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1
Raynov, Alexander Markov, Yun-Hoon Choung, Sung-Kyun Moon, and Keehyun Park. "Expression of female sex hormone receptors in human middle-ear cholesteatomas." Journal of Laryngology & Otology 119, no. 12 (December 2005): 941–45. http://dx.doi.org/10.1258/002221505775010878.
Повний текст джерелаАнотація:
The purpose of this study was to establish the eventual presence of progesterone receptor (PGR) and oestrogen receptor (EGR) in human middle-ear cholesteatoma (MECh) tissues and to compare their expression between male and female patients. An immunohistochemical technique was employed for detection of PGR- and EGR-specific immunoreactivity in MECh samples using formalin-fixed paraffin-embedded tissue sections. The positive results were verified with reverse transcriptase polymerase chain reaction (RT-PCR). The morphological study revealed stable expression of PGR in suprabasal layers of all cholesteatoma samples. Weaker immunoreactivity for PGR was demonstrated in external auditory canal skin (EACS) samples in comparison with MECh, while PGR-specific staining was not observed in retroauricular skin (RAS) samples. EGR was detected only at mRNA levels. Stronger expression of EGR PCR products was disclosed in female cholesteatoma samples, while PGR mRNA was predominantly detected in male cholesteatoma specimens. Our preliminary experimental results give us ground to assume that female sex hormones may stimulate proliferation and affect differentiation of MECh keratinocytes.
2
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.
Повний текст джерелаАнотація:
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.
3
Wu, Jun Hua, Fu Shan Zuo, and Yong Hui Zhang. "Experimental Study of EGR on Performance and Emissions of a Turbocharged DME Engine." Advanced Materials Research 886 (January 2014): 257–61. http://dx.doi.org/10.4028/www.scientific.net/amr.886.257.
Повний текст джерелаАнотація:
This paper presents anexperimental study on reduction of NOx emission of a turbochargedengine fuelled with DME by means of EGR. Effects of EGR rate on engineefficiency and emission behavior was evaluated. The results show that the EGRcould be used as an effective way to reduce NOx emission. NOx isreduced almost linearly with increase of EGR rate. At low load condition, theNOx emission is reduced by 80% with 40% EGR rate without any economypenalty. At high load condition, the same substantial reduction of NOx couldbe achieved with only 20% EGR rate. While the HC and CO emissions are increasedwith increase of EGR rate. However, it is worth noting that EGR had a negativeeffect on fuel consumption at high load. Low EGR ratio should be taken at highengine load condition.
4
Ziegelhoeffer, Tibor, Matthias Heil, Silvia Fischer, Borja Fernández, Wolfgang Schaper, Klaus T. Preissner, Elisabeth Deindl, and Judith-Irina Pagel. "Role of early growth response 1 in arteriogenesis: Impact on vascular cell proliferation and leukocyte recruitment in vivo." Thrombosis and Haemostasis 107, no. 03 (2012): 562–74. http://dx.doi.org/10.1160/th11-07-0490.
Повний текст джерелаАнотація:
SummaryBased on previous findings that early growth response 1 (Egr-1) participates in leukocyte recruitment and cell proliferation in vitro, this study was designed to investigate its mode of action during arteriogenesis in vivo. In a model of peripheral arteriogenesis, Egr-1 was significantly upregulated in growing collaterals of wild-type (WT) mice, both on mRNA and protein level. Egr-1−/− mice demonstrated delayed arteriogenesis after femoral artery ligation. They further showed increased levels of monocytes and granulocytes in the circulation, but reduced levels in adductor muscles under baseline conditions. After femoral artery ligation, elevated numbers of macrophages were detected in the perivascular zone of collaterals in Egr-1−/− mice and mRNA of leukocyte recruitment mediators was upregulated. Other Egr family members (Egr-2 to -4) were significantly upregulated only in Egr-1−/− mice, suggesting a mechanism of counterbalancing Egr-1 deficiency. Moreover, splicing factor-1, downregulated in WT mice after femoral artery ligation in the process of increased vascular cell proliferation, was upregulated in Egr-1−/− mice. αSM-actin on the other hand, significantly downregulated in WT mice, showed no differential expression in Egr-1−/− mice. While cell cycle regulator cyclin E and cdc20 were upregulated in Egr-1−/− mice, cyclin D1 expression decreased below the detection limit in collaterals, and the proliferation marker ki67 was not differentially expressed. In conclusion, compensation for deficiency in Egr-1 function in leukocyte recruitment can presumably be mediated by other transcription factors; however, Egr-1 is indispensable for effective vascular cell cycle progression in arteriogenesis.
5
Li, Lian-Jie, Jeffrey M. Weinberg, Ibrahim A. Tangoren, Joseph P. Sleater, and Lynn M. Klein. "Erythema Gyratum Repens Associated with Transitional Cell Carcinoma of the Bladder." Journal of Cutaneous Medicine and Surgery 2, no. 1 (July 1997): 50–52. http://dx.doi.org/10.1177/120347549700200113.
Повний текст джерелаАнотація:
Background: Erythema gyratum repens (EGR) is a gyrate erythema found in association with underlying malignancy, most commonly that of the lung, esophagus, and breast. Since 1952, there have been 51 cases of this condition reported. Objective: Only one case of EGR associated with transitional cell carcinoma of the bladder (TCCB) has been previously reported. Methods: The second case of EGR is the subject of a case report presentation. Results: An elderly patient presented with EGR and subsequent work-up revealed the presence of malignancy of the bladder. Conclusion: Erythema gyratum repens can be found in association with a variety of malignancies, including TCCB.
6
Smith, Jack A., and Gordon J. J. Bartley. "Stoichiometric Operation of a Gas Engine Utilizing Synthesis Gas and EGR for NOx Control." Journal of Engineering for Gas Turbines and Power 122, no. 4 (April 2, 2000): 617–23. http://dx.doi.org/10.1115/1.1289386.
Повний текст джерелаАнотація:
This paper presents the results from an internal research study conducted at the Southwest Research Institute (SwRI) on the effects of stoichiometric mixtures of natural gas and synthesis gas with exhaust gas recirculation (EGR) on engine performance and exhaust emissions. Constant load performance and emissions tests were conducted on a modified, single-cylinder, Caterpillar 1Y540 research engine at 11.0 bar (160 psi) bmep. Engine performance and emissions comparisons between natural gas with EGR, and natural gas with syngas and EGR are presented. In addition, the performance characteristics of the fuel reforming catalyst are presented. Results show that thermal efficiency increases with increasing EGR for both natural gas operation and natural gas with syngas operation at constant load. The use of syngas with natural gas extended the EGR tolerance by 44.4 percent on a mass basis compared to natural gas only, leading to a 77 percent reduction in raw NOx emissions over the lowest natural gas with EGR NOx emissions. [S0742-4795(00)00504-4]
7
Dinkel, A., W. K. Aicher, C. Haas, P. F. Zipfel, H. H. Peter, and H. Eibel. "Transcription factor Egr-1 activity down-regulates Fas and CD23 expression in B cells." Journal of Immunology 159, no. 6 (September 15, 1997): 2678–84. http://dx.doi.org/10.4049/jimmunol.159.6.2678.
Повний текст джерелаАнотація:
Abstract Activation of mature B cells via Ag receptor cross-linking induces transient expression of the transcription factor Egr-1. Although the activating signals leading to Egr-1 induction have been studied extensively, little is known about the genes that are placed further downstream within this activation cascade and that are transcriptionally regulated by Egr-1. To identify such target genes, we established Egr-1-overexpressing transfectants from the murine B cell line K46 and from human Ramos B cells. All clones derived from K46 B cells showed increased expression of CD44. Most interestingly, expression of CD95 (Fas/Apo-1) and of CD23 was down-regulated in all K46 transfectants. As a consequence, they became resistant to apoptosis induced by anti-CD95 Ab treatment. Similarly, the Egr-1-expressing Ramos cells showed reduced levels of CD95 expression. Thus, Egr-1 seems to control the expression of downstream target genes not only as a transcriptional activator, but also as a repressor molecule. In B cells, Egr-1 therefore plays a critical role in integrating the short-lived signal delivered by triggering of the Ag receptor into phenotypic changes, including repression of CD95 and CD23 transcription.
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Liang, Jinlong, Jingyi Wang, Jinshui Zeng, Zhibo Bai, Zhiyuan Zheng, Yue Zheng, Fengqi Jiang, and Di Wu. "The Landscape of Early Growth Response Family Members 1-4 in Hepatocellular Carcinoma: Their Biological Roles and Diagnostic Utility." Disease Markers 2022 (August 22, 2022): 1–8. http://dx.doi.org/10.1155/2022/3144742.
Повний текст джерелаАнотація:
The incidence of hepatocellular carcinoma (HCC), which is one of the most frequent types of cancer seen all over the world, is steadily growing from year to year. EGR genes are members of the early growth response (EGR) gene family. It has been shown that EGR genes play an increasingly essential role in the development of tumors and the progression of numerous malignancies. However, the possible diagnostic and prognostic roles of EGR genes in HCC have only been examined in a limited number of studies. Expression and methylation data on EGR family members were obtained from TCGA datasets. The prognostic values of EGR members were studied. Additionally, the correlations of EGR members with immune cells were assessed through the single-sample gene set enrichment analysis (ssGSEA). In this study, we found that the expression of EGR1, EGR2, EGR3, and EGR4 was distinctly decreased in HCC specimens compared with nontumor specimens. ROC assays confirmed that they have a strong ability in screening HCC specimens from nontumor specimens. According to the findings of Pearson’s correlation, EGR1, EGR2, EGR3, and EGR4 were found to have a negative association with the methylation level. Survival study revealed that EGR1, EGR2, and EGR3 were associated with the clinical outcome of HCC patients. Immune cell enrichment analysis demonstrated that the expressions of all EGR members were positively related to the levels of most types of immune cells, such as macrophages, NK cells, B cells, T cells, eosinophils, and CD8 T cells. Overall, the current work demonstrated the expression mode and prognostic value of EGR members in HCC in a comprehensive manner, offering insights for further research of the EGR family as possible clinical biomarkers in HCC.
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Zhou, Yanqiong, Ganggang Shi, Jinhong Zheng, Zhanqin Huang, Fenfei Gao, Yanmei Zhang, Fuxiao Guo, Qiangyong Jia, and Yanshan Zheng. "The protective effects of Egr-1 antisense oligodeoxyribonucleotide on cardiac microvascular endothelial injury induced by hypoxia–reoxygenationThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 88, no. 4 (August 2010): 687–95. http://dx.doi.org/10.1139/o10-021.
Повний текст джерелаАнотація:
Early growth response 1 (Egr-1) over-expression has been demonstrated in myocardial ischemia–reperfusion injury, which is closely associated with endothelial dysfunction. In the present study we investigated the expression of Egr-1 on cultured cardiac microvascular endothelial cells (CMECs) to help define the mechanism of myocardial ischemia–reperfusion injury. A model of cultured CMECs exposed to hypoxia–reoxygenation was developed in which synthesized Egr-1 sense and antisense oligodeoxyribonucleotide were transfected into the cells. The expression of Egr-1 was examined by Western blot analysis. Lactate dehydrogenase, malondialdehyde, superoxide dismutase, tumor necrosis factor α, and intercellular adhesion molecule 1 were measured after hypoxia–reoxygenation to assess cell function and injury. Cell morphology, cell viability, and neutrophil adhesion to the CMECs were measured to assess the degree of injury and inflammation. Only cells transfected with Egr-1 antisense oligodeoxyribonucleotide showed a significant reduction in Egr-1 protein expression following hypoxia–reoxygenation. Consistent with the down-regulation of Egr-1 expression, other forms of cell injury were significantly reduced in this group of cells, as evidenced by less alteration in cell morphology, a decrease in expression of tumor necrosis factor α and intercellular adhesion molecule 1, improved cell survival, and reduced neutrophil adhesion.
