter hepatic TAG content in response to FFA supply. To explore lipogenic flexibility after exercise, we performed lipidomics analysis on liver samples obtained 3 hours after exercise and the following day. Female mice performed a single bout of continuous exercise (CE), high intensity interval exercise (HIIE), or no exercise (CON). The total concentration of hepatic TAG rose 3 hours after exercise (P < 0.05 for both CE and HIIE vs CON), but the total concentration of all other measured lipid classes remained unchanged after exercise (NSD). Hepatic TAG declined back to control levels by the day after exercise. We performed correlation analysis to test the association of TAG (an inert lipid depot) with lipotoxic lipid classes in the liver. Hepatic TAG was positively correlated with hepatic diacylglycerol (DAG) in CON (P < 0.05); however, during the hepatic TAG pool expansion after exercise, liver TAG and DAG were no longer significantly correlated with one another (NSD). Exhibiting lipogenic flexibility after exercise appears to break the equilibration between DAG and TAG, allowing fatty acids to be drawn toward the inert lipid pool (TAG) and away from the lipotoxic lipid pool (DAG). The results suggest that the TAG pool actively expands to buffer elevated FFA supply after exercise and may act to prevent lipotoxicity.Support or Funding InformationThis work was supported by the Faculty Research Grant Program of Rutgers University, the American Diabetes Association grant # 7‐13‐JF‐27‐BR to G Henderson, and the Purdue University College of Health and Human Sciences.
The Effect of Menopause Status on the Skeletal Muscle Metaboreflex.
Authors: villarraga nicolas , Smith Joshua R. , Randall Nicholas R. , Bruhn Eric , Olson Thomas P. 
Published: April 2020

IntroductionIt is well established that the exercise pressor reflex contributes to cardiovascular control (e.g. mean arterial pressure (MAP)) during exercise. One arm of the exercise pressor reflex includes the metabolically sensitive group IV afferents (i.e. metaboreflex). The metaboreflex‐induced cardiovascular responses to exercise are incompletely understood, especially in women across the aging spectrum. For example, post‐menopausal women have greater increases in MAP and systemic vascular resistance (SVR) during locomotor muscle exercise compared to pre‐menopausal women. However, it is unclear if an exaggerated metaboreflex arising from the locomotor muscles is contributing to these cardiovascular adjustments with exercise in post‐menopausal women. We hypothesized that 1) post‐menopausal women will have an augmented MAP response with isolated metaboreflex activation compared to pre‐menopausal women and 2) the exaggerated increase in MAP in the post‐menopausal women will be primarily due to greater increases in SVR.MethodsPre‐ (n= 10, 25±3yrs, 24±3 kg/m2) and post‐menopausal women (n=12, 58±4yrs, 24±3 kg/m2) performed 2 sessions of cycling exercise at 20 W for 5 min with bilateral upper thigh pressure tourniquets inflated to 90 mmHg. At end exercise, the recovery was randomized to post‐exercise circulatory occlusion (PECO) to isolate the metaboreflex (via bilateral upper thigh pressure tourniquets rapidly inflated to suprasystolic pressure for 2 min) or normal recovery (NR) without intervention. Systolic and diastolic blood pressure were measured via manual sphygmomanometry and MAP was calculated. Cardiac output was measured via open circuit acetylene wash‐in and systemic vascular resistance (SVR) was calculated. Data is reported as the absolute change from rest to recovery.ResultsMAP was elevated during PECO compared to NR in both groups (p<0.05), while MAP during PECO was greater in post‐ compared to pre‐menopausal women (20±9 vs. 13±5 mmHg, respectively) (p<0.05). Similarly, SVR was elevated during PECO compared to NR in both groups (p<0.05), while SVR was greater during PECO in post‐ compared to pre‐menopausal women (5±3 vs. 3±1 mmHg/L/min, respectively) (p<0.05). In contrast, cardiac output was not different between NR and PECO in either pre‐ (NR: 0.3±1 vs. PECO: −0.2±1 L/min) and post‐menopausal (NR: −0.1±1 vs. PECO: −0.7±0.9 L/min) (all, p>0.05).ConclusionThese data demonstrate that isolated metaboreflex stimulation following whole‐body exercise results in exaggerated increases in MAP and SVR in post‐ compared to pre‐menopausal women. These data suggest that exercise pressor reflex‐mediated control of MAP during exercise is accentuated in post‐menopausal women with menopause status.
