bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification and quantification of anthocyanins in the transgenic tomatoes (393.8)
Authors: Su Xiaoyu , Xu Jianteng , King Brenee , Lim Wansang , Katz Benjamin , Park Sunghun , Tomich John , Wang Weiqun 
Published: June 2021

Anthocyanins, a sub‐class of flavonoids, are natural pigments derived from phenylpropanoid pathway. Most tomato cultivars found in nature have very low content of anthocyanins, but dark purple tomatoes by ectopic co‐expression of two transcription factors Delila (Del) and Rosea1 (Ros1) from snapdragon and chalcone isomerase (CHI) from onion accumulated high levels of anthocyanins. This study is to identify and quantitate anthocyanins in these transgenic tomato lines. Seven anthocyanins including two new anthocyanins [malvidin‐3‐(p‐coumaroyl)‐rutinoside‐5‐glucoside and malvidin‐3‐ (feruloyl) ‐rutinoside‐5‐glucoside] have been identified in transgenic lines by HPLC‐MS. The top two anthocyanins are petunidin 3‐(trans‐coumaroyl)‐ rutinoside‐ 5‐glucoside and delphinidin 3‐(trans‐coumaroyl)‐rutinoside‐5‐glucoside, that contribute for 85% of total anthocyanins in whole fruit. Comparing with undetectable anthocyanins in the wild type, Del/Ros1‐expressing tomatoes contain total anthocyanins at 4.95±0.42 g/kg dry matter in whole fruit, 5.09±0.62 g/kg dry matter in peel, and 5.56±0.29 g/kg dry matter in flesh, while CHIxDel/Ros1‐coexpressing tomatoes have 9.61±0.71 g/kg dry matter in whole fruit, 29.9±1.64 g/kg dry matter in peel, and 8.65±0.39 g/kg dry matter in flesh. No anthocyanins are detectable in the seeds of each line tested. Enrichment of tomato fruit with new and high anthocyanins may provide potential health‐promoting benefitsGrant Funding Source: USDA Cooperative KS511‐1001903
Insights into neural crest phosphoregulation through the antiphosphatase Paladin (541.8)
Authors: Roffers‐Agarwal Julaine , Hutt Karla , Stronge Edward , Gammill Laura 
Published: June 2021

The neural crest is a multipotent, migratory, embryonic cell type that forms a variety of derivatives including the craniofacial skeleton and peripheral nervous system. While the transcription factor network that regulates neural crest formation is heavily scrutinized, the mechanisms that control where resulting proteins act is relatively ignored. We propose that modulation of protein activity through phosphorylation also regulates the establishment of neural crest cell fate. Our previous work showed that precise levels of the antiphosphatase Paladin are required for normal neural crest specification and migration in chick, emphasizing the importance of phosphoregulation during neural crest development. To elucidate the mechanism of Paladin’s action, we identified putative Paladin interactors in an in vitro screen. One interactor, Myosin Heavy Chain 9 (MYH9), is enriched in premigratory and migratory neural crest cells and mutations are associated with human patients with neurocristopathies. We are currently working to confirm the Paladin‐MYH9 interaction in vivo, examine the regulation of MYH9 phosphorylation during neural crest development, and identify novel neural crest regulators through an in vivo Paladin interactor screen. Together, this work will expand our understanding of an underappreciated level of control within the neural crest developmental program.Grant Funding Source: Supported by NIH F32DE019973; K22DE015309; R03DE023368; Amer Assn of Anatomists; MN Med Foundation
PrPC associates with a multimolecular complex including LRP1 and glycosphingolipids within lipid rafts (601.1)
Authors: Mantuano Elisabetta , Tasciotti Vincenzo , Garofalo Tina , Sorice Maurizio , Misasi Roberta , Mattei Vincenzo 
Published: June 2021

