bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of Preparation Techniques for Optimal Hepcidin Detection in Human Hepatocyte Culture
Authors: Morehouse Zachary Patrick , Easparro Brandon , Proctor Caleb , Nash Rodney J. , Atwood James 
Published: June 2021

Approximately 40% of adults aged 65 and older are affected by Chronic Kidney Disease (CKD). Anemia is an associated symptom seen in many patients diagnosed with CKD, promoting elevated cardiovascular risk, decreased quality of life, and increased morbidity and mortality in affected populations. Hepcidin‐25 (hepcidin) is a key iron regulating hormone secreted by hepatocytes to regulate and maintain body iron homeostasis and dietary iron absorption. Hepcidin does this by stifling iron release from macrophages, preventing the normal recycling of iron in the body needed to support erythropoiesis. Elevated levels of hepcidin have been observed in both adults and children suffering from CKD, while its pathological mechanism of action is still relatively unstudied. There is a growing need to further the understanding of hepcidin's role in CDK and other iron related pathologies. Currently there is no standardized methodology for hepcidin evaluation studies on relevant human cell lines, and there is a growing need for studies to be done in this field to assist biomedical researchers in the translation of clinically relevant lab findings from the benchtop to the bedside. Hep G2 is a perpetual human hepatic cancer cell line confirmed to produce hepcidin and a commonly used lineage when studying hepatic function in vitro. While it is confirmed that Hep G2 cells produce hepcidin when cultured, there is currently no standardized procedure for detection of this peptide in vitro from these, or any other human derived cell lines. The expanding clinical and biomedical implications of hepcidin has prompted the need to determine an optimal method for detection of hepcidin in vitro. In this study we use of Hep G2 cells as a model for hepcidin peptide detection and various tissue processing techniques to prepare the cells hepcidin quantification via ELISA.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
xCT and CD44v9 Co‐Expression Mediates Pancreatic Ductal Adenocarcinoma Survival in the Presence of ROS Inducing Chemotherapeutics
Authors: Chang Julie , Holokai Loryn , Chakrabarti Jayati , Lanfranca Mirna Perusina , Frankel Timothy , Zavros Yana 
Published: June 2021

BackgroundPancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer‐related death in the United States. It has been shown that KRAS mutations, often found in PDAC, can lead to the up‐regulation of the expression of the cysteine/glutamate transporter xCT. Transporter xCT has been shown to allow cancer cells to evade ROS mediated cell death. CD44 is a transmembrane protein with many different splice varients. CD44 variant isoform 9 (CD44v9) is expressed during cellular damage and has been shown to mediate cell survival. CD44v9 stabilizes xCT expression on the surface of cancer cells. Therefore, CD44v9 stabilized the xCT transporter, which allows cancer cells to survive following treatment with chemotherapeutics that induce ROS.HypothesisTransporter xCT and CD44v9 co‐expression mediates PDAC survival in the presence of ROS inducing chemotherapeutics.MethodsHuman‐derived pancreatic cancer organoids (HuTPOs) were generated from the resected tissue of patients with PDAC. A dose response curve was performed by treating the huTPOs with eight different micromolar concentrations of oxaliplatin, gemcitabine, 5‐fluorouracil (5‐FU). These chemotherapeutics have been shown to induce ROS within PDAC cells. The susceptibility or resistance of the huTPOs to the chemotherapeutics was determined by measuring cell death by an MTS proliferation assay. HuTPOs were analyzed by immunofluorescence for the expression of the cysteine‐glutathione transporter, xCT, and cancer stem cell marker, CD44v9.ResultsThere was divergent expression of xCT and CD44v9 in huTPO lines generated from individual patients. Dose response curves performed on huTPO lines revealed that organoids not expressing xCT or only xCT were sensitive to ROS inducing chemotherapeutics (5‐FU, oxaliplatin and gemcitabine). Interestingly, huTPOs that expressed both xCT and CD44v9 were resistant to 5‐FU, oxaliplatin and gemcitabine.ConclusionCD44v9 may stabilize xCT in PDAC cancer organoids allowing for resistance to ROS inducing chemotherapeutics. Pancreatic organoids may be a good screening based model to determine efficacy of ROS inducing chemotherapeutics in PDAC.Support or Funding InformationSteven Goldman Memorial Pancreatic Cancer Research Grant (Zavros) 1RO1DK083402This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Evaluation of Antimicrobial Properties of African Basil (Ocimum gratissimum) and Tassel Flower (Emilia coccinea) Leaf Extracts
Authors: Besong Mary M. , Chintapenta Lathadevi K. , Ozbay Gulnihal , Aikins Anthea , Besong Samuel A. , Aryee Alberta N. 
Published: June 2021

