Academic literature on the topic 'Egr [Early growth response]'
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Journal articles on the topic "Egr [Early growth response]"
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Harada, Hiroaki, Vibha N. Lama, Linda N. Badri, Takashi Ohtsuka, Danica Petrovic-Djergovic, Hui Liao, Yasushi Yoshikawa, Koichiro Iwanaga, Chris L. Lau, and David J. Pinsky. "Early growth response gene-1 promotes airway allograft rejection." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 1 (July 2007): L124—L130. http://dx.doi.org/10.1152/ajplung.00285.2006.
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Chronic airway rejection, characterized by lymphocytic bronchitis, epithelial cell damage, and obliterative bronchiolitis (OB), limits long-term survival after lung transplantation. The transcription factor early growth response gene-1 (Egr-1) induces diverse inflammatory mediators, some involved in OB pathogenesis. An orthotopic mouse tracheal transplant model was used to determine whether Egr-1 promotes development of airway allograft rejection. Significantly higher Egr-1 mRNA levels were seen in allografts (3.2-fold increase vs. isografts, P = 0.012). Allografts revealed thickening of epithelial and subepithelial airway layers (51 ± 4% luminal encroachment for allografts vs. 20 ± 3% for isografts, P < 0.0001) marked by significant lymphocytic infiltration. Absence of the Egr-1 gene in donor (but not recipient) tissue resulted in significant reduction in luminal narrowing (34 ± 4%, P = 0.0001) with corresponding diminution of T cell infiltration. Egr-1 null allografts exhibited a striking reduction in inducible nitric oxide synthase (iNOS) expression. Effector cytokines previously implicated in OB pathogenesis with known Egr-1 promoter motifs (IL-1β and JE/monocyte chemoattractant protein-1) were reduced in Egr-1 null allografts. These data suggest a paradigm wherein local induction of Egr-1 in tracheal allografts drives expression of inflammatory mediators responsible for lymphocyte recruitment and tissue destruction characteristic of airway rejection.
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Suehiro, Jun-ichi, Takao Hamakubo, Tatsuhiko Kodama, William C. Aird, and Takashi Minami. "Vascular endothelial growth factor activation of endothelial cells is mediated by early growth response-3." Blood 115, no. 12 (March 25, 2010): 2520–32. http://dx.doi.org/10.1182/blood-2009-07-233478.
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Endothelial cell activation and dysfunction underlie many vascular disorders, including atherosclerosis, tumor growth, and sepsis. Endothelial cell activation, in turn, is mediated primarily at the level of gene transcription. Here, we show that in response to several activation agonists, including vascular endothelial growth factor (VEGF), tumor necrosis factor-α, and thrombin, endothelial cells demonstrate rapid and profound induction of the early growth response (Egr) genes egr-1 and egr-3. In VEGF-treated endothelial cells, induction of Egr-3 was far greater and more prolonged compared with Egr-1. VEGF-mediated stimulation of Egr-3 involved the inducible binding of NFATc, serum response factor, and CREB to their respective consensus motifs in the upstream promoter region of Egr-3. Knockdown of Egr-3 markedly impaired VEGF-mediated proliferation, migration, and tube formation of endothelial cells and blocked VEGF-induced monocyte adhesion. Egr-3 knockdown abrogated VEGF-mediated vascular outgrowth from ex vivo aortic rings and attenuated Matrigel plug vascularization and melanoma tumor growth in vivo. Together, these findings suggest that Egr-3 is a critical determinant of VEGF signaling in activated endothelial cells. Thus, Egr-3 represents a potential therapeutic target in VEGF-mediated vasculopathic diseases.
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Tsai, Jo C., Lixin Liu, Jie Zhang, Katherine C. Spokes, James N. Topper, and William C. Aird. "Epidermal growth factor induces Egr-1 promoter activity in hepatocytes in vitro and in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 5 (November 1, 2001): G1271—G1278. http://dx.doi.org/10.1152/ajpgi.2001.281.5.g1271.
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Early growth response-1 (Egr-1) is a transcription factor that couples short-term changes in the extracellular milieu to long-term changes in gene expression. Under in vitro conditions, the Egr-1 gene has been shown to respond to many extracellular signals. In most cases, these findings have not been extended to the in vivo setting. The goal of the present study was to explore the role of epidermal growth factor (EGF) in mediating Egr-1 expression in hepatocytes under both in vitro and in vivo conditions. In HepG2 cells, Egr-1 protein and mRNA were upregulated in the presence of EGF. In stable transfections of HepG2 cells, a 1,200-bp Egr-1 promoter contained information for EGF response via a protein kinase C-independent, mitogen-activated protein kinase-dependent signaling pathway. A promoter region containing the two most proximal serum response elements was sufficient to transduce the EGF signal. In transgenic mice that carry the Egr-1 promoter coupled to the LacZ reporter gene, systemic delivery of EGF by intraperitoneal injection resulted in an induction of the endogenous Egr-1 gene and the Egr-1- lacZ transgene in hepatocytes. Together, these results suggest that the 1,200-bp promoter contains information for EGF response in hepatocytes both in vitro and in intact animals.
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Tsai, Jo C., Lixin Liu, Jiazhen Guan, and William C. Aird. "The Egr-1 gene is induced by epidermal growth factor in ECV304 cells and primary endothelial cells." American Journal of Physiology-Cell Physiology 279, no. 5 (November 1, 2000): C1414—C1424. http://dx.doi.org/10.1152/ajpcell.2000.279.5.c1414.
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The early growth response (Egr)-1 transcription factor serves to couple changes in the extracellular environment to alterations in gene expression. An understanding of the mechanisms that underlie Egr-1 gene regulation should provide important insights into how environmental signals are transduced by endothelial cells. The aim of the present study was to determine whether epidermal growth factor (EGF) induces Egr-1 expression in endothelial cells. In ECV304 cells, Egr-1 mRNA and protein levels were increased in response to EGF. In stable transfection assays, the 1,200-bp promoter of the mouse Egr-1 gene contained information for EGF response via a protein kinase C-independent, mitogen-activated protein kinase-dependent pathway. The endogenous Egr-1 gene was similarly responsive to EGF in primary human umbilical vein endothelial cells, human coronary artery endothelial cells, and rat fat pad endothelial cells, but not in bovine aortic endothelial cells, calf pulmonary artery endothelial cells, or PY-4-1 endothelial cells. Together, these results suggest that the Egr-1 gene is responsive to EGF in a subset of endothelial cells.
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Bedadala, Gautam, Feng Chen, Robert Figliozzi, Matthew Balish, and Victor Hsia. "Construction and Characterization of Recombinant HSV-1 Expressing Early Growth Response-1." ISRN Virology 2014 (February 12, 2014): 1–7. http://dx.doi.org/10.1155/2014/629641.
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Early Growth response-1 (Egr-1) is a transcription factor that possesses a variety of biological functions. It has been shown to regulate HSV-1 gene expression and replication in different cellular environments through the recruitment of distinct cofactor complexes. Previous studies demonstrated that Egr-1 can be induced by HSV-1 infection in corneal cells but the level was lower compared to other cell types. The primary goal of this report is to generate a recombinant HSV-1 constitutively expressing Egr-1 and to investigate the regulation of viral replication in different cell types or in animals with Egr-1 overexpression. The approach utilized was to introduce Egr-1 into the BAC system containing complete HSV-1 (F) genome. To assist in the insertion of Egr-1, a gene cassette was constructed that contains the Egr-1 gene flanked by loxP sites. In this clone Egr-1 is expressed under control of CMV immediate-early promoter followed by another gene cassette expressing the enhanced green fluorescent protein (EGFP) under the control of the elongation factor 1α (EF-1 α) promoter. The constructed recombinant viruses were completed containing the Egr-1 gene within the viral genome and the expression was characterized by qRT-PCR and Western blot analyses. Our results showed that Egr-1 transcript and protein can be generated and accumulated upon infection of recombinant virus in Vero and rabbit corneal cells SIRC. This unique virus therefore is useful for studying the effects of Egr-1 during HSV-1 replication and gene regulation in epithelial cells and neurons.
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Abdel-Latif, M. M. M., H. J. Windle, K. A. Fitzgerald, Y. S. Ang, D. Ní Eidhin, M. Li-Weber, K. Sabra, and D. Kelleher. "Helicobacter pylori Activates the Early Growth Response 1 Protein in Gastric Epithelial Cells." Infection and Immunity 72, no. 6 (June 2004): 3549–60. http://dx.doi.org/10.1128/iai.72.6.3549-3560.2004.
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ABSTRACT The early growth response 1 (Egr-1) transcription factor is rapidly induced by various stimuli and is implicated in the regulation of cell growth, differentiation, and gene expression. The aim of this study was to examine the effect of Helicobacter pylori on the expression of Egr-1 and Egr-1-regulated genes in gastric epithelial AGS cells. Egr-1 expression was assayed by immunoblotting and electrophoretic mobility shift assays using H. pylori-stimulated AGS cells. Transient transfection experiments with promoter-reporter constructs of CD44, ICAM-1, and CD95L were used for expression studies. H. pylori induced the expression of Egr-1 in gastric epithelial cell lines in a dose-dependent manner, with the rapid kinetics that are typical of this class of transcription factors. Immunohistochemical studies of biopsies revealed that Egr-1 expression is more abundant in H. pylori-positive patients than in uninfected individuals. Reporter-promoter transfection studies indicated that Egr-1 binding is required for the H. pylori-induced transcriptional promoter activity of the CD44, ICAM-1, and CD95L (APO-1/Fas) constructs. The blocking of egr-1 with an antisense sequence prevented H. pylori-induced Egr-1 and CD44 protein expression. The MEK1/2 signaling cascade participates in H. pylori-mediated Egr-1 expression, but the p38 pathway does not. The data indicate that H. pylori induces Egr-1 expression in AGS cells in vitro and that the Egr-1 protein is readily detectable in biopsies from H. pylori-positive subjects. These observations suggest that H. pylori-associated Egr-1 expression may play a role, in part, in H. pylori-induced pathology.
