bluuebunny/crossref_metadata_2025_split huggingface dataset:
Omega‐3 Index as a risk factor of ischemic and haemorrhagic stroke: a pilot case‐control study
Authors: Park Yongsoon , Park Seonhye 
Published: June 2021

Previous studies suggested that fish consumption and blood level of omega‐3 fatty acids negatively correlated with ischemic stroke, but the relation to the risk of haemorrhagic stroke remains unclear. This study was investigated the effect of Omega‐3 Index (EPA + DHA in red blood cell, RBC) on hemorrhagic and ischemic stroke.Hemorrhagic (n=24) and ischemic stroke (n=31) cases, and controls (n=20) were included in the present study. Omega‐3 Index (8.36 ± 0.58 vs. 10.66 ± 0.68 %), total n‐3 fatty acids (15.30 ± 0.57 vs. 12.61 ± 0.78 %), and C22:6n3 (DHA; 8.93 ± 0.55 vs. 7.09 ± 0.38 %) in RBC were significantly higher in control than ischemic and haemorrhagic stroke patients. Omega‐3 Index and total n‐3 fatty acids, and DHA were significantly increased the risk for haemorrhagic stroke, but not for ischemic stroke. However, among the ischemic stroke subgroups, lacunar infarction patients had the significantly lower level of Omega‐3 Index and EPA, suggesting that low level of omga‐3 fatty acids might be a provocating factor on lacunar infarction. There was no significant difference in intake of nutrients and foods between control and patients, except low intake of brown rice, seaweed soup, bean sprouts soup, and bean paste pot stew in stroke patients. In conclusion, n‐3 fatty acids may have beneficial effect on haemorrhagic stroke and lacunar infarction, a subgroup of ischemic stroke.
Effects of dietary calcium and milk on oxidative and inflammatory stress and lifespan in wild‐type and aP2‐agouti transgenic mice
Authors: Bruckbauer Antje , Sobhani Marilyn T , Zemel Michael B 
Published: June 2021

Dietary Ca reduces oxidative and inflammatory stress, while milk exerts a greater effect than supplemental Ca. To examine the effects on lifespan and related biomarkers, aP2‐agouti transgenic mice (model of diet‐induced obesity) and wild‐type littermates were fed a low Ca (0.4% Ca), high‐Ca (1.2% Ca from CaCO3), or milk (1.2% Ca from non‐fat dry milk) obesigenic diets until death. Randomized subgroups were sacrificed at 28, 52 and 78 weeks of age for biomarker analysis. The milk diet attenuated weight and adiposity gain and prevented the age‐related muscle loss (p<0.04) and rise in reactive oxygen production (ROS) in adipose tissue (p=0.005). There was a corresponding increase in SOD3 (in wild‐type, p=0.04) and glutathione peroxidase gene expression (p<0.02) in soleus, and in liver SOD activity (p<0.04). The milk diet decreased adipose tissue IL6 (p<0.05) and TNFα (p<0.03) expression in male mice only. The survival analysis showed an overall shorter lifespan in transgenic vs. wild‐type mice. Although no diet effect was found on lifespan, the milk diet resulted in a significant increase in early (75%) survival rate in wild‐type mice (p<0.02). These data demonstrate that milk diet attenuates adiposity, protects against muscle loss and reduces oxidative and inflammatory stress. Although these effects did not influence maximum lifespan, they did suppress early mortality.Grant Funding SourceThe National Dairy Council
Neonatal birth weight according to maternal serum lipid levels and dietary intakes
Authors: Choi Hyung In , Kim Hyesook , Kim Ki Nam , Ha Eun‐Hee , Park Hye‐Sook , Ha Mina , Kim Yangho , Hong Yun‐Chul , Chang Namsoo 
Published: June 2021