The use of plant extracts and phytoconstituents with antimicrobial properties may provide therapeutic benefits and application in consumer products such lotions and soaps, and active food packaging. The objective of this study was to assess the efficacy of water, methanol, butanol and ethyl acetate extracts of Ocimum gratissimum leaf (OGL) in inhibiting the growth of selected bacteria (E. coli O157:H7 (ATCC 43894), Salmonella enterica serovar Typhimurium DT‐104 (CDC H3380), Aeromonas hydrophila K144, and Pseudomonas aeruginosa (ATCC 7700)). In a parallel study, water, methanol, and butanol extracts of Emilia coccinea leaf (ECL) and OGL were also tested against E. coli, Pseudomonas aeruginosa, and Staphylococcus aureus. To screen for antimicrobial activity, the susceptibility of these selected pathogens and non‐pathogenic bacteria was determined using the disk diffusion assay. Selected antibiotics such as tetracycline, streptomycin, ampicillin and kanamycin were used as positive control. Following incubation, zone of inhibition differed between control and extracts, with larger zone of inhibition in the OGL butanol extract than the water, methanol, and ethyl acetate extracts in all the four pathogens tested, and a smaller zone of inhibition for E. coli, Salmonella and Pseudomonas cultures. Aeromonas hydrophila K144 cultures were found to be susceptible to butanol extract showing 10 mm of clearance zone. Incubation of ampicillin with Aeromonas hydrophila K144, Salmonella enterica serovar Typhimurium DT‐104 (CDC H3380) and Pseudomonas aeruginosa (ATCC 7700) led to minor changes in the zone of inhibition of these antimicrobials. P. Aeruginosa and S. aureus were resistant and susceptible to all antibiotic controls tested, respectively. E. coli, P. aeruginosa, S. aureus were all susceptible to the methanol and butanol extracts of OGL and ECL. Butanol and methanol extracts of Ocimum gratissimum and Emilia coccinea leaf could be suitable alternative to some chemical antimicrobials, satisfying consumer demand for natural products.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Self‐serving Contagion and Mimicry in Buffet Lines: Whom You Follow Influences What and How Much You Take and Eat
Authors: Wansink Brian 
Published: June 2021

Eating companions can influence eating behavior, but can they influence self‐serving? Less is known how strangers who self‐serve food in a public place may encourage self‐serving mimicry, whether this varies with food‐type and gender, and how self‐serving behavior influences eating behavior. This study investigates self‐serving mimicry in a buffet line in an attempt to determine what people and foods are most prone to serving mimicry and what is the impact of these on subsequent items. 163 strangers were ordered female‐female‐male male and then consecutively served themselves six food items from a lunch buffet. Amounts served and eaten were measured along with demographic measures. The amount a person serves and eats is influenced by the amount served and eaten by the person immediately in front of them. This result appears to be driven mostly by females following females, and can result in an increase in caloric intake. Among these women, mimicry appeared to be stronger with hedonic foods (French fries, applesauce, and macaroni salad) than with less indulgent foods (chicken and celery). Serving contagion and mimicry exist in public places like buffet lines. There are specific implications for dieters suggesting the most indulgent foods are the ones most prone to mimicry.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Neuropeptide Y and Dipeptidyl Peptidase IV in Pre‐ and Post‐Menopausal Women
Authors: Mann Elise , Kluess Heidi A. , Neidert Leslie E. , La Mantia Anna M. , Sandage Mary , Plexico Laura 
Published: June 2021

