bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Whole Egg Consumption on Vitamin E Absorption from Co‐Consumed, Mixed‐Vegetable Salad
Authors: Kim Jung Eun , Ferruzzi Mario G , Campbell Wayne W 
Published: November 2023

The daily usual intake of vitamin E (VIT E) in nearly 90% of the US population is lower than the estimated average requirement. In addition to promoting increased VIT E intake, dietary approaches to increase the absorption of VIT E would help people meet their body's need. Vitamin E is co‐absorbed with dietary lipid, but very limited data exist on the impact of endogenous food sources of lipid on VIT E absorption. Co‐consuming whole egg with VIT E‐containing foods may increase VIT E absorption via the lipid contained in egg yolk. The objective of this study was to assess the effect of adding cooked whole egg to a raw mixed‐vegetable salad on VIT E absorption. Healthy young males (n=16) consumed the same salad (all served with 3g canola oil) with no egg (control, CON); with 75 g (1½ eggs) of scrambled whole egg (low egg, LE); and with 150 g (3 eggs) of scrambled whole egg (high egg, HE) (randomized, crossover design). The CON, LE, and HE trials contained 4.1 mg, 5.2 mg (1.1 mg from eggs), and 6.4 mg (2.3 mg from eggs) of VIT E (α‐tocopherol (α‐T) and γ‐tocopherol (γ‐T) combined), respectively, and included 3 g, 10.5 g (7.5 g from eggs), and 18 g (15 g from eggs) of total dietary lipids, respectively. Blood was collected hourly during 10 hours and triacylglycerol rich lipoprotein fractions (TRL) were isolated. α‐tocopherol and γ‐T concentrations in TRL were analyzed and composite areas under the curve (AUC) were calculated. α‐tocopherol AUC0–10h in TRL was higher for HE vs. LE and CON (981 ± 151a vs. 311 ± 151b vs. 117 ± 151b nmol • L−1 • 10h, p < 0.05) and γ‐T AUC0–10h in TRL was also higher for HE vs. CON (402 ± 50a vs. 226 ± 50ab vs. 72 ± 50b nmol • L−1 • 10h, p < 0.05). These findings support that consuming cooked whole eggs is an effective way to increase the absorption of α‐T and γ‐T from co‐consumed meals which naturally contain vitamin E such as a raw mixed‐vegetable salad. Thus, co‐consuming cooked whole eggs with a vegetable salad improves the nutritional value of the vegetables, which are under‐consumed by the majority of the US population.Support or Funding InformationAmerican Egg Board‐Egg Nutrition Center; NIH UL1TR001108; Purdue Ingestive Behavior Research Center
Impact of Microvesicles Pro‐Inflammatory Properties on Sepsis‐Induced Endothelium Dysfunction
Authors: Doursout Marie‐Francoise , Liang Yangyan , Wang Yao‐Wei W. , Devakottai Sundar , Payne JaNae A. , Wade Charles E. , Matijevic Nena 
Published: November 2023

This is the first inter‐disciplinary proposal to assess the impact of microvesicles (MVs)‐ pro‐inflammatory properties on sepsis‐induced endothelial dysfunction. Sepsis is a clinical syndrome characterized by a systemic inflammatory response to infection, leading to endothelial dysfunction with increased endothelial permeability, increased levels of nitric oxide (NO), reduced NO availability, enhanced reactive oxygen species (ROS)‐induced oxidative stress and disseminated intravascular coagulation with microvascular thrombosis.The overall goal of this research proposal was to assess phenotypic and pathophysiological implications of pro‐inflammatory MVs as strong biomarkers of sepsis‐induced vascular dysfunction over a 6 hour time course. We hypothesize that the pro‐inflammatory effects of isolated and characterized MVs from septic rats are tissue and time course‐specific. Ten rats were instrumented under isoflurane anesthesia to implant Tygon catheters into the femoral artery and vein to record mean arterial blood pressure (MAP), heart rate and for drug administration, respectively. Following recovery from surgery, rats were injected with lipopolysaccharide (LPS) at 20 mg/kg IV. Simultaneously to hemodynamic measurements, blood samples were collected from control (n=5) and experimental animals (n=5) into 0.129 mol/L sodium citrate to isolate and characterize leucocytes MVs and platelet MVs. Along with decreases in MAP, preliminary data show that LPS administration induced increases in MV counts (PMVs and LMVs) 4 hrs following LPS administration. LMVs increased from 39/μl to 68/μl and PMVs increased from 145/μl to 631/μl. We are currently exploring endothelial MVs in rat plasma subjected to LPS. This on‐going project is important because it will answer a critical question not explored until now: How the vascular system is affected in sepsis and consequently what will be the best treatment to improve endothelial dysfunction and clinical outcomes.
Beneficial cardiovascular effects of O‐GlcNAc increase in early phase of septic shock
Authors: Ferron Marine , Cadiet Julien , Prat Valentine , Erraud Angélique , Aillerie Virginie , Grabherr Amandine , Mevel Mathieu , Alraj Mohammed , Chatham John , Rozec Bertrand , Gauthier Chantal , Lauzier Benjamin 
Published: November 2023