The relationship of neonatal birth weight with maternal serum triglyceride (TG) level has been reported. This hospital‐based cohort study examined the relationship between maternal dietary intake and serum lipid levels in relation to neonatal births weights in 460 pregnant women and their babies. Maternal serum TG and HDL‐cholesterol (HDL‐C) were correlated with intakes of food and nutrients such as cereals and cereal products, meat and meat products, carbohydrates, and polyunsaturated fatty acid. After controlling for maternal age, babies' sex, income and history of low birth weight, the adjusted odds ratio of low birth weight (<2.5kg) delivery was 6.1 (95% confidence intervals, 1.202‐30.707) in women with below the median serum TG level at parturition. The adjusted odds ratio of macrosomia (=4kg) delivery was 0.4 (95% confidence intervals, 0.133‐0.931) in women with above the median serum HDL‐C level. We suggest that maternal lipid levels at parturition of which dietary intake may have partial contribution throughout the pregnancy is associated with birth weight.*This work was supported by the Ministry of Environment and the 2nd stage of Brain Korea 21 project in 2008
Dietary Supplementation with Dried Plum Prevents Ovariectomy‐Induced Bone Loss in C57BL/6 Mice and Modulates the Immune Response
Authors: Rendina Elizabeth , Lim Yin F. , Marlow Denver , Wang Yan , Clarke Stephen L. , Kuvibidila Solo , Lucas Edralin A. , Smith Brenda J. 
Published: June 2021

Due to recent evidence demonstrating the link between the immune system and skeletal health, this study was designed to determine the osteoprotective effects of dried plum (DP) on bone metabolism and the immune response. Twelve‐week old female mice (n=59) were assigned to 5 treatment groups for a duration of 4 wks: sham‐operated (Sham) control diet (AIN‐96M), ovariectomized (OVX)‐control diet and OVX animals receiving diet supplemented with 5%, 15%, or 25% DP (w/w). Bone mineral density and content of the spine was decreased (8%) by OVX, which was totally prevented by 25% DP. µCT analyses revealed the OVX compromise in spine and proximal tibial bone volume was prevented by higher doses of DP. Similar results were also observed in the trabecular number and thickness of the spine. Simulated biomechanical tests (finite element analyses) showed the improved structural properties observed with DP (15% & 25%) resulted in enhanced bone strength and stiffness. These alterations in bone mass and architecture coincided with increased serum IGF‐I and reduced bone turnover (i.e. serum PINP) in OVX mice consuming DP. Following ex vivo Con A stimulation, splenocyte TNF‐α production was suppressed by DP, but no change in IL‐6 occurred. This study supports DP's positive effects on bone in the OVX mouse model; however the role of the immune system in this response warrants further investigation. (Supported by California Dried Plum Board)Grant Funding SourceCalifornia Dried Plum Board
Xanthohumol decreases adipocyte differentiation
Authors: Teixeira Diana , Mendes Vanda , Pestana Diogo , Calhau Conceição , Azevedo Isabel , Monteiro Rosário 
Published: June 2021

Lately, some phytochemicals have been demonstrated to possess anti‐obesity properties. In this regard we investigated the effect of xanthohumol (XN), a flavonoid from hops (Humulus lupulus L.) in preadipocyte differentiation. For this, we tested the effect of XN on 3T3‐L1 cells in lipid accumulation in several periods of preadipocyte differentiation, PPARγ expression and NFκB activation. Differentiation was measured using oil red O incorporation or PPARγ expression and NFκB activation was assessed by ELISA. XN reduced culture lipid content and this effect was more pronounced when the compound was present before (46% of control) or during differentiation induction (47% of control). Supporting these results, PPARγ transcription was also reduced by treatment with 10 μM XN, corroborating an inhibitory effect of the flavonoid in adipocyte differentiation. NFκB activation was detected in preadipocytes which may account for part of the effects on differentiation, although it was unaltered in adipocytes. These results suggest that XN is able to reduce adipocyte differentiation which may contribute to increase adipocyte size. Since adipocyte hypertrophy may result in obesity‐related inflammatory events, XN may not improve the metabolic profile associated with obesity.Supported by FCT (POCI, FEDER, Programa Comunitário de Apoio, SFRH/BPD/40110/2007) and Instituto de Bebidas e Saúde (iBeSa).
Opposing effects of carbon monoxide (CO) releasing molecule (CORM3) on activation of polymorphonuclear leukocytes (PMN) and endothelial cells (HUVEC) in sepsis.
Authors: Mizuguchi Shinjiro , Stephen Jancy , Bihari Relka , Markovic Nevena , Katada Kazuhiro , Capretta Fred , Potter Richard F. , Cepinskas Gediminas 
Published: June 2021

