bluuebunny/crossref_metadata_2025_split huggingface dataset:
Holistic Neuro‐Physio Quanta Coherence‐Congruence Energy Dynamics for Exploring the Cause and Symptoms of Diseases
Authors: Tulp Orien L , Einstein George P , Rahman Michael S , Konyk Carla M 
Published: June 2021

Dynamic Congruence and Coherence is a dynamic model and framework used to understand the mathematical and quanta relationships within the biochemical and biophysical aspects of the human organism. It is an integrated or holistic model that may be utilize to explore the etiology and the observed signs and symptoms of the diseased and healthy states (stable and unstable states) With measured parameters, the model can then be used to predict which of the parameters or symptom or system disruption may have the largest influence on Dynamic Congruence and thus explore significant avenues into potential therapeutic targets. The sign and symptoms represent our Quanta or information output.This Energy model also lends to graphical representation of our body as a physiologically dynamic system, as well as an input model for the deliverance of Quanta to that system.In the model, several parameters of various systems, with appropriate correction and correlation factors, summate to provide a description of dynamic congruence. If an organism is in a state of dynamic congruence, we expect that changing one parameter will influence another parameter to change in the opposite direction, so that the equilibrium is restored. Mathematically, this means that the system will revert back to the original number, also it would suggest that the organism is a congruent system that moves away from chaos and disorder.As the spring‐like structures in figure 1 and the qualifier ‘dynamic’ suggest, it may take the system a while before it ‘swings back’ into the original state, thus representing a truly holistic model.Support or Funding InformationSupport from Institutional Resources of USAT, EMI, and UHHThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Lipid Metabolism at Two Different Walking Speeds in Obese Individuals: Pilot Study
Authors: Choi Myung Dong , Taylor Trent D 
Published: June 2021

Exercise is an important factor of obesity and overweight management. American College of Sports Medicine recommends that 150–250 minutes per week and up to 60 minutes per day of moderate‐intensity aerobic exercise should be performed for weight gain prevention or modest weight reduction. Walking is a common and relatively safe form of aerobic exercise that can easily be incorporated into weight management programs. The energy expenditure associated with walking has been reported to be either linearly or slightly exponentially related to speed. Thus, interval walking training has been developed as a novel free‐living training modality that improves physical fitness and cardiovascular risk factors in humans.PURPOSEto determine if an interval walking exercise increases fat breakdown, fat utilization, and energy expenditure to a greater extent, compared with constant walking exercise in obese adults.METHODSThis study was set as randomized crossover design. Six sedentary obese individuals (BMI ≥ 30 kg/m2 and 18–50 yrs) were recruited. Initially six subjects were randomly assigned into a constant speed walking group (CON) or an interval walking group (INT). Then, CON became INT and INT became CON. The constant speed walking consists of a single bout of 40 min walking exercise at 45% of VO2max on a treadmill. The interval walking consists of a single bout of 40 min walking exercise with cycles of alternating 3‐min slow (30% of VO2max), 3‐min moderate (45% of VO2max), and 3‐min fast (60% of VO2max) walking. Energy expenditure and fat usage were measured at rest and every 10min during walking exercises via indirect calorimetry. Blood samples were drawn at rest and every 10min during walking exercises to measure glycerol levels. Two‐way ANOVA was used to determine differences in energy expenditure and fat utilization between the groups.RESULTSThe net rates of fat utilization (g/min) and calorie expenditure (kcal/min) were not different between the groups during walking exercises. Also, blood glycerol concentrations were not different between the groups at any time points of exercise. However, the net rates of fat utilization, calorie expenditure, and blood glycerol concentrations were significantly higher at 30min and 40min of exercise, compared to those at 10min of exercise in both groups.CONCLUSIONOur data show that walking speeds might not be a primary factor to regulate fat utilization and energy expenditure during low and moderate exercise intensities. However, an increase in fat metabolism and energy expenditure during walking exercises may be attributed to the longer duration of exercise. Thus, these findings may provide a better exercise strategy to increase lipid breakdown and prevent weight gain in overweight/obese people.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Proteolytic Cleavage by House Dust Mite Impairs SPLUNC1's Ability to Modulate TH2 Inflammation in the Airway
Authors: Wu Tongde , Tarran Robert 
Published: June 2021

