bluuebunny/crossref_metadata_2025_split huggingface dataset:
Do Body Shape/Proportions predict injury? Novel insights from a 3D body scan imaging.
Authors: Talty Kevin , Thomas Diana M. , Kuiper Patrick , Morse Steven , Bigelman Kevin , Heymsfield Steven , Scioletti Michael 
Published: June 2021

BackgroundPosture, obesity, and body shape are well‐established predictors of injury and athletic performance. However, due to the manual burden in collecting numerous anthropometric measures, to date, no large database and systematic data analysis determining body shape effects on performance and injury have gone beyond using standard measurements like BMI, waist circumference and hip circumference.ObjectiveTo use machine learning based Artificial Neural Network (ANN) and decision tree analysis on a large nationally representative database of automatically captured body anthropometrics to predict basic training‐related injury.MethodsOver N=20,896soldiers (28% female) recruited for US Army basic training at Fort Jackson, SC were scanned for uniform fitting using the Human Solutions Kinect based 3D imaging technology. Each subject image consisted of 161 body shape measurements. After removing subjects with missing measurements, the remaining subjects were split into injured (91 recruits) and non‐injured (13,296 recruits) groups. 75% of each group was placed into a training group and the other 25% into a testing group. An ANN and Decision Tree model evaluated using the area under the curve(AUC) was developed to predict severe physical injury occurrence during 10 weeks of US Army basic training. Body length measurement was compared against height to evaluate whether certain body proportions were more at risk for injury.ResultsThe AUC for the ANN was 0.79 and the AUC for the Decision Tree model was 0.70. It was determined that body proportions of shorter legs and longer torso more than doubled the risk of injury during US Army basic trainingConclusionsMachine learning models that leverage data sources like those from the newly emerging 3D body image scanners may be used to predict severe injury during vigorous physical activity. These results can be used to develop personalized prevention strategies reducing injury and retaining individuals within their activity protocols.Support or Funding InformationNoneThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Investigation of the Roles of Novel Endogenous Ligand of Aryl Hydrocarbon Receptor in Neural Development
Authors: Chuang Pei‐Yun , Chan Ya‐Yun , Wu Pei‐yi , Chen Pei‐Jen , Lee Hsinyu 
Published: June 2021

Activation of aryl hydrocarbon receptor (AHR) by xenobiotic toxic chemicals such as 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin regulates a variety of cellular processes including embryogenesis, tumorigenesis and inflammation. However, the identity of endogenous AHR ligands remains elusive. A potential AHR ligand, compound X, was identified from zebrafish embryos using previous developed cell free bioassay for dioxin‐like compounds. In this study, we aim to investigate the effect of compound X in AHR activation and further explore its physiological effects. Compound X induces AHR translocation into nucleus and upregulates downstream cytochrome P450 1A1 (CYP1A1) in vitro. It also promotes neuronal differentiation in neuroblastoma (NB) cells, which is consistent with our previous studies that overexpression of AHR leads to NB cells differentiation. Furthermore, compound X enhances zCyp1a, myelin‐associated myelin basic protein (zMbp) and SRY (sex determining region Y)‐box 10 (zSox10) expression and improves the mobility of zebrafish larvae via Ahr2 pathway. Therefore, our results suggest that compound X is an endogenous AHR ligand, and plays a critical role during neural differentiation.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Myosin Light Chain Kinase‐210 Induces ER‐PM Junctions and STIM1 Puncta Formation to Augment Store‐Operated Ca2+ Entry
Authors: Srivastava Nityanand , Mohammad Tauseef , Amin Ruhul , Joshi Jagdish Chandra , Klomp Jennifer , Li Wennan , Kini Vidisha , Knezevic Nebojsa , Obukhov Alexander G. , Karginov Andrei , Komarova Yulia , Mehta Dolly 
Published: June 2021