The purpose of this study was to investigate changes in neuropeptide Y (NPY) protein and dipeptidyl peptidase IV (DPP‐IV) activity in the plasma and saliva in normally cycling women and women after menopause. We recruited seven premenopausal women and seven post‐menopausal women for the study. Blood via venipuncture and saliva samples were taken at each point in the menstrual cycle (pre‐menopausal) or once per week (post‐menopausal) for 2 months. Blood and saliva were analyzed for estrogen, neuropeptide Y using ELISA's and DPP‐IV activity using a fluorometric assay. Plasma β‐estradiol was an average of 96.45±57.04 pg/ml over 2 cycles in the pre‐menopausal group and 1.72±0.35 pg/ml over 2 months in the post‐menopausal group (p<0.05). In the pre‐menopausal group, there were no significant differences in saliva or plasma NPY or DPP‐IV over the cycle. For the post‐menopausal group, salivary NPY and DPP‐IV did not change over 2 months. Plasma NPY was lowest in the middle 2 weeks (average: 0.52±0.10 ng/ml) compared to the first and 4th weeks (average of week 1 and 4: 0.60±0.14 ng/ml; p<0.05). Plasma NPY in postmenopausal women was higher overall (0.56±0.13 ng/ml) compared to pre‐menopausal women (0.30±0.11 ng/ml; p<0.05). Plasma DPP‐IV activity was unchanged by time in the post‐menopausal group. Saliva DPP‐IV and saliva NPY in the pre‐menopausal group had a significant negative correlation (R=−0.95; p<0.05). We found that saliva measures of NPY and DPP‐IV activity are poor estimates of plasma concentrations and activities. Differences in plasma NPY concentrations between the groups and the relationship between salivary NPY and DPP‐IV suggests that there are some unique differences between these groups.Support or Funding InformationThe work presented in this poster session was supported by Award Number 1R03DC013664‐01A1 from the National Institute on Deafness and Other Communication Disorders (NIDCD). The content of this presentation is solely the responsibility of the authors and does not necessarily represent the official views of the NIDCD or the National Institutes of Health.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Chronic Intermittent Hypobaric Hypoxia Ameliorates Pulmonary Hypertension Induced by Monocrotaline in Rats
Authors: Zhang Yi , Gao Lei , ZHOU JINGJING , Li De‐Pei 
Published: June 2021

The anti‐hypertensive effect of chronic intermittent hypobaric hypoxia (CIHH) has been demonstrated, but the effect of CIHH on pulmonary hypertension (PAH) is not elucidated. This study investigated the effect of CIHH on monocrotaline (MCT)‐induced PAH in rats. Adult male rats were randomly divided into control group, PAH group, CIHH group, and CIHH+MCT group. The CIHH rats were treated with a hypobaric hypoxia simulating 5000 m altitude for 28 days, 6 hours per day in a hypobaric chamber. The PAH rats were subjected to a single‐dose injection of MCT (60 mg/kg, intraperitoneally). The CIHH+MCT rats were subjected to 28‐days CIHH treatment before MCT injection. The pulmonary arterial pressure and right ventricular pressure were measure through catheterization, and the wall thickness of pulmonary artery and right ventricle were measured. Micro‐vascular tension recording technique was used to determine the relaxation in pulmonary arterioles. Western blot and quantitative PCR were used to determine the expression of eNOS protein and mRNA in pulmonary arterioles. The mean pulmonary artery pressure and right ventricular systolic pressure were increased in MCT‐treated rats but did not changed significantly in CIHH+MCT rats compared with control rats. The wall thickness of pulmonary arterial and right ventricle were significantly increased in MCT‐treated rats and these increases were smaller in rats treated with CIHH and MCT. The endothelial‐dependent and endothelial‐independent relaxation in pulmonary arterioles rings were significantly decreased in MCT‐treated rats compared with untreated rats. The decreased relaxation was significantly ameliorated by CIHH treatment. The expression levels of eNOS mRNA and protein in pulmonary arterioles were decreased in MCT‐treated rats compared with untreated rats and this downregulation of eNOS was prevented by CIHH treatment. In conclusion, CIHH ameliorates pulmonary hypertension in MCT‐treated rats. This effect may be is related to up‐regulation of eNOS by CIHH treatment.Support or Funding InformationThis work was supported by the National Natural Sciences Foundation of China (31271223 and 31071002), National Basic Research Development Program of China (2012CB518200).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Microscopic Surface Geometries and Blood Clotting: A Computational Analysis
Authors: Riggenbach Zachary William 
Published: June 2021