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Eto, Kazuhiro, Varinderpal Kaur, and Melissa K. Thomas. "Regulation of Insulin Gene Transcription by the Immediate-Early Growth Response Gene Egr-1." Endocrinology 147, no. 6 (June 1, 2006): 2923–35. http://dx.doi.org/10.1210/en.2005-1336.
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Abstract Changes in extracellular glucose levels regulate the expression of the immediate-early response gene and zinc finger transcription factor early growth response-1 (Egr-1) in insulin-producing pancreatic β-cells, but key target genes of Egr-1 in the endocrine pancreas have not been identified. We found that overexpression of Egr-1 in clonal (INS-1) β-cells increased transcriptional activation of the rat insulin I promoter. In contrast, reductions in Egr-1 expression levels or function with the introduction of either small interfering RNA targeted to Egr-1 (siEgr-1) or a dominant-negative form of Egr-1 decreased insulin promoter activation, and siEgr-1 suppressed insulin gene expression. Egr-1 did not directly interact with insulin promoter sequences, and mutagenesis of a potential G box recognition sequence for Egr-1 did not impair the Egr-1 responsiveness of the insulin promoter, suggesting that regulation of insulin gene expression by Egr-1 is probably mediated through additional transcription factors. Overexpression of Egr-1 increased, and reduction of Egr-1 expression decreased, transcriptional activation of the glucose-responsive FarFlat minienhancer within the rat insulin I promoter despite the absence of demonstrable Egr-1-binding activity to FarFlat sequences. Notably, augmenting Egr-1 expression levels in insulin-producing cells increased the mRNA and protein expression levels of pancreas duodenum homeobox-1 (PDX-1), a major transcriptional regulator of glucose-responsive activation of the insulin gene. Increasing Egr-1 expression levels enhanced PDX-1 binding to insulin promoter sequences, whereas mutagenesis of PDX-1-binding sites reduced the capacity of Egr-1 to activate the insulin promoter. We propose that changes in Egr-1 expression levels in response to extracellular signals, including glucose, can regulate PDX-1 expression and insulin production in pancreatic β-cells.
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Yan, Shi-Fang, Jiesheng Lu, Linna Xu, Yu Shan Zou, Joern Tongers, Walter Kisiel, Nigel Mackman, David J. Pinsky, and David M. Stern. "Pulmonary expression of early growth response-1: biphasic time course and effect of oxygen concentration." Journal of Applied Physiology 88, no. 6 (June 1, 2000): 2303–9. http://dx.doi.org/10.1152/jappl.2000.88.6.2303.
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Hypoxia induces complex adaptive responses. In this report, induction of early growth response-1 (Egr-1) transcripts in lungs of mice subjected to hypoxia is shown to be dose and time dependent. Within 30 min of hypoxia, Egr-1 transcripts were ∼20-fold elevated in 6% oxygen, ∼5.2-fold increased by 10% oxygen, and returned to the normoxic baseline by 12% oxygen. Time course studies up to 48 h showed a biphasic profile with an initial steep rise in Egr-1 transcripts after 0.5 h of hypoxia and a second elevation beginning after 20–24 h. Hypoxic induction of Egr-1 was paralleled by enhanced expression of the downstream target gene tissue factor. Egr-1 and tissue factor antigen were visualized in bronchial and vascular smooth muscle and in alveolar macrophages. Egr-1 has the capacity to modulate expression of genes involved in the remodeling of the extracellular matrix and properties of smooth muscle, thus possibly contributing to the pulmonary response to chronic hypoxia.
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Hjoberg, Josephine, Louis Le, Amy Imrich, Venkat Subramaniam, Sheeba I. Mathew, Joseph Vallone, Kathleen J. Haley, Francis H. Y. Green, Stephanie A. Shore, and Eric S. Silverman. "Induction of early growth-response factor 1 by platelet-derived growth factor in human airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 4 (April 2004): L817—L825. http://dx.doi.org/10.1152/ajplung.00190.2003.
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Platelet-derived growth factors (PDGF) may contribute to the activation and growth of smooth muscle that is characteristic of airway remodeling in asthmatic patients. Early growth response 1 (EGR-1) is a transcription factor that is induced in several cell types by PDGF and may mediate some of the effects of PDGF. We show that human airway smooth muscle cells in cell culture express EGR-1 ∼1 h after addition of PDGF. Analysis of the EGR-1 promoter indicates that a serum response element located between 663 and 654 bp 5′ to the ATG start site is essential for this induction. Serum response factor, E26 transcription factor-like protein 1, and serum protein 1 bind to this region. PDGF causes phosphorylation of ERK1/2 and is temporally associated with E26 transcription factor-like protein 1 phosphorylation. Finally, the specific ERK1/2 inhibitor U-0126 abolishes PDGF-induced expression of EGR-1 in these cells. On the basis of these data, we speculated that EGR-1 would be increased in airway smooth muscle of asthmatic patients compared with nonasthmatic controls. Using immunohistochemistry, we found that EGR-1 protein was expressed in airway smooth muscle cells and epithelial cells of asthmatic patients and nonasthmatic controls; however, there was no significant difference in the intensity of staining between groups. EGR-1 was similarly expressed in the lungs of mice with and without ovalbumin-induced airway inflammation; however, there was no difference between groups by immunohistochemistry and quantitative PCR. Although EGR-1 is induced by PDGF in human airway smooth muscle cells in cell culture, the role of EGR-1 in airway remodeling and asthma remains to be established.
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Chang, Yao, Heng-Huan Lee, Yu-Te Chen, Jean Lu, Shih-Yi Wu, Chaio-Wei Chen, Kenzo Takada, and Ching-Hwa Tsai. "Induction of the Early Growth Response 1 Gene by Epstein-Barr Virus Lytic Transactivator Zta." Journal of Virology 80, no. 15 (August 1, 2006): 7748–55. http://dx.doi.org/10.1128/jvi.02608-05.
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ABSTRACT Early growth response 1 (Egr-1) is a cellular transcription factor involved in diverse biologic functions. Egr-1 has been associated with Epstein-Barr virus (EBV) infection, but it is still unknown whether any EBV protein regulates Egr-1 expression. In this study, we first showed that EBV reactivation is involved in upregulation of Egr-1 and that Egr-1 can be induced by Zta, an EBV lytic transactivator. Zta not only binds to the Egr-1 promoter but also activates the ERK signaling pathway to trigger binding of Elk-1 to the Egr-1 promoter. In addition, knockdown of Egr-1 significantly reduces the spontaneous expression of Zta and Rta in EBV-infected 293 cells, suggesting that a positive-feedback network involving Egr-1 is required for EBV reactivation. This study also implies that Zta has the potential to affect expression of certain genes through Egr-1.
Dissertations / Theses on the topic "Egr [Early growth response]"
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Omodho, Becky. "Early growth response gene (Egr) 2 and 3 control inflammatory responses of tolerant T cells." Thesis, Brunel University, 2016. http://bura.brunel.ac.uk/handle/2438/13516.
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This study investigated the role of tolerance induction in an inflammatory setting in regard to the early growth response genes Egr2 and Egr3. T cells robustly respond to pathogenic antigens during infection, but are tolerant to stimulation by self-antigens. The intrinsic mechanisms for self-tolerance in the periphery are still not clear. Egr2 and 3 are induced in tolerant T cells in response to antigen stimulation by NFAT-medicated tolerant signalling; however, their function in tolerant T cells is still unknown. The study demonstrated that Egr2 and 3, induced in tolerant T cells, are not directly involved in defective proliferation and IL-2 production, the hallmarks of T cell tolerance. However, they are essential for preventing inflammatory response of tolerant T cells. In the absence of Egr2 and 3, tolerant T cells show impaired proliferation and production of IL-2, but produce high levels of IFN-γ, a key inflammatory cytokine. This phenotype resembles CD4 T cells from autoimmune diseases such as lupus which show poor proliferative response, but hyper-inflammation. Our study demonstrated, for the first time, a distinctive mechanism to control inflammation from proliferative tolerance regulated by Egr2 and 3, which may be an important mechanism for the control of autoimmune diseases.
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Kasneci, Amanda. "Early growth factor response 1 (Egr-1) negatively regulates expression of calsequestrin (CSQ) on cardiomyocytes in vitro." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112521.
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Heart failure represents an important cause of death in Western Countries. The pathophysiology of heart failure is mainly associated with abnormalities in intracellular calcium control. We previously showed that Egr-1 negatively regulates expression of sodium-calcium exchanger (NCX) in vivo and in vitro. Here we tested the hypothesis that Egr-1 regulates expression of calcium storage proteins in the sarco-endoplasmic reticulum (SER), calsequestrin (CSQ) and/or ER, calreticulin (CRT) directly or indirectly via Egr-1:NFAT (nuclear factor of activated T-cells) formation. Secondarily, we hypothesized that this will reduce calcium mobilization. We found that undifferentiated 1293F cells, overexpressing Egr-1, have reduced CSQ compared to control H9c2 cells. We demonstrated that Egr-1 negatively regulates CSQ but not CRT expression. The Egr-1 mediated decrease in CSQ is linked to decreased calcium availability. Repression is by a novel NAB-independent (NGFI-A binding protein) activity localized to a.a. region 1-307. We conclude that Egr-1-mediated reductions in calcium storage protein expression alter calcium availability for cardiac contraction/relaxation.