Recently, it has been shown that CORM‐released CO can modulate inflammatory response. In this study we assessed the effects and potential mechanisms of water‐soluble CO‐releasing molecule, CORM3, in experimental model of sepsis.Sepsis in mice was induced by cecal ligation/puncture (CLP). CORM3 (3mg/kg; iv) was administered 15 min after CLP induction. PMN accumulation (MPO assay) in the lung was assessed 6 hr later. In in vitro experiments human PMN were primed with LPS (10ng/ml) and stimulated with fMLP (100nM). PMN production of ROS (oxidation of L‐012/DHR123 over 30 min period of time) and release of elastase (AAPV‐pNA; 1hr) were assessed. In parallel, HUVEC were stimulated with LPS (1µg/ml) and assessed for ROS production, E‐selectin/ICAM‐1 expression (RT‐PCR) and 51Cr‐PMN adhesion/migration. Some experiments were performed in the presence of CORM‐3 (1‐100 µM).The obtained results indicate that CORM3 significantly reduced PMN accumulation in the lung of septic mice. In parallel, LPS‐induced increase in HUVEC ROS production, E‐selectin/ICAM‐1 expression and PMN adhesion/migration were attenuated by CORM‐3. On the contrary, CORM3 markedly increased ROS production and potentiated release of elastase by LPS‐primed PMN.These data indicate that CORM3 reduces inflammation in the septic lung by differentially modulating PMN and endothelial cell activation (HSFO‐ NA6171 and MOP‐68848)
Protective Effect of Astragalus Polysaccharide Against High glucose‐induced Endoplasmic Reticulum Stress by Activation of AMP‐activated Protein Kinase in Human HepG2 Cells
Authors: Liu Jian , Jin Huan , Deng Juan , Ouyang Jingping 
Published: June 2021

OBJECTIVEAstragalus polysaccharide (APS) activates AMP‐activated protein kinase (AMPK) and attenuates endoplasmic reticulum (ER)stress. We investigated whether AMPK is required for the attenuation of high glucose‐induced ER stress of APS in human HepG2 cells.RESEARCH DESIGN AND METHODSHepG2 cells were exposed to low glucose (5.5mmol/L) or high glucose (30mmol/L) for 24 h. The expression of ER stress‐related marker (p‐perk) was evaluated with or without APS by western blotting analysis.RESULTSWe found that high glucose‐induced p‐perk expression was significantly inhibited by pretreatment with APS, We also found that this effect of APS was mimicked by 5‐aminoimidazole‐4‐carboxyamide‐1‐β ‐D‐ribofuranoside (AICAR), a pharmacological activator of AMPK.In parallel, Compound C, an inhibitor of AMPK, abrogated the effect of APS on p‐perk expression.CONCLUSIONSThese data suggest that APS can protect HepG2 cells against high glucose‐induced ER stress by activation of AMPK. (This work was supported by the National Natural Science Foundation of China (No. 30370673))
Roles of Prostaglandin E2 and 12‐Hydroxy‐eicosatetraenoic Acid on Promotion of Angiogenesis of Choroid‐retinal Endothelial Cells by Pigment Epithelial Cells and Leukocytes under Inflammatory Conditions
Authors: Tian Haibin , Lu Yan , Sherwood Alexander , Hong Song 
Published: June 2021

