bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immune response mediated by NRLP3 expression in children infected with Respiratory Syncytial Virus
Authors: NETO ERASMO ASSUMPCAO , DE ANGELIS KATIA , DE PAULA VIEIRA RODOLFO , CONSOLIM‐COLOMBO FERNANDA MARCIANO 
Published: June 2021

OBJECTIVETo evaluate the expression of the NRLP3 gene present in the inflammatory pathway and its regulation against pediatric infection with Respiratory Syncytial Virus (RSV)METHODS: 31 patients younger than 2 years of age were divided into RSV (n = 11) and control (n = 20) groups. Five cc of venous blood was collected in EDTA tube. The tubes were centrifuged and, after separation of the blood constituents, the buff coat was added and RNA latter Total RNA was isolated. The amount and quality (280/260) of RNA were assessed by reading spectrophotometry at Nanodrop Total sample RNA was retranscribed and the cDNA/reaction was used for relative expression analysis of the NLRP3 inflammation gene by means of gene‐specific type‐specific fluorogenic probes and qPCR. The ExpressionSuite software in the Cloud Platform was used to obtain the raw data (Ct). The GAPDH gene was used as endogenous control for raw data normalization (Ct). The gene expression data were analyzed using the comparative method of CtRESULTSThe analysis of the data obtained in the qPCR technique for the expression of the NRLP3 gene was that in the patients infected with Respiratory Syncytial Virus it has a lower expression of it in relation to the control patients. Statistical analysis was performed using GraphPad Prism® software, using t test. presenting (P <0.05) between the groups compared.CONCLUSIONWith the present analysis of the studied study we can observe a lower expression of NRLP3 in pediatric patients infected with RSV in relation to the control patients without infection, within this result we can collaborate with the literature in the description of the behavior of the NRLP3 gene that is not yet well defined as in some articles demonstrate in the bronchial epithelial cells, that when the infection is expected an increase in the expression of the gene and consequently of its products the pro‐inflammatory cytokines and the caspases for induction to cell death. However in our study we have seen that the decrease in NRLP3 expression in bloodstream cells may demonstrate a mechanism of escape of the virus so that the cell does not produce pro‐inflammatory cytokines and caspases for induction of cell death so that it can maintain alive and replicating for longer.Support or Funding InformationFAPESP
Fold change of expression mRNAimageFold change of expression mRNAThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Temporal inhibition of ERK Activity by Optogenetic Control of MAPK Phosphatase 3
Authors: Sharum Savanna R. , Mondal Payel , Cho Kelly , Zhang Kai 
Published: June 2021

The functional outcome of the Ras/ERK pathway is encoded by both signal amplitude and temporal kinetics. While a suite of optogenetic strategies allow for precise activation of the Ras/ERK pathway, inhibition of this pathway remains challenging because most negative regulators do not function through subcellular protein translocation or dimerization, features often utilized in common optogenetic strategies. Here, we developed an optogenetic split protein system to accomplish reversible inhibition of ERK activity using the MAPK phosphatase 3 (opto‐sMKP3). Opto‐sMKP3 reversibly inhibits ERK activity under patterned blue light stimulation. Scanning of a 6‐hour pERK inhibition window revealed that equal reduction of PC12 cell differentiation occurs regardless of the placement of the window, indicating that persistent pERK activity is necessary for maximum PC12 cell differentiation. In combination with current optogenetic strategies, opto‐sMKP3 provides an emerging modality to achieve bi‐directional control of the Ras/ERK pathway and helps identify how signaling dynamics encodes functional outcome.Support or Funding InformationSRS thanks the support of the Westcott Bioscience Fellowship from the Department of Biochemistry at UIUC. KZ thanks the support from the School of Molecular and Cellular Biology at UIUC.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Bio‐risk assessment research on genetically engineered cyanobacteria for sustainable biofuels
Authors: Nguyen Thu , Barnes Cherrelle , Sherazi Sana , Agola Jason , Greene Lesley , Lee James W 
Published: June 2021