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Symonds, Alistair. "The zinc finger transcription factor Early Growth Response 2 (Egr-2) is an intrinsic regulator of T cell tolerance and homeostasis." Thesis, Queen Mary, University of London, 2009. http://qmro.qmul.ac.uk/xmlui/handle/123456789/409.
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Tolerance of T cells to self-antigen is crucial to prevent the development of autoimmune disease. How self-tolerance is controlled at the transcriptional level is, however, unknown. We discovered that the transcription factor Early Growth Response 2 (Egr-2) was expressed by tolerant T cells, and by CD4+CD44high T cells in the absence of overt antigen stimulation, in vivo. To investigate the roles of Egr-2 in T cells, we generated CD2 cell specific Egr-2 deficient (Egr-2 cKO) mice. The proliferation of Egr-2 cKO CD44high T cells in vivo was markedly increased leading to progressive accumulation as the mice aged. By 15 months of age CD4+CD44high cells constituted the predominant T cell population in the peripheral lymphoid organs of Egr-2 cKO mice and expressed high levels of the activation markers CD25 and CD69. In addition to this lymphoproliferative disorder, 15 month old Egr-2 cKO mice showed signs of lupus-like autoimmune disease. This autoimmune syndrome was characterised by glomerulonephritis and proteinuria, infiltration of T cells into internal organs and, crucially, auto-antibodies directed against nuclear components; the hallmark of lupus. We observed decreased expression of the cyclin-dependent kinase inhibitor p21cip1 in Egr-2 cKO CD4+CD44high T cells while TCR stimulation induced IFN-γ, and, in particular, IL-17A and IL-17F expression was markedly increased. Consistent with these findings, we observed increased numbers of IFN-γ and IL-17 producing CD4+ T cells in Egr-2 cKO mice. The numbers of IFN-γ and IL-17 producing CD4+ T cells further increased as the mice aged in parallel with the gradual development of symptoms of lupus-like disease. These results demonstrate that Egr-2 is an intrinsic regulator of both T cell homeostasis and T cell tolerance.
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Pagel, Judith-Irina Carola. "Functional characterization of the transcription factor early growth response 1 (Egr1) in arteriogenesis." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-178078.
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The number of patients suffering from obstructive arterial disease is still increasing. Stimulation of a patient’s collateralization (arteriogenesis), though an auspicious therapeutic approach, is still not part of current therapy regimes. Further studies on the molecular level are needed to understand the genetic regulation in this process. The transcription factor early growth response 1 (Egr1) was shown to partic-ipate in leukocyte recruitment and cell proliferation in vitro. This work contributes to the acquisition of new insights into its mode of action in vivo.
Using a model of peripheral arteriogenesis, Egr1 was found significantly upregulated in growing col-laterals of wild-type mice (WT), both on mRNA (2.24fold) and protein level (2.3fold). Egr1 stained positive in EC and vSMCs of collaterals as well as in nerves. In LDI measurements conducted over the period of 21 days evidenced a delayed perfusion recovery after femoral artery ligation in Egr1-/- mice compared to WT mice (day7: 0.46±0.05 in Egr1-/- vs. WT (0.73±0.04), day 14: 0.65±0.02 in Egr1-/- vs. 0.88±0.04 in WT and day 21: 0.79 ±0.03 in Egr1-/- vs. 0.96±0.02 in WT). Under baseline conditions, Egr1-/- showed increased levels of monocytes (521.89±52.9 cells/µl vs. 326.56±21.6 cells/µl in WT) and granulocytes (811.79±79.96 cells/µl vs. WT 559.88±34.57 cells/µl) in the circulation but reduced levels in adductor muscles (18.14±2.73 cells/µl vs. 51.22±4.38 cells/µl in WT) as evidenced by FACS analyses. After femoral artery ligation, more macrophages were detected in the perivascular space of collateral arteries in Egr1-/- (8.10±0.99 per vessel) vs. WT (6.12±0.45 per vessel) mice. The mRNA of leukocyte recruitment mediators monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1) and urokinase plasminogen activator (uPA) were found upregulated in both groups. Whereas other Egr family members (Egr2-4) did not show an upregulation in WT collateral arteries, they were found significantly upregulated in Egr1-/- mice suggesting a mechanism of counter-balancing Egr1 deficiency. A closer look at cell cycle regulators revealed that cyclin E and cdc20 were found upregulated in WT as well as in Egr1-/- mice. However, cyclin D1 was hardly detectable under Egr1 deficiency conferring Egr1 an unique role for cyclin D1 transcription. vSMC phenotype switch is a critical step towards vSMC proliferation and therefore arteriogenesis. In this context, the downregu-lation of alpha smooth muscle actin (αSM-actin) and of the transcriptional repressor, splicing factor-1 (SF-1) has been shown to be critical in vitro. During arteriogenesis, SF-1 has been found downregulat-ed in collaterals of WT mice but was 1.64fold upregulated in Egr1-/-. Similar was true for αSM-actin. Whereas in WT mice αSM-actin is downregulated at 12h after ligation Egr1 deficient mice evidenced an upregulation of αSM-actin. The strong upregulation of the nonselective proliferation marker ki67 in WT mice was not detectable under Egr1 deficiency evidencing furthermore a delay in vascular cell proliferation. Conclusion: Compensation for deficiency of Egr1 function in leukocyte recruitment can be mediated by other transcription factors; however, Egr1 is indispensable for effective vascular cell cycle progression and phenotype switch in arteriogenesis.
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Mohamad, Trefa Salih. "EARLY GROWTH RESPONSE 1 (EGR1) AS A TUMOR SUPPRESSOR AND APOPTOSIS INDUCER IN RHABDOMYOSARCOMA." OpenSIUC, 2017. https://opensiuc.lib.siu.edu/dissertations/1375.
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EGR1, one of the immediate-early response genes, plays an important role as a mediator for transmitting extracellular stimuli. EGR1 is down regulated in many cancers. Many studies show that it functions as a tumor suppressor gene in a variety of cancers. EGR1 also acts as an oncogene in number of cancers. We found that in rhabdomyosarcoma (RMS), which is a muscle derived pediatric cancer, EGR1 was expressed in both RMS subtypes, embryonal and alveolar, but with a much higher expression profile in embryonal RMS. This suggests different mechanisms of down regulation of EGR1 in these two subtypes. Molecular and cellular approaches were used to characterize the functional role of EGR1 in RMS. We found that over expression of EGR1 in alveolar RMS significantly decreased cell proliferation, mobility, and anchorage-independent growth. We showed that exogenous EGR1 up regulated the cell cycle regulator, p21, which is normally repressed in RMS. EGR1 also promoted differentiation in RMS cells by up regulating several genes involved in muscle differentiation including myosin heavy chain (MyHC), MyoD and myogenin. We found that EGR1 interacts with the oncogene TBX2 in RMS cells and that TBX2 inhibits EGR1 function. To understand how TBX2 inhibits EGR1, we depleted TBX2 in RMS and we found an up regulation of the EGR1 targeted tumor suppressor gene, PTEN, and the cysteine protease inhibitor gene, CST6. Also, we performed luciferase assays and found that TBX2 decreased the expression of luciferase constructs fused with the PTEN promoter when TBX2 was co-transfected with EGR1. Our novel findings on the EGR1 function in RMS highlights the significant role of EGR1 in muscle development and tumor growth. Significantly, our work also suggests the EGR1 could promote tumor regression in RMS through inducing programmed cell death, or apoptosis. We found that EGR1 induced apoptosis through triggering the intrinsic apoptosis pathway and activating caspase cascades involving caspase 3 and caspase 9, which are essential mitochondrial apoptotic factors. Also, we observed the activation of two pro-apoptotic factors, BAX and dephosphorylated BAD, which are both located upstream of the caspase cascades in the intrinsic pathway. Also, we found in our study that EGR1 is repressed by the catalytic subunit of PRC2 complex, EZH2, which mediates gene silencing through methylation of lysine 27 on histone 3 (H3K27me3). EGR1 also sensitized RMS cells to chemotherapeutic agents, which could be a future direction for improved therapeutic targeting. Therefore, this work provides a novel and powerful molecular therapeutic target for RMS cancer.
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Young, Ada. "IL-1β Amplification of Nitric Oxide Production and Its Inhibitory Effects on Glucose Induced Early Growth Response-1 Expression in INS-1 Cells." Digital Commons @ East Tennessee State University, 2012. https://dc.etsu.edu/etd/1463.
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The pathophysiology of cytokines released by infiltrating white blood cells upon pancreatic beta cells is not fully understood. Early growth response gene-1 (Egr-1) expression is specifically and transiently up regulated in pancreatic beta cells in response to glucose. We hypothesized that interleukin-1 beta (IL-1▀) induction of nitric oxide alters glucose induced Egr-1 transcription levels. Egr-1 levels were assessed via western blot, nitric oxide was measured with a Griess Reagent kit and insulin levels via ELISA. Glucose induced both insulin and Egr-1 production in INS-1 cells. IL-1▀ dose dependently increased nitric oxide production over time and significantly attenuated glucose induced Egr-1 expression. Sodium nitroprusside dose dependently reduced glucose induced Egr-1 production. The data suggest a strong relationship between IL-1▀ induced nitric oxide production and the reduction of glucose stimulated Egr-1 production. The pathways altered by this cytokine could provide a better understanding of the pathophysiology leading to pancreatic beta cell death.
