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Journal articles on the topic 'Andakter'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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1

Bremer, Leif. "Andakt." Kirke og Kultur 113, no. 03 (2008): 213–15. http://dx.doi.org/10.18261/issn1504-3002-2008-03-07.

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2

Fyhn, Signe. "Andakt." Kirke og Kultur 113, no. 04 (2008): 341–43. http://dx.doi.org/10.18261/issn1504-3002-2008-04-10.

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3

Thomassen, Merete. "Andakt." Kirke og Kultur 113, no. 01 (2008): 53–54. http://dx.doi.org/10.18261/issn1504-3002-2008-01-07.

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4

Gyrid Gunnes. "Andakt." Kirke og Kultur 114, no. 3 (2009): 282–85. http://dx.doi.org/10.18261/issn1504-3002-2009-03-11.

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5

Reinertsen, Ellen Aasland. "Andakt – Jakobs kamp." Kirke og Kultur 113, no. 05 (2008): 402–4. http://dx.doi.org/10.18261/issn1504-3002-2008-05-06.

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6

Hansen, Trond Egil. "Andakt for de frelste." Tidsskrift for Den norske legeforening 135, no. 11 (2015): 1056. http://dx.doi.org/10.4045/tidsskr.15.0360.

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7

Vederhus, Inger. "Med salmesong, andakt og skjellsord." Kirke og Kultur 121, no. 03 (2017): 281–88. http://dx.doi.org/10.18261/issn.1504-3002-2017-03-06.

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8

Moxnes, Halvor. "Andakt – Tekst som terror." Kirke og Kultur 113, no. 02 (2008): 125–26. http://dx.doi.org/10.18261/issn1504-3002-2008-02-06.

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9

Feijoo, Alexander, and Liliana Vanessa Celis Gil. "Tres nuevas especies de Righiodrilus Zicsi 1995 (Annelida, Oligochaeta: Glossoscolecidae) de la Amazonía colombiana." Acta Amazonica 40, no. 1 (2010): 231–40. http://dx.doi.org/10.1590/s0044-59672010000100030.

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Se describieron tres nuevas especies de Righiodrilus Zicsi, 1995 para la Amazonía: R. andake sp. n., R. inga sp. n. y R. muinanei. Con las nuevas adiciones el género suma 26 especies. Se presenta una clave para las especies y algunos comentarios relacionados con las características y presencia en usos del terreno de Righiodrilus.

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10

Norheim, Bård Eirik Hallesby. "Andakt – Er vatn tjukkare enn blod?" Kirke og Kultur 114, no. 01 (2009): 82–84. http://dx.doi.org/10.18261/issn1504-3002-2009-01-09.

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11

Dokka, Åste. "Andakt – Tyven Jesus? Luk 12,35-40." Kirke og Kultur 113, no. 06 (2008): 490–93. http://dx.doi.org/10.18261/issn1504-3002-2008-06-08.

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12

Čokić, Vladan P., Olivera Mitrović-Ajtić, Bojana B. Beleslin-Čokić, et al. "Proinflammatory Cytokine IL-6 and JAK-STAT Signaling Pathway in Myeloproliferative Neoplasms." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/453020.

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The recent JAK1/2 inhibitor trial in myeloproliferative neoplasms (MPNs) showed that reducing inflammation can be more beneficial than targeting gene mutants. We evaluated the proinflammatory IL-6 cytokine and JAK-STAT signaling pathway related genes in circulating CD34+cells of MPNs. Regarding laboratory data, leukocytosis has been observed in polycythemia vera (PV) andJAK2V617F mutation positive versus negative primary myelofibrosis (PMF) patients. Moreover, thrombocytosis was reduced byJAK2V617F allele burden in essential thrombocythemia (ET) and PMF. 261 significantly changed genes have been detected in PV, 82 in ET, and 94 genes in PMF. The following JAK-STAT signaling pathway related genes had augmented expression in CD34+cells of MPNs:CCND3andIL23Aregardless ofJAK2V617F allele burden;CSF3R, IL6ST, andSTAT1/2in ET and PV withJAK2V617F mutation; andAKT2, IFNGR2, PIM1, PTPN11, andSTAT3only in PV.STAT5Agene expression was generally reduced in MPNs. IL-6 cytokine levels were increased in plasma, as well as IL-6 protein levels in bone marrow stroma of MPNs, dependent onJAK2V617F mutation presence in ET and PMF patients. Therefore, theJAK2V617F mutant allele burden participated in inflammation biomarkers induction and related signaling pathways activation in MPNs.