Development of Targeted Interleukin‐27 Gene Therapy for Disrupting Malignant Crosstalk in Prostate Cancer Bone Metastases
Authors: Salameh Janelle Weslyn , Figueiredo Marxa L. 
Published: April 2020

Although ~90% of prostate cancer patients with advanced disease will exhibit bone metastasis, current therapies focus on one aspect of the disease (either the tumor or the bone), with tumor elimination being the primary goal. Prostate cancer (PCa) cells ‘hijack’ bone homeostasis by disrupting the crosstalk between critical cells within the tumor/bone microenvironment (osteoblasts, osteoclasts, and immune cells), and utilizing this effector‐rich environment for cancer cell survival and growth. Crosstalk pathways primarily involve Interleukins (IL‐6 and IL‐11) and transforming growth factor β (TGFβ). Therefore, a key therapeutic objective in malignant skeletal disease management is to eliminate tumors while restoring bone homeostasis. Current treatments are limited to palliative radiotherapy, chemotherapy, or anti‐RANK treatments, all of which have considerable side effects such as osteonecrosis of the jaw or enhanced tumor invasion. An emerging approach to treating skeletal malignancies, osteoimmunology, investigates new multifunctional immune‐stimulatory agents that can simultaneously combat tumor growth and promote bone repair. Our group is interested in IL‐27, an immunomodulatory cytokine with great potential as a multifunctional cancer therapeutic. Its regulatory roles include antitumor immune responses (promoting Th1 differentiation), inhibition of tumor growth, and direct modification of tumor/bone crosstalk to support bone regeneration. We hypothesize that a secreted tumor‐targeted IL‐27 gene therapy approach would facilitate the accumulation of IL‐27 in the bone/tumor microenvironment, thus eliminating tumors while restoring bone. To test this hypothesis, we created a tumor‐targeted IL‐27 gene by incorporating a novel peptide (LSLITRL); an IL‐6 receptor antagonist known to inhibit angiogenesis and tumor growth; or a scrambled control peptide at the C‐terminus. To detect the expression, secretion, and tumor recognition specificity, IL‐27 constructs were fused to a NanoLuciferase expressing vector modified with a secretion signal at the N‐terminus. We have also assessed the potential for our proposed gene therapy in disrupting malignant characteristics of PCa in vitro in by assessing STAT‐1/‐3 activation and will be assessing bone cell mineralization in PCa/bone co‐cultures. Future studies will examine the therapeutic efficacy of secreted, tumor‐targeted IL‐27 in vivo.Support or Funding InformationNCI R01CA196947‐S1
SPARC: Renal Denervation Attenuates DOCA‐salt Hypertension in the Mouse
Authors: Baumann Daniel C. , Van Helden Dusty , Evans Louise , Osborn John 
Published: April 2020

Hypertension affects approximately one third of the adult population in the United States. Catheter based renal denervation (RDN) has emerged as a novel treatment for hypertension in patients. However, the mechanisms by which RDN lowers arterial pressure has not been fully determined. We hypothesize that an interaction between renal nerves (afferent and efferent) and renal inflammation contributes to hypertension. To test this hypothesis, we utilized a model of hypertension in the mouse produced by the combination of uni‐nephrectomy with deoxycorticosterone acetate (DOCA) and a high salt diet (DOCA‐salt). 