Biofouling and thrombogenesis present a challenge tobiomedical products that contact blood plasma. These devices include heartvalves and artificial blood vessels. Excessive blood‐borne protein depositionon device surfaces likely lead to clot formation and eventual device failure. Toprevent clot formations, an effective anti‐thrombotic surface is needed toallow for more viable regenerative medical devices and procedures. Previousresearch suggests superhydrophobic surfaces serve as one method to reduceprotein deposition and clot formation. The hierarchical surface features of superhydrophobicsurfaces allow fluids to rest in the fakir state which produces substantiallyreduced fluid‐to‐surface contact area and increased droplet mobility. Simple engineering techniques have successfully demonstrate that superhydrophobicsurfaces reduce clot formation compared to control surfaces. This study uses a predictive computational program to model blood droplet behavior on microscopic surface features. The computational software uses the gradient descent method to predict equilibrium droplet positions and geometries based on the surface energies of the fluid and surface features. The software predicts and visualizes the impact various surface feature dimensions have on the ability of human blood to maintain the fakir state. The new optimization builds off of prior work from previous literature by considering the non‐homogenous nature of whole human blood and the varying surface energies of coagulation cascade proteins. The optimized surface feature geometries potentially provides a more efficient anti‐clotting surface for biomedical devices.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypergravity selectively augments neuronal in vitro differentiation
Authors: Brungs Sonja , Liemersdorf Christian , Lichterfeld Yannick , Frett Timo , Anken Ralf , Jordan Jens , Hemmersbach Ruth 
Published: June 2021

Disturbed neuronal connectivity is the ultimate cause of disability in individuals with neurological disease including spinal cord injury, head trauma, and stroke. Functional neurological recovery is limited through an unfavorable balance between neuronal regrowth and glia scar formation. Neuronal growth requires dynamic cytoskeletal protein rearrangements. Because hypergravity stabilizes microtubules while de‐stabilizing actin filaments, we hypothesized that experimental hypergravity would shift the balance between neuronal and astroglial growth in vitro.We exposed murine primary hippocampal neurons during different developmental stages to 2g using the DLR hypergravity platform. The platform unlike commercial laboratory centrifuges models physiological hypergravity and allows for cell cultivation and live‐cell imaging. We assessed neuritogenesis, neuronal polarization and maturation processes including synaptogenesis and synaptic integration in mature neural networks. Moreover, we studied primary astrocytes to shed light on their role during glial scar formation at neural lesion sites.Exposure of hippocampal neurons to 24h of 2g hypergravity increased neurite number by 30% and neurite projection length by 20% compared to 1g. At later developmental stages, mature synaptic contacts were formed under hypergravity conditions. In contrast, astrocytes showed decreases in cell spreading and lamellipodial protrusions with hypergravity.We conclude that experimental hypergravity ameliorates neuronal cell growth and synaptic contacts while halting astrocyte spreading and migration in vivo. Given the importance of this balance for neuronal regeneration in human neurological disease, we will now study the underlying mechanisms in more detail using, both, DLR hypergravity and clinostat‐induced hypogravity platforms.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Endothelial TRPA1 Channels Are Activated by Hypoxia in Cerebral Arteries and Protect Against Ischemic Damage
Authors: Pires Paulo Wagner , Earley Scott 
Published: June 2021

