bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of core and skin temperatures and dehydration on heart rate response during interval exercise in warm and cool conditions
Authors: TAKEDA RYOSUKE , Imai Daiki , Kwai Eriko , Ota Akemi , Hanno Genta , Morita Emiko , Suzuki Yuta , Yokoyama Hisayo , Okazaki Kazunobu 
Published: June 2021

Heart rate (HR) gradually increases during exercise at a constant work load, which is known as cardiovascular drift (CVD). The CVD is exacerbated when exercise is performed under condition with high ambient temperatures (Ta). It is suggested that increased esophageal temperature (Tes) is associated with the level of CVD. In the present study, we examined the effect of skin temperatures (Tsk) and the dehydration on CVD during high intensity interval exercise.METHODSEight healthy young men underwent interval exercise on a cycling ergometer for 72 min (8 sets of 4 min at 80% VO2max – 5 min at 20% VO2max) in cool (Ta of 20□, 40% relative humidity) and warm (Ta of 30□, 40% relative humidity) conditions. Tes, Tsk, heart rate (HR), sweat rate (SR) and skin blood flow (SkBF) at chest were measured continuously. Blood samples were taken before and at the end of exercise, and relative change in plasma volume (%ΔPV) after exercise were determined from hematocrit and hemoglobin concentration of the blood samples.RESULTSHR increased during exercise at 80% VO2max while decreased during exercise at 20% VO2max in both trials. HR in warm condition was higher than cool condition (p < 0.05) throughout trial. More importantly, HR at the end of each set was gradually increased during exercise and the increase was significantly higher in warm than in cool condition. Tes increased during exercise at 80% VO2max while decreased during exercise at 20% VO2max in both trials, it reached the peak value at the end of the 4th set of exercise at 80% VO2max (37.93 ± 0.04□ (means ± SE) in cool and 37.84 ± 0.04□ in warm), then kept these values until the end of trial. There was no significant difference in Tes between trials throughout trial. Tsk was higher (p < 0.05) in warm than cool condition throughout trial. SR at chest was higher (p < 0.05) in warm than cool condition from 9 min to the end of exercise, while SkBF at chest was not significantly different between conditions throughout trial. The %ΔPV was not different among conditions (−13.9 ± 1.0 % in cool, −12.7 ± 1.5 % in warm).CONCLUSIONSExercise in a warm condition increased HR during interval exercise compared to a cool condition despite the level of esophageal temperature and dehydration were same between conditions. The increased HR would be associated with an increased skin temperatures.Support or Funding InformationThis work was supported by a Grant‐in‐Aid for Scientific Research (B) and a Grant‐in‐Aid for Challenging Exploratory Research (K. Okazaki) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.This 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 Transcutaneous Carbon Dioxide (CO2) on Hyperglycemia‐Induced Capillary Regression in Skeletal Muscle
Authors: Matsumoto Tomohiro , Takuwa Miho , Hirabayashi Takumi , Ikeji Takuya , Ono Kohei , Maeshige Noriaki , Kondo Hiroyo , Fujino Hidemi 
Published: June 2021

Hyperglycemia causes microvascular impairment in skeletal muscle of diabetes. Transcutaneous carbon dioxide (CO2) have been shown to increase capillary in skeletal muscle of healthy rats via the increase of angiogenic factor. The purpose of this study was to determine the effects of transcutaneous CO2 on muscle capillary impairment by exposure of hyperglycemia in streptozotocin (STZ)‐treated diabetic rats. Twenty‐four male Wistar rats (220~270g) were divided into control (CON), CO2, STZ and STZ+CO2 groups. STZ (50 mg/kg) was injected into the tail vein of rats. Blood glucose levels above 250 mg/dl after 2 days of the STZ injection confirmed the diabetic state. The lower limbs in rats were shaved and hydrogel was applied afterwards. The CO2 adaptor was attached to the limbs and sealed, and CO2 was administered into the adaptor for 30 min. This treatment was performed 5 days per week for 8 weeks. STZ resulted in capillary regression, indicated by decreases in capillary‐to‐fiber ratio. However, the capillary‐to‐fiber ratio in STZ + CO2 was higher than that in STZ. In addition, the protein expression level of vascular endothelial growth factor (VEGF), which is angiogenic factor, in STZ + CO2 was higher than that in STZ. The protein expression level of thrombospondin‐1 (TSP‐1), which is antiangiogenic factor, in STZ + CO2 was lower than that in STZ. These results indicated that transcutaneous CO2 attenuated the capillary regression via the increase of angiogenic factor and the decrease of antiangiogenic factor.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Increased Subpleural Pulmonary Arteriolar Tone Associated with Inhibition of Nitric Oxide Synthase in a Mouse Model of Type‐1 Diabetes
Authors: Roberts Andrew M. , Jagadapillai Rekha , Moulana Nayeem , Cai Lu , Gozal Evelyne 
Published: June 2021