10‐week‐old male C57BL6/J mice were implanted with radio‐telemetry probes in the carotid artery for measurement of arterial pressure. DOCA was administered via subcutaneous implantation of a silicon pellet containing 50 mg of DOCA. Sham mice received a drug free silicon pellet. Uni‐nephrectomy, pellet insertion, salt treatment, and RDN were all performed or started on the same day. RDN was performed through surgical ablation and peri‐axonal application of 10% phenol. Baseline arterial pressure was measured 3 days prior to induction of DOCA‐salt hypertension by radiotelemetry. Separate cohorts of mice were generated for protein quantification and histology, with urine and kidneys harvested 21 days post induction of DOCA‐salt hypertension. Cytokine protein quantification was obtained through Multiplex ELISA. All errors reported are SEM. Following 7 days of DOCA‐salt, mean arterial pressure (MAP) increased +44.8 ± 3.2 mmHg from baseline (153.1± 1.8 mmHg day 7 absolute value), comparted to −1.5 ± 5.5 mmHg in sham mice (105.6 ± 0.5 mmHg day 7 absolute value). RDN reduced this increase by more than 50% in RDN‐DOCA‐salt mice (+20.5 ± 5.0 mmHg delta, 131.6 ± 8.1 mmHg absolute). Renal and urinary cytokines and chemokines were increased in DOCA‐salt compared to sham treated mice. For example, renal MCP‐5 was 24.7 ± 7.2 pg/mg in DOCA‐salt mice compared to 5.0 ± 0.6 pg/mg in sham treated mice. Similarly, urinary MCP‐5 was significantly higher in in DOCA‐salt mice (12.4 ± 5.1 pg/mg) compared to sham mice (2.1 ± 1.1 pg/mg). IL‐1α and IL‐1β were both increased in DOCA‐salt kidneys (112.4 ± 19.2 pg/mg and 2.1 ± 0.4 pg/mg respectively) compared to sham kidneys (31.98 ± 4.4 pg/mg and 0.36 ± 0.06 pg/mg respectively). We also measured, by immunohistochemistry, an increase expression of the IL‐1 receptor in kidneys of DOCA‐salt mice compared to sham controls. We hypothesize that renal cytokines activate renal afferent nerves and ultimately elevate arterial pressure by activation of the sympathetic nervous system. Future studies will test this hypothesis by examining whether elimination of cytokine generated afferent nerve activity attenuates hypertension in DOCA‐salt mice.Support or Funding InformationNIH: R01HL116476, MnOPT: T32DK083250–01A1, SPARC: 5U01DK116320‐03
Sex Differences in Periaqueductal Gray Kinase Activation After Morphine Tolerance
Authors: Ram Akila , Edwards Taylor M. , McCarty Ashley , Bobeck Erin N. 
Published: April 2020

Morphine is a potent opioid analgesic with very high propensity for tolerance development. The analgesic and tolerance properties of opioids are partially regulated by the midbrain ventrolateral periaqueductal gray (vlPAG). There is a growing body of literature that highlights the sex differences in pain processing and opioid effects. However, the nature of sex differences at the level of kinase effectors of the μ‐receptor is unknown. Here, we investigate the intracellular kinase activation and localization patterns in the vlPAG of male and female mice following acute and chronic morphine treatment. Wild‐type mice were treated with morphine (10 mg/kg, i.p.) or saline in a chronic or acute administration paradigm. We performed fluorescence immunohistochemistry to map the localization and activation of extracellular signal‐regulated kinase 1/2 (ERK 1/2), protein kinase‐C (PKC), and protein kinase‐A (PKA). We observed elevated baseline levels of phosphorylated forms of the kinases ERK 1/2, PKC and PKA in females. We observed significantly greater activated ERK 1/2 in the vlPAG chronic morphine‐treated animals which co‐localized with the endosomal marker Eea1. We note that phosphorylated PKC tends to localize to the plasma membrane near the μ‐opioid receptor in the vlPAG following chronic morphine treatment. Further, we observed that although PKA activation is increased following chronic morphine treatment, there is a significant reduction in nuclear translocation of this kinase. Across these kinases, the magnitude of increase of kinase activation was more in males after morphine tolerance. Taken together, this study demonstrates a differential activation and localization of ERK 1/2, PKC and PKA across sexes and opens avenues to explore the role of chronic morphine treatment on G‐protein signaling and kinase nuclear transport.Support or Funding InformationBrain and Behavior Research Foundation to ENB. Department of Biology, Utah State University