PurposesTo determine the effects of choroid‐retinal endothelial cells (CREC), retinal pigment epithelial cells (RPE) and leukocytes on CREC angiogenesis including migration, vasculature formation, and proliferation. The lipid profiles in these process were also determined. Prostaglandin E2 (PGE2) and 12‐hydroxy‐eicosatetraenoic acid (12‐HETE) are chosen as targets to confirm the effects of lipids on CREC angiogenesis.MethodsCREC migration was carried out in 24‐transwell plate, RPE or leukocytes in low chambers stimulated with 2ng/ml IL‐1 β and 2ng/ml TNF‐α. Tube formation was performed on matrigel. Lipid profiles of CREC, RPE ad leukocytes were analyzed using LC‐UV‐MS/MS.Resultsstimulated with IL‐1 β and TNF‐α, EC, RPE and leukocytes could produce many kinds of lipid mediators including PGE2 and 12HETE, which promoted CREC migration and vasculature formation. CREC and leukocytes produced much more lipid mediators than RPE. High concentration of COX2 inhibitor NS398 and lipoxygenase inhibitor Baicalein inhibited expressions of PGE2 and 12‐HETE respectively, and subsequently reduce CREC migration and vasculature formation.ConclusionsCREC, RPE and leukocytes could promote angiogenesis by producing PGE2 and 12HETE under inflammation conditions.
Gender differences in plasma volume changes in response to arm & leg ergometer exercise
Authors: Francois Michelle Renee , Sehgal Kiran Bala , Bhayana Anuradha , Fleming Mollie , Prasad Anu , Shehane Lindsey , Sissodiya Ekta 
Published: June 2021

Plasma volume shift (PVS) in response to exercise is a well‐understood phenomenon that has not been investigated for gender differences. Ten healthy young subjects ‐ 5 men (mean age 24.8) and 5 women (mean age 24.4) ‐ each pedaled a cycle ergometer at 50 rpm starting at 0.5 kp and increasing by 0.5 kp every 2 min until heart rate (HR) reached 170. They continued for 8 min with work load adjusted to keep HR at 170±5 bpm. On a separate day, subjects turned an arm ergometer at 50 rpm starting at 0.25 kp and increasing by 0.25 kp every minute until HR reached 170, then continued for 8 min as above. Sessions were counterbalanced. Two‐mL blood samples (in EDTA) were drawn immediately before and after each exercise bout. Hematocrit (Hct) was measured using a microhematocrit reader. Hemoglobin (Hb) was measured using the cyanmethemoglobin method. PVS was calculated using the Dill & Costill equations. One‐way ANOVA revealed significant (p<0.05) pre‐ to post‐exercise increases in Hct and Hb and decreases in PV within both groups. Change in Hb was significant (p<0.05; F=18.366) between groups for arm ergometry. PVS was not significantly different between groups for either type of ergometry. Data suggest that, for a moderately high level of cardiovascular stress, upper and lower body aerobic exercise elicits similar PVS regardless of gender.This research was supported by the Department of Kinesiology and Health Studies, SLU.
Effect of depth of anaesthesia and postganglionic sympathetic blockade on reflex heart rate control in rodents during lower body negative pressure
Authors: Usselman Charlotte W , Welch Ian , Mattar Louis , Shoemaker J Kevin 
Published: June 2021

We tested the hypothesis that depth of anaesthesia affects heart rate (HR) control during orthostatic stress in rodents. Urethane (UR) and a‐chlorolose (a‐CL) were injected IP to reach either a Light (n=4; 25mg UR/100g rat mass, 3.5mg a‐CL/100g rat mass) or Deep (n=3; 40mg UR/100g rat mass, 4.0mg a‐CL/100g rat mass; IV top‐ups as needed) plane of anaesthesia, verified by the respective presence or absence of ear twitch, palpebral and pedal reflexes. Orthostatic stress was achieved with lower body negative pressure (LBNP), adapted for a rat model. Cardiac output (Q; transonic flow‐meter at descending aorta) and HR (ECG) were measured during graded bouts of LBNP between ‐1 and ‐10 mmHg, ordered randomly. At each anaesthetic depth LBNP was repeated with saline or hexamethonium (HEX; 25mg/kg IV) to block postganglionic sympathetic nerve activity. The reduction in Q during LBNP (main effect, P<0.05) was not affected by anaesthetic depth or HEX. HR increased with LBNP when suction exceeded ‐4 mmHg (main effect, P<0.05). Focusing on ‐10 mmHg, the HR increase was not different between Light (24±10 bpm) and Deep (24±7 bpm) planes, but was attenuated with HEX (4±1 and 5±5 bpm, P<0.001 vs. Light and Deep, respectively). These preliminary results suggest that the majority of the HR response to LBNP in rodents is mediated by postganglionic sympathetic outflow and is not affected by depth of anaesthesia.Support provided by CIHR and NSERC.
Age‐related alterations in the critical closing pressure of the cerebral circulation from rest to exercise in healthy humans
Authors: Ogoh Shigehiko , Fisher James P. , Young Colin N. , Fadel Paul J. 
Published: June 2021