Type‐1 diabetes, characterized by elevation of blood glucose, inflammation and oxidative stress, results in endothelial injury that alters nitric oxide (NO) signaling and impairs microvascular regulation in a variety of vascular beds. NO signaling also plays a prominent role in the modulation of alveolar perfusion. Therefore, the lungs may be particularly vulnerable to diabetes‐induced endothelial changes. We hypothesized that diabetes‐induced oxidative injury, resulting in decreased NO bioavailability and enhanced fibrinogen‐endothelial interaction, induces endothelial injury and pulmonary microvascular dysfunction in the mouse lung. The effects of acute NO synthase (NOS) inhibition with L‐NAME on subpleural arterioles were examined in streptozotocin‐treated C57BL/6J mice (STZ) and their saline‐treated controls (Control). Microvascular changes were assessed by intravital microscopy of the right lung in anesthetized mice (7 to 11 months old) with open chest and ventilated lungs. Pulmonary arteriolar diameters (ranging from 27.2 – 48.7 μm) were measured before and after acute administration of the nitric oxide synthase (NOS) inhibitor, L‐NAME (0.1mg/g body wt). L‐NAME caused a 13.6 ± 7.5% constriction (n=5, p=0.034) in Control mice. In contrast, there was an 18.0 ± 11% dilation (p<0.009, n=5) in STZ mice. Intra‐arterial administration of fluorescently‐labeled fibrinogen in STZ mice, without L‐NAME treatment, resulted in adherence of fibrinogen in the microvascular network, indicating endothelial injury. These data suggest that diabetes‐induced systemic effects may affect lung endothelial function. Control mice displayed a physiological vasoconstriction response to L‐NAME resulting from a loss of the NO vasodilator influence. In contrast, while L‐NAME may have decreased bioavailable NO in the diabetic lung, inhibition of NOS with L‐NAME appeared to have a vasodilator effect by decreasing formation of reactive nitrogen species or by unmasking another vasodilator. We conclude that diabetes may adversely affect lung microvasculature by inducing inflammation and decreasing NO bioavailability. Altered NO‐induced responses may subsequently cause significant pulmonary endothelial injury and microvascular dysfunction that could lead to ventilation‐perfusion abnormalities and exacerbate systemic complications of diabetesSupport or Funding InformationUniversity of Louisville, School of Medicine Collaborative Enhancement GrantThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hemodilution Improves Shear‐Mediated Transduction of Vasodilatory Signals in Human Cerebral and Systemic Circulations
Authors: Hoiland Ryan Leo , Tremblay Josh , Flück Daniela , Willie Chris , Smith Kurt J , Tymko Mike M , Howe Connor A , Donnelly Joseph , Stembridge Mike , Patrician Alex , Rieger Matt , Hansen Alex , Coombs Geoff , Santoro Antoinette , Green Daniel , MacLeod David , Ainslie Philip 
Published: June 2021