10
Rupprecht, H. D., P. Dann, V. P. Sukhatme, R. B. Sterzel, and D. L. Coleman. "Effect of vasoactive agents on induction of Egr-1 in rat mesangial cells: correlation with mitogenicity." American Journal of Physiology-Renal Physiology 263, no. 4 (October 1, 1992): F623—F636. http://dx.doi.org/10.1152/ajprenal.1992.263.4.f623.
Повний текст джерелаАнотація:
The early growth response gene 1 (Egr-1) is a member of the family of immediate early response genes. Egr-1 encodes a nuclear phosphoprotein that binds a specific nonameric DNA sequence through three zinc-finger domains and functions as a transcriptional activator. We tested whether the vasoactive agents platelet-derived growth factor (PDGF), arginine vasopressin (AVP), serotonin (5-HT), and angiotensin II (ANG II) induced Egr-1 mRNA in cultured rat mesangial cells (MCs) and investigated the role of protein kinase C (PKC) in mediating the induction process. PDGF, AVP, and 5-HT induced Egr-1 mRNA within 15 min, reaching peak levels at 45-60 min. After PDGF and 5-HT stimulation, Egr-1 mRNA levels returned to baseline within 4 h, whereas AVP induced a sustained increase for up to 8 h. There was a very close correlation between doses required for Egr-1 induction and induction of MC proliferation. ANG II was a very weak MC mitogen and induced only a small increase in Egr-1 mRNA. Comparison of control cells with cells depleted of PKC by 48 h of PMA treatment revealed that induction of Egr-1 by PDGF and 5-HT is independent of PKC. In contrast, however, the Egr-1 response to AVP was diminished in PKC-depleted cells. AVP induced Egr-1 mRNA 10.9-fold in control cells, compared with 7.8-fold in PKC-depleted cells. Egr-1 mRNA after AVP stimulation remained elevated in control cells for up to 8 h but returned to baseline after 120 min in PKC-depleted cells. Similar results were obtained using the PKC-inhibitor H-7. Using immunocytochemistry, PDGF and AVP were found to induce Egr-1 protein within 30 min localized to the nucleus. We conclude that there is a strong correlation between induction of Egr-1 after stimulation with PDGF, AVP, 5-HT, and ANG II and the proliferative response elicited by these agents in MCs. AVP induces Egr-1 by both PKC-dependent and PKC-independent pathways, whereas the effects of PDGF and 5-HT are independent of PKC.
11
Iwami, K., N. Ashizawa, Y. S. Do, K. Graf, and W. A. Hsueh. "Comparison of ANG II with other growth factors on Egr-1 and matrix gene expression in cardiac fibroblasts." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 6 (June 1, 1996): H2100—H2107. http://dx.doi.org/10.1152/ajpheart.1996.270.6.h2100.
Повний текст джерелаАнотація:
The purpose of the present investigation was to compare the effects of angiotensin II (ANG II) other growth factors implicated to play a role in ventricular hypertrophy on cardiac fibroblast changes associated with cardiac remodeling. These changes included induction of early growth response (Egr-1) gene and increases in message levels of extracellular matrix proteins. ANG II treatment (10(-10)-10(-6) M) of rat cardiac fibroblasts induced 1) Egr-1 and 2) a fourfold (P < 0.02) increase in fibronectin and a twofold (P = 0.05) increase in laminin mRNA levels but no increases in that of collagens I, III, or IV at 24–48 h, and 3) a decrease in AT1-receptor mRNA levels to 26% (P < 0.001) of basal at 4–6 h. These effects were all inhibited by the AT1-receptor blocker, losartan, but not AT2-receptor blockers. Immunostaining of cultured cells with antibody against rat fibronectin demonstrated positive staining of cells in serum-free medium; staining was more intense in cells treated with ANG II (10(-6) M, 48 h). Fluorescent-activated cell sorting using an antibody against rat AT1 receptor demonstrated a receptor signal in cells maintained in serum-free medium; however, the receptor signal was not detectable in ANG II-treated cells. Serum and epidermal growth factor (EGF) also induced Egr-1, but norepinephrine (NE) and endothelin (ET) had no effect. Serum increased fibronectin mRNA levels by twofold (P < 0.05). EGF, NE, and ET had no effect on matrix gene expression. Serum, EGF, and NE also transiently downregulated AT1-receptor mRNA levels at 4–6 h of treatment. These results demonstrate that 1) ANG II both induces protooncogene expression and enhances fibronectin mRNA levels in cultured cardiac fibroblasts, whereas EGF only induces Egr-1, and NE and ET have no effects on either function; 2) ANG II effects are primarily mediated by the AT1 receptor; and 3) growth factors can regulate AT1-receptor mRNA levels. Thus ANG II, relative to NE, ET, and EGF, appears to play a prominent and direct role in fibroblast changes associated with cardiac hypertrophy.
12
Yang, Chuan-lei, Xiang-huan Zu, He-Chun Wang, and Yin-yan Wang. "Optimized modelling and application of exhaust gas recirculation performance evaluation of turbocharged diesel engine." Royal Society Open Science 5, no. 6 (June 2018): 172112. http://dx.doi.org/10.1098/rsos.172112.
Повний текст джерелаАнотація:
Aimed at the problem of exhaust gas recirculation (EGR) performance evaluation and optimal EGR rate determination of turbocharged diesel engines, an optimized decision-making method, based on grey theory and entropy weight, was proposed. The internal combustion pressure, fuel consumption rate, NO X , CO and smoke were selected as the decision-making targets and the initial decision-making model was established based on the traditional grey decision-making theory. According to the characteristics and optimization requirements of EGR, the optimal compromise between combustion and emission performance is proposed to transform into decision-making target weighting problem, then an optimized subjective weighting method based on expert scoring and grey relational analysis is proposed. Finally, the entropy weight method was used to solve the objective weight and the optimized multi-objective grey decision-making model was established, which can not only weaken the human error of subjective empowerment, but also fully explore the intrinsic relationship of the evaluation indexes. At last, an optimization simulation platform for EGR performance evaluation based on MATLB/GUIDE was designed and established. The results show that the optimization simulation platform can effectively improve the efficiency of simulation calculation, which is more convenient for practical engineering applications. The optimized method can successfully realize EGR performance evaluation and optimal EGR rate determination under different working conditions. The decision-making result was consistent with the present EGR control strategies, which provide a new research idea for EGR performance optimization.
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Gibbs, John D., Alaina A. Borden, Dan A. Liebermann, and Barbara Hoffman. "Challenging E2F-1 and c-Myb Block of Myeloid Terminal Differentiation with the Tumor Suppressor-Egr1." Blood 104, no. 11 (November 16, 2004): 4330. http://dx.doi.org/10.1182/blood.v104.11.4330.4330.
Повний текст джерелаАнотація:
Abstract The proliferation and differentiation of hematopoietic cells are tightly regulated to maintain cellular homeostasis. Understanding the mechanism of this regulation may identify potential therapeutic targets against leukemia. Previous works have shown that several negative regulators of differentiation, namely oncogenes c-Myb, E2F-1 and c-Myc were capable of blocking the IL6-mediated myeloid terminal differentiation program of M1 myeloblastic leukemia cells. On the other hand, a positive regulator of differentiation, Egr-1 has been shown to activate the macrophage differentiation program of M1 cells in the absence of IL-6. Interestingly, recent work showed that Egr-1 could override the block of differentiation imparted by deregulated c-Myc in the presence of IL-6, and could reverse the leukemic phenotype associated with deregulated c-Myc. From such observations, we asked whether exogenous expression of Egr-1 in M1 cells could override the earlier block of differentiation imparted by the oncogenes c-Myb or E2F-1. The established M1Myb-Egr cells and M1E2F-Egr cells were analyzed. The M1E2F-Egr cells underwent growth arrest followed by macrophage differentiation and subsequently apoptosis. In addition, exogenous Egr-1 only partially abrogated c-Myb block of differentiation. The M1Myb-Egr cells failed to undergo growth arrest, however, were able to enter intermediate-late stage macrophage differentiation with concomitant phagocytic functionality. These data demonstrate that E2F and c-Myb each block myeloid differentiation via different mechanisms. Egr-1 can completely override the E2F block but cannot abrogate the c-Myb block to allow M1 cells to terminally differentiate or growth arrest. Furthermore, Egr-1 appears to behave as a tumor suppressor, and therefore may serve as a possible target against various forms of leukemia.
14
Chen, Lijuan, Siqing Wang, Yiming Zhou, Xiaosong Wu, Igor Entin, Joshua Epstein, Shmuel Yaccoby, et al. "Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma." Blood 115, no. 1 (January 7, 2010): 61–70. http://dx.doi.org/10.1182/blood-2009-03-210526.
Повний текст джерелаАнотація:
Abstract Tumor–bone marrow microenvironment interactions in multiple myeloma (MM) are documented to play crucial roles in plasma-cell growth/survival. In vitro coculture of MM cells with osteoclasts supported cell survival and significantly down-regulated JUN expression. JUN expression in myeloma cells from late-stage and high-risk MM was significantly lower than in plasma cells from healthy donors, monoclonal gammopathy of undetermined significance, smoldering MM, and low-risk MM; patients with low-JUN–expressing MM cells had earlier disease-related deaths. JUN overexpression in MM cells induced cell death and growth inhibition and up-regulated expression of early growth response protein 1 (EGR-1), whose low expression also carried unfavorable clinical implications. EGR-1 knockdown in MM cells abrogated JUN overexpression-induced MM cell death and growth inhibition, indicating that EGR-1 acts directly downstream of JUN. JUN modulates myeloma cell apoptosis through interacting with EGR-1, which down-regulates Survivin and triggers caspase signaling. Importantly, high JUN or EGR-1 expression was associated with improved outcome in Total Therapy 3, in which bortezomib is given throughout therapy, versus Total Therapy 2, in which bortezomib is given only at relapse. Consistently, JUN or EGR-1 knockdown in cultured MM cells enhanced their resistance to bortezomib, demonstrating the crucial role of low JUN/EGR-1 expression in MM resistance to bortezomib.
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Yang, Guang, Xuandai Nguyen, Judy Ou, Prasad Rekulapelli, David K. Stevenson, and Phyllis A. Dennery. "Unique effects of zinc protoporphyrin on HO-1 induction and apoptosis." Blood 97, no. 5 (March 1, 2001): 1306–13. http://dx.doi.org/10.1182/blood.v97.5.1306.