Myosin light chain kinase‐Long (MYLK‐L or MYLK‐210), a Ca2+‐calmodulin dependent kinase containing a unique 922‐amino acid N‐terminal domain is a predominant isoform of MYLK expressed in endothelial cells (ECs). N‐terminus of MYLK‐210 has been shown to contain several single nucleotide polymorphisms (SNPs) in an actin binding region which is associated with severity of acute lung injury (ALI). However, significance of SNPs in regulating MYLK‐210 function remains unclear. The classical function of MYLK‐210 is to catalyze the phosphorylation of myosin light chain to induce EC contraction, leading to inter‐endothelial gap formation and increase permeability, a hall mark of ALI. Intriguingly, we showed that MYLK‐210, through its actin‐binding motif, regulates store‐operated Ca2+ entry (SOCE) but not receptor‐operated Ca2+ entry (ROCE). We showed that MYLK‐210 null endothelial cells (ECs) or MYLK‐210 depleted ECs displayed diminished Ca2+ entry in response to SOCE‐activator thapsigargin and thrombin. We generated MYLK‐210 constructs lacking C‐terminus (N‐MYLK) or N‐terminus (C‐MYLK) to investigate the role of specific domains of MYLK‐210 in inducing SOCE activity. We found that N‐MYLK but not C‐MYLK rescued SOCE activity in MYLK‐210 null ECs, indicating thereby that MYLK regulates SOCE in a kinase independent manner. Additionally, SOCE activation failed to increase lung vascular hyper‐permeability in MYLK‐210 null mice. We identified unique actin binding motif, DVRGLL within N terminus of MYLK‐L which enables MYLK‐210 to induce SOCE. Stromal‐interaction molecule 1 (STIM1), upon sensing the depletion of (Ca2+) from the endoplasmic reticulum (ER) store, organizes as puncta which translocate to plasma membrane that trigger SOCE via plasmalemmal Ca2+selective channels such as transient receptor potential channel 1 (TRPC1) and Orai1. Thus, we addressed if MYLK‐L controlled STIM1 function by regulating puncta formation. We showed that STIM1 formed puncta in control ECs but these puncta were markedly reduced in MYLK depleted ECs. Formation of endoplasmic reticulum (ER)‐plasma membrane (PM) junction is required for STIM1 activation of SOCE. Using MAPPER (membrane‐attached peripheral ER) that selectively labels ER–PM junctions, we found that MYLK induced ER‐PM junction, but these junctions were markedly reduced in the density in MYLK‐knockdown cells. Our study thereby defines for the first time the clinical validity of SNPs within actin binding region of MYLK in inducing ALI through organizing ER‐PM junctions, STIM1 activity, SOCE and lung vascular hyperpermeability.Support or Funding InformationNational Institute of Health (NIH)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Oral L‐arginine treatment significantly reduces blood pressure without altering the renal T cell profile in the DOCA salt model of hypertension
Authors: Gillis Ellen E. , Crislip G. Ryan , Sullivan Jennifer C. 
Published: June 2021

The immune system plays a critical role in the development of hypertension. Our lab has previously reported that there is a sex difference in the renal T cell profile in DOCA salt hypertension, with males having more pro‐inflammatory Th17 cells, whereas females have more anti‐inflammatory regulatory T cells (Tregs). DOCA treated males also have a greater blood pressure (BP) response to DOCA than females, and we propose this is due to the relative abundance of Tregs in the female. We have also previously reported that an intact nitric oxide (NO) system is required for Treg maintenance in hypertension, and females have greater NO levels than males. In the current study, we hypothesized that treatment with L‐arginine, a substrate for NO production, would increase renal Tregs and attenuate the sex difference in hypertension in male and female DOCA treated rats. Briefly, male and female Sprague Dawley rats (n=4–6, 10 wks of age) were uni‐nephrectomized and subcutaneously implanted with a DOCA pellet (200 mg/rat, 60‐d time release) and given 0.9% NaCl to drink ad libitum. A subset of rats were treated with L‐arginine (350 mg/kg/d, via drinking water). BP was measured by tail cuff plethysmography at baseline and after 3 wks of DOCA treatment. After 3 wks of treatment, kidneys were processed for flow cytometric analysis of T cells (CD3+CD4+FOXp3+ Tregs, CD3+CD4+RORγ+ Th17 cells, and IL‐10+CD3+ T cells). BP was comparable between treatment groups within each sex at baseline, although males had a higher BP than females (Table, effect of sex, p<0.001, 2‐Way ANOVA). DOCA treatment increased BP in all groups compared to baseline values (Table, effect of DOCA, p=0.002). L‐arginine treatment attenuated DOCA‐induced increases in BP in both sexes, although this effect was greater in females (Table, effect of L‐arginine, p=0.02, interaction of sex and L‐arginine, p=0.03). Females had a more anti‐inflammatory renal T cell profile, with greater levels of Tregs and IL‐10+ cells, whereas males had more pro‐inflammatory Th17 cells (Table, effect of sex, p<0.05 for Tregs, Th17, and IL‐10). Interestingly, despite the significant BP effect observed, L‐arginine treatment did not impact the renal T cell profile in either sex (Table, effect of L‐arg, p>0.05 for Tregs, Th17, and IL‐10). Future studies will examine additional mechanisms by which L‐arginine supplementation lowers BP in both sexes. The DOCA salt model is characterized by high levels of oxidative stress, which is known to impair the NO‐NOS signaling pathway by decreasing the amount of L‐arginine available to produce NO via eNOS.Support or Funding InformationThis work was supported by NIH 5R01HL12709102This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Dietary Saturated and Unsaturated Fat and Fructose Induce Distinct Patterns of Hepatic Steatosis in Male Mice
Authors: Song Ming , Shi Hongxue , Jin Jian , Cave Matt , McClain Craig 
Published: June 2021