The cellular form of prion protein (PrPC) is a highly conserved cell surface GPI‐anchored glycoprotein that was identified in cholesterol‐enriched, detergent‐resistant microdomains (‘rafts’). Like other GPI‐anchored proteins, most of PrPC molecules were found in lipid rafts from neural and non‐neural cells. Recently, PrPC was identified as a high‐affinity receptor for Aβ oligomers. Prion protein‐mediated toxicity of Aβ oligomers requires lipid rafts and the transmembrane low density lipoprotein receptor‐related protein‐1 (LRP1). LRP1 is an endocytic and cell‐signaling receptor for diverse ligands, which control the activity of LRP1 by directing the recruited co‐receptors. LRP1 controls both the surface and intracellular trafficking of PrPC in neurons.Our results show that PrPC is strictly associated with gangliosides in microdomains of neuroblastoma cells. Scanning confocal analysis reveals a consistent co‐localization between PrPC and GM1, as well as between TrkA and GM1, indicating the existence of a glycosphingolipid‐enriched molecular complex. These data suggest that LRP1, PrPC and TrkA may function as part of a single system associated with lipid rafts, involved in receptor‐mediated neuritogenic pathway. In addition, we confirmed by co‐immunoprecipitation experiments a specific PrPC ‐ganglioside interaction. Moreover, signal transduction experiments on neuritogenic pathway were performed using human recombinant PrP (hPrPrec), and the results indicate a role for PrPC in cell signaling in neurons. We hypothesize that the ability of PrP to induce cell signaling might involve a multi receptor complex, in which LRP1, in association with other receptors, like TrkA receptor, plays a role in signal transduction within lipid rafts.These findings suggest that PrPC associates with a multimolecular complex, including, LRP1, TrkA and ganglioside GM1, which is dependent on the integrity of lipid raft and is involved in the neuritogenic signaling and trafficking.
Brain dynamics and attentional control as a function of body iron status (619.4)
Authors: Rhoten Stephanie , Wenger Michael , Murray‐Kolb Laura , Gahutu Jean‐Bosco , Lung’aho Mercy , Haas Jere 
Published: June 2021

Iron deficiency (ID) is a highly prevalent micronutrient deficiency, affecting individuals in both developing and developed countries. Previous research on children with ID report deficits in attention related to variations in brain dynamics as measured using electroencephelography (EEG). We report here the results of analysis of baseline data from a randomized, double‐blind dietary intervention study involving 257 female students (ages 18‐26) at the University of Rwanda, Huye; 54 of these participated in the behavioral and EEG testing, using 3 tasks designed to assess attentional capture and control: (a) simple reaction time (SRT), a test of perceptual processing speed; (b) Go/No‐Go (GNG), a test of inhibitory control; and (c) the Attentional Network Task (ANT), a test of three critical functions of attention. EEG data were collected using a 64‐channel system (BrainProducts, Gilching, Germany), with signals sampled at 250 Hz. We observed statistically significant relationships between blood measures of iron status and the magnitude (positive) and latency (negative) of two EEG components (P1/N1 and P3); a positive relationship with one measure of overall brain activity (global field power) and a positive relationship with one measure of brain activity specific to engaged attention (power in theta‐band activity). These results suggest a critical role for iron in brain dynamics related to attention.Grant Funding Source: HarvestPlus/IFPRI
Differences in cognitive flexibility between healthy weight and obese children: an ERP study (629.6)
Authors: Khan Naiman , Raine Lauren , Drollette Eric , Scudder Mark , Pontifex Matthew , Hillman Charles 
Published: June 2021

Obesity is associated with cognitive decline in later adulthood; however, the implication of obesity on childhood cognitive and brain health remains controversial. Accordingly, this study investigated the effect of weight status (healthy weight [HW] or obese [OB]) on behavioral and neuroelectric measures of cognitive control among 80 prepubertal children (8‐9‐years). HW (n=40) and OB (n=40) children completed a switch (cognitive flexibility) task while event‐related brain potentials were concurrently measured. Adiposity and aerobic fitness were assessed using DXA and VO2max, respectively. Groups were matched on key covariates including age, sex, IQ, SES, fat‐free VO2max, and ADHD. There were no differences in response accuracy or reaction time between groups on both the homogenous and heterogeneous trials. However, obese children exhibited greater global switch costs related to response accuracy. In addition, obese children displayed smaller central‐parietal P3 amplitude during heterogeneous trials, signifying decreased allocation of attentional resources. Given that global switch costs reflect efficiency of maintaining task sets in working memory as well as the selection of subsequent tasks, our findings indicate that obese children may exhibit lower cognitive flexibility when faced with greater executive function demands.Grant Funding Source: Supported by NIH HD055352
Glucose restriction, ketone supplementation, and hyperbaric oxygen therapy inhibit proliferation and viability and increase reactive oxygen species production in VM‐M3 glioma cells (644.18)
Authors: Poff Angela , D'Agostino Dominic 
Published: June 2021