Повний текст джерелаАнотація:
Zinc protoporphyrin (ZnPP), a naturally occurring molecule, is increased in iron deficiency and lead intoxication. ZnPP can also induce heme oxygenase (HO-1), the enzyme it competitively inhibits. In cultured cells (HA-1), ZnPP was the strongest HO-1 inducer of any metalloporphyrin (MP) tested. This was not due to increased oxidative stress, enhanced binding at metal response element, nor increased binding at activator protein-1 (AP-1) or SP-1 sites on HO-1. Only ZnPP, however, increased binding of nuclear proteins to early growth response-1 (Egr-1) protein consensus sequence. Pretreatment of HA-1 with cycloheximide inhibited ZnPP-induced HO-1 messenger RNA (mRNA) by 55%. Incubation with antisense Egr-1 oligomers decreased ZnPP-induced HO-1 expression by 47%. Furthermore, the level of HO-1 mRNA induction by ZnPP was 2-fold less in Egr-1–deficient fibroblasts than in wild-type cells. Because no Egr-1 binding site was previously identified on the HO-1 promoter, HA-1 cells were transfected with HO-1 CAT constructs containing segments of a 12.5-kb enhancer region of HO-1. A 196-bp fragment (RH) located approximately 9.5 kb upstream of the transcription start site mediated HO-1 induction by ZnPP alone. DNase I footprinting analysis further revealed that nuclear proteins bound to a 50-bp sequence in the RH. Within this sequence, a novel 9-bp region with 78% homology to the Egr-1 consensus sequence was identified further suggesting that Egr-1 partially mediates HO-1 induction by ZnPP. Lastly, increased apoptosis and nuclear localization were only seen with ZnPP, suggesting that increased ZnPP in disease states may serve as a cellular signaling mechanism.
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Halvorson, Lisa M., Ursula B. Kaiser та William W. Chin. "The Protein Kinase C System Acts through the Early Growth Response Protein 1 to Increase LHβ Gene Expression in Synergy with Steroidogenic Factor-1". Molecular Endocrinology 13, № 1 (1 січня 1999): 106–16. http://dx.doi.org/10.1210/mend.13.1.0216.
Повний текст джерелаАнотація:
Abstract Expression of the LHβ gene has been shown to be modulated by both the orphan nuclear receptor, steroidogenic factor-1 (SF-1), and the early growth response protein 1, Egr-1. It is also well known that LHβ mRNA levels are increased after hormonal activation of the protein kinase C (PKC) signaling system, for example by GnRH; however, the mechanisms by which the PKC system exerts this effect has not been fully characterized. By transient transfection of the GH3 cell line, we demonstrate that activation of the PKC system with the phorbol ester, phorbol 12-myristate 13-acetate (PMA), increases activity of region −207/+5 of the rat LHβ gene promoter (∼2-fold) and markedly augments SF-1-induced stimulation (95-fold in the presence of both factors vs. 13-fold for SF-1 alone). Mutation of the two previously identified Egr-1 sites not only prevents Egr-1 effects on the LHβ gene promoter, but also eliminates the synergistic response to PMA and SF-1 together, findings that were confirmed in a longer construct spanning region −797/+5. In the gonadotrope-derived cell line,α T3–1, these mutations eliminate the GnRH responsiveness of the− 207/+5 LHβ promoter construct. We next show that PMA treatment (GH3 and αT3–1 cells) or GnRH treatment (αT3–1 cells) induces expression of Egr-1, as detected by Egr-1 interaction with Egr-1 DNA-binding sites in the rat LHβ gene promoter sequence. Furthermore, we demonstrate that PMA increases steady-state Egr-1 mRNA levels via increased Egr-1 transcription. We conclude that PMA-induced stimulation of LHβ gene expression is achieved, at least in part, by induction of Egr-1 expression.
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Frick, K. K., L. Jiang, and D. A. Bushinsky. "Acute metabolic acidosis inhibits the induction of osteoblastic egr-1 and type 1 collagen." American Journal of Physiology-Cell Physiology 272, no. 5 (May 1, 1997): C1450—C1456. http://dx.doi.org/10.1152/ajpcell.1997.272.5.c1450.
Повний текст джерелаАнотація:
Metabolic acidosis induces net calcium efflux from bone through a decrease in osteoblastic formation and an increase in osteoclastic resorption. We tested the hypothesis that changes in external pH would alter the expression of genes critical to the function of mouse calvarial bone cells, predominantly osteoblasts. Cells were cultured in physiologically neutral pH medium until confluent and then stimulated with fresh medium at either neutral or acidic pH. Among a group of immediate early response genes, including egr-1, junB, c-jun, junD, and c-fos, only egr-1 stimulation was modulated by changes in medium pH. At pH 7.4, RNA for egr-1 was stimulated approximately 10- to 30-fold, 40 min after medium change. A progressive decrease in pH to 6.8 led to a parallel reduction in egr-1 stimulation, and an increase in pH to 7.6 led to an increase in egr-1 stimulation. The protein synthesis inhibitor cycloheximide led to a superinduction of egr-1 with preservation of the pH dependency of expression. Osteoblasts synthesize collagen, which is subsequently mineralized. RNA for type 1 collagen was stimulated approximately three- to fivefold, 40 min after medium change. Again the stimulation was inhibited by acidosis and increased by alkalosis. Cycloheximide abolished the pH dependency of expression. These results suggest that small changes in external pH have a significant effect on the expression of certain genes important for osteoblastic function.
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Saadane, Nacéra, Ping Yue, Lesley Alpert, Benjamin Mitmaker, Gordon M. Kirby, and Lorraine E. Chalifour. "Diminished molecular response to doxorubicin and loss of cardioprotective effect of dexrazoxane inEgr-1deficient female mice." Canadian Journal of Physiology and Pharmacology 79, no. 6 (June 1, 2001): 533–44. http://dx.doi.org/10.1139/y01-021.
Повний текст джерелаАнотація:
Doxorubicin (DOX) and VP16 are DNA topoisomerase II inhibitors yet only DOX induces an irreversible cardiotoxicity, likely through DOX-induced oxidative stress. Egr-1 is overexpressed after many stimuli that increase oxidative stress in vitro and after DOX-injection into adult mice in vivo. To investigate Egr-1 function in the heart, we compared the molecular and histological responses of wild type (+/+) and Egr-1 deficient (/) female mice to saline, DOX, VP16, the cardioprotectant dexrazoxane (DZR), or DOX+DZR injection. DOX, and to a lesser extent VP16, induced characteristic increases in cardiac muscle and non-muscle genes typical of cardiac damage in +/+ mice, whereas only β-MHC and Sp1 were increased in / mice. DZR-alone treated +/+ mice showed increased cardiomyocyte transnuclear width without a change to the heart to body weight (HW/BW) ratio. However, DZR-alone treated / mice had an increased HW/BW, increased cardiomyocyte transnuclear width, and gene expression changes similar to DOX-injected +/+ mice. DZR pre-injection alleviated DOX-induced gene changes in +/+ mice; in DZR+DOX injected / mice the increases in cardiac and non-muscle gene expression were equal to, or exceeded that, detected after DOX-alone or DZR-alone injections. We conclude that Egr-1 is required for DOX-induced molecular changes and for DZR-mediated cardioprotection.Key words: mice, gene expression, doxorubicin, DNA topoisomerase II inhibitors, cardioprotection.
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Vítek, Oldřich, Jan Macek, Jiří Klíma, and Martin Vacek. "Optimization of 2‑Stage Turbocharged Gas SI Engine Under Steady State Operation." Journal of Middle European Construction and Design of Cars 15, no. 2 (December 20, 2017): 9–36. http://dx.doi.org/10.1515/mecdc-2017-0006.
Повний текст джерелаАнотація:
Abstract The proposed paper deals with an optimization of a highly-turbocharged large-bore gas SI engine. Only steady state operation (constant engine speed and load) is considered. The paper is mainly focused on theoretical potential of 2-stage turbocharging concept in terms of performance and limitation. The results are obtained by means of simulation using complex 0-D/ 1-D engine model including the control algorithm. Different mixture composition concepts are considered to satisfy different levels of NOx limit - fresh air mixed with external cooled EGR is supposed to be the right approach while optimal EGR level is to be found. Considering EGR circuit, 5 different layouts are tested to select the best design. As the engine control is relatively complex (2-sage turbocharger group, external EGR, compressor blow-by, controlled air excess), 5 different control means of boost pressure were considered. Each variant based on above mentioned options is optimized in terms of compressor/turbine size (swallowing capacity) to obtain the best possible BSFC. The optimal variants are compared and general conclusions are drawn.
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Li, Yang, Meng Xue, Fang Hu, Yijie Jia, Zongji Zheng, Yanlin Yang, Xiaolian Liu, Yuelian Yang, and Yanjing Wang. "Klotho prevents epithelial–mesenchymal transition through Egr-1 downregulation in diabetic kidney disease." BMJ Open Diabetes Research & Care 9, no. 1 (June 2021): e002038. http://dx.doi.org/10.1136/bmjdrc-2020-002038.
Повний текст джерелаАнотація:
IntroductionAs a key event leading to tubulointerstitial fibrosis in diabetic kidney disease (DKD), epithelial–mesenchymal transition (EMT) has drawn increasing attention from researchers. The antiaging protein Klotho attenuates renal fibrosis in part by inhibiting ERK1/2 signaling in DKD. Early growth response factor 1 (Egr-1), which is activated mainly by ERK1/2, has been shown to play an important role in EMT. However, whether Klotho prevents EMT by inhibiting ERK1/2-dependent Egr-1 expression in DKD is unclear.The aim of this study was to investigate whether Klotho prevents EMT through Egr-1 downregulation by inhibiting the ERK1/2 signaling pathway in DKD.Research design and methodsMale C57BL/6J mice fed an high-fat diet for 4 weeks received 120 mg/kg streptozotocin (STZ), which was injected intraperitoneally. Klotho and Egr-1 expression was detected in the renal cortices of these mice on their sacrifice at 6 and 12 weeks after STZ treatment. In In vitro studies, we incubated HK2 cells under high-glucose (HG) or transforming growth factor-β1 (TGF-β1) conditions to mimic DKD. We then transfected the cells with an Klotho-containing plasmid, Klotho small interfering RNA.ResultsKlotho expression was significantly decreased in the renal cortices of mice with diabetes mellitus (DM) compared with the renal cortices of control mice at 6 weeks after treatment and even more significantly decreased at 12 weeks. In contrast, Egr-1 expression was significantly increased in mice with DM compared with control mice only at 12 weeks. We also found that Klotho overexpression downregulated Egr-1 expression and the (p-ERK1/2):(ERK1/2) ratio in HG-treated or TGF-β1-treated HK2 cells. Conversely, Klotho silencing upregulated Egr-1 expression and the (p-ERK1/2):(ERK1/2) ratio in HG-treated or TGF-β1-treated HK2 cells. Moreover, the effects of si-Klotho were abolished by the ERK1/2 inhibitor PD98059.ConclusionsKlotho prevents EMT during DKD progression, an effect that has been partially attributed to Egr-1 downregulation mediated by ERK1/2 signaling pathway inhibition.
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Irrcher, Isabella, and David A. Hood. "Regulation of Egr-1, SRF, and Sp1 mRNA expression in contracting skeletal muscle cells." Journal of Applied Physiology 97, no. 6 (December 2004): 2207–13. http://dx.doi.org/10.1152/japplphysiol.00388.2004.