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Murray, Alexander James. "The Interaction of Early Growth Response Gene 1 and Myocyte Enhancer Factor 2C in the Murine Brain Cortex." Thesis, Virginia Tech, 2021. http://hdl.handle.net/10919/105007.
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Early growth response gene – 1 (Egr1) encodes a protein widely present in mammalian body, such as connective tissue, cardiac tissue, the liver, and the brain. As a transcription factor (TF), it is involved in processes that take place in the endocrine, digestive, immune, musculo-skeletal and central nervous systems, for instance, B cell maturation upon B cell receptor activation, tendon repair upon mechano-stimulation, and long-term spatial memory formation. In mammalian brains, EGR1 controls the responses to environmental stimuli such as chronic stress and physical contact. It also participates in processes such as long-term memory consolidation and synapse re-structuring. It plays a role in enacting responses and qualities of gene transcription cascades upon neuronal stimulation. Inside the epigenetic realm, EGR1 recruits Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) to remove DNA methylation at target loci. Due to its critical functions during brain development and upon neuronal activation, mis-regulation of EGR1 is associated with neuropsychological disorders such as post-traumatic stress disorder (PTSD) and schizophrenia (SCZ) in humans. In this study, we performed bioinformatics analysis with brain methylomes and predicted EGR1 may interact with myocyte enhancer factor 2C (MEF2C), which is known to be involved in many similar processes as EGR1, such as synapse architecture, cell migration, and learning and memory. EGR1 and MEF2C ChIP-seq data derived from mouse frontal cortex suggest these two proteins may regulate a common set of downstream genes. To begin, co-immunoprecipitation experiments were performed with HEK293T cells co-transfected with EGR1-FLAG and MEF2C-HA tagged constructs, allowing for specific interaction identification without endogenous protein expression interference. Furthermore, co-immunoprecipitation experiments performed with brain tissues additionally indicated the two proteins interact with each other endogenously. Altogether, this study provides protein-protein interaction evidence for EGR1 and MEF2C in cultured HEK293 cells and in the cortices of adult male mice. This information provides a foundation for future examinations of how these two TFs interact to initiate cascading events following neuronal stimulation.Master of Science
Early growth response gene – 1 (EGR1) encodes a protein that can be found in animals such as fruit flies, mice, rats, and humans. In mammals, it is widely expressed in the cardiovascular, endocrine, digestive, immune, musculo-skeletal and central nervous systems (CNS). Within the CNS, EGR1 is known as an essential transcription factor involved in brain development. More specifically, EGR1 plays a role in how the early brain develops in response to environmental stimuli, formation of synapse architecture and certain types of memories. Many gene networks involved in growth and development rely on EGR1 to regulate functions such as synapse reformation after exposure to the environment. EGR1 is known to have numerous partners with whom it interacts to execute its functions. It is also involved in epigenetic regulation, which is a process by which genes are silenced or activated without changing DNA sequences in the genome. EGR1 may directly interact with TET1 to demethylate EGR1 target sites in the genome, and to increase gene transcription. In memory development, EGR1 plays a key role ensuring short-term auditory fear memory can be converted to long-term memory, and also ensures long-term spatial memory. In this study, our computational analyses suggest that EGR1 may interact with MEF2C. This work provides evidence of a protein-protein interaction of EGR1 and MEF2C in cultured cells and in the brain cortical areas of mice. Such an interaction may explain why these two genes regulate overlapped biological processes within the brain and sheds lights on how cascading events are initiated following neuronal stimulation.
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Lejard, Véronique. "Etude de la régulation transcriptionnelle du collagène de type I dans les fibroblastes tendineux." Paris 6, 2007. http://www.theses.fr/2007PA066465.
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L’expression du gène codant pour la chaîne1 du collagène I (Col1a1) dans les tendons nécessite la coopération des éléments cis-activateurs TSE1, TSE2 et d’éléments localisés entre – 1537 et – 220 pb du promoteur proximal de Col1a1. Mon travail de thèse avait pour but d’identifier les facteurs de transcription qui, en se liant à ces séquences, activent le promoteur de Col1a1 dans les tendons. J’ai montré (1) que scleraxis (SCX), dont l’expression est spécifique des tendons, active le promoteur de Col1a1 en se liant à TSE2 sous forme d��hétérodimère SCX/E47 ; (2) que des facteurs de transcription NFATc sont exprimés dans les fibroblastes tendineux, peuvent se lier à TSE1 et augmenter l’expression de Col1a1 ; et (3) que la protéine Egr2 active le promoteur de Col1a1 probablement en se liant à un élément localisé entre – 1537 et – 220 pb. L’ensemble de ces résultats suggère que l’expression du gène Col1a1 dans les fibroblastes tendineux nécessite la coopération de SCX et de NFATc avec Egr2.
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Billah, MD Muntasir. "Cardioprotective effect of remote ischaemic preconditioning and the role of Early growth response-1 as a master switch regulator." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18248.
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Once the blood supply is restored after heart attack by opening up the coronary artery, the heart is insulted by ischemia-reperfusion (I/R) injury. Direct ischaemic preconditioning has the ability to protect the heart against this injury for a brief period of time. Direct ischaemic preconditioning involves cycles of non-lethal occlusion of the coronary artery and releasing. Preconditioning other organs remote to the heart such as the limbs can protect the heart from I/R injury. This new therapeutic technique, known as remote ischaemic preconditioning (RIPC) is non-invasive and easy to apply compared to direct ischaemic preconditioning. However, we still do not know the mechanism through which RIPC protects the heart. This thesis explores the underlying mechanism of RIPC-induced cardioprotection from myocardial I/R injury, in experimental in vitro and in vivo models. Both intrinsic and extrinsic pathways of apoptosis contribute to cell death during heart attack. This thesis explores the relative contribution of the apoptotic pathways in I/R injury. Moreover, autophagy is associated with myocardial I/R injury sparing effect of direct ischaemic preconditioning and postconditioning. It is hypothesized that autophagy plays a key role in RIPC-mediated cardioprotection and autophagy stimulation provides therapeutic benefit. There is evidence that preconditioning can decrease the level of early growth response-1 (Egr-1), a master regulator highly expressed in heart tissue followed by heart attack. Once Egr-1 is highly expressed, a number of downstream inflammatory signalling molecules get expressed, which are well known to cause myocardial damage. It is shown that Egr-1 downregulation in the hind limb prior RIPC abolishes RIPC-induced cardioprotection. In addition, it augmented certain a number of process that are attenuated by RIPC including apoptosis, cytokine expression. This work identifies a key role for Egr-1 in the signalling mechanism of RIPC through its regulation of a number of crucial downstream genes and cardioprotective pathways. In addition, it identifies IL-6 as a potential mediator of RIPC to mitigate myocardial I/R injury.
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Pfaffenseller, Bianca, Flavio Kapczinski, Amelia L. Gallitano, and Fábio Klamt. "EGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder." FRONTIERS MEDIA SA, 2018. http://hdl.handle.net/10150/627052.
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Bipolar disorder (BD) is a severe psychiatric illness with a consistent genetic influence, involving complex interactions between numerous genes and environmental factors. Immediate early genes (IEGs) are activated in the brain in response to environmental stimuli, such as stress. The potential to translate environmental stimuli into long-term changes in brain has led to increased interest in a potential role for these genes influencing risk for psychiatric disorders. Our recent finding using network-based approach has shown that the regulatory unit of early growth response gene 3 (EGR3) of IEGs family was robustly repressed in postmortem prefrontal cortex of BD patients. As a central transcription factor, EGR3 regulates an array of target genes that mediate critical neurobiological processes such as synaptic plasticity, memory and cognition. Considering that EGR3 expression is induced by brain-derived neurotrophic factor (BDNF) that has been consistently related to BD pathophysiology, we suggest a link between BDNF and EGR3 and their potential role in BD. A growing body of data from our group and others has shown that peripheral BDNF levels are reduced during mood episodes and also with illness progression. In this same vein, BDNF has been proposed as an important growth factor in the impaired cellular resilience related to BD. Taken together with the fact that EGR3 regulates the expression of the neurotrophin receptor p75NTR and may also indirectly induce BDNF expression, here we propose a feed-forward gene regulatory network involving EGR3 and BDNF and its potential role in BD.
Books on the topic "Egr [Early growth response]"
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Capo-Arteaga, Miguel A. Early survival and growth response of five species of Pinus to plant competition and aspect in southwest Oregon and northeast Mexico. 1987.
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Sytsma, David S. Richard Baxter and the Mechanical Philosophers. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780190274870.001.0001.
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Richard Baxter, one of the most famous Puritans of the seventeenth century, is generally known as a writer of practical and devotional literature. But he also excelled in knowledge of medieval and early modern scholastic theology, and was conversant with a wide variety of seventeenth-century philosophies. Baxter was among the early English polemicists to write against the mechanical philosophy of René Descartes and Pierre Gassendi in the years immediately following the establishment of the Royal Society. At the same time, he was friends with Robert Boyle and Matthew Hale, corresponded with Joseph Glanvill, and engaged in philosophical controversy with Henry More. This book is a chronological and thematic account of Baxter’s relation to the people and concepts involved in the rise of mechanical philosophy in late seventeenth-century England. Drawing on largely unexamined works, including Baxter’s Methodus theologiae christianae (1681) and manuscript treatises and correspondence, this book discusses Baxter’s response to mechanical philosophers on the nature of substance, laws of motion, the soul, and ethics. Analysis of these topics is framed by a consideration of the growth of Christian Epicureanism in England, Baxter’s overall approach to reason and philosophy, and his attempt to understand creation as an analogical reflection of God’s power, wisdom, and goodness, understood as vestigia Trinitatis. Baxter’s views on reason, analogical knowledge of God, and vestigia Trinitatis draw on medieval precedents and directly inform a largely hostile, though partially accommodating, response to mechanical philosophy.
