bluuebunny/crossref_metadata_2025_split huggingface dataset:
Precipitation patterns and hydration status of a unique insular snake population.
Authors: Sandfoss Mark , Lillywhite Harvey 
Published: June 2021

Water is essential to survival, and thus invasion of habitats having limitations of water necessitates adaptations to maintain water balance. Climate change is expected to alter precipitation patterns worldwide. A unique population of Florida cottonmouth, Agkistrodon conanti, inhabits Seahorse Key (SHK) near coastal Levy County, Florida where they are entirely terrestrial, scavenge fish carrion, and are without permanent sources of fresh water. Insofar as cottonmouths are generally associated with freshwater habitats, this insular population of snakes is likely to exhibit adaptations for living with limited resources, especially water. Our objective is to measure the hydration status in free‐ranging snakes to better understand the possible stresses related to dehydration. We hypothesize that hydration status of cottonmouths on SHK will follow patterns of precipitation. We tested dehydration and drinking behavior of cottonmouth snakes inhabiting SHK from 2001–2017. Snakes were captured and tested for thirst immediately following capture. They were provided access to fresh water for at least 12 hours while we noted drinking and weighed snakes before and after. Mass gains reflected drinking and therefore hydration status. These data were compared to satellite data for date of last rainfall event (peak >2.5 mm/hr) preceding capture (NASA TRMM & GPM). The percentage of captured cottonmouths found to drink was found to increase with an increase in the number of days since a rainfall event. Results support the prediction that hydration status of cottonmouths on SHK correlates with rainfall patterns, suggesting that snakes rely on periodic rainfall to remain hydrated. Insular cottonmouth populations are of conservation concern as annual precipitation rates have declined over the past century and may continue to decline due to climate change.Support or Funding InformationU.S. Fish & Wildlife Service, Sigma Xi, Chicago Herpetological Society, & SSARThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Mitochondrial ROS activates PKC alpha translocation to the membrane of vagal sensory neurons.
Authors: Bahia Parmvir K. , Barannikov Ivan , Taylor‐Clark Thomas E. 
Published: June 2021

Hyperexcitability of airway sensory nerves can trigger disease‐associated reflexes resulting in cough and dyspnea. We have observed that mitochondrial ROS production increases hyperexcitability in nociceptive bronchopulmonary C‐fibers. We also found that this increased excitability can be blocked by the PKC inhibitor bisindolylmaleimide (BIM) I, but not the inactive PKC analog BIM V. In previous work we have shown, using a pan‐PKC antibody, that mitochondrial ROS production via Antimycin A (AntA; mitochondrial complex III Qi site inhibitor) causes translocation to the cell membrane. However, there are several PKC isoforms expressed in nociceptive neurons. We wanted to determine which isoforms were present, their distribution in nociceptive cells and whether specific isoforms were activated by AntA. Studies looking at mRNA expression have highlighted PKC alpha, beta1, beta2, delta and epsilon as abundant in nociceptors so our studies have focused on these particular isoforms. Sensory neuron cell bodies were isolated from mouse vagal ganglia. To identify nociceptive cells, we used a mouse strain that co‐expresses a red fluorescent protein (tdTomato) with the Transient Receptor Potential V1 ion channel. Cells were treated for 2 min with: vehicle, 10 μM AntA or 300 nM PMA then immediately fixed. We performed immunocytochemistry to determine cellular location of different isoforms. Of the TRPV1 expressing nociceptive cells, more than 50% were positive for any given isoform of PKC. All isoforms translocated to the membrane in response to PMA treatment. However, only PKC alpha exhibited translocation to the membrane in response to AntA treatment. In the case of PKC delta, AntA appeared to cause translocation of this isoform to the nucleus. Our experiments suggest that nociceptor hyperexcitability, in response to ROS produced via mitochondrial dysfunction, may occur through the translocation and activation of the PKC alpha isoform.Support or Funding InformationThis work was supported by the National Heart Lung and Blood Institute in Bethesda, USA(R01‐HL119802)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Loss of Salt Sensing Kinase, SGK1, in T cells abrogates Memory Cell Formation, Hypertension and End‐Organ Damage
Authors: Itani Hana A. , Pandey Arvind , Norlander Allison E. , Harrison David G. 
Published: June 2021