Повний текст джерелаАнотація:
The early cellular signals associated with contractile activity initiate the activation and induction of transcription factors that regulate changes in skeletal muscle phenotype. The transcription factors Egr-1, Sp1, and serum response factor (SRF) are potentially important mediators of mitochondrial biogenesis based on the prevalence of binding sites for them in the promoter regions of genes encoding mitochondrial proteins, including PGC-1α, the important regulator of mitochondrial biogenesis. Thus, to further define a role for transcription factors at the onset of contractile activity, we examined the time-dependent alterations in Egr-1, Sp1, and SRF mRNA and the levels in electrically stimulated mouse C2C12 skeletal muscle cells. Early transient increases in Egr-1 mRNA levels within 30 min ( P < 0.05) of contractile activity led to threefold increases ( P < 0.05) in Egr-1 protein by 60 min. The increase in Egr-1 mRNA was not because of increased stability, as Egr-1 mRNA half-life after 30 min of stimulation showed only a 58% decline. Stimulation of muscle cells had no effect on Sp1 mRNA but led to progressive increases ( P < 0.05) in SRF mRNA by 30 and 60 min. This was not matched by increases in SRF protein but occurred coincident with increases ( P < 0.05) in SRF-serum response element DNA binding at 30 and 60 min as a result of SRF phosphorylation on serine-103. To assess the importance of the recovery period, 12 h of continuous contractile activity was compared with four successive 3-h bouts, with an intervening 21-h recovery period after each bout. Continuous contractile activity led to a twofold increase ( P < 0.05) in Egr-1 mRNA, no change in SRF mRNA, and a 43% decrease in Sp1 mRNA expression. The recovery period prevented the decline in Sp1 mRNA, produced a decrease in Egr-1 mRNA, and had no effect on SRF mRNA. Thus continuous and intermittent contractile activity evoked different specific transcription factor expression patterns, which may ultimately contribute to divergent qualitative, or temporal patterns of, phenotypic adaptation in muscle.
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Pamminger, Michael, Buyu Wang, Carrie M. Hall, Ryan Vojtech, and Thomas Wallner. "The impact of water injection and exhaust gas recirculation on combustion and emissions in a heavy-duty compression ignition engine operated on diesel and gasoline." International Journal of Engine Research 21, no. 8 (January 8, 2019): 1555–73. http://dx.doi.org/10.1177/1468087418815290.
Повний текст джерелаАнотація:
Steady-state experiments were conducted on a 12.4L, six-cylinder heavy-duty engine to investigate the influence of port-injected water and dilution via exhaust gas recirculation (EGR) on combustion and emissions for diesel and gasoline operation. Adding a diluent to the combustion process reduces peak combustion temperatures and can reduce the reactivity of the charge, thereby increasing the ignition-delay and, allowing for more time to premix air and fuel. Experiments spanned water/fuel mass ratios up to 140mass% and exhaust gas recirculation ratios up to 20vol% for gasoline and diesel operation with different injection strategies. Diluting the combustion process with either water or EGR resulted in a significant reduction in nitrogen oxide emissions along with a reduction in brake thermal efficiency. The sensitivity of brake thermal efficiency to water and EGR varied among the fuels and injection strategies investigated. An efficiency breakdown revealed that water injection considerably reduced the wall heat transfer; however, a substantial increase in exhaust enthalpy offset the reduction in wall heat transfer and led to a reduction in brake thermal efficiency. Regular diesel operation with main and post injection exhibited a brake thermal efficiency of 45.8% and a 0.3% reduction at a water/fuel ratio of 120%. The engine operation with gasoline, early pilot, and main injection strategy showed a brake thermal efficiency of 45.0% at 0% water/fuel ratio, and a 1.2% decrease in brake thermal efficiency for a water/fuel ratio of 140%. Using EGR as a diluent reduced the brake thermal efficiency by 0.3% for diesel operation, comparing ratios of 0% and 20% EGR. However, a higher impact on brake thermal efficiency was seen for gasoline operation with early pilot and main injection strategy, with a reduction of about 0.8% comparing 0% and 20% EGR. Dilution by means of EGR exhibited a reduction in nitrogen oxide emissions up to 15 g/kWh; water injection showed only up to 10 g/kWh reduction for the EGR rates and water/fuel ratio investigated.
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Janssen, Joëlle J. E., Bart Lagerwaard, Arie G. Nieuwenhuizen, Silvie Timmers, Vincent C. J. de Boer, and Jaap Keijer. "The Effect of a Single Bout of Exercise on Vitamin B2 Status Is Not Different between High- and Low-Fit Females." Nutrients 13, no. 11 (November 16, 2021): 4097. http://dx.doi.org/10.3390/nu13114097.
Повний текст джерелаАнотація:
High-fitness individuals have been suggested to be at risk of a poor vitamin B2 (riboflavin) status due to a potentially higher vitamin B2 demand, as measured by the erythrocyte glutathione reductase (EGR) activation coefficient (EGRAC). Longer-term exercise interventions have been shown to result in a lower vitamin B2 status, but studies are contradictory. Short-term exercise effects potentially contribute to discrepancies between studies but have only been tested in limited study populations. This study investigated if vitamin B2 status, measured by EGRAC, is affected by a single exercise bout in females who differ in fitness levels, and that represents long-term physical activity. At baseline and overnight after a 60-min cycling bout at 70% V·O2peak, EGR activity and EGRAC were measured in 31 young female adults, divided into a high-fit (V·O2peak ≥ 47 mL/kg/min, N = 15) and low-fit (V·O2peak ≤ 37 mL/kg/min, N = 16) group. A single exercise bout significantly increased EGR activity in high-fit and low-fit females (Ptime = 0.006). This response was not affected by fitness level (Ptime*group = 0.256). The effect of exercise on EGRAC was not significant (Ptime = 0.079) and not influenced by EGR activity. The exercise response of EGRAC was not significantly different between high-fit and low-fit females (Ptime*group = 0.141). Thus, a single exercise bout increased EGR activity, but did not affect EGRAC, indicating that vitamin B2 status was not affected. The exercise response on EGRAC and EGR did not differ between high-fit and low-fit females.
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Straka, Hans, James C. Beck, Angel M. Pastor, and Robert Baker. "Morphology and Physiology of the Cerebellar Vestibulolateral Lobe Pathways Linked to Oculomotor Function in the Goldfish." Journal of Neurophysiology 96, no. 4 (October 2006): 1963–80. http://dx.doi.org/10.1152/jn.00334.2006.
Повний текст джерелаАнотація:
Intracellular recording and single-cell labeling were combined to investigate the oculomotor circuitry of the goldfish cerebellar vestibulolateral lobe, consisting of the eminentia granularis (Egr) and caudal lobe. Purkinje cells exhibiting highly conserved vertebrate electrophysiological and morphological properties provide the direct output from the caudal lobe to the vestibular nuclei. Biocytin labeling of the Egr distinguished numerous hindbrain precerebellar sources that could be divided into either putative mechano- or vestibulosensitive nuclei based on cellular location and axon trajectories. Precerebellar neurons in a hindbrain nucleus, called Area II, were electrophysiologically characterized after antidromic activation from the Egr (>50% bilateral) and their morphology analyzed after intracellular biocytin labeling ( n = 28). Bipolar spindle-shaped somas ranged widely in size with comparably scaled dendritic arbors exhibiting largely closed field configuration. Area II neurons (85%) projected to the ipsilateral Egr with most (93%) sending a collateral through the cerebellar commissure to the contralateral Egr; however, 15% projected to the contralateral Egr by crossing in the ventral hindbrain. Axon terminals in the vestibular nucleus were the only collaterals within the hindbrain. Every Area II neuron received a disynaptic EPSP after contralateral horizontal canal nerve stimulation and a disynaptic IPSP, preceded by a small EPSP (>50%), after ipsilateral activation. Vestibular synaptic potentials were of varying shape/amplitude, unrelated to neuron location in the nucleus, and thus likely a correlate of somadendritic size. The exceptional separation of eye position and eye velocity signals into two separate hindbrain nuclei represents an ideal model for understanding the precerebellar projection to the vestibulocerebellum.
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Wolfe, Michael W., та Gerald B. Call. "Early Growth Response Protein 1 Binds to the Luteinizing Hormone-β Promoter and Mediates Gonadotropin-Releasing Hormone-Stimulated Gene Expression". Molecular Endocrinology 13, № 5 (1 травня 1999): 752–63. http://dx.doi.org/10.1210/mend.13.5.0276.
Повний текст джерелаАнотація:
Abstract The hypothalamic neuropeptide, GnRH, regulates the synthesis and secretion of LH from pituitary gonadotropes. Furthermore, it has been shown that the LH β-subunit gene is regulated by the transcription factors steroidogenic factor-1 (SF-1) and early growth response protein 1 (Egr1) in vitro and in vivo. The present study investigated the roles played by Egr1 and SF-1 in regulating activity of the equine LHβ-subunit promoter in the gonadotrope cell line, αT3–1, and the importance of these factors and cis-acting elements in regulation of the promoter by GnRH. All four members of the Egr family were found to induce activity of the equine promoter. The region responsible for induction by Egr was localized to the proximal 185 bp of the promoter, which contained two Egr response elements. Coexpression of Egr1 and SF-1 led to a synergistic activation of the equine (e)LHβ promoter. Mutation of any of the Egr or SF-1 response elements attenuated this synergism. Endogenous expression of Egr1 in αT3–1 cells was not detectable under basal conditions, but was rapidly induced after GnRH stimulation. Reexamination of the promoter constructs harboring mutant Egr or SF-1 sites indicated that these sites were required for GnRH induction. In fact, mutation of both Egr sites within the eLHβ promoter completely attenuated its induction by GnRH. Thus, GnRH induces expression of Egr1, which subsequently activates the eLHβ promoter. Finally, GnRH not only induced expression of Egr1, but also its corepressor, NGFI-A (Egr1) binding protein (Nab1), which can repress Egr1- induced transcription of the eLHβ promoter.
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Amorino, George P., Virginia M. Hamilton, Kristoffer Valerie, Paul Dent, Guido Lammering, and Rupert K. Schmidt-Ullrich. "Epidermal Growth Factor Receptor Dependence of Radiation-induced Transcription Factor Activation in Human Breast Carcinoma Cells." Molecular Biology of the Cell 13, no. 7 (July 2002): 2233–44. http://dx.doi.org/10.1091/mbc.01-12-0572.
Повний текст джерелаАнотація:
Ionizing radiation (1–5 Gy) activates the epidermal growth factor receptor (EGFR), a major effector of the p42/44 mitogen-activated protein kinase (MAPK) pathway. MAPK and its downstream effector, p90 ribosomal S6 kinase (p90RSK), phosphorylate transcription factors involved in cell proliferation. To establish the role of the EGFR/MAPK pathway in radiation-induced transcription factor activation, MDA-MB-231 human breast carcinoma cells were examined using specific inhibitors of signaling pathways. Gel-shift analysis revealed three different profile groups: 1) transcription factors that responded to both radiation (2 Gy) and epidermal growth factor (EGF) (CREB, Egr, Ets, and Stat3); 2) factors that responded to radiation, but not EGF (C/EBP and Stat1); and 3) those that did not respond significantly to either radiation or EGF (AP-1 and Myc). Within groups 1 and 2, a two- to fivefold maximum stimulation of binding activity was observed at 30–60 min after irradiation. Interestingly, only transcription factors that responded to EGF had radiation responses significantly inhibited by the EGFR tyrosine kinase inhibitor, AG1478; these responses were also abrogated by farnesyltransferase inhibitor (FTI) or PD98059, inhibitors of Ras and MEK1/2, respectively. Moreover, radiation-induced increases in CREB and p90RSK phosphorylation and activation of Stat3 and Egr-1 reporter constructs by radiation were all abolished by AG1478. These data demonstrate a distinct radiation response profile at the transcriptional level that is dependent on enhanced EGFR/Ras/MAPK signaling.