Lung epithelial cells are often on of the first lines of defense against inhaled allergens. They also work in concert with other airway cell types to orchestrate innate immune responses, keeping inflammation under control. In allergic asthma, allergens (e.g., HDM) disrupts the normal barrier function of epithelia, as well as its interaction with other airway cells via various mechanisms. Proteolytic enzyme activity of allergen components is thought to be one of top contributors of allergic inflammation in the lung. A large body of evidence supports that the biologic activity of HDM proteases augment allergic activity by 1) directly promoting IgE synthesis; 2) damaging the lung epithelium, increasing bronchial permeability; 3) degrading epithelial tight junctions and increasing accessibility to dendritic antigen presenting cells that lie beneath the epithelium; and 4) causing the release of pro‐inflammatory cytokines from epithelial cells, mast cells and basophils.Short palate, lung and nasal epithelial clone 1 (SPLUNC1) is a 256‐amino acid, secretive protein in polarized epithelia and is present at high levels in normal airway surface liquid (ASL). SPLUNC1 is a multi‐functional protein, which regulates ion channel activity, has anti‐microbial activity and affects surface tension. We observed that 1) SPLUNC1 is reduced in asthmatic patients' sputum as well as HDM challenged human bronchial epithelial cells (HBECs). 2)SPLUNC1 was degraded by HDM in both time‐ and dose‐ dependent manners. 3) SPLUNC1 knockout (KO) mice showed more severe inflammatory phenotypes in their airways when challenged with HDM, compared to their wildtype (WT) littermate controls.Overall, we conclude that SPLUNC1 is an epithelial‐derived factor that plays a major role in dampening TH2 inflammation in airways, which is deranged in asthma patients. SPLUNC1 deficiency is partially due to its proteolytical cleavage by HDM. Identifying strategies to increase SPLUNC1 resistance to HDM proteolytic activities or SPLUNC1 in ASL may lead to novel therapies to treat allergic asthma.Support or Funding InformationAmerican Asthma Foundation NCCU‐DUKE CTSIThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Inhibition of Nitric Oxide Synthesis Eliminates Interstitial Adenosine Production During Systemic Hypoxia in Rat Skeletal Muscle
Authors: MacLean David , Fabris Sergio , Bernardo Ashley 
Published: June 2021

The purpose of this study was to examine the relationship between nitric oxide (NO) synthesis and adenosine (Ado) production in the interstitial space of skeletal muscle during systemic hypoxia. In order to accomplish this, microdialysis fibers were inserted into the hindlimb of anesthetized rats and perfused with the following solutions; 1) Ringer's (control), 20 mM SNP (NO donor), 10 mM L‐NAME (NO inhibitor), 500 μM AOPCP (Ado inhibitor) and 10 mM L‐NAME+ 500 μM AOPCP during baseline (100% O2) and hypoxia (10.5% O2). Ringer's perfusion did not result in any changes in interstitial NO concentrations during either baseline or hypoxia. The perfusion of L‐NAME, AOPCP and L‐NAME+AOPCP inhibited (p<0.05) NO production below detection limits, while SNP perfusion increased interstitial NO levels beyond detection limits throughout the experiment. During Ringer's perfusion, interstitial Ado concentrations were increased (p<0.05) during hypoxia (0.07±0.01) and decreased (P<0.05) during recovery (0.05±0.01 μM) as compared to baseline (0.04±0.01 μM). The perfusion of L‐NAME, AOPCP and L‐NAME+AOPCP all inhibited adenosine production to the point where interstitial Ado levels were below detection limits (p<0.05) during baseline, hypoxia and recovery. Surprisingly, the perfusion of SNP also dramatically decreased (p<0.05) the interstitial adenosine concentrations below detectable limits during hypoxia (undetectable) and recovery as compared to baseline. These data demonstrate that interstitial Ado production is very closely linked to NO availability and even under conditions when interstitial Ado production is stimulated (hypoxia), blocking NO availability completely eliminates all interstitial Ado production. These data further indicate that interstitial Ado production is tightly regulated within a narrow range of NO concentrations and a static pool of NO is required for normal interstitial Ado production.Support or Funding InformationSupported by NSERCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Acidity suppresses T cell function and increases memory T cell development
Authors: Wu Hao , Estrella Veronica , Enriquez‐Navas Pedro , Abrahams Dominique , Ibrahim‐Hashim Arig , Luddy Kimberly , Damaghi Mehdi , RavindranadhanPillai Smitha , Pilon‐Thomas Shari , Swietach Pawel , Gillies Robert 
Published: June 2021