Acute drops in cerebral perfusion can lead to rapid neuronal death, as seen during transient ischemic attacks and ischemic strokes. The extent of brain damage following hypoxia is linked to the ability of collateral blood vessels to adequately supply blood to the peri‐infarct region and thus prevent neuronal loss and infarct expansion. During hypoxia, reactive oxygen species (ROS) are increased and may activate the Ca2+‐permeable transient receptor potential ankyrin 1 (TRPA1) in endothelial cells, promoting vasodilation. Here, we tested the hypothesis that TRPA1 channels in endothelial cells are activated by hypoxia‐derived ROS, leading to cerebral artery dilation and reduced ischemic damage. Using a novel mouse model expressing the Ca2+ indicator GCaMP6f in endothelial cells (Tek:GCaMP6f), we show that 4‐hydroxynonenal (4‐HNE), a lipid peroxide, increased TRPA1 channel activity, detected as elementary Ca2+ influx events (TRPA1 sparklets). The TRPA1 inhibitor A967079 prevented 4‐HNE induction of TRPA1 sparklets in endothelial cells. Acute exposure of cerebral arteries to hypoxia (5% O2, 6% CO2, 89% N2) significantly increased 4‐HNE accumulation in cerebral arteries, which was linked to an increase in TRPA1 sparklets. Hypoxia induction of TRPA1 sparklets was blocked by the TRPA1 inhibitor A967079, and by PEGylated superoxide dismutase (PEG‐SOD), suggesting a role for intracellular generation of ROS. Incubation of arteries with the mitochondria‐targeted antioxidant mitoTEMPO prevented the hypoxia‐induced increase in TRPA1 sparklets, whereas extracellular SOD or the NADPH oxidase inhibitor apocynin had no effect. In pressure myography studies, hypoxia caused endothelium‐dependent dilation of isolated cerebral arteries, an effect that was prevented by the membrane‐permeable SOD mimetic tempol and by mitoTEMPO. Hypoxia‐induced dilation of cerebral arteries was partially inhibited by the TRPA1 antagonist A967079 and was reduced in arteries isolated from endothelial cell‐specific TRPA1 knockout mice (eTRPA1−/− mice). In vivo, loss of TRPA1 channels in endothelial cells increased infarct size following middle cerebral occlusion, a model of ischemic strokes. Reversely, TRPA1 activation with cinnamaldehyde (50 mg/kg) reduced infarct size in wildtype, but not eTRPA1−/−, mice. Together, these data suggest that TRPA1 channels in cerebral artery endothelial cells are early sensors of hypoxia and orchestrate a response that culminates with vasodilation, thereby reducing ischemic damage. Further, pharmacological activation of TRPA1 channels may be a putative therapeutic target to reduce cerebral ischemic damage.Support or Funding InformationSupported by the National Institutes of Health (R01HL091095 to SE) and the American Heart Association (15POST2472002 to PWP)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Acid Sensing Ion Channel 1 Contributes to Endothelium‐Derived Hyperpolarizing Factor Induced Vasodilation in Small Mesenteric Arteries.
Authors: Garcia Selina , Naik Jay S. , Resta Thomas C. , Jernigan Nikki L. 
Published: June 2021

Acid sensing ion channel 1 (ASIC1) belongs to the amiloride‐sensitive degenerin/epithelial sodium channel superfamily, and is permeable to both Na+ and Ca2+. ASIC channels have been found to regulate blood pressure through mechanotransduction in arterial baroreceptors and are also pH sensors in carotid body chemoreceptors. ASIC1 is additionally expressed in vascular smooth muscle and endothelial cells in a variety of vascular beds; yet little is known regarding the role of ASIC1 in the regulation of local vascular resistance. Although extracellular H+ is the recognized activator of ASIC1, we have previously shown this channel can be activated following G protein‐coupled receptor stimulation. In small mesenteric arteries, we found that ASIC1 contributes to acetylcholine (ACh)‐induced endothelial cell Ca2+ entry and vasodilation. However, the mechanisms involved in activating ASIC1 and its downstream effects on vasodilation are unknown. We hypothesized that ACh activates ASIC1‐mediated endothelial cell Ca2+ entry to mediate endothelium‐derived hyperpolarizing factor (EDHF)‐type vasodilation through activation of small (SK) and intermittent (IK) conductance Ca2+‐activated K+ channels. To test this hypothesis, we used pressure myography to study the effects of ASIC1 on ACh‐induced vasodilation (10−9 – 10−5 M) of freshly isolated mesenteric arteries (100–200 μm inner diameter), in the presence of Nω‐nitro‐L‐arginine (nitric oxide synthase inhibitor) and indomethacin (cyclooxygenase inhibitor). ACh‐induced vasodilation was abolished by specific inhibitors of SK and IK channels (apamin and TRAM‐34, respectively), confirming that the ACh‐induced dilation is EDHF‐dependent. The specific ASIC1 antagonist, psalmotoxin 1 (PcTX1; 20 nM) similarly blocks the EDHF‐mediated vasodilatory response, suggesting ASIC1 contributes to ACh‐induced vasodilation through an EDHF‐mediated pathway. Future studies will examine the upstream mechanisms involved in activation of endothelial ASIC1 and subsequent downstream effects to mediate EDHF‐dependent vasodilation. These studies suggest a role for ASIC1 as a novel contributor to agonist‐induced mesenteric vasodilation and cardiovascular homeostasis.Support or Funding InformationSupported by National Heart, Lung, and Blood Institute Grants R01 HL‐111084 (to N.L. Jernigan), T32 HL007736 (to T.C. Resta), and R01 HL132883 (to T.C. Resta).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.