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Duman, Ronald S. Neurotrophic Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.
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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.
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Horne, Gerald. Back to Africa. University of Illinois Press, 2018. http://dx.doi.org/10.5406/illinois/9780252041198.003.0007.
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This chapter looks at the Associated Negro Press (ANP) and its competitor, the Negro Newspaper Publishers Association (NNPA), in the early postwar era. In any case, in the early postwar era, both the ANP and the NNPA had competitors beyond the mainstream, among them the United Negro Press in Durham, North Carolina, and 13 others of the same caliber. Thus, by 1960, the NNPA agency was defunct. The ANP, on the other hand, had about 80 subscribers in the 1920s and 112 by 1945, then 60 by 1955 but 101 by 1964. This latter soaring was misleading in that it represented growth in Africa that was soon to be challenged by indigenous and mainstream competitors. In response, the ANP sought to centralize, requesting that certain sources forward information solely to their Chicago office, rather than affiliates. Nevertheless, it was evident that opportunities for ANP expansion were delimited: hence Claude Barnett's tendency to look abroad increasingly for investments.
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Gorsky, Martin. The Political Economy of Health Care in the Nineteenth and Twentieth Centuries. Edited by Mark Jackson. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780199546497.013.0024.
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The main aim of this article is to account for the coming of health systems within welfare states and to examine how these systems respond to demographic, financial, and technological changes in the contemporary period. The question of why the state entered this arena in the recent past is therefore of over-arching importance, and this article summarizes common theoretical approaches advanced to explain this process. It outlines the nineteenth-century foundations of social insurance and public provision of medical facilities on which state engagement was built. It traces the growth and development of health systems in the case-study countries, dividing events into three broad periods: the early twentieth century, in which they were largely put in place; the post-war ‘golden-age’ of the welfare state; and attempts since the 1970s to reform health systems in response to burgeoning costs and ideological critique. The conclusion reflects on how the different models adopted have impacted on population health.
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Pluckhahn, Thomas J., and Victor D. Thompson. New Histories of Village Life at Crystal River. University Press of Florida, 2018. http://dx.doi.org/10.5744/florida/9781683400356.001.0001.
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The tension between competition and cooperation has emerged as a major topic of concern in the understanding of human societies. The dynamic is epitomized by societies undergoing the transition to larger and more permanent villages, referred to as “early village” societies. This study describes archaeological research directed toward the understanding of early village formation at the Crystal River and Roberts Island sites in west-central Florida. Crystal River has long recognized as one of the preeminent sites of the Woodland period (ca. 1000 B.C. to A.D. 1000) in the American Southeast; Roberts Island has remained comparatively little known. New field investigations, combined with the reanalysis of previous work at the site, permit a fine-grained understanding of the growth and dissolution of early villages at the sites. The understandings that are gained from this case study can be contextualized to contemporaneous societies of the Gulf Coast, and to early village societies elsewhere in the world. The lessons that early villages contribute regarding cooperation and competition, in turn, contribute to contemporary debates regarding: first, individual versus collective action responsible for social welfare; and, second, the human role in and response to environmental change.
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Yamamoto, Koji. Taming Capitalism before its Triumph. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198739173.001.0001.
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This study revisits England’s culture of economic improvement between 1640 and 1720, a crucial period of its transformation into a global power backed by strong domestic industries. It is often suggested that England in this period grew confident of its prospect for unlimited growth. Merchants, inventors, and others proposed achieving profit and abundance. Such promises were then, as now, prone to perversion, however. The distinguishing feature of this study is to draw on the early modern concept of ‘projecting’ to explore the darker sides of England’s obsession with improvement. Thriving literary culture under the early Stuart kings gave rise to a predominantly negative public understanding of entrepreneurs or ‘projectors’ as people pursuing the Crown’s and their own profits at the public’s expense. The book examines how this emerging public distrust came to shape the nature of embryonic capitalism in the subseqeuent decades. By criticizing greedy projectors, the incipient public sphere helped reorient the practices of entrepreneurs and statesmen away from the most damaging of rent-seeking behaviours. Far from being a recent response to mainstream capitalism, ideas about publicly beneficial businesses have long shaped the pursuit of wealth, power, and profit. The book unravels this rich history of broken promises of public service and the ensuing public suspicion as early modern actors experienced it to throw fresh light on the emergence of consumer society and the financial revolution towards the end of the seventeenth century.
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Bergès, Sandrine, ed. Sophie de Grouchy's Letters on Sympathy. Translated by Eric Schliesser. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190637088.001.0001.
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Sophie de Grouchy (1764–1822), published her Lettres sur la Sympathie in 1798, together with her translation of Adam Smith’s The Theory of Moral Sentiments. This short text is presented as her critical commentary on Smith, but also offers original analyses of the relationship of emotional and moral development to economic, institutional, and political reform. Like Smith, Grouchy believes that sympathy is fundamental to social well-being. She improves on his theory by offering an account of its origin; and she argues it is the result of early relationships of dependence. The political conclusions Grouchy draws from her analysis are in tune with her republican views: social equality can only be the result of recognizing that we depend on each other. Deepening Smith’s position, Grouchy argues that inequality hinders the growth of sympathy and renders fruitful cooperation between the different strata of society unlikely or impossible. This new translation of the text is presented with an introduction divided into three chapters. Chapter 1 covers Sophie de Grouchy’s life, times, and sources. Chapter 2 discusses Grouchy’s work, with a special emphasis on the relationship of the Letters to Smith’s The Theory of Moral Sentiments, which the Letters were a response to, as well as a discussion of other writings by Grouchy. Chapter 3 touches on three main philosophical themes present in the Letters: political philosophy, with an emphasis on the republican aspect of Grouchy’s thought; her legal philosophy and political economy; and her aesthetics.
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Nehring, Daniel, Gerardo Gómez Michel, and Magdalena López, eds. A Post-Neoliberal Era in Latin America? Policy Press, 2019. http://dx.doi.org/10.1332/policypress/9781529200997.001.0001.
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In the mid-1970s, Latin America entered a period of profound social and economic crisis, marked by the rise of brutal military dictatorships across much of the region and the near-collapse of some of Latin America’s largest economies, in Mexico and Brazil. In response to this crisis, governments across the region adopted neoliberal structural adjustment programmes from the 1980s onwards, under the auspices of international organisations, such as the International Monetary Fund and the World Bank. These reforms typically entailed sweeping cuts to public health and welfare programmes, the privatisation of large parts of the public infrastructure, the redistribution of wealth to economic elites, and a notable growth in poverty. As a result, these structural adjustment programmes faced growing resistance from the early 1990s onwards. Social and political movements, such as the Zapatistas in Mexico, formulated powerful challenges to neoliberal orthodoxy, while the election to government of left-wing populist leaders such as Hugo Chávez (1998), Evo Morales (2005) or Rafael Correa (2006) opened the door to experiments with a range of anti-neoliberal political programmes. The failures of these programmes and ongoing conflicts between neoliberal and anti-neoliberal elites and social movements have by the mid-2010s resulted in growing social instability. This book examines cultural responses to this instability. It looks at a wide range of cultural forms, such as literature, underground cinema, street fairs and self-help books to explore how Latin Americans construct subjectivities, build communities and make meaning in their everyday lives in during a profound crisis of the social. In this context, the book emphasises the role which neoliberal and anti-neoliberal narratives of self and social relationships may come to play in popular culture and everyday lived experience in Latin America today.
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Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.
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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
Book chapters on the topic "Egr [Early growth response]"
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Pfaffenseller, Bianca, Bianca Wollenhaupt-Aguiar, and Fábio Klamt. "Early Growth Response 3 (EGR3)." In Encyclopedia of Signaling Molecules, 1477–84. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101638.
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Pfaffenseller, Bianca, Bianca Wollenhaupt-Aguiar, and Fábio Klamt. "Early Growth Response 3 (EGR3)." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101638-1.
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Vashist, Yogesh Kumar, L. Müller, J. Meyer, J. Göttsche, C. Wilms, D. C. Broering, and X. Rogiers. "Expression von Heat-Shock-Protein 70 (HSP70), Heat-Shock-Cognate 70 (HSC70), BCL-2 und Early-Growth-Response 1(Egr-1) im Pfortaderastligaturmodell der Ratte." In Chirurgisches Forum 2002, 247–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56158-0_64.
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KormuŤak, A., and B. Vooková. "Early growth characteristics of some Abies hybrids." In Genetic Response of Forest Systems to Changing Environmental Conditions, 331–38. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9839-2_27.
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Lemos, Daniela, Ana Cristina Braga, and Rosete Nogueira. "Nonlinear Regression on Growth Curves for Placental Parameters in R." In Communications in Computer and Information Science, 575–90. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-53025-8_39.
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AbstractGrowth charts play a crucial role in the evaluation and surveillance of paediatric populations, serving as indispensable tools for paediatricians and public health researchers. The development of these growth charts for fetal parameters has been extensively used in recent decades. However, investigation of placental parameters and their relationship with obstetric outcome has been relatively neglected, resulting in a significant gap in understanding their biological significance. This study presents an alternative approach for constructing reference growth curves specific to the placental parameter, Diameter 2. Our methodology uses the generalized additive models for location, scale, and shape (GAMLSS), offering distinct advantages over traditional quantile regression methods. One of the key advantages of GAMLSS is its flexibility to accommodate any statistical distribution, allowing for the modelling of various parameters that characterize the distribution of the response variable. Through the application of our proposed methodology, we demonstrated that by using P-splines as a smoothing function and Box-Cox t (BCT) as a distribution, we can achieve a representative growth curve for the Diameter 2 of the placenta throughout gestational age (GA). The resulting models demonstrated high representativeness, with $$R^2$$ R 2 values of 0.7608 and 0.7673 and AIC scores of 7953 and 7946 for the best two models, respectively. Moreover, our approach has the ultimate goal to facilitate early diagnosis of fetal complications, thereby providing valuable assistance to healthcare professionals.