BackgroundO‐GlcNAcylation, a post‐translational modification, is the end product of the hexosamine biosynthetic pathway (HBP). Recent studies showed that increased concentration of N‐acetylglucosamine has beneficial effects in acute pathologies, such as hemorrhagic shock.ObjectivesWe postulated that the increase in O‐GlcNAc at the early phase of septic shock, a systemic inflammation associated with a cardiovascular dysfunction, could improve the cardiovascular function.MethodsEndotoxemic shock was induced in rats (n=6–9) by iv injection of lipopolysaccharide (LPS, 5 mg/kg) or saline (CTRL). One hour later, fluid resuscitation (FR, 15 ml/kg of colloid, iv) was associated or not with HBP substrate (glucosamine, GlcN, 180 mg/kg, iv) or an O‐GlcNAcase inhibitor (NButGT, 10 mg/kg, iv). Two hours later, echocardiography and arterial blood pressure measures were performed. Then, heart and blood were collected to evaluate biological parameters, inflammation and autophagy.ResultsLPS rats presented a hypotension corrected by FR and O‐GlcNAc increase (mean arterial pressure: CTRL 87±1, LPS 73±5*, LPS‐FR 93±6#, LPS‐FR‐NButGT 83±5, LPS‐FR‐GlcN 92±4mmHg, *: p<0.01 vs CTRL, #: p<0.01 vs LPS). LPS rats also presented a decrease of ejection fraction by 21% and diastolic function (E/A ratio) by 29%. These parameters were normalised by NButGT and tended to be improved by GlcN. In LPS rats, plasmatic troponin T and lactate were significantly increased by 31 and 1.7‐fold respectively, they were normalised under NButGT and GlcN treatments. Interestingly, increase in O‐GlcNAc was not associated with modification of autophagic pathway (Beclin‐1, LC3, Lamp‐2) or inflammation (TNFα, IL‐6).ConclusionsOur results suggest that the increase in total O‐GlcNAc at the early phase of septic shock could be a suitable therapeutic strategy. However, it remains to be determined which cellular pathways are modulated by the O‐GlcNAc increase.
Scaffold‐dependent stimulation of CaV channels via C‐terminal phosphorylation promotes vasoconstriction in the diabetic vasculature
Authors: Nystoriak Matthew , Nieves‐Cintrón Madeline , Patriarchi Tommaso , Marotti Stefano , Grandi Eleonora , Dos Santos Fernandes Julia , Forbush Katherine , Hofmann Franz , Ward Sean , Scott John , Hell Johannes , Navedo Manuel 
Published: November 2023