Accumulating evidence indicates that high salt‐intake, aging and hypertension promote NaCl accumulation in tissues. Elevated NaCl has been shown to promote TH17 cell formation in an SGK1‐dependent fashion. We have previously shown that memory T cells play a major role in the genesis of hypertension. These long‐lived cells remain responsive to repeated hypertensive stimuli, such as repeated salt feeding, and can be mobilized to enter the kidney where they release cytokines that promote renal dysfunction. To examine mechanisms by which T cells sense salt and contribute to salt‐sensitivity, we tested the hypothesis that SGK1 in T cells is necessary for formation of memory T cells and their activation in salt‐sensitive hypertension. We produced mice with T cell specific deletion of SGK1, SGK1fl/fl × tgCD4cre mice and used SGK1fl/fl mice as controls. To impose repeated episodes of hypertension, we treated these mice with L‐NAME (0.5mg/ml) in drinking water for two weeks, allowed a two‐week normotensive interval and a then fed high salt (4% NaCl) for three weeks. L‐NAME followed by high salt increased memory T cells in the kidney, aorta and bone marrow of SGK1fl/fl control mice but not in SGK1fl/fl × tgCD4cre mice, as identified by the surface marker CD44hi. To assess markers of renal injury, we measured albumin in 24‐hour urine samples collected at the end of the L‐NAME/high salt. L‐NAME/high salt caused striking albuminuria in SGK1fl/fl mice and this was prevented in SGK1fl/fl × tgCD4cre mice. In additional studies, we found that loss of SGK1 in T cells abrogates renal and vascular inflammation and protects against hypertensive renal and vascular injury in the L‐NAME/high salt model. Thus, our data indicate that SGK1 in T cells promotes their development of salt sensitivity and mediates their ability to cause renal and vascular dysfunction in hypertension.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Colonic Indole And Hydrogen Sulfide, Gut Bacterial Metabolites, Affect Portal Blood Pressure in Healthy And Cirrhotic Rats
Authors: Ufnal Marcin , Huc Tomasz , Jurkowska Halina , Wróbel Maria , Jaworska Kinga , Onyszkiewicz Maksymilian 
Published: June 2021

Liver cirrhosis is a leading cause of portal hypertension, and is often accompanied by systemic hypotension. Accumulating evidence suggests that gut bacteria may affect hemodynamics, however, the mechanisms are not clear. We investigated the effect of colon‐administered gut bacteria metabolites on portal blood pressure (PBP), portal blood flow (PBF) and systemic arterial blood pressure (ABP) in healthy (controls) and cirrhotic rats (CRH).10‐week‐old, male, Sprague Dawley rats were maintained either on tap water (controls) or water solution of thioacetamide for 18 weeks to induce liver cirrhosis (CRH). PBP, PBF and ABP were measured in anaesthetized rats at baseline and after the intracolonic administration of either a vehicle, indole, or Na2S, a hydrogen sulfide (H2S) donor into the colon.CRH showed significantly higher PBP but lower ABP than controls. The intracolonic administration of indole increased portal blood level of indole, and peripheral blood level of indoxyl sulfate, a liver metabolite of indole. Rats treated with Na2S showed increased portal blood levels of thiosulfate and sulfane sulfur, products of H2S oxidation. The intracolonic administration of vehicle did not affect hemodynamic parameters. In controls intracolonic H2S increased PBP but decreased PBF and ABP. In contrast, intracolonic indole increased both BPB and PBF, whereas did not affect significantly ABP. In comparison to controls, CRH showed significantly greater hemodynamic responses to H2S but not to indole. Cirrhotic livers had a significantly higher concentration of H2S but lower expression of rhodanese, an enzyme converting H2S to sulfate.Colon‐administered indole and H2S increase portal blood pressure via distinct hemodynamic mechanisms. Indole increases, whereas H2S decreases portal blood flow. Indole and H2S signaling in the gut‐liver axis may be involved in the control of portal blood pressure and in the etiology of portal hypertension. Further studies on the effects of gut bacterial metabolites on portal circulation are needed.Support or Funding InformationThis work was supported by the National Science Centre, Poland grant no. UMO‐2016/22/E/NZ5/00647This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Therapeutic Administration of Probiotic VSL#3 on Dextran Sodium Sulfate‐ Induced Colitis
Authors: Prest Rebecca , Sapp Madison , Glise Joe , Moore Jaime , Walton Kristen LW. 
Published: June 2021