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Stanley, E. Richard, Yee-Guide Yeung, Karen L. Berg, and Fiona J. Pixley. "Studies of the very Early Responses of a Receptor Tyrosine Kinase to Growth Factor Binding and their Application to the Purification and Identification of Proteins that are Tyrosine Phosphorylated in the Growth Factor Response." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 45–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_4.
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Ulrich, Magda M. W. "Fetal Wound Healing." In Textbook on Scar Management, 3–9. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_1.
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AbstractFirst- and second-trimester fetal skin wounds are known to heal without scarring.Research has excluded factors like the sterile uterine environment as the cause of scarless repair, and it is believed that scarless healing is an intrinsic property of early fetal skin. However, increasing wound size and induction of the inflammatory reaction can evoke a scar response in the fetus.For decades, research is performed to elucidate the mechanisms responsible for scarless healing in fetuses. Much research has been performed in animal studies, and several mechanisms have been proposed to be involved such as the microenvironment and the extracellular matrix, a reduced inflammatory response, differences in growth factor profile, and differences in fibroblast phenotype.It is clear that the wound healing process leading to scarless healing cannot be attributed to just one factor or mechanism but will be the result of a complex of interconnected processes.This chapter describes some of the possible mechanisms which may play a role in scarless healing.
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Flew, Terry, and Fiona R. Martin. "Introduction." In Palgrave Global Media Policy and Business, 1–21. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-95220-4_1.
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AbstractOver the past decade the study of internet governance and platform regulation has evolved into a new, socially engaged regulatory field. This chapter introduces regulatory debates surrounding the rise of digital communications platforms and their similarities to media companies. It considers the growth of regulatory activism in response to platformisation and the ‘techlash’, disputes about platform companies’ intermediary liability, and their resistance to legal controls. The chapter also explores the distinction between regulation and governance strategies, emphasising the challenges of self-regulation. It introduces core concerns of the contributors including: how we might address platforms’ dire impact on public interest journalism; how we can develop coherent, transparent, and convergent regulatory frameworks for tackling platform power; how we might analyse and monitor platforms’ new datafied, participatory advertising operations; how we can foster local content and conceive the politics of discoverability in an age of global streaming services; why platforms might have more in common with telecommunications than media companies, and, fundamentally, why governments’ early support for platform self-regulation and governance has shifted in response to political and economic transformations.
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Curry, Helen Anne. "Data, Duplication, and Decentralisation: Gene Bank Management in the 1980s and 1990s." In Towards Responsible Plant Data Linkage: Data Challenges for Agricultural Research and Development, 163–82. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-13276-6_9.
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AbstractIn the 1970s, the number of accessions held in national and international seed and gene banks increased steadily. This growth, initially a source of pride, was recognised as a liability by the 1980s. Too many accessions lacked the basic information necessary for researchers to access and use samples knowledgably. Many gene banks came under scrutiny for poor management practices and several found themselves accused of mishandling a ‘global patrimony’ entrusted to their care. In this paper, I explore one response to these concerns that attracted attention from many in the germplasm conservation community: creating linked, standardised databases of collections. Calls for more and better data about accessions often emphasised that these data would make collections easier to use and therefore more valued. Here I take a close look at the early history of data collation and standardisation as a means of ‘rationalising’ collections, a motivation that was not advertised as prominently. This historical example shows the infrastructures developed to facilitate data exchange in the context of seed and gene banking to have been tied up with both mundane imperatives to cut costs and lofty goals of building political bridges—in addition to the often-repeated ambition of making plant breeding more efficient.
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Tan, Oon Seng, and Jallene Jia En Chua. "Singapore’s Endemic Approach to Education: Re-Envisioning Schools and Learning." In Schools and Society During the COVID-19 Pandemic, 193–210. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-42671-1_10.
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AbstractThe COVID-19 pandemic continues to impact lives worldwide, long beyond its initial wave of infection and emergency responses. Alongside health concerns are impacts to education pertaining not just to learning loss but also to paradigm shifts and other social and psychological effects. These include long-term shifts to curriculum and pedagogy, disproportionate effects on vulnerable populations, and ripple effects on mental health and wellness. Policymakers are prompted to rethink perspectives in education to accommodate the aftermath of the pandemic. This chapter will address Singapore’s endemic approach to public health and education, a couple of years after the start of the pandemic. The nature of our chapter is to share the Singaporean experience, which represents an Asian perspective that is someone unique in its context. Singapore continues to draw from the principles of science and social responsibility, which were the bedrock of its effective response efforts in early pandemic times. This resulted in high vaccination rates and strong research and development efforts to cushion the impact of growing infection rates, allowing citizens to continue with their daily routines with as much normalcy as possible. In education, Singapore experienced two rounds of home-based learning for students in April 2020 (lasting 28 days) and May 2021 (lasting 9 days), in tandem with national lockdowns. In-person lessons resumed after each round of home-based learning, alongside growth in digital innovation in a ground-up manner, due to the autonomy afforded to schools by ministry leadership. This helped optimize learning in the increasingly digital environment where blended learning models became commonplace. On the other hand, prominent issues related to inequity and mental health became forefront concerns and areas of development. Our chapter will discuss how educational policy will benefit from shifting priorities moving forward. We propose that an ecological perspective will be advantageous for the education sector, helping us to understand education and learning beyond school walls. We conclude the chapter by discussing future challenges and insecurities that Singapore will have to overcome.
Conference papers on the topic "Egr [Early growth response]"
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Rauschkolb, Peter, Jens-Christian Wolff, Werner Seeger, and Robert Voswinckel. "Influence Of Early Growth Response 1 (Egr1) And Tenascin C (Tnc) On Compensatory Lung Growth." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6819.
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Takihara, Takahisa, Yukie Yamaguchi, Roger Chambers, and Carol A. Feghali-Bostwick. "A Peptide Derived From Endostatin Exhibits Anti-fibrotic Activity By Reducing The Expression Of Lysyl Oxidase (LOX) And Early Growth Response-1 (Egr-1)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3503.
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Shajahan-Haq, Ayesha N., Lu Jin, Amrita K. Cheema, Simina M. Boca, Yuriy Gusev, Krithika Bhuvaneshwar, Diane M. Demas, et al. "Abstract B1-23: Early growth response (EGR1) is a critical regulator of cellular metabolism and predicts increased responsiveness to antiestrogens in breast cancer." In Abstracts: AACR Special Conference: Computational and Systems Biology of Cancer; February 8-11, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-b1-23.
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Breton, Michael E., Albert W. Schueller, and Graham E. Quinn. "The ERG A-Wave and the cGMP Phototransduction Cascade in the Developing Infant Eye." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/navs.1993.nsuc.2.
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The leading edge of the electroretinogram (ERG) a-wave undergoes change during early development that may be interpreted in terms of photoreceptor growth and maturity of the phototransduction mechanism. The a-wave of the ERG recorded in response to a brief flash of light under dark adapted conditions has long been known to reflect the collective responses of rod photoreceptors (Granit, 1933; Hagins, Penn and Yoshikami, 1970). A variety of features of the a-wave have pointed to its photoreceptor origin. Despite understanding of the photoreceptor origin of the a-wave, application to clinical populations, including differentiating normal development from disease states in infants, has been hampered by a number of factors, including the intrusion of the b-wave, which effectively truncates the a-wave in a time- and light- dependent manner.
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Kute, Stephanie M., and David A. Vorp. "Regional Association of Biological and Hemodynamic Parameters in Distal End-to-Side Vascular Anastomoses Perfused Ex Vivo." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32513.
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Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.
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Wang, Chen, Jose M. Pimiento, Kazim Husain, Anying Zhang, Zhongsheng Tong, and Mokenge P. Malafa. "Abstract 4738: The early response protein EGR-1 mediates vitamin E γ-tocotrienol-induced apoptosis in pancreatic cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4738.
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Zhao, Yi D., Keith M. Jacobs, Rowan M. Karvas, Dennis E. Hallahan, and Dinesh Thotala. "Abstract 422: Early growth response 1 is required for radiation-induced apoptosis in normal tissues." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-422.
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Bharath, Anand Nageswaran, Nitya Kalva, Rolf D. Reitz, and Christopher J. Rutland. "Use of Early Exhaust Valve Opening to Improve Combustion Efficiency and Catalyst Effectiveness in a Multi-Cylinder RCCI Engine System: A Simulation Study." In ASME 2014 Internal Combustion Engine Division Fall Technical Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/icef2014-5534.