Dysregulated influx of calcium in arterial myocytes via L‐type CaV1.2 channels (LTCCs) has recently been linked to vascular dysfunction during diabetic hyperglycemia. Functional upregulation of LTCCs under hyperglycemic conditions involves cAMP‐dependent protein kinase (PKA) activity, yet the mechanistic details of how these pathological phenomena promote vasoconstriction is unclear. Here, we report that a subpopulation of CaV1.2 channels is located within nanometer proximity of PKA catalytic subunits at the sarcolemma of native murine and human arterial myocytes. This organization requires selective scaffolding of PKA RIIα by A‐kinase anchoring protein 150 (AKAP150; murine ortholog of human AKAP79). Potentiated LTCC activity in response to elevated D‐glucose was associated with enhanced phosphorylation of CaV1.2 at the putative PKA target site serine 1928 (S1928) in murine and human arterial myocytes, as well as in arteries from mice on a high‐fat diet (HFD) and diabetic human subjects. This modification was absent in myocytes from genetically engineered mice lacking AKAP150 or expressing mutant AKAP150 unable to target PKA. Supporting a functional role for S1928 phosphorylation, hyperglycemia‐ and HFD‐induced LTCC potentiation and vasoconstriction were nearly abolished in myocytes and arteries from mice expressing mutated CaV1.2 in which S1928 was replaced by alanine. These results demonstrate a requisite functional role for CaV1.2 S1928 phosphorylation in stimulation of vascular LTCC activity and vasoconstriction by targeted subsarcolemmal PKA signaling in hyperglycemic conditions and diabetes.Support or Funding InformationThis work was supported by grants from the National Institute of Health R01‐HL098200 and R01‐HL121059 and American Heart Association 14GRNT18730054 (to MFN), American Heart Association 13POST12730001 and the Lawrence J. and Florence A. DeGeorge Charitable Trust (to MAN), American Heart Association 14POST18380011 (to SM), American Heart Association Scientist Development Grant 15SDG24910015 (to EG), National Institute of Health R01‐DK54441 and R01‐DK105542 (to JDS), and National Institutes of Health R01‐MH097887 and R01‐NS078792 (to JWH).
Activation of Toll‐like Receptor 4 (TLR4) by High Mobility Group Box 1 (HMGB1) Leads to Oxidative Stress and Inflammation in Human Aortic Endothelial Cells
Authors: Szasz Theodora , Ogbi Safia , Webb R. Clinton 
Published: November 2023

Endothelial dysfunction is a central mechanism in the vascular pathology associated with hypertension, diabetes and atherosclerosis. Key mechanisms mediating endothelial dysfunction, such as reduced NO bioavailability and increased reactive oxygen species (ROS) production are intimately linked to vascular inflammation. Recent evidence supports activation of the innate immune system by endogenous damage‐associated molecular patterns (DAMPs) as a causative factor of the chronic low‐grade sterile inflammation associated with these conditions. High mobility group box 1 (HMGB1) is a chromatin protein and a DAMP which activates Toll‐like receptor 4 (TLR4), leading to increased NFκB signaling, ROS and cytokine production in immune cells. We hypothesized that TLR4 activation by HMGB1 in human aortic endothelial cells (HAEC) leads to activation of oxidative stress and inflammatory pathways and contributes to endothelial dysfunction. Recombinant human HMGB1, time and concentration‐dependently, induced activation of TLR4 in cultured HAEC as evidenced by expression of its downstream partner MyD88. HMGB1 increased ERK phosphorylation and nuclear translocation of NFκB, as well as increased expression of cyclooxygenase (COX‐1 and COX‐2). NO production was decreased in the presence of HMGB1, however no changes were observed in eNOS phosphorylation. HMGB1 also induced an increase in ROS production, increase in the expression of Nox4 subunit of NADPH oxidase and upregulation of the mitochondrial isoform of superoxide dismutase (MnSOD). These effects closely mimicked those induced by the TLR4 agonist lipopolysaccharide (LPS) and were inhibited or reversed by pretreatment of HAEC with the TLR4 antagonist CLI‐095. Our results suggest that HMGB1 may contribute to the endothelial dysfunction associated with diabetes and cardiovascular disease via activation of inflammatory and oxidative stress pathways.Support or Funding InformationNIDDK
Assessing the Migration and Morphology of Individual Neurons within Orderly Transcription Factor Domains in the Developing Zebrafish Hindbrain
Authors: Monen Joost , Fetcho Joseph 
Published: November 2023

Neural networks within the spinal cord and hindbrain control much of the output of the nervous system. The discovery of a transcription factor code that gives rise to the cell types in spinal cord and hindbrain has revealed simple core patterns of organization that are shared by vertebrates. In zebrafish, transcription factor domains give rise to orderly stripes of neurons that extend longitudinally in hindbrain and exhibit a topographic, age related map of recruitment and input resistance. Neurons within these stripes are actively recruited in free swimming of five‐day‐old fish, suggesting that these neurons are wired to perform behaviors prior to the formation of discrete motor nuclei. To assess whether and to what extent neurons that makeup these orderly domains migrate and shift morphologically, we examine both gross morphology in fish with fluorescently labeled transcription factor types (alx [chx10], and dbx1b) and neurotransmitter phenotypes (vglut, glyt2), as well as individually labeled cells over several time points in vivo via multi‐photon microscopy over multiple time points from 3 days post fertilization up to 27 days post fertilization. We show that both the neurotransmitter and transcription factor stripes present in the early developing hindbrain undergo significant migration within the first 2 weeks of development leaving the stripe patterns of neurotransmitter phenotypes virtually undetectable and within transcription factors still apparent, but much less defined. Furthermore, single cells expressing dbx1b tracked over time demonstrate soma migration and while there is no correlation between a cells initial dorsoventral position in a stripe (a crude age indicator) and its final location, there is a correlation between the dorsoventral position of its arbors and the dorsoventral migration of its soma, suggesting that the dendritic and axonal connections established may dictate where a neuron ultimately settles.Support or Funding InformationJ.M. was supported in part by a Ruth L. Kirschstein National Research Service Award from the National Institute for Neurological Disorders and Stroke. This work was supported by an NIH grant to J.F.
Capsaicin suppressed body weight gain and pain reaction in mice
Authors: Yang William , Xu Benjamin , Xu Richard , Ouyang Kevin , Ouyang Amy , Shan Huimin , Wang Hong 
Published: November 2023