Acidity is a common microenvironmental factor in solid tumors. We and others have observed that mild acidosis (pH ~6.6) can inhibit the interferon‐γ (IFN‐γ) production by CD8+ T cells and suppress the T‐cell mediated anti‐tumor cell cytolysis. However, the mechanism by which acidosis inhibits effector fuction of T‐cells is not fully understood. Here we show the inhibition of IFN‐γ production by acidity is titratable and is not transduced through the inhibition of major proton‐sensing transporters, such as TDAG8, OGR1, ASIC‐3, or ADIC‐4, all of which we show are expressed in T cells. Neither pharmacologically blockade nor genetic knockout of these transporters could precent the inhibition of IFN‐γ or IL‐2 production by acidosis. Acidosis also inhibited the secretion of other important cytokines by T cells. However, secretion of MDC, MIG, and IP‐10, was increased under acidic pH, indicating that acidosis is not working through a general inhibition of secretion. Acid treated T cells showed the same kinetics of cytokine production compared with non‐treated cells when re‐stimulated under normal physiological pH. These together suggest the inhibition is not due to general failure of cell activity. Furthermore, we found that T cell can be successfully activated under low pH, evidenced by cell surface marker profile change, but more cells were directed to a memory T cell phenotype, suggesting that the acidity directs T cells to differentiate to memory status. Mechanically, extracellular acidification potentaly inhibited the monocarboxylated transporter, MCT1, blocking lactate and H+ efflux leading to an inhibition of glycolysis, which is required for effector T cell function.Support or Funding InformationThis work is supported by Team Science project of Moffitt Cancer CenterThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypoxia‐Induced Inactivation of 26S Proteasome Increases Immunogenicity of Allogeneic Mesenchymal Stem Cells
Authors: Dhingra Sanjiv , Abu‐El‐Rub Ejlal , Sequiera Glen Lester , Sareen Niketa , Yan Weiang , Rafieerad Alireza 
Published: June 2021

Allogeneic (donor derived) mesenchymal stem cells (MSCs) derived from bone marrow are in phase I and II clinical trials for cardiac regeneration. Even though the outcome of allogeneic MSCs based animal studies and initial clinical trials was encouraging, the overall enthusiasm of lately has come down. This is due to poor survival of transplanted cells in the recipient heart. The recent reports on allogeneic MSCs based studies found a switch in the phenotype of transplanted cells from immunoprivileged to immunogenic state that led to rejection of cells by host immune system. In the current study, we discovered a novel mechanism of immune switch in MSCs. Our studies demonstrate that hypoxia/or ischemic environment induces an immune shift in MSCs from immunoprivileged to immunogenic state. The immunoprivilege of MSCs is preserved by absence of major histocompatibility complex class II (MHC‐II) molecules. We found that 26S proteasome‐mediated degradation of MHC‐II prevents its expression on cell surface in MSCs and preserves their immunoprivilege. The exposure to hypoxia leads to dissociation of 19S and 20S subunits, and inactivation of 26S proteasome. This prevented the degradation of MHC‐II, and increased immunogenicity of MSCs. Furthermore, hypoxia‐induced downregulation of a chaperon protein HSP90α is responsible for inactivation of 26S proteasome. Maintaining HSP90α levels in hypoxic MSCs prevented 26S inactivation and preserved the immunoprivilege of MSCs. Therefore, hypoxia‐induced defects in 26S proteasome assembly causes loss of immunoprivilege of allogeneic MSCs. Maintaining 26S proteasome activity in MSCs preserves immunoprivilege and prevents rejection of allogeneic stem cells in the heart.Support or Funding InformationCanadian Institute of Health ResearchThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Polystyrene Nanoplastics on Goldfish Olfactory Function
Authors: Stoeber Hayden , Huertas Mar 
Published: June 2021