The Warburg Effect and tumor hypoxia underlie a unique cancer metabolism characterized by glucose dependency and mitochondrial dysfunction. Previous research indicates this phenotype can be exploited therapeutically with glucose restriction, ketone supplements, or hyperbaric oxygen (HBOT). We have previously shown that these conditions decrease tumor growth and metastatic spread and increase survival time in mice with VM‐M3 metastatic cancer. To further characterize the effects of these therapies, we measured proliferation, viability, and ROS production in VM‐M3 cells exposed to these conditions: high glucose (control; 25mM), low glucose (LG; 3mM), ketone supplementation (βHB; 5mM), hyperbaric oxygen (HBOT; 90 min, 2.5 ATA), or combination therapy (LG+BHB+HBOT). Proliferation of VM‐M3 cells was measured with trypan blue hemocytometry and was significantly decreased from controls at 24, 48, 72, and 96 hours (p<05). Viability of VM‐M3 cells was measured by fluorescence microscopy with calcein and EthD‐1 and was decreased by 19.2% in LG, 12.5% in βHB, and 38.2% in LG+βHB+HBOT treated cells compared to control (p<0.05). ROS production was measured by fluorescent microscopy with DHE and was increased by 46% in HBOT and by 48% in LG+βHB+HBOT treated cells compared to control (p<0.001). This study further supports the use of these metabolic therapies as a potential cancer treatment.Grant Funding Source: Supported by Office of Naval Research and a charitable donation from Scivation Inc.
Intravenous mesenchymal stem cell administration spurs endogenous hepatic mitochondrial gene expression in the diet‐induced obese mouse (693.10)
Authors: Newell Christopher , Hughey Curtis , Pihl Carin , Hittel Dustin , Shearer Jane 
Published: June 2021

Intravenous human mesenchymal stem cell (MSC) administration alleviates hepatic oxidative stress in the diet‐induced obese mouse. However, the underlying mechanisms responsible for these benefits are uncertain. Possible explanations range from direct cell engraftment to paracrine‐mediated endogenous cell stimulation. To examine this question, male C57BL/J mice (n=24) were assigned to one of two dietary groups; chow (10% kcal fat) and high fat (60% kcal fat) for 12 wk. Animals were further divided, receiving intravenous saline (0.2 mL PBS) or MSC (750,000 cells). Post‐injection (24 h), qRT‐PCR was used to identify changes in endogenous (mouse) and exogenous (human) transcripts for glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) and mouse mitochondrial protein cytochrome c oxidase subunit II (COX‐II) in the liver. Human GAPDH and COX‐II were detected in the livers of animals undergoing MSC treatment indicating successful cell targeting. Declines in mouse COX‐II caused by HF were mitigated by MSC therapy (p<0.05). Results indicate that MSC administration triggers endogenous mitochondrial gene proliferation which may explain the ability of MSC to mitigate hepatic oxidative stress in diet‐induced obesity.Grant Funding Source: Supported by MitoCanada
Students' satisfaction and burnout: cross‐sectional study at the New Medical Studies in English Program of the University of Split School of Medicine, Croatia (719.17)
Authors: Valic Zoran , Malički Mario , Bradaric Kristina , Jeličić Karlo , Bozic Josko , Marusic Matko , Ljutic Dragan , Valic Maja 
Published: June 2021

Introduction: Quality of teaching and the faculty’s teaching practices can be indirectly assessed through students’ satisfaction and burnout with their studies, factors which also influence students’ academic success and the schools prestige.Aim: To assess students’ satisfaction and burnout at the New Medical Studies in English Program (started in 2011) at the University of Split, Croatia.Methods: In October 2013, we conducted a previously designed satisfaction survey, as well as the Oldenburg Burnout Inventory (OLBI) on all students of the New Medical Studies in English in Split.Results: In total 88 (78%) of students returned the completed questionnaires. Students GPA (out of max 5.0) was 3.4 for the 2nd year and 3.0 for the 3rd year students. Most students (87%) rated campus safety as above average or excellent, 83% rated as such the staff friendliness, 73% the teaching quality, and 67% the overall satisfaction with the School, with no differences between the study years. Students scores on OLBI subscales were 3.0±0.4 for disengagement, and 2.7±0.7 for exhaustion, with first year students showing less exhaustion than higher year students (ANOVA, P=0.010).Discussion: Students grades, as well as self reported study satisfaction and burnout demonstrate the balance of high quality teaching and student engagement at the pre‐clinical courses of the New Medical Studies in English at the University of Split, Croatia.This study was supported by University of Split School of Medicine.
Clinical Anatomy League of University of São Paulo Medical School Methodology: analysis of the impact on student’s learning (721.24)
Authors: Iuamoto Leandro , Nogueira Thiago , Sousa Braian , Ribeiro João , Hojaij Flávio , Akamatsu Flávia , Andrade Mauro , Jacomo Alfredo 
Published: June 2021