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Low Temperature Combustion (LTC) strategies such as Reactivity Controlled Compression Ignition (RCCI) can result in significant improvements of fuel economy and emissions reduction. However, they can produce significant carbon monoxide and unburnt hydrocarbon emissions at low load operating conditions due to poor combustion efficiencies at these operating points, which is a consequence of the low combustion temperatures that cause the oxidation rates of these species to slow down. The exhaust gas temperature is also not high enough at low loads for effective performance of turbocharger systems and diesel oxidation catalysts (DOC). The DOC is extremely sensitive to exhaust gas temperature changes and lights off only when a certain temperature is reached, depending on the catalyst specifications. Uncooled EGR can increase combustion temperatures, thereby improving combustion efficiency, but high EGR concentrations of 50% or more are required, thereby increasing pumping work and reducing volumetric efficiency. However, with early exhaust valve opening, the exhaust gas temperature can be much higher, allowing lower EGR flow rates, and enabling activation of the DOC for more effective oxidization of unburnt hydrocarbons and CO in the exhaust. In this paper, a multi-cylinder engine system simulation of RCCI at low load operation with early exhaust valve opening is presented, along with consideration of the exhaust aftertreatment system. The combustion process is modeled using the 3D CFD code, KIVA, and the heat release rates obtained from this combustion are used in a GT-Power model of a turbocharged, multi-cylinder light-duty RCCI engine for a full system simulation. The post-turbine exhaust gas is fed into GT-Power’s aftertreatment model of the engine’s DOC to determine the catalyst response. It is confirmed that opening the exhaust valve earlier increases the exhaust gas temperature, and hence lower EGR flow rates are needed to improve combustion efficiency. It was also found that exhaust temperatures of around 457 K are required to light off the catalyst and oxidize the unburnt hydrocarbons and CO effectively. Performance of the DOC was drastically improved and higher amounts of unburnt hydrocarbons were oxidized by increasing the exhaust gas temperature.
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CIBELLI, GIUSEPPE. "REGULATION OF EARLY GROWTH RESPONSE-1 GENE EXPRESSION AND SIGNALING MECHANISMS IN NEURONAL CELLS: PHYSIOLOGICAL STIMULATION AND STRESS." In Modelling Biomedical Signals. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812778055_0018.
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Sheppard, Sheri D., and Michael Strange. "Estimation of Fatigue Crack Initiation and Early Growth in Resistance Spot Welds." In ASME 1991 Design Technical Conferences. American Society of Mechanical Engineers, 1991. http://dx.doi.org/10.1115/detc1991-0016.
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Abstract The main objective of this research is to develop a model of fatigue crack initiation and early crack growth in resistance spot welds that is specimen independent. This objective is achieved by examining the stress state around a resistance spot weld. A general expression for the structural stress around the weld is formulated that is dependent only on the loading immediately surrounding the weld. As such, the expression is specimen independent. An additional objective is to explore the feasibility of applying this fatigue crack initiation model to life estimation using structural response data from finite element analysis (FEA). This numerical technique is often used for evaluating structural integrity of assemblies. Limited verification examples show that the structural stress range as calculated from FEA reaction load data is capable of describing fatigue crack initiation and early crack growth in cyclically loaded resistance spot welds.
Reports on the topic "Egr [Early growth response]"
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Ahmed, Mansoor M. Role of Early Growth Response-1 (Egr-1) Gene in Radiation-Induced Apoptosis of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada398097.
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Philosoph-Hadas, Sonia, Peter B. Kaufman, Shimon Meir, and Abraham H. Halevy. Inhibition of the Gravitropic Shoot Bending in Stored Cut Flowers Through Control of Their Graviperception: Involvement of the Cytoskeleton and Cytosolic Calcium. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586533.bard.
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Original objectives: The basic goal of the present project was to study the mechanism involved in shoot graviperception and early transduction, in order to determine the sequence of events operating in this process. This will enable to control the entire process of gravity-induced differential growth without affecting vertical growth processes essential for development. Thus, several new postulated interactions, operating at the perception and early transduction stages of the signaling cascade leading to auxin-mediated bending, were proposed to be examined in snapdragon spikes and oat shoot pulvini, according to the following research goals: 1) Establish the role of amyloplasts as gravireceptors in shoots; 2) Investigate gravity-induced changes in the integrity of shoot actin cytoskeleton (CK); 3) Study the cellular interactions among actin CK, statoliths and cell membranes (endoplasmic reticulum - ER, plasma membrane - PM) during shoot graviperception; 4) Examine mediation of graviperception by modulations of cytosolic calcium - [Ca2+]cyt, and other second messengers (protein phosphorylation, inositol 1,4,5-trisphosphate - IP3). Revisions: 1) Model system: in addition to snapdragon (Antirrhinum majus L.) spikes and oat (Avena sativa) shoot pulvini, the model system of maize (Zea mays) primary roots was targeted to confirm a more general mechanism for graviperception. 2) Research topic: brassinolide, which were not included in the original plan, were examined for their regulatory role in gravity perception and signal transduction in roots, in relation to auxin and ethylene. Background to the topic: The negative gravitropic response of shoots is a complex multi-step process that requires the participation of various cellular components acting in succession or in parallel. Most of the long-lasting studies regarding the link between graviperception and cellular components were focused mainly on roots, and there are relatively few reports on shoot graviperception. Our previous project has successfully characterized several key events occurring during shoot bending of cut flowers and oat pulvini, including amyloplast displacement, hormonal interactions and differential growth analysis. Based on this evidence, the present project has focused on studying the initial graviperception process in flowering stems and cereal shoots. Major conclusions and achievements: 1) The actin and not the microtubule (MT) CK is involved in the graviperception of snapdragon shoots. 2) Gravisensing, exhibited by amyloplast displacement, and early transduction events (auxin redistribution) in the gravitropic response of snapdragon spikes are mediated by the acto-myosin complex. 3) MTs are involved in stem directional growth, which occurs during gravitropism of cut snapdragon spikes, but they are not necessary for the gravity-induced differential growth. 4) The role of amyloplasts as gravisensors in the shoot endodermis was demonstrated for both plant systems. 5) A gravity-induced increase in IP.
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Miller, James H., Bruce R. Zutter, Shepard M. Zedaker, M. Boyd Edwards, and Ray A. Newbold. A Regional Framework of Early Growth Response for Loblolly Pine Relative to Herbaceous, Woody, and Complete Competition Control: The COMProject. New Orleans, LA: U.S. Department of Agriculture, Forest Service, Southern Forest Experiment Station, 1995. http://dx.doi.org/10.2737/so-gtr-117.
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Phillips, Peter C. Early Detection of NF1 Brain Tumor Growth and Treatment Response by MRI, MRS and PET in a Trial of Novel Antitumor Drugs. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada376214.
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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.
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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Dickman, Martin B., and Oded Yarden. Regulation of Early Events in Hyphal Elongation, Branching and Differentiation of Filamentous Fungi. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580674.bard.
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In filamentous fungi, hyphal elongation, branching and morphogenesis are in many cases the key to successful saprophytic and pathogenic fungal proliferation. The understanding of the fungal morphogenetic response to environmental cues is in its infancy. Studies concerning the regulation of fungal growth and development (some of which have been obtained by the participating collaborators in this project) point to the fact that ser/thr protein kinases and phosphatases are (i) involved in the regulation of such processes and (ii) share common structural and functional features between saprophytes and pathogens. It is our objective to combine a pharmaceutical and a genetic approach in order to identify, characterize and functionally dissect some of the regulatory factors involved in hyphal growth, branching and differentiation. Using an immunohistochemical approach, a ser/thr protein kinase involved in hyphal elongation in both Neurospora crassa and Colletotrichum trifolii has been localized in order to identify the physical arena of regulation of hyphal elongation. The analysis of additional kinases and phosphatases (e.g. Protein kinase C, cAMP-dependent kinase, lipid-activated protein kinase, components of the type 2A protein phosphatase) as well as a RAS-related gene (an additional key participant in signal transduction) has been performed. In order to succeed in advancing the goals of this project, we have taken advantage of available elongation/branching mutants in N. crassa and continuously combined the accumulated information obtained while studying the two systems in order to dissect the elements involved in these processes. The various inhibitors/effectors analyzed can serve as a basis for modification to be used as anti-fungal compounds. Understanding the regulation of hyphal proliferation is a key requirement for identifying novel target points for either curbing fungal growth (as in the case of pathogenesis) or affecting growth patterns in various biotechnological processes. The major objective of our joint project was to advance our understanding of regulation of hyphal growth, especially during early events of fungal germination. Towards achieving this goal, we have coupled the analysis of a genetically tractable organism (N. crassa) with a plant pathogen o economic importance (C. trifolii). As the project progressed we believe that the results obtained have provided a reinforcement to our basic approach which called for combining the two fungal systems for a joint research project. On the one hand, we feel that much of the advance made was possible due to the amenability of N. crassa to genetic manipulations. The relevance of some of the initial findings obtained in Neurospora have been proven to be relevant to the plant pathogen while unique features of the pathogen have been identified in Colletotrichum. Most of the results obtained from this research project have been published. Thus, the main volume of this report is comprised of the relevant publications describing the research and results obtained.
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Philosoph-Hadas, Sonia, Peter Kaufman, Shimon Meir, and Abraham Halevy. Signal Transduction Pathway of Hormonal Action in Control and Regulation of the Gravitropic Response of Cut Flowering Stems during Storage and Transport. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7695838.bard.