Inflammatory bowel disease (IBD) affects as many as 1.6 million Americans every year. This condition is a chronic intestinal disease that includes Crohn's disease and ulcerative colitis. Probiotic bacteria, including specific species of Lactobacillus and Bacteroides, have previously been shown to have beneficial effects in some intestinal disorders such as pouchitis, irritable bowel syndrome, and some models of IBD. We examined the effects of the probiotic cocktail VSL#3 administration for 3 days of recovery after a 5‐day treatment with 3% dextran sodium sulfate (DSS). Clinical signs of colitis, including weight loss, fecal occult blood, and fecal consistency, were monitored daily during the treatment and recovery period. At the end of the experiment, samples were collected for histological scoring, fecal bacterial analysis by quantitative PCR, and RNA isolation and analysis of colonic pro‐inflammatory cytokine expression by quantitative PCR. As expected, clinical signs of colitis were observed more frequently in DSS treated mice than in non‐DSS treated mice. However, probiotic‐treated colitic mice had clinical signs of disease similar to those of non‐probiotic treated colitic mice. Histological scoring of colitis showed a trend towards decreased histological colitis with VSL#3 treatment compared to colitic mice. Quantitative PCR for the pro‐inflammatory cytokine KC suggested decreased expression in probiotic‐treated mice compared to colitic mice. In conclusion, 3 days of treatment with VSL#3 following acute DSS‐induced colitis did not significantly improve recovery from colitis at the macroscopic level, but may improve inflammation at this time point.Support or Funding InformationSupported by the PORTAL program, Missouri Western State University.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The impact of cognitive fatigue on aerobic output in a 6‐minute walk test among older adults
Authors: Goodwin Aurora , Avolio Abby , Boolani Ali 
Published: June 2021

PurposeThe purpose of this study was to determine the impact of cognitive fatigue on aerobic output during a 6‐minute walk test (6MWT) in older adults.MethodsHealthy older adults (N=9, age= 67.39±4.58 yrs, height=168.01±55.82 cm, weight=60.80±12.41 kg) were involved in 2 days of testing. One day was a 2‐hour protocol of cognitively fatiguing tasks (S3 and S7, continuous performance task (CPT), rapid visual input processing (RVIP),) after which they were tasked to complete a 6MWT at their normal speed and VO2 was measured using the Cosmed Fitmate Pro. The other day, a baseline 6MWT was performed and VO2 were measured. A One‐Sample Kolmogorov‐Smirnov Test to determine distribution of peak VO2 scores prior to performing an independent sample T‐test to determine differences between cognitive fatigue and non‐cognitive fatigue days.ResultsResults yielded a normal distribution (Mean=871,33, SD=265.89) and T‐test analysis yielded no significant differences (p=.734) between cognitive fatigue and non‐cognitive fatigue days.ConclusionAlthough analysis yielded no difference in peak VO2 scores between days, it should be noted that 6 out of the 9 subjects had lower peak VO2 on cognitive fatigue days than on non‐cognitive fatigue days. Further research needs to be conducted to determine whether cognitive fatigue does decrease aerobic performance in older adults.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Alpha adrenergic inputs to PVN do not play a role in the sympathetic, phrenic or cardiovascular responses to intravenous sodium cyanide
Authors: Beig Irfan , Schreihofer Ann , Mifflin Steve 
Published: June 2021