Genetically engineered (GE) cyanobacteria are an attractive photosynthetic platform for sustainable biofuels and bioproducts. A number of biofuels such as ethanol, isobutanol, and 1‐butanol have been experimentally produced using GE cyanobacteria. Even though this approach is promising, there are still questions regarding the biosafety of these GE organisms. What happens to the plasmids that are used for introducing transgenes into the cyanobacterial cells? Studies have shown that E. coli can transfer plasmids into cyanobacteria. We are interested in knowing if the reverse direction is possible? Furthermore, can the transgenes be horizontally transferred into other organisms after they are already integrated into the genomic DNA of the cyanobacteria? These questions need to be addressed before this approach can be commercialized. In order to answer these questions, we conducted an experiment by co‐incubating wild‐type E. coli DH5α with different sets of GE Thermosynechococcus elongatus BP1 carrying either plasmid transgenes or solely integrated transgenes. The transfer event was monitored using selection markers. Our results showed that the transgenes in the form of plasmids were transferred from these GE cyanobacteria into wild‐type E. coli DH5α even without the help of a nitrocellulose membrane while there was no detectable transfer event for the integrated transgenes observed so far. In addition, the frequency of the plasmid transfer event appeared to decrease gradually over time. These results suggested that even though GE cyanobacteria carrying integrated transgenes possess a more permanent change in the genomic DNA, the bio‐risk of these GE organisms in the context of gene sharing is less severe than plasmids‐carrying GE cyanobacteria.Support or Funding InformationThis work is supported by Biotechnology Risk Assessment Grant Program competitive grant award no. 2016‐33522‐25624 from the U.S. Department of Agriculture to JWL and LHG.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
EXPRESSION OF IRISIN AND ITS RELATION WITH ANTHROPOMETRIC AND BIOCHEMICAL PARAMETERS IN DIABETES MELLITUS TYPE II PATIENTS
Authors: Mendonça Maria Isabel Sacchi , Mathia Vanessa Lopes , Simões Diogo Pimenta , Perez Matheus Moreira , Bacci Marcelo Rodrigues , Murad Neif , Encinas Jessica Araújo , da Costa Aguiar Alves Beatriz , Fonseca Fernando Luiz Affonso , da Veiga Glaucia Luciano 
Published: June 2021

AimTo evaluate the gene expression of irisin in patients with type 2 diabetes mellitus (DM2) and its possible involvement in the metabolic changes and obesity in this pathophysiological situation.MethodsPatients anthropometric data were obtained, as well as samples of blood were collected in the clinic of specialties from Faculty of Medicine of ABC. A list of healthy individuals CT (n=14) and DM2 patients (n=16) diagnosed for less than 10 years was obtained. The criteria for the diagnosis of DM2 were the one used by the American Diabetes Association (ADA). Volunteers filled in terms of consent, and all of them were greater than or equal to 21 years old. After collection, it was evaluated complete hemogram and biochemical parameters: glucose and glycated hemoglobin (A1C). The expression of molecular biomarker irisin in peripheral blood leukocytes was performed by RT‐qPCR technique. Results were expressed as mean ± standard deviation (SD) and analyzed by the program GraphPad Prism® 6.0, using the Student's t‐test and Mann‐Whitney test. As for the analyzes of correlation, it was done the Spearman correlation test. The significance level was 5% (descriptive value *p<0.05).ResultsThe mean age of the patients studied was 51±15 years for the CT group (n=14) and 64±10 years for the DM2 (n=16). As for the biochemical parameters, the following results were obtained: glucose (CT 92±13, n=14 DM2 versus 143±40 mg/dL, n=16 *p<0.05); A1C (CT 5.6±0.5, n=14 DM2 versus 7.1±1.6%, n=16 *p<0.05); irisin gene expression in peripheral blood was obtained by the formula 2^‐ΔCT and values found in CT group were 8.506e‐006±1.412e‐005, n=6. The ones found in DM2 group were 0.02288± 0.08050 n=14, p=0.06. The correlation test between the expression of irisin versus Body Mass Index (BMI) in DM2 was r=0.5221, p=0.06. There was no correlation between the glucose levels and A1C with irisin expression.ConclusionDespite the preliminary findings, the data showed a tendency toward a positive correlation between the expression of irisin and BMI in diabetic patients. These data suggest that irisin is associated to possible changes in adiposity which happen in obesity associated to DM2.Support or Funding InformationFinancial Support: CAPES, CNPq.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Quantifying the Contribution of Cardiomyocyte Metabolic Dysfunction to the Heart Mechanical Function
Authors: Lopez Rachel , Gao Xin , Van den Bergh Françoise , Beard Daniel 
Published: June 2021