ObjectiveNonalcoholic fatty liver disease (NAFLD) is a major cause of liver disease, with a global prevalence of 25.24%. The etiology of NAFLD is complex, and dietary nutrients and their interactions play a critical role. The aim of this study was to determine the effect of different types of dietary fat‐fructose interactions on the pathogenesis of NAFLD and to explore the potential underlying mechanism(s).MethodsMale adult C57BL/6J mice were assigned to six groups and fed with diets (AIN‐93G based) enriched with different types of fat (with or without fructose added in the water), such as saturated fat (SF‐‐beef tallow), n−6 polyunsaturated fat (n6USF‐‐corn oil), or n−3 polyunsaturated fat (n3USF‐‐menhaden fish oil), respectively, for 20 weeks. 42% of calories was derived from the fat. Tap water or tap water containing 10% fructose (w/v) was given ad lib during the entire experiment. Body weight and energy efficiency ratio were monitored. Liver histology, fat accumulation, and liver enzymes, as well as glucose tolerance test were evaluated.ResultsBoth SF and n6USF fed mice developed obesity and hepatic steatosis, but with distinct phenotypes. n3USF fed mice with or without fructose exhibited a lean shape with normal liver histology and liver enzymes. There was no difference between SF and n6USF fed mice in terms of body weight (BW). Mice fed with SF displayed more severe hepatic steatosis and liver injury as well as hepatic fibrosis compared to n6USF fed mice. Fructose feeding led to significantly increased liver weight and liver weight:body weight ratio in SF fed mice, but not in the n6USF or n3USF fed mice. While the energy efficiency ratio was the highest in n6USF fed mice, the hepatic triglyceride content in n6USF fed mice was significantly lower than that of SF fed mice. Interestingly, n6USF fed mice displayed marked glucose intolerance which was worsened by fructose feeding, and this effect was not obvious in SF fed mice.ConclusionOur data demonstrated that dietary SF‐fructose and n6USF‐fructose interactions differentially contribute to the development of obesity and hepatic steatosis. n3USF plays a beneficial role in the prevention of obesity and fatty liver, even with the consumption of excess fructose. The underlying mechanism(s) are currently under investigation.Support or Funding InformationSupported by grants from NIH and Veterans AdministrationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
ROLE OF ESTRADIOL RECEPTOR BETA (ERβ) ON BRAIN MITOCHONDRIAL FUNCTIONS AND CARDIO‐RESPIRATORY CONTROL IN AGED FEMALE MICE
Authors: LAOUAFA Sofien , ROUSSEL Damien , MARCOUILLER François , SOLIZ Jorge , BAIRAM Aida , JOSEPH Vincent 
Published: June 2021