Previous studies from our lab indicate that catecholaminergic inputs to the hypothalamic paraventricular nucleus (PVN) mediate at least part of the hypertension induced by exposure to intermittent hypoxia. The present study was designed to examine the role of alpha adrenergic inputs to PVN in the cardiovascular and phrenic nerve responses to chemoreceptor activation induced by sodium cyanide (NaCN). Rats were anesthetized with chloralose and urethane and vagotomized. Mean arterial pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), phrenic nerve activity (PNA) and end tidal CO2 recorded. The rat was placed in a stereotaxic frame for PVN microinjections, ventilated with O2‐enriched room air and paralyzed with pancuronium. Chemoreceptor activation was induced by iv. NaCN (200mcg/kg) to obtain baseline levels of responses. After return of MAP to baseline, bilateral injection of vehicle or either α1 antagonist prazosin (500nmol) or α2 antagonist idazoxin (5nMol) was made into PVN. A 2nd and 3rd iv. injection of NaCN was given 15 minutes and 1 hour after PVN microinjections of vehicle or drug. At the end of experiment brain was removed for localization of PVN injection sites. NaCN induced significant increases in MAP (Δ 32.5±4.5 mmHg, n=9), RSNA (Δ63.5±8.6% n=7) and PNA frequency (Δ 28.4±4.7%, n=7) and no change in HR. Bilateral administration of either prazosin or idazoxin into PVN did not alter the MAP, HR, RSNA or PNA responses to iv. NaCN. In separate set of experiments, bilateral injection of the α1–adrenergic agonist phenylephrine (200 ng) into the PVN increased RSNA within 5min. RSNA remained elevated by 36±12% for at least 60min after the injections, which did not change MAP and HR. Our study indicates that alpha adrenergic inputs to PVN do not appear to play a significant role in the MAP, RSNA, PNA and HR responses to chemoreceptor activation.Support or Funding InformationThis work supported by HL088052This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Ventilatory, Arterial Blood Gas, pH, and Electrolyte Adaptations to Chronic Hypercapnia in Healthy Goats
Authors: Buchholz Kirstyn , Burgraff Nicholas , Neumueller Suzanne , Hodges Matthew , Pan Lawrence , Langer Thomas , Forster Hubert 
Published: June 2021

Respiratory diseases, such as chronic obstructive pulmonary disease (COPD), affect ~24 million U.S adults and cost $49B annually. Many of these patients hypoventilate, leading to chronic hypercapnia, cognitive dysfunction, and high mortality rates. To gain insight into hypercapnia induced changes in neural and physiological function, we studied the breathing, arterial blood gases, pH, electrolytes, and cognitive function in goats during 30 days of chronic hypercapnia (inspired CO2 (InCO2) of 6%) or normocapnia. PaCO2 increased 10 mmHg during the first day of hypercapnia, continued to rise to a maximum of 16 mmHg above control between days 11–12, and remained near this level thereafter. PaO2 remained ~20 mmHg above control throughout the exposure to hypercapnia. Minute ventilation increased by 319% above control on day 1 of hypercapnia (n=7), but declined to 249% above control by day 2 of hypercapnia (n=7). Thereafter, ventilation progressively decreased to a nadir around day 12 at 211% above control (n=6) and remained near this level for the remainder of CO2 exposure. The initial hyperpnea during hypercapnic exposure was due to increases in both tidal volume and breathing frequency. However, breathing frequency returned to near control levels during the first week of hypercapnia, while tidal volume remained elevated. Arterial blood was acidic (−0.05) during day 1 of hypercapnia, followed by a partial compensation by day 8 due to increased arterial [HCO3+] (+7.4 mEq/L). VI/PaCO2 and VI/H+ at 6% InCO2 initially increased ~250% above control and remained elevated for the duration of hypercapnic exposure. Arterial [Cl−] decreased ~4 mmol/L during the first day of CO2 exposure and remained below control (−4–5 mmol/L) for the remainder of the 30 days. Arterial [K+] increased ~0.5 mmol/L during the first week of hypercapnia, and remained above control. No changes were found in arterial [Na+] or [Ca2+]. Accuracy of shape selection (index of cognitive function) decreased nearly 50% during hypercapnia. There were no apparent changes in any physiologic measurement for up to 30 days in goats maintained in room air conditions. In conclusion, we have established a model for future study of neuroadaptive responses, that potentially underlie compromised phenotypic/cognitive function, in COPD patients.Support or Funding InformationDepartment of Veterans Affairs; NIH HL007852This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
CAROM, a novel gene suppressing endothelial cell migration.
Authors: Xia Jixiang , Xiong Xinyu , Saredy Jason Jonathan , Xu Yanjie , Liu Suxuan , Yang Xiao‐Feng , Wang Hong 
Published: June 2021