Shear stress (SS) regulates blood flow within the systemic and cerebral circulation. For example, in clinical populations (e.g. hemochromatosis), endothelium‐dependent flow‐mediated dilation (FMD) is improved and impaired by increases and decreases in whole blood viscosity (WBV), respectively. We tested the hypothesis that reductions in WBV would attenuate both cerebrovascular CO2 reactivity and brachial FMD in healthy males (n=9). Internal carotid (ICA) and brachial artery (BA) blood flow, as well as cerebrovascular CO2 reactivity and FMD, were measured prior to and following isovolumic hemodilution with 5% human serum albumin (20% removal/replacement of blood volume). Hemodilution reduced hematocrit (42.7±2.5 vs. 34.7±2.0 %; P<0.01) and WBV (3.6±0.2 vs. 2.7±0.2 cP; P<0.01). Resting ICA blood flow increased by 19% (328.7±66.3 vs. 389.9±91.0 mL · dL−1; P<0.01) while SS was unaltered (13.4±3.2 vs. 12.5±2.6 dyn · cm−2; P=0.17). BA blood flow (41.0±18.9 vs. 54.6±34.1 mL · min−1; P=0.31) and SS (2.54±1.15 vs. 3.00±2.83 dyn · cm−2; P=0.66) were unaltered following hemodilution. Despite a similarly unaltered SS area under the curve stimulus (733.4±296.6 vs. 996.1±571.1 au3; P=0.20), BA FMD increased by 130% (3.9±2.3 vs. 9.0±4.3%; P=0.02). In contrast, however, neither absolute [24.3±7.4 vs. 30.1±13.5 ΔCBF (mL/dL) · ΔmmHg PaCO2; P=0.10] or relative [7.6±3.1 vs. 8.5±4.1 %ΔCBF · mmHg PaCO2; P=0.28) CO2 reactivity were altered following hemodilution despite a reduced SS stimulus throughout the reactivity test (main effect, P<0.01). Therefore, despite the differing influence of hemodilution on cerebral and systemic circulations, both were more responsive for a given SS stimulus following hemodilution.Support or Funding InformationRyan L. Hoiland was supported by a Natural Sciences and Engineering Research Council of Canada Post Graduate Scholarship. Dr. David MacLeod is supported through the Duke University Human Physiology & Pharmacology Laboratory. Prof. Philip Ainslie is supported by the Natural Sciences and Engineering Research Council of Canada and Canada Research Chairs.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Sodium Nitroprusside Induced Vasodilatation Encompasses Cerebral Blood Flow in Young Men
Authors: Olesen Niels Damkjar , Fischer Mads , Secher Niels Henry 
Published: June 2021

PurposeSodium nitroprusside (SNP) reduces blood pressure by vasodilatation, but is reported to lower cerebral blood flow (CBF). We evaluated the influence of SNP on CBF when mean arterial pressure (MAP) was reduced by 20% and by 40%, while keeping MAP ≥ 50 mmHg.MethodsIn 19 healthy men (age 24 ± 4 years; mean ± SD) right internal carotid (ICA) and vertebral artery (VA) blood flow was evaluated by duplex ultrasound. Cerebral CO2 reactivity was determined during hyperventilation and CBF ((ICA + VA flow) × 2) also ‘corrected’ according to reduction in arterial CO2 tension. Evaluation of MAP was by brachial artery catheterisation and total peripheral resistance was derived by pulse contour analysis (Modelflow). Analysis was by a repeated measure mixed model and comparison of the relative change in ICA vs. VA flow was by paired t‐test. Values are presented as mean ± SD or median (IQR) and changes as mean (95% CI). The study was registered at clinicaltrials.gov (NCT03317652) prior to subject enrolment.ResultsThree subjects developed presyncopal symptoms during the large reduction in MAP and data obtained at that time was not included in the analysis. Infusion of SNP at 2.0 μg kg–1 min–1 (1.5–2.5) reduced MAP by 17 ± 5% and at 8.6 μg kg–1 min–1 (6.0–9.4) by 31 ± 6% (both P < 0.0001) as total peripheral resistance decreased from 17 ± 4 to 10 ± 2 and 7 ± 1 l min−1 mmHg−1 (both P < 0.001). The PaCO2 decreased from 5.5 ± 0.3 to 5.2 ± 0.4 and 4.9 ± 0.6 kPa (both P < 0.001) at the low and high SNP rate. With no ‘correction’ for change in PaCO2, ICA flow increased at the low infusion rate (from 336 ± 66 to 365 ± 69 ml min−1; P = 0.013) with no change in VA flow and CBF while ICA and VA vascular conductance increased with increasing SNP rate. With ‘correction’ for the reduction in PaCO2, ICA flow increased similarly at the two levels of MAP with maintained VA flow with a larger increase in ICA than VA flow (16 ± 14% vs. 5 ± 21%; P = 0.023) during moderate reduction in MAP. Thus, CBF increased by 50 (95% CI: 27–72) and 50 ml min−1 (95% CI: 26–73; both P < 0.001) at the two rates of SNP infusion.ConclusionInfusion of SNP reduces MAP by vasodilatation and by determination of ICA and VA flow in young men vasodilatation encompasses the brain and more so ICA than VA. The results indicate that CBF is controlled not only by its perfusion pressure when blood pressure is reduced.Support or Funding InformationThis study was supported by the University of Copenhagen.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypo‐phosphorylated hnRNPK promotes migration of triple negative breast cancer cells through an Aurora‐A‐independent manner
Authors: Tsai Hsin‐Yu , Lin Chao‐Hsiung 
Published: June 2021