We tested the hypothesis that ERβ is involved in brain mitochondrial function and cardio‐respiratory control in aged female mice. We used aged (17–18 months‐old) ERβKO and wild‐type controls (WT) female mice to assess arterial blood pressure (via a tail‐cuff sensor) and indices of respiratory pattern (sighs and apneas – recorded by whole body plethysmography at rest). We also measured respiratory parameters at rest and in response to brief (<10 minutes) exposure to hypoxia (12% O2) or hypercapnia (5% CO2). Because ERβ is localized in mitochondria, and because estradiol and ERβ agonist increase mitochondrial O2 consumption, we used fresh brain cortex tissue (~2 mg) permeabilized with saponin to assess mitochondrial respiration with high‐resolution respirometry (O2k‐ Oroboros) and in‐vitro activity of the complex I of the electron transport chain. In ERβKO female mice, mean arterial blood pressure was lower than in old WT mice (88±4 vs 110±3 mmHg, P<0.05), the frequency of sighs was similar in ERβKO than in WT micez (26±3 vs 19±2 sighs/h P=ns) and the frequency of apneas much lower (4±2 vs 26±9 apnea/h, P=0.01). In ERβKO mice, minute ventilation is reduced in response to hypoxia (−50%, P<0.01) and hypercapnia (−39%, P<0.01) compared to WT mice. Concerning mitochondrial function, with substrates of complex I (Pyruvate/Glutamate/Malate) and in presence of ADP, ERβKO mice have a reduced O2 consumption compared to WT mice (60±7 vs 98±4 pmol O2/s/mg tissue, p<0.05). With the substrate of complex II (succinate) and ADP, there was no difference between ERβKO and WT mice. In vitro activity of complex I is 70% lower in ERβKO mice compared to WT (P<0.01). We conclude that the deletion of ERβ reduces chemoreflex functions and reduces mitochondrial function in the central nervous system. This role ERβ may be relevant in pathological or physiological conditions in which O2 homeostasis is compromised (sleep apnea, altitude, lung diseases).Support or Funding InformationCIHR, Région Rhône Alpes and consulat de France in QuébecThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Sirt3 Restores Lipid Homeostasis in Bovine Hepatocytes Exposed to NEFA
Authors: Liu Lei , Xing Dongmei , Su Jianming , Peng Tao , Wang Jianguo , Wen Lixin , Cheng Tianyin 
Published: June 2021

IntroductionSirt3, a major deacetylase in mitochondria, plays a pivotal role in the regulation of lipid metabolism in mice and humans. Dynamic changes of Sirt3 expression are observed in ruminants during the transition period, a time when fat mobilization initiates and non‐esterified fatty acids (NEFA) sore in plasma, and also a time when most of lipid metabolism disorders in ruminants take place, like fatty liver and ketosis etc. However, the rationale between Sirt3 and fat metabolism disturbance in dairy cows has not been characterized yet. The current study aims to investigate interrelations of Sirt3 and NEFA on expressions of key factors involved in fat metabolism in bovine hepatocytes.MethodsHepatocytes from a calf were isolated, and primarily cultured by a modified 2 steps of collagenase perfusion method. NEFA ranging from 0 mM to 1.2 mM were added, and their effects on the expression of Sirt3 was studied. Sirt3 overexpression was induced by adenovirus (AdMAX system), and expressions of key fat metabolism factors, namely acetyl‐CoA carboxylase‐1 (ACC‐1), fatty acid synthase (FAS), carnitine palmitoyltransterase‐1 (CPT‐1), CPT‐2, acyl‐CoA oxidase (ACO), apolipoprotein B (ApoB) and ApoE were investigated. The level of supernatant very low‐density lipoprotein (VLDL) content and cellular triacylglycerol (TG) contents were also measured. Then 1.2 mM NEFA and Sirt3 overexpression vectors were co‐incubated with hepatocytes. All above mentioned parameters were also tested.ResultsThe mRNA level of Sirt3 was significantly up‐regulated by 0.3 mM NEFA, but was significantly down‐regulated by 1.2 mM NEFA (p<0.01). Sirt3 overexpression significantly induced expressions of ACC‐1, CPT‐1, CPT‐2, ACO, ApoB and ApoE (p<0.01), and elevated cellular TG contents (p<0.01). However, Ad‐Sirt3 treatment did not change mRNA level of FAS and supernatant VLDL level compared with controls. Ad‐Sirt3 + 1.2 mM NEFA treatment increased the mRNA level of Sirt3 by 4‐fold compared to Ad‐GFP controls (p<0.01), and regained expressions of CPT‐1, CPT‐2 and ACO previous inhibited by 1.2 mM NEFA. Moreover, cellular TG contents were lowered in Ad‐Sirt3 + 1.2 mM NEFA group compared 1.2 mM NEFA treatments (p<0.01).ConclusionThose data indicated that Sirt3 was involved in the regulation of lipid metabolism in bovine hepatocytes exposed to high level NEFA by restoring lipid homeostasis. Further investigations are needed to explore the potential role of Sirt3 as a therapeutic target for maintenance of perinatal health in dairy cows.Support or Funding InformationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Mapping Hair Cortisol Concentrations Across Body Sites to Study Health Disparities
Authors: Marquez Hilda F. , Samayoa Cathy , Marquez‐Magaña Leticia 
Published: June 2021