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13

Khwanraj, Kawinthra, Suriyat Madlah, Khwanthana Grataitong, and Permphan Dharmasaroja. "Comparative mRNA Expression of eEF1A Isoforms and a PI3K/Akt/mTOR Pathway in a Cellular Model of Parkinson’s Disease." Parkinson's Disease 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8716016.

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The PI3K/Akt/mTOR pathway is one of dysregulated pathways in Parkinson’s disease (PD). Previous studies in nonneuronal cells showed that Akt regulation can be increased by eukaryotic protein elongation factor 1 alpha 2 (eEF1A2). eEF1A2 is proposed to contribute protection against apoptotic death, likely through activation of the PI3K/Akt pathway. Whether eEF1A2 plays a role in the prevention of cell death in PD has not been investigated. Recently, gene profiling on dopaminergic neurons from postmortem PD patients showed both upregulation and downregulation of some PI3K and mTOR genes. In this paper, the expression of all gene members of the PI3K/Akt/mTOR pathway in relation to those of the eEF1A isoforms in a cellular model of PD was investigated at the mRNA level. The results showed a similar trend of upregulation of genes of the eEF1A isoforms (eEF1A1andeEF1A2) and of the PI3K (classes I–III)/Akt (Akt1,Akt2, andAkt3)/mTOR (mTORC1andmTORC2) pathway in both nondifferentiated and differentiated SH-SY5Y dopaminergic cells treated with 1-methyl-4-phenylpyridinium (MPP+). Upregulation ofeEF1A2,Akt1, andmTORC1was consistent with the relative increase of eEF1A2, Akt, phospho-Akt, and mTORC1 proteins. The possible role of eEF1A isoforms in the regulation of the PI3K/Akt/mTOR pathway in PD is discussed.

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14

Zeng, Guangyuan, Frederick H. Nystrom, Lingamanaidu V. Ravichandran, et al. "Roles for Insulin Receptor, PI3-Kinase, andAktin Insulin-Signaling Pathways Related to Production of Nitric Oxide in Human Vascular Endothelial Cells." Circulation 101, no. 13 (2000): 1539–45. http://dx.doi.org/10.1161/01.cir.101.13.1539.

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15

Wang, Ya-Xin, Jiu-Ru Zhao, Yue-Ying Xu, Wei-Bin Wu, and Hui-Juan Zhang. "miR-21 Is Overexpressed in Hydatidiform Mole Tissues and Promotes Proliferation, Migration, and Invasion in Choriocarcinoma Cells." International Journal of Gynecologic Cancer 27, no. 2 (2017): 364–74. http://dx.doi.org/10.1097/igc.0000000000000861.

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ObjectiveThe aims of this study were to make clear whether miR-21 was dysregulated in hydatidiform mole (HM) tissues and choriocarcinoma (CCA) cells, to elucidate whether aberrant miR-21 expression would affect the function of CCA cells, and to find out whether there was a relationship between miR-21 andAKT,PDCD4, andPTENin CCA cells.MethodsFresh and formalin-fixed, paraffin-embedded trophoblastic tissues (normal first trimester placentas and HMs) were retrieved from the biobank in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University. Choriocarcinoma JAR and JEG-3 cells were cultured. Expression of miR-21 in trophoblast cells and tissues was examined by quantitative real-time polymerase chain reaction. Location and distribution of miR-21 in trophoblast tissues were determinated by in situ hybridization and fluorescent in situ hybridization. The effect of miR-21 on JAR and JEG-3 cells was tested by miR-21 mimics and inhibitor transfection, followed by cell viability assay, flow cytometric analysis, and Transwell analysis. Interaction between miR-21 and its target genes in CCA cells was verified by quantitative real-time polymerase chain reaction, Western blot, and luciferase report system.ResultsWe originally found miR-21 was markedly upregulated in HM tissues compared with normal first trimester placentas. The expression of miR-21 was exclusively confined in trophoblastic layers. Furthermore, we discovered miR-21 was significantly increased in JAR and JEG-3 cells compared with normal primary human trophoblastic cells. Moreover, we demonstrated miR-21 could promote proliferation, migration, and invasion of CCA cells. We furthermore proved miR-21 negatively regulated PDCD4 and PTEN in CCA cells and targeted toPDCD43′UTR directly. In addition, we confirmed that miR-21 could activate Akt pathway by phosphorylating Akt at Ser 473.ConclusionsOur results suggested miR-21 was responsible for aggressive phenotype of gestational trophoblastic disease and had the potential diagnostic and therapeutic values for gestational trophoblastic neoplasm.

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