We sought to examine the influence of age on exercise‐induced changes in cerebral vascular tone. The critical closing pressure (CCP), or pressure at which cerebral blood flow ceases, was estimated by linear extrapolation from arterial blood pressure (ABP) and middle cerebral artery blood velocity (MCAV) waveforms at rest and during moderate intensity steady‐state cycling at 50% heart rate reserve in 12 young (24±1 yr) and 12 older middle‐aged (57±2 yr) healthy subjects. No age‐group differences were observed in end‐tidal PCO2 at rest or during exercise (P=0.181). The increases in ABP during exercise were greater in older subjects (P<0.001), while changes in mean MCAV from rest were similar between groups (P=0.395). Importantly, the CCP was significantly elevated in both young (Δ +12.1 mmHg, P=0.005) and older (Δ +21.4 mmHg, P<0.001) subjects during exercise. Moreover, this change in CCP from rest was significantly greater in the older subjects (P=0.025). These data suggest that compared to younger subjects, older subject's exhibit larger exercise‐induced increases in cerebral vascular tone. We speculate that the greater increases in CCP may serve to protect the blood‐brain barrier from the higher blood pressure responses evoked by dynamic exercise in older subjects.Supported by R01‐HL093167.
Interrupting reperfusion suppresses the activation and expression of NADPH oxidase after global ischemia in mice
Authors: SHEN Jia , BAI Xiaoyin , ZHOU Jingyi , BRUCE Iain C , XIA Qiang 
Published: June 2021

OBJECTIVECerebral ischemia/reperfusion increases the activity and expression of NADPH oxidase which is a major enzymatic source of reactive oxygen species (ROS). Interrupting reperfusion therapy has been demonstrated to protect against global and focal cerebral ischemia injury. The purpose of this study was to determine whether the interrupting reperfusion therapy suppress the increasing activity and expression of NADPH oxidase induced by global ischemia/reperfusion.METHODSMale C57BL/6 mice (23‐28g) were randomly divided into a sham operated group, control (15 min global ischemia/reperfusion) group, interrupting reperfusion (15 min global ischemia, 3 circles of 15 sec reperfusion/15 sec occlusion before permanent reperfusion) group. Second and seventh day after reperfusion, NADPH oxidase activity, gp91phox expression, p47phox expression and transportation were measured.RESLUTSThe enzymatic activity of control group was sharply higher than that in PC group at day 2 and day 7 after reperfusion. The enzymatic activity in PC group increased at day 2 after reperfusion while decreased at day 7 after reperfusion. p47phox and gp91phox expression, p47phox transportation were significantly decreased in the PC group, and reduced to the pre‐ischemic level at the day 7 after reperfusion.CONCLUSIONInterrupting reperfusion suppresses NADPH oxidase activation and expression induced by global ischemia/reperfusion.
Blocking peripheral leukotrienes decreases plasma vasopressin concentration during the early phase of experimental sepsis
Authors: Rocha Maria Jose Alves , Martins Thalita Freitas , Coelho Camila Henriques , Oliveira‐Pelegrin Gabriela Ravanelli 
Published: June 2021