Perceived discrimination, poverty, and environmental stress stimulates the release of cortisol, the primary stress hormone, through the hypothalamic–pituitary–adrenal (HPA) axis. Chronic stress, a long‐term form of stress, increases the risk of various diseases, including; diabetes, hypertension, and inflammatory and autoimmune disorders among all populations. Unfortunately, ethnic minorities experience higher levels of chronic stress, and bear the burden of health disparities. Hair cortisol is a retrospective biological marker for cortisol exposure and can be used as an integrated measure of long‐term HPA activity and chronic stress. However, studies that use hair from the scalp may face collection challenges due to the symbolic and spiritual meaning that is carried by locks of hair among populations particularly affected by health disparities. Therefore, identifying alternatives for the measurement of chronic cortisol exposure would enable inclusion of diverse population in health disparities research. The purpose of this study is to determine if hair across body sites can be used for cortisol analysis to investigate chronic stress among populations affected by health disparities. I hypothesized that hair from arms, legs, and pelvic area will be correlated to scalp hair cortisol levels, and could be used to assess chronic cortisol levels. In this study, participants were asked to provide hair samples from the following four regions of the body; the scalp, arms, legs, and pelvic region. Hair samples were processed, and cortisol was extracted using the established methanol method. Cortisol was quantified using an Enzyme‐Linked Immunosorbent Assay. A total of eight participants were recruited, five females and three males. Participants represented 4 different ethnic groups and were of recruited from a University. 25% of participants provided samples from all four hair sites, while 62.5% provided all but pubic hair. Average cortisol levels ranged from 236 pg/ml in the scalp to 1020 pg/ml in the legs. Linear correlation analysis was conducted to determine the relationship between hair cortisol concentration (HCC) from the scalp and other areas of the body. Our preliminary analysis shows trends suggesting that arm and leg hair may be culturally appropriate samples for hair cortisol analysis. In conclusion, this study revealed cortisol levels across body hair sites, and highlights the need to incorporate culturally acceptable biomarkers to address and eliminate health disparities.Support or Funding InformationCCSF/SMCCD/SFSU BRIDGES TO THE BACCALAUREATE PROGRAM: R25 GM050078SFSU SF BUILD: ENABLING STUDENTS TO REPRESENT IN SCIENCE‐ TL4 GM118986This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Inflammatory Reflex Controls Inflammation in Response to Viral Challenges
Authors: Martelli Davide , Farmer David G. S. , Komegae Evilin N. , McKinley Michael Joseph , McAllen Robin Michael 
Published: June 2021

The nervous and immune systems talk to and influence each other. In particular, the nervous system helps maintain inflammation within appropriate limits. It is known that a neural reflex, termed the inflammatory reflex, is engaged and inhibits inflammation in response to lipopolysaccharide, a component of the wall of gram negative bacteria. This reflex has its efferent motor arm in the splanchnic nerves. Viral infections are different from bacterial infections and the innate immune system detects and responds differently to them.The aim of this study was to test the hypothesis that the inflammatory reflex is involved in the control of inflammation triggered by viruses as well as bacteria.For this purpose, we investigated whether the injection of polyinosinic:polycytidylic acid (Poly I:C; 1mg/kg i.v.), which mimics viral challenge, is able to activate splanchnic sympathetic nerve activity (SSNA) in urethane anesthetized rats. We also studied the effect of bilateral section of the greater splanchnic nerves on the systemic inflammatory response 90 minutes after the injection of the same dose of Poly I:C.Our results showed that poly I:C induces an activation of the SSNA that lasted for at least 7 hours. Furthermore, splanchnic nerve section resulted respectively in 3‐fold higher and 4‐fold lower levels of the pro‐inflammatory cytokine plasma tumor necrosis factor α (TNF) and the anti‐inflammatory cytokine interleukin 10.These results show that a viral challenge activates the inflammatory reflex in the same way as a bacterial challenge. Viral infections can lead to secondary bacterial infections. Because viral stimulation of the inflammatory reflex would suppress innate immune function, this may be why the host's ability to fight off a secondary attack by bacteria is compromised.Support or Funding InformationThis work was supported by project grant number 1098887 from the National Health and Medical Research Council (NHMRC) of Australia and from the Victorian Government Operational Infrastructure Support Program. E. N. Komegae was the recipient of a postdoctoral fellowship from Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP 2016/1555‐6).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.