Capsaicin is a hot pepper extracts and has been reported as an anti‐inflammatory and anti‐oxidant agent. It was suggested that Capsaicin may potentially control peripheral nerve pain and has anti‐obesity effect. To test this hypothesis, we examined the effect of Capsacin on body weight gain, general metabolism and pain reaction in the C57BL/6J mice. Male mice at 6 weeks of age were fed with capsaicin (2 mg/kg body weight) or vehicle (0.9% saline, 3% ethanol and 10% Tween 80) every other day for a total of 90 days (n=10). The average weight of mice is about 18.1 grams at 6 weeks of age. The control mice fed with vehicle has a normal body weight gain and grown to 26.3 grams by the end of the experiments at 4.5 month of age. Capsacin fed mice reached 24.1 grams by the end of the experiments, a 12% suppression on body weight gain. Mouse metabolism was assessed in a metabolic cage for 24h and was found not altered by Capsaicin supplement. Finally, we tested mouse pain reaction on a 52–54°C hot plate (Ugo Basile, Varese, Italy) by using either jumping or hind‐paw licking as the nociceptive endpoint. We found that Capsaicin delayed the pain reaction. Hot plate pain reaction time was 7.5 seconds in the control mice and extended to 14.5 seconds in mice fed Capsaicin for 30 days. After 90 days of Capsaicin treatment, pain reaction remained latent as 12.9 seconds as compared with that 7.7 seconds in the control mice. We conclude that Capsaicin can control body weight gain and suppress peripheral nerve pain reaction in adult mice. Our study support the hypothesis that hot pepper is beneficial to prevent obesity and suppress pain reaction. Study is ongoing to take advantage of this common dietary ingredient to prevent the onset and progression of obesity in metabolic disease mice and to test its clinical relevance.Support or Funding InformationThis study was supported by research funding from NIHR01HL077288
How does Estrogen Influence Attention? Impact of 17‐beta Estradiol on Performance in an Attentional Set Shifting Task
Authors: Chen Sandi , Kolangara Shiva , Mokler David 
Published: November 2023

Estrogens have been shown to affect learning and memory in female rats. ADHD is 3–9× more prevalent in males, suggesting that gonadal hormones may be in part responsible for the observed disparity between the sexes. In this disorder dopamine and norepinephrine levels in the ventromedial prefrontal cortex may be deficient, as evidenced by the use of stimulants to treat this disorder. Estrogen has been shown to inhibit dopamine reuptake in the prefrontal cortex this increasing extracellular levels of dopamine. Our previous work has suggested that in ovariectomized female rats, estradiol supplementation yielded higher levels of dopamine in the PFC than in male rats (1). The purpose of the present study was to evaluate the effect of estrogen in ovariectomized (OVX) female Long‐Evans rats in the attentional set‐shifting task (ASST)(2), a measure of attention which is strongly associated with monoamine levels in the vmPFC. Adult female rats were ovariectomized (OVX) or underwent a sham surgery. OVX rats were then randomized into two groups and given injections of 21 ug/kg 17‐B‐estradiol or vehicle every other day for the remainder of the study, while sham surgery animals were given vehicle injections. Rats were then tested in the ASST, wherein rats are trained to dig in pots for food reward. Pots are labeled with three dimensions, scent, digging material and texture of the pot and trained to dig for a food reward. Once the animal reaches criteria performance in a simple discrimination (SD) and then a complex discrimination (CD), the animal is then tested for performance in the intradimensional shift (ID), followed by a reversal (IDR). The animal is then exposed to an extradimensional shift (odor to digging material) (ED), followed by the reversal within this ED (EDR). This study found that OVX rats performed better in the ASST than sham or OVX + E animals, possibly reflecting a complicated dose‐response relationship to 17‐B‐estradiol administration. Further studies are underway to assess the levels of dopamine, norepinephrine, and serotonin in the ventromedial prefrontal cortex of these animals using in vivo microdialysis.Support or Funding InformationSC supported by a Morgane Research Fellowship from UNECOM.
Systemic and Central Nervous System Levels of Neutrophil Gelatinase‐Associated Lipocalin after Cardiac Surgery Are Associated with Postoperative Cognitive Impairment
Authors: Schoemaker Regien G , Hovens Iris B 
Published: November 2023