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Longkumer, Toshisangba, Chih-Yun Chen, Marco Biancucci, Govinal Badiger Bhaskara, and Paul E. Verslues. "Spatial differences in stoichiometry of EGR phosphatase and Microtubule-associated Stress Protein 1 control root meristem activity during drought stress." Plant Cell 34, no. 2 (December 1, 2021): 742–58. http://dx.doi.org/10.1093/plcell/koab290.
Повний текст джерелаАнотація:
Abstract During moderate severity drought and low water potential (ψw) stress, poorly understood signaling mechanisms restrict both meristem cell division and subsequent cell expansion. We found that the Arabidopsis thaliana Clade E Growth-Regulating 2 (EGR2) protein phosphatase and Microtubule-Associated Stress Protein 1 (MASP1) differed in their stoichiometry of protein accumulation across the root meristem and had opposing effects on root meristem activity at low ψw. Ectopic MASP1 or EGR expression increased or decreased, respectively, root meristem size and root elongation during low ψw stress. This, along with the ability of phosphomimic MASP1 to overcome the EGR-mediated suppression of root meristem size and the observation that ectopic EGR expression had no effect on unstressed plants, indicated that during low ψw EGR activation and attenuation of MASP1 phosphorylation in their overlapping zone of expression determines root meristem size and activity. Ectopic EGR expression also decreased root cell size at low ψw. Conversely, both the egr1-1 egr2-1 and egr1-1 egr2-1 masp1-1 mutants had similarly increased root cell size but only egr1-1egr2-1 had increased cell division. These observations demonstrated that EGRs affect meristem activity via MASP1 but affect cell expansion via other mechanisms. Interestingly, EGR2 was highly expressed in the root cortex, a cell type important for growth regulation and environmental response.
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Omar, Abdirizak, Mouadh Addassi, Volker Vahrenkamp, and Hussein Hoteit. "Co-Optimization of CO2 Storage and Enhanced Gas Recovery Using Carbonated Water and Supercritical CO2." Energies 14, no. 22 (November 10, 2021): 7495. http://dx.doi.org/10.3390/en14227495.
Повний текст джерелаАнотація:
CO2-based enhanced gas recovery (EGR) is an appealing method with the dual benefit of improving recovery from mature gas reservoirs and storing CO2 in the subsurface, thereby reducing net emissions. However, CO2 injection for EGR has the drawback of excessive mixing with the methane gas, therefore, reducing the quality of gas produced and leading to an early breakthrough of CO2. Although this issue has been identified as a major obstacle in CO2-based EGR, few strategies have been suggested to mitigate this problem. We propose a novel hybrid EGR method that involves the injection of a slug of carbonated water before beginning CO2 injection. While still ensuring CO2 storage, carbonated water hinders CO2-methane mixing and reduces CO2 mobility, therefore delaying breakthrough. We use reservoir simulation to assess the feasibility and benefit of the proposed method. Through a structured design of experiments (DoE) framework, we perform sensitivity analysis, uncertainty assessment, and optimization to identify the ideal operation and transition conditions. Results show that the proposed method only requires a small amount of carbonated water injected up to 3% pore volumes. This EGR scheme is mainly influenced by the heterogeneity of the reservoir, slug volume injected, and production rates. Through Monte Carlo simulations, we demonstrate that high recovery factors and storage ratios can be achieved while keeping recycled CO2 ratios low.
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Saravanan, P., M. Ettappan, Nallapaneni Manoj Kumar, and N. Elangkeeran. "Exhaust Gas Recirculation on a Nano-Coated Combustion Chamber of a Diesel Engine Fueled with Waste Plastic Oil." Sustainability 14, no. 3 (January 20, 2022): 1148. http://dx.doi.org/10.3390/su14031148.
Повний текст джерелаАнотація:
Managing waste plastic is becoming a severe challenge. The industry and researchers have been looking at various opportunities in line with circular economy principles for effective plastic waste management. In that context, plastic waste valorization to oil as a substitute to fossil fuel has gained recent attention. In the literature, there exist few studies showing the use of oil derived from waste plastics in blends with other conventional fuels in compression ignition (CI) engines; however, studies on CI engines that use 100% waste-derived fuels are limited. Additionally, the exhaust gas recirculation (EGR) concepts and the use of nano-coated chambers (like pistons, valves and cylinders heads) have been gaining interest purely from the engine performance enhancement perspective in recent years. Therefore, this study investigates engine performance by combining exhaust gas from the EGR technique and waste plastic oil (WPO) as inputs, followed by thermal coatings in the CI engine chambers for performance enhancement. The experimental setup of the engine is developed, and the engine’s piston, valve and cylinder heads are coated with Al2O3-SiO4 material. The CI engine’s energy, emission, and combustion characteristics are tested, followed by a scenario analysis compared with diesel-only fuel. The tested scenarios include a WPO + Al2O3-SiO4, WPO + Al2O3-SiO4 + 10% EGR, and WPO + Al2O3-SiO4 + 20% EGR. The results show that the piston crown’s thermal coating increased the combustion performance. Significant impacts on the carbon monoxide, hydrocarbons, and smoke characteristics are observed for different %EGR rates. The results also showed that the cooled EGR engine has decreased nitric oxide emissions. Overall, the results show that WPO combined with exhaust gas could be a potential fuel for future CI engines.
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REISER, O. A. Christian, Thomas LANZ, Fred HOFMANN, Gerhard HOFER, D. Harald RUPPRECHT, and Margarete GOPPELT-STRUEBE. "Lysophosphatidic acid-mediated signal-transduction pathways involved in the induction of the early-response genes prostaglandin G/H synthase-2 and Egr-1: a critical role for the mitogen-activated protein kinase p38 and for Rho proteins." Biochemical Journal 330, no. 3 (March 15, 1998): 1107–14. http://dx.doi.org/10.1042/bj3301107.
Повний текст джерелаАнотація:
During inflammatory processes of the kidney, lesions of the glomerulus lead to aggregation of thrombocytes and infiltration of macrophages, which can release bioactive mediators. One of these important signalling molecules is lysophosphatidic acid (LPA). Incubation of rat mesangial cells with LPA induced mRNA and protein expression of the early-response genes pghs-2 (for prostaglandin G/H synthase-2/cyclo-oxygenase-2) and egr-1. As shown by antisense experiments, induction of egr-1 was related to the strong mitogenic effect of LPA. LPA-mediated gene expression was inhibited by pertussis toxin, indicating coupling to G-proteins of the Gi family. Specific inhibition of proteins of the small G-protein subfamily Rho with toxin B from Clostridium difficile led to changes in mesangial cell morphology without induction of apoptosis. LPA-mediated expression of pghs-2 and egr-1 was reduced to base-line levels by toxin B, indicating a role for Rho proteins in LPA-mediated gene induction. Of the two mitogen-activated protein kinase (MAPK) pathways investigated, the MAPK kinase-extracellular signal-regulated kinase pathway was involved in the induction of both pghs-2 and egr-1 mRNA expression, as shown by the inhibitory effect of PD98059. Activation of the MAPK p38, however, was only related to pghs-2 expression, whereas egr-1 expression was not affected by treatment of mesangial cells with the specific inhibitor SB203580. Taken together our data provide evidence that LPA-mediated activation of MAPK kinase and Rho proteins leads to the induction of the functionally distinct early-response genes pghs-2 and egr-1, whereas activation of MAPK p38 revealed considerable differences between the regulation of these two genes.
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Lin, Tzu-Keng, and Bieng-Zih Hsieh. "Prevention of Seabed Subsidence of Class-1 Gas Hydrate Deposits via CO2-EGR: A Numerical Study with Coupled Geomechanics-Hydrate Reaction-Multiphase Fluid Flow Model." Energies 13, no. 7 (April 1, 2020): 1579. http://dx.doi.org/10.3390/en13071579.
Повний текст джерелаАнотація:
The geomechanics effects and seabed subsidence are critical issues that should be considered in the development of a hydrate reservoir. The purpose of this study is to couple the geomechanics, hydrate reaction, and multiphase fluid flow modules to investigate the feasibility of CO2 enhanced gas recovery (CO2-EGR) of a Class-1 hydrate deposit by observing the formation deformation, and the seabed subsidence. The production methods of depressurization and CO2-EGR are modeled, respectively. The production behaviors and seabed subsidence of different production methods are compared. The positive influence on the gas recovery for a Class-1 hydrate deposit via CO2-EGR is observed. The calculations of seabed subsidence showed a significant improvement can be achieved when CO2-EGR was used. The subsidence is only 6.8% of that from the pure depressurization in the case of a pressure drop of 30%. The effects of production pressure drop and production gas rate are investigated. The association between the gas production and the pressure drop of the well is different from the cases of pure depressurization and the CO2-EGR. The appropriate initial time for the CO2 injection is tested. Slighter seabed subsidence is observed when the CO2 injection is initiated earlier. The case of different injection pressure control showed that a lower injection pressure leads to a heavier seabed subsidence. A higher CO2 fraction allowed in the produced gas stream results in a higher cumulative gas production, but there is no significant impact on the seabed subsidence.
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FU, Mingui, Jifeng ZHANG, Yimin LIN, Xiaojun ZHU, Luning ZHAO, Mushtaq AHMAD, Markus U. EHRENGRUBER, and Yuqing E. CHEN. "Early stimulation and late inhibition of peroxisome proliferator-activated receptor gamma (PPARgamma) gene expression by transforming growth factor beta in human aortic smooth muscle cells: role of early growth-response factor-1 (Egr-1), activator protein 1 (AP1) and Smads." Biochemical Journal 370, no. 3 (March 15, 2003): 1019–25. http://dx.doi.org/10.1042/bj20021503.
Повний текст джерелаАнотація:
Transforming growth factor β (TGFβ) and peroxisome proliferator-activated receptor γ (PPARγ) play major roles in the development of vascular diseases. It has been documented that PPARγ activation inhibits the TGFβ signal pathway in vascular smooth muscle cells (VSMC). Here we examined whether TGFβ can regulate PPARγ expression. Northern blot analyses revealed that both TGFβ1 and 2 exert a biphasic effect (early stimulation and late repression) on PPARγ gene expression in VSMC. TGFβ rapidly and transiently induced early growth-response factor-1 (Egr-1) expression through the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK1)/ERK-mediated pathway. Inhibition of MEK1/ERK by PD98059 not only abrogated the induction of Egr-1 but also abolished the rapid and transient induction of PPARγ by TGFβ. Furthermore, overexpression of NAB2, a repressor of Egr-1 activation, also blocked the induction of PPARγ by TGFβ in VSMC, suggesting that Egr-1 mediates the rapid and transient induction of PPARγ by TGFβ. With regard to the TGFβ repression of PPARγ expression, activator protein 1 (AP1) and Smad3/4 dramatically inhibited the PPARγ promoter activity in transient-transfection studies. In contrast, adenovirus-mediated overexpression of a dominant-negative form of c-Jun partially rescued the TGFβ-induced PPARγ repression in VSMC. Taken together, our data demonstrate that Egr-1, AP1 and Smad are part components of the TGFβ signal transduction pathway that regulates PPARγ expression.