Hydrolysis of ATP provides the chemical free energy to drive the molecular processes underlying cardiac pumping. Under normal conditions the heart hydrolyzes and resynthesizes the entire ATP pool several times per minute. In the failing heart, cardiomyocyte metabolic dysfunction leads to a reduction in the chemical potential (free energy of ATP hydrolysis) at which ATP is synthesized and is made available to drive cellular processes. We hypothesize that this metabolic/energetic dysfunction causes contractile dysfunction of the myocardium in heart failure, contributing to the whole‐body phenotype (venous congestion, exercise intolerance) of heart failure in humans. To test this hypothesis, we used a rat transverse aortic constriction (TAC) model of cardiac decompensation/heart failure to measure the relationships between functional parameters (cardiac output, ejection fraction, etc.) and myocardial energetic state, determined based on measurements of myocardial metabolite pools and mitochondrial oxidative capacity. Cardiac function was measured by echocardiography and hearts were harvested for mitochondrial isolation and phosphate metabolite measurements at the end‐point, either 15 weeks post‐surgery, or 18 weeks post‐surgery. Cardiac phosphate metabolites levels were measured using NADH dependent enzymatic assays and mitochondrial oxidative capacity was measured using an Oroboros O2k Oxygraph. In both cohorts of rats, there was an overall reduction in fatty acid and carbohydrate oxidative capacity, with an increase in the ratio of maximal carbohydrate to fatty acid oxidative capacity in the 18‐week TAC rats compared to sham controls. In addition, we also observed differences in phosphate metabolite levels in both 15‐week TAC and 18‐week TAC rats compared to controls and correlations between metabolite mechanical functional changes. Furthermore, we used multi‐scale computational models of myocardial metabolism and metabolic state‐dependent contractile dynamics to quantify the contribution of reductions in oxidative capacity and metabolite pools levels to heart mechanical function. Our results suggest that there is a causal link between a reduction in free energy of ATP hydrolysis and kinetic impairment of the myosin ATPase cross‐bridge cycle in decompensated hypertrophy/heart failure.Support or Funding InformationFunded by NIH Grants 5T32GM008322‐28 and U01HL122199This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Control of Cardiac Mitochondrial Fuel Selection by Calcium
Authors: Jones Edith , Van den Bergh Françoise , Kandel Sunil M. , Dasika Santosh K. , Dash Ranjan K. , Beard Daniel A. 
Published: June 2021

Calcium ion concentration modulates the function of several mitochondrial enzymes. Specifically, the kinetic operations of the decarboxylating dehydrogenases pyruvate dehydrogenase, isocitrate dehydrogenase, alpha‐ketoglutarate dehydrogenase are all affected by [Ca2+]. Previous studies have shown that, despite its ability to affect the function of specific dehydrogenases, [Ca2+] does not substantially alter mitochondrial ATP synthesis in vitro or in vivo in the heart. We hypothesize that, rather than contributing to respiratory control, [Ca2+] plays a role in contributing to fuel selection. Specifically, cardiac mitochondria are able to use different primary carbon substrates (carbohydrates, fatty acids, and ketones) to synthesize ATP aerobically in the living cells. To determine if and how [Ca2+] affects the relative use of carbohydrates versus fatty acids in vitro we measured oxygen consumption and TCA cycle intermediate concentrations in suspensions of cardiac mitochondria with different combinations of pyruvate and palmitoyl‐L‐carnitine in the media at various [Ca2+] and ADP infusion rates. Stoichiometric analysis of the data reveals that when both fatty acid and carbohydrate substrates are available, fuel selection is sensitive to both the rate of ADP infusion and to the calcium concentration. With increasing both the rate of oxidative ATP synthesis and [Ca2+], the fuel utilization ratio shifts to increased fractional consumption of pyruvate. Thus, our results indicate that the effects of ATP synthesis rate and [Ca2+] are interdependent.Support or Funding InformationThis work supported by NIH grants HL122199 and T32GM008322This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Adaptive effects of prolonged mitochondrial‐targeted catalase on adipocyte differentiation
Authors: Yang Sophia , Esterly Harrison , Tavares Kendall , Christian Brooke 
Published: June 2021