Increased plastic pollution has begun to affect aquatic environments from oceans to freshwater streams with little signs of it slowing down since plastics are a cheap and durable resource to use for manufacturing. Due to increased plastic material waste in natural aquatic ecosystems, fish are threatened by the natural break down of these plastics into sizes and molecules that can be easily ingested and absorbed by tissue. When plastics are broken down and are present in the water, the absorption of these molecules becomes less regulated by tissue. Most of the studies regarding plastic effects at this point in time on aquatic organisms are focused on the transfer of plastic particles through generation. We hypothesized that polystyrene nanoplastic (PS NP) particles on Carassius auratus are incorporated through the nose to the brain, dampening olfaction and compromising several physiological responses associated with the sense of smell. We analyzed the physiological effect PS NPs have on the brain and olfactory system of C. auratus. After the fish were exposed to Nanocs 20 nm Fluorescein isothiocyanate (FITC) labeled PS NPs in water for 24 hours in a dark aquarium, or injected directly in the nose, several organs were dissected. The brain, nose, intestines, kidney, liver, and gills were all snap frozen, mounted in OCT and immediately cut at 20 μm on a cryotome before organs were viewed with fluorescent microscopy. PS NP fluorescence was observed mainly in the nose, brain and intestines while the other organs are still in the process of being analyzed. Accumulation of nanoparticles in the brain was stronger in hypothalamic and olfactory bulb areas. Behavioral and electrophysiology studies of olfactory function after nanoplastic exposure are under development to more closely look at the direct possible effects that nanoplastic materials in the brain might have on behavior. The observed fluorescence supported the existence and ability of PS NPs to infiltrate nervous tissues in C. auratus and points to a possible interference with the sense of smell.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Interleukin‐22, a Pro‐inflammatory Cytokine, is Increased in the Serum of Canines with Inflammatory Bowel Disorder
Authors: Panickar Kiran S , Hollar Regina L 
Published: June 2021

Inflammatory Bowel Disease (IBD) is characterized by a chronic and/or recurrent inflammatory condition associated with adverse gastrointestinal signs including diarrhea, vomiting, and weight loss. Inflammation plays a key role in the initiation and continual progression of IBD. Interleukin 22 (IL‐22) is a pro‐inflammatory cytokine that is expressed by various cells of the immune system including dendritic cells, natural killer cells, and T cells. IL‐22 is a cytokine that can have either a helpful or a deleterious role in the intestine. The protective role of IL‐22 includes promoting mucosal barrier integrity and epithelial cell regeneration. Its deleterious actions may depend on the presence of other cytokines as well including IL‐23 and IL‐22 binding proteins. Regardless, a continually increased level in IL‐22 can increase associated gastrointestinal inflammatory processes. We tested the circulating levels of IL‐22 in the serum of dogs that were clinically diagnosed as having IBD following an endoscopy conducted by a veterinarian. Blood was collected from dogs with IBD (n=6; 2.2–13.1 yr) and control dogs (n=5; 2.2–11.3 yr) which did not show any signs of IBD. Blood was collected at two different time points (~1 year apart) from the same dogs. Using an ELISA technique, we found that the mean levels of serum IL‐22 from both time points were significantly higher in IBD (286.5 ± 69.32 pg/ml) when compared to controls (104.2 ± 17.8; p<0.05). The levels of IL‐22 in IBD dogs were higher than controls at both individual time points assessed as well. Our results identify IL‐22 as a promising biomarker of inflammatory bowel disorder in dogs and strategies to decrease a continual and elevated level of IL‐22 may be an effective way to reduce the adverse conditions associated with IBD. Further, an optimal anti‐inflammatory nutritional therapy may be a promising option to pursue as a therapeutic measure for IBD in caninesSupport or Funding InformationFunded by Hills PNCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Effects of Acute Hyperglycemia on Cardiac Autonomic Balance Between Sexes
Authors: Skalk Alexandra , Saran Gary , Rampuri Zahrah , Soriano Jan Elaine , Lorida Jeena , Joki Tysen , Hewitt Sarah , Day Trevor A 
Published: June 2021