IntroductionEvidence suggests that leukotrienes and nitric oxide may have a role in vasopressin secretion that occurs during the early phase of sepsis. Moreover, leukotrienes are thought to affect nitric oxide production. Our objective was to analyze the effect of blocking leukotrienes on plasma nitric oxide and vasopressin levels. Materials and Methods: Male Wistar rats received i.p. injections of MK‐886 (1.0, 2.0 or 4.0 mg/kg) or vehicle (DMSO 5%) 1h before cecal ligation and puncture (CLP) or sham operation. In one group the survival rate was monitored for 3 days. In another group, the animals were decapitated at 0, 4, and 24h after CLP or sham operation, and blood was collected for hematocrit, sodium, vasopressin and nitrate measurement.ResultsWe observed an increase in NO production at 24 h and in hematocrit and vasopressin at 4h after CLP; serum sodium levels remained unchanged. The survival rate after 3 days was 20% in the CLP group. Pretreatment with any dose of MK‐886 did not diminish NO production or affect serum sodium levels, nor did it alter the survival rate. However, vasopressin secretion was affected in a dose‐dependent manner, while hematocrit decreased only with 1mg of the drug.ConclusionThe results suggest that peripheral leukotrienes affect the secretion of vasopressin in the early phase of sepsis and that this alteration seems to be independent of nitric oxide production.
Pulmonary Surfactant Protein D Inhibits Lipopolysaccharide (LPS)‐Induced Inflammatory Cell Responses by Altering LPS Binding to Its Receptors
Authors: Nishitani Chiaki , Yamazoe Masami , Takahashi Motoko , Katoh Tsuyoshi , Ariki Shigeru , Shimizu Takeyuki , Hiroaki Mitsuzawa , Sawada Kaku , Voelker Dennis R. , Takahashi Hiroki , Kuroki Yoshio 
Published: June 2021

Pulmonary sufactant protein D (SP‐D), member of the collectin family, plays an important role in regulating innate immunity of the lung. We examined the mechanisms by which SP‐D modulates lipopolysaccharide (LPS)‐elicited inflammatory cell responses. SP‐D bound to a complex of Toll‐like receptor 4 (TLR4) and MD‐2, and down‐regulated TNF‐α secretion and NF‐κB activation elicited by LPS, in alveolar macrophages and TLR4/MD‐2‐transfected HEK293 cells. Cell surface binding of LPS to TLR4/MD‐2‐expressing cells was attenuated by SP‐D. In addition, SP‐D significantly reduced MD‐2 binding to both serotypes of LPS. A chimera containing the amino‐terminal region and the collagenous domain of surfactant protein A, and the coiled‐coil neck and lectin domains of SP‐D, was a weak inhibitor of LPS‐induced cell responses and MD‐2 binding to LPS, compared to native SP‐D. The collagenase‐resistant fragment consisting of the neck plus the carbohydrate recognition domain of SP‐D also was a very weak inhibitor of LPS activation. This study demonstrates that SP‐D down‐regulates LPS‐elicited inflammatory responses by altering LPS binding to its receptors, and reveals the importance of the correct oligomeric structure of the protein in this process.This works was supported in part by a Grant‐in‐Aid for scientific research from the MEXT, Japan.
Effect of the thioredoxin system in IGF‐1‐mediated de‐remodeling of cardiac K+ channels; role of ASK1‐JNK signaling
Authors: Tang Kang , Zheng Ming‐Qi , Rozanski George J 
Published: June 2021

c‐Jun NH2‐terminal kinase (JNK) plays a major role in the response of cells to oxidative stress. We found that JNK was activated in rat heart with chronic myocardial infarction (MI) compared with controls, as assessed by Western blotting and JNK assay. In voltage‐clamp studies of post‐MI ventricular myocytes down‐regulation of transient outward K+ current (Ito) was reversed by the JNK inhibitor SP600125 or peptide inhibitor JNKI‐1. We also examined apoptosis signal‐regulating kinase (ASK1), which activates JNK and which is normally inhibited by reduced thioredoxin (Trx). Using a co‐immunoprecipitation assay we found that ASK1‐Trx binding was decreased post‐MI, which is consistent with activation of ASK1‐JNK signaling. To further probe the impact of the Trx system on ASK1‐JNK signaling we studied the effects of IGF‐1 which regulates anti‐apoptotic and cell survival pathways. In voltage‐clamp studies IGF‐1 increased Ito density in myocytes from MI hearts and this effect was blocked by the thioredoxin reductase (TrxR) inhibitor auranofin. In isolated MI hearts perfused with IGF‐1, JNK activity was decreased and auranofin blocked this effect. IGF‐1 also increased TrxR and K+ channel protein expression in MI hearts. Our data suggest that K+ channel expression is regulated by the Trx system whose loss of function post‐MI underlies Ito remodeling via activation of ASK1‐JNK signaling.Supported by NIH grant HL066446.