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Wang, Li, Zhaoming Huang, Wang Tao, Kai Shen, and Weiguo Chen. "Economy and emission characteristics of the optimal dilution strategy in lean combustion based on GDI gasoline engine equipped with prechamber." Advances in Mechanical Engineering 13, no. 12 (December 2021): 168781402110381. http://dx.doi.org/10.1177/16878140211038100.
Повний текст джерелаАнотація:
EGR and excess-air dilution have been investigated in a 1.5 L four cylinders gasoline direct injection (GDI) turbocharged engine equipped with prechamber. The influences of the two different dilution technologies on the engine performance are explored. The results show that at 2400 rpm and 12 bar, EGR dilution can adopt more aggressive ignition advanced angle to achieve optimal combustion phasing. However, excess-air dilution has greater fuel economy than that of EGR dilution owing to larger in-cylinder polytropic exponent. As for prechamber, when dilution ratio is greater than 37.1%, the combustion phase is advanced, resulting in fuel economy improving. Meanwhile, only when the dilution ratio is under 36.2%, the HC emissions of excess-air dilution are lower than the original engine. With the increase of dilution ratio, the CO emissions decrease continuously. The NOX emissions of both dilution technologies are 11% of those of the original engine. Excess-air dilution has better fuel economy and very low CO emissions. EGR dilution can effectively reduce NOX emissions, but increase HC emissions. Compared with spark plug ignition, the pre chamber ignition has lower HC, CO emissions, and higher NO emissions. At part load, the pre-chamber ignition reduces NOX emissions to 49 ppm.
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Hoke, Kim L., Michael J. Ryan, and Walter Wilczynski. "Candidate neural locus for sex differences in reproductive decisions." Biology Letters 4, no. 5 (July 8, 2008): 518–21. http://dx.doi.org/10.1098/rsbl.2008.0192.
Повний текст джерелаАнотація:
Sexual selection and signal detection theories predict that females should be selective in their responses to mating signals in mate choice, while the response of males to signals in male competition should be less selective. The neural processes underlying this behavioural sex difference remain obscure. Differences in behavioural selectivity could result from differences in how sensitive sensory systems are to mating signals, distinct thresholds in motor areas regulating behaviour, or sex differences in selectivity at a gateway relaying sensory information to motor systems. We tested these hypotheses in frogs using the expression of egr-1 to quantify the neural responses of each sex to mating signals. We found that egr-1 expression in a midbrain auditory region was elevated in males in response to both conspecific and heterospecific calls, whereas in females, egr-1 induction occurred only in response to conspecific signals. This differential neural selectivity mirrored the sex differences in behavioural responsiveness to these stimuli. By contrast, egr-1 expression in lower brainstem auditory centres was not different in males and females. Our results support a model in which sex differences in behavioural selectivity arise from sex differences in the neural selectivity in midbrain areas relaying sensory information to the forebrain.
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Racke, Frederick, Cordelle Tanega, Karen Zeller, Anna Janiak, Sema Rosinbum, Chi Dang, and Michael McDevitt. "Identification of Signaling-Induced Transcription Pathway Determinants that Influence Erythro-Megakaryocytic Lineage Commitment." Blood 104, no. 11 (November 16, 2004): 1607. http://dx.doi.org/10.1182/blood.v104.11.1607.1607.
Повний текст джерелаАнотація:
Abstract Erythroid and megakaryocytic cells are derived from a common precursor and share many of the same transcriptional regulators. We and others have demonstrated a critical role for sustained activation of extracellular-related (ERK) kinase in PKC-induced megakaryocytic differentiation of K562 cells. However, the transcriptional mechanisms underlying this process are largely unknown. Our prior studies have focused on late stage megakaryocyte specific genes such as glycoprotein IIb/CD41. In order to understand the early transcriptional events regulating this process, we have begun to examine the mechanisms regulating the expression of CD9, a tetraspanin molecule that is currently the earliest identified marker of megakaryocyte differentiation. The PKC agonist ingenol 3,20 dibenzoate (IDB) rapidly induced CD9 expression in both K562 cells as well as in primary human CD34+ progenitor cells, much earlier than the kinetics for CD41 induction. CD9 induction by PKC was dependent on ERK activation. Recently, it has been shown that immediate early gene expression, including the transcription factor Egr-1, is highly sensitive to the duration and amplitude of ERK activity. Egr-1 has been previously implicated in the regulation of hematopoietic lineage commitment. PKC/ERK activation rapidly and strongly induced Egr-1 expression, which remained elevated for up to 96 hrs after IDB treatment of K562 cells. Egr-1 induction was closely followed by CD9 induction, suggesting a causal relationship. This was supported by chromatin immunoprecipitation (ChIP) analysis, which showed strong recruitment of Egr-1 to the CD9 promoter during PKC/ERK-induced differentiation. KLF5, a known downstream target of Egr-1, was identified as an additional target of PKC/ERK signaling during megakaryocytic differentiation. KLF5, a novel GC binding factor, was found to be expressed in primary megakaryocytes and not in erythroid cells. KLF5 expression was induced by IDB treatment, and ChIP analysis showed that Egr-1 was recruited to the KLF5 promoter during PKC/ERK-induced differentiation. KLF5 has been shown previously to regulate known megakaryocyte-expressed genes PDGF-A and TGF-β expression in vascular smooth muscle, but a role in megakaryocyte gene expression has not been previously suggested. To better understand the regulation of Egr-1 in erythromegakaryocytic differentiation, Nab2, a natural co-repressor of Egr-1 was also evaluated. Control K562 cells strongly expressed c-myc and Nab2. ChIP studies show that c-myc binds to the Nab2 promoter in control K562 cells and both c-myc and Nab2 expression strongly declined during the first 24 hours after PKC stimulation. Enforced expression of Nab2 not only blocked CD9 induction by IDB, but also induced marked hemoglobinization of K562 cells. Taken together, these findings suggest a novel and critical role for the balance in Egr-1/Nab2 activity as a regulatory mechanism in erythroid versus megakaryocytic differentiation pathways.
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Han, Peng, Hilda Guerrero-Netro, Anthony Estienne, Binyun Cao, and Christopher A. Price. "Regulation and action of early growth response 1 in bovine granulosa cells." Reproduction 154, no. 4 (October 2017): 547–57. http://dx.doi.org/10.1530/rep-17-0243.
Повний текст джерелаАнотація:
Fibroblast growth factors (FGF) modify cell proliferation and differentiation through receptor tyrosine kinases, which stimulate the expression of transcription factors including members of the early growth response (EGR) family. In ovarian granulosa cells, most FGFs activate typical response genes, although the role of EGR proteins has not been described. In the present study, we determined the regulation of EGR mRNA by FGFs and explored the role of EGR1 in the regulation of FGF-response genes. Addition of FGF1, FGF2, FGF4 or FGF8b increased EGR1 and EGR3 mRNA levels, whereas FGF18 increased only EGR1 mRNA abundance. No mRNA encoding EGR2 or EGR4 was detected. Overexpression of EGR1 increased EGR3 mRNA levels as well as the FGF-response genes SPRY2, NR4A1 and FOSL1 and also increased the phosphorylation of MAPK3/1. Knockdown of EGR3 did not alter the ability of FGF8b to stimulate SPRY2 mRNA levels. These data demonstrate the regulation of EGR1 and EGR3 mRNA abundance by FGFs in granulosa cells and suggest that EGR1 is likely an upstream component of FGF signaling in granulosa cells.
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Besson, Philippe, Luise J. Fischer, Sebastian Schemm, and Michael Sprenger. "A global analysis of the dry-dynamic forcing during cyclone growth and propagation." Weather and Climate Dynamics 2, no. 4 (October 27, 2021): 991–1009. http://dx.doi.org/10.5194/wcd-2-991-2021.
Повний текст джерелаАнотація:
Abstract. Mechanisms driving the intensification and propagation direction of extratropical cyclones are an active field of research. Dry-dynamic forcing factors have been established as fundamental drivers of the deepening and propagation of extratropical cyclones, but their climatological interplay, geographical distribution, and relatedness to the observed cyclone deepening and propagation direction remain unknown. This study considers two key dry-dynamic forcing factors, the Eady growth rate (EGR) and the upper-level induced quasi-geostrophic lifting (QGω), and relates them to the surface deepening rates and the propagation direction during the cyclones' growth phase. To this aim, a feature-based cyclone tracking is used, and the forcing environment is climatologically analysed based on ERA-Interim data. The interplay is visualized by means of a forcing histogram, which allows one to identify different combinations of EGR and QGω and their combined influence on the cyclone deepening (12 h sea-level pressure change) and propagation direction. The key results of the study are as follows. (i) The geographical locations of four different forcing categories, corresponding to cyclone growth in environments characterized by low QGω and low EGR (Q↓E↓), low QGω but high EGR (Q↓E↑), high QGω and low EGR (Q↑E↓), and high QGω and EGR (Q↑E↑), display distinct hot spots with only mild overlaps. For instance, cyclone growth in a Q↑E↑ forcing environment is found in the entrance regions of the North Pacific and Atlantic storm tracks. Category Q↓E↑ is typically found over continental North America, along the southern tip of Greenland, over parts of East Asia, and over the western North Pacific. In contrast, category Q↑E↓ dominates the subtropics. (ii) The four categories are associated with different stages of the cyclones' growth phase: large EGR forcing typically occurs earlier, during the growth phase at genesis, while large QGω forcing attains its maximum amplitude later towards maturity. (iii) Poleward cyclone propagation is strongest over the North Pacific and North Atlantic, and the poleward propagation tendency becomes more pronounced as the deepening rate gets larger. Zonal, or even equatorward, propagation on the other hand is characteristic for cyclones developing in the lee of mountain ranges, e.g. to the lee of the Rocky Mountains. The exact location of maximum QGω forcing relative to the surface cyclone centre is found to be a good indicator for the direction of propagation, while no information on the propagation direction can be inferred from the EGR. Ultimately, the strength of the poleward propagation and of the deepening is inherently connected to the two dry-dynamic forcing factors, which allow cyclone development in distinct environments to effectively be identified.
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Mohammed, Nuhu, Abubakar Jibrin Abbas, Godpower C. Enyi, Salihu M. Suleiman, Donatus E. Edem, and Muhammad Kabir Abba. "Alternating N2 gas injection as a potential technique for enhanced gas recovery and CO2 storage in consolidated rocks: an experimental study." Journal of Petroleum Exploration and Production Technology 10, no. 8 (June 20, 2020): 3883–903. http://dx.doi.org/10.1007/s13202-020-00935-z.