One cause of obesity is an increase in the total number adipocytes by hyperplasia. To increase fat cell number, adipocyte precursors undergo differentiation into mature fat cells, a process which requires reactive oxygen species (ROS). ROS are generated in the mitochondria during oxidative phosphorylation, and previous studies have shown that short‐term treatment with mitochondria‐targeted antioxidants can reduce adipogenesis. This suggests that antioxidant therapy might be useful to treat obesity, although the efficacy of antioxidants for long‐term treatment has not been investigated. Mice that have catalase targeted to mitochondria (mCAT mice) have increased levels of the antioxidant enzyme throughout life. We tested whether mCAT mice would display reduced fat pad mass or body weight due to a reduction in mitochondrial hydrogen peroxide. At 12 weeks of age, mCAT mice showed no significant decrease in size or weight of subcutaneous fat depots compared to wild‐type mice, which suggests that mCAT pre‐adipocytes were able to bypass the requirement for ROS and differentiate normally. To test this, we isolated preadipocytes from subcutaneous fat pads of mCAT mice and compared their differentiation profiles to cells transiently transfected with a plasmid encoding mitochondrial catalase. As expected, short‐term antioxidant treatment resulted in little to no differentiation. Although preadipocytes from mCAT mice differentiated more slowly in culture, they were ultimately able to reach full differentiation. Gene expression profiles of regulatory proteins that function during differentiation in cells with short‐term antioxidant treatment were different than those with long‐term exposure. Current work involves understanding how these gene expression changes are directly affected by mitochondrial hydrogen peroxide.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
That's Swell! The Role of Aquaporin in an Inflammatory Response
Authors: Arnholt Mark , Betts Lilly , Hawkins Abigail , Herro Madeleine , Hoefs Alisha , Powers Farren , Sill Brooke , Munzenmaier Diane H 
Published: June 2021

Death due to lung inflammation has increased 31 percent over the last 35 years. A protein that influences this mortality rate is aquaporin‐4. This tetramer protein is a water channel that is water permeable. This integral protein, made up of six transmembrane helices and two pore helices, creates an hourglass shape. The structure of aquaporin is vital to its function due to pore helices preventing large molecules from passing through the membrane, only facilitating the movement of water molecules or small solutes. These two pore helices allow one molecule to pass at a time, making the net water movement facilitation easier. All types of aquaporins have NPA (asparagine‐proline‐alanine) motifs which are located in the central channel and are responsible for water permeation and intracellular processing. In aquaporin‐4, there are two NPA motifs at residues 97–99 and 213–215. Scientists discovered that aquaporin's response to bacterial stimuli can alter its pore size. Trauma, toxins or injury to tissue can cause a cell to become hypotonic. Aquaporin‐4 is specifically related to lung injury and inflammation because it is highly expressed in humans. The HUHS MAPS Team (Modeling A Protein Story) has designed a model of the wild form of AQP4 with 3D printing technology to investigate structure‐function relationships. The extensive research on aquaporins in relation to lung inflammation can contribute to the scientific and medical world and eventually target new pharmacological therapies.Support or Funding InformationThe MSOE Center for BioMolecular Modeling would like to acknowledge and thank the National Institutes of Health Clinical and Translational Science Award (NIH_CTSA UL1RR031973) and the Milwaukee School of Engineering for their support in funding the 2018_2019 SMART Team program.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Multifaceted Role of Lipid A 1‐phosphatase in Bacterial Envelope Biogenesis
Authors: Zhao Jinshi , An Jinsu , Hwang Dohyeon , Wu Qinglin , Wang Su , Gillespie Robert A , Yang Eun Gyeong , Chung Hak Suke , Zhou Pei 
Published: June 2021