IntroductionPostoperative cognitive dysfunction (POCD) is a debilitating surgical complication, with cardiac surgery patients at particular risk. The systemic and central inflammatory response to surgery is considered to be a key factor in POCD development. Neutrophil gelatinase‐associated lipocalin (NGAL), a sensitive marker for inflammatory damage, has previously been associated with development of depressive symptoms in patients with cardiac disease. The current study aimed to investigate the association of systemic and central NGAL concentrations with postoperative cognitive performance in a rat‐model for POCD.MethodsMale Wistar rats were subjected to ischemia reperfusion of the left coronary artery (cardiac surgery), received thoracic sham surgery or remained naïve. Cognitive performance was assessed in the second postoperative week. Two weeks following surgery plasma (ELISA) and brain (immunohistochemistry) NGAL levels were determined.ResultsNGAL was increased from 80±7 ng/ml in control rats to 321±48 ng/ml (p<0.01) and 278±53 ng/ml (p<0.01) in rats that had undergone thoracic sham surgery or cardiac surgery respectively (F2,33=9.4, p<0.01). NGAL in the paraventricular nucleus of the hypothalamus (PVN) was increased significantly after cardiac surgery only (F2,29=9.2, p<0.01; control: 13±1%; sham: 15±1%; cardiac: 18±1%, p<0.01). The route of anesthesia did not affect NGAL levels. Plasma NGAL concentrations in cardiac surgery and control rats were significantly correlated with performance in the novel location test (r=−0.46, p=0.04), and learning (r=0.50, p=0.30) and reversal learning (r=0.66, p=<0.01) in the Morris water maze, while PVN NGAL was correlated with novel location recognition only (r=−0.53, p<0.01).ConclusionsOpening of the thorax appears to be associated with a marked long‐lasting rise in systemic NGAL concentrations, but only in cardiac surgery this is associated in increased NGAL in the brain, specifically in the PVN. These surgery‐specific alterations in NGAL may provide a lead towards understanding the cognitive sequelae of cardiac surgery
Baseline levels and baroreflex control of cardiac sympathetic nerve activity during renovascular hypertension
Authors: Ramchandra Rohit , George Bindu , Mahesh Darvina 
Published: November 2023

Globally, hypertension affects one in three adults and the sympathetic nervous system has been implicated in the development of hypertension. In this context, increased sympathetic drive to the heart promotes arrhythmias and sudden death in patients, but the level of cardiac sympathetic nerve activity (CSNA) in hypertension has been assessed only by indirect methods. We tested the hypothesis that directly recorded CSNA is increased in renovascular hypertension. Renovascular hypertension was induced by clipping of one renal artery. Following three weeks post‐clip, resting levels of mean arterial pressure, heart rate CSNA and renal SNA (RSNA) were recorded in conscious ewes. Baroreflex control of heart rate and CNSA was assessed using intravenous infusions of phenylephrine and sodium nitroprusside. The same protocol was repeated in sham clip ewes (n=5). Renal clipping was associated with a significant increase in resting MAP (108±4 vs. 87±6 mmHg; n=10) and resting CSNA (38±3 vs. 30±2 bursts/min; n=5 and 7). In contrast, there was no difference in resting RSNA levels (67±11 vs. 70±8 bursts/min; n=4 and 3) between the groups. The sensitivity of baroreflex control of CSNA and RSNA was unchanged. This study provides the first direct evidence that CSNA is increased in a sheep model of renovascular hypertension. This increase in SNA was specific to the heart at this stage of hypertension since resting RSNA levels were unchanged. This study indicates an important role for CSNA in mediating the chronic elevation in MAP in renovascular hypertensive animals.Support or Funding InformationSupported by The University of Auckland Faculty Research Development Fund and the Maurice and Phyllis Paykel Trust