Повний текст джерелаАнотація:
Abstract The promotion of enhanced gas recovery (EGR) and CO2 storage is still shrouded in contention and is not well accepted, due to the excessive in situ CO2 mixing with the nascent natural gas. This adulterates the recovered CH4 and thus results in a high sweetening process cost thereby making the technique impractical. This has not only limited the field application of EGR in actual projects to a few trails but renders it uneconomical. This study aims to present, experimentally, alternating N2 injection as a potential technique for EGR and CO2 storage in sandstone rock cores. A laboratory core flooding experiment was carried out to simulate a detailed process of unsteady-state methane (CH4) displacement using Bandera grey core plug. This was carried out at 40 °C, 1500 psig, and 0.4 ml/min injection rate by alternative injection of N2 and CO2 in succession designed to suit the application based on optimum operating conditions. The results show that both CO2 storage capacity and CH4 recovery improved significantly when gas alternating gas (GAG) injection was considered. The best results were observed at lower N2 cushion volumes (1 and 2 PV). Therefore, the GAG injection method with N2 as cushion gas can potentially increase both CO2 storage and CH4 recovery of the gas reservoir. This technique if employed will assert the current position and provide vital information for further researches aimed at promoting environmental sustainability and economic viability of the EGR and CO2 sequestration processes.
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Silva, Fagner Taiano Dos Santos, Fabiane Pereira Machado Dias, Poliana Dos Santos de Farias, Flávia Melo Moreira, Ludmila De Oliveira De Amorim, Juan Manuel Anda Rocabado, Felipe Torres Sampaio, and Júlio César Azevedo Nóbrega. "Soil Physical Attributes and Organic Carbon in a Cohesive Yellow Latosol (Oxisol) Under Different Soil Management Systems in the Coastal Plains of Bahia, Brazil." Journal of Agricultural Science 10, no. 6 (May 6, 2018): 272. http://dx.doi.org/10.5539/jas.v10n6p272.
Повний текст джерелаАнотація:
Although soil physical attributes are determining factors of soil quality and for root development of crops, they are often neglected when dealing with soil management, which refers only to fertility. The objective of this work was to evaluate soil physical characteristics, organic carbon content and carbon stock levels in yellow Latosol cohesive distrophic coastal plains of Bahia, Brazil, where different soil management systems were implemented. Soil texture, water dispersible clay, flocculation index, soil density and porosity, liquid limit, plastic limit, plasticity index, stability of aggregates, organic carbon content and resistance to penetration were evaluated from soil samples collected in the 40 cm-top soil. The different soil plot covers consisted of (i) Eucalyptus with grasses (EGR), (ii) Eucalyptus with spontaneous vegetation (EVE), (iii) fallow (POU), (iv) pasture (PAS), and (v) native forest (MN). It was found that EVE and MN contributed to greater stability of larger aggregates in the 20-40 cm-soil layer compared to EGR, PAS and POU. The high organic matter contents of soils of the cultivated plots (EVE and EGR) increased the limits of consistency. Soil management systems with Eucalyptus and pasture contributed to accelerate the oxidation process and the loss of C.
40
Yun, Seongseok, Nicole D. Vincelette, Katherine L. B. Knorr, Luciana L. Almada, Paula A. Schneider, Kevin L. Peterson, Karen S. Flatten, et al. "mTOR Dual Inhibitor Induced Cytotoxicity Depends on 4EBP1/c-Myc/Puma and NFkB/Egr-1/Bim Pathways in Human Lymphoid Malignancies." Blood 126, no. 23 (December 3, 2015): 3705. http://dx.doi.org/10.1182/blood.v126.23.3705.3705.
Повний текст джерелаАнотація:
Abstract The mammalian target of rapamycin (mTOR), a kinase that regulates proliferation and apoptosis, has been extensively evaluated as a therapeutic target in hematologic malignancies. Rapamycin analogues, which partially inhibit mTOR complex 1 (mTORC1), showed limited anti-tumor activity due to feedback mechanisms involving mTORC2 and incomplete inhibition of mTORC1. Thus, attention has turned to agents targeting both mTOR complexes by binding the mTOR kinase domain. The purpose of this study was to delineate the mechanisms of mTOR dual inhibitor induced apoptosis in human neoplastic lymphoid cells in vitro. MTS assays and propidium iodide staining followed by flow cytometry for subdiploid populations demonstrated that OSI-027 and MLN0128 inhibited cell proliferation and induced apoptosis in a wide range of lymphoid cell lines including Jurkat, Nalm-6, Molt-4, and SeAX. Raptor and Rictor knockdown in Jurkat and Nalm-6 increased cell death, suggesting both mTOR complexes play a role in apoptosis. 4EBP1 phosphorylation was inhibited by mTOR dual inhibitors, but not by rapamycin. Expression of 4EBP1 T37A/T46A and 4EBP1 T37A/T46A/S65A/T70A, which mimic dephosphorylated 4EBP1, increased Puma mRNA and protein levels as well as apoptosis. Moreover, 4EBP1 knockdown abrogated mTOR dual inhibitor induced Puma upregulation and cell death, further supporting the role of 4EBP1 dephosphorylation in mTORC1 dependent apoptosis. In accord with the known dependence of c-Myc translation on the eIF4E/eIF4G complex, we also observed c-Myc downregulation after treatment with OSI-027, MLN0128 and 4EGI-1, but not rapamycin. Puma induction mirrored c-Myc downregulation under a variety of conditions, including expression of nonphosphorylatable 4EBP1 in parental Jurkat cells or wt 4EBP1 in 4EBP1 deficient cells. Furthermore, c-Myc knockdown induced Puma mRNA and protein as well as increased apoptosis. Collectively, these results support a model in which mTORC1 inhibition, acting through 4EBP1, induces Puma upregulation and apoptosis through c-Myc downregulation. In order to assess the parallel mTORC2-dependent Bim-mediated apoptotic mechanism, we utilized reporter assays and RNAseq experiments. OSI-027-induced Bim promoter activity decreased markedly when the nucleotides -29 to -18 were removed, suggesting that this response element is critical for OSI-027-induced promoter activation. In silico analysis identified eight transcription factors, including SP1, Egr-1, and Myb, that potentially bind this 12-bp region. In RNAseq experiments, we detected a 9-fold increase in Egr-1. Egr-1 upregulation was confirmed by qRT-PCR and immunoblotting after dual inhibitors treatment or Rictor knockdown. Moreover, dominant negative Egr-1 or Egr-1 knockdown diminished dual inhibitor-induced Bim promoter activation and Bim upregulation. Chromatin immunoprecipitation assays demonstrated that OSI-027 enhances binding of Egr-1 to a region of the Bim promoter including bp -29 to -18, further confirming that Egr-1 functions as a direct transcriptional activator for Bim upon mTOR dual inhibitor treatment. NFκB is a known transcription factor for Egr-1 and we observed increased p65 in the nucleus and increased NFκB transcriptional activity after dual inhibitor treatment. Overexpression of S32A/S36A IκB impaired the ability of dual inhibitors to induce NFκB transcriptional activation, Egr-1 mRNA and protein, Bim promoter activation and Bim mRNA and protein upregulation. Collectively, these results suggest that mTORC2 inhibition induces Bim upregulation and apoptosis through NFκB and Egr-1 transactivation. When fresh clinical ALL isolates were exposed to OSI-027 or MLN0128 ex vivo, inhibition of 4EBP1 phosphorylation along with upregulation of Egr-1 and Bim and/or c-Myc downregulation accompanied by Puma induction occurred, indicating that the pathways identified in ALL cell lines can also potentially be engaged in clinical ALLs. These observations not only provide new insight into the survival roles of mTOR in lymphoid malignancies, but also identify alterations that potentially modulate the action of mTOR dual inhibitors. Disclosures No relevant conflicts of interest to declare.
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AOYAGI, Yuzo. "Improvement of BSFC and effective NOx and PM reduction by high EGR rates in heavy duty diesel engine." Combustion Engines 171, no. 4 (November 1, 2017): 4–10. http://dx.doi.org/10.19206/ce-2017-401.
Повний текст джерелаАнотація:
The test engine was a turbocharged 10.5L engine with an intercooler. A performance target was set at a rated power of 300 kW (BMEP = 1.7 MPa) and peak torque of 1842 Nm (BMEP = 2.2 MPa). Emission targets were set at a level of near future and stringent regulation standards in Japan. The engine was equipped with new technologies such as a high pressure common rail system, FCD piston, a high pressure ratio VGT and an aftertreatment system. The high and low pressure loop EGR system was installed and this system with a VGT had a high performance and could increase an EGR rate in order to reduce BSNOx while maintaining the satisfied BSFC and PM performance simultaneously not only in the steady state condition but also in the transient condition.
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Murtaza, Ghulam, Aamir I. Bhatti, and Yasir A. Butt. "Super twisting controller-based unified FDI and FTC scheme for air path of diesel engine using the certainty equivalence principle." Proceedings of the Institution of Mechanical Engineers, Part D: Journal of Automobile Engineering 232, no. 12 (October 24, 2017): 1623–33. http://dx.doi.org/10.1177/0954407017732860.
Повний текст джерелаАнотація:
This paper proposes a combination of higher order sliding mode and adaptive control for unified fault detection and isolation and fault tolerant control (FTC) of the air path of a diesel engine. Current diesel engines are equipped with features such as variable geometry turbochargers (VGT) and exhaust gas recirculation (EGR) for exhaust emission control. Since EGR and VGT systems are present in the exhaust channel, they are strongly coupled and are prone to both structured as well as unstructured faults. The proposed controller detects and estimates the structured faults by means of adaptation laws, designed by making use of the certainty equivalence principle. Fault effects are compensated by repositioning the actuators. This allows relaxation of the boundedness condition of the super twisting algorithm, as sliding mode controller gains are required to dominate the unstructured parts only, which consequently reduces chattering. A nonlinear multi-input multi-output reduced state control-oriented model has been employed for working out the FTC strategy for EGR and VGT actuators. The stability of the overall system has been analysed using the Lyapunov stability criterion. Faults and proposed controllers are simulated using a fully validated industrial scale diesel engine model to establish the effectiveness of the algorithm.
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Pulver-Kaste, Renee A., Christy A. Barlow, Jeffery Bond, Anjanette Watson, Paul L. Penar, Bruce Tranmer, and Karen M. Lounsbury. "Ca2+ source-dependent transcription of CRE-containing genes in vascular smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (July 2006): H97—H105. http://dx.doi.org/10.1152/ajpheart.00753.2005.
Повний текст джерелаАнотація:
Altered Ca2+ handling has immediate physiological and long-term genomic effects on vascular smooth muscle function. Previously we showed that Ca2+ entry through voltage-dependent Ca2+ channels (VDCCs) or store-operated Ca2+ channels (SOCCs) results in phosphorylation of the Ca2+/cAMP response element (CRE)-binding protein in cerebral arteries. Here, oligonucleotide array analysis was used to determine gene transcription profiles resulting from these two Ca2+ entry pathways in human cerebrovascular smooth muscle cell cultures. Results were confirmed and expanded using quantitative RT-PCR, Western blot, and immunofluorescence. A distinct, yet overlapping, set of CRE-regulated genes was induced by VDCC activation using K+ membrane depolarization vs. SOCC activation by thapsigargin (TG). Membrane depolarization selectively induced a sustained increase in early growth response-1 (Egr-1) mRNA and protein, which were inhibited by the VDCC blocker nimodipine and the SOCC inhibitor 2-aminoethoxydiphenylborate (2-APB). TG selectively induced a sustained increase in MAPK phosphatase-1 (MKP-1) mRNA and protein, and these effects were decreased by 2-APB, but not by nimodipine. The physiological agonist ANG II also stimulated expression of Egr-1 and MKP-1. Coadministration of 2-APB prevented expression of Egr-1 and MKP-1, whereas nimodipine blocked only Egr-1 expression. TG and ANG II induced phosphorylation of ERK, which was sensitive to 2-APB and was selectively required for CRE-binding protein phosphorylation. Our findings thus indicate that Ca2+ entry through VDCCs and store-operated Ca2+ entry can differentially regulate CRE-containing genes in vascular smooth muscle and also imply that agonist-induced signals involved in modulation of gene transcription can be controlled by multiple sources of Ca2+.