Gram‐negative bacterial cell envelope consists of a phospholipid bilayer inner membrane, a peptidoglycan layer and an asymmetric bilayer outer membrane with lipopolysaccharide (LPS) covering the outer leaflet and phospholipid the inner leaflet. Here we report that the lipid A 1‐phosphatase (LpxE) functionally connects the biogenesis of multiple membrane components by utilizing a variety of lipid substrates. We found that the LpxE from Aquifex aeolicus (LpxEAA) is capable of dephosphorylating lipid A (the hydrophobic anchor of LPS), phosphatidyl glycerol phosphate (PGP, an intermediate in the phosphatidyl glycerol synthetic pathway), and undecaprenyl pyrophosphate (C55‐PP, an essential lipid carrier for syntheses of both peptidoglycan and O‐antigen of LPS). Overexpression of LpxEAA in E. coli complements lethal deletion strains deficient in PGP or C55‐PP synthesis. In Francisella novicida, an animal pathogen, deletion of LpxEFN leads to sensitivity to bacitracin, an antibiotic targeting C55‐PP phosphatase. In a F. novicida C55‐PP phosphatase deficient strain carrying a plasmid harboring LpxEFN, suppression of LpxE expression causes cell deformation, loss of O‐antigen and ultimately cell death. Intriguingly, LpxEAA is an efficient phosphatase to lipid A species without the 3‐Deoxy‐D‐manno‐oct‐2‐ulosonic acid (KDO) moiety. Such a unique property of LpxEAA has enabled us to engineer E. coli strains carrying an LpxEAA‐harboring plasmid to produce novel lipid A species as the major component of LPS, implicating its potential usage for biotechnology applications.Support or Funding InformationThis work was supported by the Intramural Research Program of KIST, by the Pioneer Research Center Program (2014M3C1A3054141) through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning, by the National Research Foundation of Korea (NRF) grant founded by the Korea government (MSIT) (2018R1A2B2008995) and National Institutes of Health (NIH) grants (GM51310 to C.R.H.R. and P.Z. and GM115355 to P.Z.).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Dietary Rice Bran Oil and γ‐Oryzanol Attenuates Toll Like Receptor‐mediated IκBα Phosphorylation, NF‐κB p65 Activation and Matrix Metallo Protease‐9 Expression in Peritoneal Macrophages from Rats Fed Partially Hydrogenated Vegetable Fat and thereby Exhibit Anti‐Inflammatory Activity
Authors: Yalagala Poorna C , Dhavamani Sugasini , Pandugala Pavan Kumar , Lokesh B.R. 
Published: June 2021

In spite of warning issued by regulatory agencies all over the world, South Asian countries are continuing to use Partially Hydrogenated Vegetable Fat (PHVF) in many food products. PHVF contains trans fatty acid known as elaidic acid which is pro‐inflammatory. NF‐κB p65 and Matrix Metallo Proteases‐9 (MMP‐9) play an important role in promoting inflammation. Dietary Rice bran oil (RBO) and γ‐ORY reduce the secretion of inflammatory mediators from macrophages as compared to those obtained from rats fed diet containing PHVF and thereby exhibit anti‐inflammatory activity. The present study was focused on specific role of RBO and γ‐ORY on the phosphorylation of IκBα, subsequent activation of NF‐κB p65 and secretion of Matrix Metallo Proteases (MMP‐9) a mechanism by which RBO and γ‐ORY may be exhibiting their anti‐inflammatory activity. Male wistar rats were fed AIN‐93 diet for 60 days. The diet was supplemented with one of the following fat/oil at 10wt%level: PHVF, RBO‐N (unfrationated oil), RBO‐MCR (Minor Constituents Removed oil), RBO‐MCR+Unsaponifiable Matter from Rice Bran Oil added back to RBO‐MCR (UM RBO‐MCR), RBO‐MCR+ γ‐ORY(700mg/kg diet), PHVF+RBO‐N (5.0+5.0wt%), PHVF+ γ‐ORY (700mg/kg diet). The macrophages from rats fed diet containing PHVF showed increased phosphorylation of IκB, translocation of NF‐κB p65, enhanced secretion of MMP‐9 indicating pro‐inflammatory nature of dietary PHVF. Diet containing RBO‐N, RBO‐MCR, UM RBO‐MCR and RBO‐MCR+ γ‐ORY significantly reduced phosphorylation of IκB, translocation of NF‐κB p65 and expression of MMP‐9 in macrophages all of which were enhanced when PHVF diets were fed to rats. Thus RBO and its components like γ‐ORY exhibit anti‐inflammatory activity by modulating expression of NF‐κB p65 which ultimately results in decreased secretion of pro‐inflammatory mediators by macrophages.Support or Funding InformationDepartment of Biotechnology, IndiaThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.