Anatomical knowledge plays an important role in medical education and practice. Learning anatomy is frequently associated with memorization. Studies have suggested that the way Anatomy is taught at Medical School is rather inappropriate and that the ability to reason and to apply this knowledge is more important than structure names memorization. The Clinical Anatomy League of University of São Paulo Medical School represents acomplementary way of learning this subject by promoting cadaver dissection activities and lectures that aim to elucidate the clinical and anatomical correlations regarding frequent procedures in the practice of medicine.A 20‐question examination was used to assess the anatomy knowledge of 33 FMUSP students. 14 of those students were League members and the other 19 students composed the control group. The grades of the students on the undergraduate topographical anatomy course and on this research project’s examination were used in order to compare the capability of retaining the anatomy knowledge acquired during the undergraduate course. The data was analyzed on Minitab 16 statistics package.No statistical difference was observed between the grades of the two groups on the undergraduate topographic anatomy course. League members had a better performance on the research project examination. This difference was markedly observed between the more than 1‐year long members and the same grade nonmember students.A still better performance was observed for students who had one full year of activities on the League as compared to students from the same grade that did not, suggesting that it may be an important element for knowledge fixation.
The utilization of positive psychology and multiple modalities in the treatment of mentally ill persons (728.17)
Authors: Cartier William , Cartier Earnestine , Einstein George , Tulp Orien 
Published: June 2021

To determine the contributions of positive psychology along with the integration of multiple behavioural modalities such as Cognitive Behavioral Therapy [CBT], Rational Emotive Behavioral Therapy [R.E.B.T], Individual and group psychotherapy were integrated with a positive orientated interdisciplinary team. Scientist and researchers have barely determined the full capabilities of the human brain and its unknown/hidden powers in terms of commanding/healing of the human body. It became apparent to our research team early on with correctional offenders, that “traditional” patient therapy simply wasn’t working and hence, the offender patient was not presenting any positive results or benefits for them. This study will present several case studies along with other data to illustrate the positive results obtained from correctional offender patient treated with positive results, utilizing the therapies/modalities mentioned above. This has been 5 years of intensive research (phase I) to determine a possible solution to our question. The next phase (phase II) will require 2 years of further intensive research. This will include research utilizing bio‐feedback, neuro‐biofeedback, Imaging (MRI), CAT and PET scan data. Additional research in this area is demanded along with dedicated efforts on the part of multidisciplinary research teams for years to come. Our changing world environment demands this of all of us define ourselves as research scientist when investigating the nature and outcomes of such client populations.Grant Funding Source: Institutional Resources
Structure and evolution guided investigations of terpene synthase mechanism (769.11)
Authors: Peters Reuben 
Published: June 2021

Structure and evolution guided investigations of terpene synthase mechanism Reuben J. Peters Department of Biochem., Biophys. & Mol. Biol., Iowa State University Terpene synthases catalyze wonderfully complex reactions, involving cyclization and/or rearrangements of isoprenyl diphosphate precursors. These reactions are driven by carbocationic cascades, which can be initiated in two distinct ways. Class I terpene synthases catalyze heterolytic cleavage of an allylic diphosphate ester bond to initiate their reactions, while class II terpene synthases utilize protonation for the same purpose. Building on our recent determination of high‐resolution crystal structures for both classes of terpene synthases, along with the conservation pattern underlying the evolution of novel function, we are probing the underlying enzymatic structure‐function relationships. Our results have revealed the ability of single residues changes to dramatically remodel reaction outcome, highlighting the role of electrostatic effects and providing significant insights into the catalyzed complex reactions.Grant Funding Source: GM076324
G‐protein beta‐gamma regulation of Golgi to cell surface transport (802.11)
Authors: Klayman Lauren , Wedegaertner Philip 
Published: June 2021