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Noble, Peter J. M., Geraint Wilde, Michael R. H. White, Steven R. Pennington, Graham J. Dockray, and Andrea Varro. "Stimulation of gastrin-CCKB receptor promotes migration of gastric AGS cells via multiple paracrine pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 1 (January 1, 2003): G75—G84. http://dx.doi.org/10.1152/ajpgi.00300.2002.
Повний текст джерелаАнотація:
Responses to G protein-coupled receptor stimulation may be mediated by paracrine factors. We have developed a coculture system to study paracrine regulation of migration of gastric epithelial (AGS) cells after stimulation of gastrin-CCKBreceptors. In cells expressing this receptor, G-17 stimulated migration by activation of protein kinase C. However, G-17 also stimulated the migration of cells expressing green fluorescent protein, but not the receptor, when they were cocultured with receptor-expressing cells consistent with activation of paracrine signals. The use of various pharmacological inhibitors indicated that gastrin stimulated migration via activation of the EGF receptor (EGR-R), the erbB-2 receptor tyrosine kinase, and the MAP kinase pathway. However, gastrin also released fibroblast growth factor (FGF)-1, and migration was inhibited by the FGF receptor tyrosine kinase inhibitor SU-5402. Flow cytometry indicated that in both cell types, gastrin increased MAP kinase via activation of EGF-R but not FGF-R1 or erbB-2. We conclude that gastrin-CCKB receptors stimulate epithelial cell migration partly via paracrine mechanisms; transactivation of EGF-R is only one component of the paracrine pathway.
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Kenzel, Sybille, Sandra Santos-Sierra, Sachin D. Deshmukh, Inga Moeller, Bilge Ergin, Katherine A. Fitzgerald, Egil Lien, Shizuo Akira, Douglas T. Golenbock, and Philipp Henneke. "Role of p38 and Early Growth Response Factor 1 in the Macrophage Response to Group B Streptococcus." Infection and Immunity 77, no. 6 (March 30, 2009): 2474–81. http://dx.doi.org/10.1128/iai.01343-08.
Повний текст джерелаАнотація:
ABSTRACT Group B streptococcus (GBS), the most frequent single isolate in neonatal sepsis and meningitis, potently activates inflammatory macrophage genes via myeloid differentiation antigen 88 (MyD88). However, events parallel to and downstream of MyD88 that instruct the macrophage response are incompletely understood. In this study, we found that only MyD88, not the Toll-like receptor (TLR) adapter proteins MAL/TIRAP, TRIF, and TRAM, essentially mediates the cytokine (tumor necrosis factor [TNF] and interleukin-6) and chemokine (RANTES) responses to whole GBS organisms, although MAL, TRIF, and TRAM have been shown to mediate the responses to substructures in other gram-positive and gram-negative bacteria. GBS-induced, MyD88-dependent phosphorylation of the mitogen-activated protein kinase p38 activated the transcription factor AP-1 and early growth response factor 1 (Egr-1) but not NF-κB. Furthermore, phosphorylation of Ets-like molecule 1 (Elk-1) was mediated by p38. However, in contrast to Egr-1 and AP-1, Elk-1 was dispensable for transcriptional activation of TNF by GBS organisms. Studies of macrophages from Elk-1-deficient mice revealed that Elk-1 was furthermore nonessential for the TNF responses to purified TLR2 and TLR4 agonists, which was in notable contrast to what was revealed in studies employing in vitro expression systems. In conclusion, MyD88, p38, and Egr-1, but not Elk-1, essentially mediate the inflammatory cytokine response to GBS organisms.
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Chen, Ye, Elizabeth Montcalm-Smith, Christine Schlaerth, Charles Auker, and Richard M. McCarron. "Acclimation to decompression: stress and cytokine gene expression in rat lungs." Journal of Applied Physiology 111, no. 4 (October 2011): 1007–13. http://dx.doi.org/10.1152/japplphysiol.01402.2010.
Повний текст джерелаАнотація:
Previous studies demonstrated that animals exposed to repeated compression-decompression stress acclimated (i.e., developed reduced susceptibility) to rapid decompression. This study endeavored to characterize inflammatory and stress-related gene expression and signal transduction associated with acclimation to rapid decompression. Rats were divided into four groups: 1) control-sham: pressure naïve rats; 2) acclimation-sham: nine acclimation dives [70 feet seawater (fsw), 30 min]; 3) control-dive: test dive only (175 fsw, 60 min); and 4) acclimation-dive: nine acclimation dives and a test dive. After the test dive, rats were observed for decompression sickness (DCS). Expression of 13 inflammatory and stress-related genes and Akt (or PKB, a serine/threonine protein kinase) and MAPK phosphorylation of lung tissue were examined. The expression of immediate early gene/transcription factor early growth response gene 1 (Egr-1) was observed in both control and acclimation animals with DCS but not in animals without DCS. Increased Egr-1 in control-dive animals with DCS was significantly greater than in acclimation-dive animals with DCS. TNF-α, IL-1β, IL-6, and IL-10 were significantly elevated in control-DCS animals. Acclimation-DCS animals had increased TNF-α, but there was no change in IL-1β, IL-6, and IL-10. High levels of Akt phosphorylation were observed in lungs of acclimation-sham, acclimation-dive, and control-dive animals; phosphorylated ERK1/2 was only observed in animals with DCS. This study suggests that activation of ERK1/2 and upregulation of Egr-1 and its target cytokine genes by rapid decompression may play a role in the initiation and progression of DCS. It may be that the downregulated expression of these genes in animals with DCS is associated with previous exposure to repeated compression-decompression cycles. This study represents an initial step toward understanding the molecular mechanisms associated with acclimation to decompression.
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Saadane, Nacéra, Lesley Alpert, and Lorraine E. Chalifour. "TAFII250, Egr-1, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 3 (March 1, 1999): H803—H814. http://dx.doi.org/10.1152/ajpheart.1999.276.3.h803.
Повний текст джерелаАнотація:
Differential display identified that gene fragment HA220 homologous to the transcriptional activator factor II 250 (TAFII250) gene, or CCG1, was increased in hypertrophied rodent heart. To determine whether TAFII250 gene expression is modified after cardiac damage, we measured TAFII250 expression in vivo in mouse hearts after injection of the cardiotoxic agent doxorubicin (DXR) and in vitro in DXR-treated isolated rat neonatal cardiomyocytes. In vivo atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), Egr-1, and TAFII250 expression increased with dose and time after a single DXR injection, but only ANF and β-MHC expression were increased after multiple injections. After DXR treatment of neonatal cardiomyocytes we found decreased ANF, α-MHC, Egr-1, and TAFII250 expression. Expression of the TAFII250-regulated genes, the D-type cyclins, was increased after a single injection in adult mice and was decreased in DXR-treated cardiomyocytes. Thus expression of Erg-1, TAFII250, and the D-type cyclins is modulated after cardiotoxic damage in adult and neonatal heart.
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Wu, Yanna, Shanshan Ma, Yong Xia, Yangpeng Lu, Shiyin Xiao, Yali Cao, Sidian Zhuang, et al. "Loss of GCN5 leads to increased neuronal apoptosis by upregulating E2F1- and Egr-1-dependent BH3-only protein Bim." Cell Death & Disease 8, no. 1 (January 26, 2017): e2570-e2570. http://dx.doi.org/10.1038/cddis.2016.465.
Повний текст джерела
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Cook, Peter, Yildiray Cinar, Guy Allinson, Charles Jenkins, Sandeep Sharma, Michael Soroka, and Jo Ann Tan. "Enhanced gas recovery, CO2 storage and implications from the CO2CRC Otway Project." APPEA Journal 51, no. 2 (2011): 684. http://dx.doi.org/10.1071/aj10064.
Повний текст джерелаАнотація:
Successful completion of the first stage of the CO2CRC Otway Project demonstrated safe and effective CO2 storage in the Naylor depleted gas field and confirmed our ability to model and monitor subsurface behaviour of CO2. It also provided information of potential relevance to CO2 enhanced gas recovery (EGR) and to opportunities for CO2 storage in depleted gas fields. Given the high CO2 concentration of many gas fields in the region, it is important to consider opportunities for integrating gas production, CO2 storage in depleted gas fields, and CO2-EGR optimisation within a production schedule. The use of CO2-EGR may provide benefits through the recovery of additional gas resources and a financial offset to the cost of geological storage of CO2 from gas processing or other anthropogenic sources, given a future price on carbon. Globally, proven conventional gas reserves are 185 trillion m3 (BP Statistical Review, 2009). Using these figures and Otway results, a replacement efficiency of 60 % (% of pore space available for CO2 storage following gas production) indicates a global potential storage capacity—in already depleted plus reserves—of approximately 750 Gigatonnes of CO2. While much of this may not be accessible for technical or economic reasons, it is equivalent to more than 60 years of total global stationary emissions. This suggests that not only gas—as a lower carbon fuel—but also depleted gas fields, have a major role to play in decreasing CO2 emissions worldwide.
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Peltsch, Heather, Sandhya Khurana, Collin J. Byrne, Phong Nguyen, Neelam Khaper, Aseem Kumar, and T. C. Tai. "Cardiac phenylethanolamine N-methyltransferase: localization and regulation of gene expression in the spontaneously hypertensive rat." Canadian Journal of Physiology and Pharmacology 94, no. 4 (April 2016): 363–72. http://dx.doi.org/10.1139/cjpp-2015-0303.
Повний текст джерелаАнотація:
Phenylethanolamine N-methyltransferase (PNMT) is the terminal enzyme in the catecholamine biosynthetic pathway responsible for adrenaline biosynthesis. Adrenaline is involved in the sympathetic control of blood pressure; it augments cardiac function by increasing stroke volume and cardiac output. Genetic mapping studies have linked the PNMT gene to hypertension. This study examined the expression of cardiac PNMT and changes in its transcriptional regulators in the spontaneously hypertensive (SHR) and wild type Wistar-Kyoto (WKY) rats. SHR exhibit elevated levels of corticosterone, and lower levels of the cytokine IL-1β, revealing systemic differences between SHR and WKY. PNMT mRNA was significantly increased in all chambers of the heart in the SHR, with the greatest increase in the right atrium. Transcriptional regulators of the PNMT promoter show elevated expression of Egr-1, Sp1, AP-2, and GR mRNA in all chambers of the SHR heart, while protein levels of Sp1, Egr-1, and GR were elevated only in the right atrium. Interestingly, only AP-2 protein-DNA binding was increased, suggesting it may be a key regulator of cardiac PNMT in SHR. This study provides the first insights into the molecular mechanisms involved in the dysregulation of cardiac PNMT in a genetic model of hypertension.