Hyperhomocysteinemia (HHcy), a syndrome displayed by high concentration of homocysteine (Hcy) in blood has been demonstrated as a significant risk factor for cardiovascular disease (CVD). We have shown that Hcy leaded to endothelial cells (EC) injuries through inhibition of proliferation and migration. However, the comprehensive disclosure of mechanisms accounted for Hcy mediated EC injuries are still lacking up to date. It's compelling to discover more molecules that participate in the pathogenesis of diseases involving HHcy. Through differential display screening of cDNA from Hcy stimulated cultured EC, we discovered a highly induced gene and it was identified as CAROM, which was also called FCHSD2 (FCH and double SH3 domains 2). CAROM protein belongs to Bin‐Amphiphysin‐Rvs (BAR) superfamily and specifically it is a FBAR protein since it displays Fes/CIP homology (FCH) domain on N‐terminus. Proteins in this family are usually involved in endocytosis and other cellular trafficking regulation. The function of CAROM has been poorly characterized. Three major areas were focused for this study: 1) Genomic alignment among species and prediction of interacting partners through bioinformatics; 2) Mass Spectrometry (MS) analysis for discovering interacting proteins; 3) Characterizing its role of regulating EC function. This gene displays highly conservative homology among mammalian species, with 96.5% identity of amino acids between human and mouse homologue. Information collected from multiple interactome databases showed CAROM could bind to more than thirty proteins, although most of them haven't been experimentally verified. We used samples from CAROM overexpression EC for MS analysis. Our data disclosed that CAROM complexes covered a lot proteins regulating endocytosis, vesicle trafficking and cytoskeleton dynamics. These partners included EEA1(Early Endosome Antigen 1), Filamin, Vinculin, Importin‐5, Dynein et al, suggesting it could regulate motility, migration and other cell behaviors. CAROM expression was reduced more than 80% by siRNA targeted at different regions of its transcript. With gain and loss of function strategies, we tested its potential effect on EC function. Our preliminary data showed that inhibition on EC migration by Hcy were partially reversed after CAROM downregulation, indicating its interference with EC repair after vascular injury. Further studies are needed to unveil the underlying mechanisms mediated by CAROM.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Assessment of Cardiac Function of Rbm 20−/− Rats Using Pressure‐Volume Loop Analysis After 28 Days of Angiotensin II Treatment
Authors: Ahuja Hanna , Zhu Chaoqun , Willoughby Ashley , Pedrei Filipa Monteiro , Guo Wei , Chew Herbert G. 
Published: June 2021

RNA binding motif 20 (Rbm20), a muscle specific splicing factor for the sarcomeric protein titin, affects diastolic and systolic properties of the heart per the Frank‐Starling mechanism. Failure to alter titin expression from the predominant fetal isoform N2BA to the shorter, adult N2B isoform in Rbm20−/− (KO) rats, results in impaired cardiomyocyte relaxation, increased compliance of the ventricular walls, and dilated cardiomyopathy. These pathologies are similar to those seen in humans with this mutation, which often results in early, sudden death in both species. Angiotensin II (AII) acutely causes vasoconstriction, and chronically results in cardiac hypertrophy, characterized by an increase in cardiac wall stiffness. We hypothesized that 28 days of treatment with AII would increase the stiffness of the myocardium, resulting in improved cardiac function in KO rats. KO rats and age‐matched wild type (WT) controls were fitted with subdermal osmotic pumps, delivering AII continuously (0.25 μL·hr −1) for 28 days. After AII exposure, cardiac function was assessed in vivo using pressure‐volume loop analysis. Under isoflurane anesthesia, loops were recorded under baseline, brief inferior vena cava occlusion, and hypertonic saline infusion (20–40 μL) conditions. The rat was then heparinized, and blood collected for cuvette calibration. No group differences (p<0.05) were found in cardiac output (23.3±0.8 KO; 26.9±2.5 mL·min−1 WT), heart rate (295±21 KO; 341±16 b·min−1 WT), and stroke volume (80.8±9.1 KO; 79.5±7.6 μL WT). However, significant reductions were found in contractility (preload recruitable stroke work; 41.6±10.8 KO; 86.9±8.2 mmHg WT), stroke work (5.13±0.73; 8.13±0.86 mmHg·min WT), and ejection fraction (49.8±4.2 KO; 74.7±7.4 % WT) in KO rats. KO rats were able to maintain stroke volume, despite impaired contractility, due to a significant increase in preload (169±16 KO; 113±7 μL WT) and decrease in afterload (84.4±8.7 KO; 113±9 mmHg WT). We conclude that KO rats failed to improve contractility with 28 days of AII treatment, but maintained normal cardiac output through compensatory changes in preload and afterload.Support or Funding InformationThis project is supported in part by a grant from the National Institute of General Medical Sciences (2P20GM103432) from the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of 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.