HnRNPK, a member of heterogeneous nuclear ribonucleoprotein (hnRNP) family, is well known as a poly(C)‐binding protein that participates in RNA processing and translational regulations. Importance of hnRNPK in tumorigenesis has been implicated by its persistent amplification in a wide range of cancers, whereas diverse post‐transcriptional modifications (PTMs) of hnRNPK also have been shown to regulate its protein function. We previously reported a novel Aurora‐A‐mediated phosphorylation of hnRNPK, but the cellular function of such phosphorylation remains unknown. Because Aurora‐A has been known as an oncogenic kinase and promotes transformation, growth and migration of cancer cells, we further investigated the functional role of hnRNPK phosphorylation in MDA‐MB‐231 cell line, a triple negative breast cancer cell with amplification of Aurora‐A. Accordingly, two stable clones replacing endogenous hnRNPK with either phosphorylation‐defective or phosphorylation‐mimic mutants were established, namely MDA‐MB‐231‐SA and MDA‐MB‐231‐SD. To determine whether such hnRNPK phosphorylation participates in the Aurora‐A‐mediated migration signaling, migration ability was compared between the hnRNPK phosphorylation‐defective and phosphorylation‐enhancing cells. Our results showed that migration ability of MDA‐MB‐231‐SA cells is higher than the control MDA‐MB‐231 cells but migration ability of MDA‐MB‐231‐SD cells is less than control, suggesting that Aurora‐A‐mediated hnRNPK phosphorylation does not promote cell migration but instead suppresses it, likely through an Aurora‐A‐independent manner. Therefore, it is proposed that such hnRNPK phosphorylation is not only mediated by Aurora‐A amplification but also regulated by other factors. It has been shown that different PTMs of hnRNPK are able to crosstalk with each other, and synergistically influence protein functions. My data showed that such Aurora‐A‐mediated phosphorylation was inhibited by arginine methylation of hnRNPK, whereas cell migration was decreased upon deficiency of hnRNPK arginine methylation in MDA‐MB‐231 cells. Further verification of migration‐associated signaling pathway showed that levels of EMT‐related proteins, Twist and β‐catenin, and RNA levels of MMP family were increased in MDA‐MB‐231‐SA cells. In conclusion, our results imply that a hypo‐phosphorylated status of hnRNPK may promote cell migration through hnRNPK‐β‐catenin‐MMP pathway.This 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 AN AEROBIC PHYSICAL EXERCISE SESSION ON INFLAMMATORY MARKERS IL‐6, IL‐10 AND TNF‐alpha IN PATIENTS WITH CHRONIC RENAL DISEASE (DRC) STAGE 3.
Authors: Pinto Walter Pereira , Rezende Rafael Andrade , Júnior Armando Morales , De Oliveira Barguena Renato , Dalboni Maria Aparecida , Tinucci Tais 
Published: June 2021

IntroductionLoss of renal function results in serum accumulation of toxic substances in chronic kidney disease (CKD) patients. These substances increase the inflammatory response, which in turn contributes to the pathophysiology of cardiovascular disease in this population.It has been described in the general population that aerobic physical exercise is capable of exerting anti‐inflammatory effects. However, the impact of physical exercise in CKD stage 3 patients (CKD3; creatinine clearance 29–69 ml/min) is unclear. Thus, the objective of this study was to evaluate the effects of a session of aerobic exercise on inflammation markers in CKD stage 3 patients.Methods10 subjects with CKD3, (55 ± 6 years, creatinine clearance between 29 and 69 ml/min/1.73 m2), and 10 subjects with normal renal function (51 ± 5 years creatinine clearance> 100 ml/min/1.73m2) were selected to performed aerobic exercise (cycle ergometer, 45 min, 50% VO2peak). Before and after the sessions, blood samples were collected for analysis of the inflammatory markers: TNF‐alpha, IL‐6 and IL‐10.Statistical analysisThe normality of the data was tested by the Shapiro‐Wilk test. Data were compared through two‐factor ANOVA (groups × times) for parametric data, and the FRIEDMAN test used for non‐parametric comparisons. A significant difference was considered when p <0.05. The software used was IBM SPSS STATISTICS 24.0.ResultsAerobic physical exercise reduced IL‐6 levels in the CKD3 group (2.13 ± 0.36 vs. 1.86 ± 0.45; p = 0.04). IL‐10 levels increased after an aerobic exercise session compared to the control group (p <0.001). Physical exercise had no effect on TNF‐alpha levels (P> 0.05).ConclusionWhen compared CKD3 with healthy individuals, patients with CKD3 are more inflamed. However, in this study the aerobic exercise decreased IL‐6 (pro‐inflammatory) and increased IL‐10 (anti‐inflammatory) in these patients. In conclusion, aerobic physical exercise played an anti‐inflammatory effect in CKD stage 3 patients, suggesting that this practice may to benefit this population.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Empagliflozin Inhibits NHE3 Activity in the Proximal Tubule of Normotensive and Hypertensive Rats
Authors: Borges Flávio Araújo , Silva Corina Albuquerque , Crajoinas Renato Oliveira , Castelo‐Branco Regiane Cardoso , Luchi Weverton Machado , Girardi Adriana Castello Costa 
Published: June 2021