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Original objectives: The basic goal of the present project was to increase our understanding of the cellular mechanisms operating during the gravitropic response of cut flowers, for solving their bending problem without affecting flower quality. Thus, several elements operating at the 3 levels o the gravity-induced signal transduction pathway, were proposed to be examined in snapdragon stems according to the following research goals: 1) Signaling: characterize the signal transduction pathway leading to the gravitropic response, regarding the involvement of [Ca2+]cyt as a mediator of IAA movement and sensitivity to auxin. 2) Transduction by plant hormones: a) Examine the involvement of auxin in the gravitropic response of flower stems with regard to: possible participation of auxin binding protein (ABP), auxin redistribution, auxin mechanism of action (activation of H+-ATPase) mediation by changes in [Ca2+]cyt and possible regulation of auxin-induced Ca2+ action b: calmodulin-activated or Ca2+-activated protein kinases (PK). b) Examine the involvement of ethylene in the gravitropic response of flower stems with regard to auxin-induced ethylene production and sensitivity of the tissue to ethylene. 3) Response: examine the effect of gravistimulation on invertase (associated with growth and elongation) activity and invertase gene expression. 4) Commercial practice: develop practical and simple treatments to prevent bending of cut flowers grown for export. Revisions: 1) Model systems: in addition to snapdragon (Antirrhinum majus L.), 3 other model shoe systems, consisting of oat (Avena sativa) pulvini, Ornithogalun 'Nova' cut flowers and Arabidopsis thaliana inflorescence, were targeted to confirm a more general mechanism for shoot gravitropism. 2 Research topics: the involvement of ABP, auxin action, PK and invertase in the gravitropic response of snapdragon stems could not be demonstrated. Alternatively, the involvement in the gravity signaling cascade of several other physiological mediators apart of [Ca2+]cyt such as: IP3, protein phosphorylation and actin cytoskeleton, was shown. Additional topics introduced: starch statolith reorientation, differential expression of early auxin responsive genes, and differential shoot growth. Background to the topic: The gravitropic bending response of flowering shoots occurring upon their horizontal placement during shipment exhibits a major horticultural problem. In spite of extensive studies in various aboveground organs, the gravitropic response was hardly investigated in flowering shoots. Being a complex multistep process that requires the participation of various cellular components acting in succession or in parallel, analysis of the negative gravitropic response of shoot includes investigation of signal transduction elements and various regulatory physiological mediators. Major achievements: 1) A correlative role for starch statoliths as gravireceptors in flowering shoot was initially established. 2) Differentially phosphorylated proteins and IP3 levels across the oat shoe pulvini, as well as a differential appearance of 2 early auxin-responsive genes in snapdragon stems were all detected within 5-30 minutes following gravistimulation. 3) Unlike in roots, involvement of actin cytoskeleton in early events of the gravitropic response of snapdragon shoots was established. 4) An asymmetric IAA distribution, followed by an asymmetric ethylene production across snapdragon stems was found following gravistimulation. 5) The gravity-induced differential growth in shoots of snapdragon was derived from initial shrinkage of the upper stem side and a subsequent elongation o the lower stem side. 6) Shoot bending could be successfully inhibited by Ca2+ antagonists (that serve as a basis for practical treatments), kinase and phosphatase inhibitors and actin-cytoskeleton modulators. All these agents did not affect vertical growth. The essential characterization of these key events and their sequence led us to the conclusion that blocking gravity perception may be the most powerful means to inhibit bending without hampering shoot and flower growth after harvest. Implications, scientific and agriculture: The innovative results of this project have provided some new insight in the basic understanding of gravitropism in flower stalks, that partially filled the gap in our knowledge, and established useful means for its control. Additionally, our analysis has advanced the understanding of important and fundamental physiological processes involved, thereby leading to new ideas for agriculture. Gravitropism has an important impact on agriculture, particularly for controlling the bending of various important agricultural products with economic value. So far, no safe control of the undesired bending problem of flower stalks has been established. Our results show for the first time that shoot bending of cut flowers can be inhibited without adverse effects by controlling the gravity perception step with Ca2+ antagonists and cytoskeleton modulators. Such a practical benefit resulting from this project is of great economic value for the floriculture industry.
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Uni, Zehava, and Peter Ferket. Enhancement of development of broilers and poults by in ovo feeding. United States Department of Agriculture, May 2006. http://dx.doi.org/10.32747/2006.7695878.bard.
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The specific objectives of this research were the study of the physical and nutritional properties of the In Ovo Feeding (IOF) solution (i.e. theosmostic properties and the carbohydrate: protein ratio composition). Then, using the optimal solution for determining its effect on hatchability, early nutritional status and intestinal development of broilers and turkey during the last quarter of incubation through to 7 days post-hatch (i.e. pre-post hatch period) by using molecular, biochemical and histological tools. The objective for the last research phase was the determination of the effect of in ovo feeding on growth performance and economically valuable production traits of broiler and turkey flocks reared under practical commercial conditions. The few days before- and- after hatch is a critical period for the development and survival of commercial broilers and turkeys. During this period chicks make the metabolic and physiological transition from egg nutriture (i.e. yolk) to exogenous feed. Late-term embryos and hatchlings may suffer a low glycogen status, especially when oxygen availability to the embryo is limited by low egg conductance or poor incubator ventilation. Much of the glycogen reserve in the late-term chicken embryo is utilized for hatching. Subsequently, the chick must rebuild that glycogen reserve by gluconeogenesis from body protein (mostly from the breast muscle) to support post-hatch thermoregulation and survival until the chicks are able to consume and utilize dietary nutrients. Immediately post-hatch, the chick draws from its limited body reserves and undergoes rapid physical and functional development of the gastrointestinal tract (GIT) in order to digest feed and assimilate nutrients. Because the intestine is the nutrient primary supply organ, the sooner it achieves this functional capacity, the sooner the young bird can utilize dietary nutrients and efficiently grow at its genetic potential and resist infectious and metabolic disease. Feeding the embryo when they consume the amniotic fluid (IOF idea and method) showed accelerated enteric development and elevated capacity to digest nutrients. By injecting a feeding solution into the embryonic amnion, the embryo naturally consume supplemental nutrients orally before hatching. This stimulates intestinal development to start earlier as was exhibited by elevated gene expression of several functional genes (brush border enzymes an transporters , elvated surface area, elevated mucin production . Moreover, supplying supplemental nutrients at a critical developmental stage by this in ovo feeding technology improves the hatchling’s nutritional status. In comparison to controls, administration of 1 ml of in ovo feeding solution, containing dextrin, maltose, sucrose and amino acids, into the amnion of the broiler embryo increased dramatically total liver glycogen in broilers and in turkeys in the pre-hatch period. In addition, an elevated relative breast muscle size (% of broiler BW) was observed in IOF chicks to be 6.5% greater at hatch and 7 days post-hatch in comparison to controls. Experiment have shown that IOF broilers and turkeys increased hatchling weights by 3% to 7% (P<0.05) over non injected controls. These responses depend upon the strain, the breeder hen age and in ovo feed composition. The weight advantage observed during the first week after hatch was found to be sustained at least through 35 days of age. Currently, research is done in order to adopt the knowledge for commercial practice.
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Chen, Weixing. PR-378-083601-R02 Effect of Pressure Fluctuations on Growth Rate of Near-Neutral pH SCC. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), August 2017. http://dx.doi.org/10.55274/r0011010.
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This report summarizes the work completed in Phase 1 and Phase 2 of PRCI SCC-2-12 project: Effect of Pressure Fluctuations on Growth Rate of Near-Neutral pH SCC. The following two insights from the two-phase PRCI SCC 2-12 project can be proven to be the most important: 1) The identification of three types of pressure fluctuations and their different susceptibility to crack growth; 2) The importance of load interaction effects during variable amplitude pressure fluctuations in the prediction of crack growth rate. The work has enabled us to divide near-neutral pH SCC cracking into the following two governing processes: the dissolution growth process for crack initiation and early stage crack growth and the hydrogen facilitated fatigue growth after crack initiation and dormancy. The first process features very high rate of dissolution at the pipe surface caused by various forms of galvanic processes and reduced crack growth in the depth direction leading to crack dormancy. The hydrogen facilitated fatigue growth process has been determined to be predominant for the crack growth after crack initiation and dormancy. Depending on the location of pipeline sections, the pressure fluctuations could be characterized into three types based on the relative pressure levels of the large loading events and the minor cycles. It has been determined from extensive experimental investigations that crack growth under Type I pressure fluctuations with frequent underload cycles, which is often found within 30 km downstream of a compressor station, can be enhanced significantly because of effects of load interactions of variable amplitude of cyclic loading. The load-interactions during SCC of pipeline steels in near-neutral pH environments are complex, which include both the time independent load-history interactions and the time dependent load interactions related to the rate of diffusion of hydrogen and hydrogen embrittlement in response to various scenarios of pressure fluctuations. Based on the experimental findings obtained, strategies for mitigating near-neutral pH crack initiation and crack growth during field operations have been proposed. The experimental findings have also been integrated into a software, namely the Pipe-Online, for making crack growth and remaining life prediction. For the purpose of capturing all the crack-growth contributing events of pressure fluctuations for life predictions, a method of recording pressure fluctuations has also been developed.
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Lillehoj, Hyun, Dan Heller, and Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, November 1992. http://dx.doi.org/10.32747/1992.7561056.bard.
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Coccidiosis, ubiquitous diseases of poultry, seriously impair the growth and feed utilization of livestock and poultry. Coccidiosis causes over $600 million annual losses world-wide and no vaccine is currently available. The goal of this study was to investigate the cellular and molecular mechanisms controlling protective immune responses to coccidia parasites in order to develop immunological control strategy against coccidiosis. The major findings of this study were: 1) cell-mediated immunity plays a major role in protection against coccidiosis, 2) when different genetic lines showing different levels of disease susceptibility were compared, higher T-cell response was seen in the strains of chickens showing higher disease resistance, 3) early interferon secretion was observed in more coccidia-resistant chicken strains, 4) both sporozoite and merozoite antigens were able to induce interferon production, and 5) chicken monoclonal antibodies which detect immunogenic coccidia proteins have been developed. This study provided a good background work for future studies toward the development of recombinant coccidial vaccine. Availability of chicken monoclonal antibodies which detect immunogenic coccidia proteins will enhance our ability to identify potential coccidial vaccine antigens.