Non‐canonical G‐protein signaling has been shown to regulate intracellular transport and secretion. G‐protein beta‐gamma localizes to the trans‐Golgi network and activates Protein Kinase D (PKD), resulting in fission of vesicles destined for the plasma membrane. While basolaterally‐targeted (BL) or secretory vesicle release is known to be downstream of PKD activation, apically‐targeted (AP) vesicle release from the Golgi occurs via a PKD‐independent pathway. A similar cargo selectivity for beta‐gamma has not been tested. Here, we generate GRK2ct variants that inhibit beta‐gamma in a spatial or temporal manner. We test regulation of AP and BL cargo trafficking via a temperature shift immunofluorescence transport assay, as well as trafficking of other AP and BL candidate cargoes. We find that lipid‐association of the GRK2ct is critical for its inhibitory function on beta‐gamma. We also generate an inducible system of recruitment of GRK2ct variants to distinct subcellular locations, towards the goal of inhibiting solely Golgi‐localized beta‐gamma signaling. Our system can also be used to inhibit beta‐gamma signaling at other endomembrane locations. The results indicate that beta‐gamma is an upstream regulator of vesicle transport from the Golgi to the cell surface.Grant Funding Source: NIH GM056444
Characterization of tumor‐derived B56γ mutations and their effect on the tumor suppressor function of B56γ‐PP2A (802.21)
Authors: Nobumori Yumiko , Liu Xuan 
Published: June 2021

Protein phosphatase 2A (PP2A) is a family of serine/threonine phosphatases with diverse cellular functions. Previous study reported that B56γ subunit directs PP2A toward tumor suppressive function by dephosphorylating and activating tumor suppressor p53. B56γ‐PP2A also inhibits cell transformation by an unknown p53‐independent mechanism. In this study, we investigate the inactivation mechanism of B56γ tumor suppressive function through characterization of B56γ mutations identified in human cancer. The first class mutations disrupt interaction between B56γ and AC core, and thus B56γ fails to regulate its substrates and completely lose tumor suppressive function. Further, we show that C39R mutation within HEAT repeat1 disrupts B56γ binding with AC core, providing structural insight that intact HEAT repeat1 is required for B56γ‐PP2A holoenzyme assembly. The second class mutations prevent specific substrates from binding B56γ and cause partial reduction of tumor suppressive function of B56γ. We find that A383G and F395C mutations disrupt B56γ from interacting p53. Mutants are unable to dephosphorylate p53 and thus lack p53‐dependent tumor suppressive function, implying that bridging interaction between B56γ and p53 is required for p53 activation by B56γ‐PP2A. In addition, we identified S220N mutation that specifically disrupts p53‐independent function of B56γ, suggesting that it may disrupt the binding of unknown substrates. Although it remains to be investigated how frequently these mutations occur, our results underline the importance of B56γ tumor suppressive function in human cancer.Grant Funding Source: Supported by NIH
Post‐phosphorylation control of dopamine transporter by peptidyl prolyl cis‐trans isomerase PIN1 (803.6)
Authors: Challasivakanaka Sathyavathi , Smith Margaret , Foster James , Vaughan Roxanne 
Published: June 2021

The rat dopamine transporter (DAT) is phosphorylated at the N‐terminus on T53, a site that is followed by proline, making it specific for proline‐directed kinases such as ERK. We found that amphetamine (AMPH) stimulates DAT T53 phosphorylation and mutating this site affects DA transport and AMPH‐stimulated efflux, suggesting a role for T53 phosphorylation in these processes. Phosphorylation of proline‐directed residues strongly impacts protein conformation by reducing the rate of cis‐trans isomerization of the phospho (p)‐S/T‐P peptide bond. This in turn slows the rate of p‐S/T‐P dephosphorylation by preventing actions of phosphatases. The peptidyl prolyl cis‐trans isomerase, PIN1, specifically isomerizes p‐S/T‐P motifs and catalyzes the return of the bond to the trans configuration allowing dephosphorylation to occur. To test for such activities on DAT we have used the PIN1‐specific inhibitor juglone. In both rat striatal synaptosomes and heterologous expression systems juglone treatment rapidly increased the p‐T53 level suggesting that PIN1 acts on DAT and regulates dephosphorylation of T53. In addition, juglone strongly stimulated [3H]DA efflux from rat striatal synaptosomes, supporting a mechanistic link between efflux and p‐T53. These results identify a novel mechanism for regulation of DA efflux and suggest PIN1 as an enzyme that functions in post‐phosphorylation control of DAT function.Grant Funding Source: Supported by NIDA R01 DA 13147