BackgroundA growing body of evidence suggests an interplay between extracellular volume and glucose homeostasis. NHE3 is the main pathway for Na reabsorption in the proximal tubule (PT). The sodium glucose cotransporter SGLT2 reabsorbs most of the glucose filtered by the kidneys and colocalizes with NHE3 in the apical membrane of PT. Thus, we tested the hypothesis that SGLT2 and NHE3 functionally interact. Given that SGLT2 inhibitors confer blood‐pressure lowering effects in T2DM patients, we also tested the hypothesis that the antihypertensive effects of SGLT2 inhibitors may be associated with PT NHE3 inhibition.MethodsThe acute and long‐term effects of the SGLT2 inhibitor empagliflozin on PT NHE3 activity were determined by in vivo stationary microperfusion in fourteen‐week‐old male Wistar rats and SHR‐treated rats. Additionally, twelve‐week‐old SHRs were treated with empagliflozin (10 mg/kg/day) or vehicle (control) for two weeks. Tail‐cuff blood pressure and renal function were measured before (baseline) and after treatment (post‐treatment). NHE3 expression and phosphorylation levels were evaluated by immunoblotting.ResultsEmpagliflozin acutely inhibited PT NHE3 activity in both Wistar (1.73 ± 0.07 vs. 2.55 ± 0.14 nmol/cm2.s, P < 0.001) and SHR (0.82 ± 0.07 vs. 1.21 ± 0.10 nmol/cm2.s, P < 0.01). Blood pressure (BP) of empagliflozin‐treated SHR was lower than baseline levels (176 ± 4 vs. 194 ± 4 mm Hg, P < 0.01) whereas no change in BP was observed in vehicle‐treated SHR (194 ± 6 vs. 192 ± 5 mm Hg). Compared to baseline, empagliflozin‐treatment enhanced cumulative urinary flow, calcium, sodium and glucose excretion whereas in vehicle‐treated SHR these parameters remained unchanged. Lower BP in empagliflozin‐treated SHR was associated with lower PT NHE3 activity (0.67 ± 0.10 vs. 1.18 ± 0.10 nmol/cm2.s, P < 0.001). No differences were observed on renal cortical NHE3 protein expression or NHE3 phosphorylation levels between the two groups of rats.ConclusionThese results suggest that NHE3 and SGLT2 functionally interact in the PT. Inhibition of NHE3 by SGLT2 inhibitors may underlie, at least in part, the antihypertensive effect of empagliflozin.Support or Funding InformationFAPESPThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Mulberry extract protects from diet‐induced obesity in association with modulation of gut microbiota in mice
Authors: Song Haizhao 
Published: June 2021

Mulberry, a natural source of flavonoids, phenolics and anthocyanins, has been widely used in edible food and medicine due to its pharmacological effect. Growing evidence indicates that gut microbiota contributes to obesity, type II diabetes and many other related metabolic disorders. The present study was designed to evaluate the influence of the mulberry water extract (ME) on high‐fat diet induced obesity and determine whether the beneficial effects of ME are associated with the modulation of gut microbiota. Forty‐five male C57BL/6J mice were divided into three groups and fed with low‐fat diet, high‐fat diet or high‐fat diet plus ME administration of 300 mg/kg/day for 15 weeks. 16S rDNA sequencing was performed to analyze the composition of gut microbiota. Our results showed that dietary ME reduced HFD‐induced body weight gain and ameliorated adipose tissue hypertrophy and insulin resistance. Moreover, metagenomic analysis indicated that ME supplement significantly changed the ratio of Firmicutes and Bacteroidetes at the phylum level.In conclusion, ME protects from diet‐induced obesity and its related metabolic disorders, which is associated with the modulation of gut microbiota in mice. These findings suggested a dietary choice of mulberry in the nutrition therapy of obesity and its metabolic disorders.Support or Funding InformationNational Natural Science Foundation of China (Grant No. 31701031) China Postdoctoral Science Foundation (Grant No. 2016M601006)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.