Males and females have differential cardiac autonomic functioning, possibly contributing to high rates of cardiovascular disease in men with aging. In addition, there is still a general lack of understanding regarding normal physiology and disease risk in women. In young, healthy populations, a sex difference in cardiovascular autonomic function has not been established. Acute glucose ingestion has been shown to stimulate a cardiovascular sympathetic response, likely through carotid body activation. We hypothesized that young men would have a greater cardiovascular sympathetic response following glucose loading than women, measured through heart rate variability (HRV) metrics. We aimed to test the effects of acute relative hyperglycemia on HRV metrics to study cardiovascular autonomic function between young, healthy men and women. We recruited 40 healthy participants (21.6±1.7 yrs; BMI 24.1±4.2 kg/m2; 19 females), and instrumented them with electrocardiogram (ECG) to measure heart rate (HR) and finger photoplethysmography to measure mean arterial pressure (MAP). Blood glucose was tested using a glucometer and capillary draw via sterile lancets. Cardiovascular measures were recorded at rest in a fasted state and 30‐min after an acute relative hyperglycemic load (75g glucose, 300ml; 4.8±0.4 vs. 7.5±1.3 mmol/L; P<0.0001). HRV was quantified in two ways: frequency domain, with low frequency (LF; sympathetic activity), and high frequency (HF; parasympathetic activity), and with Poincaré plots, deriving SD1 (parasympathetic activity) and SD2 (sympathetic activity). Frequency domain metrics were minimally affected by glucose loading, increasing HF (P=0.03) and decreasing LF (P=0.02). In both fasted and glucose loaded states, LF and HF domains were different between males and females, with males having increased LF values (P<0.001) and females having increased HF domain (P<0.001). SD1 was also significantly increased in females in both fasted and glucose loaded sates (P=0.013). Our data demonstrates a sex difference in cardiovascular autonomic functioning using HRV metrics. Specifically, we observed increased resting sympathetic activity in males, possibly contributing to high rates of cardiovascular disease later in life. Females had increased resting parasympathetic activity, possibly offering clinical relevance in understanding reduced cardiovascular disease risk in women over the lifespan.Support or Funding InformationNSERC Discovery and MRU Faculty of Science and TechnologyThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effect of Beta‐hydroxybutyrate on Myoblast Proliferation and Differentiation
Authors: Melanson Joshua R. , Olsen Zachary E , Walton Chase M. , Bikman Benjamin T. , Thomson David M. 
Published: June 2021

Ketogenic diets (KDs) and fasting have been promoted for weight loss and health. KDs cause an increase in circulating levels of ketone bodies, including beta‐hydroxybutyrate (βHB). The effects of amplified levels of βHB on skeletal muscle proliferation and differentiation are largely unknown. Therefore, we tested whether βHB has an effect on proliferation and differentiation of C2C12 myoblast cells in vitro. Experiment 1: to assess proliferation, myoblasts were plated sparsely and incubated in growth media for 6 hours. They were then incubated overnight (~12 hours) with 0 – 10 mM bHB followed by the addition of BrDU to the media for an additional 2 hours to label proliferating cells. The cells were fixed and stained for BrDU and DAPI and proliferation index was calculated as the percentage of BrDU+ nuclei/total nuclei. We found that myoblast proliferation did not increase significantly with βHB. Experiment 2: to assess differentiation, myoblasts were grown to 60% confluence in growth media, followed by differentiation media for 4 days with 0–10 mM bHB. The myotubes were then fixed and stained with DAPI and antibodies against myosin heavy chain. Differentiation index was calculated as the percentage of nuclei associated with MHC+ myotubes. We found that myoblast differentiation increased 22% with 0.6125 mM βHB, and tended to increase (p = 0.12) at 1.25 mM bHB. This suggests that moderate levels of bHB (similar to those achieved in those on KDs or fasting) may be beneficial to muscle repair and/or regeneration.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.